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2,331,100 | Prevention of endotoxin-induced cardiomyopathy using sodium tanshinone IIA sulfonate: Involvement of augmented autophagy and NLRP3 inflammasome suppression. | Increasing evidence indicates that patients or experimental animals exposure to endotoxin (lipopolysaccharides, LPS) exert deleterious cardiac functions that greatly contribute to morbidity and mortality. The pathophysiologic processes, including NLRP3 inflammasome overactivation and cardiac inflammatory injury, are complicated. Sodium tanshinone IIA sulfonate (STS), a water-soluble derivative of tanshinone IIA, is a naturally occurring compound extracted from Salvia miltiorrhiza and has anti-inflammatory and cardioprotective properties. In this study we examined the effect of STS on endotoxin-induced cardiomyopathy and investigated the underlying mechanisms. An endotoxemic mouse model was established by injecting LPS (10 mg/kg). Different doses of STS were administered intraperitoneally (5, 10, or 50 mg/kg) at different time points (2/12 h, 4/12 h, and 8/12 h) after LPS challenge to assess its effect on survival of mice with endotoxemia. In parallel, cardiac function, myocardial inflammatory cytokines, cardiomyocyte pyroptosis and autophagy were evaluated to determine the extent of myocardial damage due to sepsis in the presence and absence of STS at the optimal dose (10 mg/kg) and time-point (2/12 h). The results demonstrated that STS increased the survival rates, improved the compromised cardiac function and reduced myocardial inflammatory injury associated with enhanced autophagy and mitigated NLRP3 inflammasome activation. Moreover, inhibiting of autophagy or blocking the AMPK pathway reversed STS-elicited prevention of cardiomyopathy and activated the NLRP3 inflammasome in endotoxemic mice. Collectively, our study demonstrates that STS attenuates endotoxemia-induced mortality and cardiomyopathy, which may be associated with promotion of autophagy and inhibition of NLRP3 inflammasome overactivation. |
2,331,101 | New Insights into the Development and Morphogenesis of the Cardiac Purkinje Fiber Network: Linking Architecture and Function. | The rapid propagation of electrical activity through the ventricular conduction system (VCS) controls spatiotemporal contraction of the ventricles. Cardiac conduction defects or arrhythmias in humans are often associated with mutations in key cardiac transcription factors that have been shown to play important roles in VCS morphogenesis in mice. Understanding of the mechanisms of VCS development is thus crucial to decipher the etiology of conduction disturbances in adults. During embryogenesis, the VCS, consisting of the His bundle, bundle branches, and the distal Purkinje network, originates from two independent progenitor populations in the primary ring and the ventricular trabeculae. Differentiation into fast-conducting cardiomyocytes occurs progressively as ventricles develop to form a unique electrical pathway at late fetal stages. The objectives of this review are to highlight the structure-function relationship between VCS morphogenesis and conduction defects and to discuss recent data on the origin and development of the VCS with a focus on the distal Purkinje fiber network. |
2,331,102 | Differential inflammatory responses of the native left and right ventricle associated with donor heart preservation. | Dysfunction and inflammation of hearts subjected to cold ischemic preservation may differ between left and right ventricles, suggesting distinct strategies for amelioration.</AbstractText>Explanted murine hearts subjected to cold ischemia for 0, 4, or 8 h in preservation solution were assessed for function during 60 min of warm perfusion and then analyzed for cell death and inflammation by immunohistochemistry and western blotting and total RNA sequencing. Increased cold ischemic times led to greater left ventricle (LV) dysfunction compared to right ventricle (RV). The LV experienced greater cell death assessed by TUNEL+</sup> cells and cleaved caspase-3 expression (n = 4). While IL-6 protein levels were upregulated in both LV and RV, IL-1β, TNFα, IL-10, and MyD88 were disproportionately increased in the LV. Inflammasome components (NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), adaptor molecule apoptosis-associated speck-like protein containing a CARD (ASC), cleaved caspase-1) and products (cleaved IL-1β and gasdermin D) were also more upregulated in the LV. Pathway analysis of RNA sequencing showed increased signaling related to tumor necrosis factor, interferon, and innate immunity with ex-vivo ischemia, but no significant differences were found between the LV and RV. Human donor hearts showed comparable inflammatory responses to cold ischemia with greater LV increases of TNFα, IL-10, and inflammasomes (n = 3).</AbstractText>Mouse hearts subjected to cold ischemia showed time-dependent contractile dysfunction and increased cell death, inflammatory cytokine expression and inflammasome expression that are greater in the LV than RV. However, IL-6 protein elevations and altered transcriptional profiles were similar in both ventricles. Similar changes are observed in human hearts.</AbstractText>© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.</CopyrightInformation> |
2,331,103 | The method to generate pulsatile circulatory fluid flow using microfluidics. | Microfluidic chips provide versatile tools to mimic the biological effect of blood flow on pluripotent stem cells (PSC). This paper presents methods for the use of microfluidics to model embryonic circulation using differentiated PSC. Pulsatile circulatory flow is created with a microfluidics device with pressure-driven microvalves and ventricles. Silicone rubber devices are cast from moulds manufactured using standard and 3D laser lithography. The surface chemistry is modified to support the growth of human umbilical vein endothelial cells and pluripotent stem cells. Pulsatile circulatory fluid flow can be applied at specific stages of cell differentiation with direct observation of cellular responses by time-lapse fluorescent microscopy.•Replicable manufacturing protocol of lab scale microfluidic device generating pulsatile fluid flow mimicry embryonic blood circulation.•Integration of human cell lines on microfluidic chip. |
2,331,104 | Electrophysiologic Mapping of the Extraocular Motor Nuclei. | Mapping the floor of the fourth ventricle to identify the motonuclei of cranial nerves VII-XII has been well-described. Though there are some reports of stimulating the pontomesencephalic surface to identify the extraocular motor nuclei, there is a debate as to its efficacy and utility in helping to identify safe entry zones for medullary incision in an intra-axial resection. We present two cases where we positively and negatively mapped the surface of the midbrain and rostral pons to assist in surgical decision-making. Both patients had gross total resections of cavernomas, and both awoke without any new onset extraocular motor deficits. |
2,331,105 | White Matter Microstructural Damage Associated With Gait Abnormalities in Idiopathic Normal Pressure Hydrocephalus. | <b>Background</b>: Idiopathic normal pressure hydrocephalus (iNPH) is a common disease in elderly adults. Patients with iNPH are generally characterized by progressive gait impairment, cognitive deficits, and urinary urgency and/or incontinence. A number of radiographic studies have shown that iNPH patients have enlarged ventricles and altered brain morphology; however, few studies have focused on the relationships between altered brain structure and gait dysfunction due to iNPH. Thus, this study aimed to evaluate the abnormalities of white matter (WM) correlated with gait impairment in iNPH patients and to gain a better understanding of its underlying pathology. <b>Methods</b>: Fifteen iNPH patients (five women, 10 men) were enrolled in this study, and each patient's demographic and gait indices were collected. First, we performed a correlation analysis between the demographic and gait indices. Then, all gait indices were grouped according to the number of WM hyperintensities (WMH) among each WM tract (JHU WM tractography atlas), to perform comparative analysis. <b>Results</b>: Considering sex and illness duration as covariates, correlation analysis showed a significantly negative correlation between step length (<i>r</i> = -0.80, <i>p</i> = 0.001), pace (<i>r</i> = -0.84, <i>p</i> = 2.96e-4), and age. After removing the effects of age, sex, and illness duration, correlation analysis showed negative correlation between step length (<i>r</i> = -0.73, <i>p</i> = 0.007), pace (<i>r</i> = -0.74, <i>p</i> = 0.005), and clinical-grade score and positive correlation between 3-m round trip time (<i>r</i> = 0.66, <i>p</i> = 0.021), rising time (<i>r</i> = 0.76, <i>p</i> = 0.004), and clinical-grade score. Based on WMH of each white matter tract, gait indices showed significant differences (<i>p</i> < 0.05/48, corrected by Bonferroni) between fewer WMH patients and more WMH in the middle cerebellar peduncle, left medial lemniscus, left posterior limb of the internal capsule (IC), and right posterior limb of the IC. <b>Conclusions</b>: Our results indicated that iNPH patients exhibited gait-related WM abnormalities located in motor and sensory pathways around the ventricle, which is beneficial to understand the underlying pathology of iNPH. |
2,331,106 | Completion Posterior Quadrant Disconnection After Failed Temporal Lobectomy: 2-Dimensional Operative Video. | Epilepsy is a chronic seizure disorder that affects about 1% of the global population.1 When seizure freedom cannot be obtained solely through antiseizure medicines (ASMs), the condition is termed medically refractory epilepsy (MRE).2,3 Though posterior quadrant disconnection (PQD) is underutilized in our experience, it is a highly effective surgical procedure for MRE restricted to the temporal, parietal, and/or occipital lobes.4-12 In this operative video, we demonstrate a right-sided completion PQD following failed temporal lobectomy in an 8-yr-old female with focal MRE. We review technical nuances, including (1) extension/revision of prior scalp incision, (2) placement of subdural strip for the identification of phase reversal and central sulcus, (3) disconnection of parietal and occipital lobes, (4) extension of the corticectomy to the pia overlying the falcotentorial junction and into the prior temporal lobectomy defect, and (5) posterior disconnection of the corpus callosum. Postoperatively, the patient experienced subtle left-arm weakness and central fever, both of which resolved. An external ventricular drain (EVD) was placed in the ventricle/operative cavity and left for 3 to 4 d until the draining cerebrospinal fluid (CSF) cleared. As of 3-mo follow-up, she has been seizure-free without complications. In summary, PQD is a safe and effective treatment option for MRE that can be utilized not only as an initial operation but also after failed surgery.  Appropriate patient consent was obtained to perform this procedure and present this clinical case and surgical video for academic purposes.  Image at 4:00 licensed under CC BY-2.5, 2006, modified from http://upload.wikimedia.org/wikipedia/commons/7/70/Lateral_head_skull.jpg (flipped and rotated). Image at 4:42, Public Domain: Gray H. Anatomy of the Human Body. 1918. Bartleby.com, https://commons.wikimedia.org/wiki/File:Lobes_of_the_brain_NL.svg; flipped, modified. Image at 6:42, Public Domain: House EL, Pansky B. A Functional Approach to Neuroanatomy. 1960. McGraw-Hill Book Company; https://upload.wikimedia.wikipedia.commons/5/52/Lawrence_1960_2.3.png; modified. |
