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2,329,700 | Endoscopic endonasal approach for infradiaphragmatic craniopharyngiomas: a multicentric Italian study. | Infradiaphragmatic craniopharyngiomas (ICs) represent a distinct subtype, harboring a sellar-suprasellar origin and generally growing in the extra-arachnoidal space contained by the diaphragma sellae. They have been considered ideal for surgical removal through the transsphenoidal approach since the 1960s. The authors present a multicentric national study, intending to selectively analyze IC behavior and the impact of the transsphenoidal endoscopic endonasal approach (EEA) on surgical outcomes.</AbstractText>Craniopharyngiomas that were intraoperatively recognized as infradiaphragmatic and removed with standard EEA between 2000 and 2021 at 6 Italian neurosurgical departments were included in the study. Clinical, radiological, and surgical findings and outcomes were evaluated and reviewed.</AbstractText>In total, 84 patients were included, with 45.23% identified as pediatric cases and 39.28% as having recurrent tumors. The most common presenting symptoms were endocrine (75%), visual (59.52%), and hypothalamic (26.19%) disorders. ICs were classified as extending below (6 intrasellar and 41 occupying the suprasellar cistern) or above (26 obliterating the anterior recesses of the third ventricle and 11 extending up to the foramina of Monro) the chiasmatic cistern. Gross-total resection (GTR) was achieved in 54 cases (64.28%). Tumor extension above the chiasmatic cistern and calcifications were associated with lower likelihood of GTR. The cumulative rate of postoperative complications was 34.53%, with CSF leak being the most common (14.28%). Endocrine, visual, and hypothalamic functions deteriorated postoperatively in 41/78 patients (52.56%), 5/84 (5.95%), and 14/84 (16.67%), respectively. Twenty-eight patients (33.33%) had recurrence during follow-up (mean 63.51 months), with a mean 5-year progression-free survival (PFS) rate of 58%. PFS was greater in patients who achieved GTR than patients with other extent of resection.</AbstractText>This is the largest series in the literature to describe ICs removed with standard EEA, without the need for additional bone and dural opening over the planum sphenoidale. EEA provides a direct route to ICs, the opportunity to manage lesions extending up to the third ventricle without breaching the diaphragma, and high rates of GTR and satisfactory clinical outcomes. Increased surgical complexity and morbidity should be expected in patients with extensive suprasellar extension and involvement of the surrounding vital neurovascular structures.</AbstractText> |
2,329,701 | Extra-axial endoscopic third ventriculostomy: preliminary experience with a technique to circumvent conventional endoscopic third ventriculostomy complications. | Endoscopic third ventriculostomy (ETV) is mostly safe but may have serious complications. Most of the complications are inherent to the procedure's intra-axial nature. This study aimed to explore an alternative route to overcome inherent issues with conventional ETV. The authors performed supraorbital, subfrontal extra-axial ETV (EAETV) via the lamina terminalis.</AbstractText>This prospective study began in October 2021 and included patients with obstructive triventricular hydrocephalus with a Glasgow Coma Scale score of 8 or more and a minimum follow-up of 3 months. Patients with multiloculated hydrocephalus and those younger than 1 year of age were excluded. The preoperative parameters etiology, symptoms, Evans' Index, frontal occipital horn ratio (FOHR), and third ventricle index were recorded. The surgical procedure is described. Postoperative evaluation included clinical (modified Rankin Scale [mRS]) and radiological assessment with CT and cine phase-contrast MRI. Preoperative and postoperative parameters were compared statistically.</AbstractText>Ten patients were included in this study. Six patients had acute hydrocephalus, and 4 had chronic hydrocephalus. After EAETV, all patients showed clinical improvement. An mRS score of 0 or 1 was achieved in 9 patients, but the mRS score remained at 4 in a patient with tectal tuberculoma. There was a significant reduction in Evans' Index, FOHR, and third ventricle index after EAETV (p < 0.05). The mean percent reduction in Evans' Index was 20.80% ± 13.89%, the mean percent reduction in FOHR was 20.79% ± 12.98%, and the mean percent reduction in the third ventricle index was 37.45% ± 14.74%. CSF flow voids were seen in all cases. The results of CSF flow quantification parameters were as follows: mean peak velocity 3.82 ± 0.93 cm/sec, mean average velocity 0.10 ± 0.05 cm/sec, mean average flow rate 46.60 ± 28.58 μL/sec, mean forward volume 39.90 ± 23.29 μL, mean reverse volume 34.10 ± 15.98 μL, mean overall flow amplitude 74.00 ± 27.61 μL, and mean stroke volume 37.00 ± 13.80 μL. One patient developed a minor frontal lobe contusion. The frontal air sinus was breached in 5 patients, but none had CSF rhinorrhea. Transient supraorbital hypesthesia was seen in 3 patients. No patient had electrolyte disturbance or change in thirst or fluid intake habits.</AbstractText>EAETV is a feasible, safe, and effective surgical alternative to conventional ETV.</AbstractText> |
2,329,702 | Median trans-atlanto-occipital membrane microsurgical approach to the posterior cranial fossa without craniotomy. | Minimally invasive approaches are becoming increasingly popular and contributing to improving the results of the surgical treatment of a wide variety of intracranial pathologies. Fifteen patients with posterior cranial fossa tumors underwent microsurgery through the atlanto-occipital membrane without resection of any bone structures. Tumors were localized in the brainstem in 8 patients and in the fourth ventricle in 7 patients. According to preoperative MRI and CT scans, the distance between the posterior arch of the atlas and the opisthion ranged from 9.9 to 16.5 mm (median 13 mm). The surgery was performed with the patient in the prone position and the head flexed. The trajectory of the surgical approach was directed from the skin incision located above the C2 spinous process 3.5-4 cm rostral along the midline. Total tumor resection was performed in 10 patients, subtotal resection in 2 patients, partial resection in 1 patient, and open biopsy in 2 patients. Surgical complications occurred in only 1 patient (meningoencephalitis). This minimally invasive trans-atlanto-occipital membrane approach for posterior cranial fossa tumors provides adequate visualization of the caudal part of the fourth ventricle and brainstem when the anthropometric parameters of the patient are suitable. |
2,329,703 | Intraventricular metastasis from carcinoma breast masquerading as choroid plexus neoplasm: A case report. | Metastatic tumors in the brain represent the most common type of intracranial neoplasm, comprising 8-10% of all brain tumors. 30% of such tumors are primarily of breast origin in females. Brain parenchymal metastasis is the more common presentation. Intraventricular spread is rare, seen in less than 5% of cases in a metastatic scenario. Here, we report a case of 41-year-old female presenting with intraventricular brain metastasis in a follow-up case of carcinoma breast. Five years post-surgery, the patient presented with complaints of headache. On evaluation, magnetic resonance imaging (MRI) brain showed an intraventricular lesion in the fourth ventricle. She was operated on for the same and the biopsy revealed a tumor with a complex papillary pattern resembling choroid plexus papilloma. On immunohistochemistry (IHC), the tumor cells were positive for cytokeratin 7 (CK7), Epithelial membrane antigen (EMA), GATA3, and mammaglobin favoring a metastasis from breast origin. Hence, a possibility of brain metastasis should be kept in mind in patients presenting with solitary ventricular masses due to the lack of definite radiological characteristics in such locations and histological overlap. Also, organ-specific IHC is a must in today's evidence-based era as is reflected in our case. |
2,329,704 | Use of a telovelar approach for complete resection of a choroid plexus tumor in a dog. | To describe a telovelar approach to the fourth ventricle for excision of a choroid plexus tumor within the ventricle.</AbstractText>A 3-year-old entire male Chihuahua.</AbstractText>Case report METHODS: A 3-year-old dog with two-month history of progressive vestibular signs and subdued mentation was diagnosed with a fourth ventricle tumor. Gross total resection of the tumor was achieved through a telovelar approach to the fourth ventricle.</AbstractText>Complete removal of the tumor was confirmed on immediate postoperative MRI. The dog recovered from the surgical procedure without complications, displaying some neurological deficits as preoperatively. His neurological examination was normal 2 weeks after surgery and remained so until the time of writing this case report (28 months) without additional treatment.</AbstractText>The telovelar approach allowed complete excision of a choroid plexus tumor located in the fourth ventricle of the dog reported here.</AbstractText>© 2022 The Authors. Veterinary Surgery published by Wiley Periodicals LLC on behalf of American College of Veterinary Surgeons.</CopyrightInformation> |
2,329,705 | Estimation of biological heart age using cardiovascular magnetic resonance radiomics. | We developed a novel interpretable biological heart age estimation model using cardiovascular magnetic resonance radiomics measures of ventricular shape and myocardial character. We included 29,996 UK Biobank participants without cardiovascular disease. Images were segmented using an automated analysis pipeline. We extracted 254 radiomics features from the left ventricle, right ventricle, and myocardium of each study. We then used Bayesian ridge regression with tenfold cross-validation to develop a heart age estimation model using the radiomics features as the model input and chronological age as the model output. We examined associations of radiomics features with heart age in men and women, observing sex-differential patterns. We subtracted actual age from model estimated heart age to calculate a "heart age delta", which we considered as a measure of heart aging. We performed a phenome-wide association study of 701 exposures with heart age delta. The strongest correlates of heart aging were measures of obesity, adverse serum lipid markers, hypertension, diabetes, heart rate, income, multimorbidity, musculoskeletal health, and respiratory health. This technique provides a new method for phenotypic assessment relating to cardiovascular aging; further studies are required to assess whether it provides incremental risk information over current approaches. |
2,329,706 | Guanidinoacetic acid provides superior cardioprotection to its combined use with betaine and (or) creatine in HIIT-trained rats. | This study aimed to determine how guanidinoacetic acid (GAA) or its combined administration with betaine (B) or creatine (C) influences the cardiac function, morphometric parameters, and redox status of rats subjected to high-intensity interval training (HIIT). This research was conducted on male Wistar albino rats exposed to HIIT for 4 weeks. The animals were randomly divided into five groups: HIIT, HIIT + GAA, HIIT + GAA + C, HIIT + GAA + B, and HIIT + GAA + C + B. After completing the training protocol, GAA (300 mg/kg), C (280 mg/kg), and B (300 mg/kg) were applied daily per os for 4 weeks. GAA supplementation in combination with HIIT significantly decreased the level of both systemic and cardiac prooxidants ( <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mi>O</mml:mi> <mml:mn>2</mml:mn> <mml:mo>-</mml:mo></mml:msubsup> </mml:math> , H<sub>2</sub>O<sub>2</sub>, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msubsup><mml:mi>NO</mml:mi> <mml:mn>2</mml:mn> <mml:mo>-</mml:mo></mml:msubsup> </mml:math> , and thiobarbituric acid reactive substances) compared with nontreated HIIT (<i>p</i> < 0.05). Also, GAA treatment led to an increase in glutathione and superoxide dismutase levels. None of the treatment regimens altered cardiac function. A larger degree of cardiomyocyte hypertrophy was observed in the HIIT + GAA group, which was reflected through an increase of the cross-sectional area of 27% (<i>p</i> < 0.05) and that of the left ventricle wall thickness of 27% (<i>p</i> < 0.05). Since we showed that GAA in combination with HIIT may ameliorate oxidative stress and does not alter cardiac function, the present study is a basis for future research exploring the mechanisms of cardioprotection induced by this supplement in an HIIT scenario. |
2,329,707 | Tubulinopathy Presenting as Developmental and Epileptic Encephalopathy. | Tubulin proteins play a role in the cortical development. Mutations in the tubulin genes affect patients with brain malformations. The present report describes two cases of developmental and epileptic encephalopathy (DEE) due to tubulinopathy. Case 1, a 23-year-old boy, was found to have a brain malformation with moderate ventriculomegaly prenatally. Hypotonia was noted at birth. Seizures were noted on the 1st day with multifocal discharges on the EEGs, which became intractable to many anticonvulsants. Brain MRI showed marked dilated ventricles and pachy/polymicrogyri. He became a victim of DEE. A de novo mutation in TUBB2B was proven through next-generation sequencing (NGS). Case 2, a mature male baby, began to have myoclonic jerks of his limbs 4 h after birth. EEG showed focal sharp waves from central and temporal regions. Brain MRI showed lissencephaly, type I. The seizures were refractory initially. A de novo mutation in TUBA1A was proven at the 6th week through NGS. He showed the picture of DEE at 1 year and 2 months of age. The clinical features of the tubulinopathies include motor delay, intellectual disabilities, epilepsy, and other deficits. Our cases demonstrated the severe form of tubulinopathy due to major tubulin gene mutations. NGS makes the early identification of genetic etiology possible for clinical evaluation. |
2,329,708 | Hippocampal semaphorin 3B improves depression-like behaviours in mice by upregulating synaptic plasticity and inhibiting neuronal apoptosis. | Depression is a global health problem, and there is a pressing need for a better understanding of its pathogenesis. Semaphorin 3B (Sema 3B) is an important axon guidance molecule that is primarily expressed in neurons and contributes to synaptic plasticity. Our previous studies using a high-throughput microarray assay suggested that Sema 3B expression was tremendously decreased during the development of depression, but the specific role and mechanisms of Sema 3B in depression are still unknown. Herein, we report that levels of Sema 3B protein are decreased in the hippocampus and serum of chronic mild stress (CMS)-treated mice. Increasing the levels of Sema 3B, either by injecting AAV-Sema 3B into the hippocampus or by injecting recombinant Sema 3B protein into the lateral ventricles, alleviated CMS-induced depression-like behaviours and enhanced the resistance to acute stress by increasing dendritic spine density in hippocampal neurons. In contrast, interfering with the function of Sema 3B by injecting anti-Sema 3B antibody into the lateral ventricles decreased the resistance to acute stress. In vitro, corticosterone (CORT) treatment decreased the survival rate and protein levels of Sema 3B and synapse-associated proteins in HT22 cells. Overexpression of Sema 3B improved the decreased survival rate caused by CORT by inhibiting apoptosis and increasing levels of synaptic-associated proteins, and knockdown of Sema 3B reduces the cellular resistance to CORT and the levels of synapse-associated proteins. These findings represent the first evidence for the neuroprotective mechanism of Sema 3B against stresses, suggesting that Sema 3B could be a promising novel target for the prevention and treatment of depression. |
2,329,709 | Spatial distribution and network morphology of epicardial, endocardial, interstitial, and Purkinje cell-associated elastin fibers in porcine left ventricle. | Cardiac extracellular matrices (ECM) play crucial functional roles in cardiac biomechanics. Previous studies have mainly focused on collagen, the major structural ECM in heart wall. The role of elastin in cardiac mechanics, however, is poorly understood. In this study, we investigated the spatial distribution and microstructural morphologies of cardiac elastin in porcine left ventricles. We demonstrated that the epicardial elastin network had location- and depth-dependency, and the overall epicardial elastin fiber mapping showed certain correlation with the helical heart muscle fiber architecture. When compared to the epicardial layer, the endocardial layer was thicker and has a higher elastin-collagen ratio and a denser elastin fiber network; moreover, the endocardial elastin fibers were finer and more wavy than the epicardial elastin fibers, all suggesting various interface mechanics. The myocardial interstitial elastin fibers co-exist with the perimysial collagen to bind the cardiomyocyte bundles; some of the interstitial elastin fibers showed a locally aligned, hinge-like structure to connect the adjacent cardiomyocyte bundles. This collagen-elastin combination reflects an optimal design in which the collagen provides mechanical strength and elastin fibers facilitate recoiling during systole. Moreover, cardiac elastin fibers, along with collagen network, closely associated with the Purkinje cells, indicating that this ECM association could be essential in organizing cardiac Purkinje cells into "fibrous" and "branching" morphologies and serving as a protective feature when Purkinje fibers experience large deformations in vivo. In short, our observations provide a structural basis for future in-depth biomechanical investigations and biomimicking of this long-overlooked cardiac ECM component. |
2,329,710 | Effects of Gold Nanoparticles Functionalized with Bioactive Compounds from <i>Cornus mas</i> Fruit on Aorta Ultrastructural and Biochemical Changes in Rats on a Hyperlipid Diet-A Preliminary Study. | Cornus mas L. extract (CM) presents hypolipidemic, antioxidant and anti-inflammatory activity. Gold nanoparticles (AuNPs) are considered potent delivery systems and may be used to release pharmaceutical compounds at the level of injury. In our study, we used gold nanoparticles functionalized with bioactive compounds from Cornus mas L. (AuNPsCM) in an experimental model of a high-fat diet (HFD), and we assessed their effects on aorta wall but also in the serum, as compared to Cornus mas (CM) administration. Sprague Dawley female rats were fed for 9 months with an HFD. During the last month of the experiment, we randomly allocated the animals into three groups that received, by oral gavage: saline solution, CM solution (0.158 mg/mL polyphenols) or AuNPsCM solution (260 μg Au/kg/day), while a Control group received a standard diet and saline solution. At the end of the experiment, we performed an ultrasonography of the aorta and left ventricle and a histology and transmission electron microscopy of the aorta walls; we investigated the oxidative stress and inflammation in aorta homogenates and in serum and, in addition, the lipid profile. AuNPsCM presented better effects in comparison with the natural extract (CM) on lipid peroxidation (p < 0.01) and TNF-alpha (p < 0.001) in aorta homogenates. In serum, both CM and AuNPsCM decreased the triglycerides (p < 0.001) and C-reactive protein (CM, p < 0.01; AuNPsCM, p < 0.001) and increased the antioxidant protection (p < 0.001), in comparison with the HFD group. In intima, AuNPsCM produced ultrastructural lesions, with the disorganization of intima and subendothelial connective layer, whereas CM administration preserved the intima normal aspect, but with a thinned subendothelial connective layer. AuNPsCM oral administration presented certain antioxidant, anti-inflammatory and hypolipidemic effects in an experimental model of HFD, but with a negative impact on the ultrastructure of aorta walls, highlighted by the intima disorganization. |
2,329,711 | Effects of Maternal Nutrient Restriction and Melatonin Supplementation on Cardiomyocyte Cell Development Parameters Using Machine Learning Techniques. | The objective of the current study was to examine the effects of maternal feed restriction and melatonin supplementation on fetal cardiomyocyte cell development parameters and predict binucleation and hypertrophy using machine learning techniques using pregnant beef heifers. Brangus heifers (n = 29) were assigned to one of four treatment groups in a 2 × 2 factorial design at day 160 of gestation: (1) 100% of nutrient requirements (adequately fed; ADQ) with no dietary melatonin (CON); (2) 100% of nutrient requirements (ADQ) with 20 mg/d of dietary melatonin (MEL); (3) 60% of nutrient requirements (nutrient-restricted; RES) with no dietary melatonin (CON); (4) 60% of nutrient requirements (RES) with 20 mg/d of dietary melatonin (MEL). On day 240 of gestation, fetuses were removed, and fetal heart weight and thickness were determined. The large blood vessel perimeter was increased in fetuses from RES compared with ADQ (<i>p</i> = 0.05). The total number of capillaries per tissue area exhibited a nutrition by treatment interaction (<i>p</i> = 0.01) where RES-MEL increased capillary number compared (<i>p</i> = 0.03) with ADQ-MEL. The binucleated cell number per tissue area showed a nutrition by treatment interaction (<i>p</i> = 0.010), where it was decreased in RES-CON vs. ADQ-CON fetuses. Hypertrophy was estimated by dividing ventricle thickness by heart weight. Based on machine learning results, for the binucleation and hypertrophy target variables, the Bagging model with 5 Decision Tree estimators and 3 Decision Tree estimators produced the best results without overfitting. In the prediction of binucleation, left heart ventricular thickness feature had the highest Gin importance weight followed by fetal body weight. In the case of hypertrophy, heart weight was the most important feature. This study provides evidence that restricted maternal nutrition leads to a reduction in the number of cardiomyocytes while melatonin treatment can mitigate some of these disturbances. |
2,329,712 | Neurotrophic factor-secreting cells restored endogenous hippocampal neurogenesis through the Wnt/β-catenin signaling pathway in AD model mice. | Impairment in neurogenesis correlates with memory and  cognitive dysfunction in AD patients. In the recent decade, therapies with stem cell bases are growing and proved to be efficient. This study is a preliminary attempt to explore the impact of NTF-SCs on hippocampal neurogenesis mediated by the Wnt/β-catenin signaling cascade in AD-like mouse brain parenchyma.</AbstractText>The BALB/c mice were divided into four groups: Control, AD +Vehicle, AD+ TF-SCs-CM and AD+NTF-SCs (n = 10). For AD induction, 100 µM Aβ1-42</sub> was injected into lateral ventricles. The AD-like model was confirmed via passive avoidance test and Thioflavin-S staining 21 days following Aβ injection. Next, NTF-SCs were differentiated from ADMSCs, and both NTF-SCs and supernatant (NTF-SCs-CM) were injected into the hippocampus after AD confirmation. Endogenous neural stem cells (NSCs) proliferation capacity was assessed after 50 mg/kbW BrdU injection for 4 days using immunofluorescence (IF) staining. The percent of BrdU/Nestin and BrdU/NeuN positive NSCs were calculated. Real-time RT-PCR was used to detect genes related to the Wnt/β-catenin signaling cascade. The spatial learning and memory alternation was evaluated using the Morris water maze (MWM).</AbstractText>Data showed the reduction in escape latency over 5 days in the AD mice compared to the control group. The administration of NTF-SCs and NTF-SCs-CM increased this value compared to the AD-Vehicle group. Both NTF-SCs and NTF-SCs-CM were the potential to reduce the cumulative distance to the platform in AD mice compared to the AD-Vehicle group. The time spent in target quadrants was ameliorated following NTF-SCs and NTF-SCs-CM transplantation followed by an improved MWM performance. IF imaging revealed the increase in BrdU/Nestin+</sup> and BrdU/NeuN+</sup> in AD mice that received NTF-SCs and NTF-SCs-CM, indicating enhanced neurogenesis. Based on real-time PCR analysis, the expression of PI3K, Akt, MAPK, ERK, Wnt, and β-catenin was upregulated and coincided with the suppression of GSK-3β after injection of NTF-SCs-CM and NTF-SCs. In this study, NTF-SCs had superior effects in AD mice that received NTF-SCs compared to NTF-SCs-CM.</AbstractText>The activation of Wnt/β-catenin pathway via NTF-SCs can be touted as a possible therapeutic approach to restore neurogenesis in AD mice.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,713 | Outcomes after gamma knife radiosurgery for intraventricular meningiomas. | Intraventricular meningiomas (IVMs) are rare tumors with considerable treatment-associated morbidity due to their challenging location. Treatment with stereotactic radiosurgery (SRS) is sparsely reported in the literature. We describe our experience over the last 35 years using Gamma knife radiosurgery (GKRS) for IVMs.</AbstractText>We retrospectively reviewed the GKRS database identifying 2501 meningiomas treated at the University of Pittsburgh Medical Center over the last 35 years. Nineteen patients with (12 males, mean age = 53.2 years, range 14-84) 20 IVMs were identified. Headache was the most frequent presenting symptom (N = 12), and the trigone of the lateral ventricle was the most common location (N = 18). The median tumor volume was 4.8 cc (range, 0.8-17). The median margin dose was 14 Gy (range, 12-25) delivered at 50% isodose line.</AbstractText>At a median follow-up of 63.1 months (range, 6-322.4) symptom control was achieved in 18 (94.7%) patients. The overall progression-free survival (PFS) was 95% at 5 years, and 85% at 10-years. After Log-rank test, patients who underwent GKRS within 12 months after diagnosis (vs. ≥ 12 months, X2</sup>: 4.455, p = 0.035), patients treated with primary GKRS without prior biopsy (vs. prior biopsy, X2</sup>: 4.000, p = 0.046), and patients with WHO grade I meningioma (vs. WHO II, X2</sup>: 9.000, p = 0.003) had a longer PFS. Imaging showed peritumoral edema in seven cases at a median of 10.5 (range, 6.13-24.3) months after GKRS. Only three of these patients were symptomatic and were successfully managed with oral medications. Cox´s regression revealed that a V12Gy ≥ 10 cc [HR: 10.09 (95% CI: 2.11-48.21), p = 0.004], and tumor volume ≥ 8 cc [HR: 5.87 (95% CI: 1.28-26.97), p = 0.023] were associated with a higher risk of peritumoral edema.</AbstractText>GKRS is an effective and safe management option for intraventricular meningiomas. Early GKRS should be considered as a primary management modality for small and medium sized IVM and adjuvant management for residual IVMs.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation> |
2,329,714 | Towards the interpretability of deep learning models for multi-modal neuroimaging: Finding structural changes of the ageing brain. | Brain-age (BA) estimates based on deep learning are increasingly used as neuroimaging biomarker for brain health; however, the underlying neural features have remained unclear. We combined ensembles of convolutional neural networks with Layer-wise Relevance Propagation (LRP) to detect which brain features contribute to BA. Trained on magnetic resonance imaging (MRI) data of a population-based study (n = 2637, 18-82 years), our models estimated age accurately based on single and multiple modalities, regionally restricted and whole-brain images (mean absolute errors 3.37-3.86 years). We find that BA estimates capture ageing at both small and large-scale changes, revealing gross enlargements of ventricles and subarachnoid spaces, as well as white matter lesions, and atrophies that appear throughout the brain. Divergence from expected ageing reflected cardiovascular risk factors and accelerated ageing was more pronounced in the frontal lobe. Applying LRP, our study demonstrates how superior deep learning models detect brain-ageing in healthy and at-risk individuals throughout adulthood. |
2,329,715 | Choroid plexus tissue perfusion and blood to CSF barrier function in rats measured with continuous arterial spin labeling. | The choroid plexus (ChP) of the cerebral ventricles is a source of cerebrospinal fluid (CSF) production and also plays a key role in immune surveillance at the level of blood-to-CSF-barrier (BCSFB). In this study, we quantify ChP blood perfusion and BCSFB mediated water exchange from arterial blood into ventricular CSF using non-invasive continuous arterial spin labelling magnetic resonance imaging (CASL-MRI). Systemic administration of anti-diuretic hormone (vasopressin) was used to validate BCSFB water flow as a metric of choroidal CSF secretory function. To further investigate the coupling between ChP blood perfusion and BCSFB water flow, we characterized the effects of two anesthetic regimens known to have large-scale differential effects on cerebral blood flow. For quantification of ChP blood perfusion a multi-compartment perfusion model was employed, and we discovered that partial volume correction improved measurement accuracy. Vasopressin significantly reduced both ChP blood perfusion and BCSFB water flow. ChP blood perfusion was significantly higher with pure isoflurane anesthesia (2-2.5%) when compared to a balanced anesthesia with dexmedetomidine and low-dose isoflurane (1.0 %), and significant correlation between ChP blood perfusion and BCSFB water flow was observed, however there was no significant difference in BCSFB water flow. In summary, here we introduce a non-invasive, robust, and spatially resolved in vivo imaging platform to quantify ChP blood perfusion as well as BCSFB water flow which can be applied to study coupling of these two key parameters in future clinical translational studies. |
2,329,716 | Thyroid-stimulating hormone and mortality in pulmonary arterial hypertension.<ELocationID EIdType="pii" ValidYN="Y">e001348</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjresp-2022-001348</ELocationID><Abstract><AbstractText Label="INTRODUCTION">Pulmonary arterial hypertension (PAH) remains a serious and life-threatening illness. Thyroid dysfunction is relatively understudied in individuals with PAH but is known to affect cardiac function and vascular tone in other diseases. The aim of this observational study was to evaluate the association between thyroid-stimulating hormone (TSH), mortal and non-mortal outcomes in individuals with PAH.</AbstractText><AbstractText Label="METHODS">The Seattle Right Ventricle Translational Science (Servetus) Study is an observational cohort that enrolled participants with PAH between 2014 and 2016 and then followed them for 3 years. TSH was measured irrespective of a clinical suspicion of thyroid disease for all participants in the cohort. Linear regression was used to estimate the relationships between TSH and right ventricular basal diameter, tricuspid annular plane systolic excursion and 6-minute walk distance. Logistic regression was used to estimate the relationship with New York Heart Association Functional Class, and Cox proportional hazards were used to estimate the relationship with mortality. Staged models included unadjusted models and models accounting for age, sex at birth and aetiology of pulmonary hypertension with or without further adjustment for N-terminal-pro hormone brain natriuretic peptide.</AbstractText><AbstractText Label="RESULTS">Among 112 participants with PAH, TSH was strongly associated with mortality irrespective of adjustment. There was no clear consistent association between TSH and other markers of severity in a cohort with PAH.</AbstractText><AbstractText Label="DISCUSSION">This report reinforces the important observation that TSH is associated with survival in patients with PAH, and future study of thyroid dysfunction as a potential remediable contributor to mortality in PAH is warranted.</AbstractText><CopyrightInformation>© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pi</LastName><ForeName>Hongyang</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rayner</LastName><ForeName>Samuel G</ForeName><Initials>SG</Initials><AffiliationInfo><Affiliation>Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ralph</LastName><ForeName>David D</ForeName><Initials>DD</Initials><AffiliationInfo><Affiliation>Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nolley</LastName><ForeName>Stephanie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barros</LastName><ForeName>Lia M</ForeName><Initials>LM</Initials><AffiliationInfo><Affiliation>Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Steinberg</LastName><ForeName>Zachary L</ForeName><Initials>ZL</Initials><AffiliationInfo><Affiliation>Cardiology, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leary</LastName><ForeName>Peter J</ForeName><Initials>PJ</Initials><Identifier Source="ORCID">0000-0001-5716-248X</Identifier><AffiliationInfo><Affiliation>Pulmonary, Critical Care, and Sleep Medicine, University of Washington, Seattle, Washington, USA learyp@uw.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Epidemiology, University of Washington, Seattle, Washington, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>KL2 TR000421</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI137111</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open Respir Res</MedlineTA><NlmUniqueID>101638061</NlmUniqueID><ISSNLinking>2052-4439</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9002-71-5</RegistryNumber><NameOfSubstance UI="D013972">Thyrotropin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D065627" MajorTopicYN="N">Familial Primary Pulmonary Hypertension</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006976" MajorTopicYN="Y">Hypertension, Pulmonary</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000081029" MajorTopicYN="Y">Pulmonary Arterial Hypertension</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013972" MajorTopicYN="N">Thyrotropin</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Clinical Epidemiology</Keyword><Keyword MajorTopicYN="N">Primary Pulmonary Hypertension</Keyword></KeywordList><CoiStatement>Competing interests: None declared.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>6</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>25</Day><Hour>21</Hour><Minute>13</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35879020</ArticleId><ArticleId IdType="pmc">PMC9328089</ArticleId><ArticleId IdType="doi">10.1136/bmjresp-2022-001348</ArticleId><ArticleId IdType="pii">9/1/e001348</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501–9. 10.1056/NEJM200102153440707</Citation><ArticleIdList><ArticleId IdType="doi">10.1056/NEJM200102153440707</ArticleId><ArticleId IdType="pubmed">11172193</ArticleId></ArticleIdList></Reference><Reference><Citation>Marvisi M, Balzarini L, Mancini C, et al. . Thyroid gland and pulmonary hypertension. What’s the link? Panminerva Med 2013;55:93–7.</Citation><ArticleIdList><ArticleId IdType="pubmed">23474667</ArticleId></ArticleIdList></Reference><Reference><Citation>Li JH, Safford RE, Aduen JF, et al. . Pulmonary hypertension and thyroid disease. Chest 2007;132:793–7. 10.1378/chest.07-0366</Citation><ArticleIdList><ArticleId IdType="doi">10.1378/chest.07-0366</ArticleId><ArticleId IdType="pubmed">17646226</ArticleId></ArticleIdList></Reference><Reference><Citation>Silva DR, Gazzana MB, John AB, et al. . Pulmonary arterial hypertension and thyroid disease. J Bras Pneumol 2009;35:179–85. 10.1590/s1806-37132009000200012</Citation><ArticleIdList><ArticleId IdType="doi">10.1590/s1806-37132009000200012</ArticleId><ArticleId IdType="pubmed">19287922</ArticleId></ArticleIdList></Reference><Reference><Citation>Curnock AL, Dweik RA, Higgins BH, et al. . High prevalence of hypothyroidism in patients with primary pulmonary hypertension. Am J Med Sci 1999;318:289–92. 10.1016/S0002-9629(15)40640-8</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/S0002-9629(15)40640-8</ArticleId><ArticleId IdType="pubmed">10555089</ArticleId></ArticleIdList></Reference><Reference><Citation>Chu JW, Kao PN, Faul JL, et al. . High prevalence of autoimmune thyroid disease in pulmonary arterial hypertension. Chest 2002;122:1668–73. 10.1378/chest.122.5.1668</Citation><ArticleIdList><ArticleId IdType="doi">10.1378/chest.122.5.1668</ArticleId><ArticleId IdType="pubmed">12426269</ArticleId></ArticleIdList></Reference><Reference><Citation>Richter MJ, Sommer N, Schermuly R, et al. . The prognostic impact of thyroid function in pulmonary hypertension. J Heart Lung Transplant 2016;35:1427–34. 10.1016/j.healun.2016.05.022</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.healun.2016.05.022</ArticleId><ArticleId IdType="pubmed">27373820</ArticleId></ArticleIdList></Reference><Reference><Citation>Warner MH, Beckett GJ. Mechanisms behind the non-thyroidal illness syndrome: an update. J Endocrinol 2010;205:1–13. 10.1677/JOE-09-0412</Citation><ArticleIdList><ArticleId IdType="doi">10.1677/JOE-09-0412</ArticleId><ArticleId IdType="pubmed">20016054</ArticleId></ArticleIdList></Reference><Reference><Citation>Tonelli AR, Arelli V, Minai OA, et al. . Causes and circumstances of death in pulmonary arterial hypertension. Am J Respir Crit Care Med 2013;188:365–9. 10.1164/rccm.201209-1640OC</Citation><ArticleIdList><ArticleId IdType="doi">10.1164/rccm.201209-1640OC</ArticleId><ArticleId IdType="pmc">PMC3778730</ArticleId><ArticleId IdType="pubmed">23600433</ArticleId></ArticleIdList></Reference><Reference><Citation>Grais IM, Sowers JR. Thyroid and the heart. Am J Med 2014;127:691–8. 10.1016/j.amjmed.2014.03.009</Citation><ArticleIdList><ArticleId IdType="doi">10.1016/j.amjmed.2014.03.009</ArticleId><ArticleId IdType="pmc">PMC4318631</ArticleId><ArticleId IdType="pubmed">24662620</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35878741</PMID><DateRevised><Year>2022</Year><Month>08</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-9488</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>22</Day></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg</ISOAbbreviation></Journal>Decellularized vs Non-decellularized Allogeneic Pulmonary Artery Patches for Pulmonary Arterioplasty. | We studied pulmonary artery size, reinterventions, and panel reactive antibodies in patients with single-ventricle physiology who underwent a pulmonary arterioplasty with decellularized (DAPAP) and non-decellularized allogeneic pulmonary artery patches (non-DAPAP). Retrospective review identified 59 patients with single-ventricle physiology who underwent pulmonary arterioplasty from 2008 to 2017: 28 patients underwent arterioplasty with DAPAP and 31 patients with non-DAPAP. Demographic and operative variables were similar between groups. Among patients who underwent a Norwood procedure, a right ventricle to pulmonary artery shunt was more commonly used in the DAPAP group (12/20, 60%) and a modified Blalock-Taussig shunt was more commonly used in the non-DAPAP group (17/22, 77%). On multivariable analysis, the use of DAPAP was associated with higher pre-Fontan angiography Z-scores in right (estimate = 0.17, standard error = 0.04, P = 0.0005) and left pulmonary arteries (estimate = 0.12, standard error = 0.05, P = 0.01). No areas of calcification, discrete coarctation, or pulmonary dilation were noted in any of the pulmonary arteries. On multivariable analysis, the use of DAPAP was associated with higher freedom from pulmonary artery reinterventions (Hazard ratio = 0.36, 95% confidence interval = 0.13-0.9, P = 0.04). The median value for Class I panel reactive antibodies was 0% (IQR 0, 4) in the DAPAP and 23% (IQR 14, 36) in the non-DAPAP group. The median value for Class II panel reactive antibodies was 15% (IQR 0, 17) in the DAPAP and 21% (IQR 10, 22) in the non-DAPAP group. Pulmonary arterioplasty with DAPAP was associated with higher pre-Fontan pulmonary artery Z-scores and higher freedom from pulmonary artery reinterventions. |
2,329,717 | Histological Identification and Quantification of Eosinophils and Ascites in Leghorn Chickens Treated with High Oral Concentrations of NaCl-Pilot Study. | The purpose of this pilot study was to determine the role played by eosinophils in NaCl poisoning and right cardiac hypertrophy (ascitic syndrome) in Leghorn chickens, as well as the histological findings in the central nervous system (CNS), liver, and kidney. Moreover, the hypertrophy of the right ventricle index (HRVI) as an indicator of ascites was evaluated. Male SPF Leghorn birds at 28 days of age were submitted to two experiments. Food and water (FW) experiment: birds were treated with food plus 3.3% NaCl for the next 27 days and 1% NaCl in their drinking water from days 22 to 27. Water experiment (W): birds were treated with 1% NaCl in their drinking water for 5 days. In both experiments, the chickens exhibited loss of appetite, diuresis, and watery, green diarrhea during treatment days; at 24−27 td-FW and experiment W, the birds showed nervous signology (prostration, running movements, tremors, and comatose state). In the leukogram at 28 td-FW, an increase (p < 0.05) in heterophiles and basophils was observed. CNS eosinophilia was not observed in birds intoxicated with NaCl, though they did present demyelination in the brain and spinal cord, hepatic degeneration, mesangial proliferative glomerulopathy, and acute proximal renotubular necrosis. |
2,329,718 | Severe cerebellar malformations in mutant mice demonstrate a role for PDGF-C/PDGFRα signalling in cerebellar development. | Formation of the mouse cerebellum is initiated in the embryo and continues for a few weeks after birth. Double-mutant mice lacking platelet-derived growth factor C (PDGF-C) and that are heterozygous for platelet-derived growth factor receptor alpha (Pdgfc-/-; PdgfraGFP/+) develop cerebellar hypoplasia and malformation with loss of cerebellar lobes in the posterior vermis. This phenotype is similar to those observed in Foxc1 mutant mice and in a human neuroimaging pattern called Dandy Walker malformation. Pdgfc-Pdgfra mutant mice also display ependymal denudation in the fourth ventricle and gene expression changes in cerebellar meninges, which coincide with the first visible signs of cerebellar malformation. Here, we show that PDGF-C/PDGFRα signalling is a critical component in the network of molecular and cellular interactions that take place between the developing meninges and neural tissues, and which are required to build a fully functioning cerebellum. |
2,329,719 | Costs and Its Determinants in Pituitary Tumour Surgery. | Value-based healthcare (VBHC) provides a framework to improve care by improving patient outcomes and reducing healthcare costs. To support value-based decision making in clinical practice we evaluated healthcare costs and cost drivers in perioperative care for pituitary tumour patients.</AbstractText>We retrospectively assessed financial and clinical data for surgical treatment up to the first year after surgery of pituitary tumour patients treated between 2015 and 2018 in a Dutch tertiary referral centre. Multivariable regression analyses were performed to identify determinants of higher costs.</AbstractText>271 patients who underwent surgery were included. Mean total costs (SD) were €16339 (13573) per patient, with the following cost determinants: surgery time (€62 per minute; 95% CI: 50, 74), length of stay (€1331 per day; 95% CI 1139, 1523), admission to higher care unit (€12154 in total; 95% CI 6413, 17895), emergency surgery (€10363 higher than elective surgery; 95% CI: 1422, 19305) and postoperative cerebrospinal fluid leak (€14232; 95% CI 9667, 18797). Intradural (€7128; 95% CI 10421, 23836) and combined transsphenoidal/transcranial surgery (B: 38494; 95% CI 29191, 47797) were associated with higher costs than standard. Further, higher costs were found in these baseline conditions: Rathke's cleft cyst (€9201 higher than non-functioning adenoma; 95% CI 1173, 17230), giant adenoma (€19106 higher than microadenoma; 95% CI 12336, 25877), third ventricle invasion (€14613; 95% CI 7613, 21613) and dependent functional status (€12231; 95% CI 3985, 20477). In patients with uncomplicated course, costs were €8879 (3210) and with complications €17551 (14250).</AbstractText>Length of hospital stay, and complications are the main drivers of costs in perioperative pituitary tumour healthcare as were some baseline features, e.g. larger tumors, cysts and dependent functional status. Costs analysis may correspond with healthcare resource utilization and guide further individualized care path development and capacity planning.</AbstractText>Copyright © 2022 Dekkers, de Vries, Najafabadi, van der Hoeven, Verstegen, Pereira, van Furth and Biermasz.</CopyrightInformation> |
2,329,720 | Bone Specific Alkaline Phosphatase and Serum Calcification Propensity Are Not Influenced by Etelcalcetide vs. Alfacalcidol Treatment, and Only Bone Specific Alkaline Phosphatase Is Correlated With Fibroblast Growth Factor 23: Sub-Analysis Results of the ETACAR-HD Study. | Secondary hyperparathyroidism in chronic kidney disease poses a major risk factor for vascular calcification and high bone turnover, leading to mineralization defects. The aim was to analyze the effect of active vitamin D and calcimimetic treatment on fibroblast growth factor 23 (FGF23), serum calcification propensity (T50), a surrogate marker of calcification stress and bone specific alkaline phosphatase (BAP) in hemodialysis. This is a subanalysis of a randomized trial comparing etelcalcetide vs. alfacalcidol in 62 hemodialysis patients for 1 year. We compared the change of BAP and serum calcification propensity between the two medications and assessed the influence of FGF23 change over time. We found no significant differences in the change of BAP or serum calcification propensity (T50) levels from baseline to study end between treatment arms (difference in change of marker between treatment with etelcalcetide vs. alfacalcidol: BAP : 2.0 ng/ml [95% CI-1.5,5.4], p</i> = 0.3; T50: -15 min [95% CI -49,19], p</i> = 0.4). Using FGF23 change over time, we could show that BAP levels at study end were associated with FGF23 change (-0.14 [95% CI -0.21, -0.08], p</i> < 0.001). We did not observe the same association between FGF23 change and T50 (effect of FGF23 change on T50: 3.7 [95% CI -5.1, 12], p</i> = 0.4; R</i> 2</sup> = 0.07 vs. R</i> 2</sup> = 0.06). No significant difference was found in serum calcification propensity (T50) values between treatment arms. FGF23 was not associated with serum calcification propensity (T50), but was negatively correlated with BAP underlying its role in the bone metabolism.</AbstractText>[www.ClinicalTrials.gov], identifier [NCT03182699].</AbstractText>Copyright © 2022 Dörr, Hödlmoser, Kammer, Reindl-Schwaighofer, Lorenz, Reiskopf, Jagoditsch, Marculescu and Oberbauer.</CopyrightInformation> |
2,329,721 | [Development and Evaluation of Prognostic Nomogram Model for Adult Ventricle Glioma Patients].<Pagination><StartPage>588</StartPage><EndPage>596</EndPage><MedlinePgn>588-596</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.12182/20220760203</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="UNASSIGNED">To explore the prognostic factors of adult ventricle glioma (AVG) and to construct and evaluate a survival-related prognostic nomogram model, which could provide further reference for the clinical management of AVG patients.</AbstractText><AbstractText Label="METHODS" NlmCategory="UNASSIGNED">The patients covered in the study were selected from the Surveillance Epidemiology and End Results (SEER) database (1973-2016). They all had definite histological diagnosis of AVG. They were assigned randomly to the training cohort and the validation cohort by random number table at a 2/1 ratio. Survival analysis was performed by Kaplan-Meier analysis. Cox regression analysis was employed to determine the independent prognostic factors for overall survival (OS) and cancer-specific survival (CSS). Then, integrating the basic characteristics of patients, the survival-related nomogram predictive model for OS and CSS in the training cohort was constructed, respectively. After that, internal cross validation and external validation of the model were carried out with the training cohort and the validation cohort in succession. The authenticity and reliability of the nomogram model were evaluated by calculating the concordance index (C-index). Calibration plots were constructed to assess the agreement between the predicted values and the observed values in the training cohort and the validation cohort.</AbstractText><AbstractText Label="RESULTS" NlmCategory="UNASSIGNED">A total of 369 AVG patients, including 218 males and 151 females, were included. The median age of the patients was 53. According to the WHO classification of gliomas, 66 (17.9%) patients had grade Ⅱ gliomas, 73 (19.8%) had grade Ⅲ gliomas, and 230 (62.3%) had grade Ⅳ gliomas. Regarding the extent of resection (EOR), 59 (16.0%) had gross total resection (GTR) and 145 (39.3%) had subtotal resection (STR) or partial resection (PR). Of all the patients, 167 (45.3%) received postoperative radiotherapy and 143 (38.8%) received postoperative chemotherapy. Patients were randomized into the training cohort ( <i>n</i>=246) and the validation cohort ( <i>n</i>=123), and there was no significant difference ( <i>P</i>>0.05) in the basic clinical characteristics between the training cohort and the validation cohort. In the training cohort, Cox regression analysis revealed that the independent prognostic factors for OS and CSS included age≥65, grades Ⅲ and Ⅳ according to the WHO classification of gliomas, and not receiving radiotherapy. Furthermore, 5 variables, including age, gender, WHO grades, surgery, and radiotherapy, were used to construct the nomogram model for predicting 6-month, 1-year, and 2-year OS and CSS. The results of internal cross validation in the training cohort showed that the C-indexes of OS and CSS were 0.758 and 0.765, respectively. The external validation results of the validation cohort showed that the C-indexes of OS and CSS were 0.733 and 0.719, respectively. Calibration plots for 6-month, 1-year, and 2-year OS in the training cohort showed relatively good agreement, while in the validation cohort the agreement was relatively low. The 6-month, 1-year, and 2-year CSS calibration plots had results similar to the calibration plots of OS.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="UNASSIGNED">This nomogram predictive model of OS and CSS showed moderately reliable predictive performance, providing helpful reference information for clinicians to make quick and simple assessment of the survival probability of AVG patients.</AbstractText><CopyrightInformation>Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Hao-Dong-Fang</ForeName><Initials>HD</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Niu</LastName><ForeName>Xiao-Dong</ForeName><Initials>XD</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Xing-Wang</ForeName><Initials>XW</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yuan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jiao-Ming</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Sichuan Cancer Hospital, Chengdu 610042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gan</LastName><ForeName>You-Jun</ForeName><Initials>YJ</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Medical Center Hospital of Qionglai City, Qionglai 611530, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xiang</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yan-Hui</ForeName><Initials>YH</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mao</LastName><ForeName>Qing</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu 610041, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Sichuan Da Xue Xue Bao Yi Xue Ban</MedlineTA><NlmUniqueID>101162609</NlmUniqueID><ISSNLinking>1672-173X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005910" MajorTopicYN="Y">Glioma</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049451" MajorTopicYN="Y">Nomograms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015203" MajorTopicYN="N">Reproducibility of Results</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018426" MajorTopicYN="N">SEER Program</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cancer-specific survival.</Keyword><Keyword MajorTopicYN="N">Nomogram</Keyword><Keyword MajorTopicYN="N">Overall survival</Keyword><Keyword MajorTopicYN="N">Prognostic model</Keyword><Keyword MajorTopicYN="N">SEER</Keyword><Keyword MajorTopicYN="N">Ventricleglioma</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>24</Day><Hour>23</Hour><Minute>32</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35871728</ArticleId><ArticleId IdType="doi">10.12182/20220760203</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">33085352</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK563205</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17973">Atrioventricular Dissociation<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Rahman</LastName><ForeName>Mohammed Faraaz F.</ForeName><Initials>MFF</Initials></Author><Author ValidYN="Y"><LastName>Yandrapalli</LastName><ForeName>Srikanth</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>New York Medical College/Westchester Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The term atrioventricular (AV) dissociation describes a family of arrhythmias where independent pacemakers control the atria and ventricles. The standard activation of the cardiac circuits works in the order of impulse transmission from the sinoatrial (SA) node to the atria, the AV node, and ventricular activation via the His-Purkinje system. Disruption in this pathway leads to a dissociation between the conduction rates of the atria and ventricle. The severity of this event varies, from benign in cases of isorhythmic AV dissociation to complete heart block, which in cases might be fatal if not treated with a permanent pacemaker. Another important cause of this condition is ventricular tachycardia, which is lethal if not recognized or treated appropriately.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s6">Toxicokinetics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Littmann L, Monroe MH, Letts DP. 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Ann Transl Med. 2015 Mar;3(3):42.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4356861</ArticleId><ArticleId IdType="pubmed">25815303</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33085352</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32809599</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK560764</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-23696">Intracranial Hypotension<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Swyden</LastName><ForeName>Shelbi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Wyckoff Heights Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carter</LastName><ForeName>Carley</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>University of Kansas Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shah</LastName><ForeName>Sumir u.</ForeName><Initials>SU</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The intracranial cavity consists of three components: cerebrospinal fluid (CSF), blood, and brain tissue. CSF is contained within the subarachnoid space between the arachnoid and pia layers of the meninges. CSF is produced by a specialized vascular structure called choroid plexus within each ventricle of the brain. A blood-CSF barrier is formed by ependymal cells that line the ventricles and choroid epithelial cells that line the surrounding capillaries within the choroid plexus. The ventricular system includes two lateral ventricles, a third ventricle, and the fourth ventricle, which is encompassed by the brainstem and cerebellum. The interventricular foramen of Monro connects the third and lateral ventricles while the third and fourth ventricles communicate via the cerebral aqueduct, also known as the Aqueduct of Sylvius. CSF enters the subarachnoid space surrounding the brain and spinal cord via the foramina of Luschka and Magendie. It then travels within and around the brain and spinal cord until it is eventually reabsorbed by the arachnoid granules to finally make its way into the dural venous sinuses, back into the bloodstream. Normal CSF pressure falls approximately within 65 to 195 mm of water or CSF within the subarachnoid space. Intracranial hypotension (ICH) is defined as CSF pressure less than 60 mm H2O. It is hypothesized that low CSF volume, as opposed to low CSF pressure, is the primary cause of symptoms of ICH. Historically, Heinrich Irenaeus Quincke was credited with performing the first lumbar puncture (LP) in 1891. In 1898 it was August Bier, also known as the father of spinal anesthesia, who reported his observations on post-dural puncture headaches and proposed the hypothesis that ongoing leak of CSF from the dural puncture site was the inciting factor of such symptoms. His studies led to the proposition that the CSF leak exceeded the rate of CSF production. George Schaltenbrand, a German Neurologist, studied the pressure system of CSF within the cranial system. He proposed three mechanisms in which spontaneous ICH, which he termed "aliquorrhea," induce a clinical presentation identical to that of a post-LP headache. These mechanisms are a decrease in CSF production, an increase in CSF absorption, and loss of CSF volume via a leak.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s6">Histopathology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Mokri B. 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Neurology. 2005 Apr 12;64(7):1282-4.</Citation><ArticleIdList><ArticleId IdType="pubmed">15824366</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32809599</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644365</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK558939</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-617">Aortic Valve Repair<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Talha</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>University Of Maryland</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Puckett</LastName><ForeName>Yana</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>West Virginia University School of Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Aortic valve functional unit is a central outflow tract of the left side of the heart. The operational unit of the left outflow tract consists of aortic valve cusps, commissures, annulus, and sinuses at the root of the aorta. This functional unit of the left ventricular outflow tract is responsible for maintaining the laminar flow of blood after ejection from the left ventricle. Aortic valve pathologies can have a severe generalized impact on the body based on the perfusion deficit. Aortic valve insufficiency is mostly due to the underlying shear force causing stretch, dilation, rupture of the valve. Moreover, conditions of the aortic root, including coarctation, dissection, and aneurysm, can increase the aortic valve pathology due to increase shear force of blood at the aortic valve disrupting the laminar flow. Aortic valve pathologies can be managed by repair or replacement. Aortic valve replacement with a biological or prosthetic valve has been the cornerstone of the management of aortic valve pathologies. However, aortic valve repair has been the topic of debate as compared to replacement in specific subsets of patients. Over the last decade, aortic valve repair and preservation gained exceptional significance in the treatment of aortic root disease with and without insufficiencies. Successful aortic valve repair and preservation methods have been performed worldwide with a prevalence of procedures, less than 2%, as it needs excellent expertise.  The prevalence of procedure performed is low as compared to mitral valve repair as calcific aortic stenosis is the most common valvular pathology seen, which has less success. As compared to repair, aortic valve replacement seems to be relatively simpler, but it has the downside of causing long term complications of structural deterioration, restenosis, infection, and bleeding due to anticoagulation. Therefore, aortic valve preservation procedures have become a reasonable alternative in preventing complications of replacement by maintaining nearby normal anatomy and physiology of the aortic valve functional unit.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s3">Anatomy and Physiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s4">Indications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s5">Contraindications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s6">Equipment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s7">Personnel</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s8">Preparation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s9">Technique or Treatment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s11">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s13">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s18">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Chester AH, El-Hamamsy I, Butcher JT, Latif N, Bertazzo S, Yacoub MH. 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Eur J Cardiothorac Surg. 2012 Jan;41(1):2-3.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3241134</ArticleId><ArticleId IdType="pubmed">22219496</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32644365</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491734</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557802</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-26594">Anatomy, Thorax, Heart Papillary Muscles<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Rich</LastName><ForeName>Natalie L.</ForeName><Initials>NL</Initials></Author><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>Yusuf S.</ForeName><Initials>YS</Initials><AffiliationInfo><Affiliation>Vision (Alfarabi) College of Medicine, Riyadh, KSA</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The papillary muscles of the heart are pillar-like muscles seen within the cavity of the ventricles, attached to their walls. They have an integral role in proper cardiac valvular function. They arise from the inner walls of the left and right ventricle and attach to mitral and tricuspid valve leaflets respectively via chordae tendinae. Historical documentation of the existence of papillary muscles as a component of cardiac anatomy exists at least as early as the 16th century. This article will describe the structure, function, embryology, blood supply, lymphatics, nerves, physiologic variants, surgical considerations, and clinical significance of the papillary muscles of the heart.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s9">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Bestetti RB, Restini CB, Couto LB. 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Tex Heart Inst J. 2009;36(3):252-4.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2696506</ArticleId><ArticleId IdType="pubmed">19568400</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491734</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491596</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557664</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17975">Atrioventricular Node<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Heaton</LastName><ForeName>Joseph</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Brooklyn Hospital Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goyal</LastName><ForeName>Amandeep</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Kansas Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The atrioventricular (AV) node is a small structure in the heart, located in the Koch triangle, near the coronary sinus on the interatrial septum. In a right-dominant heart, the atrioventricular node is supplied by the right coronary artery. The purpose of this structure is to connect the electrical systems of the atria and the ventricles, providing electrical impedance from the atria and an intrinsic pacemaker in its absence. The intrinsic rate of the AV node is 40 to 60 beats per minute (bpm).</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s1">Definition/Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s2">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s3">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s4">Nursing, Allied Health, and Interprofessional Team Interventions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s5">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s8">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Kurian T, Ambrosi C, Hucker W, Fedorov VV, Efimov IR. 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West J Emerg Med. 2016 Jul;17(4):469-70.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4944806</ArticleId><ArticleId IdType="pubmed">27429700</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491596</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491346</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557414</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-74451">Neuroanatomy, Neural Tube Development and Stages<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Kuwar Chhetri</LastName><ForeName>Parvat</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Rajshahi university</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>M Das</LastName><ForeName>Joe</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Bahrain Specialist Hospital, Juffair, Bahrain</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The entire nervous system forms via the process called neurulation in which neural tube and neural crest form initially. In the third week of embryogenesis, three germ layers arise, namely, ectoderm, mesoderm, and endoderm, through the process of gastrulation. The overlying ectoderm is induced and thickened by the notochord and the neural plate forms. The neural plate then gives rise to the neural tube by folding upon itself, which makes up the central nervous system, which includes the brain, brainstem, and the spinal cord. The brainstem and spinal cord are composed of plates separated by the sulcus limitans, which is in the fourth ventricle of the brain. It separates the alar plate, which gives rise to sensory neurons and a basal plate, which gives rise to motor neurons.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s5">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Moghadasi Boroujeni S, Koontz A, Tseropoulos G, Kerosuo L, Mehrotra P, Bajpai VK, Selvam SR, Lei P, Bronner ME, Andreadis ST. 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Neuroimaging Clin N Am. 2019 Aug;29(3):411-421.</Citation><ArticleIdList><ArticleId IdType="pubmed">31256862</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491346</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32119344</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK554457</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-18391">Anatomy, Blood Flow<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Matienzo</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>American University of the Caribbean</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordoni</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Foundation Don Carlo Gnocchi IRCCS</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Blood flow through the body delivers oxygen, nutrients, hormones, cells, products of defense mechanisms for wound healing, and platelets. The heart pumps these products to the organs, while the vessels transport them to and from the organs. Arteries perfuse the organs and veins drain the organs of waste products. The lymphatic system helps in draining excess tissue fluid to the bloodstream. Two circulatory loops are most important to survival: the pulmonary circulation and the systemic circulation. The pulmonary circulation pumps blood from the right ventricle to the pulmonary artery. Blood exchanges carbon dioxide for oxygen while passing through the lung and the newly oxygenated blood drains into the left atrium from the pulmonary veins. The other circulatory loop is the systemic circulation, which pumps blood from the left ventricle to the aorta to the rest of the body. It transports nutrients to the intestines and hormones to endocrine glands. Waste excretion then occurs via the kidneys, intestines, lungs, and skin. Blood returns to the right atrium from the superior and inferior vena cava.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s7">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s8">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Sun XG. 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Cureus. 2019 Jun 03;11(6):e4819.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6682397</ArticleId><ArticleId IdType="pubmed">31404386</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32119344</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31869070</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK551589</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-24901">Neuroanatomy, Medulla Oblongata<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Iordanova</LastName><ForeName>Radostina</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>LECOM</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reddivari</LastName><ForeName>Anil Kumar Reddy</ForeName><Initials>AKR</Initials><AffiliationInfo><Affiliation>University of Illinois</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The medulla oblongata is the connection between the brainstem and the spinal cord, carrying multiple important functional centers. It is comprised of the cardiovascular-respiratory regulation system, descending motor tracts, ascending sensory tracts, and origin of cranial nerves IX, X, XI, and XII. Motor neurons cross from the left motor cortex to the right side of the spinal cord in the medulla. The medulla is the most caudal aspect of the brainstem, approximately at the level of the foramen magnum. Anterior to the medulla oblongata is the median fissure, which connects with the median fissure of the spinal cord. The posterior surface of the medulla can divide into two parts, the inferior part, which has median sulcus continuous with the spinal cord, and the superior part, which forms the lower floor of the fourth ventricle. The medulla, including the pons and the midbrain, is divided into three laminae, from dorsal to ventral, called the tectum, tegmentum, and basis, respectively. The tectum of the medulla involves the inferior medullary velum, which is the most inferior posterior part of the fourth ventricle. The tegmentum consists of the inferior olivary nucleus and the cranial nerve nuclei of IX, X, XI, XII. The basis, most ventral layer, has the pyramid decussation at the medulla.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s6">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s7">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s8">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Angeles Fernández-Gil M, Palacios-Bote R, Leo-Barahona M, Mora-Encinas JP. 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J Neurol. 2006 Nov;253(11):1442-6.</Citation><ArticleIdList><ArticleId IdType="pubmed">16775654</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31869070</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31855391</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK551564</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-146">Cardiac Electrical and Structural Remodeling<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Liaquat</LastName><ForeName>Muhammad Talha</ForeName><Initials>MT</Initials><AffiliationInfo><Affiliation>St. Joseph's University Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Makaryus</LastName><ForeName>Amgad N.</ForeName><Initials>AN</Initials><AffiliationInfo><Affiliation>Zucker School Medicine/Hofstra/Northwell</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Even with the falling rates of cardiovascular deaths, the events of deaths attributable to sudden cardiac death keep rising. A total of 350000 events of sudden cardiac death are estimated to occur in the United States every year. Coronary artery disease often leads to complex electrical and structural remodeling of the heart due to myocardial injury. This remodeling is the root cause that precipitates ventricular arrhythmias, which often lead to sudden cardiac death. Cardiac remodeling occurs in response to stress, either functional stress or structural stress. This remodeling plays a vital role in the disease process that ensues. Initially, the electrical and structural remodeling helps in compensating the cardiac performance. But over time, these compensatory mechanisms often lead to pump failure and/or fatal arrhythmias. Both atria and ventricles are affected by electrical remodeling. This process eventually leads to atrial fibrillation and fatal ventricular arrhythmias. Structural remodeling of the heart can be physiologic growth occurring in response to exercise, pregnancy, or during the postnatal period. It can also be pathologic hypertrophy in response to neurohumoral activation, injury to myocardium, or hypertension. Heart failure and malignant arrhythmia are often precipitated by pathological hypertrophy of the heart. However, they don’t occur with the physiological growth of the heart.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s2">Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s3">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s4">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s5">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s7">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Thom T, Haase N, Rosamond W, Howard VJ, Rumsfeld J, Manolio T, Zheng ZJ, Flegal K, O'Donnell C, Kittner S, Lloyd-Jones D, Goff DC, Hong Y, Adams R, Friday G, Furie K, Gorelick P, Kissela B, Marler J, Meigs J, Roger V, Sidney S, Sorlie P, Steinberger J, Wasserthiel-Smoller S, Wilson M, Wolf P, American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart disease and stroke statistics--2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. 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J Eval Clin Pract. 2016 Jun;22(3):329-40.</Citation><ArticleIdList><ArticleId IdType="pubmed">26552842</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31855391</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31751074</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK549884</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-37651">Anatomy, Thorax, Mitral Valve<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Sanchez Vaca</LastName><ForeName>Felipe</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Pontificia Universidad Catolica, Ecuador</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordoni</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Foundation Don Carlo Gnocchi IRCCS</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The heart has four chambers; the right and left atria and right and left ventricles. The heart also has valves that help with blood circulation, the mitral and tricuspid valves are called “atrioventricular” because of their location that is between the atriums and ventricles, and the aortic and pulmonary valves are the “arterioventricular” valves located between the ventricles and arteries. (Figure-1) The name of the mitral valve derives from the liturgical headgear (miter) of the Catholic/Christian tradition. The mitral valve also called bicuspid valve, is located between the left atrium and left ventricle and is composed of the mitral annulus, papillary muscles, anterior leaflet, and posterior leaflet and chordae tendinae, all these components form the valve apparatus which prevents the blood backflow from the left ventricle to the left atrium during systole, and during diastole allows normal blood flow from the left atrium to the left ventricle. </AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Rajput FA, Zeltser R. 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Indian Heart J. 2001 Jan-Feb;53(1):35-7.</Citation><ArticleIdList><ArticleId IdType="pubmed">11456138</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31751074</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31613486</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK547706</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28065">Anatomy, Thorax, Heart Pulmonic Valve<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Sundjaja</LastName><ForeName>Joshua Henrina</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Atma Jaya Catholic University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordoni</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Foundation Don Carlo Gnocchi IRCCS</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The heart is a four-chambered organ hemodynamically functioning as a reservoir and a pump; it receives deoxygenated blood from the systemic circulation through the superior and inferior vena cava in the right atrium and oxygenated blood from the lung via the four pulmonary veins. The heart pumps deoxygenated blood from the right ventricle to the lungs and at the same time pumps oxygenated blood from the left ventricle into the aorta. These processes are orchestrated by the electric conduction system which coordinates the rhythmic contractions of the atria and ventricles, and the opening and closure of the heart valves. The heart valves are especially important to effectively maintain the systolic and diastolic phase of the cardiac cycle. There are two types of heart valves; the atrioventricular valves (mitral, tricuspid) and the semilunar valves (aortic and pulmonic). The pulmonic valve physically separates the right ventricle from the pulmonary trunk. While there is more literature on the other heart valves, little is known about the intricate function of the pulmonary valve and its role in various disorders.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s10">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Ho SY, Nihoyannopoulos P. 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Fetal Pediatr Pathol. 2019 Feb;38(1):57-62.</Citation><ArticleIdList><ArticleId IdType="pubmed">30661433</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31613486</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31082032</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK540988</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-43039">Neuroanatomy, Cerebral Aqueduct (Sylvian)<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Rubino</LastName><ForeName>Jessica M.</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>West Virginia University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hogg</LastName><ForeName>Jeffery P.</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>West Virginia University School of Med.</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Galen initially described the ventricular system of the brain. As more information arose about the anatomy of the brain, anatomists described the cerebral aqueduct as a narrow communication duct between the third and fourth ventricles. The word aqueduct comes from the Latin word “aqueductus" which translates to a canal used for taking water through a structure to another location. It is unclear when the eponym ‘Aqueduct of Sylvius’ first appeared; it is believed to be traced back to the well-known anatomist Franciscus Sylvius. The cerebral aqueduct (of Sylvius) plays an essential role in the ventricular system of the brain and when disrupted can have some significant clinical manifestations.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Mortazavi MM, Adeeb N, Griessenauer CJ, Sheikh H, Shahidi S, Tubbs RI, Tubbs RS. 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Neurosurg Clin N Am. 2012 Jan;23(1):165-77.</Citation><ArticleIdList><ArticleId IdType="pubmed">22107867</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31082032</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30844183</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK538156</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19499">Neuroanatomy, Choroid Plexus<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Javed</LastName><ForeName>Kinaan</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Upike-KYCOM</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reddy</LastName><ForeName>Vamsi</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>McKinsey & Company</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lui</LastName><ForeName>Forshing</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>CA Northstate Uni, College of Med</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The choroid plexus is a complex network of capillaries lined by specialized cells and has various functions. One of the primary functions is to produce cerebrospinal fluid (CSF) via the ependymal cells that line the ventricles of the brain. Secondly, the choroid plexus serves as a barrier in the brain separating the blood from the CSF, known as the blood-CSF barrier. In addition to these vital functions, the choroid plexus also secretes various growth factors that maintain the stem cell pool in the subventricular zone. Not only are these functions necessary for successful brain development, but they are also essential to protect against harmful microbes and toxins.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s7">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Lun MP, Monuki ES, Lehtinen MK. Development and functions of the choroid plexus-cerebrospinal fluid system. Nat Rev Neurosci. 2015 Aug;16(8):445-57.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4629451</ArticleId><ArticleId IdType="pubmed">26174708</ArticleId></ArticleIdList></Reference><Reference><Citation>Strazielle N, Ghersi-Egea JF. Choroid plexus in the central nervous system: biology and physiopathology. J Neuropathol Exp Neurol. 2000 Jul;59(7):561-74.</Citation><ArticleIdList><ArticleId IdType="pubmed">10901227</ArticleId></ArticleIdList></Reference><Reference><Citation>Kaur C, Rathnasamy G, Ling EA. The Choroid Plexus in Healthy and Diseased Brain. J Neuropathol Exp Neurol. 2016 Mar;75(3):198-213.</Citation><ArticleIdList><ArticleId IdType="pubmed">26888305</ArticleId></ArticleIdList></Reference><Reference><Citation>Dziegielewska KM, Ek J, Habgood MD, Saunders NR. Development of the choroid plexus. Microsc Res Tech. 2001 Jan 01;52(1):5-20.</Citation><ArticleIdList><ArticleId IdType="pubmed">11135444</ArticleId></ArticleIdList></Reference><Reference><Citation>Lopez JA, Reich D. Choroid plexus cysts. J Am Board Fam Med. 2006 Jul-Aug;19(4):422-5.</Citation><ArticleIdList><ArticleId IdType="pubmed">16809660</ArticleId></ArticleIdList></Reference><Reference><Citation>Okano A, Ogiwara H. Long-term follow-up for patients with infantile hydrocephalus treated by choroid plexus coagulation. J Neurosurg Pediatr. 2018 Dec 01;22(6):638-645.</Citation><ArticleIdList><ArticleId IdType="pubmed">30215586</ArticleId></ArticleIdList></Reference><Reference><Citation>Trevisi G, Frassanito P, Di Rocco C. Idiopathic cerebrospinal fluid overproduction: case-based review of the pathophysiological mechanism implied in the cerebrospinal fluid production. Croat Med J. 2014 Aug 28;55(4):377-87.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4157373</ArticleId><ArticleId IdType="pubmed">25165051</ArticleId></ArticleIdList></Reference><Reference><Citation>Lay CM. Low Cerebrospinal Fluid Pressure Headache. Curr Treat Options Neurol. 2002 Sep;4(5):357-363.</Citation><ArticleIdList><ArticleId IdType="pubmed">12162924</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30844183</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30844167</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK538140</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17732">Anatomy, Thorax, Heart Aorta<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shahoud</LastName><ForeName>James S.</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>Lake Erie College of Osteopathic Med.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miao</LastName><ForeName>Julia H.</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Cornell University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bolla</LastName><ForeName>Srinivasa Rao</ForeName><Initials>SR</Initials><AffiliationInfo><Affiliation>Imam Abdulrahman Bin Faisal University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The aorta is the largest vessel within the human body. It originates from the left ventricle of the heart anterior to the pulmonary artery before arching posteriorly and descending along the posterior mediastinum. It descends to the level of the L4 vertebral body where it bifurcates into the left and right common iliac arteries. It is the main artery in the body and distributes oxygenated blood to the entire systemic circulation. This section will be limited to the thoracic portion of the aorta, which includes the ascending aorta, aortic arch, and descending thoracic aorta before it crosses the level of the diaphragm where it becomes the abdominal aorta. The thoracic aorta is responsible for supplying oxygenated blood to multiple structures, including the head, neck, upper extremities, and thoracic structures.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s4">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s5">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s9">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Kau T, Sinzig M, Gasser J, Lesnik G, Rabitsch E, Celedin S, Eicher W, Illiasch H, Hausegger KA. Aortic development and anomalies. Semin Intervent Radiol. 2007 Jun;24(2):141-52.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3036416</ArticleId><ArticleId IdType="pubmed">21326792</ArticleId></ArticleIdList></Reference><Reference><Citation>Dungan DH, Heiserman JE. The carotid artery: embryology, normal anatomy, and physiology. Neuroimaging Clin N Am. 1996 Nov;6(4):789-99.</Citation><ArticleIdList><ArticleId IdType="pubmed">8824131</ArticleId></ArticleIdList></Reference><Reference><Citation>Bamforth SD, Chaudhry B, Bennett M, Wilson R, Mohun TJ, Van Mierop LH, Henderson DJ, Anderson RH. Clarification of the identity of the mammalian fifth pharyngeal arch artery. Clin Anat. 2013 Mar;26(2):173-82.</Citation><ArticleIdList><ArticleId IdType="pubmed">22623372</ArticleId></ArticleIdList></Reference><Reference><Citation>Stout KK, Daniels CJ, Aboulhosn JA, Bozkurt B, Broberg CS, Colman JM, Crumb SR, Dearani JA, Fuller S, Gurvitz M, Khairy P, Landzberg MJ, Saidi A, Valente AM, Van Hare GF. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Apr 02;139(14):e698-e800.</Citation><ArticleIdList><ArticleId IdType="pubmed">30586767</ArticleId></ArticleIdList></Reference><Reference><Citation>Karaosmanoglu AD, Khawaja RD, Onur MR, Kalra MK. CT and MRI of aortic coarctation: pre- and postsurgical findings. AJR Am J Roentgenol. 2015 Mar;204(3):W224-33.</Citation><ArticleIdList><ArticleId IdType="pubmed">25714305</ArticleId></ArticleIdList></Reference><Reference><Citation>Campbell M. 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What is the appropriate size criterion for resection of thoracic aortic aneurysms? J Thorac Cardiovasc Surg. 1997 Mar;113(3):476-91; discussion 489-91.</Citation><ArticleIdList><ArticleId IdType="pubmed">9081092</ArticleId></ArticleIdList></Reference><Reference><Citation>Coady MA, Rizzo JA, Goldstein LJ, Elefteriades JA. Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin. 1999 Nov;17(4):615-35; vii.</Citation><ArticleIdList><ArticleId IdType="pubmed">10589336</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30844167</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30726042</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537357</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28593">Anatomy, Thorax, Heart Right Coronary Arteries<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Saxton</LastName><ForeName>Anthony</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Miami</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaudhry</LastName><ForeName>Raheel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Ross University School Of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manna</LastName><ForeName>Biagio</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>RWJUH/Barnabas Health System</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The coronary arteries are the first vessels to branch from the aorta, and they provide a crucial supply of oxygen and nutrients to the layers of the heart. The right coronary artery and its branches mostly supply the right side of the heart, although they also reach part of the left atrium, a posterior portion of the left ventricle, and even the posterior third of the interventricular septum. Unlike vessels in peripheral locations of the body, these vessels dilate during exertion to meet the increased demands of the myocardium. However, the lack of anastomoses amongst the coronary arteries leaves the heart at risk of ischemia and infarction if blood flow through the vessels is severely compromised, such as with atherosclerosis.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s10">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Villa AD, Sammut E, Nair A, Rajani R, Bonamini R, Chiribiri A. Coronary artery anomalies overview: The normal and the abnormal. World J Radiol. 2016 Jun 28;8(6):537-55.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4919754</ArticleId><ArticleId IdType="pubmed">27358682</ArticleId></ArticleIdList></Reference><Reference><Citation>Murphy C, Lazzara R. Current concepts of anatomy and electrophysiology of the sinus node. J Interv Card Electrophysiol. 2016 Jun;46(1):9-18.</Citation><ArticleIdList><ArticleId IdType="pubmed">27142063</ArticleId></ArticleIdList></Reference><Reference><Citation>Melnikova NB, Svitenkov AI, Hose DR, Hoekstra AG. A cell-based mechanical model of coronary artery tunica media. J R Soc Interface. 2017 Jul;14(132)</Citation><ArticleIdList><ArticleId IdType="pmc">PMC5550961</ArticleId><ArticleId IdType="pubmed">28679664</ArticleId></ArticleIdList></Reference><Reference><Citation>Joyner MJ, Casey DP. Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiol Rev. 2015 Apr;95(2):549-601.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4551211</ArticleId><ArticleId IdType="pubmed">25834232</ArticleId></ArticleIdList></Reference><Reference><Citation>Nishimiya K, Matsumoto Y, Shimokawa H. Viewpoint: Recent Advances in Intracoronary Imaging for Vasa Vasorum Visualisation. Eur Cardiol. 2017 Dec;12(2):121-123.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6223353</ArticleId><ArticleId IdType="pubmed">30416583</ArticleId></ArticleIdList></Reference><Reference><Citation>Senst B, Kumar A, Diaz RR. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2022. Sep 12, Cardiac Surgery.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Bachar BJ, Manna B. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2023. 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Jan 19, Coronary CT Angiography.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30726042</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30726004</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537319</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-42474">Anatomy, Abdomen and Pelvis: Aorta<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>White</LastName><ForeName>Hunter J.</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>Alabama College of Osteopathic Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordes</LastName><ForeName>Stephen J.</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Surgery, Louisiana State University Health Sciences Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Borger</LastName><ForeName>Judith</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Campbell Un. School of Osteopathic Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The aorta is the first and largest artery in the body. It is responsible for transporting nutrient-rich blood to the systemic circulation following ejection from the left ventricle of the heart. The aorta extends from the aortic valve of the left ventricle to the proximal iliac bifurcation at the L4 vertebral level. The vessel can be divided into various segments depending on course and location. The thoracic aorta consists of the ascending aorta, aortic arch, and descending aorta. The descending thoracic aorta passes through the diaphragm’s aortic hiatus at the T12 vertebral level at which point it continues as the abdominal aorta. The abdominal aorta terminates as it bifurcates into common iliac arteries, which subsequently provide arterial supply to the pelvis and lower limbs.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Collins JA, Munoz JV, Patel TR, Loukas M, Tubbs RS. 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Anatomical significance in aortoiliac occlusive disease. Clin Anat. 2014 Nov;27(8):1264-74.</Citation><ArticleIdList><ArticleId IdType="pubmed">25065617</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30726004</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725672</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK536987</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-27862">Prosthetic Heart Valve<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mathew</LastName><ForeName>Philip</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>St. Luke's at Des Peres Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanmanthareddy</LastName><ForeName>Arun</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Texas Houston</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The heart is a specialized vascular structure with an intrinsic pumping mechanism to direct oxygenated blood and nutrients to the tissues of the body.  Basic physics informs us that pressure gradients provide the physical impetus for fluid flow and the force generated by myocardial contraction drives blood flow into systemic and pulmonary circulation.  Myocardial relaxation generates a drop in pressure that promotes retrograde blood flow. Prevention of this retrograde blood flow is by the presence of heart valves which open and close due to changes in pressure. The heart has four valves: the mitral valve, aortic valve, tricuspid valve, and pulmonic valve.  The mitral and tricuspid valves are collectively known as the <i>atrioventricular valves</i> due to their anatomical location at the junction of the atrium and ventricle. Their primary function is to prevent retrograde blood flow into the atria during ventricular systole. The aortic and pulmonic valves are collectively known as the <i>semilunar valves</i>, and their primary function is to prevent retrograde blood flow into the ventricles during diastole.  They are at the junction of the ventricle and their respective great artery.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-27862" sec="article-27862.s1">Definition/Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-27862" sec="article-27862.s2">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-27862" sec="article-27862.s3">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-27862" sec="article-27862.s4">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-27862" sec="article-27862.s6">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Mazine A, El-Hamamsy I, Verma S, Peterson MD, Bonow RO, Yacoub MH, David TE, Bhatt DL. 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Am J Cardiol. 2018 Nov 15;122(10):1738-1744.</Citation><ArticleIdList><ArticleId IdType="pubmed">30449326</ArticleId></ArticleIdList></Reference><Reference><Citation>Pibarot P, Clavel MA. Prosthesis-Patient Mismatch After Transcatheter Aortic Valve Replacement: It Is Neither Rare Nor Benign. J Am Coll Cardiol. 2018 Dec 04;72(22):2712-2716.</Citation><ArticleIdList><ArticleId IdType="pubmed">30497556</ArticleId></ArticleIdList></Reference><Reference><Citation>Pibarot P, Weissman NJ, Stewart WJ, Hahn RT, Lindman BR, McAndrew T, Kodali SK, Mack MJ, Thourani VH, Miller DC, Svensson LG, Herrmann HC, Smith CR, Rodés-Cabau J, Webb J, Lim S, Xu K, Hueter I, Douglas PS, Leon MB. Incidence and sequelae of prosthesis-patient mismatch in transcatheter versus surgical valve replacement in high-risk patients with severe aortic stenosis: a PARTNER trial cohort--a analysis. J Am Coll Cardiol. 2014 Sep 30;64(13):1323-34.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4237285</ArticleId><ArticleId IdType="pubmed">25257633</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30725672</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30521233</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK534812</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28002">Anatomy, Thorax, Heart Pulmonary Arteries<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Tucker</LastName><ForeName>William D.</ForeName><Initials>WD</Initials><AffiliationInfo><Affiliation>ETSU Quillen College of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weber</LastName><ForeName>Carly</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Lake Erie College of Osteopathic Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burns</LastName><ForeName>Bracken</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>East Tennessee State University (ETSU)</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The main pulmonary artery and the subsequent right and left pulmonary arteries sit within the middle mediastinum. They arise from the right ventricle of the four-chambered heart and transport blood to the lungs. De-oxygenated blood from the body's somatic cells travels to the right atrium, then into the right ventricle, and through the main pulmonary artery and its branches before blood enters the lungs for oxygenation and gas exchange. These steps are all prerequisites for normal human physiologic function.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Kandathil A, Chamarthy M. 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Radiology. 1997 Nov;205(2):447-52.</Citation><ArticleIdList><ArticleId IdType="pubmed">9356627</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30521233</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30422527</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK532932</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32436">Neuroanatomy, Ventricular System<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shenoy</LastName><ForeName>Saraswati Satyanarayan</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Seth G S Med College & KEM Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lui</LastName><ForeName>Forshing</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>CA Northstate Uni, College of Med</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The ventricular system of the brain is an interconnected series of cavities filled with cerebrospinal fluid (CSF) that cushions the brain. Though the presence of cerebral ventricles was known since ancient times, its function was obscure. Early scientists believed ventricles to be the site of thought, emotions, reasoning, and memory. Leonardo da Vinci, the famed artist who drew Mona Lisa, performed the first ventriculography on the brain of an ox. However, in the 17th century, it was Domenico Felice Antonio Cotugno who first described the connection between cerebral ventricles and subarachnoid space, a fact later confirmed by Francis Jean Magendie.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s7">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s8">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Schiller F. 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Neuroimage. 2012 Jan 02;59(1):154-67.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3319053</ArticleId><ArticleId IdType="pubmed">21787868</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30422527</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30247839</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK525964</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-40416">Anatomy, Abdomen and Pelvis: Abdominal Aorta<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Clement T.</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>California Northstate College Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Cheng Ying</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Ross University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordes</LastName><ForeName>Stephen J.</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Surgery, Louisiana State University Health Sciences Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lui</LastName><ForeName>Forshing</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>CA Northstate Uni, College of Med</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The aorta is the main artery of the human body. It arises from the left ventricle of the heart and travels superiorly to form the ascending aorta. It then loops inferiorly to form the arch of the aorta and through the thorax to form the thoracic aorta. After crossing the diaphragm into the abdomen, the aptly-named abdominal aorta eventually bifurcates into the common iliac arteries in the lower abdomen. Along the way, the aorta gives rise to the arterial branches that are responsible for transmitting oxygenated blood to all the tissues of the body. As such, pathology arising in the aorta frequently results in serious consequences. Thus, it is important for the clinician to be aware of the functional, anatomical, surgical, and clinical considerations about the aorta.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Loukas M, Bilinsky E, Bilinsky S, Blaak C, Tubbs RS, Anderson RH. 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Vasa. 2012 May;41(3):163-76.</Citation><ArticleIdList><ArticleId IdType="pubmed">22565618</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30247839</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30020697</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK513325</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32314">Anatomy, Thorax, Phrenic Nerves<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Oliver</LastName><ForeName>Kaitlin A.</ForeName><Initials>KA</Initials></Author><Author ValidYN="Y"><LastName>Ashurst</LastName><ForeName>John V.</ForeName><Initials>JV</Initials><AffiliationInfo><Affiliation>Kingman Regional Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The phrenic nerve originates from the anterior rami of C3 through C5 and traverses the neck, heart, and lungs to reach the diaphragm. From its origin, the phrenic nerve descends vertically caudad and adjacent to the internal jugular vein. In the neck and upper thorax, the left phrenic nerve tracts proximal to the subclavian artery. The right phrenic nerve runs superficial to the anterior scalene muscle and the second part of the right subclavian artery. In the thorax, the right and left phrenic nerve will continue to descend anteriorly to the root of the lung and between the mediastinal surface of the parietal pleura and fibrous pericardium. The right phrenic nerve passes lateral to the right atrium and right ventricle and will continue to descend through the vena cava hiatus in the diaphragmatic opening at the level of T8. The left phrenic nerve descends anterior to the pericardial sac of the left ventricle and terminates at the central tendon of the diaphragm.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s5">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Bains KNS, Kashyap S, Lappin SL. 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Clin Anat. 2017 Nov;30(8):1077-1082.</Citation><ArticleIdList><ArticleId IdType="pubmed">28726261</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang J, Li J, Liu G, Deslauriers J. Nerves of the mediastinum. Thorac Surg Clin. 2011 May;21(2):239-49, ix.</Citation><ArticleIdList><ArticleId IdType="pubmed">21477774</ArticleId></ArticleIdList></Reference><Reference><Citation>Khong P, Lazzaro A, Mobbs R. Phrenic nerve stimulation: the Australian experience. J Clin Neurosci. 2010 Feb;17(2):205-8.</Citation><ArticleIdList><ArticleId IdType="pubmed">20056422</ArticleId></ArticleIdList></Reference><Reference><Citation>Loukas M, Kinsella CR, Louis RG, Gandhi S, Curry B. Surgical anatomy of the accessory phrenic nerve. Ann Thorac Surg. 2006 Nov;82(5):1870-5.</Citation><ArticleIdList><ArticleId IdType="pubmed">17062263</ArticleId></ArticleIdList></Reference><Reference><Citation>Morgan JA, Morales DL, John R, Ginsburg ME, Kherani AR, Vigilance DW, Cheema FH, Smith CR, Oz MC, Argenziano M. Endoscopic, robotically assisted implantation of phrenic pacemakers. J Thorac Cardiovasc Surg. 2003 Aug;126(2):582-3.</Citation><ArticleIdList><ArticleId IdType="pubmed">12928662</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30020697</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29261997</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK470179</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28281">Anatomy, Head and Neck, Larynx Recurrent Laryngeal Nerve<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Allen</LastName><ForeName>Evan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Ohio University HCOM</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Minutello</LastName><ForeName>Katrina</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Michigan State University College of Osteopathic Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murcek</LastName><ForeName>Benjamin W.