2,331,107 | Menkes disease diagnosed by a <i>novel ATP7A</i> frameshift mutation in a patient with infantile spasms-a case report. | Menkes disease (MD) is a rare congenital copper deficiency disease caused by an adenosine triphosphatase copper transporting alpha (<i>ATP7A</i>) gene mutation. It is a progressive and systemic disease that primarily involves the central nervous system and connective tissues. The clinical manifestation of these patients with MD is curly hair, progressive muscle tone reduction, and convulsions, and often leads to death in early infancy. Herein, we present a case of a 9-month-old Chinese male who displayed developmental regression, followed by convulsions, which were characterized by infantile spasms (ISs). The proband also had curly hair, hypopigmented skin, cutis laxa, decreased muscle tone, and micrognathia. The patient's ceruloplasmin levels were below the reference values. Brain magnetic resonance imaging (MRI) showed abnormal signals bilaterally that were symmetrically distributed in the caudate nucleus, globus pallidus, and subcortical white matter of the temporal parietal cortex, white matter in the anterior and posterior corners of the ventricles and the anterior limb of the internal capsule. The electroencephalograph (EEG) showed hypsarrhythmia. Genetic testing revealed a novel frameshift mutation in the <i>ATP7A</i> gene exon 13 and premature termination codon. Copper replacement therapy was initiated after the delayed diagnosis was established. However, the patient still died several months later due to disease progression. Our case reveals a novel frameshift mutation of the <i>ATP7A</i> gene, which expands the gene spectrum of MD. The infants with uncontrollable convulsions, regressive development, curly hair, MD should be considered at early stage and also need the further genetic analysis to confirm MD finally. The correct and timely diagnosis and initiating copper replacement therapy may improve the prognosis. |
2,331,108 | Rosette-forming glioneuronal tumor of the fourth ventricle; A case report and review of the literature. | Despite mostly indolent course and favorable postoperative outcome long-term follow-up studies are needed to identify the most appropriate therapeutic strategies to minimize surgical morbidity and neurologic injury in patients with RGNT. |
2,331,109 | Cardiac magnetic resonance assessment of right ventricular remodeling after anthracycline therapy. | There are limited data on the effects of anthracyclines on right ventricular (RV) structure, function, and tissue characteristics. The goal of this study was to investigate the effects of anthracyclines on the RV using cardiac magnetic resonance (CMR). This was a post-hoc analysis of a prospective study of 27 breast cancer (BC) patients (51.8 ± 8.9 years) using CMR prior, and up to 3-times after anthracyclines (240 mg/m<sup>2</sup>) to measure RV volumes and mass, RV extracellular volume (ECV) and cardiomyocyte mass (CM). Before anthracyclines, LVEF (69.4 ± 3.6%) and RVEF (55.6 ± 9%) were normal. The median follow-up after anthracyclines was 399 days (IQR 310-517). The RVEF reached its nadir (46.3 ± 6.8%) after 9-months (P < 0.001). RV mass-index and RV CM decreased to 13 ± 2.8 g/m<sup>2</sup> and 8.13 ± 2 g/m<sup>2</sup>, respectively, at 16-months after anthracyclines. The RV ECV expanded from 0.26 ± 0.07 by 0.14 (53%) to 0.40 ± 0.1 (P < 0.001). The RV ECV expansion correlated with a decrease in RV mass-index (r = -0.46; P < 0.001) and the increase in CK-MB. An RV ESV index at baseline above its median predicted an increased risk of LV dysfunction post-anthracyclines. In BC patients treated with anthracyclines, RV atrophy, systolic dysfunction, and a parallel increase of diffuse interstitial fibrosis indicate a cardiotoxic response on a similar scale as previously seen in the systemic left ventricle. |
2,331,110 | Cardioprotective effects of the proline-rich oligopeptide Bj-PRO-7a in spontaneously hypertensive rats. | The proline-rich oligopeptide from Bothrops jararaca snake venom, Bj-PRO-7a, promotes acute effects in blood pressure in hypertensive animals. However, the cardiac effects of this heptapeptide are completely unknown. Thus, we sought to evaluate whether the Bj-PRO-7a could protect against cardiac remodelling in spontaneously hypertensive rats (SHR). SHR were treated with Bj-PRO-7a (71 nmol/kg/day, s.c.) or saline for 28 days. Wistar rats were used as control. Systolic blood pressure (SBP) and heart rate (HR) were measured by tail-cuff plethysmography. Cardiomyocyte diameter and interstitial and perivascular fibrosis of the left ventricle (LV) were evaluated using Picrosirius staining. Immunofluorescence was used to detect collagen I and III. Fibroblast proliferation was assessed by immunohistochemistry to detect proliferating cell nuclear antigen (PCNA). Protein expression was assessed by western blot. The superoxide dismutase and catalase activities and the concentration of lipid peroxidation products were evaluated in the LV. The SBP and HR were not different between treated and non-treated SHR at the end of the treatment. However, Bj-PRO-7a attenuated the cardiomyocyte hypertrophy, deposition of interstitial and perivascular fibrosis and collagen I, and positive PCNA-labelled fibroblasts. This peptide also reduced the increased levels of TBARS, expression and activity of catalase, and activity of SOD in LV from SHR. Also, the Bj-PRO-7a increased the expression of metalloproteinases-2 in SHR hearts. These findings demonstrate that the Bj-PRO-7a reduced the pathological cardiac remodelling in a pressure-independent manner in hypertensive rats through mechanisms mediated by oxidative stress regulation. |
2,331,111 | Importance of extracellular vesicle secretion at the blood-cerebrospinal fluid interface in the pathogenesis of Alzheimer's disease. | Increasing evidence indicates that extracellular vesicles (EVs) play an important role in the pathogenesis of Alzheimer's disease (AD). We previously reported that the blood-cerebrospinal fluid (CSF) interface, formed by the choroid plexus epithelial (CPE) cells, releases an increased amount of EVs into the CSF in response to peripheral inflammation. Here, we studied the importance of CP-mediated EV release in AD pathogenesis. We observed increased EV levels in the CSF of young transgenic APP/PS1 mice which correlated with high amyloid beta (Aβ) CSF levels at this age. The intracerebroventricular (icv) injection of Aβ oligomers (AβO) in wild-type mice revealed a significant increase of EVs in the CSF, signifying that the presence of CSF-AβO is sufficient to induce increased EV secretion. Using in vivo, in vitro and ex vivo approaches, we identified the CP as a major source of the CSF-EVs. Interestingly, AβO-induced, CP-derived EVs induced pro-inflammatory effects in mixed cortical cultures. Proteome analysis of these EVs revealed the presence of several pro-inflammatory proteins, including the complement protein C3. Strikingly, inhibition of EV production using GW4869 resulted in protection against acute AβO-induced cognitive decline. Further research into the underlying mechanisms of this EV secretion might open up novel therapeutic strategies to impact the pathogenesis and progression of AD. |
2,331,112 | Long-Standing Overt Ventriculomegaly in Adults (LOVA): Diagnostic Aspects, CSF Dynamics with Lumbar Infusion Test and Treatment Options in a Consecutive Series with Long-Term Follow-Up. | Long-standing overt ventriculomegaly in adults is a chronic form of hydrocephalus without a clear pathophysiological description and a consensus about the treatment. We present the results of endoscopic third ventriculostomy (ETV) in a consecutive series with a mean follow-up of 79 ± 23 months, highlighting how the preoperative lumbar infusion test could facilitate understanding the pathophysiology of the disease.</AbstractText>We retrospectively collected data regarding clinical assessment, neuroradiological findings, and preoperative lumbar infusion tests in 22 symptomatic patients.</AbstractText>In the majority of cases, patients reported imbalance and gait disorders, and 8 subjects had headaches. The preoperative lumbar infusion test demonstrated a mean opening pressure of 13.95 ± 2.88 mm Hg, with plateau values ranging from 22 to 39 mm Hg. The resistance to outflow was 11.21 ± 2.00 mm Hg/mL/min. After the procedure, all patients reported improvement or halted progression in their presenting symptoms, whereas no significant reduction was demonstrated in Evans' index. One subject underwent a second ETV procedure after more than 2 years because of the failure of the endoscopic approach.</AbstractText>A progressive exhaustion of brain compliance plays an important role in explaining the dichotomy between severe ventriculomegaly and mild clinical symptoms in patients with long-standing overt ventriculomegaly in adults. The role of the aqueductal stenosis as a diagnostic criterion might be reconsidered. The preoperative infusion test data support this observation. Preoperative assessment should include not only clinical and neuroradiological evaluation but also the study of cerebrospinal fluid dynamics. ETV should be considered the treatment of choice because of its safety and efficacy. Long-term follow-up is mandatory.</AbstractText>Copyright © 2021 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,331,113 | De-differentiated metastatic adenosquamous carcinoma arising from germ cell tumor in the brain and spine. | Intracranial germ cell tumors have an estimated incidence of 0.4-3.4% in the Western Hemisphere. Patients can present with a variety of differing clinical signs and symptoms including headache, nausea/vomiting, hydrocephalus, obtundation, pyramidal tract signs, ataxia, and hypothalamic/pituitary dysfunction. Rarely germ cell tumors can transform into alternative malignancy. In these cases, treatment options may be difficult. Metastasis to the brain is not uncommon in germ cell tumors and is frequently reported within the pineal region; however, they are less common intraventricularly, within the posterior fossa and have never been reported after malignant transformation. Herein, we present the first reported case of a metastatic adenosquamous carcinoma transformed from a yolk sac tumor with diffuse cerebral metastasis in atypical locations of the brain including intraventricular and posterior fossa. A 53-year-old right-handed Caucasian female was transferred from an outside hospital for a chief complaint of altered mental status with CT head showing right side intraventricular mass and cerebellar hemorrhage. MRI of the brain found multifocal contrast-enhancing lesions of the right lateral ventricle, right cerebellum, right frontal lobe, diffuse lumbar dural enhancement, and an intramedullary lesion at the cervico-medullary junction of the brainstem. The right lateral ventricular lesion and right cerebellar lesions were resected. Pathology findings support a diagnosis of adenosquamous carcinoma, and the morphologic and immunophenotypic features suggest development as a somatic malignancy in a germ cell neoplasm with features of a yolk sac tumor. Germ cell tumors are typically included within the differential of pineal region masses; however, other locations such as intraventricular and posterior fossa are rarely seen. Even rarer are cases with malignant transformation to an alternative lesion for which treatment options are exceptionally scarce. Neurosurgeons and oncologists alike should be aware of this rare possible lesion to add to a broad differential diagnosis. |
2,331,114 | Developmental genes controlling neural circuit formation are expressed in the early postnatal hypothalamus and cellular lining of the third ventricle. | The arcuate nucleus of the hypothalamus is central in the regulation of body weight homeostasis through its ability to sense peripheral metabolic signals and relay them, through neural circuits, to other brain areas, ultimately affecting physiological and behavioural changes. The early postnatal development of these neural circuits is critical for normal body weight homeostasis, such that perturbations during this critical period can lead to obesity. The role for peripheral regulators of body weight homeostasis, including leptin, insulin and ghrelin, in this postnatal development is well described, yet some of the fundamental processes underpinning axonal and dendritic growth remain unclear. Here, we hypothesised that molecules known to regulate axonal and dendritic growth processes in other areas of the developing brain would be expressed in the postnatal arcuate nucleus and/or target nuclei where they would function to mediate the development of this circuitry. Using state-of-the-art RNAscope<sup>®</sup> technology, we have revealed the expression patterns of genes encoding Dcc/Netrin-1, Robo1/Slit1 and Fzd5/Wnt5a receptor/ligand pairs in the early postnatal mouse hypothalamus. We found that individual genes had unique expression patterns across developmental time in the arcuate nucleus, paraventricular nucleus of the hypothalamus, ventromedial nucleus of the hypothalamus, dorsomedial nucleus of the hypothalamus, median eminence and, somewhat unexpectedly, the third ventricle epithelium. These observations indicate a number of new molecular players in the development of neural circuits regulating body weight homeostasis, as well as novel molecular markers of tanycyte heterogeneity. |
2,331,115 | A Transmural Path Model Improves the Definition of the Orthotropic Tissue Structure in Heart Simulations. | In the past decades, the structure of the heart, human as well as other species, has been explored in a detailed way, e.g., via histological studies or diffusion tensor magnetic resonance imaging. Nevertheless, the assignment of the characteristic orthotropic structure in a patient-specific finite element model remains a challenging task. Various types of rule-based models, which define the local fiber and sheet orientation depending on the transmural depth, have been developed. However, the correct assessment of the transmural depth is not trivial. Its accuracy has a substantial influence on the overall mechanical and electrical properties in rule-based models. The main purpose of this study is the development of a finite element-based approach to accurately determine the transmural depth on a general unstructured grid. Instead of directly using the solution of the Laplace problem as the transmural depth, we make use of a well-established model for the assessment of the transmural thickness. It is based on two hyperbolic first-order partial differential equations for the definition of a transmural path, whereby the transmural thickness is defined as the arc length of this path. Subsequently, the transmural depth is determined based on the position on the transmural path. Originally, the partial differential equations were solved via finite differences on structured grids. In order to circumvent the need of two grids and mapping between the structured (to determine the transmural depth) and unstructured (electromechanical heart simulation) grids, we solve the equations directly on the same unstructured tetrahedral mesh. We propose a finite-element-based discontinuous Galerkin approach. Based on the accurate transmural depth, we assign the local material orientation of the orthotropic tissue structure in a usual fashion. We show that this approach leads to a more accurate definition of the transmural depth. Furthermore, for the left ventricle, we propose functions for the transmural fiber and sheet orientation by fitting them to literature-based diffusion tensor magnetic resonance imaging data. The proposed functions provide a distinct improvement compared to existing rules from the literature. |
2,331,116 | Subventricular zone/white matter microglia reconstitute the empty adult microglial niche in a dynamic wave. | Microglia, the brain's resident myeloid cells, play central roles in brain defense, homeostasis, and disease. Using a prolonged colony-stimulating factor 1 receptor inhibitor (CSF1Ri) approach, we report an unprecedented level of microglial depletion and establish a model system that achieves an empty microglial niche in the adult brain. We identify a myeloid cell that migrates from the subventricular zone and associated white matter areas. Following CSF1Ri, these amoeboid cells migrate radially and tangentially in a dynamic wave filling the brain in a distinct pattern, to replace the microglial-depleted brain. These repopulating cells are enriched in disease-associated microglia genes and exhibit similar phenotypic and transcriptional profiles to white-matter-associated microglia. Our findings shed light on the overlapping and distinct functional complexity and diversity of myeloid cells of the CNS and provide new insight into repopulating microglia function and dynamics in the mouse brain. |
2,331,117 | A Dense RNN for Sequential Four-Chamber View Left Ventricle Wall Segmentation and Cardiac State Estimation. | The segmentation of the left ventricle (LV) wall in four-chamber view cardiac sequential image is significant for cardiac disease diagnosis and cardiac mechanisms study; however, there is no successful reported work on sequential four-chambered view LV wall segmentation due to the complex four-chamber structure and diversity of wall motion. In this article, we propose a dense recurrent neural network (RNN) algorithm to achieve accurately LV wall segmentation in a four-chamber view MRI time sequence. In the cardiac sequential LV wall process, not only the sequential accuracy but also the accuracy of each image matters. Thus, we propose a dense RNN to provide compensation for the first long short-term memory (LSTM) cells. Two RNNs are combined in this work, the first one aims at providing information for the first image, and the second RNN generates segmentation result. In this way, the proposed dense RNN improves the accuracy of the first frame image. What is more is that, it improves the effectiveness of information flow between LSTM cells. Obtaining more competent information from the former cell, frame-wise segmentation accuracy is greatly improved. Based on the segmentation result, an algorithm is proposed to estimate cardiac state. This is the first time that deals with both cardiac time-sequential LV segmentation problems and, robustly, estimates cardiac state. Rather than segmenting each frame separately, utilizing cardiac sequence information is more stable. The proposed method ensures an Intersection over Union (IoU) of 92.13%, which outperforms other classical deep learning algorithms. |
2,331,118 | Diagnosis and Treatment of Right Heart Failure in Pulmonary Vascular Diseases: A National Heart, Lung, and Blood Institute Workshop. | Right ventricular dysfunction is a hallmark of advanced pulmonary vascular, lung parenchymal, and left heart disease, yet the underlying mechanisms that govern (mal)adaptation remain incompletely characterized. Owing to the knowledge gaps in our understanding of the right ventricle (RV) in health and disease, the National Heart, Lung, and Blood Institute (NHLBI) commissioned a working group to identify current challenges in the field. These included a need to define and standardize normal RV structure and function in populations; access to RV tissue for research purposes and the development of complex experimental platforms that recapitulate the <i>in vivo</i> environment; and the advancement of imaging and invasive methodologies to study the RV within basic, translational, and clinical research programs. Specific recommendations were provided, including a call to incorporate precision medicine and innovations in prognosis, diagnosis, and novel RV therapeutics for patients with pulmonary vascular disease. |
2,331,119 | Incidental Detection of Ischemic Myocardium on <sup>68</sup> Ga-FAPI PET/CT. | Recent studies using Ga-68-labeled fibroblast activation protein inhibitors (FAPI) PET have shown strong association between focal uptake of FAPI in myocardium and presence of coronary artery disease. We present an interesting case of a 76-year-old female with breast cancer with incidental uptake on FAPI PET in apex and septal wall of left ventricle myocardium correlating with findings of ischemia on dobutamine stress myocardial perfusion imaging and anatomical stenosis on coronary angiography. |
2,331,120 | YAP/TAZ maintain the proliferative capacity and structural organization of radial glial cells during brain development. | The Hippo pathway regulates the development and homeostasis of many tissues and in many species. It controls the activity of two paralogous transcriptional coactivators, YAP and TAZ (YAP/TAZ). Although previous studies have established that aberrant YAP/TAZ activation is detrimental to mammalian brain development, whether and how endogenous levels of YAP/TAZ activity regulate brain development remain unclear. Here, we show that during mammalian cortical development, YAP/TAZ are specifically expressed in apical neural progenitor cells known as radial glial cells (RGCs). The subcellular localization of YAP/TAZ undergoes dynamic changes as corticogenesis proceeds. YAP/TAZ are required for maintaining the proliferative potential and structural organization of RGCs, and their ablation during cortical development reduces the numbers of cortical projection neurons and causes the loss of ependymal cells, resulting in hydrocephaly. Transcriptomic analysis using sorted RGCs reveals gene expression changes in YAP/TAZ-depleted cells that correlate with mutant phenotypes. Thus, our study has uncovered essential functions of YAP/TAZ during mammalian brain development and revealed the transcriptional mechanism of their action. |
2,331,121 | Development of an In Vitro Hemorrhagic Hydrocephalus Model for Functional Evaluation of Magnetic Microactuators Against Shunt Obstructions. | Occlusion of ventriculoperitoneal shunts placed after intraventricular hemorrhage occurs frequently. The objective of this study was to develop a hemorrhagic hydrocephalus model to assess the ability of an oscillating microactuator within the ventricular catheter (VC) to prevent shunt obstruction.</AbstractText>An in vitro hydrocephalus model with extreme risk of shunt obstruction was created. Phosphate-buffered saline, blood, and thrombin were driven through ventriculoperitoneal shunts for 8 hours. Five VCs were fitted with a microactuator and compared with 5 control VCs. The microactuator was actuated by an external magnetic field for 30 minutes. Pressure within the imitation lateral ventricle was measured.</AbstractText>In the 5 control shunts, 6 obstructions developed (3 VC, 3 valve-distal catheter) compared with 1 obstruction (VC) in the 5 microactuator shunts. In the control and microactuator groups, the median volume exiting the shunts in 8 hours was 30 mL versus 256 mL. Median time to reach an intraventricular pressure of 40 mm Hg (13.8 minutes vs. >8 hours), median total time >40 mm Hg (6.2 hours vs. 0.0 hours), and median maximum pressure (192 mm Hg vs. 36 mm Hg) were significantly improved in the microactuator group (P < 0.01).</AbstractText>In addition to protecting the VC, the microactuator appeared to prevent hematoma obstructing the valve or distal catheter, resulting in a much longer duration of low intraventricular pressures. A microactuator activated by placing the patient's head in an external magnetic field could reduce shunt obstructions in hemorrhagic hydrocephalus.</AbstractText>Copyright © 2021 Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,331,122 | Short-time total-body dynamic PET imaging performance in quantifying the kinetic metrics of <sup>18</sup>F-FDG in healthy volunteers.<Pagination><StartPage>2493</StartPage><EndPage>2503</EndPage><MedlinePgn>2493-2503</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00259-021-05500-2</ELocationID><Abstract><AbstractText Label="PURPOSE">To investigate the performance of short-time dynamic imaging in quantifying kinetic metrics of 2-[<sup>18</sup>F]-fluoro-2-deoxy-D-glucose (<sup>18</sup>F-FDG).</AbstractText><AbstractText Label="METHODS">Dynamic total-body positron emission tomography (PET) imaging was performed in 11 healthy volunteers for 75 min. The data were divided into 30-, 45- and 75-min groups. Nonlinear regression (NLR) generated constant rates (k<sub>1</sub> to k<sub>3</sub>) and NLR-based Ki in various organs. The Patlak method calculated parametric Ki images to generate Patlak-based Ki values. Paired samples t-test or the Wilcoxon signed-rank test compared the kinetic metrics between the groups, depending on data normality. Deming regression and Bland-Altman analysis assessed the correlation and agreement between NLR- and Patlak-based Ki. A two-sided P < 0.05 was considered statistically significant.