</ForeName><Initials>BW</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The larynx is a dynamic, flexible structure composed of a cartilaginous core with interconnecting membranes and associated musculature. The larynx is a midline structure positioned at the interface between the digestive and respiratory tracts. In addition to housing the vocal cords and producing phonation, the larynx assists with multiple other functions including but not limited to: airway protection, regulating intrathoracic pressures, and regulating intra-abdominal pressures. The anatomical position, composition, associated musculature and innervation of the larynx all contribute to this structure’s capabilities. <b>Laryngeal Position</b> The anatomical position of the larynx is also dynamic in nature and varies from birth to maturity. Initially, at birth and for the first couple years of life, the larynx is further superior in the neck than in adults. In infants, this high position results in direct contact between the soft palate and epiglottis. This allows inspired air to move from the nose to the trachea directly. It is because of this anatomical relationship; an infant is able to swallow liquids and breathe almost simultaneously. By adulthood, the larynx descends inferiorly to its final position. The larynx is found within the visceral compartment of the neck and serves as the “floor” of the anterior triangle of the neck. The larynx is the superior portion of the respiratory tract and aligned on its long axis, is vertically adjacent to the trachea, which lies directly inferior to the larynx and is connected via the cricotracheal ligament. Anterosuperiorly, the larynx articulates with the hyoid bone via the thyrohyoid membrane. Dorsally, the larynx attaches to the muscular walls of the pharynx. <b>Laryngeal Skeleton</b> The larynx is composed of nine contributing cartilages: three unpaired cartilages and three paired cartilages, which share connections to each other, the hyoid (superiorly), and the trachea (inferiorly). The epiglottic, thyroid, and cricoid cartilages make up the three unpaired cartilages and are arranged superior to inferior respectively. The thyroid cartilage, with the epiglottic cartilage superior, predominates anteriorly and forms the laryngeal prominence (i.e., Adam’s Apple), while the predominate cartilage dorsally is the cricoid cartilage which sits inferior to the thyroid cartilage. The three paired cartilages include the arytenoid, corniculate, and cuneiform cartilages. The paired arytenoid cartilages are found on the dorsal aspect of the larynx, attached superiorly to the cricoid cartilage. Both arytenoid cartilages give off a lateral extension (muscular process) and anterior extension (vocal process) which aid in supporting the vocal ligaments. Additionally, each arytenoid cartilage has an associated corniculate and cuneiform cartilage. These two small, paired cartilages border the opening into the laryngeal vestibule both dorsally and laterally. The corniculate cartilage can be found at the apex of both arytenoid cartilages. The cuneiform cartilage can be found sitting anterior and lateral to both arytenoids. These cartilages form connections via numerous membranes, ligaments, and synovial joints. There are two essential synovial joints associated with the larynx. One pair of synovial joints exists between the thyroid and cricoid cartilages. This joint allows the thyroid cartilage to rotate about the cricoid cartilage and allows the cricoid cartilage to separate from or approximate to the thyroid cartilage anteriorly. The second set of synovial joints exists between the cricoid and arytenoids (cricoarytenoid synovial joint). The cricoarytenoid synovial joint allows the arytenoid cartilages to translate on both an anterior-posterior axis and lateral-medial axis, as well as rotate about a cranial-caudal axis. <b>Laryngeal Folds and Membranes</b> The aryepiglottic folds extend over the lateral aspects of epiglottic, cuneiform, corniculate and arytenoid cartilages. The aryepiglottic folds demarcate the opening into the laryngeal lumen. The piriform sinus can be found just lateral to the aryepiglottic folds, which form the medial border of these sinuses. This is sometimes referred to as the lateral food channel. The aryepiglottic folds serve as a protective wall that prevents food from passing into the laryngeal aditus and together, with the associated cartilages forms a protective ring. This ring is not uniform in height, at the dorsal-most aspect, there is a reduction in the height of this fold creating susceptibility to food or liquid incursions. This is called the interarytenoid notch. The laryngeal ventricle is the fossa or sinus that lies between the vocal and vestibular folds on either side. The vocal folds are commonly referred to as the vocal cords and the vestibular folds as the false vocal cords. The laryngeal ventricle also demarcates the separation between the quadrangular membrane superiorly, and the cricovocal membrane found inferiorly. These two membranes together cover the entire interior portion of the larynx from the epiglottic and arytenoid cartilages superiorly to the cricoid cartilage inferiorly. These membranes are bilateral. The quadrangle membrane gives support to the aryepiglottic folds superiorly and continues inferiorly as the vestibular folds. The vestibular folds contain the vestibular ligament, which extends from the arytenoid cartilage to the thyroid cartilage. The vestibular folds appear to have no role in phonation and are relatively immobile structures. The laryngeal ventricle begins inferiorly to the free edge of the vestibular fold and continues laterally. The ventricle exists bilaterally, and secretes mucus over the superior surface of the vocal folds, forming a protective layer. The lateral cricothyroid ligament is contained within the cricovocal membrane. Like the vestibular ligament, this ligament also extends from the arytenoid cartilage to the thyroid cartilage. However, the lateral cricothyroid ligament also follows the cricoid cartilage as it extends inferiorly. In addition, this ligament gives rise to the vocal ligament as it thickens superiorly. The vocal ligament extends from the thyroid cartilage [luminal surface] to the vocal process of the arytenoid cartilage. The conus elasticus is a collective term for the cricovocal membrane and its contained ligaments. The medial convergence of these ligaments support the vocal folds. The vocal folds, also known as the true vocal cords, are medial projections of the walls of the larynx that can approximate to each other in the midline to completely obstruct the lumen of the larynx. These vocal folds delineate the plane referred to as the glottis. Within these vocal folds is a muscle known as vocalis muscle which runs aside the vocal ligament. The ligament and lack of blood vessels on the surface of the folds result in the characteristic white appearance of the pair of vocal folds. This provides visual distinction compared to the pink appearing vestibular folds. The space found between the vocal folds is termed the rima glottides. <b>Laryngeal Cavity</b> The laryngeal inlet/aditus is used to refer to the entrance of the cavity of the larynx. Superior to the inlet is the laryngopharynx. The cavity of the larynx is divided into three regions: Supraglottic space: at the level of the vestibular folds. Bounded anteriorly by epiglottis, laterally by the aryepiglottic folds and posteriorly by the inter arytenoid mucosa. Laryngeal ventricles: The middle region of the laryngeal cavities is composed of the paired laryngeal ventricles that fall between the vestibular and vocal folds. Subglottic space: also referred to as the infraglottic space, continues downward as far inferior as the junction between the cricoid and trachea.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s2">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s3">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s4">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s5">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Sun H, Wu CW, Zhang D, Makay Ö, Zhao Y, Carcofaro P, Kim HY, Dionigi G, Pino A, Caruso E, Pontin A, Pappalardo V. New Paradigms for Neural Monitoring in Thyroid Surgery. Surg Technol Int. 2019 May 15;34:79-86.</Citation><ArticleIdList><ArticleId IdType="pubmed">30664223</ArticleId></ArticleIdList></Reference><Reference><Citation>Cirocchi R, Arezzo A, D'Andrea V, Abraha I, Popivanov GI, Avenia N, Gerardi C, Henry BM, Randolph J, Barczyñski M. Intraoperative neuromonitoring versus visual nerve identification for prevention of recurrent laryngeal nerve injury in adults undergoing thyroid surgery. Cochrane Database Syst Rev. 2019 Jan 19;1(1):CD012483.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6353246</ArticleId><ArticleId IdType="pubmed">30659577</ArticleId></ArticleIdList></Reference><Reference><Citation>Bakalinis E, Makris I, Demesticha T, Tsakotos G, Skandalakis P, Filippou D. Non-Recurrent Laryngeal Nerve and Concurrent Vascular Variants: A Review. 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Paediatr Respir Rev. 2018 Jun;27:74-85.</Citation><ArticleIdList><ArticleId IdType="pubmed">29336933</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29261997</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29261906</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK470522</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32357">Anatomy, Thorax, Heart Arteries<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaudhry</LastName><ForeName>Raheel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Ross University School Of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rahman</LastName><ForeName>Sajedur</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Law</LastName><ForeName>Mark A.</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Childrens of AL, Un of AL at Birmingham</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The coronary arteries provide the main blood supply to the heart. The coronary arteries also supply the myocardium with oxygen to allow for the contraction of the heart and thus causing circulation of the blood throughout the body. Two main coronary arteries originate from the base of the aorta as it exits the left ventricle: the left and right coronary arteries. These arteries further branch into smaller arteries to supply specific parts of the heart like the atria, ventricles, SA, and AV nodes. It is important to realize that the paths these arteries take may vary slightly from person to person.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s3">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s4">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s5">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s6">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s7">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s8">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Lee YJ, Park KS, Kil HR. Change of coronary artery indices according to coronary dominance pattern in early childhood. Korean J Pediatr. 2019 Jun;62(6):240-243.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6584238</ArticleId><ArticleId IdType="pubmed">30463399</ArticleId></ArticleIdList></Reference><Reference><Citation>Saedi S, Parsaee M, Farrashi M, Noohi F, Mohebbi B. The role of echocardiography in anomalous origin of coronary artery from pulmonary artery (ALCAPA): Simple tool for a complex diagnosis. Echocardiography. 2019 Jan;36(1):177-181.</Citation><ArticleIdList><ArticleId IdType="pubmed">30620101</ArticleId></ArticleIdList></Reference><Reference><Citation>Angelini P, Cheong BY, Lenge De Rosen VV, Lopez A, Uribe C, Masso AH, Ali SW, Davis BR, Muthupillai R, Willerson JT. High-Risk Cardiovascular Conditions in Sports-Related Sudden Death: Prevalence in 5,169 Schoolchildren Screened via Cardiac Magnetic Resonance. Tex Heart Inst J. 2018 Aug;45(4):205-213.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6183627</ArticleId><ArticleId IdType="pubmed">30374227</ArticleId></ArticleIdList></Reference><Reference><Citation>Kuang H, Zhou X, Li L, Yi Q, Shou W, Lu T. Early severe coronary heart disease and ischemic heart failure in homozygous familial hypercholesterolemia: A case report. Medicine (Baltimore) 2018 Oct;97(42):e12869.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6211926</ArticleId><ArticleId IdType="pubmed">30335000</ArticleId></ArticleIdList></Reference><Reference><Citation>Ahmad M, Mehta P, Reddivari AKR, Mungee S. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2022. Sep 30, Percutaneous Coronary Intervention.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Fakhri Y, Sejersten M, Schoos MM, Melgaard J, Graff C, Wagner GS, Clemmensen P, Kastrup J. Algorithm for the automatic computation of the modified Anderson-Wilkins acuteness score of ischemia from the pre-hospital ECG in ST-segment elevation myocardial infarction. J Electrocardiol. 2017 Jan-Feb;50(1):97-101.</Citation><ArticleIdList><ArticleId IdType="pubmed">27889057</ArticleId></ArticleIdList></Reference><Reference><Citation>Ayer A, Terkelsen CJ. Difficult ECGs in STEMI: lessons learned from serial sampling of pre- and in-hospital ECGs. J Electrocardiol. 2014 Jul-Aug;47(4):448-58.</Citation><ArticleIdList><ArticleId IdType="pubmed">24792903</ArticleId></ArticleIdList></Reference><Reference><Citation>Warner MJ, Tivakaran VS. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2023. Feb 12, Inferior Myocardial Infarction.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Chatterjee A, Watts TE, Mauchley DC, Iskandrian AE, Law MA. Multimodality Imaging of Rare Adult Presentation of ALCAPA Treated With Takeuchi Repair. JACC Cardiovasc Interv. 2018 Jan 08;11(1):98-99.</Citation><ArticleIdList><ArticleId IdType="pubmed">29248407</ArticleId></ArticleIdList></Reference><Reference><Citation>Kastellanos S, Aznaouridis K, Vlachopoulos C, Tsiamis E, Oikonomou E, Tousoulis D. Overview of coronary artery variants, aberrations and anomalies. World J Cardiol. 2018 Oct 26;10(10):127-140.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6205847</ArticleId><ArticleId IdType="pubmed">30386490</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29261906</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29083815</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK459286</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19195">Anatomy, Head and Neck: Cerebrospinal Fluid | The term atrioventricular (AV) dissociation describes a family of arrhythmias where independent pacemakers control the atria and ventricles. The standard activation of the cardiac circuits works in the order of impulse transmission from the sinoatrial (SA) node to the atria, the AV node, and ventricular activation via the His-Purkinje system. Disruption in this pathway leads to a dissociation between the conduction rates of the atria and ventricle. The severity of this event varies, from benign in cases of isorhythmic AV dissociation to complete heart block, which in cases might be fatal if not treated with a permanent pacemaker. Another important cause of this condition is ventricular tachycardia, which is lethal if not recognized or treated appropriately.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s6">Toxicokinetics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17973" sec="article-17973.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Littmann L, Monroe MH, Letts DP. 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Ann Transl Med. 2015 Mar;3(3):42.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4356861</ArticleId><ArticleId IdType="pubmed">25815303</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33085352</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32809599</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK560764</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-23696">Intracranial Hypotension</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Swyden</LastName><ForeName>Shelbi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Wyckoff Heights Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carter</LastName><ForeName>Carley</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>University of Kansas Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shah</LastName><ForeName>Sumir u.</ForeName><Initials>SU</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The intracranial cavity consists of three components: cerebrospinal fluid (CSF), blood, and brain tissue. CSF is contained within the subarachnoid space between the arachnoid and pia layers of the meninges. CSF is produced by a specialized vascular structure called choroid plexus within each ventricle of the brain. A blood-CSF barrier is formed by ependymal cells that line the ventricles and choroid epithelial cells that line the surrounding capillaries within the choroid plexus. The ventricular system includes two lateral ventricles, a third ventricle, and the fourth ventricle, which is encompassed by the brainstem and cerebellum. The interventricular foramen of Monro connects the third and lateral ventricles while the third and fourth ventricles communicate via the cerebral aqueduct, also known as the Aqueduct of Sylvius. CSF enters the subarachnoid space surrounding the brain and spinal cord via the foramina of Luschka and Magendie. It then travels within and around the brain and spinal cord until it is eventually reabsorbed by the arachnoid granules to finally make its way into the dural venous sinuses, back into the bloodstream. Normal CSF pressure falls approximately within 65 to 195 mm of water or CSF within the subarachnoid space. Intracranial hypotension (ICH) is defined as CSF pressure less than 60 mm H2O. It is hypothesized that low CSF volume, as opposed to low CSF pressure, is the primary cause of symptoms of ICH. Historically, Heinrich Irenaeus Quincke was credited with performing the first lumbar puncture (LP) in 1891. In 1898 it was August Bier, also known as the father of spinal anesthesia, who reported his observations on post-dural puncture headaches and proposed the hypothesis that ongoing leak of CSF from the dural puncture site was the inciting factor of such symptoms. His studies led to the proposition that the CSF leak exceeded the rate of CSF production. George Schaltenbrand, a German Neurologist, studied the pressure system of CSF within the cranial system. He proposed three mechanisms in which spontaneous ICH, which he termed "aliquorrhea," induce a clinical presentation identical to that of a post-LP headache. These mechanisms are a decrease in CSF production, an increase in CSF absorption, and loss of CSF volume via a leak.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s6">Histopathology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s7">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s8">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s9">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s10">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s11">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s12">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s13">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s14">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s15">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-23696" sec="article-23696.s16">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Mokri B. 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Headache. 2018 Sep;58(8):1244-1255.</Citation><ArticleIdList><ArticleId IdType="pubmed">30238694</ArticleId></ArticleIdList></Reference><Reference><Citation>Schievink WI, Maya MM, Louy C. Cranial MRI predicts outcome of spontaneous intracranial hypotension. Neurology. 2005 Apr 12;64(7):1282-4.</Citation><ArticleIdList><ArticleId IdType="pubmed">15824366</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32809599</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32644365</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK558939</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-617">Aortic Valve Repair</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Talha</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>University Of Maryland</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Puckett</LastName><ForeName>Yana</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>West Virginia University School of Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Aortic valve functional unit is a central outflow tract of the left side of the heart. The operational unit of the left outflow tract consists of aortic valve cusps, commissures, annulus, and sinuses at the root of the aorta. This functional unit of the left ventricular outflow tract is responsible for maintaining the laminar flow of blood after ejection from the left ventricle. Aortic valve pathologies can have a severe generalized impact on the body based on the perfusion deficit. Aortic valve insufficiency is mostly due to the underlying shear force causing stretch, dilation, rupture of the valve. Moreover, conditions of the aortic root, including coarctation, dissection, and aneurysm, can increase the aortic valve pathology due to increase shear force of blood at the aortic valve disrupting the laminar flow. Aortic valve pathologies can be managed by repair or replacement. Aortic valve replacement with a biological or prosthetic valve has been the cornerstone of the management of aortic valve pathologies. However, aortic valve repair has been the topic of debate as compared to replacement in specific subsets of patients. Over the last decade, aortic valve repair and preservation gained exceptional significance in the treatment of aortic root disease with and without insufficiencies. Successful aortic valve repair and preservation methods have been performed worldwide with a prevalence of procedures, less than 2%, as it needs excellent expertise.  The prevalence of procedure performed is low as compared to mitral valve repair as calcific aortic stenosis is the most common valvular pathology seen, which has less success. As compared to repair, aortic valve replacement seems to be relatively simpler, but it has the downside of causing long term complications of structural deterioration, restenosis, infection, and bleeding due to anticoagulation. Therefore, aortic valve preservation procedures have become a reasonable alternative in preventing complications of replacement by maintaining nearby normal anatomy and physiology of the aortic valve functional unit.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s3">Anatomy and Physiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s4">Indications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s5">Contraindications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s6">Equipment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s7">Personnel</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s8">Preparation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s9">Technique or Treatment</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s10">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s11">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s12">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s13">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-617" sec="article-617.s18">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Chester AH, El-Hamamsy I, Butcher JT, Latif N, Bertazzo S, Yacoub MH. 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They have an integral role in proper cardiac valvular function. They arise from the inner walls of the left and right ventricle and attach to mitral and tricuspid valve leaflets respectively via chordae tendinae. Historical documentation of the existence of papillary muscles as a component of cardiac anatomy exists at least as early as the 16th century. This article will describe the structure, function, embryology, blood supply, lymphatics, nerves, physiologic variants, surgical considerations, and clinical significance of the papillary muscles of the heart.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s9">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-26594" sec="article-26594.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Bestetti RB, Restini CB, Couto LB. 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Tex Heart Inst J. 2009;36(3):252-4.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2696506</ArticleId><ArticleId IdType="pubmed">19568400</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491734</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491596</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557664</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17975">Atrioventricular Node</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Heaton</LastName><ForeName>Joseph</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Brooklyn Hospital Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goyal</LastName><ForeName>Amandeep</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Kansas Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The atrioventricular (AV) node is a small structure in the heart, located in the Koch triangle, near the coronary sinus on the interatrial septum. In a right-dominant heart, the atrioventricular node is supplied by the right coronary artery. The purpose of this structure is to connect the electrical systems of the atria and the ventricles, providing electrical impedance from the atria and an intrinsic pacemaker in its absence. The intrinsic rate of the AV node is 40 to 60 beats per minute (bpm).<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s1">Definition/Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s2">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s3">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s4">Nursing, Allied Health, and Interprofessional Team Interventions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s5">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17975" sec="article-17975.s8">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Kurian T, Ambrosi C, Hucker W, Fedorov VV, Efimov IR. 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West J Emerg Med. 2016 Jul;17(4):469-70.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4944806</ArticleId><ArticleId IdType="pubmed">27429700</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491596</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491346</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557414</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-74451">Neuroanatomy, Neural Tube Development and Stages</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Kuwar Chhetri</LastName><ForeName>Parvat</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Rajshahi university</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>M Das</LastName><ForeName>Joe</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Bahrain Specialist Hospital, Juffair, Bahrain</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The entire nervous system forms via the process called neurulation in which neural tube and neural crest form initially. In the third week of embryogenesis, three germ layers arise, namely, ectoderm, mesoderm, and endoderm, through the process of gastrulation. The overlying ectoderm is induced and thickened by the notochord and the neural plate forms. The neural plate then gives rise to the neural tube by folding upon itself, which makes up the central nervous system, which includes the brain, brainstem, and the spinal cord. The brainstem and spinal cord are composed of plates separated by the sulcus limitans, which is in the fourth ventricle of the brain. It separates the alar plate, which gives rise to sensory neurons and a basal plate, which gives rise to motor neurons.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s5">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-74451" sec="article-74451.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Moghadasi Boroujeni S, Koontz A, Tseropoulos G, Kerosuo L, Mehrotra P, Bajpai VK, Selvam SR, Lei P, Bronner ME, Andreadis ST. 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Neuroimaging Clin N Am. 2019 Aug;29(3):411-421.</Citation><ArticleIdList><ArticleId IdType="pubmed">31256862</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491346</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">32119344</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK554457</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-18391">Anatomy, Blood Flow</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Matienzo</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>American University of the Caribbean</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordoni</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Foundation Don Carlo Gnocchi IRCCS</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Blood flow through the body delivers oxygen, nutrients, hormones, cells, products of defense mechanisms for wound healing, and platelets. The heart pumps these products to the organs, while the vessels transport them to and from the organs. Arteries perfuse the organs and veins drain the organs of waste products. The lymphatic system helps in draining excess tissue fluid to the bloodstream. Two circulatory loops are most important to survival: the pulmonary circulation and the systemic circulation. The pulmonary circulation pumps blood from the right ventricle to the pulmonary artery. Blood exchanges carbon dioxide for oxygen while passing through the lung and the newly oxygenated blood drains into the left atrium from the pulmonary veins. The other circulatory loop is the systemic circulation, which pumps blood from the left ventricle to the aorta to the rest of the body. It transports nutrients to the intestines and hormones to endocrine glands. Waste excretion then occurs via the kidneys, intestines, lungs, and skin. Blood returns to the right atrium from the superior and inferior vena cava.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s7">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s8">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-18391" sec="article-18391.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Sun XG. 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Cureus. 2019 Jun 03;11(6):e4819.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6682397</ArticleId><ArticleId IdType="pubmed">31404386</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32119344</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31869070</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK551589</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-24901">Neuroanatomy, Medulla Oblongata</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Iordanova</LastName><ForeName>Radostina</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>LECOM</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reddivari</LastName><ForeName>Anil Kumar Reddy</ForeName><Initials>AKR</Initials><AffiliationInfo><Affiliation>University of Illinois</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The medulla oblongata is the connection between the brainstem and the spinal cord, carrying multiple important functional centers. It is comprised of the cardiovascular-respiratory regulation system, descending motor tracts, ascending sensory tracts, and origin of cranial nerves IX, X, XI, and XII. Motor neurons cross from the left motor cortex to the right side of the spinal cord in the medulla. The medulla is the most caudal aspect of the brainstem, approximately at the level of the foramen magnum. Anterior to the medulla oblongata is the median fissure, which connects with the median fissure of the spinal cord. The posterior surface of the medulla can divide into two parts, the inferior part, which has median sulcus continuous with the spinal cord, and the superior part, which forms the lower floor of the fourth ventricle. The medulla, including the pons and the midbrain, is divided into three laminae, from dorsal to ventral, called the tectum, tegmentum, and basis, respectively. The tectum of the medulla involves the inferior medullary velum, which is the most inferior posterior part of the fourth ventricle. The tegmentum consists of the inferior olivary nucleus and the cranial nerve nuclei of IX, X, XI, XII. The basis, most ventral layer, has the pyramid decussation at the medulla.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s6">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s7">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s8">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-24901" sec="article-24901.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Angeles Fernández-Gil M, Palacios-Bote R, Leo-Barahona M, Mora-Encinas JP. 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J Neurol. 2006 Nov;253(11):1442-6.</Citation><ArticleIdList><ArticleId IdType="pubmed">16775654</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31869070</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31855391</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK551564</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-146">Cardiac Electrical and Structural Remodeling</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Liaquat</LastName><ForeName>Muhammad Talha</ForeName><Initials>MT</Initials><AffiliationInfo><Affiliation>St. Joseph's University Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Makaryus</LastName><ForeName>Amgad N.</ForeName><Initials>AN</Initials><AffiliationInfo><Affiliation>Zucker School Medicine/Hofstra/Northwell</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Even with the falling rates of cardiovascular deaths, the events of deaths attributable to sudden cardiac death keep rising. A total of 350000 events of sudden cardiac death are estimated to occur in the United States every year. Coronary artery disease often leads to complex electrical and structural remodeling of the heart due to myocardial injury. This remodeling is the root cause that precipitates ventricular arrhythmias, which often lead to sudden cardiac death. Cardiac remodeling occurs in response to stress, either functional stress or structural stress. This remodeling plays a vital role in the disease process that ensues. Initially, the electrical and structural remodeling helps in compensating the cardiac performance. But over time, these compensatory mechanisms often lead to pump failure and/or fatal arrhythmias. Both atria and ventricles are affected by electrical remodeling. This process eventually leads to atrial fibrillation and fatal ventricular arrhythmias. Structural remodeling of the heart can be physiologic growth occurring in response to exercise, pregnancy, or during the postnatal period. It can also be pathologic hypertrophy in response to neurohumoral activation, injury to myocardium, or hypertension. Heart failure and malignant arrhythmia are often precipitated by pathological hypertrophy of the heart. However, they don’t occur with the physiological growth of the heart.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s2">Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s3">Issues of Concern</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s4">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s5">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-146" sec="article-146.s7">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Thom T, Haase N, Rosamond W, Howard VJ, Rumsfeld J, Manolio T, Zheng ZJ, Flegal K, O'Donnell C, Kittner S, Lloyd-Jones D, Goff DC, Hong Y, Adams R, Friday G, Furie K, Gorelick P, Kissela B, Marler J, Meigs J, Roger V, Sidney S, Sorlie P, Steinberger J, Wasserthiel-Smoller S, Wilson M, Wolf P, American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart disease and stroke statistics--2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. 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J Eval Clin Pract. 2016 Jun;22(3):329-40.</Citation><ArticleIdList><ArticleId IdType="pubmed">26552842</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31855391</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31751074</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK549884</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-37651">Anatomy, Thorax, Mitral Valve</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Sanchez Vaca</LastName><ForeName>Felipe</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Pontificia Universidad Catolica, Ecuador</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordoni</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Foundation Don Carlo Gnocchi IRCCS</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The heart has four chambers; the right and left atria and right and left ventricles. The heart also has valves that help with blood circulation, the mitral and tricuspid valves are called “atrioventricular” because of their location that is between the atriums and ventricles, and the aortic and pulmonary valves are the “arterioventricular” valves located between the ventricles and arteries. (Figure-1) The name of the mitral valve derives from the liturgical headgear (miter) of the Catholic/Christian tradition. The mitral valve also called bicuspid valve, is located between the left atrium and left ventricle and is composed of the mitral annulus, papillary muscles, anterior leaflet, and posterior leaflet and chordae tendinae, all these components form the valve apparatus which prevents the blood backflow from the left ventricle to the left atrium during systole, and during diastole allows normal blood flow from the left atrium to the left ventricle. <CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-37651" sec="article-37651.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Rajput FA, Zeltser R. 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Indian Heart J. 2001 Jan-Feb;53(1):35-7.</Citation><ArticleIdList><ArticleId IdType="pubmed">11456138</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31751074</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31613486</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK547706</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28065">Anatomy, Thorax, Heart Pulmonic Valve</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Sundjaja</LastName><ForeName>Joshua Henrina</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Atma Jaya Catholic University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordoni</LastName><ForeName>Bruno</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Foundation Don Carlo Gnocchi IRCCS</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The heart is a four-chambered organ hemodynamically functioning as a reservoir and a pump; it receives deoxygenated blood from the systemic circulation through the superior and inferior vena cava in the right atrium and oxygenated blood from the lung via the four pulmonary veins. The heart pumps deoxygenated blood from the right ventricle to the lungs and at the same time pumps oxygenated blood from the left ventricle into the aorta. These processes are orchestrated by the electric conduction system which coordinates the rhythmic contractions of the atria and ventricles, and the opening and closure of the heart valves. The heart valves are especially important to effectively maintain the systolic and diastolic phase of the cardiac cycle. There are two types of heart valves; the atrioventricular valves (mitral, tricuspid) and the semilunar valves (aortic and pulmonic). The pulmonic valve physically separates the right ventricle from the pulmonary trunk. While there is more literature on the other heart valves, little is known about the intricate function of the pulmonary valve and its role in various disorders.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s10">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28065" sec="article-28065.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Ho SY, Nihoyannopoulos P. 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Fetal Pediatr Pathol. 2019 Feb;38(1):57-62.</Citation><ArticleIdList><ArticleId IdType="pubmed">30661433</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31613486</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">31082032</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK540988</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-43039">Neuroanatomy, Cerebral Aqueduct (Sylvian)</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Rubino</LastName><ForeName>Jessica M.</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>West Virginia University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hogg</LastName><ForeName>Jeffery P.</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>West Virginia University School of Med.</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Galen initially described the ventricular system of the brain. As more information arose about the anatomy of the brain, anatomists described the cerebral aqueduct as a narrow communication duct between the third and fourth ventricles. The word aqueduct comes from the Latin word “aqueductus" which translates to a canal used for taking water through a structure to another location. It is unclear when the eponym ‘Aqueduct of Sylvius’ first appeared; it is believed to be traced back to the well-known anatomist Franciscus Sylvius. The cerebral aqueduct (of Sylvius) plays an essential role in the ventricular system of the brain and when disrupted can have some significant clinical manifestations.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-43039" sec="article-43039.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Mortazavi MM, Adeeb N, Griessenauer CJ, Sheikh H, Shahidi S, Tubbs RI, Tubbs RS. 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Pineal region tumors: Clinical symptoms and syndromes. Neurochirurgie. 2015 Apr-Jun;61(2-3):106-12.</Citation><ArticleIdList><ArticleId IdType="pubmed">24439798</ArticleId></ArticleIdList></Reference><Reference><Citation>Recinos PF, Rahmathulla G, Pearl M, Recinos VR, Jallo GI, Gailloud P, Ahn ES. Vein of Galen malformations: epidemiology, clinical presentations, management. Neurosurg Clin N Am. 2012 Jan;23(1):165-77.</Citation><ArticleIdList><ArticleId IdType="pubmed">22107867</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31082032</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30844183</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK538156</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-19499">Neuroanatomy, Choroid Plexus</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Javed</LastName><ForeName>Kinaan</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Upike-KYCOM</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reddy</LastName><ForeName>Vamsi</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>McKinsey & Company</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lui</LastName><ForeName>Forshing</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>CA Northstate Uni, College of Med</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The choroid plexus is a complex network of capillaries lined by specialized cells and has various functions. One of the primary functions is to produce cerebrospinal fluid (CSF) via the ependymal cells that line the ventricles of the brain. Secondly, the choroid plexus serves as a barrier in the brain separating the blood from the CSF, known as the blood-CSF barrier. In addition to these vital functions, the choroid plexus also secretes various growth factors that maintain the stem cell pool in the subventricular zone. Not only are these functions necessary for successful brain development, but they are also essential to protect against harmful microbes and toxins.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s7">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-19499" sec="article-19499.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Lun MP, Monuki ES, Lehtinen MK. Development and functions of the choroid plexus-cerebrospinal fluid system. Nat Rev Neurosci. 2015 Aug;16(8):445-57.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4629451</ArticleId><ArticleId IdType="pubmed">26174708</ArticleId></ArticleIdList></Reference><Reference><Citation>Strazielle N, Ghersi-Egea JF. Choroid plexus in the central nervous system: biology and physiopathology. J Neuropathol Exp Neurol. 2000 Jul;59(7):561-74.</Citation><ArticleIdList><ArticleId IdType="pubmed">10901227</ArticleId></ArticleIdList></Reference><Reference><Citation>Kaur C, Rathnasamy G, Ling EA. The Choroid Plexus in Healthy and Diseased Brain. J Neuropathol Exp Neurol. 2016 Mar;75(3):198-213.</Citation><ArticleIdList><ArticleId IdType="pubmed">26888305</ArticleId></ArticleIdList></Reference><Reference><Citation>Dziegielewska KM, Ek J, Habgood MD, Saunders NR. Development of the choroid plexus. Microsc Res Tech. 2001 Jan 01;52(1):5-20.</Citation><ArticleIdList><ArticleId IdType="pubmed">11135444</ArticleId></ArticleIdList></Reference><Reference><Citation>Lopez JA, Reich D. Choroid plexus cysts. J Am Board Fam Med. 2006 Jul-Aug;19(4):422-5.</Citation><ArticleIdList><ArticleId IdType="pubmed">16809660</ArticleId></ArticleIdList></Reference><Reference><Citation>Okano A, Ogiwara H. Long-term follow-up for patients with infantile hydrocephalus treated by choroid plexus coagulation. J Neurosurg Pediatr. 2018 Dec 01;22(6):638-645.</Citation><ArticleIdList><ArticleId IdType="pubmed">30215586</ArticleId></ArticleIdList></Reference><Reference><Citation>Trevisi G, Frassanito P, Di Rocco C. Idiopathic cerebrospinal fluid overproduction: case-based review of the pathophysiological mechanism implied in the cerebrospinal fluid production. Croat Med J. 2014 Aug 28;55(4):377-87.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4157373</ArticleId><ArticleId IdType="pubmed">25165051</ArticleId></ArticleIdList></Reference><Reference><Citation>Lay CM. Low Cerebrospinal Fluid Pressure Headache. Curr Treat Options Neurol. 2002 Sep;4(5):357-363.</Citation><ArticleIdList><ArticleId IdType="pubmed">12162924</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30844183</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30844167</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK538140</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17732">Anatomy, Thorax, Heart Aorta</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shahoud</LastName><ForeName>James S.</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>Lake Erie College of Osteopathic Med.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miao</LastName><ForeName>Julia H.</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Cornell University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bolla</LastName><ForeName>Srinivasa Rao</ForeName><Initials>SR</Initials><AffiliationInfo><Affiliation>Imam Abdulrahman Bin Faisal University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The aorta is the largest vessel within the human body. It originates from the left ventricle of the heart anterior to the pulmonary artery before arching posteriorly and descending along the posterior mediastinum. It descends to the level of the L4 vertebral body where it bifurcates into the left and right common iliac arteries. It is the main artery in the body and distributes oxygenated blood to the entire systemic circulation. This section will be limited to the thoracic portion of the aorta, which includes the ascending aorta, aortic arch, and descending thoracic aorta before it crosses the level of the diaphragm where it becomes the abdominal aorta. The thoracic aorta is responsible for supplying oxygenated blood to multiple structures, including the head, neck, upper extremities, and thoracic structures.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s4">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s5">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s6">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17732" sec="article-17732.s9">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Kau T, Sinzig M, Gasser J, Lesnik G, Rabitsch E, Celedin S, Eicher W, Illiasch H, Hausegger KA. 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Cardiol Clin. 1999 Nov;17(4):615-35; vii.</Citation><ArticleIdList><ArticleId IdType="pubmed">10589336</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30844167</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30726042</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537357</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28593">Anatomy, Thorax, Heart Right Coronary Arteries</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Saxton</LastName><ForeName>Anthony</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Miami</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaudhry</LastName><ForeName>Raheel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Ross University School Of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manna</LastName><ForeName>Biagio</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>RWJUH/Barnabas Health System</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The coronary arteries are the first vessels to branch from the aorta, and they provide a crucial supply of oxygen and nutrients to the layers of the heart. The right coronary artery and its branches mostly supply the right side of the heart, although they also reach part of the left atrium, a posterior portion of the left ventricle, and even the posterior third of the interventricular septum. Unlike vessels in peripheral locations of the body, these vessels dilate during exertion to meet the increased demands of the myocardium. However, the lack of anastomoses amongst the coronary arteries leaves the heart at risk of ischemia and infarction if blood flow through the vessels is severely compromised, such as with atherosclerosis.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s10">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28593" sec="article-28593.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Villa AD, Sammut E, Nair A, Rajani R, Bonamini R, Chiribiri A. 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Jan 19, Coronary CT Angiography.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30726042</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30726004</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK537319</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-42474">Anatomy, Abdomen and Pelvis: Aorta</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>White</LastName><ForeName>Hunter J.</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>Alabama College of Osteopathic Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordes</LastName><ForeName>Stephen J.</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Surgery, Louisiana State University Health Sciences Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Borger</LastName><ForeName>Judith</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Campbell Un. School of Osteopathic Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The aorta is the first and largest artery in the body. It is responsible for transporting nutrient-rich blood to the systemic circulation following ejection from the left ventricle of the heart. The aorta extends from the aortic valve of the left ventricle to the proximal iliac bifurcation at the L4 vertebral level. The vessel can be divided into various segments depending on course and location. The thoracic aorta consists of the ascending aorta, aortic arch, and descending aorta. The descending thoracic aorta passes through the diaphragm’s aortic hiatus at the T12 vertebral level at which point it continues as the abdominal aorta. The abdominal aorta terminates as it bifurcates into common iliac arteries, which subsequently provide arterial supply to the pelvis and lower limbs.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-42474" sec="article-42474.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Collins JA, Munoz JV, Patel TR, Loukas M, Tubbs RS. 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Clin Anat. 2014 Nov;27(8):1264-74.</Citation><ArticleIdList><ArticleId IdType="pubmed">25065617</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30726004</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30725672</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK536987</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-27862">Prosthetic Heart Valve</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mathew</LastName><ForeName>Philip</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>St. Luke's at Des Peres Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanmanthareddy</LastName><ForeName>Arun</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Texas Houston</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The heart is a specialized vascular structure with an intrinsic pumping mechanism to direct oxygenated blood and nutrients to the tissues of the body.  Basic physics informs us that pressure gradients provide the physical impetus for fluid flow and the force generated by myocardial contraction drives blood flow into systemic and pulmonary circulation.  Myocardial relaxation generates a drop in pressure that promotes retrograde blood flow. Prevention of this retrograde blood flow is by the presence of heart valves which open and close due to changes in pressure. The heart has four valves: the mitral valve, aortic valve, tricuspid valve, and pulmonic valve.  The mitral and tricuspid valves are collectively known as the <i>atrioventricular valves</i> due to their anatomical location at the junction of the atrium and ventricle. Their primary function is to prevent retrograde blood flow into the atria during ventricular systole. 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They arise from the right ventricle of the four-chambered heart and transport blood to the lungs. De-oxygenated blood from the body's somatic cells travels to the right atrium, then into the right ventricle, and through the main pulmonary artery and its branches before blood enters the lungs for oxygenation and gas exchange. These steps are all prerequisites for normal human physiologic function.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28002" sec="article-28002.s13">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Kandathil A, Chamarthy M. 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Radiology. 1997 Nov;205(2):447-52.</Citation><ArticleIdList><ArticleId IdType="pubmed">9356627</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30521233</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30422527</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK532932</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32436">Neuroanatomy, Ventricular System</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Shenoy</LastName><ForeName>Saraswati Satyanarayan</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Seth G S Med College & KEM Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lui</LastName><ForeName>Forshing</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>CA Northstate Uni, College of Med</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The ventricular system of the brain is an interconnected series of cavities filled with cerebrospinal fluid (CSF) that cushions the brain. Though the presence of cerebral ventricles was known since ancient times, its function was obscure. Early scientists believed ventricles to be the site of thought, emotions, reasoning, and memory. Leonardo da Vinci, the famed artist who drew Mona Lisa, performed the first ventriculography on the brain of an ox. However, in the 17th century, it was Domenico Felice Antonio Cotugno who first described the connection between cerebral ventricles and subarachnoid space, a fact later confirmed by Francis Jean Magendie.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s7">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s8">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32436" sec="article-32436.s10">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Schiller F. 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Neuroimage. 2012 Jan 02;59(1):154-67.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC3319053</ArticleId><ArticleId IdType="pubmed">21787868</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30422527</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30247839</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK525964</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-40416">Anatomy, Abdomen and Pelvis: Abdominal Aorta</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Tran</LastName><ForeName>Clement T.</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>California Northstate College Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Cheng Ying</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Ross University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bordes</LastName><ForeName>Stephen J.</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Surgery, Louisiana State University Health Sciences Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lui</LastName><ForeName>Forshing</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>CA Northstate Uni, College of Med</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The aorta is the main artery of the human body. It arises from the left ventricle of the heart and travels superiorly to form the ascending aorta. It then loops inferiorly to form the arch of the aorta and through the thorax to form the thoracic aorta. After crossing the diaphragm into the abdomen, the aptly-named abdominal aorta eventually bifurcates into the common iliac arteries in the lower abdomen. Along the way, the aorta gives rise to the arterial branches that are responsible for transmitting oxygenated blood to all the tissues of the body. As such, pathology arising in the aorta frequently results in serious consequences. Thus, it is important for the clinician to be aware of the functional, anatomical, surgical, and clinical considerations about the aorta.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s5">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s6">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s7">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s8">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s9">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s10">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-40416" sec="article-40416.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Loukas M, Bilinsky E, Bilinsky S, Blaak C, Tubbs RS, Anderson RH. 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Vasa. 2012 May;41(3):163-76.</Citation><ArticleIdList><ArticleId IdType="pubmed">22565618</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30247839</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30020697</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK513325</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32314">Anatomy, Thorax, Phrenic Nerves</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Oliver</LastName><ForeName>Kaitlin A.</ForeName><Initials>KA</Initials></Author><Author ValidYN="Y"><LastName>Ashurst</LastName><ForeName>John V.</ForeName><Initials>JV</Initials><AffiliationInfo><Affiliation>Kingman Regional Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The phrenic nerve originates from the anterior rami of C3 through C5 and traverses the neck, heart, and lungs to reach the diaphragm. From its origin, the phrenic nerve descends vertically caudad and adjacent to the internal jugular vein. In the neck and upper thorax, the left phrenic nerve tracts proximal to the subclavian artery. The right phrenic nerve runs superficial to the anterior scalene muscle and the second part of the right subclavian artery. In the thorax, the right and left phrenic nerve will continue to descend anteriorly to the root of the lung and between the mediastinal surface of the parietal pleura and fibrous pericardium. The right phrenic nerve passes lateral to the right atrium and right ventricle and will continue to descend through the vena cava hiatus in the diaphragmatic opening at the level of T8. The left phrenic nerve descends anterior to the pericardial sac of the left ventricle and terminates at the central tendon of the diaphragm.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s5">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32314" sec="article-32314.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Bains KNS, Kashyap S, Lappin SL. 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J Thorac Cardiovasc Surg. 2003 Aug;126(2):582-3.</Citation><ArticleIdList><ArticleId IdType="pubmed">12928662</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30020697</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29261997</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK470179</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28281">Anatomy, Head and Neck, Larynx Recurrent Laryngeal Nerve</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Allen</LastName><ForeName>Evan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Ohio University HCOM</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Minutello</LastName><ForeName>Katrina</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Michigan State University College of Osteopathic Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murcek</LastName><ForeName>Benjamin W.</ForeName><Initials>BW</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The larynx is a dynamic, flexible structure composed of a cartilaginous core with interconnecting membranes and associated musculature. The larynx is a midline structure positioned at the interface between the digestive and respiratory tracts. In addition to housing the vocal cords and producing phonation, the larynx assists with multiple other functions including but not limited to: airway protection, regulating intrathoracic pressures, and regulating intra-abdominal pressures. The anatomical position, composition, associated musculature and innervation of the larynx all contribute to this structure’s capabilities. <b>Laryngeal Position</b> The anatomical position of the larynx is also dynamic in nature and varies from birth to maturity. Initially, at birth and for the first couple years of life, the larynx is further superior in the neck than in adults. In infants, this high position results in direct contact between the soft palate and epiglottis. This allows inspired air to move from the nose to the trachea directly. It is because of this anatomical relationship; an infant is able to swallow liquids and breathe almost simultaneously. By adulthood, the larynx descends inferiorly to its final position. The larynx is found within the visceral compartment of the neck and serves as the “floor” of the anterior triangle of the neck. The larynx is the superior portion of the respiratory tract and aligned on its long axis, is vertically adjacent to the trachea, which lies directly inferior to the larynx and is connected via the cricotracheal ligament. Anterosuperiorly, the larynx articulates with the hyoid bone via the thyrohyoid membrane. Dorsally, the larynx attaches to the muscular walls of the pharynx. <b>Laryngeal Skeleton</b> The larynx is composed of nine contributing cartilages: three unpaired cartilages and three paired cartilages, which share connections to each other, the hyoid (superiorly), and the trachea (inferiorly). The epiglottic, thyroid, and cricoid cartilages make up the three unpaired cartilages and are arranged superior to inferior respectively. The thyroid cartilage, with the epiglottic cartilage superior, predominates anteriorly and forms the laryngeal prominence (i.e., Adam’s Apple), while the predominate cartilage dorsally is the cricoid cartilage which sits inferior to the thyroid cartilage. The three paired cartilages include the arytenoid, corniculate, and cuneiform cartilages. The paired arytenoid cartilages are found on the dorsal aspect of the larynx, attached superiorly to the cricoid cartilage. Both arytenoid cartilages give off a lateral extension (muscular process) and anterior extension (vocal process) which aid in supporting the vocal ligaments. Additionally, each arytenoid cartilage has an associated corniculate and cuneiform cartilage. These two small, paired cartilages border the opening into the laryngeal vestibule both dorsally and laterally. The corniculate cartilage can be found at the apex of both arytenoid cartilages. The cuneiform cartilage can be found sitting anterior and lateral to both arytenoids. These cartilages form connections via numerous membranes, ligaments, and synovial joints. There are two essential synovial joints associated with the larynx. One pair of synovial joints exists between the thyroid and cricoid cartilages. This joint allows the thyroid cartilage to rotate about the cricoid cartilage and allows the cricoid cartilage to separate from or approximate to the thyroid cartilage anteriorly. The second set of synovial joints exists between the cricoid and arytenoids (cricoarytenoid synovial joint). The cricoarytenoid synovial joint allows the arytenoid cartilages to translate on both an anterior-posterior axis and lateral-medial axis, as well as rotate about a cranial-caudal axis. <b>Laryngeal Folds and Membranes</b> The aryepiglottic folds extend over the lateral aspects of epiglottic, cuneiform, corniculate and arytenoid cartilages. The aryepiglottic folds demarcate the opening into the laryngeal lumen. The piriform sinus can be found just lateral to the aryepiglottic folds, which form the medial border of these sinuses. This is sometimes referred to as the lateral food channel. The aryepiglottic folds serve as a protective wall that prevents food from passing into the laryngeal aditus and together, with the associated cartilages forms a protective ring. This ring is not uniform in height, at the dorsal-most aspect, there is a reduction in the height of this fold creating susceptibility to food or liquid incursions. This is called the interarytenoid notch. The laryngeal ventricle is the fossa or sinus that lies between the vocal and vestibular folds on either side. The vocal folds are commonly referred to as the vocal cords and the vestibular folds as the false vocal cords. The laryngeal ventricle also demarcates the separation between the quadrangular membrane superiorly, and the cricovocal membrane found inferiorly. These two membranes together cover the entire interior portion of the larynx from the epiglottic and arytenoid cartilages superiorly to the cricoid cartilage inferiorly. These membranes are bilateral. The quadrangle membrane gives support to the aryepiglottic folds superiorly and continues inferiorly as the vestibular folds. The vestibular folds contain the vestibular ligament, which extends from the arytenoid cartilage to the thyroid cartilage. The vestibular folds appear to have no role in phonation and are relatively immobile structures. The laryngeal ventricle begins inferiorly to the free edge of the vestibular fold and continues laterally. The ventricle exists bilaterally, and secretes mucus over the superior surface of the vocal folds, forming a protective layer. The lateral cricothyroid ligament is contained within the cricovocal membrane. Like the vestibular ligament, this ligament also extends from the arytenoid cartilage to the thyroid cartilage. However, the lateral cricothyroid ligament also follows the cricoid cartilage as it extends inferiorly. In addition, this ligament gives rise to the vocal ligament as it thickens superiorly. The vocal ligament extends from the thyroid cartilage [luminal surface] to the vocal process of the arytenoid cartilage. The conus elasticus is a collective term for the cricovocal membrane and its contained ligaments. The medial convergence of these ligaments support the vocal folds. The vocal folds, also known as the true vocal cords, are medial projections of the walls of the larynx that can approximate to each other in the midline to completely obstruct the lumen of the larynx. These vocal folds delineate the plane referred to as the glottis. Within these vocal folds is a muscle known as vocalis muscle which runs aside the vocal ligament. The ligament and lack of blood vessels on the surface of the folds result in the characteristic white appearance of the pair of vocal folds. This provides visual distinction compared to the pink appearing vestibular folds. The space found between the vocal folds is termed the rima glottides. <b>Laryngeal Cavity</b> The laryngeal inlet/aditus is used to refer to the entrance of the cavity of the larynx. Superior to the inlet is the laryngopharynx. The cavity of the larynx is divided into three regions: Supraglottic space: at the level of the vestibular folds. Bounded anteriorly by epiglottis, laterally by the aryepiglottic folds and posteriorly by the inter arytenoid mucosa. Laryngeal ventricles: The middle region of the laryngeal cavities is composed of the paired laryngeal ventricles that fall between the vestibular and vocal folds. Subglottic space: also referred to as the infraglottic space, continues downward as far inferior as the junction between the cricoid and trachea.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s2">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s3">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s4">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s5">Muscles</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s6">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s7">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s8">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28281" sec="article-28281.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Sun H, Wu CW, Zhang D, Makay Ö, Zhao Y, Carcofaro P, Kim HY, Dionigi G, Pino A, Caruso E, Pontin A, Pappalardo V. 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Paediatr Respir Rev. 2018 Jun;27:74-85.</Citation><ArticleIdList><ArticleId IdType="pubmed">29336933</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29261997</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29261906</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK470522</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-32357">Anatomy, Thorax, Heart Arteries</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaudhry</LastName><ForeName>Raheel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Ross University School Of Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rahman</LastName><ForeName>Sajedur</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Law</LastName><ForeName>Mark A.</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Childrens of AL, Un of AL at Birmingham</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The coronary arteries provide the main blood supply to the heart. The coronary arteries also supply the myocardium with oxygen to allow for the contraction of the heart and thus causing circulation of the blood throughout the body. Two main coronary arteries originate from the base of the aorta as it exits the left ventricle: the left and right coronary arteries. These arteries further branch into smaller arteries to supply specific parts of the heart like the atria, ventricles, SA, and AV nodes. It is important to realize that the paths these arteries take may vary slightly from person to person.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s3">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s4">Nerves</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s5">Physiologic Variants</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s6">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s7">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s8">Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s9">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-32357" sec="article-32357.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>25</Day></ContributionDate><ReferenceList><Reference><Citation>Lee YJ, Park KS, Kil HR. 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It occupies the central spinal canal, the ventricular system, and the subarachnoid space. It is produced mostly by the choroidal plexus of the ventricular system as well as its ependymal lining. The CSF has a physiologic volume of about 150 ml with a daily turnover of about 500 ml. Produced mostly in the lateral ventricles, the CSF passes through the interventricular foramen (of Monro), into the third ventricle. It exits the third ventricle through the cerebral aqueduct (of Sylvius) into the fourth ventricle. It exits the fourth ventricle into the cerebral subarachnoid space through the median aperture of Magendie and the two lateral apertures of Luschka. The CSF continues into the spinal subarachnoid space through the central canal of the spinal cord. Normal CSF pressure (8 mmHg to 15 mmHg supine and about 20 mmHg erect) is a function of a tightly maintained equilibrium in rates of production and resorption of CSF. The out-pouching of the arachnoid mater called arachnoid granulations are responsible for the resorption of  CSF into the dural venous sinuses. Disequilibrium in synthesis and resorption or obstruction of circulation results in  CSF accumulation and raised intracranial pressure called hydrocephalus. |
2,329,722 | T1 values and extracellular volume fraction in asymptomatic subjects: variations in left ventricular segments and correlation with cardiovascular risk factors. | To evaluate variations in pre-contrast (preT1) and post-contrast (postT1) myocardial T1 values and extracellular volume fraction (ECV) according to left ventricular (LV) segments and to find correlations between them and cardiovascular risk factors. The 233 asymptomatic subjects (210 men, 23 women; aged 54.1 ± 6.0 years) underwent cardiac magnetic resonance imaging with preT1 and postT1 mapping on a 1.5-T scanner. T1 values and ECVs were evaluated according to LV segments, age, sex, and estimated glomerular filtration rate (eGFR). Based on the presence of hypertension (HTN) and diabetes mellitus (DM), subjects were subdivided into the control, HTN, DM, and HTN and DM (HTN-DM) groups. T1 values and ECV showed significant differences between septal and lateral segments at the mid-ventricular and basal levels (p ≤ 0.003). In subgroup analysis, the HTN-DM group showed a significantly higher ECV (0.260 ± 0.023) than the control (0.240 ± 0.021, p = 0.011) and HTN (0.241 ± 0.024, p = 0.041) groups. Overall postT1 and ECV of the LV had significant correlation with eGFR (r = 0.19, p = 0.038 for postT1; r =  - 0.23, p = 0.011 for ECV). Septal segments show higher preT1 and ECV but lower postT1 than lateral segments at the mid-ventricular and basal levels. ECV is significantly affected by HTN, DM, and eGFR, even in asymptomatic subjects. |
2,329,723 | Diagnosis and Surgical Management of Neonatal Hydrocephalus. | Neonatal hydrocephalus represents an important pathological condition with significant impact on medical care and neurocognitive development. This condition requires early recognition, appropriate medical and surgical management, and long-term surveillance by clinicians and pediatric neurosurgeons. Common etiologies of neonatal and infant hydrocephalus include intraventricular hemorrhage related to prematurity with subsequent post-hemorrhagic hydrocephalus, myelomeningocele, and obstructive hydrocephalus due to aqueductal stenosis. Clinical markers of elevated intracranial pressure include rapid increases in head circumference across percentiles, elevation and firmness of the anterior fontanelle, splitting or splaying of cranial sutures, upgaze palsy, lethargy, frequent emesis, or episodic bradycardia (unrelated to other comorbidities). Complementing these clinical markers, imaging modalities used for the diagnosis of neonatal hydrocephalus include head ultrasonography, brain magnetic resonance imaging, and head computed tomography in urgent or emergent situations. Following diagnosis, temporizing measures may be employed prior to definitive treatment and include ventricular access device or ventriculo-subgaleal shunt insertion. Definitive surgical management involves permanent cerebrospinal fluid (CSF) diversion via CSF shunt insertion, or endoscopic third ventriculostomy with or without choroid plexus cauterization. Surgical decision-making and approaches vary based on patient age, hydrocephalus etiology, neuroanatomy, imaging findings, and medical comorbidities. Indications, surgical techniques, and clinical outcomes of these procedures continue to evolve and elicit significant attention in the research environment. In this review we describe the epidemiology, pathophysiology, clinical markers, imaging findings, early management, definitive surgical management, and clinical outcomes of pediatric patients with neonatal hydrocephalus. |
2,329,724 | Proteomic and Metabolomic Analyses of Right Ventricular Failure due to Pulmonary Arterial Hypertension.<Pagination><StartPage>834179</StartPage><MedlinePgn>834179</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">834179</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fmolb.2022.834179</ELocationID><Abstract><AbstractText>Right ventricular failure (RVF) is the independent and strongest predictor of mortality in pulmonary arterial hypertension (PAH), but, at present, there are no preventive and therapeutic strategies directly targeting the failing right ventricle (RV). The underlying mechanism of RV hypertrophy (RVH) and dysfunction needs to be explored in depth. In this study, we used myocardial proteomics combined with metabolomics to elucidate potential pathophysiological changes of RV remodeling in a monocrotaline (MCT)-induced PAH rat model. The proteins and metabolites extracted from the RV myocardium were identified using label-free liquid chromatography-tandem mass spectrometry (LC-MS/MS). The bioinformatic analysis indicated that elevated intracellular Ca<sup>2+</sup> concentrations and inflammation may contribute to myocardial proliferation and contraction, which may be beneficial for maintaining the compensated state of the RV. In the RVF stage, ferroptosis, mitochondrial metabolic shift, and insulin resistance are significantly involved. Dysregulated iron homeostasis, glutathione metabolism, and lipid peroxidation related to ferroptosis may contribute to RV decompensation. In conclusion, we depicted a proteomic and metabolomic profile of the RV myocardium during the progression of MCT-induced PAH, and also provided the insights for potential therapeutic targets facilitating the retardation or reversal of RV dysfunction in PAH.</AbstractText><CopyrightInformation>Copyright © 2022 Qin, Lei, Yan, Sun, Liu, Guo, Sun, Guo and Fang.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Qin</LastName><ForeName>Xiaohan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>Chuxiang</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Haidan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Zhengguang</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Wei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Xiaoxiao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Quan</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Mol Biosci</MedlineTA><NlmUniqueID>101653173</NlmUniqueID><ISSNLinking>2296-889X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ferroptosis</Keyword><Keyword MajorTopicYN="N">metabolome</Keyword><Keyword MajorTopicYN="N">proteome</Keyword><Keyword 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Res. 19 (1), 94. 10.1186/s12931-018-0800-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1186/s12931-018-0800-5</ArticleId><ArticleId IdType="pmc">PMC5948901</ArticleId><ArticleId IdType="pubmed">29751839</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35864813</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>22</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Single ventricular strain measures correlate with peak oxygen consumption in children and adolescents with Fontan circulation. | Right ventricular failure (RVF) is the independent and strongest predictor of mortality in pulmonary arterial hypertension (PAH), but, at present, there are no preventive and therapeutic strategies directly targeting the failing right ventricle (RV). The underlying mechanism of RV hypertrophy (RVH) and dysfunction needs to be explored in depth. In this study, we used myocardial proteomics combined with metabolomics to elucidate potential pathophysiological changes of RV remodeling in a monocrotaline (MCT)-induced PAH rat model. The proteins and metabolites extracted from the RV myocardium were identified using label-free liquid chromatography-tandem mass spectrometry (LC-MS/MS). The bioinformatic analysis indicated that elevated intracellular Ca<sup>2+</sup> concentrations and inflammation may contribute to myocardial proliferation and contraction, which may be beneficial for maintaining the compensated state of the RV. In the RVF stage, ferroptosis, mitochondrial metabolic shift, and insulin resistance are significantly involved. Dysregulated iron homeostasis, glutathione metabolism, and lipid peroxidation related to ferroptosis may contribute to RV decompensation. In conclusion, we depicted a proteomic and metabolomic profile of the RV myocardium during the progression of MCT-induced PAH, and also provided the insights for potential therapeutic targets facilitating the retardation or reversal of RV dysfunction in PAH.<CopyrightInformation>Copyright © 2022 Qin, Lei, Yan, Sun, Liu, Guo, Sun, Guo and Fang.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Qin</LastName><ForeName>Xiaohan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>Chuxiang</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Haidan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Zhengguang</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Wei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Core Facility of Instrument, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Xiaoxiao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Quan</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Mol Biosci</MedlineTA><NlmUniqueID>101653173</NlmUniqueID><ISSNLinking>2296-889X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ferroptosis</Keyword><Keyword MajorTopicYN="N">metabolome</Keyword><Keyword MajorTopicYN="N">proteome</Keyword><Keyword MajorTopicYN="N">pulmonary 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Res. 19 (1), 94. 10.1186/s12931-018-0800-5</Citation><ArticleIdList><ArticleId IdType="doi">10.1186/s12931-018-0800-5</ArticleId><ArticleId IdType="pmc">PMC5948901</ArticleId><ArticleId IdType="pubmed">29751839</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35864813</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>22</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal><ArticleTitle>Single ventricular strain measures correlate with peak oxygen consumption in children and adolescents with Fontan circulation.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>7</EndPage><MedlinePgn>1-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1017/S1047951122002323</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Children with a single ventricle post-Fontan palliation are at increased risk of poor outcomes with peak oxygen consumption acting as a surrogate outcome marker. The purpose of this study is to evaluate the relationship between peak oxygen consumption and echocardiographic measures of ventricular function and deformation, including ventricular global longitudinal strain and dyssynchrony, in children and adolescents following Fontan palliation.<AbstractText Label="METHODS" NlmCategory="METHODS">Patients (age 8-21 years) with single ventricle post-Fontan palliation were prospectively recruited and participated in an echocardiogram, including views optimised for two-dimensional speckle tracking, and a cardiopulmonary exercise test on a cycle ergometer to maximal volitional fatigue.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Thirty-eight patients (mean age 13.7 ± 2.3 years) post-Fontan palliation had either a single left ventricular (n = 20), single right ventricular (n = 14), or biventricular (n = 4) morphology. Peak oxygen consumption (24.9 ± 5.6 ml/kg/minute) was correlated with global longitudinal strain (r = -0.435, p = 0.007), a strain discoordination time to peak index (r = -0.48, p = 0.003), and the presence of an electro-mechanical dyssynchrony strain pattern (p = 0.008). On multivariate regression modelling, these three variables were associated with peak oxygen consumption independently of age and sex. The single right ventricular group had evidence of possible diastolic dysfunction by E/e' compared to the single left ventricular and biventricular groups (p = 0.001).<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Strain analysis measures are correlated with peak oxygen consumption in this cohort of children, adolescents, and young adults following Fontan palliation, suggesting that ventricular mechanics may influence the efficiency of the Fontan circulation. |
2,329,725 | Ventriculocholecystal Shunt as a Salvage Procedure in Shunt Dependent Hydrocephalic Children with Compromised Peritoneal Cavity. | Multiple shunt revisions are a formidable challenge in neurosurgery, as the surgeon faces progressive difficulties in finding suitable distal sites for implantation. Gallbladder offers an alternative safe implantation site of distal catheter in case of repeated peritoneal failures. We describe two such cases done in our institute in this brief report. One case has long term functioning shunt, whist other had complications. Relevant literature is also briefly reviewed here. |
2,329,726 | Cerebrospinal Fluid Flow Analysis in Tuberculous Meningitis Using Phase Contrast Technique on 3 Tesla MRI: A New Paradigm and Our Initial Experience. | Phase-contrast magnetic resonance imaging (PC-MRI) has been used for studying cerebrospinal fluid (CSF) dynamics in various CSF related disorders at aqueduct of Sylvius.</AbstractText>To analyze the CSF flow dynamics qualitatively and quantitatively using PC-MRI across the aqueduct of Sylvius in diagnosed patients of tuberculous meningitis.</AbstractText>Thirty patients, clinically diagnosed with tuberculous meningitis and mean age of 24 years (range: 12-60 years) were taken up to study the changes in CSF flow dynamics using PC-MRI with retrospective cardiac gating. Thirty age and sex matched healthy volunteers were also included for comparison and reference values. Flow quantification was done by through-plane scans acquired in the axial plane perpendicular to the aqueduct. For qualitative examination, in-plane phase contrast scans were acquired in the mid-sagittal plane. Encoding velocity was kept in craniocaudal direction. Calculated parameters were peak velocity (cm/s), average velocity (cm/s), average flow (mL/s), net forward volume (mL), and stroke volume (μL).</AbstractText>Qualitatively, loss of normal sinusoidal waveform of CSF flow was noted in two cases of hydrocephalus with exaggerated flows. Quantitatively, CSF flow parameters showed marked numerical difference in tuberculous meningitis patients with hydrocephalus on comparison with healthy volunteers and with cases without hydrocephalus.</AbstractText>PC-MRI is a sensitive technique to analyze altered CSF flow dynamics in tuberculous meningitis patients. This is a useful adjunct in imaging these patients to extract both the qualitative and quantitative information about CSF flow for comprehensive evaluation.</AbstractText> |
2,329,727 | Risk Factors for and Outcomes of Postoperative Entrapped Temporal Horn in Trigone Meningiomas. | Meningioma in the ventricle triangle area is a benign tumor that can be cured by surgery, but postoperative entrapped temporal horn may seriously affect the patient's quality of life and even require a second operation. Currently, there are few reports on this complication.</AbstractText>The risk factors and prognosis of postoperative ETH in trigone meningiomas were investigated.</AbstractText>A retrospective analysis of the clinical data of 87 patients with trigone meningioma from 2010 to 2018 was performed, and univariate and multivariate analyses were used to assess the risk factors associated with postoperative ETH. The degree of ETH was evaluated using the modified ventriculocranial ratio.</AbstractText>The incidence of postoperative ETH in trigone meningioma was 29.9% (26/87). Preoperative ETH [odds ratio (OR): 4.826, 95% confidence interval (CI): 1.820-12.796, P = 0.002] and postoperative meningitis (OR: 12.811, 95%CI: 1.615-101.605, P = 0.016) are independent risk factors for postoperative ETH. Of the 18 patients with ETH syndrome, 12 improved after medical treatment, and finally, a total of 6 patients received ETH surgery. The mean duration from tumor resection to the appearance of ETH syndrome was 3.1 ± 1.9 months (range: 9 days-7 months). Patients with ETH grade II and III are more prone to clinical symptoms.</AbstractText>: The incidence of postoperative ETH for trigone meningiomas is high, and clinical symptoms generally appear delayed after surgery. Reducing postoperative infections can reduce the occurrence of postoperative ETH. Patients with symptoms of ETH who have failed medical treatment have clear indications for surgery.</AbstractText> |
2,329,728 | Surgical Treatment of IV Ventricle Calcifying Pseudoneoplasm of the Neuraxis (CAPNON) Operative Nuances. | Calcifying pseudoneoplasm of the neuroaxis (CAPNON) is a rare, slow growing, and generally benign fibro osseous mass that can emerge throughout the entire central nervous system (CNS). When diagnosed, prompt surgical treatment can determine a good neurological outcome and possibly curative resolution. The objective of the present work is to present a step by step technical report with its video. We present a 37 year old female presented with occipital headache and cervical pain associated with dysphagia, nausea, and gait disturbances. Computed tomography (CT) scan showed a focal calcified lesion on the floor of the IV ventricle projecting toward the vermis with associated supratentorial hydrocephalus and transependymal edema. The telovelar approach was chosen for the procedure. The outcome was favorable, with no complications. Postoperative CT was performed, which revealed no residual lesion. A step by step report of a IV ventricle CAPNON that manifested with hydrocephalus is described. |
2,329,729 | Unveiling the gut-brain axis: structural and functional analogies between the gut and the choroid plexus vascular and immune barriers. | The vasculature plays an essential role in the development and maintenance of blood-tissue interface homeostasis. Knowledge on the morphological and functional nature of the blood vessels in every single tissue is, however, very poor, but it is becoming clear that each organ is characterized by the presence of endothelial barriers with different properties fundamental for the maintenance of tissue resident immune homeostasis and for the recruitment of blood-trafficking immune cells. The tissue specificity of the vascular unit is dependent on the presence of differentiated endothelial cells that form continues, fenestrated, or sinusoidal vessels with different grades of permeability and different immune receptors, according to how that particular tissue needs to be protected. The gut-brain axis highlights the prominent role that the vasculature plays in allowing a direct and prompt exchange of molecules between the gut, across the gut vascular barrier (GVB), and the brain. Recently, we identified a new choroid plexus vascular barrier (PVB) which receives and integrates information coming from the gut and is fundamental in the modulation of the gut-brain axis. Several pathologies are linked to functional dysregulation of either the gut or the choroid plexus vascular barriers. In this review, we unveil the structural and functional analogies between the GVB and PVB, comparing their peculiar features and highlighting the functional role of pitcher and catcher of the gut-brain axis, including their role in the establishment of immune homeostasis and response upon systemic stimuli. We propose that when the gut vascular barrier-the main protecting system of the body from the external world-is compromised, the choroid plexus gatekeeper becomes a second barrier that protects the central nervous system from systemic inflammation. |
2,329,730 | Dimorphic evaluation of hippocampal changes in rat model of demyelination: A comparative functional, morphometric, and histological study. | Multiple sclerosis (MS) is the most common autoimmune disease. Progressive depletion of the brain and spinal cord tissue appears at the onset of the disease. Several studies have shown the increased size of the ventricles of the brain and decreases in the area of the corpus callosum and the width of the brain. Other important symptoms of this disease are cognitive, learning, and memory disorders.</AbstractText>The aim of this study was to compare morphometric, histological, and functional changes in the demyelination model in both sexes.</AbstractText>In this experimental study, male and female Wistar rats were studied in four experimental groups. Demyelination was induced by the injection of ethidium bromide in the ventricular region. The chronic effect of demyelination on spatial memory, movement, and coordination was investigated using the Morris Water Maze (MWM), and clinical and balance beam tests, respectively. Myelin degradation, cell death and neurogenesis were estimated using Luxol Fast Blue staining and immunohistochemistry (Caspase-3 and Nestin markers). In addition, morphometric findings were recorded for the brain and hippocampus (weight, volume, length, width).</AbstractText>Demyelination increased the time and distance index and decreased the residence time in the target quarter in the water maze test (p < .001). It also increases the neuromuscular and modified neurological severity score (p < .01). Demyelination increases caspase-3 (p < .05) expression and decreases Nestin expression (p < .001), which are directly related to the extent of damage.</AbstractText>This study showed an interaction between hippocampal structural and functional networks in explaining spatial learning and memory in the early stages of MS.</AbstractText>© 2022 The Authors. Brain and Behavior published by Wiley Periodicals LLC.</CopyrightInformation> |
2,329,731 | A novel stem cell type at the basal side of the subventricular zone maintains adult neurogenesis. | According to the current consensus, murine neural stem cells (NSCs) apically contacting the lateral ventricle generate differentiated progenitors by rare asymmetric divisions or by relocating to the basal side of the ventricular-subventricular zone (V-SVZ). Both processes will ultimately lead to the generation of adult-born olfactory bulb (OB) interneurons. In contrast to this view, we here find that adult-born OB interneurons largely derive from an additional NSC-type resident in the basal V-SVZ. Despite being both capable of self-renewal and long-term quiescence, apical and basal NSCs differ in Nestin expression, primary cilia extension and frequency of cell division. The expression of Notch-related genes also differs between the two NSC groups, and Notch activation is greatest in apical NSCs. Apical downregulation of Notch-effector Hes1 decreases Notch activation while increasing proliferation across the niche and neurogenesis from apical NSCs. Underscoring their different roles in neurogenesis, lactation-dependent increase in neurogenesis is paralleled by extra activation of basal but not apical NSCs. Thus, basal NSCs support OB neurogenesis, whereas apical NSCs impart Notch-mediated lateral inhibition across the V-SVZ. |
2,329,732 | Mechanisms of central brain atrophy in multiple sclerosis. | Change in ventricular volume has been suggested as surrogate measure of central brain atrophy (CBA) applicable to the everyday management of multiple sclerosis (MS) patients.</AbstractText>We investigated the contribution of inflammatory activity (including the severity of lesional tissue damage) to CBA.</AbstractText>Fifty patients with relapsing-remitting multiple sclerosis (RRMS) were enrolled. Lesional activity during 4 years of follow-up was analysed using custom-build software, which segmented expanding part of the chronic lesions, new confluent lesions and new free-standing lesions. The degree of lesional tissue damage was assessed by change in mean diffusivity (MD). Volumetric change of lateral ventricles was used to measure CBA.</AbstractText>During follow-up, ventricles expanded on average by 12.6% ± 13.7% (mean ± SD</i>). There was a significant increase of total lesion volume, 69.3% of which was due to expansion of chronic lesions. Correlation between volume of combined lesional activity and CBA (r</i>2</sup> = 0.67) increased when lesion volume was adjusted by the degree of tissue damage severity (r</i>2</sup> = 0.81). Regression analysis explained 90% of CBA variability, revealing that chronic lesion expansion was by far the largest contributor to ventricular enlargement.</AbstractText>CBA is almost entirely explained by the combination of the volume and severity of lesional activity. The expansion of chronic lesions plays a central role in this process.</AbstractText> |
2,329,733 | Conservation of miR combo based direct cardiac reprogramming. | There is considerable interest in regenerating the injured heart by reprogramming resident fibroblasts into new functional cardiomyocytes. Cardiac reprogramming has been achieved via transcription factors or miRNAs. Transcription factor combinations appear to be species-specific as evidenced by the fact that combinations of transcription factors which are effective for the reprogramming of mouse fibroblasts are ineffective in pigs and humans. Whether miRNA based cardiac reprogramming suffers from the same limitation is unknown. We have previously demonstrated that mouse cardiac fibroblasts can be directly converted into cardiomyocytes both in vitro and in vivo via a combination of four microRNAs (miR-1, miR-133a, miR-208a and miR-499) termed "miR combo." To assess species-specificity, miR combo was transfected into cardiac fibroblasts isolated from the left ventricle of dogs, pigs and humans. QPCR analysis indicated that miR combo effectively reprogrammed fibroblasts from all of the tested mammalian species. Significant upregulation of cardiac developmental, sarcomere, and cardiac ion channel genes was observed. Through Actn2+ staining, we also found that miR combo transfection induced dog, pig and human cardiac fibroblasts to develop into cardiomyocyte-like cells. In conclusion, we have demonstrated that in contrast to transcription factor based approaches, miR combo effectively reprograms mammalian cardiac fibroblasts into cardiomyocyte-like cells. |
2,329,734 | A case of McKusick-Kaufman syndrome with perinatal diagnosis: Case report and literature review. | and importance: McKusick-Kaufman syndrome (MKS) is a rarely reported autosomal recessive syndrome characterized by hydrometrocolpos (HMC), polydactyly and various gastrointestinal and renal manifestations.</AbstractText>We present a case of suspected MKS in a prenatal ultrasound with dilated lateral ventricles of the brain and HMC.</AbstractText>Main differential diagnosis includes Bardet-Beidel syndrome (BBS) which can present with HMC and polydactyly but retinal manifestations are a differentiating feature from MKS.</AbstractText>Both of the disease syndromes are diagnosed clinically after birth.Keywords: McKusick Syndrome, Bardet-beidel syndrome, hydrometrocolpos, case report.</AbstractText>© 2022 The Authors.</CopyrightInformation> |
2,329,735 | Decreased Brain Ventricular Volume in Psychiatric Inpatients with Serotonin Reuptake Inhibitor Treatment. | Brain ventricles have been reported to be enlarged in several neuropsychiatric disorders and in aging. Whether human cerebral ventricular volume can decrease over time with psychiatric treatment is not well-studied. The aim of this study was to examine whether inpatients taking serotonin reuptake inhibitors (SRI) exhibited reductions in cerebral ventricular volume.</AbstractText>Psychiatric inpatients, diagnosed mainly with depression, substance use, anxiety, and personality disorders, underwent two imaging sessions (Time 1 and Time 2, approximately 4 weeks apart). FreeSurfer was used to quantify volumetric features of the brain, and ANOVA was used to analyze ventricular volume differences between Time 1 and Time 2. Inpatients' brain ventricle volumes were normalized by dividing by estimated total intracranial volume (eTIV). Clinical features such as depression and anxiety levels were collected at Time 1, Time 1.5 (approximately 2 weeks apart), and Time 2.</AbstractText>Inpatients consistently taking SRIs (SRI + , n = 44) showed statistically significant reductions of brain ventricular volumes particularly for their left and right lateral ventricular volumes. Reductions in their third ventricular volume were close to significance (p</i> = .068). The inpatients that did not take SRIs (SRI-, n = 25) showed no statistically significant changes in brain ventricular volumes. The SRI + group also exhibited similar brain structural features to the healthy control group based on the 90% confidence interval comparsions on brain ventricular volume parameters, whereas the SRI- group still exhibited relatively enlarged brain ventricular volumes after treatment.</AbstractText>SRI treatment was associated with decreased brain ventricle volume over treatment.</AbstractText>© The Author(s) 2022.</CopyrightInformation> |
2,329,736 | Effect of taurine administration on symptoms, severity, or clinical outcome of dilated cardiomyopathy and heart failure in humans: a systematic review.<Pagination><StartPage>9</StartPage><MedlinePgn>9</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">9</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.12688/wellcomeopenres.17505.3</ELocationID><Abstract><AbstractText><b>Background:</b> Taurine, 2-aminoethanesulfonic acid, is an amino acid found in animal products. Taurine is produced for human consumption as a supplement and ingredient in beverages. Supplementation is a safe, inexpensive, and effective treatment for dilated cardiomyopathy (DCM) in domestic mammals, however it is currently unlicensed in Europe and the United States for human medical treatment. Recent genome-wide association studies of DCM have identified the locus of the taurine transporter ( <i>SLC6A6</i>). To assess whether taurine supplementation may be a novel therapeutic option for DCM, we undertook a systematic review. <b>Methods:</b> Four electronic databases (PubMed, Cochrane Central Register, Web of Science, Biomed Central) were searched until 11/03/21. Included studies of human participants reported measured phenotypes or symptoms for cardiomyopathy, heart failure (HF), or altered left ventricle structure or function, administering taurine in any formulation, by any method. Non-English articles were excluded. Meta-analysis was completed in R software (version 3.6.0). The Newcastle-Ottawa Scale quality assessment score (NOQAS) tool was used to assess bias. <b>Results:</b> 285 articles were identified, of which eleven met our criteria for inclusion. Only one paper was deemed "high quality" using the NOQAS tool. Taurine supplementation varied across studies; by dose (500 mg to 6g per day), frequency (once to thrice daily), delivery method (tablet, capsule, drink, powder), and duration (2 to 48 weeks). Patient inclusion was all-cause HF patients with ejection fraction (EF) <50% and no study was specific to DCM. While improvements in diastolic and systolic function, exercise capacity, and haemodynamic parameters were described, only EF and stroke volume were measured in enough studies to complete a meta-analysis; the association was not significant with all-cause HF (P<0.05). No significant safety concerns were reported. <b>Conclusions:</b> A formal clinical trial is needed to address whether taurine supplementation is beneficial to the approximately 1/250 individuals with DCM in the population.</AbstractText><CopyrightInformation>Copyright: © 2022 McGurk KA et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McGurk</LastName><ForeName>Kathryn A</ForeName><Initials>KA</Initials><Identifier Source="ORCID">0000-0002-5445-6906</Identifier><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kasapi</LastName><ForeName>Melpomeni</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ware</LastName><ForeName>James S</ForeName><Initials>JS</Initials><Identifier Source="ORCID">0000-0002-6110-5880</Identifier><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MRC London Institute of Medical Sciences, Imperial College London, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Royal Brompton & Harefield Hospitals, Guy's and St. Thomas' NHS Foundation Trust, London, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MC_UP_1102/20</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Wellcome Open Res</MedlineTA><NlmUniqueID>101696457</NlmUniqueID><ISSNLinking>2398-502X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cardiomyopathy</Keyword><Keyword MajorTopicYN="N">DCM</Keyword><Keyword MajorTopicYN="N">Heart Failure</Keyword><Keyword MajorTopicYN="N">Taurine</Keyword></KeywordList><CoiStatement>Competing interests: J.S.W. has consulted for MyoKardia, Inc. and Foresite Labs.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>21</Day><Hour>2</Hour><Minute>38</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>22</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35855073</ArticleId><ArticleId IdType="pmc">PMC9257265</ArticleId><ArticleId IdType="doi">10.12688/wellcomeopenres.17505.3</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Pinto YM, Elliott PM, Arbustini E, et al. : Proposal for a revised definition of dilated cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for clinical practice: A position statement of the ESC working group on myocardial and pericardial diseases. 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The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in meta-analyses.