</AbstractText><AbstractText Label="RESULTS">The 45- and 75-min groups were similar in NLR-based kinetic metrics. The relative difference ranges were as follows: k<sub>1</sub>, from 3.4% (P = 0.627) in the spleen to 57.9% (P = 0.130) in the white matter; k<sub>2</sub>, from 6.0% (P = 0.904) in the spleen to 60.7% (P = 0.235) in the left ventricle (LV) myocardium; k<sub>3</sub>, from 45.6% (P = 0.302) in the LV myocardium to 96.3% (P = 0.478) in the liver; Ki, from 14.0% (P = 0.488) in the liver to 77.8% (P = 0.067) in the kidney. Patlak-based Ki values were also similar between these groups in all organs, except the grey matter (9.6%, P = 0.029) and cerebellum (14.4%, P = 0.002). However, significant differences in kinetic metrics were found between the 30-min and 75-min groups in most organs both in NLR- and Patlak-based analyses. The NLR- and Patlak-based Ki values significantly correlated, with no bias in any of the organs.</AbstractText><AbstractText Label="CONCLUSION">Dynamic imaging using a high-sensitivity total-body PET scanner for a shorter time of 45 min could achieve relevant kinetic metrics of <sup>18</sup>F-FDG as done by long-time imaging.</AbstractText><CopyrightInformation>© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Guobing</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Haojun</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Dai</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Pengcheng</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Hui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yiqiu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Hongyan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Hongcheng</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China. shi.hongcheng@zs-hospital.sh.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Nuclear Medicine, Fudan University, Shanghai, 200032, China. shi.hongcheng@zs-hospital.sh.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Medical Imaging, Shanghai, 200032, China. shi.hongcheng@zs-hospital.sh.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cancer Prevention and Treatment Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. shi.hongcheng@zs-hospital.sh.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2021</Year><Month>08</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Eur J Nucl Med Mol Imaging</MedlineTA><NlmUniqueID>101140988</NlmUniqueID><ISSNLinking>1619-7070</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0Z5B2CJX4D</RegistryNumber><NameOfSubstance UI="D019788">Fluorodeoxyglucose F18</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D019985" MajorTopicYN="Y">Benchmarking</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019788" MajorTopicYN="Y">Fluorodeoxyglucose F18</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064368" MajorTopicYN="N">Healthy Volunteers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="N">Positron-Emission Tomography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">2-[18F]-fluoro-2-deoxy-D-glucose (18F-FDG)</Keyword><Keyword MajorTopicYN="N">Dynamic imaging</Keyword><Keyword MajorTopicYN="N">Short-time imaging</Keyword><Keyword MajorTopicYN="N">Total-body Positron emission tomography</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>4</Month><Day>4</Day></PubMedPubDate><PubMedPubDate 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J Nucl Med. 2006;47(6):945–9.</Citation><ArticleIdList><ArticleId IdType="pubmed">16741303</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">34417133</PMID><DateRevised><Year>2021</Year><Month>10</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2173-5743</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2021</Year><Month>Aug</Month><Day>17</Day></PubDate></JournalIssue><Title>Reumatologia clinica</Title><ISOAbbreviation>Reumatol Clin (Engl Ed)</ISOAbbreviation></Journal>Takotsubo Syndrome in a Rheumatoid Arthritis Patient Under Tofacitinib: A Case Report. | We describe a case of a 57-year-old white woman treated for rheumatoid arthritis (RA) with tofacitinib 10mg daily (started one year ago) and prednisolone 5mg daily. She presented to the emergency department with a tight squeezing chest pain and shortness of breath for 7h and the clinical evaluation revealed regional systolic dysfunction of the left ventricle, mimicking a myocardial infarction, in the absence of angiographic evidence of obstructive coronary artery disease or acute plaque rupture. All changes were transient and resolved completely within 4 days. The diagnosis of Takotsubo cardiomyopathy (TKM) was established. This is, as far as we know, the first report of a case of TKM in a RA patient taking tofacitinib. Although the association has not been previously described and the precise cause cannot be identified in this patient, the association with tofacitinib should be considered given the etiopathogenic rationale and the absence of any other identifiable cause. |
2,331,123 | Tumor characteristics and surgical outcomes of intracranial subependymomas: a systematic review and meta-analysis. | The tumor characteristics and surgical outcomes of intracranial subependymomas are poorly defined. In this study the authors aimed to provide a comprehensive review of all clinical, pathological, radiological, and surgical aspects of this important neoplasm to inform future management strategies.</AbstractText>A systematic review and meta-analysis of MEDLINE, EMBASE, Cochrane, and Google Scholar databases adherent to PRISMA guidelines was conducted.</AbstractText>Of the 1145 articles initially retrieved, 24 studies encompassing 890 cases were included. The authors identified 3 retrospective cohort studies and 21 case series, but no controlled trials. Mean age at presentation was 46.7 ± 18.1 years with a male predominance (70.2%). Common sites of tumor origin were the lateral ventricle (44.5%) and fourth ventricle (43.1%). Cumulative postoperative mortality and morbidity rates were 3.4% and 24.3% respectively. Meta-analysis revealed that male sex (HR 3.15, 95% CI 1.39-7.14, p = 0.006) was associated with poorer 5-year overall mortality rates. All-cause mortality rates were similar when performing subgroup meta-analyses for age (HR 0.50, 95% CI 0.03-7.36, p = 0.61), smaller subependymoma size (HR 1.51, 95% CI 0.78-2.92, p = 0.22), gross-total resection (HR 0.65, 95% CI 0.35-1.23, p = 0.18), and receipt of postoperative radiation therapy (HR 0.88, 95% CI 0.27-2.88, p = 0.84). Postoperative Karnofsky Performance Index scores improved by a mean difference of 1.62 ± 12.14 points (p = 0.42). The pooled overall 5-year survival rate was 89.2%, while the cumulative recurrence rate was 1.3% over a median follow-up ranging from 15.3 to 120.0 months. The pure subependymoma histopathological subtype was most prevalent (85.6%), followed by the mixed subependymoma-ependymoma tumor variant (13.7%).</AbstractText>Surgical extirpation without postoperative radiotherapy results in excellent postoperative survival and functional outcomes in the treatment of intracranial subependymomas. Aggressive tumor behavior should prompt histological reevaluation for a mixed subependymoma-ependymoma subtype. Further high-quality controlled trials are still required to investigate this rare tumor.</AbstractText> |
2,331,124 | Transitory and Vestigial Structures of the Developing Human Nervous System. | As with many body organs, the human central nervous system contains many structures and cavities that may have had functions in embryonic and fetal life but are vestigial or atrophic at maturity. Examples are the septum pellucidum, remnants of the lamina terminalis, Cajal-Retzius neurons, induseum griseum, habenula, and accessory olfactory bulb. Other structures are transitory in fetal or early postnatal life, disappearing from the mature brain. Examples are the neural crest, subpial granular glial layer of Brun over cerebral cortex, radial glial cells, and subplate zone of cerebral cortex. At times persistent fetal structures that do not regress may cause neurological problems or indicate a pathologic condition, such as Blake pouch cyst. Transitory structures thus can become vestigial. Examples are an excessively wide cavum septi pellucidi, suprapineal recess of the third ventricle, trigeminal artery of the posterior fossa circulation, and hyaloid ocular artery. Arrested maturation might be considered another aspect of vestigial structure. An example is the persistent microcolumnar cortical architecture in focal cortical dysplasia type Ia, in cortical zones of chronic fetal ischemia, and in some metabolic/genetic congenital encephalopathies. Some transitory structures in human brain are normal adult structures in lower vertebrates. Recognition of transitory and vestigial structures by fetal or postnatal neuroimaging and neuropathologically enables better understanding of cerebral ontogenesis and avoids misinterpretations. |
2,331,125 | Defining the reference range for right ventricular systolic strain by echocardiography in healthy subjects: A meta-analysis. | Right ventricular (RV) systolic strain has recently demonstrated prognostic value in various cardiovascular diseases. Despite this, the reference range including the lower limit of normal (LLN) and factors associated with RV strain measurements are not well-established. This meta-analysis aimed to determine the mean and LLN of two- (2D) and three-dimensional (3D) right ventricular global (RVGLS), free wall (RVFWLS) and interventricular septal wall (IVSLS) longitudinal strains in healthy individuals and factors that affect strain measurements.</AbstractText>In this meta-analysis, Pubmed, Embase and Cochrane databases were searched until 31 July 2020 for eligible studies reporting RVGLS, RVFWLS and/or IVSLS in at least 30 healthy subjects. We pooled the means and LLNs of RV strains by two- (2D) and three- (3D) dimensional echocardiography, and performed meta-regression analyses.</AbstractText>From 788 articles screened, 45 eligible studies totaling 4439 healthy subjects were eligible for analysis. Pooled means and LLNs with 95% confidence intervals for 2D- RV strains were RVGLS -23.4% (-24.2%, -22.6%) and -16.4% (-17.3%, -15.5%) in 27 studies; RVFWLS -26.9% (-28.0%, -25.9%) and -18.0% (-19.2%, -16.9%) in 32 studies; and IVSLS -20.4% (-22.0%, -18.9%) and -11.5% (-13.6%, -9.6%) in 10 studies, and similar results for 3D- RV strains. Right ventricular fractional area change and vendor software were associated with 2D-RVGLS and RVFWLS means and LLNs.</AbstractText>We reported the pooled means and LLNs of RV systolic strains in healthy subjects, to define thresholds for abnormal, borderline and normal strains. Important factors associated with RV systolic strains include right ventricular fractional area change and vendor software.</AbstractText> |