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Zenodo. 2021. 10.5281/zenodo.5785673</Citation><ArticleIdList><ArticleId IdType="doi">10.5281/zenodo.5785673</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35858644</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-8785</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>12</Day></PubDate></JournalIssue><Title>American journal of perinatology</Title><ISOAbbreviation>Am J Perinatol</ISOAbbreviation></Journal>Fetal Echocardiographic Findings to Predict Early Surgical Repair and Neonatal Outcomes in Fetuses with Isolated Coarctation of the Aorta. | <b>Background:</b> Taurine, 2-aminoethanesulfonic acid, is an amino acid found in animal products. Taurine is produced for human consumption as a supplement and ingredient in beverages. Supplementation is a safe, inexpensive, and effective treatment for dilated cardiomyopathy (DCM) in domestic mammals, however it is currently unlicensed in Europe and the United States for human medical treatment. Recent genome-wide association studies of DCM have identified the locus of the taurine transporter ( <i>SLC6A6</i>). To assess whether taurine supplementation may be a novel therapeutic option for DCM, we undertook a systematic review. <b>Methods:</b> Four electronic databases (PubMed, Cochrane Central Register, Web of Science, Biomed Central) were searched until 11/03/21. Included studies of human participants reported measured phenotypes or symptoms for cardiomyopathy, heart failure (HF), or altered left ventricle structure or function, administering taurine in any formulation, by any method. Non-English articles were excluded. Meta-analysis was completed in R software (version 3.6.0). The Newcastle-Ottawa Scale quality assessment score (NOQAS) tool was used to assess bias. <b>Results:</b> 285 articles were identified, of which eleven met our criteria for inclusion. Only one paper was deemed "high quality" using the NOQAS tool. Taurine supplementation varied across studies; by dose (500 mg to 6g per day), frequency (once to thrice daily), delivery method (tablet, capsule, drink, powder), and duration (2 to 48 weeks). Patient inclusion was all-cause HF patients with ejection fraction (EF) <50% and no study was specific to DCM. While improvements in diastolic and systolic function, exercise capacity, and haemodynamic parameters were described, only EF and stroke volume were measured in enough studies to complete a meta-analysis; the association was not significant with all-cause HF (P<0.05). No significant safety concerns were reported. <b>Conclusions:</b> A formal clinical trial is needed to address whether taurine supplementation is beneficial to the approximately 1/250 individuals with DCM in the population.<CopyrightInformation>Copyright: © 2022 McGurk KA et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McGurk</LastName><ForeName>Kathryn A</ForeName><Initials>KA</Initials><Identifier Source="ORCID">0000-0002-5445-6906</Identifier><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kasapi</LastName><ForeName>Melpomeni</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ware</LastName><ForeName>James S</ForeName><Initials>JS</Initials><Identifier Source="ORCID">0000-0002-6110-5880</Identifier><AffiliationInfo><Affiliation>National Heart and Lung Institute, Imperial College London, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>MRC London Institute of Medical Sciences, Imperial College London, London, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Royal Brompton & Harefield Hospitals, Guy's and St. Thomas' NHS Foundation Trust, London, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MC_UP_1102/20</GrantID><Acronym>MRC_</Acronym><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D000078182">Systematic Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Wellcome Open Res</MedlineTA><NlmUniqueID>101696457</NlmUniqueID><ISSNLinking>2398-502X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cardiomyopathy</Keyword><Keyword MajorTopicYN="N">DCM</Keyword><Keyword MajorTopicYN="N">Heart Failure</Keyword><Keyword MajorTopicYN="N">Taurine</Keyword></KeywordList><CoiStatement>Competing interests: J.S.W. has consulted for MyoKardia, Inc. and Foresite Labs.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>21</Day><Hour>2</Hour><Minute>38</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>22</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35855073</ArticleId><ArticleId IdType="pmc">PMC9257265</ArticleId><ArticleId IdType="doi">10.12688/wellcomeopenres.17505.3</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Pinto YM, Elliott PM, Arbustini E, et al. : Proposal for a revised definition of dilated cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for clinical practice: A position statement of the ESC working group on myocardial and pericardial diseases. Eur Heart J. 2016;37(23):1850–1858. 10.1093/eurheartj/ehv727</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/eurheartj/ehv727</ArticleId><ArticleId IdType="pubmed">26792875</ArticleId></ArticleIdList></Reference><Reference><Citation>Hershberger RE, Hedges DJ, Morales A: Dilated cardiomyopathy: The complexity of a diverse genetic architecture. Nat Rev Cardiol. 2013;10(9):531–547. 10.1038/nrcardio.2013.105</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/nrcardio.2013.105</ArticleId><ArticleId IdType="pubmed">23900355</ArticleId></ArticleIdList></Reference><Reference><Citation>Ware JS, Cook SA: Role of titin in cardiomyopathy: From DNA variants to patient stratification. Nat Rev Cardiol. 2018;15(4):241–252. 10.1038/nrcardio.2017.190</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/nrcardio.2017.190</ArticleId><ArticleId IdType="pubmed">29238064</ArticleId></ArticleIdList></Reference><Reference><Citation>McNally EM, Mestroni L: Dilated cardiomyopathy: Genetic determinants and mechanisms. Circ Res. 2017;121(7):731–748. 10.1161/CIRCRESAHA.116.309396</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCRESAHA.116.309396</ArticleId><ArticleId IdType="pmc">PMC5626020</ArticleId><ArticleId IdType="pubmed">28912180</ArticleId></ArticleIdList></Reference><Reference><Citation>Garnier S, Harakalova M, Weiss S, et al. : Genome-wide association analysis in dilated cardiomyopathy reveals two new players in systolic heart failure on chromosomes 3p25.1 and 22q11.23. Eur Heart J. England; 2021;42(20):2000–2011. 10.1093/eurheartj/ehab030</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/eurheartj/ehab030</ArticleId><ArticleId IdType="pmc">PMC8139853</ArticleId><ArticleId IdType="pubmed">33677556</ArticleId></ArticleIdList></Reference><Reference><Citation>Tadros R, Francis C, Xu X, et al. : Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect. Nat Genet. 2021;53(2):128–134. 10.1038/s41588-020-00762-2</Citation><ArticleIdList><ArticleId IdType="doi">10.1038/s41588-020-00762-2</ArticleId><ArticleId IdType="pmc">PMC7611259</ArticleId><ArticleId IdType="pubmed">33495596</ArticleId></ArticleIdList></Reference><Reference><Citation>Aguet F, Barbeira AN, Bonazzola R, et al. : The GTEx Consortium atlas of genetic regulatory effects across human tissues. Science. 2020;369(6509):1318–1330. 10.1126/science.aaz1776</Citation><ArticleIdList><ArticleId IdType="doi">10.1126/science.aaz1776</ArticleId><ArticleId IdType="pmc">PMC7737656</ArticleId><ArticleId IdType="pubmed">32913098</ArticleId></ArticleIdList></Reference><Reference><Citation>Ansar M, Ranza E, Shetty M, et al. : Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. Hum Mol Genet. 2020;29(4):618–623. 10.1093/hmg/ddz303</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/hmg/ddz303</ArticleId><ArticleId IdType="pmc">PMC7068170</ArticleId><ArticleId IdType="pubmed">31903486</ArticleId></ArticleIdList></Reference><Reference><Citation>Schaffer SW, Shimada-Takaura K, Jong CJ, et al. : Impaired energy metabolism of the taurine-deficient heart. Amino Acids. 2016;48(2):549–58. 10.1007/s00726-015-2110-2</Citation><ArticleIdList><ArticleId IdType="doi">10.1007/s00726-015-2110-2</ArticleId><ArticleId IdType="pubmed">26475290</ArticleId></ArticleIdList></Reference><Reference><Citation>Pion PD, Kittleson MD, Rogers QR, et al. : Myocardial failure in cats associated with low plasma taurine: A reversible cardiomyopathy. Science. 1987;237(4816):764–768. 10.1126/science.3616607</Citation><ArticleIdList><ArticleId IdType="doi">10.1126/science.3616607</ArticleId><ArticleId IdType="pubmed">3616607</ArticleId></ArticleIdList></Reference><Reference><Citation>Pion PD, Kittleson MD, Thomas WP, et al. : Response of cats with dilated cardiomyopathy to taurine supplementation. 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Zenodo. 2021. 10.5281/zenodo.5785673</Citation><ArticleIdList><ArticleId IdType="doi">10.5281/zenodo.5785673</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35858644</PMID><DateRevised><Year>2022</Year><Month>11</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-8785</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Sep</Month><Day>12</Day></PubDate></JournalIssue><Title>American journal of perinatology</Title><ISOAbbreviation>Am J Perinatol</ISOAbbreviation></Journal><ArticleTitle>Fetal Echocardiographic Findings to Predict Early Surgical Repair and Neonatal Outcomes in Fetuses with Isolated Coarctation of the Aorta.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1055/a-1904-9519</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE"> The aim of this study was to investigate fetal echocardiographic findings in predicting the need for surgical repair in fetuses with coarctation of the aorta (CoA) and to evaluate perinatal outcomes.<AbstractText Label="STUDY DESIGN" NlmCategory="METHODS"> In this retrospective study, fetuses diagnosed with CoA in a tertiary center between January 2015 and June 2021 were analyzed. Fetal echocardiographic measurements and quantitative findings, middle cerebral artery (MCA) and umbilical artery (UA) Doppler indices, and perinatal outcomes were recorded.<AbstractText Label="RESULTS" NlmCategory="RESULTS"> A total of 57 fetuses with CoA were included in the study. In total, 51 (89.5%) pregnancies resulted in live births and 32 (62.8%) of the neonates underwent surgical repair. The left ventricle/right ventricle width ratio and aortic isthmus <i>z</i>-score were significantly lower in fetuses who underwent surgical repair (<i>p</i> = 0.004 0.001, respectively). Retrograde flow in the aortic isthmus (odds ratio [OR]:7.43; 95% confidence interval [CI]: 1.98-27.76), left-to-right foramen ovale shunt (OR: 8.50; 95% CI: 1.68-42.98), and ventricular septal defect (OR: 9.63; 95% CI: 1.90-48.74) were associated with the need for surgical repair. A new scoring system integrating these echocardiographic findings had 89% specificity and 54% sensitivity in predicting surgical repair. Fetal growth restriction rates, preterm birth rates, mean MCA pulsatility index (PI), and mean UA PI were similar in fetuses with and without surgical repair.<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS"> A scoring system integrating echocardiographic findings in fetuses with CoA may improve the prediction of surgical repair need. There is no evidence of an increased risk of FGR, preterm birth, and brain sparing effect in fetuses with CoA who require surgical repair.<AbstractText Label="KEY POINTS" NlmCategory="CONCLUSIONS">· Coarctation of the aorta is one of the most difficult congenital heart defects to diagnose.. · A new scoring system may improve the prediction of surgical repair need.. · There is no increased risk of fetal growth restriction in fetuses requiring early surgical repair.. |
2,329,737 | Quantitative Neuroanatomical Phenotyping of the Embryonic Mouse Brain. | Congenital neurodevelopmental anomalies are present from birth and are characterized by an abnormal development of one or more structures of the brain. Brain structural anomalies are highly comorbid with neurodevelopmental and neuropsychiatric disorders such as intellectual disability, autism spectrum disorders, epilepsy, and schizophrenia, and 80% are of genetic origin. We aim to address an important neurobiological question: How many genes regulate the normal anatomy of the brain during development. To do so, we developed a quantitative approach for the assessment of a total of 106 neuroanatomical parameters in mouse mutant embryos at embryonic day 18.5 across two planes commonly used in brain anatomical studies, the coronal and sagittal planes. In this article we describe the techniques we developed and explain why ultrastandardized procedures involving embryonic mouse brains are even more of prime importance for morphological phenotyping than adult mouse brains. We focus our analysis on brain size anomalies and on the most frequently altered brain regions including the cortex, corpus callosum, hippocampus, ventricles, caudate putamen, and cerebellum. Our protocols allow a standardized histology pipeline from embryonic mouse brain preparation to sectioning, staining, and scanning and neuroanatomical analyses at well-defined positions on the coronal and sagittal planes. Together, our protocols will help scientists in deciphering congenital neurodevelopmental anomalies and anatomical changes between groups of mouse embryos in health and genetic diseases. © 2022 The Authors. Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1: Fixation and preparation of embryonic mouse brain samples Basic Protocol 2: Sectioning, staining, and scanning of embryonic mouse brain sections Basic Protocol 3: Coronal neuroanatomical measurements of embryonic mouse brain structures Basic Protocol 4: Sagittal neuroanatomical measurements of embryonic mouse brain structures. |
2,329,738 | Stereotactic surgery for neurocysticercosis of the 4th ventricle: illustrative cases. | Neurocysticercosis, caused by the larval stage of Taenia solium</i>, affects the cerebral ventricles in 20-30% of cases and may lead to hydrocephalus and other neurological morbidity. Conventional treatment for cysts in the 4th ventricle includes open surgery (suboccipital approach) and neuroendoscopy, with the latter being the option of choice. Stereotactic surgery, minimally invasive, offers a good alternative for this type of deep lesion.</AbstractText>The authors report the cases of two women, 30 and 45 years old, who presented with headache, dizziness, and ataxia and were diagnosed with 4th ventricle cysticercosis. Magnetic resonance imaging (MRI) revealed dilated 4th ventricles (approximately 2.5 cm in both cases, with cystic images inside the ventricular cavity). Both patients were treated with stereotactic surgery via a suboccipital transcerebellar approach. Cyst material was extracted, and the diagnosis was confirmed by pathological examination. The surgeries had no complications and resulted in clinical improvement. Control MRI scans showed reduction of the volume of the ventricle without residual cysts.</AbstractText>Minimally invasive stereotactic surgery provided a safe alternative for 4th ventricle neurocysticercosis cysts, with more benefits than risks in comparison with conventional techniques.</AbstractText>© 2021 The authors.</CopyrightInformation> |
2,329,739 | Posttraumatic Parinaud's syndrome as a contrecoup injury in a case of closed head trauma. | The purpose of the study was to present a rare case of post-traumatic Parinaud's syndrome with a history of closed head injury. The clinical characteristics, examination, and management are presented in a 12-year-old boy who was a victim of physical violence at the hands of a young boy who punched him in his chin with his fists, with associated paralysis of the upward gaze of the left eyeball, and convergence nystagmus with pupillary involvement. CT examination indicated posttraumatic lesions in the dorsal midbrain and in the cavity of third ventricle, suggestive of acute hemorrhages. Posttraumatic Parinaud's syndrome is a rare phenomenon that can occur in a case of closed head trauma as contrecoup injury. |
2,329,740 | COVID-19 Resulting in Global Stress Cardiomyopathy in a Young Female. | Takotsubo cardiomyopathy, also called stress cardiomyopathy, is a form of reversible cardiomyopathy that occurs during periods of emotional or physical stress. There are many variants of takotsubo. They are classified depending on the region of hypokinesis: the most common four variants include the apical/typical variant (left ventricular apical hypokinesis), the midventricular type (midventricular hypokinesis), the basal type (basal hypokinesis), and the focal type (isolated segmental dysfunction of the left ventricle). Rarely takotsubo presents as a global variant where there is global left ventricular hypokinesis. Takotsubo cardiomyopathy has had an increasing incidence since the COVID-19 pandemic. We report a case of a 29-year-old woman with no prior cardiac history who presented with a seizure and was found to have COVID-19. The patient's echocardiogram showed global cardiomyopathy, a rare type of takotsubo cardiomyopathy. |
2,329,741 | Diagnostic Value of Abdominal B-Ultrasound for Congenital Heart Disease Complicated with Extracardiac Malformation in the Second Trimester of Pregnancy. | To explore the diagnostic value of abdominal B-ultrasound in the diagnosis of congenital heart disease complicated with extracardiac malformations in the second trimester of pregnancy.</AbstractText>50 pregnant women with congenital cardiac malformations and extracardiac malformations diagnosed in our hospital from 2015 to 2019 were retrospectively analyzed. The diagnostic results and the types of congenital heart disease complicated with extracardiac malformations were compared to analyze the diagnostic value of abdominal B-ultrasound.</AbstractText>In the diagnosis of 50 fetuses with congenital heart disease and extracardiac malformation, the tetralogy of Fallot syndrome accounts for the largest proportion. Abdominal B-ultrasound in the second trimester was associated with a higher detection rate of fetal heart malformation (72%) versus in the third trimester (40%) (P</i> < 0.05). The single atrium and single ventricle had the highest diagnostic accuracy of fetal congenital heart malformation in the second trimester. The highest success rate of detection at different gestational weeks was observed at the 14th gestational week (P</i> < 0.05). Four-chamber cardiac section (4CV) had the lowest diagnostic accuracy (62%) for cardiac malformations, and the 4CV + three-vessel-trachea plane (3VVT) had the highest diagnostic accuracy (90%) for cardiac malformations.</AbstractText>Abdominal B-ultrasound features a high diagnostic value for congenital heart disease complicated with extracardiac malformations in the second trimester of pregnancy, and the second trimester is the optimal detection timing with the highest detection accuracy.</AbstractText>Copyright © 2022 Yanming Deng et al.</CopyrightInformation> |
2,329,742 | Ventricular volume in relation to lumbar CSF levels of amyloid-β 1-42, tau and phosphorylated tau in iNPH, is there a dilution effect? | Levels of the biomarkers amyloid-β 1-42 (Aβ42), tau and phosphorylated tau (p-tau) are decreased in the cerebrospinal fluid (CSF) of patients with idiopathic normal pressure hydrocephalus (iNPH). The mechanism behind this is unknown, but one potential explanation is dilution by excessive CSF volumes. The aim of this study was to investigate the presence of a dilution effect, by studying the relationship between ventricular volume (VV) and the levels of the CSF biomarkers.</AbstractText>In this cross-sectional observational study, preoperative magnetic resonance imaging (MRI) and lumbar CSF was acquired from 136 patients with a median age of 76 years, 89 men and 47 females, selected for surgical treatment for iNPH. The CSF volume of the lateral and third ventricles was segmented on MRI and related to preoperative concentrations of Aβ42, tau and p-tau.</AbstractText>In the total sample VV (Median 140.7 mL) correlated weakly (rs</sub> = - 0.17) with Aβ42 (Median 534 pg/mL), but not with tau (Median 216 pg/mL) nor p-tau (Median 31 pg/mL). In a subgroup analysis, the correlation between VV and Aβ42 was only present in the male group (rs</sub> = - 0.22, p = 0.038). Further, Aβ42 correlated positively with tau (rs</sub> = 0.30, p = 0.004) and p-tau (rs</sub> = 0.26, p = 0.012) in males but not in females.</AbstractText>The findings did not support a major dilution effect in iNPH, at least not in females. The only result in favor for dilution was a weak negative correlation between VV and Aβ42 but not with the other lumbar CSF biomarkers. The different results between males and females suggest that future investigations of the CSF pattern in iNPH would gain from sex-based subgroup analysis.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,743 | Anatomy of the Ventricles, Subarachnoid Spaces, and Meninges. | The ventricular system, subarachnoid spaces, and meninges are structures that lend structure, support, and protection to the brain and spinal cord. This article provides a detailed look at the anatomy of the intracranial portions of these structures with a particular focus on neuroimaging methods. |
2,329,744 | Percutaneous jugular leadless pacemaker implantation in a pediatric patient.<Pagination><StartPage>2111</StartPage><EndPage>2115</EndPage><MedlinePgn>2111-2115</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jce.15620</ELocationID><Abstract><AbstractText Label="INTRODUCTION">Leadless cardiac pacing has not been widely utilized in pediatric patients, in part due to concerns regarding size of the delivery sheath and the potential for vascular injury.</AbstractText><AbstractText Label="METHODS">We present a case of leadless pacemaker implantation via internal jugular vein without a surgical cutdown.</AbstractText><AbstractText Label="RESULTS">A leadless pacemaker was successfully implanted in the right ventricle via internal jugular approach in a pediatric patient with congenital heart disease.</AbstractText><AbstractText Label="CONCLUSION">This is a novel approach to leadless pacemaker implantation that could broaden the utilization of this technology to the vulnerable population of children, especially those with congenital heart disease.</AbstractText><CopyrightInformation>© 2022 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kumthekar</LastName><ForeName>Rohan N</ForeName><Initials>RN</Initials><Identifier Source="ORCID">0000-0002-2224-276X</Identifier><AffiliationInfo><Affiliation>Division of Cardiology, Nationwide Children's Hospital, Columbus, Ohio, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Augostini</LastName><ForeName>Ralph S</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Division of Cardiology, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamp</LastName><ForeName>Anna N</ForeName><Initials>AN</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Nationwide Children's Hospital, Columbus, Ohio, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kertesz</LastName><ForeName>Naomi J</ForeName><Initials>NJ</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Nationwide Children's Hospital, Columbus, Ohio, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Cardiovasc Electrophysiol</MedlineTA><NlmUniqueID>9010756</NlmUniqueID><ISSNLinking>1045-3873</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010138" MajorTopicYN="Y">Pacemaker, Artificial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019736" MajorTopicYN="N">Prostheses and Implants</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Micra™</Keyword><Keyword MajorTopicYN="N">leadless</Keyword><Keyword MajorTopicYN="N">pacemaker</Keyword><Keyword MajorTopicYN="N">pediatrics</Keyword><Keyword MajorTopicYN="N">transjugular</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>6</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>7</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>9</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Eur Heart J. 2016;37:2503.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">29489273</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK482171</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-22900">Neuroanatomy, Hippocampus<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Fogwe</LastName><ForeName>Leslie A.</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>University of Missouri Columbia</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reddy</LastName><ForeName>Vamsi</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>McKinsey & Company</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mesfin</LastName><ForeName>Fassil B.</ForeName><Initials>FB</Initials><AffiliationInfo><Affiliation>MU School of Medicine</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>The hippocampus is the "flash drive" of the human brain and is often associated with memory consolidation and decision making, but it is far more complex in structure and function than a flash drive. The hippocampus is a convex elevation of gray matter tissue within the parahippocampal gyrus inside the inferior temporal horn of the lateral ventricle. One can describe it more holistically as a curved and recurved sheet of the cortex that folds into the temporal lobe's medial surface. The hippocampus has three distinct zones: the dentate gyrus, the hippocampus proper, and the subiculum—the dentate gyrus and hippocampus proper form two C-shaped rings that interlock. The subiculum is thus a transition zone, linking the hippocampus proper with the dentate gyrus. The parahippocampal gyrus and cingulate sulci are located on the medial surface of the hemisphere, forming a C-shaped ring. The medial temporal lobe cortex includes major subdivisions such as the hippocampus and the entorhinal cortex. This five-centimeter-long hippocampus (from the anterior end at the amygdala to the posterior end near the splenium of the corpus callosum) divides into a head, body, and tail. the head is expanded and bears two or three shallow grooves called pes hippocampi. The head of the hippocampus is part of the posterior half of the triangular uncus and is separated inferiorly from the parahippocampal gyrus by the uncal sulcus. The alveus, which is the surface of the hippocampus, is covered by the ependymal inside the ventricular cavity. The fornix, which is the main outflow bundle out of the hippocampus, wraps around the thalamus, where it then becomes separated by the choroidal fissure and the choroid plexus. The hippocampus contains parts like the fimbria, crus, body, and column—the fimbria forms where alveus fibers converge along the medial portion of the lateral ventricle's inferior horn. The white matter of the fimbria separates to form a crux of the ipsilateral fornix at a point beyond the splenium of the corpus callosum. The Cornu Ammonis (CA) is a seahorse-like or ram's horn-like structure that describes the different layers of the hippocampus. There are four hippocampal subfields CA1, CA2, CA3, and CA4. CA3 and CA2 border the hilus of the dentate gyrus on either side. CA3 is the largest in the hippocampus and receives fibers from the dentate granule cells on their proximal dendrites. The pyramidal cell layer is about ten cells thick.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s7">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>18</Day></ContributionDate><ReferenceList><Reference><Citation>AbuHasan Q, Reddy V, Siddiqui W. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2022. Jul 19, Neuroanatomy, Amygdala.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Daugherty AM, Bender AR, Raz N, Ofen N. Age differences in hippocampal subfield volumes from childhood to late adulthood. Hippocampus. 2016 Feb;26(2):220-8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4718822</ArticleId><ArticleId IdType="pubmed">26286891</ArticleId></ArticleIdList></Reference><Reference><Citation>Kizilirmak JM, Schott BH, Thuerich H, Sweeney-Reed CM, Richter A, Folta-Schoofs K, Richardson-Klavehn A. Learning of novel semantic relationships via sudden comprehension is associated with a hippocampus-independent network. Conscious Cogn. 2019 Mar;69:113-132.</Citation><ArticleIdList><ArticleId IdType="pubmed">30763808</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang EW, Du G, Lewis MM, Lee EY, De Jesus S, Kanekar S, Kong L, Huang X. Multimodal MRI evaluation of parkinsonian limbic pathologies. Neurobiol Aging. 2019 Apr;76:194-200.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6461740</ArticleId><ArticleId IdType="pubmed">30739076</ArticleId></ArticleIdList></Reference><Reference><Citation>Spallazzi M, Dobisch L, Becke A, Berron D, Stucht D, Oeltze-Jafra S, Caffarra P, Speck O, Düzel E. Hippocampal vascularization patterns: A high-resolution 7 Tesla time-of-flight magnetic resonance angiography study. Neuroimage Clin. 2019;21:101609.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6413539</ArticleId><ArticleId IdType="pubmed">30581106</ArticleId></ArticleIdList></Reference><Reference><Citation>Uda T, Kunihiro N, Nakajo K, Kuki I, Fukuoka M, Ohata K. Seizure freedom from temporal lobe epilepsy with mesial temporal lobe tumor by tumor removal alone without hippocampectomy despite remaining abnormal discharges on intraoperative electrocorticography: Report of two pediatric cases and reconsideration of the surgical strategy. Surg Neurol Int. 2018;9:181.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6157038</ArticleId><ArticleId IdType="pubmed">30283714</ArticleId></ArticleIdList></Reference><Reference><Citation>Li N, Li Y, Li LJ, Zhu K, Zheng Y, Wang XM. Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer's disease. Neural Regen Res. 2019 Jun;14(6):1037-1045.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6404481</ArticleId><ArticleId IdType="pubmed">30762016</ArticleId></ArticleIdList></Reference><Reference><Citation>Bhusal A, Rahman MH, Lee IK, Suk K. Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy. Front Endocrinol (Lausanne) 2019;10:25.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6363678</ArticleId><ArticleId IdType="pubmed">30761088</ArticleId></ArticleIdList></Reference><Reference><Citation>Tan B, Fox S, Kruger C, Lynch M, Shanagher D, Timmons S. Investigating the healthcare utilisation and other support needs of people with young-onset dementia. Maturitas. 2019 Apr;122:31-34.</Citation><ArticleIdList><ArticleId IdType="pubmed">30797527</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29489273</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29083579</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK459381</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28595">Right Heart Failure<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mandras</LastName><ForeName>Stacy A.</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Ochsner Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Desai</LastName><ForeName>Sapna</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Ochsner</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>When addressing heart failure, most commonly, the left ventricle (LV) is the topic of discussion, and the right heart overlooked. However, the right ventricle (RV) is unique in structure and function and is affected by a set of disease processes that rival that of the LV. This article will review the normal structure and function of the RV, describe the pathophysiology of RV failure (RVF), and detail the medical and surgical management of the various disease processes during which RVF occurs.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s10">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s12">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>18</Day></ContributionDate><ReferenceList><Reference><Citation>Malamba-Lez D, Ngoy-Nkulu D, Steels P, Tshala-Katumbay D, Mullens W. Heart Failure Etiologies and Challenges to Care in the Developing World: An Observational Study in the Democratic Republic of Congo. J Card Fail. 2018 Dec;24(12):854-859.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6635643</ArticleId><ArticleId IdType="pubmed">30359689</ArticleId></ArticleIdList></Reference><Reference><Citation>Zhuravleva MV, Prokofiev AB, Shih EV, Serebrova SY, Gorodetskaya GI. [Novel Possibilities in Pharmacotherapy of Patients With Chronic Heart Failure]. Kardiologiia. 2018 Oct;(10):88-95.</Citation><ArticleIdList><ArticleId IdType="pubmed">30359220</ArticleId></ArticleIdList></Reference><Reference><Citation>Westphal JG, Bekfani T, Schulze PC. What's new in heart failure therapy 2018? Interact Cardiovasc Thorac Surg. 2018 Dec 01;27(6):921-930.</Citation><ArticleIdList><ArticleId IdType="pubmed">30304450</ArticleId></ArticleIdList></Reference><Reference><Citation>Uduman J. Epidemiology of Cardiorenal Syndrome. Adv Chronic Kidney Dis. 2018 Sep;25(5):391-399.</Citation><ArticleIdList><ArticleId IdType="pubmed">30309456</ArticleId></ArticleIdList></Reference><Reference><Citation>Nochioka K, Querejeta Roca G, Claggett B, Biering-Sørensen T, Matsushita K, Hung CL, Solomon SD, Kitzman D, Shah AM. Right Ventricular Function, Right Ventricular-Pulmonary Artery Coupling, and Heart Failure Risk in 4 US Communities: The Atherosclerosis Risk in Communities (ARIC) Study. JAMA Cardiol. 2018 Oct 01;3(10):939-948.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6233815</ArticleId><ArticleId IdType="pubmed">30140848</ArticleId></ArticleIdList></Reference><Reference><Citation>Cannavo A, Bencivenga L, Liccardo D, Elia A, Marzano F, Gambino G, D'Amico ML, Perna C, Ferrara N, Rengo G, Paolocci N. Aldosterone and Mineralocorticoid Receptor System in Cardiovascular Physiology and Pathophysiology. Oxid Med Cell Longev. 2018;2018:1204598.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6169243</ArticleId><ArticleId IdType="pubmed">30327709</ArticleId></ArticleIdList></Reference><Reference><Citation>Hamada-Harimura Y, Seo Y, Ishizu T, Nishi I, Machino-Ohtsuka T, Yamamoto M, Sugano A, Sato K, Sai S, Obara K, Yoshida I, Aonuma K, ICAS-HF Investigators Incremental Prognostic Value of Right Ventricular Strain in Patients With Acute Decompensated Heart Failure. Circ Cardiovasc Imaging. 2018 Oct;11(10):e007249.</Citation><ArticleIdList><ArticleId IdType="pubmed">30354477</ArticleId></ArticleIdList></Reference><Reference><Citation>Sano H, Tanaka H, Motoji Y, Mukai J, Suto M, Takada H, Soga F, Hatani Y, Matsuzoe H, Hatazawa K, Shimoura H, Ooka J, Nakayama K, Matsumoto K, Yamada H, Emoto N, Hirata KI. Echocardiography during preload stress for evaluation of right ventricular contractile reserve and exercise capacity in pulmonary hypertension. Echocardiography. 2018 Dec;35(12):1997-2004.</Citation><ArticleIdList><ArticleId IdType="pubmed">30328154</ArticleId></ArticleIdList></Reference><Reference><Citation>Ibrahim NE, Januzzi JL. Established and Emerging Roles of Biomarkers in Heart Failure. Circ Res. 2018 Aug 17;123(5):614-629.</Citation><ArticleIdList><ArticleId IdType="pubmed">30355136</ArticleId></ArticleIdList></Reference><Reference><Citation>Rohit S, Rahul M. Efficacy of heart failure reversal treatment in patients with low ejection fraction. J Ayurveda Integr Med. 2018 Oct-Dec;9(4):285-289.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6314236</ArticleId><ArticleId IdType="pubmed">30287144</ArticleId></ArticleIdList></Reference><Reference><Citation>Peterson PN, Allen LA, Heidenreich PA, Albert NM, Piña IL, American Heart Association The American Heart Association Heart Failure Summit, Bethesda, April 12, 2017. Circ Heart Fail. 2018 Oct;11(10):e004957.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6211812</ArticleId><ArticleId IdType="pubmed">30354400</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29083579</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35842401</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-0938</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiovascular revascularization medicine : including molecular interventions</Title><ISOAbbreviation>Cardiovasc Revasc Med</ISOAbbreviation></Journal>Benign chronic mid left anterior descending artery perforation in the setting of coronary intervention with a large fistula formation into the right ventricular cavity. | The hippocampus is the "flash drive" of the human brain and is often associated with memory consolidation and decision making, but it is far more complex in structure and function than a flash drive. The hippocampus is a convex elevation of gray matter tissue within the parahippocampal gyrus inside the inferior temporal horn of the lateral ventricle. One can describe it more holistically as a curved and recurved sheet of the cortex that folds into the temporal lobe's medial surface. The hippocampus has three distinct zones: the dentate gyrus, the hippocampus proper, and the subiculum—the dentate gyrus and hippocampus proper form two C-shaped rings that interlock. The subiculum is thus a transition zone, linking the hippocampus proper with the dentate gyrus. The parahippocampal gyrus and cingulate sulci are located on the medial surface of the hemisphere, forming a C-shaped ring. The medial temporal lobe cortex includes major subdivisions such as the hippocampus and the entorhinal cortex. This five-centimeter-long hippocampus (from the anterior end at the amygdala to the posterior end near the splenium of the corpus callosum) divides into a head, body, and tail. the head is expanded and bears two or three shallow grooves called pes hippocampi. The head of the hippocampus is part of the posterior half of the triangular uncus and is separated inferiorly from the parahippocampal gyrus by the uncal sulcus. The alveus, which is the surface of the hippocampus, is covered by the ependymal inside the ventricular cavity. The fornix, which is the main outflow bundle out of the hippocampus, wraps around the thalamus, where it then becomes separated by the choroidal fissure and the choroid plexus. The hippocampus contains parts like the fimbria, crus, body, and column—the fimbria forms where alveus fibers converge along the medial portion of the lateral ventricle's inferior horn. The white matter of the fimbria separates to form a crux of the ipsilateral fornix at a point beyond the splenium of the corpus callosum. The Cornu Ammonis (CA) is a seahorse-like or ram's horn-like structure that describes the different layers of the hippocampus. There are four hippocampal subfields CA1, CA2, CA3, and CA4. CA3 and CA2 border the hilus of the dentate gyrus on either side. CA3 is the largest in the hippocampus and receives fibers from the dentate granule cells on their proximal dendrites. The pyramidal cell layer is about ten cells thick.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s2">Structure and Function</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s3">Embryology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s4">Blood Supply and Lymphatics</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s5">Surgical Considerations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s6">Clinical Significance</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s7">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-22900" sec="article-22900.s11">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>18</Day></ContributionDate><ReferenceList><Reference><Citation>AbuHasan Q, Reddy V, Siddiqui W. StatPearls [Internet] StatPearls Publishing; Treasure Island (FL): 2022. Jul 19, Neuroanatomy, Amygdala.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference><Reference><Citation>Daugherty AM, Bender AR, Raz N, Ofen N. Age differences in hippocampal subfield volumes from childhood to late adulthood. Hippocampus. 2016 Feb;26(2):220-8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4718822</ArticleId><ArticleId IdType="pubmed">26286891</ArticleId></ArticleIdList></Reference><Reference><Citation>Kizilirmak JM, Schott BH, Thuerich H, Sweeney-Reed CM, Richter A, Folta-Schoofs K, Richardson-Klavehn A. Learning of novel semantic relationships via sudden comprehension is associated with a hippocampus-independent network. Conscious Cogn. 2019 Mar;69:113-132.</Citation><ArticleIdList><ArticleId IdType="pubmed">30763808</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang EW, Du G, Lewis MM, Lee EY, De Jesus S, Kanekar S, Kong L, Huang X. Multimodal MRI evaluation of parkinsonian limbic pathologies. Neurobiol Aging. 2019 Apr;76:194-200.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6461740</ArticleId><ArticleId IdType="pubmed">30739076</ArticleId></ArticleIdList></Reference><Reference><Citation>Spallazzi M, Dobisch L, Becke A, Berron D, Stucht D, Oeltze-Jafra S, Caffarra P, Speck O, Düzel E. Hippocampal vascularization patterns: A high-resolution 7 Tesla time-of-flight magnetic resonance angiography study. Neuroimage Clin. 2019;21:101609.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6413539</ArticleId><ArticleId IdType="pubmed">30581106</ArticleId></ArticleIdList></Reference><Reference><Citation>Uda T, Kunihiro N, Nakajo K, Kuki I, Fukuoka M, Ohata K. Seizure freedom from temporal lobe epilepsy with mesial temporal lobe tumor by tumor removal alone without hippocampectomy despite remaining abnormal discharges on intraoperative electrocorticography: Report of two pediatric cases and reconsideration of the surgical strategy. Surg Neurol Int. 2018;9:181.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6157038</ArticleId><ArticleId IdType="pubmed">30283714</ArticleId></ArticleIdList></Reference><Reference><Citation>Li N, Li Y, Li LJ, Zhu K, Zheng Y, Wang XM. Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer's disease. Neural Regen Res. 2019 Jun;14(6):1037-1045.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6404481</ArticleId><ArticleId IdType="pubmed">30762016</ArticleId></ArticleIdList></Reference><Reference><Citation>Bhusal A, Rahman MH, Lee IK, Suk K. Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy. Front Endocrinol (Lausanne) 2019;10:25.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6363678</ArticleId><ArticleId IdType="pubmed">30761088</ArticleId></ArticleIdList></Reference><Reference><Citation>Tan B, Fox S, Kruger C, Lynch M, Shanagher D, Timmons S. Investigating the healthcare utilisation and other support needs of people with young-onset dementia. Maturitas. 2019 Apr;122:31-34.</Citation><ArticleIdList><ArticleId IdType="pubmed">30797527</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29489273</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29083579</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK459381</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28595">Right Heart Failure</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Mandras</LastName><ForeName>Stacy A.</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Ochsner Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Desai</LastName><ForeName>Sapna</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Ochsner</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>When addressing heart failure, most commonly, the left ventricle (LV) is the topic of discussion, and the right heart overlooked. However, the right ventricle (RV) is unique in structure and function and is affected by a set of disease processes that rival that of the LV. This article will review the normal structure and function of the RV, describe the pathophysiology of RV failure (RVF), and detail the medical and surgical management of the various disease processes during which RVF occurs.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s10">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s11">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-28595" sec="article-28595.s12">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>18</Day></ContributionDate><ReferenceList><Reference><Citation>Malamba-Lez D, Ngoy-Nkulu D, Steels P, Tshala-Katumbay D, Mullens W. Heart Failure Etiologies and Challenges to Care in the Developing World: An Observational Study in the Democratic Republic of Congo. J Card Fail. 2018 Dec;24(12):854-859.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6635643</ArticleId><ArticleId IdType="pubmed">30359689</ArticleId></ArticleIdList></Reference><Reference><Citation>Zhuravleva MV, Prokofiev AB, Shih EV, Serebrova SY, Gorodetskaya GI. [Novel Possibilities in Pharmacotherapy of Patients With Chronic Heart Failure]. Kardiologiia. 2018 Oct;(10):88-95.</Citation><ArticleIdList><ArticleId IdType="pubmed">30359220</ArticleId></ArticleIdList></Reference><Reference><Citation>Westphal JG, Bekfani T, Schulze PC. What's new in heart failure therapy 2018? Interact Cardiovasc Thorac Surg. 2018 Dec 01;27(6):921-930.</Citation><ArticleIdList><ArticleId IdType="pubmed">30304450</ArticleId></ArticleIdList></Reference><Reference><Citation>Uduman J. Epidemiology of Cardiorenal Syndrome. Adv Chronic Kidney Dis. 2018 Sep;25(5):391-399.</Citation><ArticleIdList><ArticleId IdType="pubmed">30309456</ArticleId></ArticleIdList></Reference><Reference><Citation>Nochioka K, Querejeta Roca G, Claggett B, Biering-Sørensen T, Matsushita K, Hung CL, Solomon SD, Kitzman D, Shah AM. Right Ventricular Function, Right Ventricular-Pulmonary Artery Coupling, and Heart Failure Risk in 4 US Communities: The Atherosclerosis Risk in Communities (ARIC) Study. JAMA Cardiol. 2018 Oct 01;3(10):939-948.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6233815</ArticleId><ArticleId IdType="pubmed">30140848</ArticleId></ArticleIdList></Reference><Reference><Citation>Cannavo A, Bencivenga L, Liccardo D, Elia A, Marzano F, Gambino G, D'Amico ML, Perna C, Ferrara N, Rengo G, Paolocci N. Aldosterone and Mineralocorticoid Receptor System in Cardiovascular Physiology and Pathophysiology. 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Circ Heart Fail. 2018 Oct;11(10):e004957.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6211812</ArticleId><ArticleId IdType="pubmed">30354400</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29083579</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35842401</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-0938</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>09</Day></PubDate></JournalIssue><Title>Cardiovascular revascularization medicine : including molecular interventions</Title><ISOAbbreviation>Cardiovasc Revasc Med</ISOAbbreviation></Journal><ArticleTitle>Benign chronic mid left anterior descending artery perforation in the setting of coronary intervention with a large fistula formation into the right ventricular cavity.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S1553-8389(22)00646-7</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.carrev.2022.07.004</ELocationID><Abstract>Coronary perforations occurring during percutaneous coronary intervention can be life-threatening and usually requires immediate intervention to seal the perforation. Here, a case of chronic large persistent left anterior descending artery perforation into the right ventricle that was left alone without any significant clinical sequela is presented. This case is the first case report of this interesting benign complication followed by a review of the literature of reported cases with coronary perforation in any cardiac chamber. |
2,329,745 | Factors Influencing Craniospinal Relapse of Intracranial Germinoma After Complete Remission. | To evaluate the pathomechanism of the recurrence of intracranial germinoma after complete response and to confirm the association of the initial magnetic resonance imaging and therapeutic factors with recurrence.</AbstractText>This study included patients who were followed up for ≥5 years and who were treated in our hospital from 1980 to 2021. Those with germinoma and germinoma with syncytiotrophoblastic giant cells were diagnosed pathologically. Data were categorizedbased on "gender," "single region," "intraventricular dissemination at the initial diagnosis," "hydrocephalus," "types of radiation therapy (RT)," and "chemotherapy." Fisher's exact probability test was used to assess differences between the no recurrence and recurrence groups.</AbstractText>Among 43 patients, 34 had no recurrence, 5 had delayed recurrence (≥60 months), and 4 had early recurrence (<60 months). Follow-up periods were 143.5 (60-380), 198 (88-222), and 132.5 (75-291) months for the no recurrence, delayed recurrence, and early recurrence groups, respectively. Five patients with delayed recurrence showed 3 intracranial lesions and 2 spinal lesions. Four patients with early recurrence showed 3 intracranial lesions and 1 spinal lesion. Differences in delayed recurrences (focal RT vs. RT including whole-ventricle system; P = 0.0491) were significant in Fisher's exact test.</AbstractText>RT including the whole-ventricle system reduces delayed craniospinal relapses including dissemination, local, and distant recurrences even ≥5 years after complete response in patients with primary central nervous system germinoma.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,746 | Synergistic effects of hIAPP and Aβ<sub>1</sub><sub>-</sub><sub>42</sub> impaired the olfactory function associated with the decline of adult neurogenesis in SVZ. | According to many in the field，the prevalence of Alzheimer's disease (AD) in type II diabetes (T2DM) populations is considerably higher than that in the normal population. Human islet amyloid polypeptide (hIAPP) is considered to be a common risk factor for T2DM and AD. Preliminary observations around T2DM animal model show that the decrease of adult neural stem cells (NSCs) in the subventricular zone (SVZ) is accompanied by olfactory dysfunction. Furthermore, impaired olfactory function could serve as to an early predictor of neurodegeneration，which is associated with cognitive impairment. However, the synergistic effects between hIAPP and amyloid-beta (Aβ) <sub>1</sub><sub>-</sub><sub>42</sub> in the brain and the neurodegeneration remains to be further clarified. In this study, olfactory capacity, synaptic density, status of NSC in SVZ, and status of newborn neurons in olfactory bulb (OB) were assessed 6 months after stereotactic injection of oligomer Aβ<sub>1</sub><sub>-</sub><sub>42</sub> into the dens gyrus (DG) of hIAPP-/+ mice or wild-type homogenous mice. Our results set out that Aβ<sub>42</sub> and amylin co-localized into OB and raised Aβ<sub>42</sub> deposition in hIAPP<sup>-/+</sup> mice compared with wild-type brood mice. In addition, 6 months after injection of Aβ<sub>1</sub><sub>-</sub><sub>42</sub> in hIAPP<sup>-/+</sup> mice, these mice showed increased olfactory dysfunction, significant loss of synapses, depletion of NSC in SVZ, and impaired cell renewal in OB. Our present study suggested that the synergistic effects between hIAPP and Aβ<sub>1</sub><sub>-</sub><sub>42</sub> impairs olfactory function and was associated with decreased neurogenesis in adults with SVZ. |
2,329,747 | Accurate image-based CSF volume calculation of the lateral ventricles. | The size/volume of the brain's ventricles is essential in diagnosing and treating many neurological disorders, with various forms of hydrocephalus being some of the most common. Initial ventricular size and changes, if any, in response to disease progression or therapeutic intervention are monitored by serial imaging methods. Significant variance in ventricular size is readily noted, but small incremental changes can be challenging to appreciate. We have previously reported using artificial intelligence to determine ventricular volume. The values obtained were compared with those calculated using the inaccurate manual segmentation as the "gold standard". This document introduces a strategy to measure ventricular volumes where manual segmentation is not employed to validate the estimations. Instead, we created 3D printed models that mimic the lateral ventricles and measured those 3D models' volume with a tuned water displacement device. The 3D models are placed in a gel and taken to the magnetic resonance scanner. Images extracted from the phantoms are fed to an artificial intelligence-based algorithm. The volumes yielded by the automation must equal those yielded by water displacement to assert validation. Then, we provide certified volumes for subjects in the age range (1-114) months old and two hydrocephalus patients. |
2,329,748 | Third Ventricle Craniopharyngioma Intraventricular Tumor: A Case Report and a Brief Literature Review. | Craniopharyngioma is a rare embryonic malformation, usually benign, of the sellar or parasellar regions. In this study, an uncommon case of third ventricle craniopharyngioma and a succinct review of its prevalence are presented. Even with low mortality rates, these injuries involve a high degree of endocrinological, visual, and neuropsychological morbidities, which have a huge impact on the patient's quality of life. Thus, surgical resection is the preferred therapy for tumors that compromise the flow of cerebrospinal fluid. However, due to the location of the craniopharyngioma, surgical management is accompanied by the risk of injury to important adjacent areas with postoperative repercussions. Therefore, the neurosurgeon's experience and the choice of the best surgical approach, are crucial for increasing prognosis. |
2,329,749 | Diagnosis of symmetric bilateral lateral ventricular subependymomas: A case report. | Subependymomas are rare benign tumors that are hypovascular and noninvasive. Subependymomas tend to present as solitary lesions in the fourth ventricle or the frontal horn of the lateral ventricle. When multiple lesions are present, determining the correct diagnosis between subependymoma and other intraventricular neoplasms can be challenging. The characterization of imaging features and enhancement patterns can help narrow down the list of potential differential diagnoses. In this article, we describe a case of bilateral subependymomas in the lateral ventricles in a 40-year-old Asian man, including the clinical features, imaging results from conventional magnetic resonance imaging, magnetic resonance spectroscopy, and magnetic resonance perfusion, histological outcomes, and the disease management approach. |
2,329,750 | Schizencephaly as an Unusual Cause of Adult-Onset Epilepsy: A Case Report. | Schizencephaly is a very rare anatomical malformation of the cerebrum characterized by a cleft extending from the cortex to the ventricles. Usually, this disease is diagnosed at a very young age or in early adulthood. Symptoms may vary depending on the site and the size of the malformation. Here, we are describing the unique case of a 21-year-old female, with a past medical history of migraine-type headaches, who presented after the first-onset seizure and was found to have open-lip schizencephaly. She was started on levetiracetam with no complications. In this report, we are trying to describe the proposed etiology and discuss the typical clinical presentation of schizencephaly and compare it to our adult patient who survived childhood without significant cognitive or neurological impairment. |
2,329,751 | Fast acquisition of left and right ventricular function parameters applying cardiovascular magnetic resonance in clinical routine - validation of a 2-shot compressed sensing cine sequence.<Pagination><StartPage>266</StartPage><EndPage>275</EndPage><MedlinePgn>266-275</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/14017431.2022.2099010</ELocationID><Abstract><AbstractText Label="UNLABELLED"><i>Objectives.</i> To evaluate if cine sequences accelerated by compressed sensing (CS) are feasible in clinical routine and yield equivalent cardiac morphology in less time. <i>Design.</i> We evaluated 155 consecutive patients with various cardiac diseases scanned during our clinical routine. LV and RV short axis (SAX) cine images were acquired by conventional and prototype 2-shot CS sequences on a 1.5 T CMR. The 2-shot prototype captures the entire heart over a period of 3 beats making the acquisition potentially even faster. Both scans were performed with identical slice parameters and positions. We compared LV and RV morphology with Bland-Altmann plots and weighted the results in relation to pre-defined tolerance intervals. Subjective and objective image quality was evaluated using a 4-point score and adapted standardized criteria. Scan times were evaluated for each sequence. <i>Results.</i> In total, no acquisitions were lost due to non-diagnostic image quality in the subjective image score. Objective image quality analysis showed no statistically significant differences. The scan time of the CS cines was significantly shorter (<i>p</i> < .001) with mean scan times of 178 ± 36 s compared to 313 ± 65 s for the conventional cine. All cardiac function parameters showed excellent correlation (<i>r</i> 0.978-0.996). Both sequences were considered equivalent for the assessment of LV and RV morphology. <i>Conclusions.</i> The 2-shot CS SAX cines can be used in clinical routine to acquire cardiac morphology in less time compared to the conventional method, with no total loss of acquisitions due to nondiagnostic quality.</AbstractText><AbstractText Label="TRIAL REGISTRATION">ISRCTN12344380. Registered 20 November 2020, retrospectively registered.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gröschel</LastName><ForeName>Jan</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-7268-9041</Identifier><AffiliationInfo><Affiliation>Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Working Group on Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a Joint Cooperation Between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine Charité Campus Buch, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ammann</LastName><ForeName>Clemens</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000-0002-5962-4008</Identifier><AffiliationInfo><Affiliation>Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Working Group on Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a Joint Cooperation Between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine Charité Campus Buch, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zange</LastName><ForeName>Leonora</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Working Group on Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a Joint Cooperation Between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine Charité Campus Buch, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology and Nephrology, HELIOS Hospital Berlin-Buch, Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Viezzer</LastName><ForeName>Darian</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Working Group on Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a Joint Cooperation Between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine Charité Campus Buch, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Forman</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Siemens Healthineers, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmidt</LastName><ForeName>Michaela</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Siemens Healthineers, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blaszczyk</LastName><ForeName>Edyta</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Working Group on Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a Joint Cooperation Between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine Charité Campus Buch, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schulz-Menger</LastName><ForeName>Jeanette</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Working Group on Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a Joint Cooperation Between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine Charité Campus Buch, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Berlin, Germany.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Cardiology and Nephrology, HELIOS Hospital Berlin-Buch, Berlin, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Scand Cardiovasc J</MedlineTA><NlmUniqueID>9708377</NlmUniqueID><ISSNLinking>1401-7431</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D062485" MajorTopicYN="N">Breath Holding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007090" MajorTopicYN="N">Image Interpretation, Computer-Assisted</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019028" MajorTopicYN="Y">Magnetic Resonance Imaging, Cine</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011237" MajorTopicYN="N">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015203" MajorTopicYN="N">Reproducibility of Results</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016278" MajorTopicYN="Y">Ventricular Function, Right</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Magnetic resonance imaging</Keyword><Keyword MajorTopicYN="N">cardiovascular magnetic resonance</Keyword><Keyword MajorTopicYN="N">compressed sensing</Keyword><Keyword MajorTopicYN="N">fast imaging</Keyword><Keyword MajorTopicYN="N">left ventricle</Keyword><Keyword MajorTopicYN="N">right ventricle</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>15</Day><Hour>2</Hour><Minute>13</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35836407</ArticleId><ArticleId IdType="doi">10.1080/14017431.2022.2099010</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35836381</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Utilizing technology to expand home monitoring to high-risk infants with CHD. | Infants born with single ventricle physiology that require an aorto-pulmonary shunt are at high risk for sudden cardiac death, particularly during the interstage period between the first-stage palliation and the second-stage palliation. Home monitoring programs have decreased interstage mortality in the hypoplastic left heart syndrome population prompting programs to expand the home monitoring program to other high-risk populations. At our mid-sized program, we implemented the Locus Health home monitoring platform first in the hypoplastic left heart syndrome population, then expanding to the single ventricle shunt population. Interstage mortality for the hypoplastic left heart syndrome population after initiation of the home monitoring program went from 18% prior to 2009 to 7% as of the end of 2020 (n = 99), with 2.8% mortality from 2013 to 2020 and 0% mortality since initiation of the Locus program in 2017. Caregiver surveys done prior to discharge and then 3 weeks later were used to document caregiver experience using the digital home monitoring program. Caregivers reported overall positive experience with the digital application, with 91.8% stating that they felt confident taking care of their baby at home. Transitioning the home monitoring program from a traditional binder to an iPad with the Locus Health application allowed us to expand the program, utilize the electronic medical record, bill for the service, and demonstrate positive experiences for caregivers. Overall engagement and adherence with the program by caregivers were 50.94 and 45.45%, with a total of 112 patient episodes. Reimbursement from private insurance providers was 22% of the billed amount for 2020. |
2,329,752 | Diffuse Myocardial Fibrosis at Cardiac MRI in Young Adults Born Prematurely: A Cross-sectional Cohort Study. | To measure native T1 values, a marker of diffuse fibrosis, by using cardiac MRI (CMR) in young adults born prematurely.</AbstractText>This secondary analysis of a prospective cohort study included young adults born moderately to extremely preterm and age-matched, term-born participants. CMR was performed with a 3.0-T imager that included cine imaging for the quantification of left ventricular (LV) and right ventricular (RV) volumes and function and native saturation recovery T1 mapping for the assessment of diffuse myocardial fibrosis. Values between preterm and term were compared by using the Student t</i> test. Associations between T1 values and other variables were analyzed by using linear regression and multivariate regression.</AbstractText>Of the 50 young-adult participants, 32 were born preterm (mean age, 25.8 years ± 4.2 [SD]; 23 women) and 18 were born at term (mean age, 26.2 years ± 5.4; 10 women). Native T1 values were significantly higher in participants born preterm than in participants born at term (1477 msec ± 77 vs 1423 msec ± 71, respectively; unadjusted P</i> = .0019). Native T1 values appeared to be positively associated with indexed LV end-diastolic and end-systolic volumes (β = 2.1, standard error = 0.7 and β = 3.8, standard error = 1.2, respectively), the RV end-diastolic volume index (β = 1.3, standard error = 0.6), and the LV mass index (β = 2.5, standard error = 0.9). Higher T1 values may be associated with reduced cardiac systolic strain measures and diastolic strain measures. Five-minute Apgar scores were inversely associated with native T1 values.</AbstractText>Young adults born moderately to extremely preterm exhibited significantly higher native T1 values than age-matched, term-born young adults.Keywords:</b> MRI, Cardiac, Heart, Left Ventricle, CardiomyopathiesClinical trial registration no. NCT03245723Published under a CC BY 4.0 license Supplemental material is available for this article.</i></AbstractText>© 2022 by the Radiological Society of North America, Inc.</CopyrightInformation> |
2,329,753 | Clinically important changes in right ventricular volume and function in pulmonary arterial hypertension assessed with cardiac magnetic resonance imaging. | Right ventricular (RV) dilatation predicts clinical worsening in pulmonary arterial hypertension (PAH) and RV volumes can be measured with high precision using cardiovascular magnetic resonance imaging. In regular follow-up of patients and in studies of improvement in RV function, knowledge of clinically significant changes of RV volumes and function are of relevance. Patients with PAH were followed with cardiovascular magnetic resonance imaging and clinical assessment at 6-month intervals. Changes in RV volumes associated with changes in clinical status were assessed. Twenty-five patients with PAH (Group 1) were included and examined every 6 months for 2.5 years, with a total of 107 MRI scans. For a step change in WHO functional class, the associated change in RV volume was 11% (confidence interval 7%-14%, <i>p</i> < 0.0001) and in stroke volume 9% (confidence interval 3%-15%, <i>p</i> = 0.003). This study found an 11% change in RV volume to be clinically significant. The combination of clinically significant changes and the known precision in the measurements enables individualized follow-up of RV-function in PAH. To our knowledge, this study is the first to use repeated assessments to suggest clinically significant changes of RV volume based on changes in clinical presentation. |
2,329,754 | Symptomatic care of late-onset Alexander disease presenting with area postrema-like syndrome with prednisolone; a case report. | Alexander disease (AxD) is classified into AxD type I (infantile) and AxD type II (juvenile and adult form). We aimed to determine the potential genetic cause(s) contributing to the AxD type II manifestations in a 9-year-old male who presented area postrema-like syndrome and his vomiting and weight loss improved after taking prednisolone.</AbstractText>A normal cognitive 9-year-old boy with persistent nausea, vomiting, and a significant weight loss at the age of 6 years was noticed. He also experienced an episode of status epilepticus with generalized atonic seizures. He showed non-febrile infrequent multifocal motor seizures at the age of 40 days which were treated with phenobarbital. He exhibited normal physical growth and neurologic developmental milestones by the age of six. Occasionally vomiting unrelated to feeding was reported. Upon examination at 9 years, a weak gag reflex, prominent drooling, exaggerated knee-deep tendon reflexes (3+), and nasal tone speech was detected. All gastroenterological, biochemical, and metabolic assessments were normal. Brain magnetic resonance imaging (MRI) revealed bifrontal confluent deep and periventricular white matter signal changes, fine symmetric frontal white matter and bilateral caudate nucleus involvements with garland changes, and a hyperintense tumefactive-like lesion in the brain stem around the floor of the fourth ventricle and area postrema with contrast uptake in post-contrast T1-W images. Latter MRI at the age of 8 years showed enlarged area postrema lesion and bilateral middle cerebellar peduncles and dentate nuclei involvements. Due to clinical and genetic heterogeneities, whole-exome sequencing was performed and the candidate variant was confirmed by Sanger sequencing. A de novo heterozygous mutation, NM_001242376.1:c.262 C > T;R88C in exon 1 of the GFAP (OMIM: 137,780) was verified. Because of persistent vomiting and weight loss of 6.0 kg, prednisolone was prescribed which brought about ceasing vomiting and led to weight gaining of 3.0 kg over the next 3 months after treatment. Occasional attempts to discontinue prednisolone had been resulting in the reappearance of vomiting.</AbstractText>This study broadens the spectrum of symptomatic treatment in leukodystrophies and also shows that R88C mutation may lead to a broad range of phenotypes in AxD type II patients.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,755 | Ventriculomegaly in Cavalier King Charles Spaniels with Chiari-like malformation: relationship with clinical and imaging findings. | The objective of this study was to calculate lateral ventricles dimension in Cavalier King Charles Spaniel dogs with Chiari-like malformation and investigate the association between ventriculomegaly and signalment, clinical signs, ventricular asymmetry, grade of Chiari-like malformation, syringomyelia and index of medullary kinking. Retrospectively, 43 client-owned Cavalier King Charles Spaniels, older than 1 year of age, with magnetic resonance imaging diagnosis of Chiari-like malformation were enrolled. Initial and follow-up (up to 36 months) clinical status was graded. Images were reviewed to quantify the enlargement of lateral ventricles, evaluate ventricular symmetry, grade of Chiari-like malformation, grade of syringomyelia and medullary kinking index. Cases presenting epileptic seizures during the evaluation period were also recorded. The most common initial clinical signs were scratching and neck pain. Ventriculomegaly was identified in 70% of dogs, Chiari-like malformation grade 2 was observed in 77% of cases, ventricular asymmetry and syringomyelia were identified in 54% and 80% of dogs, respectively; the median medullary kinking index was 37.77%. Moreover, 28% of dogs presented epileptic seizures. No significant association was identified between dimension of lateral ventricles and signalment, clinical signs, and imaging findings; no significant association was identified between ventriculomegaly and epilepsy (P≥0.05). In conclusion, the prevalence of ventriculomegaly in Cavalier King Charles Spaniels is high but this finding does not seem related to the severity of clinical signs, presence of Chiari-like malformation, syringomyelia and craniocervical junction abnormalities such as medullary kinking. |
2,329,756 | Leptin receptor-expressing cells in the ventromedial nucleus of the hypothalamus contribute to enhanced CCK-induced satiety following central leptin injection. | Others have shown that leptin and cholecystokinin (CCK) act synergistically to suppress food intake. Experiments described here tested whether leptin in the ventromedial hypothalamus (VMH) contributes to the synergy with peripheral CCK in male Sprague Dawley rats. A subthreshold injection of 50-ng leptin into the VMH 1 h before a peripheral injection of 1 µg/kg CCK did not change the response to CCK in rats offered chow or low-fat purified diet, but did exaggerate the reduction in intake of high-fat diet 30 min and 1 h after injection in rats that had been food deprived for 8 h. By contrast, deletion of leptin receptor-expressing cells in the VMH using leptin-conjugated saporin (Lep-Sap) abolished the response to peripheral CCK in chow-fed rats. Lateral ventricle injection of 2-µg leptin combined with peripheral CCK exaggerated the inhibition of chow intake for up to 6 h in control rats treated with Blank-saporin, but not in Lep-Sap rats. Blank-Saporin rats offered low- or high-fat purified diet also demonstrated a dose-response inhibition of intake that reached significance with 1 µg/kg of CCK for both diets. CCK did not inhibit intake of Lep-Sap rats in either low- or high-fat-fed rats. Thus, although basal activation of VMH leptin receptors makes a significant contribution to the synergy with CCK, increased leptin activity in the VMH does not exaggerate the response to CCK in intact rats offered low-fat diets, but does enhance the response in those offered high-fat diet.<b>NEW & NOTEWORTHY</b> Leptin is a feedback signal in the control of energy balance, whereas cholecystokinin (CCK) is a short-term satiety signal that inhibits meal size. The two hormones synergize to promote satiety. We tested whether leptin receptors in the ventromedial nucleus of the hypothalamus (VMH) contribute to the synergy. The results suggest that there is a requirement for a baseline level of activation of leptin receptors in the VMH in order for CCK to promote satiety. |
2,329,757 | Pineal cysts without hydrocephalus: microsurgical resection via an infratentorial-supracerebellar approach-surgical strategies, complications, and their avoidance. | Indications for surgery of pineal cysts without ventriculomegaly are still under debate. In view of the limited data for pineal cyst resection in the absence of hydrocephalus, and the potential risk of this approach, we have analyzed our patient cohort focusing on strategies to avoid complications according to our experience in a series of 73 pineal cyst patients. From 2003 to 2015, we reviewed our database retrospectively for all patients operated on a pineal cyst. Furthermore, we prospectively collected patients from 2016 to 2020. In summary, 73 patients with a pineal cyst were treated surgically between 2003 and 2020. All patients were operated on via a microscopic supracerebellar-infratentorial (SCIT) approach. The mean follow-up period was 26.6 months (range: 6-139 months). Seventy-three patients underwent surgery for a pineal cyst. An absence of enlarged ventricles was documented in 62 patients (51 female, 11 male, mean age 28.1 (range 4-59) years). Main presenting symptoms included headache, visual disturbances, dizziness/vertigo, nausea/emesis, and sleep disturbances. Complete cyst resection was achieved in 59/62 patients. Fifty-five of 62 (89%) patients improved after surgery with good or even excellent results according to the Chicago Chiari Outcome Scale, with complete or partial resolution of the leading symptoms. Pineal cysts resection might be an indication in certain patients for surgery even in the absence of ventriculomegaly. The high percentage of postoperative resolution of quality-of-life impairing symptoms in our series seems to justify surgery. Preoperatively, other causes of the leading symptoms have to be excluded. |
2,329,758 | Efficacy of endoscopic management of primary central nervous system lymphoma: a multicentric study and literature review. | To date, confined intra-ventricular localization of primary central nervous system lymphoma (PCNSL) has been usually managed with open surgical resection and/or stereotactic biopsy; nonetheless, the endoscopic approach to such localization can provide many advantages over standard microsurgery and/or stereotactic biopsy. Here we present our experience in managing such a rare pathology through the endoscopic approach.</AbstractText>In order to gather more information about such a rare pathology, a retrospective multicentric study on a prospectively built database has been performed during a 5 year period. Ten different European centers have been involved.</AbstractText>A total of 60 patients, 25 women and 35 men, have been enrolled in the study. The mean age was 65.3 years. The mean lesion size was 40.3 mm. Among all selected patients, 40 (66.6%) had superficial lesions within the ventricle, whereas the remaining 20 (33.4%) had lesions involving/extending to deeper structures. All surgical procedures were uneventful and ETV was deemed necessary only in 20/60 cases.</AbstractText>In our experience, endoscopic management of intraventricular PCNSL is an effective option. It should be considered after a careful examination of neurological and immunological status, alternative options for diagnostic sampling, location of the lesion, and presence or absence of hydrocephalus. Endoscopic management could be considered as a safe and minimally invasive option to obtain: (a) a biopsy sample of the lesion for further diagnostic workup, (b) CSF diversion through third ventriculostomy or VP shunt for the management of hydrocephalus, and (c) insertion of ventricular access devices for long term medical management and whenever necessary as a rescue option for ventricular tap.</AbstractText>© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</CopyrightInformation> |
2,329,759 | Intraventricular CNS aspergillosis in a patient with prior history of COVID-19: Case report and review of literature. | Although some immunocompetent patients have developed invasive aspergillosis, the vast majority of cases are seen in immunocompromised patients. COVID-19 infection has been proposed to cause immune dysfunction or suppression, which predisposes patients to fungal co-infections such as mucormycosis and aspergillosis.</AbstractText>A 58-year-old woman was admitted to the hospital with confusion, dysarthria, and loss of consciousness. The patient had a 1-month prior history of severe COVID-19 infection. A computerized tomography (CT) scan and a magnetic resonance imaging (MRI) revealed an intraventricular lesion with perilesional edema and a significant midline shift, which was initially thought to be an intraventricular tumor. Following a posterior parietal craniotomy, the lesion was resected via a transcortical approach from the posterior parietal region to the right lateral ventricle. Histopathological findings confirmed intraventricular aspergillosis (IVA). The patient was treated with intravenous amphotericin B for two months and discharged with oral variconazole for 4 months.</AbstractText>Covid-19 infections can result in- dissemination of fungal diseases such as aspergillosis. As a minor component of cerebral aspergillosis with a poor prognosis, intraventricular aspergillosis necessitates prompt treatment, which includes surgical resection and the administration of anti-fungal medications.</AbstractText>Infection with COVID-19 causes immune dysfunction, which leads to fungal co-infection, including CNS aspergillosis. As a result, all COVID-19 patients who present with acute neurologic symptoms should have CNS aspergillosis considered in their differential diagnosis.</AbstractText>© 2022 Published by Elsevier Ltd on behalf of IJS Publishing Group Ltd.</CopyrightInformation> |
2,329,760 | Detection of Spontaneous Bone Metastases of Solid Human Tumor Xenografts in Mice. | The formation of bone metastases from solid primary tumors comprises several processes following each other in a sequential order in terms of the metastatic cascade. The most widely used preclinical models of bone metastasis formation do not reflect this pathophysiological situation as they are based on intracardiac (left ventricle) or intracaudal artery injection of tumor cells. These attempts circumvent all early steps of the metastatic cascade taking place within primary tumors (e.g., epithelial-mesenchymal transition), the passage of circulating tumor cells through upstream organ "filters" like the lung, and the initial establishment of single disseminated tumor cells/cell clusters within the bone marrow. In this chapter, we describe how the entire cascade of bone metastasis formation can be modelled in vivo using bioluminescence techniques. The cascade ranges from the formation of a primary tumor to the outgrowth of single disseminated tumor cells to micro-metastases within the bone marrow. In addition, we describe how the disseminated tumor cells and bone metastases can be visualized by histological and immunohistochemical staining. The described methodology provides the opportunity to investigate the basic mechanisms of spontaneous bone metastasis formation of solid human tumors in partly immunodeficient hosts in vivo. |
2,329,761 | Glioblastoma disrupts the ependymal wall and extracellular matrix structures of the subventricular zone. | Glioblastoma (GBM) is the most aggressive and common type of primary brain tumor in adults. Tumor location plays a role in patient prognosis, with tumors proximal to the lateral ventricles (LVs) presenting with worse overall survival, increased expression of stem cell genes, and increased incidence of distal tumor recurrence. This may be due in part to interaction of GBM with factors of the subventricular zone (SVZ), including those contained within the cerebrospinal fluid (CSF). However, direct interaction of GBM tumors with CSF has not been proved and would be hindered in the presence of an intact ependymal cell layer.</AbstractText>Here, we investigate the ependymal cell barrier and its derived extracellular matrix (ECM) fractones in the vicinity of a GBM tumor. Patient-derived GBM cells were orthotopically implanted into immunosuppressed athymic mice in locations distal and proximal to the LV. A PBS vehicle injection in the proximal location was included as a control. At four weeks post-xenograft, brain tissue was examined for alterations in ependymal cell health via immunohistochemistry, scanning electron microscopy, and transmission electron microscopy.</AbstractText>We identified local invading GBM cells within the LV wall and increased influx of CSF into the LV-proximal GBM tumor bulk compared to controls. In addition to the physical disruption of the ependymal cell barrier, we also identified increased signs of compromised ependymal cell health in LV-proximal tumor-bearing mice. These signs include increased accumulation of lipid droplets, decreased cilia length and number, and decreased expression of cell channel proteins. We additionally identified elevated numbers of small fractones in the SVZ within this group, suggesting increased indirect CSF-contained molecule signaling to tumor cells.</AbstractText>Our data is the first to show that LV-proximal GBMs physically disrupt the ependymal cell barrier in animal models, resulting in disruptions in ependymal cell biology and increased CSF interaction with the tumor bulk. These findings point to ependymal cell health and CSF-contained molecules as potential axes for therapeutic targeting in the treatment of GBM.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,762 | Differential spatial distribution of white matter lesions in Parkinson's and Alzheimer's diseases and cognitive sequelae. | White Matter Lesions (WML) are a radiological finding common in aged subjects. We explored the impact of WML on underlying neurodegenerative processes. We focused on the impact of WML on two neurodegenerative diseases with different pathology. In this cross-sectional study of 137 subjects (78 female, 59 men, mean age 67.2; 43-87 years), we compared WML in healthy controls (HC; n = 55), patients with Alzheimer's disease and amnestic Mild Cognitive Impairment (aMCI), and Parkinson's disease patients with normal cognition and with MCI. Subjects with AD and aMCI were treated as one group (n = 40), subjects with PD and PDMCI were another group (n = 42). MRI T2_FLAIR sequences were analyzed. WML were divided into periventricular (pWML) or subcortical (sWML) depending on their distance from the ventricles. Subjects from the AD + aMCI group, had a significantly greater volume of WML than both HC and the PD + PDMCI group. The volume of WML was greater in the PD + PDMCI than in HC but the difference was not significant. In AD + aMCI subjects, sWML and not pWML were related to a decrease in global cognitive functioning despite greater volume of pWML. In PD + PDMCI, pWML correlate with decline in executive functions and working memory. In HC, pWML correlated with the multidomain decrease corresponding with the aging. This points to a difference between normal aging and pathological aging due to AD and PD brain pathology. The WML location together with underlying disease related neurodegeneration may play a role in determining the effect of WML on cognition. Our results suggest that the impact of WML is not uniform in all patients; rather, their volume, location and cognitive effect may be disease-specific. |
2,329,763 | Cardiac remodeling in amateur triathletes after 24 weeks of exercise training for a half-Ironman event: a brief report.<Pagination><StartPage>367</StartPage><EndPage>372</EndPage><MedlinePgn>367-372</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.23736/S0022-4707.22.14108-3</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Triathletes' physiological adaptations to exercise training can have a different impact on cardiac remodeling based on the extreme exercise preparation. Moreover, cardiac remodeling might be different depending on whether triathletes have trained for many years or if they just decided to be more active. Nevertheless, data are limited in amateur endurance athletes and studies about them are key for their safety. Therefore, we investigated the effects of exercise training for a half-ironman on cardiac remodeling.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A total of 24 amateur athletes underwent a 24-week exercise program and were followed by three-dimensional echocardiography to assess its global impact on cardiac remodeling. Subanalyses were performed based on participants past-training experience (low versus high).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We found significant group effects on the right and left ventricle, significant time effect on the right ventricle. No significant interaction effects were observed. We observed significant correlations between the right ventricle, clinical and performance characteristics where the peak power output explained 38% of the variance, while the body surface area, weight and power at the second ventilatory threshold explained 34%, 31% and 30%, respectively.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Changes in cardiac remodeling in response to an exercise program for a half-ironman are not homogeneous across the ventricles and are influenced by participants' past-training experience. This study strengthens our knowledge of extreme exercise training for a half-ironman to further develop better training programs and medical follow-up in amateur triathletes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lalonde</LastName><ForeName>François</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Division of Cardiology, University of Montreal Hospital Research Center, Montreal, QC, Canada - triathlonfrank@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Exercise Sciences, Faculty of Sciences, University of Quebec at Montreal, Montreal, QC, Canada - triathlonfrank@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caru</LastName><ForeName>Maxime</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Penn State College of Medicine, Department of Pediatric Hematology and Oncology, Hershey, PA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Penn State College of Medicine, Department of Public Health Sciences, Hershey, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baudet</LastName><ForeName>Mathilde</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Cardiology, University of Montreal Hospital Research Center, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ribeiro</LastName><ForeName>Paula Ab</ForeName><Initials>PA</Initials><AffiliationInfo><Affiliation>Division of Cardiology, University of Montreal Hospital Research Center, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>Sarah-Maude</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Division of Cardiology, University of Montreal Hospital Research Center, Montreal, QC, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Exercise Sciences, Faculty of Sciences, University of Quebec at Montreal, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Comtois</LastName><ForeName>Alain S</ForeName><Initials>AS</Initials><AffiliationInfo><Affiliation>Department of Exercise Sciences, Faculty of Sciences, University of Quebec at Montreal, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tournoux</LastName><ForeName>François B</ForeName><Initials>FB</Initials><AffiliationInfo><Affiliation>Department of Exercise Sciences, Faculty of Sciences, University of Quebec at Montreal, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>J Sports Med Phys Fitness</MedlineTA><NlmUniqueID>0376337</NlmUniqueID><ISSNLinking>0022-4707</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010807" MajorTopicYN="Y">Physical Endurance</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020257" MajorTopicYN="Y">Ventricular Remodeling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015444" MajorTopicYN="N">Exercise</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056352" MajorTopicYN="N">Athletes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>11</Day><Hour>10</Hour><Minute>40</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35816147</ArticleId><ArticleId IdType="doi">10.23736/S0022-4707.22.14108-3</ArticleId><ArticleId IdType="pii">S0022-4707.22.14108-3</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35815747</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1467-1107</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>11</Day></PubDate></JournalIssue><Title>Cardiology in the young</Title><ISOAbbreviation>Cardiol Young</ISOAbbreviation></Journal>Mid-term follow-up by speckle tracking and cardiac MRI of children post-transcatheter closure of large atrial septal defects. | This is a case-control study of our experience of mid-term follow-up of 40 children who had a transcatheter closure of very large atrial septal defects group (1). All cases had an atrial septal defect device size more than 1.5 times their weight, a ratio considered a contraindication for trans catheter closure (TCC) in some previous reports. The aim of this study is to report the outcomes and mid-term follow-up of transcatheter closure of large atrial septal defects using two-dimensional conventional echocardiography, tissue Doppler imaging, and four-dimensional speckle tracking imaging, and as such to compare results of same echocardiographic examination of age-matched control group of 40 healthy children group (2). Cardiac MRI was performed on cases group (1) only to detect right ventricle and left ventricle volumes and function and early signs of complications. There was no difference between cases and matched healthy controls in terms of the assessment of left ventricle and right ventricle by two-dimensional echocardiography, tissue Doppler imaging, and four-dimensional speckle tracking imaging. Similarly, there was no statistically significant difference between four-dimensional echocardiography and cardiac MRI in their respective assessment of both left ventricle and right ventricle volumes and function. We also detected no complications by echo or by cardiac MRI after a median follow-up period of 2 years and recorded a complete remodelling of right ventricle volumes in all children studied. This points to the safety and efficiency of transcatheter closure of large atrial septal defects in children on mid-term follow-up. |
2,329,764 | Bilateral Vocal Cord Paralysis Associated with Meningeal Carcinomatosis from Lung Adenocarcinoma. | Cranial neuropathy is a clinical manifestation of meningeal carcinomatosis (MC); however, the glossopharyngeal and vagus nerves are rarely impaired. Therefore, dysphagia and bilateral vocal cord paralysis (BVCP) are extremely rare manifestations of MC. Here, we present a case of MC from a lung adenocarcinoma presenting with dysphagia and BVCP. An 84-year-old man with a 4-year history of left lung adenocarcinoma developed dysphagia and hoarseness. Flexible nasopharyngoscopy revealed BVCP. Ten days later, the patient developed stridor and respiratory distress. A tracheotomy was performed to prevent airway obstruction. Gadolinium-enhanced magnetic resonance imaging (MRI) of the brain showed enhancement of the bilateral glossopharyngeal and vagus nerves, and several enhancing lesions in the right internal auditory canal, left cerebellum, fourth ventricle, pons, cerebral aqueduct, and right frontal lobe, suggesting MC and brain metastasis. Based on the clinical history of malignancy and the MRI findings, the patient was diagnosed with MC. As the patient refused additional treatment, including chemotherapy and radiation, only palliative care was provided. To the best of our knowledge, this was the first case of MC from a solid tumor presenting with BVCP. When patients with malignancy present with BVCP, MC should be considered. |
2,329,765 | Resuscitation of Term Compromised and Asphyctic Newborns: Better with Intact Umbilical Cord? | The authors hypothesize that particularly severely compromised and asphyctic term infants in need of resuscitation may benefit from delayed umbilical cord clamping (after several minutes). Although evidence is sparse, the underlying pathophysiological mechanisms support this assumption. For this review the authors have analyzed the available research. Based on these data they conclude that it may be unfavorable to immediately clamp the cord of asphyctic newborns (e.g., after shoulder dystocia) although recommended in current guidelines to provide quick neonatological support. Compression of the umbilical cord or thorax obstructs venous flow to the fetus more than arterial flow to the placenta. The fetus is consequently cut off from a supply of oxygenated, venous blood. This may cause not only hypoxemia and consecutive hypoxia during delivery but possibly also hypovolemia. Immediate cord clamping may aggravate the situation of the already compromised newborn, particularly if the cord is cut before the lungs are ventilated. By contrast, delayed cord clamping leads to fetoplacental transfusion of oxygenated venous blood, which may buffer an existing acidosis. Furthermore, it may enhance blood volume by up to 20%, leading to higher levels of various blood components, such as red and white blood cells, thrombocytes, mesenchymal stem cells, immunoglobulins, and iron. In addition, the resulting increase in pulmonary perfusion may compensate for an existing hypoxemia or hypoxia. Early cord clamping before lung perfusion reduces the preload of the left ventricle and hinders the establishment of sufficient circulation. Animal models and clinical trials support this opinion. The authors raise the question whether it would be better to resuscitate compromised newborns with intact umbilical cords. Obstetric and neonatal teams need to work even closer together to improve neonatal outcomes. |
2,329,766 | Prediction of high and low disease activity in early MS patients using multiple kernel learning identifies importance of lateral ventricle intensity. | Lack of easy-to-interpret disease activity prediction methods in early MS can lead to worse patient prognosis.</AbstractText>Using machine learning (multiple kernel learning - MKL) models, we assessed the prognostic value of various clinical and MRI measures for disease activity.</AbstractText>Early MS patients (n</i> = 148) with at least two associated clinical and MRI visits were investigated. T2-weighted MRIs were cropped to contain mainly the lateral ventricles (LV). High disease activity was defined as surpassing NEDA-3 Criteria more than once per year. Clinical demographic, MRI-extracted image-derived phenotypes (IDP), and MRI data were used as inputs for separate kernels to predict future disease activity with MKL. Model performance was compared using bootstrapped effect size analysis of mean differences.</AbstractText>A total of 681 visits were included, where 81 (55%) patients had high disease activity in a combined end point measure using all follow-up visits. MKL model discrimination performance was moderate (AUC ≥ 0.62); however, modelling with combined clinical and cropped LV kernels gave the highest prediction performance (AUC = 0.70).</AbstractText>MRIs contain valuable information on future disease activity, especially in and around the LV. MKL techniques for combining different data types can be used for the prediction of disease activity in a relatively small MS cohort.</AbstractText>© The Author(s), 2022.</CopyrightInformation> |
2,329,767 | Revisiting the Concept of Recurrence of Primary Central Nervous System Lymphomas After Complete Response to Methotrexate-Based Therapy: Periventricular Reseeding as the Predominant Mechanism of Recurrence. | Understanding patterns of relapse for primary central nervous system lymphoma (PCNSL) may inform mechanisms of recurrence and optimal consolidation strategies. In this study, we report patterns of relapse among patients with PCNSL who achieved a complete response to high-dose methotrexate (HD-MTX)-based chemotherapy with or without consolidation radiation therapy (RT).</AbstractText>We conducted an institutional retrospective analysis of patients with PCNSL who received HD-MTX-based chemotherapy between November 2001 and May 2019. Relapses were characterized as in-field (within original T1 contrasted lesion), marginal (within T2 fluid-attenuated inversion recovery but not T1), local (in-field or marginal), distant brain (no overlap), or distant (distant brain, cerebrospinal fluid, vitreous or extra-axial) and further characterized with respect to periventricular location (≤10 mm of ventricles).</AbstractText>Seventy-eight patients with PCNSL met inclusion criteria, of whom 29 (37%) underwent consolidation RT. Median progression-free survival and overall survival were 57.0 and 66.7 months, respectively. After a median follow-up of 38.9 months, a total of 32 patients (41%) experienced recurrence. Most patients (21 [65.6%]) had a periventricular failure. Surprisingly, local recurrences (n = 11) were exclusively observed within periventricular lesions, whereas distant recurrences (n = 21) were seen in both periventricular and nonperiventricular locations (P </i>= .009). The median time to progression was shorter for locally recurrent lesions compared with distant recurrences (13.8 vs 26.1 months; P </i>= .03).</AbstractText>After complete response to HD-MTX, few failures occurred within initial T1 contrast-enhancing lesions and many of these may have been alternatively classified as periventricular failures. These observations argue against the use of purely focal RT consolidation for patients who achieve a complete response after HD-MTX-based chemotherapy and suggest that periventricular reseeding may have a central role in PCNSL recurrence.</AbstractText>© 2022 The Authors.</CopyrightInformation> |
2,329,768 | [Septo optic dysplasia plus: about a case]. | Septo optic dysplasia plus is a rare disease seen in children. Its diagnosis is radiological, based on brain magnetic resonance imaging (MRI). We report the case of a child aged 2 years and 4 months, with no particular pathological history; who consulted for psychomotor retardation, strabismus and low vision behavior. An endocrine biological assessment exploring the hypothalomo-pituitary function was carried out, revealing no abnormality. The diagnosis of septo-optic dysplasia plus was retained on the brain MRI data, in front of the agenesis of the septum pellucidum and of the splenium of the corpus callosum, the hypoplasia of the optic pathways and of the pituitary stalk as well as in front of the agenesis of the posterior pituitary. It was associated with a closed schizencephaly. Septo-optic dysplasia is a rare congenital malformation. Our objective is to recall its semiology in imaging and to underline the importance of MRI to establish the diagnosis. Septo-optic dysplasia is a rare clinical entity typically involving midline brain abnormalities, optic nerve hypoplasia, and pituitary insufficiency. The association with cortical malformations such as schizencephaly and polymicrogyria denotes the term septo-optic dysplasia plus. Advances in imaging currently allow early diagnosis, which is essential for adequate management. Antenatal ultrasound may suspect dysplasia, and brain MRI confirms the diagnosis.<CopyrightInformation>Copyright: Lamiaa Chahidi El Ouazzani et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ouazzani</LastName><ForeName>Lamiaa Chahidi El</ForeName><Initials>LCE</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jadib</LastName><ForeName>Abdelhamid</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laoudiyi</LastName><ForeName>Dalal</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Youssef</LastName><ForeName>Sara</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chbani</LastName><ForeName>Kamilia</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salam</LastName><ForeName>Siham</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ouzidane</LastName><ForeName>Lahcen</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Service de la Radiologie Pédiatrique, Hôpital Ibn Rochd, Casablanca, Maroc.</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><VernacularTitle>Dysplasie septo optique plus: à propos d’un cas.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2022</Year><Month>05</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Uganda</Country><MedlineTA>Pan Afr Med J</MedlineTA><NlmUniqueID>101517926</NlmUniqueID></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007018" MajorTopicYN="Y">Hypopituitarism</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D065707" MajorTopicYN="Y">Schizencephaly</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D025962" MajorTopicYN="Y">Septo-Optic Dysplasia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012688" MajorTopicYN="N">Septum Pellucidum</DescriptorName><QualifierName UI="Q000002" MajorTopicYN="N">abnormalities</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre">La dysplasie septo optique plus est une pathologie rare qui se voit chez l´enfant. Son diagnostic est radiologique, reposant sur l'imagerie par résonnance magnétique (IRM) cérébrale. Nous rapportons le cas d´un enfant âgé de 2 ans et 4 mois, sans antécédents pathologiques particuliers, qui a consulté pour un retard psycho moteur, un strabisme et des comportements de malvoyance. Un bilan biologique endocrinien explorant la fonction hypothalomo-hypophysaire a été réalisé, ne révélant pas d´anomalie. Le diagnostic de dysplasie septo-optique plus a été retenu sur les données de l´IRM encéphalique, devant l´agénésie du septum pellucidum et du splénium du corps calleux, l´hypoplasie des voies optiques et de la tige pituitaire ainsi que devant l´agénésie de la post hypophyse. Il s´y associait une schizencéphalie fermée. La dysplasie septo-optique est une malformation congénitale rare. Notre objectif est de rappeler sa sémiologie en imagerie et de souligner l´importance de l´IRM pour établir le diagnostic. La dysplasie septo-optique est une entité clinique rare associant classiquement des anomalies encéphaliques de la ligne médiane, une hypoplasie des nerfs optiques et une insuffisance hypophysaire. L´association à des malformations corticales comme la schizencéphalie et la polymicrogyrie désigne le terme dysplasie septo-optique plus. Les progrès de l´imagerie permettent actuellement un diagnostic précoce, ce qui est primordial pour une prise en charge adéquate. L´échographie anténatale peut suspecter la dysplasie, et l´IRM encéphalique confirme le diagnostic. |
2,329,769 | Evaluation of Intracranial Structures of Fetuses With Congenital Heart Defects.<Pagination><StartPage>419</StartPage><EndPage>425</EndPage><MedlinePgn>419-425</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/jum.16049</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">We classified congenital heart defects (CHDs) according to cerebral blood flow oxygenation and aimed to evaluate the effect on the size of brain structures in these fetuses.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">The study which was designed retrospectively, included 28 patients with fetal CHDs and 76 patients without fetal anomalies.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The width and length of the cavum septum pellucidum significantly increased in the CHD group (P = .002, P = .004). The biparietal diameter and z scores were significantly lower in the single ventricle (SV) (P = .006, P = .019), and the head circumference (HC) and z scores were significantly lower in the transposition of great arteries (TGA) (P = .013, P = .038). The transverse cerebellar diameter, the cerebellar HC and the cerebellar hemisphere area values were lower in the SV (P = .005, P = .017, P = .044).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Brain structure changes are more pronounced in groups with low cerebral oxygenation, especially in the SV and the TGA.</AbstractText><CopyrightInformation>© 2022 American Institute of Ultrasound in Medicine.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Turgut</LastName><ForeName>Ezgi</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0002-5509-7888</Identifier><AffiliationInfo><Affiliation>School of Medicine, Department of Obstetrics and Gynecology, Gazi University, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Özdemir</LastName><ForeName>Halis</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0002-9194-8504</Identifier><AffiliationInfo><Affiliation>School of Medicine, Department of Obstetrics and Gynecology, Gazi University, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Turan</LastName><ForeName>Gokce</ForeName><Initials>G</Initials><Identifier Source="ORCID">0000-0002-2443-1927</Identifier><AffiliationInfo><Affiliation>School of Medicine, Department of Obstetrics and Gynecology, Gazi University, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karcaaltıncaba</LastName><ForeName>Deniz</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0001-5276-9303</Identifier><AffiliationInfo><Affiliation>School of Medicine, Department of Obstetrics and Gynecology, Gazi University, Ankara, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bayram</LastName><ForeName>Merih</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0003-1299-2433</Identifier><AffiliationInfo><Affiliation>School of Medicine, Department of Obstetrics and Gynecology, Gazi University, Ankara, Turkey.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Ultrasound Med</MedlineTA><NlmUniqueID>8211547</NlmUniqueID><ISSNLinking>0278-4297</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014188" MajorTopicYN="Y">Transposition of Great Vessels</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006257" MajorTopicYN="N">Head</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016216" MajorTopicYN="N">Ultrasonography, Prenatal</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">brain structures</Keyword><Keyword MajorTopicYN="N">cerebral blood flow oxygenation</Keyword><Keyword MajorTopicYN="N">congenital heart defect</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>5</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>2</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>6</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>1</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>11</Day><Hour>1</Hour><Minute>33</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35811400</ArticleId><ArticleId IdType="doi">10.1002/jum.16049</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>Massaro AN, El-dib M, Glass P, et al. 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Can J Cardiol 2021; 37:425-432.</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">29494015</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK482408</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-28072">Physiology, Pulse Pressure | Pulse pressure is the difference between systolic and diastolic blood pressures. <b>Pulse Pressure = Systolic Blood Pressure – Diastolic Blood Pressure.</b> The systolic blood pressure is defined as the maximum pressure experienced in the aorta when the heart contracts and ejects blood into the aorta from the left ventricle (approximately 120 mmHg). The diastolic blood pressure is the minimum pressure experienced in the aorta when the heart is relaxing before ejecting blood into the aorta from the left ventricle (approximately 80 mmHg). Normal pulse pressure is, therefore, approximately 40 mmHg. A change in pulse pressure (delta Pp) is proportional to volume change (delta-V) but inversely proportional to arterial compliance (C): <b>Delta Pp =  Delta V/C.</b> Because the change in volume is due to the stroke volume of blood ejected from the left ventricle (SV), we can approximate pulse pressure as: <b>Pp = SV/C.</b> A normal young adult at rest has a stroke volume of approximately 80 mL. Arterial compliance is approximately 2 mL/mm Hg, which confirms that normal pulse pressure is approximately 40 mm Hg. Arterial compliance is equal to the change in volume (Delta V) over a given change in pressure (Delta P): <b>C = Delta V/Delta P.</b> Because the aorta is the most compliant portion of the human arterial system, the pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again. This concept requires an understanding of the effect of pressure wave reflection on the amplification of aortic pressure and thus pulse pressure. The phenomenon mainly occurs in the lower body, especially the lower extremities where pressure waves reflect back due to vessel branching, and the vessels are less compliant (stiffer) When a reflected wave is in phase with a forward wave, it generates a wave with higher amplitude. An analogy here is waves bouncing off a seawall and interacting with an incoming wave. If they are in phase, the wave height is greater. A pulse pressure that is less than 25% of the systolic pressure is inappropriately low or narrowed, whereas a pulse pressure of greater than 100 is high or widened. |