2,331,126 | Small Endogeneous Peptide Mitigates Myocardial Remodeling in a Mouse Model of Cardioselective Galectin-3 Overexpression. | Myocardial Gal3 (galectin-3) expression is associated with cardiac inflammation and fibrosis. Increased Gal3 portends susceptibility to heart failure and death. There are no data reporting the causative role of Gal3 to mediate cardiac fibro-inflammatory response and heart failure.</AbstractText>We developed a cardioselective Gal3 gain-of-function mouse (Gal3+/+</i>) using α-myosin heavy chain promotor. We confirmed Gal3-transgene expression with real-time polymerase chain reaction and quantified cardiac/circulating Gal3 with Western blot and immunoassays. We used echocardiogram and cardiac magnetic resonance imaging to measure cardiac volumes, function, and myocardial velocities. Ex vivo, we studied myocardial inflammation/fibrosis and downstream TGF (transforming growth factor) β1-mRNA expression. We examined the effects of acute myocardial ischemia in presence of excess Gal3 by inducing acute myocardial infarction in mice. Two subsets of mice including mice treated with N-acetyl-seryl-aspartyl-lysyl-proline (a Gal3-inhibitor) and mice with genetic Gal3 loss-of-function (Gal3</i>-/-) were studied for comparative analysis of Gal3 function.</AbstractText>Gal3+/+</i> mice had increased cardiac/circulating Gal3. Gal3+/+</i> mice showed excess pericardial fat pad, dilated ventricles and cardiac dysfunction, which was partly normalized by N-acetyl-seryl-aspartyl-lysyl-proline. Cardiac magnetic resonance imaging showed reduced myocardial contractile velocities in Gal3+/+</i>. The majority of Gal3+/+</i> mice did not survive acute myocardial infarction, and the survivors had profound cardiac dysfunction. Myocardial histology of Gal3+/+</i> mice showed macrophage/mast-cell infiltration, fibrosis and higher TGFβ1-mRNA expression, which were mitigated by both Gal3 gene deletion and N-acetyl-seryl-aspartyl-lysyl-proline administration.</AbstractText>Our study shows that cardioselective Gal3 overexpression leads to multiple cardiac phenotypic defects including ventricular dilation and cardiac dysfunction. Pharmacological Gal3 inhibition conferred protective effects with reduction of inflammation and fibrosis. Our study highlights the importance of translational studies to counteract Gal3 function and prevent cardiac dysfunction.</AbstractText> |
2,331,127 | Electroacupuncture Pretreatment Prevents Cognitive Impairment Induced by Cerebral Ischemia-Reperfusion via Adenosine A1 Receptors in Rats. | A previous study has demonstrated that pretreatment with electroacupuncture (EA) induces rapid tolerance to focal cerebral ischemia. In the present study, we investigated whether adenosine receptor 1 (A1 R) is involved in EA pretreatment-induced cognitive impairment after focal cerebral ischemia in rats. Two hours after EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120 min in male Sprague-Dawley rats. The neurobehavioral score, cognitive function [as determined by the Morris water maze (MWM) test], neuronal number, and the Bax/Bcl-2 ratio was evaluated at 24 h after reperfusion in the presence or absence of CCPA (a selective A1 receptor agonist), DPCPX (a selective A1 receptor antagonist) into left lateral ventricle, or A1 short interfering RNA into the hippocampus area. The expression of the A1 receptor in the hippocampus was also investigated. The result showed that EA pretreatment upregulated the neuronal expression of the A1 receptor in the rat hippocampus at 90 min. And EA pretreatment reversed cognitive impairment, improved neurological outcome, and inhibited apoptosis at 24 h after reperfusion. Pretreatment with CCPA could imitate the beneficial effects of EA pretreatment. But the EA pretreatment effects were abolished by DPCPX. Furthermore, A1 receptor protein was reduced by A1 short interfering RNA which attenuated EA pretreatment-induced cognitive impairment. |
2,331,128 | Multi-Racial Normative Data for Lobar and Subcortical Brain Volumes in Old Age: Korean and Caucasian Norms May Be Incompatible With Each Other<sup>†</sup>. | Brain aging is becoming an increasingly important topic, and the norms of brain structures are essential for diagnosing neurodegenerative diseases. However, previous studies of the aging brain have mostly focused on Caucasians, not East Asians. The aim of this paper was to examine ethnic differences in the aging process of brain structures or to determine to what extent ethnicity affects the normative values of lobar and subcortical volumes in clinically normal elderly and the diagnosis in multi-racial patients with Alzheimer's disease (AD). Lobar and subcortical volumes were measured using FreeSurfer from MRI data of 1,686 normal Koreans (age range 59-89) and 851 Caucasian, non-Hispanic subjects in the ADNI and OASIS datasets. The regression models were designed to predict brain volumes, including ethnicity, age, sex, intracranial volume (ICV), magnetic field strength (MFS), and MRI scanner manufacturers as independent variables. Ethnicity had a significant effect for all lobar (|β| > 0.20, <i>p</i> < 0.001) and subcortical regions (|β| > 0.08, <i>p</i> < 0.001) except left pallidus and bilateral ventricles. To demonstrate the validity of the z-score for AD diagnosis, 420 patients and 420 normal controls were selected evenly from the Korean and Caucasian datasets. The four validation groups divided by race and diagnosis were matched on age and sex using a propensity score matching. We analyzed whether and to what extent the ethnicity adjustment improved the diagnostic power of the logistic regression model that was built using the only z-scores of six regions: bilateral temporal cortices, hippocampi, and amygdalae. The performance of the classifier after ethnicity adjustment was significantly improved compared with the classifier before ethnicity adjustment (ΔAUC = 0.10, <i>D</i> = 7.80, <i>p</i> < 0.001; AUC comparison test using bootstrap). Korean AD dementia patients may not be classified by Caucasian norms of brain volumes because the brain regions vulnerable to AD dementia are bigger in normal Korean elderly peoples. Therefore, ethnicity is an essential factor in establishing normative data for regional volumes in brain aging and applying it to the diagnosis of neurodegenerative diseases. |
2,331,129 | Cardiac MR images of thalassemia major patients with myocardial iron overload: a data note. | Patients with thalassemia major (TM) have the highest mortality rate due to heart failure induced by myocardial iron overload. However, T2* weighted MR imaging is currently a gold standard approach for measuring iron overload. Examining ventricular volumes with magnetic resonance imaging (MR imaging) and measuring myocardial iron overload in TM patients allows for an early prediction of heart failure. This dataset includes cardiac MR images of TM patients and the control group with clinical and echocardiographic data. This dataset may be useful to researchers investigating myocardial iron overload. This dataset can also be used for medical image processing applications, such as ventricle segmentation.</AbstractText>This study provides open-source cardiac MR images of 50 subjects and clinical and echocardiographic data. From February 2016 to January 2019, all images and clinical data were obtained from the MRI department of a general hospital in Mashhad, Iran. All the images are 16-bit gray-scale and stored in DICOM format. All patient-specific information is removed from image headers to preserve patient privacy. In addition, all images associated with each subject are compressed and saved in the RAR format.</AbstractText>© 2021. The Author(s).</CopyrightInformation> |
2,331,130 | Orientational changes of white matter fibers in Alzheimer's disease and amnestic mild cognitive impairment. | White matter abnormalities represent early neuropathological events in neurodegenerative diseases such as Alzheimer's disease (AD), investigating these white matter alterations would likely provide valuable insights into pathological changes over the course of AD. Using a novel mathematical framework called "Director Field Analysis" (DFA), we investigated the geometric microstructural properties (i.e., splay, bend, twist, and total distortion) in the orientation of white matter fibers in AD, amnestic mild cognitive impairment (aMCI), and cognitively normal (CN) individuals from the Alzheimer's Disease Neuroimaging Initiative 2 database. Results revealed that AD patients had extensive orientational changes in the bilateral anterior thalamic radiation, corticospinal tract, inferior and superior longitudinal fasciculus, inferior fronto-occipital fasciculus, and uncinate fasciculus in comparison with CN. We postulate that these orientational changes of white matter fibers may be partially caused by the expansion of lateral ventricle, white matter atrophy, and gray matter atrophy in AD. In contrast, aMCI individuals showed subtle orientational changes in the left inferior longitudinal fasciculus and right uncinate fasciculus, which showed a significant association with the cognitive performance, suggesting that these regions may be preferential vulnerable to breakdown by neurodegenerative brain disorders, thereby resulting in the patients' cognitive impairment. To our knowledge, this article is the first to examine geometric microstructural changes in the orientation of white matter fibers in AD and aMCI. Our findings demonstrate that the orientational information of white matter fibers could provide novel insight into the underlying biological and pathological changes in AD and aMCI. |
2,331,131 | Maternal outcome of selective feticide due to fetal anomaly in late trimester: A retrospective 10 years' experience in Taiwan. | Feticide was suggested to avoid delivering children with abnormalities. Recently, twin pregnancies have increased. Selective feticide was proposed to achieve a good outcome of pregnancy. This study aimed to evaluate the performance of feticide in twin pregnancy with fetal anomaly.</AbstractText>This was a retrospective study enrolled from 2009 to 2018. A total of 68 pregnancies with fetal anomalies received feticide. Potassium chloride was injected into the left ventricle to induce fetal asystole. Maternal and fetal characteristics of 16 dichorionic twins were documented to compare before and after 24th gestational week.</AbstractText>All pregnant women received feticide without any maternal or fetal complication. The reasons for choosing feticide were divided into four groups, including morphologic defect (61.8%), genetic-chromosomal abnormality (30.9%), obstetrical complication (5.9%), and maternal request (1.5%). Mean gestational age at delivery was significantly higher in dichorionic twins who underwent selective feticide before than after 24th gestational week (36.7 vs 33.4, p = 0.04).</AbstractText>Intracardiac injection of potassium chloride was effective for feticide and safe for mothers and fetuses. Selective feticide served as an alternative approach for twin pregnancy with fetal anomaly after sufficient discussion.</AbstractText>Copyright © 2021, the Chinese Medical Association.</CopyrightInformation> |
2,331,132 | N-methyl-D-aspartate receptor antibody and the choroid plexus in schizophrenia patients with tardive dyskinesia. | Immune disturbance has been postulated to be one of the mechanisms underlying the pathogenesis of tardive dyskinesia (TD). Recently, the role of autoimmune abnormality in TD has been increasingly recognized. Autoantibodies against neuronal N-methyl-D-aspartate receptor (NMDAR) may be cross-reactive in the brain in neuropsychiatric disorders, and the choroid plexus (CP) is a crucial immune barrier in the central nervous system (CNS). We supposed that NMDAR antibodies might underlie the pathophysiological process of TD through the mediation of CP.</AbstractText>Serum NMDAR antibody levels were assessed by enzyme-linked immunosorbent assay, CP and ventricle volumes were assessed by magnetic resonance imaging in schizophrenia patients with TD (n = 61), without TD (NTD, n = 61), and in healthy controls (n = 74). Psychopathology and TD severity were assessed by the Positive and Negative Syndrome Scale and Abnormal Involuntary Movement Scale (AIMS).</AbstractText>NMDAR antibody levels were significantly higher, CP volumes were larger in the TD group than in the NTD group (p = 0.022; p = 0.019, respectively). In the TD group, higher NMDAR antibody level was correlated with larger CP volume (β = 0.406, p = 0.002). An elevated NMDAR antibody level and enlarged CP volume were correlated with orofacial AIMS score (β = 0.331, p = 0.011; β = 0.459, p = 3.34 × 10-4</sup>, respectively). In a mediation model, the effect of NMDAR antibody level on the orofacial AIMS score was mediated by the CP volume (indirect effect: β = 0.08, 95% confidence interval = 0.002-0.225; direct effect: β = 0.14, p = 0.154).</AbstractText>Our findings highlight a potential NMDAR antibody-associated mechanism in orofacial TD, which may be mediated by increased CP volume.</AbstractText>Copyright © 2021 Elsevier Ltd. All rights reserved.</CopyrightInformation> |
2,331,133 | Antisiphon device: A review of existing mechanisms and clinical applications to prevent overdrainage in shunted hydrocephalic patients. | Overdrainage of cerebrospinal fluid is one of the most notorious complications after ventriculoperitoneal shunt implantation. Siphon effect plays a major role in the development of overdrainage. Various overdrainage-preventing devices have been invented to counteract the siphon effect. Though some of the devices are designed to reduce the flow instead of providing antisiphoning effect, they are generally called antisiphon devices (ASDs). The basics of siphoning, the mechanisms and physical properties of currently available devices are described in this article. The clinical efficacy, shunt survival, and considerations on patient factors are also discussed. There are three kinds of ASD design, diaphragm, gravitational, and flow reducing devices. Flow reducing ASD is always open and the flow it controls is relatively stable. On the other hand, it may not provide sufficient flow in nocturnal intracranial pressure elevations. Diaphragm and gravitational devices are sensitive to the position of the patients. Diaphragm device is sensitive to the external pressure and the relative position of the device to the mastoid process. The gravitational device is sensitive to the angle between the axis of the device and the head. Many studies showed encouraging results with gravitational devices. Studies regarding diaphragm devices either showed better or similar outcomes comparing to differential pressure valves. Clinical studies regarding flow-reducing devices and head-to-head comparison between different mechanisms are warranted. This review aims to provide a useful reference for clinical practice of hydrocephalus. |
2,331,134 | Cardiac remodeling after anthracycline and radiotherapy exposure in adult survivors of childhood cancer: A report from the St Jude Lifetime Cohort Study. | Limited data exist regarding left ventricular remodeling patterns observed in adult survivors of childhood cancer after therapy.</AbstractText>Among 1190 adult survivors diagnosed with childhood cancer (median age at diagnosis, 9 years [interquartile range (IQR), 3.8-14.4 years]; age at evaluation, 35.6 years [IQR, 29.5-42.8 years]), treatment exposures included anthracyclines (n = 346), chest radiotherapy (n = 174), both (n = 245), or neither (n = 425). Prospective echocardiographic assessment compared survivors with 449 noncancer controls classified according to left ventricle geometric patterns. Associations between left ventricle geometric patterns and decreased exercise tolerance were assessed.</AbstractText>Overall, 28.2% of survivors (95% confidence interval [CI], 25.6%-30.8%) exhibited concentric remodeling, 2.4% (95% CI, 1.6%-3.5%) exhibited eccentric hypertrophy, and 1.1% (95% CI, 0.6%-1.9%) exhibited concentric hypertrophy. A greater proportion of survivors who received only chest radiotherapy (41%) had concentric remodeling compared with those who received only anthracyclines (24%), both (27%), or neither (27%; all P < .001), and all were greater than the proportions in noncancer controls (18%; all P < .05). Concentric remodeling was associated with radiation exposure, but not with anthracycline exposure, in multivariable models. Survivors who had concentric remodeling were more likely to have a maximal oxygen uptake peak <85% compared with those who had normal geometry (81.0% vs 66.3%; odds ratio, 1.75; 95% CI, 1.15-2.68).</AbstractText>Chest radiation therapy, but not anthracycline therapy, increased the risk for concentric remodeling in survivors of childhood cancer. The presence of concentric remodeling was associated with increased exercise intolerance.</AbstractText>© 2021 American Cancer Society.</CopyrightInformation> |
2,331,135 | Small Brain Lesion Enhancement and Gadolinium Deposition in the Rat Brain: Comparison Between Gadopiclenol and Gadobenate Dimeglumine. | The aim of the set of studies was to compare gadopiclenol, a new high relaxivity gadolinium (Gd)-based contrast agent (GBCA) to gadobenate dimeglumine in terms of small brain lesion enhancement and Gd retention, including T1 enhancement in the cerebellum.</AbstractText>In a first study, T1 enhancement at 0.1 mmol/kg body weight (bw) of gadopiclenol or gadobenate dimeglumine was evaluated in a small brain lesions rat model at 2.35 T. The 2 GBCAs were injected in an alternated and cross-over manner separated by an interval of 4.4 ± 1.0 hours (minimum, 3.5 hours; maximum, 6.1 hours; n = 6). In a second study, the passage of the GBCAs into cerebrospinal fluid (CSF) was evaluated by measuring the fourth ventricle T1 enhancement in healthy rats at 4.7 T over 23 minutes after a single intravenous (IV) injection of 1.2 mmol/kg bw of gadopiclenol or gadobenate dimeglumine (n = 6/group). In a third study, Gd retention at 1 month was evaluated in healthy rats who had received 20 IV injections of 1 of the 2 GBCAs (0.6 mmol/kg bw) or a similar volume of saline (n = 10/group) over 5 weeks. T1 enhancement of the deep cerebellar nuclei (DCN) was assessed by T1-weighted magnetic resonance imaging at 2.35 T, performed before the injection and thereafter once a week up to 1 month after the last injection. Elemental Gd levels in central nervous system structures, in muscle and in plasma were determined by inductively coupled plasma mass spectrometry (ICP-MS) 1 month after the last injection.</AbstractText>The first study in a small brain lesion rat model showed a ≈2-fold higher number of enhanced voxels in lesions with gadopiclenol compared with gadobenate dimeglumine. T1 enhancement of the fourth ventricle was observed in the first minutes after a single IV injection of gadopiclenol or gadobenate dimeglumine (study 2), resulting, in the case of gadopiclenol, in transient enhancement during the injection period of the repeated administrations study (study 3). In terms of Gd retention, T1 enhancement of the DCN was noted in the gadobenate dimeglumine group during the month after the injection period. No such enhancement of the DCN was observed in the gadopiclenol group. Gadolinium concentrations 1 month after the injection period in the gadopiclenol group were slightly increased in plasma and lower by a factor of 2 to 3 in the CNS structures and muscles, compared with gadobenate dimeglumine.</AbstractText>In the small brain lesion rat model, gadopiclenol provides significantly higher enhancement of brain lesions compared with gadobentate dimeglumine at the same dose. After repeated IV injections, as expected for a macrocyclic GBCA, Gd retention is minimalized in the case of gadopiclenol compared with gadobenate dimeglumine, resulting in no T1 hypersignal in the DCN.</AbstractText>Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc.</CopyrightInformation> |
2,331,136 | Bilateral hyperplasia of choroid plexus with severe CSF production: a case report and review of the glymphatic system. | An important feature of hydrocephalus is the alteration of the cerebral spinal fluid (CSF) homeostasis. New insights in the understanding of production, secretion, and absorption of CSF, along with the discovery of the glymphatic system (GS), can be useful for a better understanding and treatment of hydrocephalus in disorders with CSF overproduction.</AbstractText>A 1-year-old patient was diagnosed with communicating hydrocephalus; ventricle peritoneal shunt (VPS) is installed and ascites developed. VPS is exposed, yielding volumes of 1000-1200ml/day CSF per day. MRI is performed showing generalized choroidal plexus hyperplasia. Bilateral endoscopic coagulation of thechoroid plexus was performed in 2 stages (CPC) however the high rate of CSF production persisted, needing a bilateral plexectomy through septostomy, which finally decreased the CSF outflow.</AbstractText>New knowledge about the CSF physiology will help to propose better treatment depending on the cause of the hydrocephalus. The GS is becoming an additional reason to better study and develop new therapies focused of the modulation of alternative CSF reabsorption.</AbstractText>Despite the current knowledge about hydrocephalus, we remain without a complete understanding of the pathophysiology of this condition. GS could be more important than conventional concept of reabsorption of CSF in the arachnoid villi, therefore GS could be a new key point, which will guide future investigations.</AbstractText>© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation> |
2,331,137 | Invasion of the choroid plexus epithelium by Neisseria meningitidis is differently mediated by Arp2/3 signaling and possibly by dynamin dependent on the presence of the capsule. | Neisseria meningitis (Nm) is a human-specific bacterial pathogen that can cause sepsis and meningitis. To cause meningitis Nm must enter the central nervous system (CNS) across one of the barriers between the blood and the brain. We have previously shown that a capsule-depleted Serogroup B strain of Nm displays enhanced invasion into human choroid plexus (CP) epithelial papilloma (HIBCPP) cells, which represent an in vitro model of the blood-cerebrospinal fluid barrier (BCSFB). Still, the processes involved during CNS invasion by Nm, especially the role of host cell actin cytoskeleton remodeling, are not investigated in detail. Here, we demonstrate that invasion into CP epithelial cells by encapsulated and capsule-depleted Nm is mediated by distinct host cell pathways. Whereas a Serogroup B wild-type strain enters HIBCPP cells by a possibly dynamin-independent, but actin related protein 2/3 (Arp2/3)-dependent mechanism, invasion by a capsule-depleted mutant is reduced by the dynamin inhibitor dynasore and Arp2/3-independent. Both wild-type and mutant bacteria require Src kinase activity for entry into HIBCPP cells. Our data show that Nm can employ different mechanisms for invasion into the CP epithelium dependent on the presence of a capsule. |
2,331,138 | A Rare, yet Classic Case of Colloid Cyst of Third Ventricle. | Colloid cyst of third ventricle is a rare, benign, congenital lesion that usually presents with headache, and associated with altered cognition, nausea, vomiting, gait ataxia, and blurred vision. A large cyst/growing cyst can cause obstructive hydrocephalus leading to acute rapid neurological deterioration and sudden death. Here we report a classic clinical presentation and histopathological features of colloid cyst of third ventricle with specific emphasis on the importance of rapid diagnosis and management to avoid potentially fatal complications of this otherwise benign lesion. Newer modalities like neuroendoscopy or stereotactic aspiration of cyst are now the preferred choices of management. Awareness of this entity for early diagnosis and management with minimally invasive procedures such as neuroendoscopy or stereotactic aspiration of cyst is crucial for better prognosis and patient care. |
2,331,139 | Evaluation of CSF flow dynamics in patients with schizophrenia using phase-contrast cine MRI. | Patients with schizophrenia show progressive clinical deterioration. Brain abnormalities have been suggested in these patients, including enlargement of the lateral ventricles, increased cerebrospinal fluid (CSF) volume and reductions in the frontal and temporal lobes. CSF flow pathology is a central factor in the development of many neurological disorders, but much less is known about the role of CSF flow dynamics in schizophrenia. In this study, parameters of CSF flow dynamics at the aqueduct level of 50 schizophrenic patients were compared to those of 50 controls using phase-contrast cine magnetic resonance imaging. Patients had lower peak velocity, lower net forward volume, and lower average flow over the range studied than controls. The average velocity was significantly lower in patients exhibiting violent behavior compared to non-violent patients. The aqueduct tendedto be larger in schizophrenic patients with earlier age of onset of the disorder. Furthermore, as the number of hospitalizations increased, the average velocity and flow over the range studied decreased commensurately. This study demonstrated that CSF flow dynamics are altered in patients with schizophrenia. The results indicated that additional studies of CSF flow dynamics in schizophrenia are needed, along with volumetric examinations of the brain, to elucidate the pathophysiology of the disease. |