2,329,770 | Feasibility, Prediction and Association of Right Ventricular Free Wall Longitudinal Strain with 30-Day Mortality in Severe COVID-19 Pneumonia: A Prospective Study. | Introduction: Right ventricular (RV) systolic dysfunction (RVsD) is a common complication of coronavirus infection 2019 disease (COVID-19). The right ventricular free wall longitudinal strain parameter (RV-FWLS) is a powerful predictor of mortality. We explored the performance of RVsD parameters for predicting 30-day mortality and the association between RV-FWLS and 30-day mortality. Methods: COVID-19 patients hospitalized at Amiens University Hospital in the critical care unit with transthoracic echocardiography were included. We measured tricuspid annular plane systolic excursion (TAPSE), the RV S’ wave, RV fractional area change (RV-FAC), and RV-FWLS. The diagnostic performance of RVsD parameters as predictors for 30-day mortality was evaluated by the area under the receiver operating characteristic (ROC) curve (AUC). RVsD was defined by an RV-FWLS < 21% to explore the association between RVsD and 30-day mortality. Results: Of the 116 patients included, 20% (n = 23/116) died and 47 had a RVsD. ROC curve analysis showed that RV-FWLS failed to predict 30-day mortality, as did conventional RV parameters (all p > 0.05). TAPSE (21 (19−26) mm vs. 24 (21−27) mm; p = 0.024) and RV-FAC (40 (35−47)% vs. 47 (41−55)%; p = 0.006) were lowered in the RVsD group. In Cox analysis, RVsD was not associated with 30-day mortality (hazard ratio = 1.12, CI 95% (0.49−2.55), p = 0.78). Conclusion: In severe COVID-19 pneumonia, RV-FWLS was not associated with 30-day mortality. |
2,329,771 | Effects of an Exercise Program Combining Aerobic and Resistance Training on Protein Expressions of Neurotrophic Factors in Obese Rats Injected with Beta-Amyloid. | In this study, the effects of a 12-week exercise program combining aerobic and resistance training on high-fat diet-induced obese Sprague Dawley (SD) rats after the injection of beta-amyloid into the cerebral ventricle were investigated. Changes in physical fitness, cognitive function, blood levels of beta-amyloid and metabolic factors, and protein expressions of neurotrophic factors related to brain function such as BDNF (brain-derived neurotrophic factor) in the quadriceps femoris, hippocampus, and cerebral cortex were analyzed. The subjects were thirty-two 10-week-old SD rats (DBL Co., Ltd., Seoul, Korea). The rats were randomized into four groups: β-Non-Ex group (n = 8) with induced obesity and βA25-35 injection into the cerebral ventricle through stereotactic biopsy; β-Ex group (n = 8) with induced obesity, βA25-35 injection, and exercise; S-Non-Ex group (n = 8) with an injection of saline in lieu of βA25-35 as the control; and S-Ex group (n = 8) with saline injection and exercise. The 12-week exercise program combined aerobic training and resistance training. As for protein expressions of the factors related to brain function, the combined exercise program was shown to have a clear effect on activating the following factors: PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), FNDC5 (fibronectin type III domain-containing protein 5), and BDNF in the quadriceps femoris; TrkB (Tropomyosin receptor kinase B), FNDC5, and BDNF in the hippocampus; PGC-1α, FNDC5, and BDNF in the cerebral cortex. The protein expression of β-amyloid in the cerebral cortex was significantly lower in the β-Ex group than in the β-Non-Ex group (p < 0.05). The 12-week intervention with the combined exercise program of aerobic and resistance training was shown to improve cardiopulmonary function, muscular endurance, and short-term memory. The results demonstrate a set of positive effects of the combined exercise program, which were presumed to have arisen mainly due to its alleviating effect on β-amyloid plaques, the main cause of reduced brain function, as well as the promotion of protein expressions of PGC-1α, FNDC5, and BDNF in the quadriceps femoris, hippocampus, and cerebral cortex. |
2,329,772 | Endogenous Neural Stem Cell Mediated Oligodendrogenesis in the Adult Mammalian Brain. | Oligodendrogenesis is essential for replacing worn-out oligodendrocytes, promoting myelin plasticity, and for myelin repair following a demyelinating injury in the adult mammalian brain. Neural stem cells are an important source of oligodendrocytes in the adult brain; however, there are considerable differences in oligodendrogenesis from neural stem cells residing in different areas of the adult brain. Amongst the distinct niches containing neural stem cells, the subventricular zone lining the lateral ventricles and the subgranular zone in the dentate gyrus of the hippocampus are considered the principle areas of adult neurogenesis. In addition to these areas, radial glia-like cells, which are the precursors of neural stem cells, are found in the lining of the third ventricle, where they are called tanycytes, and in the cerebellum, where they are called Bergmann glia. In this review, we will describe the contribution and regulation of each of these niches in adult oligodendrogenesis. |
2,329,773 | The Interaction of <i>mTOR</i> and <i>Nrf2</i> in Neurogenesis and Its Implication in Neurodegenerative Diseases. | Neurogenesis occurs in the brain during embryonic development and throughout adulthood. Neurogenesis occurs in the hippocampus and under normal conditions and persists in two regions of the brain-the subgranular zone (SGZ) in the dentate gyrus of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles. As the critical role in neurogenesis, the neural stem cells have the capacity to differentiate into various cells and to self-renew. This process is controlled through different methods. The mammalian target of rapamycin (<i>mTOR</i>) controls cellular growth, cell proliferation, apoptosis, and autophagy. The transcription factor <i>Nrf2</i> (nuclear factor erythroid 2-related factor 2) is a major regulator of metabolism, protein quality control, and antioxidative defense, and is linked to neurogenesis. However, dysregulation in neurogenesis, <i>mTOR</i>, and <i>Nrf2</i> activity have all been associated with neurodegenerative diseases such as Alzheimer's, Huntington's, and Parkinson's. Understanding the role of these complexes in both neurogenesis and neurodegenerative disease could be necessary to develop future therapies. Here, we review both <i>mTOR</i> and <i>Nrf2</i> complexes, their crosstalk and role in neurogenesis, and their implication in neurodegenerative diseases. |
2,329,774 | Study on Antidepressant Effect and Mechanism of Crocin Mediated by the mTOR Signaling Pathway. | Crocin is a monomer of Chinese traditional herbs extracted from saffron, relieving depression-like behavior. However, its underlying mechanism of action remains unclear. Herein, we explored whether crocin's antidepressant effect depended on the mammalian target of the rapamycin (mTOR) signaling pathway. The model of PC12 cells injury was established by corticosterone, the changes in cell survival rate were tested by the CCK-8 method, and the changes in cellular morphology were observed under a fluorescence microscope. The depression model was established by chronic unpredictable mild stress (CUMS), and its antidepressant effect was estimated by open field test (OFT), forced swimming test (FST), and tail suspension test (TST). Western blot was used to monitor the protein expression. The results showed that crocin could effectively improve cell survival rate and cellular synaptic growth, alleviate the depressive behavior of CUMS mice, and promote the expression of BDNF, P-mTOR, P-ERK, and PSD95. However, when rapamycin was pretreated, the antidepressant effects of crocin were inhibited. In summary, crocin plays a significant antidepressant effect. After pretreatment with rapamycin, the anti-depression effect of crocin was significantly inhibited. It is suggested that the mechanism of the anti-depression effect of crocin may be related to the mTOR signaling pathway. |
2,329,775 | Pleural and transpulmonary pressures to tailor protective ventilation in children. | This review aims to: (1) describe the rationale of pleural (P<sub>PL</sub>) and transpulmonary (P<sub>L</sub>) pressure measurements in children during mechanical ventilation (MV); (2) discuss its usefulness and limitations as a guide for protective MV; (3) propose future directions for paediatric research. We conducted a scoping review on P<sub>L</sub> in critically ill children using PubMed and Embase search engines. We included peer-reviewed studies using oesophageal (P<sub>ES</sub>) and P<sub>L</sub> measurements in the paediatric intensive care unit (PICU) published until September 2021, and excluded studies in neonates and patients treated with non-invasive ventilation. P<sub>L</sub> corresponds to the difference between airway pressure and P<sub>PL</sub> Oesophageal manometry allows measurement of P<sub>ES</sub>, a good surrogate of P<sub>PL</sub>, to estimate P<sub>L</sub> directly at the bedside. Lung stress is the P<sub>L</sub>, while strain corresponds to the lung deformation induced by the changing volume during insufflation. Lung stress and strain are the main determinants of MV-related injuries with P<sub>L</sub> and P<sub>PL</sub> being key components. P<sub>L</sub>-targeted therapies allow tailoring of MV: (1) Positive end-expiratory pressure (PEEP) titration based on end-expiratory P<sub>L</sub> (direct measurement) may be used to avoid lung collapse in the lung surrounding the oesophagus. The clinical benefit of such strategy has not been demonstrated yet. This approach should consider the degree of recruitable lung, and may be limited to patients in which PEEP is set to achieve an end-expiratory P<sub>L</sub> value close to zero; (2) Protective ventilation based on end-inspiratory P<sub>L</sub> (derived from the ratio of lung and respiratory system elastances), might be used to limit overdistention and volutrauma by targeting lung stress values < 20-25 cmH<sub>2</sub>O; (3) P<sub>PL</sub> may be set to target a physiological respiratory effort in order to avoid both self-induced lung injury and ventilator-induced diaphragm dysfunction; (4) P<sub>PL</sub> or P<sub>L</sub> measurements may contribute to a better understanding of cardiopulmonary interactions. The growing cardiorespiratory system makes children theoretically more susceptible to atelectrauma, myotrauma and right ventricle failure. In children with acute respiratory distress, P<sub>PL</sub> and P<sub>L</sub> measurements may help to characterise how changes in PEEP affect P<sub>PL</sub> and potentially haemodynamics. In the PICU, P<sub>PL</sub> measurement to estimate respiratory effort is useful during weaning and ventilator liberation. Finally, the use of P<sub>PL</sub> tracings may improve the detection of patient ventilator asynchronies, which are frequent in children. Despite these numerous theoritcal benefits in children, P<sub>ES</sub> measurement is rarely performed in routine paediatric practice. While the lack of robust clincal data partially explains this observation, important limitations of the existing methods to estimate P<sub>PL</sub> in children, such as their invasiveness and technical limitations, associated with the lack of reference values for lung and chest wall elastances may also play a role. P<sub>PL</sub> and P<sub>L</sub> monitoring have numerous potential clinical applications in the PICU to tailor protective MV, but its usefulness is counterbalanced by technical limitations. Paediatric evidence seems currently too weak to consider oesophageal manometry as a routine respiratory monitoring. The development and validation of a noninvasive estimation of P<sub>L</sub> and multimodal respiratory monitoring may be worth to be evaluated in the future. |
2,329,776 | Giant Colloid Cyst. | Giant colloid cysts are defined as cysts of more than 3 cm in maximal diameter. Few cases of giant colloid cysts have been reported in the literature. We herein describe a giant colloid cyst. A 15-year-old female presented with headache, blurred vision, and episodic behavioral changes for 3 months. Neurological examination was limited due to agitation and confusion. Fundoscopy was notable for bilateral papilledema. Brain computed tomography revealed a giant third-ventricular lesion, causing obstructive hydrocephalus. The patient underwent urgent ventriculoperitoneal shunt insertion initially and then cyst excision. The histopathological sections of the lesion were compatible with a colloid cyst. Five years following surgical resection, a brain magnetic resonance imaging did not demonstrate any evidence of residual or cyst recurrence. To our knowledge, giant colloid cysts have been rarely reported and pose a management dilemma in the literature. The present article highlights the symptomatology, radiological findings, and outcome of a giant colloid cyst. |
2,329,777 | Curcumin analogue BDDD-721 exhibits more potent anticancer effects than curcumin on medulloblastoma by targeting Shh/Gli1 signaling pathway. | Medulloblastoma (MB) is a malignant tumor in the fourth ventricle of children. The clinical treatment is mainly surgical resection combined with radiotherapy and chemotherapy, but the curative effect is not ideal, and the 3-year survival rate is very low. Previous study confirmed that curcumin attenuated the proliferation of medulloblastoma both <i>in vitro</i> and <i>in vivo</i>. In present study, we found a curcumin analogue named BDDD-721, exhibited more potent anti-tumor activity than curcumin. Compared with curcumin, BDDD-721 more effectively inhibited the proliferation, migration, invasion, and increased apoptosis of medulloblastoma cells. Furthermore, BDDD-721 treatment led to activation of glioma-associated oncogene homolog (Gli), reduced expression of Shh and its downstream target Smo, Gli1 and Ptch1. In addition, SAG (Shh signaling pathway agonist) antagonized the pro-apoptotic effects of BDDD-721 on medulloblastomas as confirmed by CCK8 assays and flow cytometry; while cyclopamine (Shh signaling pathway inhibitor) enhanced its effects on medulloblastomas. In conclusion, these results indicate that curcumin analogue BDDD-721 has more potent anticancer effects than curcumin on medulloblastomas by targeting Shh/Gli1 signaling pathway. |
2,329,778 | Brain Damage-linked ATP Promotes P2X7 Receptors Mediated Pineal N-acetylserotonin Release. | The pineal gland is a key player in surveillance and defense responses. In healthy conditions, nocturnal circulating melatonin (MEL) impairs the rolling and adhesion of leukocytes to the endothelial layer. Fungi, bacteria, and pro-inflammatory cytokines block nocturnal pineal MEL synthesis, facilitating leukocyte migration to injured areas. ATP is a cotransmitter of the noradrenergic signal and potentiates noradrenaline (NAd)-induced MEL synthesis via P2Y<sub>1</sub> receptor (P2Y<sub>1</sub>R) activation. Otherwise, ATP low-affinity P2X7 receptor (P2X7R) activation impairs N-acetylserotonin (NAS) into MEL conversion in NAd incubated pineals. Here we mimicked a focal increase of ATP by injecting low (0.3 and 1.0 µg) and high (3.0 µg) ATP in the right lateral ventricle of adult rats. Nocturnal pineal activity mimicked the in culture data. Low ATP doses increased MEL output, while high ATP dose and the P2X7R agonist BzATP (15.0-50.0 ng) increased NAS pineal and blood content. In the brain, the response was structure-dependent. There was an increase in cortical and no change in cerebellar MEL. These effects were mediated by changes in the expression of coding genes to synthetic and metabolizing melatonergic enzymes. Thus, the pineal gland plays a role as a first-line structure to respond to the death of cells inside the brain by turning NAS into the darkness hormone. |
2,329,779 | Bilateral Dacryoadenitis and Central Nervous System Involvement in a Child With Kimura Disease. | Kimura's disease (KD) is a systemic inflammatory condition characterized by lymphadenopathy and subcutaneous nodules in the head and neck region. The lesions have a distinctive histopathological pattern formed by follicular hyperplasia, eosinophilic infiltrates, fibrosis, and vessel proliferation. The disease may occur at all ages but predominates among young males with autoimmune dysfunctions. Visceral and orbital involvement is uncommon. We report a girl with KD who developed bilateral enlargement of the lacrimal glands and a lesion in the left lateral ventricle of the brain indistinguishable from a central nervous system neoplasia. A biopsy of both the lacrimal gland and the lateral ventricle was consistent with KD. |
2,329,780 | Neuropathy-associated Fars2 deficiency affects neuronal development and potentiates neuronal apoptosis by impairing mitochondrial function. | Neurodegenerative diseases encompass an extensive and heterogeneous group of nervous system disorders which are characterized by progressive degeneration and death of neurons. Many lines of evidence suggest the participation of mitochondria dysfunction in these diseases. Mitochondrial phenylalanyl-tRNA synthetase, encoded by FARS2, catalyzes the transfer of phenylalanine to its cognate tRNA for protein synthesis. As a member of mt-aaRSs genes, FARS2 missense homozygous mutation c.424G > T (p.D142Y) found in a Chinese consanguineous family first built the relationship between pure hereditary spastic paraplegia (HSP) and FARS2 gene. More FARS2 variations were subsequently found to cause heterogeneous group of neurologic disorders presenting three main phenotypic manifestations: infantile-onset epileptic mitochondrial encephalopathy, later-onset spastic paraplegia and juvenile onset refractory epilepsy. Studies showed that aminoacylation activity is frequently disrupt in cases with FARS2 mutations, indicating a loss-of-function mechanism. However, the underlying pathogenesis of neuropathy-associated Fars2 deficiency is still largely unknown.</AbstractText>Early gestation lethality of global Fars2 knockout mice was observed prior to neurogenesis. The conditional Fars2 knockout-mouse model delayed lethality to late-gestation, resulting in a thinner cortex and an enlarged ventricle which is consist with the MRI results revealing cortical atrophy and reduced cerebral white matter volume in FARS2-deficient patients. Delayed development of neurite outgrowth followed by neuronal apoptosis was confirmed in Fars2-knockdown mouse primary cultured neurons. Zebrafish, in which fars2 was knocked down, exhibited aberrant motor neuron function including reduced locomotor capacity which well restored the spastic paraplegia phenotype of FARS2-deficient patients. Altered mitochondrial protein synthesis and reduced levels of oxidative phosphorylation complexes were detected in Fars2-deficient samples. And thus, reduced ATP, total NAD levels and mitochondrial membrane potential, together with increased ROS production, revealed mitochondrial dysfunction both in vitro and in vivo. Dctn3 is a potential downstream molecule in responds to Fars2 deficient in neurons, which may provide some evidence for the development of pathogenesis study and therapeutic schedule.</AbstractText>The Fars2 deficiency genetic models developed in this study cover the typical clinical manifestations in FARS2 patients, and help clarify how neuropathy-associated Fars2 deficiency, by damaging the mitochondrial respiratory chain and impairing mitochondrial function, affects neuronal development and potentiates neuronal cell apoptosis.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,781 | Spatial and temporal variation of routine parameters: pitfalls in the cerebrospinal fluid analysis in central nervous system infections. | The cerebrospinal fluid (CSF) space is convoluted. CSF flow oscillates with a net flow from the ventricles towards the cerebral and spinal subarachnoid space. This flow is influenced by heartbeats, breath, head or body movements as well as the activity of the ciliated epithelium of the plexus and ventricular ependyma. The shape of the CSF space and the CSF flow preclude rapid equilibration of cells, proteins and smaller compounds between the different parts of the compartment. In this review including reinterpretation of previously published data we illustrate, how anatomical and (patho)physiological conditions can influence routine CSF analysis. Equilibration of the components of the CSF depends on the size of the molecule or particle, e.g., lactate is distributed in the CSF more homogeneously than proteins or cells. The concentrations of blood-derived compounds usually increase from the ventricles to the lumbar CSF space, whereas the concentrations of brain-derived compounds usually decrease. Under special conditions, in particular when distribution is impaired, the rostro-caudal gradient of blood-derived compounds can be reversed. In the last century, several researchers attempted to define typical CSF findings for the diagnosis of several inflammatory diseases based on routine parameters. Because of the high spatial and temporal variations, findings considered typical of certain CNS diseases often are absent in parts of or even in the entire CSF compartment. In CNS infections, identification of the pathogen by culture, antigen detection or molecular methods is essential for diagnosis. |
2,329,782 | [Effect mechanism of blistering moxibustion on visceral hypersensitivity of irritable bowel syndrome in mice based on 5-HT signal pathway]. | <b>目的：</b>观察天灸法对内脏高敏性肠易激综合征（IBS）小鼠结肠组织5-羟色胺（5-HT）及其受体蛋白表达的影响，探讨天灸法治疗IBS的作用机制。<b>方法：</b>将40只SPF级新生昆明小鼠随机分为正常组、模型组、拮抗组和天灸组，每组10只。造模前拮抗组于侧脑室注射0.2 mL对氯苯丙氨酸（PCPA），模型组、拮抗组和天灸组小鼠应用直肠内冰乙酸刺激结合夹尾刺激制备内脏高敏性IBS模型。造模后，天灸组小鼠行天灸法干预，穴取“中脘”“天枢”“足三里”，每周各穴贴药1次，每次贴药2 h，共3周。采用腹壁回缩反射（AWR）评分和腹壁肌电波幅评价小鼠内脏高敏状态；HE法观察小鼠结肠组织形态变化；免疫组化法检测小鼠结肠组织5-HT及其受体蛋白表达。<b>结果：</b>与正常组比较，20、40 mm Hg（1 mm Hg=0.133 kPa）压力下模型组腹壁肌电波幅升高（<i>P</i><0.05），60、80 mm Hg压力下模型组AWR评分及腹壁肌电波幅均升高（<i>P</i><0.05）；与模型组比较，20 mm Hg压力下天灸组腹壁肌电波幅降低（<i>P</i><0.05），40 mm Hg压力下天灸组与拮抗组AWR评分均升高（<i>P</i><0.05），60、80 mm Hg压力下天灸组与拮抗组AWR评分及腹壁肌电波幅均降低（<i>P</i><0.05）。与正常组比较，模型组黏膜上层结构轻度紊乱，黏膜下层可见中度炎性细胞；与模型组比较，天灸组与拮抗组黏膜上层固有腺体形状规则，可见少量炎性细胞。与正常组比较，模型组结肠组织5-HT及5-羟色胺受体3（5-HT<sub>3</sub>R）蛋白平均阳性面积率增加、5-羟色胺受体4（5-HT<sub>4</sub>R）蛋白平均阳性面积率降低（<i>P</i><0.05）；与模型组比较，天灸组和拮抗组结肠组织5-HT及5-HT<sub>3</sub>R蛋白平均阳性面积率降低（<i>P</i><0.05）。<b>结论：</b>天灸法可改善内脏高敏性IBS小鼠内脏高敏状态，可能与5-HT信号通路介导的肠脑轴的调节有关。. |
2,329,783 | Magnetic resonance imaging features of isolated periventricular heterotopia in pediatric epilepsy: a comparative study. | Periventricular nodular heterotopia is a neurodevelopmental disorder in which neurons fail to migrate to the cortical surface, forming discrete areas of grey matter adjacent to the lateral ventricles. Given that periventricular nodular heterotopia is seen as an incidental finding in patients without epilepsy, causality between periventricular nodular heterotopia and epilepsy cannot be assumed. Furthermore, the structural characteristics of periventricular nodular heterotopia in patients with epilepsy are poorly defined and can be misleading. In this article, we investigate whether structural radiological characteristics of heterotopia can predict epileptogenicity in pediatric patients.</AbstractText>Pediatric patients with periventricular nodular heterotopia, but no other epilepsy-associated cortical abnormalities on magnetic resonance imaging, were identified and divided into two groups: with epilepsy and without epilepsy. Radiological characteristics of laterality, regionalization, largest dimension and number of nodules were compared between the two groups.</AbstractText>Only periventricular nodular heterotopia spreading across several regions was associated with a statistically higher chance of epilepsy. Other features including laterality, individual region, number and largest dimension did not reliably predict epileptogenicity.</AbstractText>Most radiological characteristics of periventricular nodular heterotopia are similar in patients with and without epilepsy. The involvement of multiple periventricular regions with heterotopia was the only feature that inferred a higher risk of epilepsy. Periventricular nodular heterotopia requires a comprehensive work-up and should be interpreted in the context of each individual patient and not assumed to be directly causative of epilepsy, nor unrelated to it. Therefore, further studies using additional structural and functional imaging modalities are needed to determine the radiological features of epileptogenic periventricular nodular heterotopia.</AbstractText> |
2,329,784 | Analysis of L1CAM gene mutation and imaging appearance in three Chinese families with L1 syndrome: Three case reports. | The molecular mutations of the L1CAM gene and the imaging appearances of four fetuses with L1 syndrome from three independent Chinese families with a history of hydrocephalus were reported in this study. Two of the three are novel L1CAM variants.</AbstractText>Results of clinical and imaging examinations of three Chinese families were collected. Fetal samples were collected by puncture, genomic DNA was extracted, whole-exome sequencing was performed, and the L1CAM gene mutation sites were verified by PCR and Sanger sequencing.</AbstractText>In this case report, we described the imaging appearance and investigated the mutations of the L1CAM gene in three Chinese families with a history of L1 syndrome; these included two nonsense mutations (c.262C>T and c.261C>G) and one splice-site mutation (c.524-1G>A). Two of these three are novel L1CAM variants: c.262C>T and c.261C>G. The results of the sonographic images of the affected fetuses showed severe hydrocephalus. Bilateral lateral ventricles were dilated in the fetuses with c.262C>T and c.261C>G mutations. The left ventricle was about 14 mm wide and the right was about 14 mm in the fetus with c.262C>T mutation. The left ventricle was about 24.9 mm wide and the right was about 23.9 mm in the fetus with c.261C>G mutation. The ultrasound examination of the fetus with c.524-1G>A mutation showed that the third ventricle (7.5 mm wide) was raised, and the fourth ventricle was communicated with the cisterna magna. The parents requested termination of the above pregnancy.</AbstractText>The current study emphasizes the importance of combining family history, prenatal ultrasonography, and L1CAM mutation testing positive for the diagnosis of the L1 syndrome.</AbstractText>© 2022 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals LLC.</CopyrightInformation> |
2,329,785 | Long-term quality of life after ETV or ETV with consecutive VP shunt placement in hydrocephalic pediatric patients. | Endoscopic third ventriculostomy (ETV) and ventriculoperitoneal shunting are well-established treatments of obstructive hydrocephalus (HCP) in adult and pediatric patients. However, there is a lack of data with regard to the quality of life (QoL) of these patients during long-term follow-up METHODS: Inclusion criteria were pediatric patients with endoscopic treatment of hydrocephalus at the University Medicine Greifswald between 1993 and 2016. Patients older than 14 years at present were assessed with the Short Form-12 (SF-12) questionnaire. Patients younger than 14 years of age were assessed with the KINDL-R questionnaire that was completed by their parents. Patients' values were compared with the scores of a corresponding age-matched group of the healthy population and with patients who received later shunt treatment. Information about comorbidities, current symptoms, and educational level were gained by an additional part. Comparative analysis between patients with ETV success and failure (defined as shunt implantation after ETV) was performed.</AbstractText>A total of 107 patients (53 m, 54f) were included. Fifty-seven/107 patients (53.3%) were considered as ETV success. Mean age at ETV was 6.9 ± 5.9 years. Fifty-four statements of 89 patients that are still alive were gained (response rate 63%). Of these, 49 questionnaires were complete and evaluable (23 m, 26f; mean age 19.8 ± 10.0 years with an average follow-up period of 13.7 ± 7.2 years). Twenty-six/49 patients (53.1%) are considered ETV success. No statistically significant differences could be obtained between patients with ETV success and ETV failure. Patients older 14 years show QoL within normal range, patients younger than 14 years show significantly lower result regarding their environment of peers and social contacts. Patients younger than 6 months at the time of ETV and patients with posthemorrhagic HCP show significantly lower physical QoL. Gait disturbance, fatigue, and seizures are associated with a lower QoL, and educational level is lower than in the normal population.</AbstractText>Patients who underwent ETV in childhood do not have a lower health-related QoL in general. Subsequent insertions of ventriculoperitoneal (vp) shunts do not lower QoL. Certain subgroups of the patients show lower results compared to the healthy population.</AbstractText>© 2022. The Author(s).</CopyrightInformation> |
2,329,786 | Effects of Spring Warming on Seasonal Neuroendocrinology and Activation of the Reproductive Axis in Hibernating Arctic Ground Squirrels. | Many animals adjust the timing of seasonal events, such as reproduction, molt, migration, and hibernation, in response to interannual variation and directional climate-driven changes in temperature. However, the mechanisms by which temperature influences seasonal timing are relatively under-explored. Seasonal timing involves retrograde signaling in which thyrotropin (TSH) in the pars tuberalis (PT) alters expression of thyroid hormone (TH) deiodinases (Dio2/Dio3) in tanycyte cells lining the third ventricle of the hypothalamus. This, in turn, affects the availability of triiodothyronine (T3) within the mediobasal hypothalamus-increased hypothalamic T3 restores a summer phenotype and activates the reproductive axis in long-day breeders. Recently, we showed that retrograde TH signaling is activated during late hibernation in arctic ground squirrels (Urocitellus parryii) held in constant darkness and constant ambient temperature. Sensitivity of seasonal pathways to nonphotic cues, such as temperature, is likely particularly important to hibernating species that are sequestered in hibernacula during spring. To address this issue, we exposed captive arctic ground squirrels of both sexes to an ecologically relevant increase in ambient temperature (from -6 to -1°C) late in hibernation and examined the effects of warming on the seasonal retrograde TSH/Dio/T3 signaling pathway, as well as downstream elements of the reproductive axis. We found that warmed males tended to have higher PT TSHβ expression and significantly heavier testis mass whereas the TSH/Dio/T3 signaling pathway was unaffected by warming in females, although warmed females exhibited a slight decrease in ovarian mass. Our findings suggest that temperature could have different effects on gonadal growth in male and female arctic ground squirrels, which could lead to mismatched timing in response to rapid climate change. |
2,329,787 | An unusual origin of a papillary muscle of the right ventricle.<Pagination><StartPage>147</StartPage><EndPage>150</EndPage><MedlinePgn>147-150</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.morpho.2022.03.002</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1286-0115(22)00030-3</ELocationID><Abstract><AbstractText>Knowledge of anatomical variations of the heart are important to cardiac surgeons, cardiologists, and radiologist. During routine dissection of a 77-year-old male cadaver, we observed an unusual origin of a papillary muscle of the right ventricle arising from the atrioventricular aspect of the moderator band. This papillary muscle was 6.7mm long and 2.6mm wide. It gave rise to two chordae tendineae: one to the inferior (posterior) papillary muscle of the right ventricle and one directly to the inferior (posterior) leaflet of the tricuspid valve. Variants of the internal anatomy of the heart as exemplified in the present case report should be born in mind during image interpretation and invasive procedures of the right ventricle of the heart.</AbstractText><CopyrightInformation>Copyright © 2022 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hampel</LastName><ForeName>G A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Tulane University School of Medicine, New Orleans, LA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olewnik</LastName><ForeName>Ł</ForeName><Initials>Ł</Initials><AffiliationInfo><Affiliation>Department of Anatomical Dissection and Donation, Medical University of Lodz, Lodz, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iwanaga</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA; Department of Neurology, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA. Electronic address: iwanagajoeca@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loukas</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Anatomical Sciences, Saint-George's University, Saint-George's, Grenada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tubbs</LastName><ForeName>R S</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA; Department of Neurology, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA; Department of Anatomical Sciences, Saint-George's University, Saint-George's, Grenada; Department of Structural & Cellular Biology, Tulane University School of Medicine, New Orleans, LA, USA; Department of Surgery, Tulane University School of Medicine, New Orleans, LA, USA; Department of Neurosurgery and Ochsner Neuroscience Institute, Ochsner Health System, New Orleans, LA, USA; University of Queensland, Brisbane, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Morphologie</MedlineTA><NlmUniqueID>9814314</NlmUniqueID><ISSNLinking>1286-0115</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010210" MajorTopicYN="Y">Papillary Muscles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000033" MajorTopicYN="N">anatomy & histology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002815" MajorTopicYN="N">Chordae Tendineae</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014261" MajorTopicYN="N">Tricuspid Valve</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002102" MajorTopicYN="N">Cadaver</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Inferior papillary muscle</Keyword><Keyword MajorTopicYN="N">Moderator band</Keyword><Keyword MajorTopicYN="N">Papillary muscle</Keyword><Keyword MajorTopicYN="N">Septomarginal trabeculation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>3</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>3</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>5</Day><Hour>17</Hour><Minute>22</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35787342</ArticleId><ArticleId IdType="doi">10.1016/j.morpho.2022.03.002</ArticleId><ArticleId IdType="pii">S1286-0115(22)00030-3</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35786695</PMID><DateCompleted><Year>2022</Year><Month>07</Month><Day>06</Day></DateCompleted><DateRevised><Year>2022</Year><Month>07</Month><Day>24</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>184</Issue><PubDate><Year>2022</Year><Month>Jun</Month><Day>16</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Dissection Techniques and Histological Sampling of the Heart in Large Animal Models for Cardiovascular Diseases. | Knowledge of anatomical variations of the heart are important to cardiac surgeons, cardiologists, and radiologist. During routine dissection of a 77-year-old male cadaver, we observed an unusual origin of a papillary muscle of the right ventricle arising from the atrioventricular aspect of the moderator band. This papillary muscle was 6.7mm long and 2.6mm wide. It gave rise to two chordae tendineae: one to the inferior (posterior) papillary muscle of the right ventricle and one directly to the inferior (posterior) leaflet of the tricuspid valve. Variants of the internal anatomy of the heart as exemplified in the present case report should be born in mind during image interpretation and invasive procedures of the right ventricle of the heart.<CopyrightInformation>Copyright © 2022 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hampel</LastName><ForeName>G A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Tulane University School of Medicine, New Orleans, LA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Olewnik</LastName><ForeName>Ł</ForeName><Initials>Ł</Initials><AffiliationInfo><Affiliation>Department of Anatomical Dissection and Donation, Medical University of Lodz, Lodz, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iwanaga</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA; Department of Neurology, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA. Electronic address: iwanagajoeca@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Loukas</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Anatomical Sciences, Saint-George's University, Saint-George's, Grenada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tubbs</LastName><ForeName>R S</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA; Department of Neurology, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine, New Orleans, LA, USA; Department of Anatomical Sciences, Saint-George's University, Saint-George's, Grenada; Department of Structural & Cellular Biology, Tulane University School of Medicine, New Orleans, LA, USA; Department of Surgery, Tulane University School of Medicine, New Orleans, LA, USA; Department of Neurosurgery and Ochsner Neuroscience Institute, Ochsner Health System, New Orleans, LA, USA; University of Queensland, Brisbane, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Morphologie</MedlineTA><NlmUniqueID>9814314</NlmUniqueID><ISSNLinking>1286-0115</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010210" MajorTopicYN="Y">Papillary Muscles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000033" MajorTopicYN="N">anatomy & histology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002815" MajorTopicYN="N">Chordae Tendineae</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014261" MajorTopicYN="N">Tricuspid Valve</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002102" MajorTopicYN="N">Cadaver</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Inferior papillary muscle</Keyword><Keyword MajorTopicYN="N">Moderator band</Keyword><Keyword MajorTopicYN="N">Papillary muscle</Keyword><Keyword MajorTopicYN="N">Septomarginal trabeculation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>3</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>3</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2023</Year><Month>2</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>5</Day><Hour>17</Hour><Minute>22</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35787342</ArticleId><ArticleId IdType="doi">10.1016/j.morpho.2022.03.002</ArticleId><ArticleId IdType="pii">S1286-0115(22)00030-3</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35786695</PMID><DateCompleted><Year>2022</Year><Month>07</Month><Day>06</Day></DateCompleted><DateRevised><Year>2022</Year><Month>07</Month><Day>24</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>184</Issue><PubDate><Year>2022</Year><Month>Jun</Month><Day>16</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>Dissection Techniques and Histological Sampling of the Heart in Large Animal Models for Cardiovascular Diseases.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/63809</ELocationID><Abstract>The standard gross examination and sampling are key elements in the reproducibility and success of experimental studies of cardiovascular diseases carried out in large animals. Considering the complex anatomy of the heart, interspecies differences, and the types of compensatory and pathological reactions, consistent protocols are challenging to implement. The utilization of multiple dissection protocols is usually adapted to suit the prosector's experience, and personal preference continues to be a source of experimental and interobserver variability. Here, the aim is to present the main anatomical features and landmarks, dissection protocols, and histological sampling standards of the heart in some commonly used species (including dogs, pigs, ruminants, and cats) as models of cardiovascular diseases. Two standard gross examination protocols are presented here. First, the inflow-outflow method, which follows the physiological blood flow direction through the heart and large vessels (frequently used in dogs, ruminants, and pigs), and second, the four-chamber dissection technique (exemplified in cats). Both techniques can be adapted to any species in certain experimental circumstances. The sampling protocols include all the areas of interest (sinoatrial node, ventricles, interventricular septum, atria, valves, and aorta), and if properly carried out, improve both the reproducibility and reliability of experimental studies. |
2,329,788 | [Clinicopathological features of polymorphous low-grade neuroepithelial tumor of the young]. | <b>Objective:</b> To investigate the clinicopathological features and differential diagnosis of polymorphous low-grade neuroepithelial tumor of the young (PLNTY). <b>Methods:</b> Five cases of PLNTY diagnosed at the First Affiliated Hospital and Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China from 2019 to 2021 were collected. All cases were evaluated using clinical and imaging data, histology, immunohistochemical staining and molecular genetics. The relevant literature was reviewed. <b>Results:</b> There were two male and three female patients, aged 10 to 39 years, with an average age of 25 years. Clinically, the tumors were in the temporal lobe (3 cases), the lateral ventricle (1 case) and the left head of caudate nucleus (1 case). The clinical manifestations included epilepsy in 3 cases, right visual disturbance in 1 case, and post-trauma incidental finding in 1 case. Microscopically, the lesions were characterized with infiltrative growth, cellular pleomorphism (oligodendroglioma-like cells were always present, with low-grade, pleomorphic nuclei) and variable calcifications. Immunohistochemically, the tumor cells were positive for GFAP and Olig2. They also showed intense and diffuse expression of CD34 while CD34 expressing ramified neural elements were present in regional cortex. Ki-67 proliferation index was less than 3%. Molecular genetics showed the BRAF V600E mutation in 2 cases, the PAK5-Q337R missense mutation in 1 case, the FGFR2-CTNNA3 fusion in 1 case, and the FGFR2-INA and FGFR2-PPRC1 concomitant fusion in 1 case. No postoperative chemoradiotherapy was given. Follow-up intervals ranged from 3 to 29 months while no recurrence or metastasis was identified. <b>Conclusions:</b> PLNTY is uncommon. A definite diagnosis of PLNTY relies on histopathological examination and molecular genetics. It is important to distinguish PLNTY from high grade gliomas and avoid overtreatment. The recently reported the PAK5-Q337R missense mutation and the FGFR2-PPRC1 gene fusion in PLNTY may help diagnose and understand the pathogenesis of PLNTY.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pathology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pathology, Brain Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>M N</ForeName><Initials>MN</Initials><AffiliationInfo><Affiliation>Department of Pathology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Pathology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>M H</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>Department of Pathology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Kun</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Pathology, Brain Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Bing Li Xue Za Zhi</MedlineTA><NlmUniqueID>0005331</NlmUniqueID><ISSNLinking>0529-5807</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001932" MajorTopicYN="Y">Brain Neoplasms</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005910" MajorTopicYN="Y">Glioma</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018302" MajorTopicYN="Y">Neoplasms, Neuroepithelial</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009837" MajorTopicYN="Y">Oligodendroglioma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>目的：</b> 探讨青少年多形性低级别神经上皮肿瘤（polymorphous low-grade neuroepithelial tumor of the young，PLNTY）的临床病理特征、诊断及鉴别诊断要点。 <b>方法：</b> 收集2019—2021年南京医科大学第一附属医院和南京医科大学附属脑科医院手术诊治经病理确诊的PLNTY 5例，对其临床及影像学特点、组织学形态、免疫表型及分子遗传学改变进行分析总结，并复习文献。 <b>结果：</b> 患者男性2例，女性3例；年龄10~39岁，平均年龄25岁；肿瘤位于颞叶3例，侧脑室、左尾状核各1例；临床表现癫痫3例、右眼视力下降1例，1例因外伤后体检发现。镜下观察：肿瘤特征性表现为浸润性生长、瘤细胞多形性（均可见少突胶质细胞瘤样细胞、细胞核呈低级别、多形性）及不同程度钙化。免疫组织化学：肿瘤细胞胶质纤维酸性蛋白、少突胶质细胞转录因子阳性，CD34弥漫强阳性，周围脑组织可见散在CD34阳性细胞，Ki-67阳性指数均小于3%。分子遗传学：BRAF V600E突变2例，PAK5-Q337R基因错义突变1例，FGFR2-CTNNA3基因融合1例，1例伴有FGFR2-INA和FGFR2-PPRC1基因融合。术后均未行放化疗，随访3~29个月，未见复发转移。 <b>结论：</b> PLNTY罕见，确诊依赖于病理形态及分子遗传学，认识该肿瘤的重要性在于与高级别胶质瘤鉴别，避免过度治疗，本研究新报道PAK5-Q337R错义突变和FGFR2-PPRC1基因融合，拓宽了PLNTY的分子遗传学谱系。. |
2,329,789 | Single-Center Retrospective Analysis of Risk Factors for Hydrocephalus After Lateral Ventricular Tumor Resection. | There is no general consensus on the placement of preoperative and intraoperative external ventricular drainage (EVD) in patients with lateral ventricular tumors (LVTs). The aim of this study was to identify the predictors of postoperative acute and persistent hydrocephalus need for postoperative cerebrospinal fluid (CSF) drainage and guide the management of postoperative EVD in patients with LVTs.</AbstractText>We performed a single-institution, retrospective analysis of patients who underwent resection of LVTs in our Department between January 2011 and March 2021. Patients were divided between one group that required CSF drainage and another group without the need for CSF drainage. We analyzed the two groups by univariate and multivariate analyses to identify the predictors of the requirement for postoperative CSF drainage due to symptomatic intracranial hypertension caused by hydrocephalus.</AbstractText>A total of 97 patients met the inclusion criteria, of which 31 patients received preoperative or intraoperative EVD. Ten patients without prophylactic EVD received postoperative EVD for postoperative acute hydrocephalus. Eleven patients received postoperative ventriculoperitoneal(VP) shunt subsequently. Logistic regression analysis showed that tumor invasion of the anterior ventricle (OR = 7.66), transependymal edema (OR = 8.76), and a large volume of postoperative intraventricular hemorrhage (IVH) (OR = 6.51) were independent risk factors for postoperative acute hydrocephalus. Perilesional edema (OR = 33.95) was an independent risk factor for postoperative VP shunt due to persistent hydrocephalus.</AbstractText>Postoperative hydrocephalus is a common complication in patients with LVTs. These findings might help to determine whether to conduct earlier interventions.</AbstractText>Copyright © 2022 Zhang, Ge, Li, Zhang and Chen.</CopyrightInformation> |
2,329,790 | Magnetic resonance imaging measures of brain volumes across the EXPEDITION trials in mild and moderate Alzheimer's disease dementia. | Solanezumab is a monoclonal antibody that preferentially binds soluble amyloid beta and promotes its clearance from the brain. The aim of this post hoc analysis was to assess the effect of low-dose solanezumab (400 mg) on global brain volume measures in patients with mild or moderate Alzheimer's disease (AD) dementia quantified using volumetric magnetic resonance imaging (vMRI) data from the EXPEDITION clinical trial program.</AbstractText>Patients with mild or moderate AD (EXPEDITION and EXPEDITION2) and mild AD (EXPEDITION3), were treated with either placebo or solanezumab (400 mg) every 4 weeks (Q4W) for 76 weeks. vMRI scans were acquired at baseline and at 80 weeks from 427 MRI facilities using a standardized imaging protocol. Whole brain volume (WBV) and ventricle volume (VV) changes were estimated at 80 weeks using either boundary shift integral (EXPEDITION and EXPEDITION2) or tensor-based morphometry (EXPEDITION3).</AbstractText>The pooled cohort used for this study consisted of participants with vMRI at baseline and week 80 across the three trials. Analyzed patient subgroups comprised full patient cohort (N</i> = 2933), apolipoprotein E (APOE</i>) ε4+</sup> carriers (N</i> = 1835), and patients with mild (N</i> = 2497) or moderate AD dementia (N</i> = 428). No significant effect (all P</i>-values ≥.05) of treatment was observed in the pooled sample, individual trials, or subgroups of patients with mild or moderate AD or APOE</i> ε4 carriers, in either WBV or VV change.</AbstractText>Analysis of patients with mild or moderate AD dementia from baseline to 80 weeks using vMRI measures of WBV and VV changes suggested that low-dose solanezumab was not linked to changes in volumes at 80 weeks. Analysis of the pooled cohort did not demonstrate an effect on brain volumes with treatment. Evaluation of a higher dose of solanezumab in the preclinical stage of AD is currently being undertaken.</AbstractText>© 2022 Eli Lilly and Company. Alzheimer's & Dementia: Translational Research & Clinical Interventions published by Wiley Periodicals LLC on behalf of Alzheimer's Association.</CopyrightInformation> |