2,331,140 | Dynamic Contrast Magnetic Resonance Lymphangiography Localizes Lymphatic Leak to the Duodenum in Protein-Losing Enteropathy. | Protein-losing enteropathy (PLE) is a disorder of intestinal lymphatic flow resulting in leakage of protein-rich lymph into the gut lumen. Our primary aim was to report the imaging findings of dynamic contrast magnetic resonance lymphangiography (DCMRL) in patients with PLE. Our secondary objective was to use these imaging findings to characterize lymphatic phenotypes.</AbstractText>Single-center retrospective cohort study of patients with PLE unrelated to single-ventricle circulation who underwent DCMRL. We report imaging findings of intranodal (IN), intrahepatic (IH), and intramesenteric (IM) access points for DCMRL.</AbstractText>Nineteen patients 0.3-58 years of age (median 1.2 years) underwent 29 DCMRL studies. Primary intestinal lymphangiectasia (PIL) was the most common referring diagnosis (42%). Other etiologies included constrictive pericarditis, thoracic insufficiency syndrome, and genetic disorders. IN-DCMRL demonstrated a normal central lymphatic system in all patients with an intact thoracic duct and localized duodenal leak in one patient (1/19, 5%). IH-DCMRL detected a duodenal leak in 12 of 17 (71%), and IM-DCMRL detected duodenal leak in 5 of 6 (83%). Independent of etiology, lymphatic leak was only visualized in the duodenum.</AbstractText>In patients with PLE, imaging via DCMRL reveals that leak is localized to the duodenum regardless of etiology. Comprehensive imaging evaluation with three access points can provide detailed information about the site of duodenal leak.</AbstractText>Copyright © 2021 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition.</CopyrightInformation> |
2,331,141 | Quantitative evaluation of computed tomography findings in patients with pulmonary embolism: the link between D-Dimer level and thrombus volume.<Pagination><StartPage>218</StartPage><EndPage>223</EndPage><MedlinePgn>218-223</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1590/1806-9282.67.02.20200539</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0104-42302021000300218</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To investigate the correlation of D-dimer levels and computed tomography properties of pulmonary embolism.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A total of 58 treated patients with diagnosis of properties of pulmonary embolism were retrospectively studied. All patients underwent a D-dimer blood test. In computed tomography images, septal angle, interventricular septal thickness, and the diameters of all cardiac chambers and pulmonary arteries were measured. The thrombus volume (load) and density at all pulmonary arteries (main, right, left pulmonary arteries, and segmental arteries) were calculated.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">A significant correlation was found between D-dimer and total thrombus volume (p=0.009, r=0.342). Total thrombus volume and total thrombus density were calculated with mean value of 23.40±60.63 ml and 66.16±38.48 hounsfield unit (HU), respectively. Right ventricle/left ventricle ratio showed positive correlation with the D-dimer level (p=0.02).</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Increased D-dimer levels with RV/LV ratio and their correlation with total thrombus volume suggest that it may be a prognostic factor.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sasani</LastName><ForeName>Hadi</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0001-6236-4123</Identifier><AffiliationInfo><Affiliation>Tekirdag Namik Kemal University, Faculty of Medicine, Department of Radiology - Tekirdag, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mutlu</LastName><ForeName>Levent Cem</ForeName><Initials>LC</Initials><Identifier Source="ORCID">0000-0002-3535-5704</Identifier><AffiliationInfo><Affiliation>Tekirdag Namik Kemal University, Faculty of Medicine, Department of Chest Diseases - Tekirdag, Turkey.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Brazil</Country><MedlineTA>Rev Assoc Med Bras (1992)</MedlineTA><NlmUniqueID>9308586</NlmUniqueID><ISSNLinking>0104-4230</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005338">Fibrin Fibrinogen Degradation Products</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C036309">fibrin fragment D</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005338" MajorTopicYN="N">Fibrin Fibrinogen Degradation Products</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011655" MajorTopicYN="Y">Pulmonary Embolism</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013927" MajorTopicYN="Y">Thrombosis</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014057" MajorTopicYN="N">Tomography, X-Ray Computed</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>8</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>11</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2021</Year><Month>8</Month><Day>18</Day><Hour>12</Hour><Minute>24</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2021</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2021</Year><Month>8</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">34406245</ArticleId><ArticleId IdType="doi">10.1590/1806-9282.67.02.20200539</ArticleId><ArticleId IdType="pii">S0104-42302021000300218</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">34406144</PMID><DateRevised><Year>2023</Year><Month>05</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1473-5628</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2021</Year><Month>Aug</Month><Day>17</Day></PubDate></JournalIssue><Title>Nuclear medicine communications</Title><ISOAbbreviation>Nucl Med Commun</ISOAbbreviation></Journal>Parametric mapping for 11C-metomidate PET-computed tomography imaging in the study of primary aldosteronism. | To investigate the correlation of D-dimer levels and computed tomography properties of pulmonary embolism.</AbstractText>A total of 58 treated patients with diagnosis of properties of pulmonary embolism were retrospectively studied. All patients underwent a D-dimer blood test. In computed tomography images, septal angle, interventricular septal thickness, and the diameters of all cardiac chambers and pulmonary arteries were measured. The thrombus volume (load) and density at all pulmonary arteries (main, right, left pulmonary arteries, and segmental arteries) were calculated.</AbstractText>A significant correlation was found between D-dimer and total thrombus volume (p=0.009, r=0.342). Total thrombus volume and total thrombus density were calculated with mean value of 23.40±60.63 ml and 66.16±38.48 hounsfield unit (HU), respectively. Right ventricle/left ventricle ratio showed positive correlation with the D-dimer level (p=0.02).</AbstractText>Increased D-dimer levels with RV/LV ratio and their correlation with total thrombus volume suggest that it may be a prognostic factor.</AbstractText> |
2,331,142 | Transmitral resection of left ventricular lipoma by right mini-thoracotomy using a rolled up flexible ruler. | Left ventricular lipoma is a rare intracardiac tumour that is usually resected through sternotomy to effectively explore the left ventricular cavity. We introduce a simple technique to expose the left ventricular cavity and resect the intraventricular lipoma using a rolled up flexible ruler through right mini-thoracotomy. Imaging studies and gross and microscopic photography of intraventricular lipoma are presented in this report. |
2,331,143 | MultiPole pacing in non-responders to cardiac resynchronization therapy: Results from the QP ExCELs/MPP sub-study. | Multisite LV stimulation therapy allows for stimulation of two different left ventricular pacing vectors within a single LV lead and may improve responsiveness to cardiac resynchronization therapy (CRT). This study prospectively evaluated the safety and efficacy of the MultiPole Pacing (MPP) feature in CRT non-responder patients.</AbstractText>CRT non-responders with a standard CRT-D indication were eligible for enrollment into the MPP Sub-Study. Patient status, NYHA classification, Patient Global Assessment (PGA), and adverse events were collected at follow-up. A clinical composite score (CCS) was determined at the 6 month follow-up visit. The primary objective was defined as the proportion of patients with an improved CCS. Safety was evaluated as freedom from MPP system related adverse events requiring additional invasive intervention to resolve. A total of 53 patients were enrolled across 26 U.S. centers. The cumulative follow-up duration was 24.1 years. CCS was improved in 35.6% of patients (p < .0001 when compared to a performance goal of 3%) after 6 months of MPP therapy. When incorporating patient feedback into a modified CCS, 60.0% of patients showed an improvement. Three patients (5.7%) experienced hospitalization for heart failure, and three patient deaths occurred over the follow-up period. No MPP system-related events were reported for an AE-free rate of 100% (95% CI 93.28% to 100.0%).</AbstractText>The results of this small, non-randomized study suggest that the MPP feature is safe, and may be effective at converting a percentage of CRT non-responders to responders. Larger, randomized studies are needed to confirm this result.</AbstractText>© 2021 Wiley Periodicals LLC.</CopyrightInformation> |
2,331,144 | School-Age Outcome of Fetuses with Isolated Complete Septum Pellucidum Agenesis at Prenatal Magnetic Resonance Imaging. | To the best of our knowledge, there have not been studies to address the issue of long-term follow-up of patients with prenatal diagnosis of isolated complete septum pellucidum agenesis (SPA). The aim of this study was to acquire information about the school-age outcome of such patients as a resource for counseling parents receiving this prenatal finding.</AbstractText>From a large fetal magnetic resonance (MR) database, we selected only those cases with isolated complete SPA as confirmed by two senior pediatric neuroradiologists in consensus; we then gathered information from the parents of those children who had reached the school age.</AbstractText>None among the 12 cases (mean age at follow-up: 8.7 years, range: 6-13 year) of the resulting final cohort presented visual or stature deficits; only one required special teaching assistance in school. All other 11 children resulted without any notable academic issue.</AbstractText>Our report may provide information of practical value about the school-age outcome of fetuses detected by prenatal MR imaging to carry isolated complete SPA.</AbstractText>Thieme. All rights reserved.</CopyrightInformation> |
2,331,145 | Transplantation of 3D bio-printed cardiac mesh improves cardiac function and vessel formation via ANGPT1/Tie2 pathway in rats with acute myocardial infarction. | A novel tissue engineering strategy using 3D bio-print technology has become a promising therapeutic method for acute myocardial infarction (AMI) in an animal model. However, the application of 3D bio-printed tissue remains limited due to poor graft survival. Therefore, it is a scientific priority to enhance graft survival by precisely adjusting the 3D environment of encapsulated cells. In this study, novel transplantable 3D cardiac mesh (cMesh) tissue with a porous mesh structure was presented using human cardiomyocytes, human cardiac fibroblasts, and gelatin-methacryloyl-collagen hydrogel. Cardiomyocytes and cardiac fibroblasts were well spreaded. The cardiomyocytes were connected with a gap junction channel in bio-printed cMesh and a 3D cardiac patch with an aggregated structure. Porous cMesh demonstrated structural advantages by increased phosphorylation of mTOR, AKT, and ERK signals associated with cell survival. Transplanted cMesh in rats with AMI improved long-term graft survival, vessel formation, and stabilization, reduced fibrosis, increased left ventricle thickness, and enhanced cardiac function. Our results suggest that porous cMesh provides structural advantages and a positive therapeutic effect in an AMI animal model. |