2,329,791 | Unraveling the interplay between dipeptidyl peptidase 4 and the renin-angiotensin system in heart failure.<Pagination><StartPage>120757</StartPage><MedlinePgn>120757</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lfs.2022.120757</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0024-3205(22)00457-X</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Emerging evidence suggests the existence of a crosstalk between dipeptidyl peptidase 4 (DPP4) and the renin-angiotensin system (RAS). Therefore, combined inhibition of DPP4 and RAS may produce similar pharmacological effects rather than being additive. This study tested the hypothesis that combining an inhibitor of DPP4 with an angiotensin II (Ang II) receptor blocker does not provide additional cardioprotection compared to monotherapy in heart failure (HF) rats.</AbstractText><AbstractText Label="MAIN METHODS" NlmCategory="METHODS">Male Wistar rats were subjected to left ventricle (LV) radiofrequency ablation or sham operation. Six weeks after surgery, radiofrequency-ablated rats who developed HF were assigned into four groups and received vehicle (water), vildagliptin, valsartan, or both drugs, for four weeks by oral gavage.</AbstractText><AbstractText Label="KEY FINDINGS" NlmCategory="RESULTS">Vildagliptin and valsartan in monotherapy reduced LV hypertrophy, alleviated cardiac interstitial fibrosis, and improved systolic and diastolic function in HF rats, with no additional effect of combination treatment. HF rats displayed higher cardiac and serum DPP4 activity and abundance than sham. Surprisingly, not only vildagliptin but also valsartan in monotherapy downregulated the catalytic function and expression levels of systemic and cardiac DPP4. Moreover, vildagliptin and valsartan alone or in combination comparably upregulate the components of the cardiac ACE2/Ang-(1-7)/MasR while downregulating the ACE/Ang II/AT1R axis.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">Vildagliptin or valsartan alone is as effective as combined to treat cardiac dysfunction and remodeling in experimental HF. DPP4 inhibition downregulates classic RAS components, and pharmacological RAS blockade downregulates DPP4 in the heart and serum of HF rats. This interplay between DPP4 and RAS may affect HF progression and pharmacotherapy.</AbstractText><CopyrightInformation>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Arruda-Junior</LastName><ForeName>Daniel F</ForeName><Initials>DF</Initials><AffiliationInfo><Affiliation>Laboratório de Genética e Cardiologia Molecular, Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salles</LastName><ForeName>Thiago A</ForeName><Initials>TA</Initials><AffiliationInfo><Affiliation>Laboratório de Genética e Cardiologia Molecular, Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martins</LastName><ForeName>Flavia L</ForeName><Initials>FL</Initials><AffiliationInfo><Affiliation>Laboratório de Genética e Cardiologia Molecular, Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Antonio</LastName><ForeName>Ednei L</ForeName><Initials>EL</Initials><AffiliationInfo><Affiliation>Departamento de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tucci</LastName><ForeName>Paulo J F</ForeName><Initials>PJF</Initials><AffiliationInfo><Affiliation>Departamento de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gowdak</LastName><ForeName>Luís Henrique W</ForeName><Initials>LHW</Initials><AffiliationInfo><Affiliation>Laboratório de Genética e Cardiologia Molecular, Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tavares</LastName><ForeName>Caio A M</ForeName><Initials>CAM</Initials><AffiliationInfo><Affiliation>Unidade de Cardiogeriatria, Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil; Academic Research Organization (ARO), Hospital Israelita Albert Eistein, São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Girardi</LastName><ForeName>Adriana C</ForeName><Initials>AC</Initials><AffiliationInfo><Affiliation>Laboratório de Genética e Cardiologia Molecular, Instituto do Coração (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. Electronic address: adriana.girardi@incor.usp.br.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>06</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Life Sci</MedlineTA><NlmUniqueID>0375521</NlmUniqueID><ISSNLinking>0024-3205</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>80M03YXJ7I</RegistryNumber><NameOfSubstance UI="D000068756">Valsartan</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber><NameOfSubstance UI="D018819">Dipeptidyl Peptidase 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>I6B4B2U96P</RegistryNumber><NameOfSubstance UI="D000077597">Vildagliptin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018819" MajorTopicYN="Y">Dipeptidyl Peptidase 4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012084" MajorTopicYN="N">Renin-Angiotensin System</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000068756" MajorTopicYN="N">Valsartan</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077597" MajorTopicYN="N">Vildagliptin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ACE2</Keyword><Keyword MajorTopicYN="N">Angiotensin II</Keyword><Keyword MajorTopicYN="N">Cardiac remodeling</Keyword><Keyword MajorTopicYN="N">Dipeptidyl peptidase-4</Keyword><Keyword MajorTopicYN="N">Gliptins</Keyword><Keyword MajorTopicYN="N">Heart failure</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>4</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>6</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>6</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>5</Day><Hour>8</Hour><Minute>43</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35780844</ArticleId><ArticleId IdType="doi">10.1016/j.lfs.2022.120757</ArticleId><ArticleId IdType="pii">S0024-3205(22)00457-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32491360</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK557428</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-78333">Aortic Insufficiency<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Patibandla</LastName><ForeName>Saikrishna</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Brooklyn Hospital Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heaton</LastName><ForeName>Joseph</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Brooklyn Hospital Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Azzam</LastName><ForeName>Joseph S.</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>St. Mary's Medical Center</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Aortic regurgitation (AR), also known as aortic insufficiency, is a form of valvular heart disease in which the integrity of the aortic valve is compromised and leads to inadequate closure of the valve leaflets. A normal aortic valve is comprised of three semilunar cusps that attach to the aortic wall. Loss of function occurs when the valves themselves become diseased or if there is aortic root involvement. In AR, there is retrograde blood flow from the aorta into the left ventricle which occurs in diastole in the cardiac cycle. Chronic AR was initially described by Corrigan in 1832 in syphilitic patients who suffered from aortic root dilation. The clinical presentation of AR depends on its acuity of onset.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>5</Day></ContributionDate><ReferenceList><Reference><Citation>Akinseye OA, Pathak A, Ibebuogu UN. 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Transcatheter Aortic Valve Replacement in Pure Native Aortic Valve Regurgitation. J Am Coll Cardiol. 2017 Dec 05;70(22):2752-2763.</Citation><ArticleIdList><ArticleId IdType="pubmed">29191323</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491360</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29763100</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK499925</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-16999">A Wave<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Goyal</LastName><ForeName>Amandeep</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Kansas Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Basit</LastName><ForeName>Hajira</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Brookdale University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bhyan</LastName><ForeName>Poonam</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Sandeep</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Mery Fitzgerald Hospital</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Cannon A waves are large-amplitude waves seen in the jugular veins during a physical exam. They are caused by simultaneous contraction of atria and ventricle leading to exaggerated right atrial pressure. Usually, Cannon A waves are irregular and intermittent. They are seen in patients with cardiac conduction defects or certain cardiac dysrhythmias. Cannon A waves can also be seen on the EKG.</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s2">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s3">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s4">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s5">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s6">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s7">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s8">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s9">Consultations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s10">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s11">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s12">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>5</Day></ContributionDate><ReferenceList><Reference><Citation>Ranjith MP, Shajudeen K, Prasanth S. 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The Jugular Venous Pressure and Pulse Contour. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd. Butterworths; Boston: 1990.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29763100</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29083674</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK459390</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-785">Physiology, Starling Relationships | Aortic regurgitation (AR), also known as aortic insufficiency, is a form of valvular heart disease in which the integrity of the aortic valve is compromised and leads to inadequate closure of the valve leaflets. A normal aortic valve is comprised of three semilunar cusps that attach to the aortic wall. Loss of function occurs when the valves themselves become diseased or if there is aortic root involvement. In AR, there is retrograde blood flow from the aorta into the left ventricle which occurs in diastole in the cardiac cycle. Chronic AR was initially described by Corrigan in 1832 in syphilitic patients who suffered from aortic root dilation. The clinical presentation of AR depends on its acuity of onset.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-78333" sec="article-78333.s17">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>5</Day></ContributionDate><ReferenceList><Reference><Citation>Akinseye OA, Pathak A, Ibebuogu UN. 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J Am Coll Cardiol. 2017 Dec 05;70(22):2752-2763.</Citation><ArticleIdList><ArticleId IdType="pubmed">29191323</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32491360</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29763100</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK499925</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-16999">A Wave</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Goyal</LastName><ForeName>Amandeep</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>University of Kansas Medical Center</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Basit</LastName><ForeName>Hajira</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Brookdale University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bhyan</LastName><ForeName>Poonam</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Sandeep</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Mery Fitzgerald Hospital</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Cannon A waves are large-amplitude waves seen in the jugular veins during a physical exam. They are caused by simultaneous contraction of atria and ventricle leading to exaggerated right atrial pressure. Usually, Cannon A waves are irregular and intermittent. They are seen in patients with cardiac conduction defects or certain cardiac dysrhythmias. Cannon A waves can also be seen on the EKG.<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s1">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s2">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s3">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s4">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s5">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s6">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s7">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s8">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s9">Consultations</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s10">Pearls and Other Issues</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s11">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s12">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-16999" sec="article-16999.s14">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>5</Day></ContributionDate><ReferenceList><Reference><Citation>Ranjith MP, Shajudeen K, Prasanth S. 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Butterworths; Boston: 1990.</Citation><ArticleIdList><ArticleId IdType="pubmed">0</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29763100</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">29083674</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK459390</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-785">Physiology, Starling Relationships</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>LaCombe</LastName><ForeName>Philip</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>SUNY Upstate Medical University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jose</LastName><ForeName>Alvin</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>William Carey College of Osteopathic Medicine</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Basit</LastName><ForeName>Hajira</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Brookdale University</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lappin</LastName><ForeName>Sarah L.</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Upstate University Hospital</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>The systolic performance of the left ventricle is determined by three factors: preload, afterload, and contractility. 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2,329,792 | First Cardiac Magnetic Resonance Experience in Bangladesh: A Case of Arrhythmogenic Right Ventricular Dysplasia.<Pagination><StartPage>876</StartPage><EndPage>881</EndPage><MedlinePgn>876-881</MedlinePgn></Pagination><Abstract><AbstractText>Arrhythmogenic right ventricular dysplasia (ARVD) is a progressive degeneration and replacement of the right ventricular (RV) myocardial tissue by fat and fibrosis and produce clinical condition. Desmosome gene mutations are only the causative state for ARVD hereditary disorder. The arrhythmogenic right ventricular cardiomyopathy incidence is about 1/1000-5000. Mostly young people and athletes are bearing the clinical presentations include presyncope, syncope, ventricular tachycardias or ventricular fibrillation leading to cardiac arrest. We report about the first case of Cardiac magnetic resonance (CMR) imaging to diagnose a case Arrhythmogenic right ventricular dysplasia (ARVD) of a 34-year-old male from Savar, Dhaka, Bangladesh who was referred to cardiac emergency for the evaluation recurrent dizzy spells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Osmany</LastName><ForeName>M F</ForeName><Initials>MF</Initials><AffiliationInfo><Affiliation>Dr Din-E-Mujahid Mohammad Faruque Osmany, Medical Officer, Department of Cardiology, University Cardiac Center (UCC), Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh; E-mail: dr.osmanybsmmu@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zaman</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Islam</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ferdous</LastName><ForeName>Z</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Hasan</LastName><ForeName>I</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Haque</LastName><ForeName>M S</ForeName><Initials>MS</Initials></Author><Author ValidYN="Y"><LastName>Safiuddin</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Haque</LastName><ForeName>K S</ForeName><Initials>KS</Initials></Author><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>C M</ForeName><Initials>CM</Initials></Author><Author ValidYN="Y"><LastName>Shakil</LastName><ForeName>S S</ForeName><Initials>SS</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Bangladesh</Country><MedlineTA>Mymensingh Med J</MedlineTA><NlmUniqueID>9601799</NlmUniqueID><ISSNLinking>1022-4742</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019571" MajorTopicYN="Y">Arrhythmogenic Right Ventricular Dysplasia</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001459" MajorTopicYN="N" Type="Geographic">Bangladesh</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>3</Day><Hour>5</Hour><Minute>52</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35780378</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32310500</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK556040</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17964">Atrial Myxoma<Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>Tran</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>George Washington University Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vaidya</LastName><ForeName>Yash</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>SUNY Upstate Medical University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract><AbstractText>Myxomas are the most common primary cardiac tumor. It is estimated that more than 75% of myxomas originate in the left atrium either at the mitral annulus or the fossa ovalis border of the interatrial septum; 20% arise from the right atrium while 5% stem from both atria and the ventricle. Atrial myxomas are associated with a triad of complications, including obstruction, emboli, and constitutional symptoms (such as fever, weight loss).</AbstractText><CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>4</Day></ContributionDate><ReferenceList><Reference><Citation>Ha JW, Kang WC, Chung N, Chang BC, Rim SJ, Kwon JW, Jang Y, Shim WH, Cho SY, Kim SS, Cho SH. 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Braz J Cardiovasc Surg. 2015 Sep-Oct;30(5):571-8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4690663</ArticleId><ArticleId IdType="pubmed">26735605</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32310500</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30085549</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK519007</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-38475">Physiology, Cerebral Spinal Fluid | Arrhythmogenic right ventricular dysplasia (ARVD) is a progressive degeneration and replacement of the right ventricular (RV) myocardial tissue by fat and fibrosis and produce clinical condition. Desmosome gene mutations are only the causative state for ARVD hereditary disorder. The arrhythmogenic right ventricular cardiomyopathy incidence is about 1/1000-5000. Mostly young people and athletes are bearing the clinical presentations include presyncope, syncope, ventricular tachycardias or ventricular fibrillation leading to cardiac arrest. We report about the first case of Cardiac magnetic resonance (CMR) imaging to diagnose a case Arrhythmogenic right ventricular dysplasia (ARVD) of a 34-year-old male from Savar, Dhaka, Bangladesh who was referred to cardiac emergency for the evaluation recurrent dizzy spells.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Osmany</LastName><ForeName>M F</ForeName><Initials>MF</Initials><AffiliationInfo><Affiliation>Dr Din-E-Mujahid Mohammad Faruque Osmany, Medical Officer, Department of Cardiology, University Cardiac Center (UCC), Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh; E-mail: dr.osmanybsmmu@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zaman</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Islam</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ferdous</LastName><ForeName>Z</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Hasan</LastName><ForeName>I</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Haque</LastName><ForeName>M S</ForeName><Initials>MS</Initials></Author><Author ValidYN="Y"><LastName>Safiuddin</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Haque</LastName><ForeName>K S</ForeName><Initials>KS</Initials></Author><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>C M</ForeName><Initials>CM</Initials></Author><Author ValidYN="Y"><LastName>Shakil</LastName><ForeName>S S</ForeName><Initials>SS</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Bangladesh</Country><MedlineTA>Mymensingh Med J</MedlineTA><NlmUniqueID>9601799</NlmUniqueID><ISSNLinking>1022-4742</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019571" MajorTopicYN="Y">Arrhythmogenic Right Ventricular Dysplasia</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001459" MajorTopicYN="N" Type="Geographic">Bangladesh</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>3</Day><Hour>5</Hour><Minute>52</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35780378</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">32310500</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK556040</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-17964">Atrial Myxoma</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>Tran</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>George Washington University Hospital</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vaidya</LastName><ForeName>Yash</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>SUNY Upstate Medical University</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Myxomas are the most common primary cardiac tumor. It is estimated that more than 75% of myxomas originate in the left atrium either at the mitral annulus or the fossa ovalis border of the interatrial septum; 20% arise from the right atrium while 5% stem from both atria and the ventricle. Atrial myxomas are associated with a triad of complications, including obstruction, emboli, and constitutional symptoms (such as fever, weight loss).<CopyrightInformation>Copyright © 2023, StatPearls Publishing LLC.</CopyrightInformation></Abstract><Sections><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s1">Continuing Education Activity</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s2">Introduction</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s3">Etiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s4">Epidemiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s5">Pathophysiology</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s6">History and Physical</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s7">Evaluation</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s8">Treatment / Management</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s9">Differential Diagnosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s10">Prognosis</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s11">Complications</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s12">Deterrence and Patient Education</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s13">Enhancing Healthcare Team Outcomes</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s14">Review Questions</SectionTitle></Section><Section><SectionTitle book="statpearls" part="article-17964" sec="article-17964.s15">References</SectionTitle></Section></Sections><ContributionDate><Year>2022</Year><Month>7</Month><Day>4</Day></ContributionDate><ReferenceList><Reference><Citation>Ha JW, Kang WC, Chung N, Chang BC, Rim SJ, Kwon JW, Jang Y, Shim WH, Cho SY, Kim SS, Cho SH. 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Arch Neurol. 2007 Aug;64(8):1115-20.</Citation><ArticleIdList><ArticleId IdType="pubmed">17698701</ArticleId></ArticleIdList></Reference><Reference><Citation>Ma G, Wang D, He Y, Zhang R, Zhou Y, Ying K. Pulmonary embolism as the initial manifestation of right atrial myxoma: A case report and review of the literature. Medicine (Baltimore) 2019 Dec;98(51):e18386.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC6940114</ArticleId><ArticleId IdType="pubmed">31861001</ArticleId></ArticleIdList></Reference><Reference><Citation>Gavrielatos G, Letsas KP, Pappas LK, Dedeilias P, Sioras E, Kardaras F. Large left atrial myxoma presented as fever of unknown origin: a challenging diagnosis and a review of the literature. Cardiovasc Pathol. 2007 Nov-Dec;16(6):365-7.</Citation><ArticleIdList><ArticleId IdType="pubmed">18005878</ArticleId></ArticleIdList></Reference><Reference><Citation>Shetty Roy AN, Radin M, Sarabi D, Shaoulian E. Familial recurrent atrial myxoma: Carney's complex. 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Braz J Cardiovasc Surg. 2015 Sep-Oct;30(5):571-8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC4690663</ArticleId><ArticleId IdType="pubmed">26735605</ArticleId></ArticleIdList></Reference></ReferenceList></BookDocument><PubmedBookData><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32310500</ArticleId></ArticleIdList></PubmedBookData></PubmedBookArticle><PubmedBookArticle><BookDocument><PMID Version="1">30085549</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK519007</ArticleId></ArticleIdList><Book><Publisher><PublisherName>StatPearls Publishing</PublisherName><PublisherLocation>Treasure Island (FL)</PublisherLocation></Publisher><BookTitle book="statpearls">StatPearls</BookTitle><PubDate><Year>2023</Year><Month>01</Month></PubDate><BeginningDate><Year>2023</Year><Month>01</Month></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="statpearls" part="article-38475">Physiology, Cerebral Spinal Fluid</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Telano</LastName><ForeName>Lauren N.</ForeName><Initials>LN</Initials><AffiliationInfo><Affiliation>University Health</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baker</LastName><ForeName>Stephen</ForeName><Initials>S</Initials></Author></AuthorList><PublicationType UI="D000072643">Study Guide</PublicationType><Abstract>Cerebrospinal fluid (CSF) is an ultrafiltrate of plasma contained within the ventricles of the brain and the subarachnoid spaces of the cranium and spine. It performs vital functions, including providing nourishment, waste removal, and protection to the brain. Adult CSF volume is estimated to be 150 ml, with a distribution of 125 ml within the subarachnoid spaces and 25 ml within the ventricles. CSF is predominantly secreted by the choroid plexus with other sources playing a more poorly defined role. In the adult population, its secretion varies between individuals, usually ranging from 400 to 600 ml per day. The constant secretion of CSF contributes to complete CSF renewal four to five times per 24-hour period in the average young adult. The reduction of CSF turnover may contribute to the accumulation of metabolites seen in aging and neurodegenerative diseases. The composition of CSF is strictly regulated, and any variation can be useful for diagnostic purposes. |
2,329,793 | Effects of Cranioplasty on Contralateral Subdural Effusion After Decompressive Craniectomy: A Literature Review.<Pagination><StartPage>147</StartPage><EndPage>153</EndPage><MedlinePgn>147-153</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.wneu.2022.06.117</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1878-8750(22)00901-9</ELocationID><Abstract><AbstractText Label="BACKGROUND">Contralateral subdural effusion (CSE) after decompressive craniectomy (CSEDC) is occasionally observed. Cranioplasty is routinely performed for reconstruction and has recently been associated with improving contralateral subdural effusion. We sought to systematically review all available literature and evaluate the effectiveness of cranioplasty for CSE.</AbstractText><AbstractText Label="METHODS">A PubMed, Web of Science, and Google Scholar search was conducted for preferred reporting items following the guidelines of systematic review and meta-analysis, including studies reporting patients who underwent cranioplasty because of CSEDC.</AbstractText><AbstractText Label="RESULTS">The search yielded 8 articles. A total of 56 patients ranging in age from 21 to 71 years developed CSEDC. Of them, 32 patients underwent cranioplasty. Eighteen cases with symptomatic CSE underwent cranioplasty alone, 2 cases received Ommaya drainage later because of a recurrence of CDC, and 1 case underwent a ventriculoperitoneal shunt because the CSE did not resolve completely and the ventricle was dilated again. The symptoms of 14 cases lessened without recurrence after simultaneous cranioplasty and drainage or a shunt. The total success rate (CSE disappeared without recurrence) was 90.6% for patients who underwent cranioplasty; however, the total incidence of hydrocephalus was 40.1%.</AbstractText><AbstractText Label="CONCLUSIONS">This review suggests that cranioplasty is effective for the treatment of CSEDC, particularly intractable cases, but early cranioplasty may be more effective. In addition, hydrocephalus is fairly common after cranioplasty and requires further treatment.</AbstractText><CopyrightInformation>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Wu</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Zhihua</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Huaxin</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Zhiping</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yeyu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chengcai</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>Shenke</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Jilai</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Meihua</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China. Electronic address: limeihua2000@sina.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Jianguo</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Jiangxi Academy of Medical Sciences, Nanchang, Jiangxi Province, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>06</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>World Neurosurg</MedlineTA><NlmUniqueID>101528275</NlmUniqueID><ISSNLinking>1878-8750</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056424" MajorTopicYN="Y">Decompressive Craniectomy</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006849" MajorTopicYN="Y">Hydrocephalus</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013353" MajorTopicYN="Y">Subdural Effusion</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Contralateral subdural effusion</Keyword><Keyword MajorTopicYN="N">Cranioplasty</Keyword><Keyword MajorTopicYN="N">Decompressive craniectomy</Keyword><Keyword MajorTopicYN="N">Hydrocephalus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>6</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>6</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>9</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>2</Day><Hour>19</Hour><Minute>26</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35779748</ArticleId><ArticleId IdType="doi">10.1016/j.wneu.2022.06.117</ArticleId><ArticleId IdType="pii">S1878-8750(22)00901-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35779604</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1552-6259</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jun</Month><Day>30</Day></PubDate></JournalIssue><Title>The Annals of thoracic surgery</Title><ISOAbbreviation>Ann Thorac Surg</ISOAbbreviation></Journal>A Risk Prediction Model for Reintervention After Total Anomalous Pulmonary Venous Connection Repair. | Contralateral subdural effusion (CSE) after decompressive craniectomy (CSEDC) is occasionally observed. Cranioplasty is routinely performed for reconstruction and has recently been associated with improving contralateral subdural effusion. We sought to systematically review all available literature and evaluate the effectiveness of cranioplasty for CSE.</AbstractText>A PubMed, Web of Science, and Google Scholar search was conducted for preferred reporting items following the guidelines of systematic review and meta-analysis, including studies reporting patients who underwent cranioplasty because of CSEDC.</AbstractText>The search yielded 8 articles. A total of 56 patients ranging in age from 21 to 71 years developed CSEDC. Of them, 32 patients underwent cranioplasty. Eighteen cases with symptomatic CSE underwent cranioplasty alone, 2 cases received Ommaya drainage later because of a recurrence of CDC, and 1 case underwent a ventriculoperitoneal shunt because the CSE did not resolve completely and the ventricle was dilated again. The symptoms of 14 cases lessened without recurrence after simultaneous cranioplasty and drainage or a shunt. The total success rate (CSE disappeared without recurrence) was 90.6% for patients who underwent cranioplasty; however, the total incidence of hydrocephalus was 40.1%.</AbstractText>This review suggests that cranioplasty is effective for the treatment of CSEDC, particularly intractable cases, but early cranioplasty may be more effective. In addition, hydrocephalus is fairly common after cranioplasty and requires further treatment.</AbstractText>Copyright © 2022 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,794 | First-pass perfusion cardiovascular magnetic resonance parameters as surrogate markers for left ventricular diastolic dysfunction: a validation against cardiac catheterization.<Pagination><StartPage>8131</StartPage><EndPage>8139</EndPage><MedlinePgn>8131-8139</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00330-022-08938-6</ELocationID><Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">The non-invasive assessment of left ventricular (LV) diastolic dysfunction remains a challenge. The role of first-pass perfusion cardiac magnetic resonance (CMR) parameters in quantitative hemodynamic analyses has been reported. We therefore aimed to validate the diagnostic ability and accuracy of such parameters against cardiac catheterization for LV diastolic dysfunction in patients with left heart disease (LHD).</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We retrospectively enrolled 77 LHD patients who underwent CMR imaging and cardiac catheterization. LV diastolic dysfunction was defined as pulmonary capillary wedge pressure (PCWP) or LV end-diastolic pressure (LVEDP) > 12 mmHg on catheterization. On first-pass perfusion CMR imaging, pulmonary transit time (PTT) was measured as the time for blood to pass from the left ventricle to the right ventricle (RV) through the pulmonary vasculature. Pulmonary transit beat (PTB) was the number of cardiac cycles within the interval, and pulmonary blood volume indexed to body surface area (PBVi) was the product of PTB and RV stroke volume index (RVSVi).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Of the 77 LHD patients, 53 (68.83%) were found to have LV diastolic dysfunction, and showed significantly higher PTTc, PTB, and PBVi (p < 0.05) compared with those without. In multivariate analyses, only PTTc and PTB were identified as independent predictors of LV diastolic dysfunction (p < 0.05). With an optimal cutoff of 11.9 s, PTTc yielded the best diagnostic performance for LV diastolic dysfunction (area under the curve = 0.83, p < 0.001).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">PTTc may represent a non-invasive quantitative surrogate marker for the detection and assessment of diastolic dysfunction in LHD patients.</AbstractText><AbstractText Label="KEY POINTS" NlmCategory="CONCLUSIONS">• PTTc yielded the best diagnostic accuracy for diastolic dysfunction, with an optimal cutoff of 11.9 s, and a specificity of 100%. • PTTc and PTB were found to be independent predictors of LV diastolic dysfunction across different multivariate models with high reproducibility. • PTTc is a promising non-invasive surrogate marker for the detection and assessment of diastolic dysfunction in LHD patients.</AbstractText><CopyrightInformation>© 2022. The Author(s), under exclusive licence to European Society of Radiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Guo</LastName><ForeName>Xinli</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Gong</LastName><ForeName>Chao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Song</LastName><ForeName>Rizhen</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Ke</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan Province, 610041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Yuchi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medicine (Cardiovascular Division), University of Pennsylvania, Philadelphia, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yucheng</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0001-8480-4054</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, 610041, China. chenyucheng2003@126.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>No. ZYJC18013 and No. Z2018A08</GrantID><Agency>the 1·3·5 Project for Disciplines of Excellence-Clinical Research Incubation Project, West China Hospital, Sichuan University</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>07</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Eur Radiol</MedlineTA><NlmUniqueID>9114774</NlmUniqueID><ISSNLinking>0938-7994</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="Y">Ventricular Function, Left</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019028" MajorTopicYN="N">Magnetic Resonance Imaging, Cine</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015203" MajorTopicYN="N">Reproducibility of Results</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="Y">Ventricular Dysfunction, Left</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006328" MajorTopicYN="N">Cardiac Catheterization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009682" MajorTopicYN="N">Magnetic Resonance Spectroscopy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010477" MajorTopicYN="N">Perfusion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cardiac catheterization</Keyword><Keyword MajorTopicYN="N">Cardiomyopathies</Keyword><Keyword MajorTopicYN="N">Magnetic resonance imaging</Keyword><Keyword MajorTopicYN="N">Ventricular dysfunction, left</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>3</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>5</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>5</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>12</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>2</Day><Hour>11</Hour><Minute>13</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35779091</ArticleId><ArticleId IdType="doi">10.1007/s00330-022-08938-6</ArticleId><ArticleId IdType="pii">10.1007/s00330-022-08938-6</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Nagueh SF (2020) Left ventricular diastolic function: understanding pathophysiology, diagnosis, and prognosis with echocardiography. 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J Magn Reson Imaging 50:779–786</Citation><ArticleIdList><ArticleId IdType="doi">10.1002/jmri.26684</ArticleId><ArticleId IdType="pubmed">30838716</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35778853</PMID><DateRevised><Year>2022</Year><Month>10</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-8494</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>Anatomical record (Hoboken, N.J. : 2007)</Title><ISOAbbreviation>Anat Rec (Hoboken)</ISOAbbreviation></Journal>Cerebral arterial and ventricular morphology of the dogfish (Squalus acanthias), American bullfrog (Rana catesbeiana), and green iguana (Iguana iguana): Arterial high-resolution micro-CT, dissection, and radiography study. | This study's objective was to investigate obtaining high-resolution micro-computed tomography (CT) imaging of the injected arterial circulation of the brains of the dogfish (Squalus acanthias), American bullfrog (Rana catesbeiana), and green iguana (Iguana iguana). No micro-CT images of the arterial morphology of the brains of these vertebrates were previously published. Micro-CT imaging was performed on brains that had the cerebral arterial and ventricular systems injected with a radiopaque barium-gelatin compound in the early 1970s. These specimens were dissected and placed in a preservative fluid for 35 years, until imaged with micro-CT. The obtained micro-CT images were processed with a software program that provided 3D rotational motion rendering, and sequential display of 2D renderings of the micro-CT data. The anatomic information provided by the high-resolution micro-CT is not reproducible by any other radiopaque contrast currently available, without tissue removal corrosion, and enhanced the dissection information. The digital videos of the micro-CT 3D rotational motion rendering and sequential display of 2D renderings of the dogfish, bullfrog, and green iguana, demonstrate the extent of the arterial network within the brain, the arterial segments obscured by overlying structures such as nerves, and identified in the bullfrog the venous cerebral circulation resulting from the centrifugal leptomeningeal arterial capillaries. The rotational 3D images separated superimposed arterial structures, and the sequential display of the 2D renderings clarifies the relationship of cut or overlapped arterial branches. Comparing the brain and arterial morphology of the dogfish, bullfrog, and green iguana demonstrates some of the evolutionary modifications in these vertebrates. |
2,329,795 | Early prediction of failure to progress in single ventricle palliation: A step toward personalizing care for severe congenital heart disease.<Pagination><StartPage>1268</StartPage><EndPage>1276</EndPage><MedlinePgn>1268-1276</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.healun.2022.06.002</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1053-2498(22)01975-1</ELocationID><Abstract><AbstractText Label="BACKGROUND">Advances in surgical technique and medical surveillance have improved outcomes of single ventricle (SV) palliation, particularly during the first interstage period. However, there remains a considerable mortality risk beyond this period.</AbstractText><AbstractText Label="METHODS">Patients born between January 2004 and December 2011 who required SV palliation were retrospectively identified. Patients who survived stage 1 palliation, were discharged home, and then were evaluated for Glenn candidacy, and continued care at our institution were included. Perioperative echocardiographic, hemodynamic, and operative data were analyzed at each surgical stage. The primary outcome was death or need for transplant. Univariate and multivariate analysis was completed using Cox proportional-hazards modeling.</AbstractText><AbstractText Label="RESULTS">A total of 175 patients were included. Three patients died after pre-operative evaluation before Glenn. Glenn was completed in 168 patients, 16 died before Fontan. Fontan was completed in 149 patients; 117 were alive without need for transplant, 17 died post-Fontan, and 1 required transplantation. Twenty-one patients were lost to follow-up throughout the study period and were censored at time of last follow-up. Pre-Glenn moderate or severe atrioventricular valve regurgitation (AVVR) was an independent risk factor for death/transplant (HR 2.41; p-value .026). Pre-Glenn moderate ventricular dysfunction was also an independent risk factor (HR 5.29; p-value .012). Other risk factors included right ventricular (RV) dominant morphology and perinatal acidosis.</AbstractText><AbstractText Label="CONCLUSIONS">Despite advances in SV palliation, a subset of these children remains at increased risk for poor outcomes. Early risk factors include RV dominant morphology and perinatal acidosis. Patients with substantial AVVR or ventricular dysfunction before Glenn palliation are also at significantly higher risk for death or requirement of transplantation later in childhood.</AbstractText><CopyrightInformation>Copyright © 2022 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Weisert</LastName><ForeName>Molly</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California; Heart Institute, Children's Hospital Los Angeles, Los Angeles, California; Keck School of Medicine, University of Southern California, Los Angeles, California. Electronic address: mweisert@chla.usc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Menteer</LastName><ForeName>JonDavid</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California; Heart Institute, Children's Hospital Los Angeles, Los Angeles, California; Keck School of Medicine, University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Durazo-Arvizu</LastName><ForeName>Ramon</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Keck School of Medicine, University of Southern California, Los Angeles, California; The Saban Research Instititute, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wood</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California; Heart Institute, Children's Hospital Los Angeles, Los Angeles, California; Keck School of Medicine, University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, California; Heart Institute, Children's Hospital Los Angeles, Los Angeles, California; Keck School of Medicine, University of Southern California, Los Angeles, California.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>06</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Heart Lung Transplant</MedlineTA><NlmUniqueID>9102703</NlmUniqueID><ISSNLinking>1053-2498</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018729" MajorTopicYN="Y">Fontan Procedure</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="Y">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010166" MajorTopicYN="N">Palliative Care</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000080039" MajorTopicYN="Y">Univentricular Heart</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018754" MajorTopicYN="Y">Ventricular Dysfunction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">bidirectional Glenn</Keyword><Keyword MajorTopicYN="N">fontan</Keyword><Keyword MajorTopicYN="N">heart transplant</Keyword><Keyword MajorTopicYN="N">pediatrics</Keyword><Keyword MajorTopicYN="N">single ventricle</Keyword></KeywordList><CoiStatement>Disclosure statement Dr John Wood is the recipient of an Additional Ventures Single Ventricle grant. This grant was not used for this study. The other authors have no financial disclosures or conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>11</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>4</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>6</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>7</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>9</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>7</Month><Day>1</Day><Hour>22</Hour><Minute>6</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35778260</ArticleId><ArticleId IdType="doi">10.1016/j.healun.2022.06.002</ArticleId><ArticleId IdType="pii">S1053-2498(22)01975-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle>
<PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35777369</PMID><DateRevised><Year>2022</Year><Month>07</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1438-8782</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>Ultraschall in der Medizin (Stuttgart, Germany : 1980)</Title><ISOAbbreviation>Ultraschall Med</ISOAbbreviation></Journal>Prenatal Diagnosis, Associated Findings, and Postnatal Outcome in Fetuses with Double Inlet Ventricle (DIV). | Advances in surgical technique and medical surveillance have improved outcomes of single ventricle (SV) palliation, particularly during the first interstage period. However, there remains a considerable mortality risk beyond this period.</AbstractText>Patients born between January 2004 and December 2011 who required SV palliation were retrospectively identified. Patients who survived stage 1 palliation, were discharged home, and then were evaluated for Glenn candidacy, and continued care at our institution were included. Perioperative echocardiographic, hemodynamic, and operative data were analyzed at each surgical stage. The primary outcome was death or need for transplant. Univariate and multivariate analysis was completed using Cox proportional-hazards modeling.</AbstractText>A total of 175 patients were included. Three patients died after pre-operative evaluation before Glenn. Glenn was completed in 168 patients, 16 died before Fontan. Fontan was completed in 149 patients; 117 were alive without need for transplant, 17 died post-Fontan, and 1 required transplantation. Twenty-one patients were lost to follow-up throughout the study period and were censored at time of last follow-up. Pre-Glenn moderate or severe atrioventricular valve regurgitation (AVVR) was an independent risk factor for death/transplant (HR 2.41; p-value .026). Pre-Glenn moderate ventricular dysfunction was also an independent risk factor (HR 5.29; p-value .012). Other risk factors included right ventricular (RV) dominant morphology and perinatal acidosis.</AbstractText>Despite advances in SV palliation, a subset of these children remains at increased risk for poor outcomes. Early risk factors include RV dominant morphology and perinatal acidosis. Patients with substantial AVVR or ventricular dysfunction before Glenn palliation are also at significantly higher risk for death or requirement of transplantation later in childhood.</AbstractText>Copyright © 2022 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,329,796 | Isolation of Adult Mouse Neural Stem Cells and Assessment of Self-Renewal by ELDA. | The generation of new neurons in the adult brain throughout life is integral to brain plasticity and repair. Adult neural stem cells (aNSCs), present in the subventricular zone (SVZ) of the lateral ventricle wall and the subgranular zone (SGZ) of the hippocampal dentate gyrus, divide symmetrically or asymmetrically to maintain the stem cell pool or become committed progenitors and differentiate into various cell lineages. Depletion or dysregulation of aNSCs impairs proper brain connectivity and function and can contribute to several brain diseases including cognitive and neurodegenerative disorders and brain cancer. In this chapter, we present our optimized method to obtain and maintain reproducible neurosphere cultures from the adult mouse brain followed by evaluation of self-renewal using the extreme limiting dilution assay (ELDA) software. We use this assay routinely on aNSCs obtained from patient mouse models to generate log fraction plots and provide confidence intervals for all limiting dilution assay (LDA) data. At the same time, given the low number of NSCs required for the completion of the ELDA experiment, it is feasible to employ this approach to conduct high-content compound screening for therapeutic interventions aimed at enhancing the stem cell pool or combating a cohort of genetic and epigenetic disorders. |
2,329,797 | MRI abnormalities in a severe cognitive impairment mimicking a forebrain lesion in a geriatric dog. | Canine Cognitive Dysfunction is a neurological condition, that causes dogs to experience a wide variety of clinical signs. On rare occasions the symptoms may be unusual and severe, therefore they reminiscent of another disease. In this case report a 16 year and 8-month-old intact female poodle presented with circling, head pressing, and generalized ataxia. Prior clinical and neurologic examinations indicated the neurolocalisation to be forebrain. Morphometric brain parameters in MRI indicated otherwise. Quantitative MRI parameters such as the ventricle-brain index, interthalamic adhesion thickness, area, and the ratio of the interthalamic adhesion thickness to brain height may aid in the diagnosis of CCD.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Burbaitė</LastName><ForeName>Evelina</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0003-1540-2697</Identifier><AffiliationInfo><Affiliation>Faculty of Veterinary Veterinary Academy Lithuanian University of Health Sciences Kaunas Lithuania Veterinarian, Kriaučeliūnas Small Animal Veterinary Clinic, Faculty of Veterinary, Veterinary Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gradeckienė</LastName><ForeName>Aistė</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0001-9020-7280</Identifier><AffiliationInfo><Affiliation>Faculty of Veterinary Veterinary Academy Lithuanian University of Health Sciences Kaunas Lithuania Veterinarian, Kriaučeliūnas Small Animal Veterinary Clinic, Faculty of Veterinary, Veterinary Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Juodžentė</LastName><ForeName>Dalia</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0001-7854-3003</Identifier><AffiliationInfo><Affiliation>Faculty of Veterinary Veterinary Academy Lithuanian University of Health Sciences Kaunas Lithuania Veterinarian, Kriaučeliūnas Small Animal Veterinary Clinic, Faculty of Veterinary, Veterinary Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jankauskas</LastName><ForeName>Martinas</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0001-8702-8855</Identifier><AffiliationInfo><Affiliation>Faculty of Veterinary Veterinary Academy Lithuanian University of Health Sciences Kaunas Lithuania Veterinarian, Kriaučeliūnas Small Animal Veterinary Clinic, Faculty of Veterinary, Veterinary Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>06</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>Brazil</Country><MedlineTA>Braz J Vet Med</MedlineTA><NlmUniqueID>9918435088106676</NlmUniqueID></MedlineJournalInfo><OtherAbstract Type="Publisher" Language="por">A Disfunção Cognitiva Canina é uma condição neurológica, que faz com que os cães apresentem uma grande variedade de sinais clínicos. Em raras ocasiões, os sintomas podem ser incomuns e graves, portanto, lembram outras doenças. Neste relato de caso, uma cadela, da raça poodle, inteira de 16 anos e 8 meses de idade apresentou-se com movimentos circulares, pressão de cabeça e ataxia generalizada. Exames clínicos e neurológicos prévios indicaram que a neurolocalização era prosencéfalo. Os parâmetros morfométricos do cérebro na ressonância magnética indicaram o contrário. Parâmetros quantitativos de RM, como índice ventrículo-cérebro, espessura de adesão intertalâmica, área e a relação entre a espessura de adesão intertalâmica e a altura do cérebro podem auxiliar no diagnóstico de DCC. |
2,329,798 | Hypothesis: By-products of vascular disruption carried in the CSF affect prenatal brain development. | Prenatal CNS disruptions can be associated with physically separate findings. Examples include cognitive issues in septo-optic dysplasia and sporadic and WNT1-related unilateral cerebellar hypoplasia, and physical findings such as thinning of the corpus callosum, ventriculomegaly, hippocampal abnormalities, olfactory tract and bulb hypoplasia, and distant cortical dysplasias with schizencephaly. Similar effects to toxicities with intraventricular hemorrhage in prematurity could occur earlier in development. CSF transportation of disruption by-products would provide access to vulnerable areas through inflammatory effects on blood-brain barrier permeability. Outcomes are influenced by location and volume of byproducts in the CSF, timing, transport, and inflammatory responses. A particular association of vermis disruption with cognitive issues may be related to CSF flow distortions that avoid toxin dilutions in the third ventricle. Symmetrical contralateral cortical dysplasia with schizencephaly may reflect immunovascular field-related vulnerabilities seen in situations such as vitiligo. |
2,329,799 | Application of Light-Sheet Mesoscopy to Image Host-Pathogen Interactions in Intact Organs. | Human African Trypanosomiasis (HAT) is a disease caused by the extracellular parasite <i>Trypanosoma brucei</i> that affects the central nervous system (CNS) during the chronic stage of the infection, inducing neuroinflammation, coma, and death if left untreated. However, little is known about the structural change happening in the brain as result of the infection. So far, infection-induced neuroinflammation has been observed with conventional methods, such as immunohistochemistry, electron microscopy, and 2-photon microscopy only in small portions of the brain, which may not be representative of the disease. In this paper, we have used a newly-developed light-sheet illuminator to image the level of neuroinflammation in chronically infected mice and compared it to naïve controls. This system was developed for imaging in combination with the Mesolens objective lens, providing fast sub-cellular resolution for tens of mm<sup>3</sup>-large imaging volumes. The mouse brain specimens were cleared using CUBIC+, followed by antibody staining to locate Glial Fibrillary Acid Protein (GFAP) expressing cells, primarily astrocytes and ependymocytes, used here as a proxy for cell reactivity and gliosis. The large capture volume allowed us to detect GFAP<sup>+</sup> cells and spatially resolve the response to <i>T. brucei</i> infection. Based on morphometric analyses and spatial distribution of GFAP<sup>+</sup> cells, our data demonstrates a significant increase in cell dendrite branching around the lateral ventricle, as well as dorsal and ventral third ventricles, that are negatively correlated with the branch extension in distal sites from the circumventricular spaces. To our knowledge, this is the first report highlighting the potential of light-sheet mesoscopy to characterise the inflammatory responses of the mouse brain to parasitic infection at the cellular level in intact cleared organs, opening new avenues for the development of new mesoscale imaging techniques for the study of host-pathogen interactions. |
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