2,331,146 | miR-141-3p inhibits the activation of astrocytes and the release of inflammatory cytokines in bacterial meningitis through down-regulating HMGB1. | Bacterial meningitis (BM) is a serious infectious disease of the central nervous system that often occurs in children and adolescents. Many studies have suggested that microRNAs (miRNAs) are involved in BM. This study aimed to address the effects of miR-141-3p on astrocyte activation and inflammatory response in BM through HMGB1.</AbstractText>The 3-week-old rats were injected with Streptococcus pneumoniae (SP) into the lateral ventricle to establish a BM model. Loeffler scoring method was used to evaluate the recovery of neurological function. Brain pathological damage was observed by hematoxylin and eosin (H&E) staining. Primary astrocytes were isolated from brain tissues of BM or non-infected SD rats. The levels of TNF-α, IL-1β, and IL-6 in brain tissues and astrocyte culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The targeting relationship between miR-141-3p and HMGB1 was tested using dual-luciferase reporter assay. The expression of miR-141-3p, HMGB1, and the astrocytic marker glial fibrillary acidic protein (GFAP) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blotting. Methylation-specific PCR (MSP) analysis was performed to measure the methylation status of miR-141 promoter.</AbstractText>The results showed that lower Loeffler scores were exhibited in rats with BM. The subarachnoid space of brain tissues of BM rats was widened, and obvious inflammatory cells were observed. miR-141-3p expression was reduced in BM rats and SP-treated astrocytes. Additionally, we found that overexpression of miR-141-3p led to the downregulation of HMGB1, GFAP, and inflammatory cytokines (TNF-α, IL-1β, and IL-6) in astrocytes. Furthermore, the results of dual-luciferase reporter assay confirmed that miR-141-3p directly targeted HMGB1. Overexpression of miR-141-3p inhibited the levels of GFAP, TNF-α, IL-1β, and IL-6 in astrocytes, which was eliminated by the up-regulation of HMGB1. The results of MSP analysis indicated that miR-141 promoter was highly methylated in brain tissues and astrocytes. DNMT1 was involved in the methylation of miR-141 promoter in BM.</AbstractText>The present study verified that miR-141-3p affected inflammatory response by suppressing HMGB1 in SP-induced astrocytes and BM rat model.</AbstractText>Copyright © 2021 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,331,147 | The importance of first trimester screening of cranial posterior fossa in predicting posterior fossa malformations which may be identified in the following weeks of gestation. | We aimed to investigate the value of posterior fossa ultrasonography measurements in predicting fetal posterior fossa anomaly at 11-14 weeks of gestation.</AbstractText>The study was performed at Zeynep Kamil Women and Children's Diseases Training and Research Hospital. Measurements were made in two groups: the control group consisted of 328 fetuses with normal postnatal outcome and the study group consisted of 22 fetuses with enlarged 4th</sup> ventricle. In the study group, we questioned the value of intracranial translucency (IT) and brainstem (BS) measurements and the BS/brainstem-to-occipital bone (BSOB) ratio in order to predict possible posterior fossa anomalies that may be identified in advanced gestational weeks. The differences of ultrasonographic measurements between groups with p < 0.05 were considered statistically significant.</AbstractText>IT value, BSOB value, and BS/BSOB ratio were determined as ultrasonographic variables in predicting normal development of the fetal posterior fossa, with cutoff values of 2.7, 5.1, and 0.3. Negative predictive values of these three measurements for posterior fossa abnormalities were 100%. There was no statistically significant difference between the three variables for other diagnostic accuracy values (specifities and positive predictive values) (p > 0.05).</AbstractText>IT, BSOB, and BS/BSOB ratio can be used as ultrasonographic markers to predict the normal development of the fetal posterior fossa.</AbstractText>© 2021 Wiley Periodicals LLC.</CopyrightInformation> |
2,331,148 | Upregulation of FoxM1 protects against ischemia/reperfusion-induced myocardial injury. | Ischemia/reperfusion (I/R) induced lethal tissue injury in myocardium. FoxM1 (Forkhead Box M1), expressed in proliferating cardiac progenitor cells, could regulate myocardial development. However, the role of FoxM1 in I/R-induced myocardial injury has not been reported yet.</AbstractText>Rats were conducted with regional ischemia followed by reperfusion in myocardium through ligation of the left anterior descending coronary artery. Triphenyl-tetrazolium chloride staining was utilized to assess the infarct size. ELISA was performed to detect activities of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH). Protein expression of FoxM1 in heart tissues and H9c2 were determined by western blot. H9c2 cells were used to establish a hypoxia/reoxygenation cell model, and the cell viability, proliferation and apoptosis were evaluated by MTT, EdU (5-ethynyl-2'-deoxyuridine) staining and TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) staining, respectively. Adenovirus (Ad)-mediated over-expression of FoxM1 was injected into the anterior wall of the left ventricle of rats to evaluate the role of FoxM1 on in vivo I/R-induced myocardial injury.</AbstractText>FoxM1 was reduced in heart tissues isolated from rats post myocardial I/R injury. Forced FoxM1 expression increased cell viability and proliferation of hypoxia/reoxygenation-induced H9c2, while repressed the cell apoptosis with increased Bcl-2 and decreased Bax and cleaved caspase-3. Injection of Ad-FoxM1 suppressed infarct size of the heart and decreased activities of CK-MB and LDH.</AbstractText>FoxM1 attenuated I/R-induced myocardial injury, providing potential therapeutic target for the disease.</AbstractText> |
2,331,149 | Right ventricular longitudinal fractional shortening: a substitute to right ventricular free wall longitudinal strain? | Because of its diagnostic and prognostic value, right ventricular strain assessed by speckle-tracking imaging (RVS) has been incorporated into echocardiographic guidelines. However, it suffers from limitations including the need of good image quality and of dedicated software with inter-vendor variability. We hypothesized that RV free wall longitudinal fractional shortening (LFS) could be used as a substitute to RVS, without suffering from the aforementioned limitations.</AbstractText>We aimed to establish in a series of non-selected consecutive patients in sinus rhythm the value of LFS, calculated as [-(TAPSE/RVdiastolic length)] and of several common echocardiographic and Doppler parameters to predict an abnormal RV function, defined as RVS > - 20.2%.</AbstractText>Among 144 consecutive patients, poor image quality precluded the assessment of RVS and of LFS in 31 and 4 patients, respectively (P = 0.0018), resulting in a final study group of 113 patients. The intraclass correlation coefficients for inter- and intra-observer variability were 0.97 (95% CI 0.92; 0.98) and 0.93 (CI 0.92; 0.98) for LFS and RVS, respectively. Among all tested RV function indices, LFS best correlated with RVS (R 0.97, 95% CI 0.81; 0.91). Bland-Altman analysis for the comparison between LFS and RVS showed no systematic bias. The area under the ROC-curve of the various RV function indices to detect abnormal RVS was best for LFS (0.97, 95% CI 0.94-1), with sensitivity, specificity, negative and positive predictive value of 83%, 96%, 96%, and 83%, respectively.</AbstractText>LFS performs reasonably well to predict abnormal RVS and is more often feasible than RVS.</AbstractText>© 2021. Springer Japan KK, part of Springer Nature.</CopyrightInformation> |
2,331,150 | Salt-inducible kinase 2 regulates energy metabolism in rats with cerebral ischemia-reperfusion. | To investigate the effects of salt-inducible kinase 2 (SIK2) on energy metabolism in rats with cerebral ischemia-reperfusion. Adult SD male rats were divided into 5 groups: sham group, ischemia group, reperfusion group, adenovirus no-load group, and SIK2 overexpression group with 5 animals in each group. The middle cerebral artery occlusion (MCAO) was induced with the modified Zea-Longa line thrombus method to establish the cerebral ischemia reperfusion model. Eight days before the MCAO, SIK2 overexpression was induced by injecting 7 μL adenovirus in the right ventricle, then MCAO was performed for followed by reperfusion HE staining was used to observe the pathological changes of cerebral tissue in rats; TTC staining was used to observe the volume of cerebral infarct. The levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) in rat brain tissue were detected by ELISA; the levels of SIK2 and hypoxia-inducible factor 1α (HIF-1α) in the rat brain tissues were detected by RT-qPCR and Western blotting. Compared with the sham group, SIK2 level was decreased in the ischemia group, and it was further declined in the reperfusion group (<0.05). Compared with the sham group and ischemic group, the pathological injury in reperfusion group were more severe, and the infarct size was larger; compared with the reperfusion group and adenovirus no-load group, the pathological injury of the SIK2 overexpression group was milder, and the infarct size is less. Compared with the sharn group, HIF-1α was increased in both ischemia group and reperfusion group, especially in ischemia group (all <0.05); HIF-1α level in the SIK2 overexpression group was higher than that in the reperfusion group and adenovirus no-load group (all <0.05). ATP level in ischemia group and reperfusion group was lower than that in the sham group, and the reperfusion group decreased more significantly than the ischemia group (<0.05); ADP content was increased in the ischemia and reperfusion group, and the ADP content in reperfusion group was significantly higher than that in the ischemia group (<0.05). ATP level in the SIK2 overexpression group was higher than that in the reperfusion group and adenovirus no-load group (all <0.05), and ADP was decreased in the SIK2 overexpression group (all <0.05). SIK2 can up-regulate the ATP level and down-regulate the ADP level in rat brain tissue and alleviate cerebral ischemia-reperfusion injury by increase the level of HIF-1α.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Ran</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Clinical Colloge of Wannan Medical College.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yun</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Clinical Colloge of Wannan Medical College.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Cui</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Clinical Colloge of Wannan Medical College.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Mengyao</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Clinical Colloge of Wannan Medical College.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Shu</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Clinical Colloge of Wannan Medical College.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>Yun</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Clinical Colloge of Wannan Medical College.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhejiang Da Xue Xue Bao Yi Xue Ban</MedlineTA><NlmUniqueID>100927946</NlmUniqueID><ISSNLinking>1008-9292</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051795">Hypoxia-Inducible Factor 1, alpha Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C583272">SIK2 protein, rat</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002545" MajorTopicYN="Y">Brain Ischemia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004734" MajorTopicYN="N">Energy Metabolism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051795" MajorTopicYN="N">Hypoxia-Inducible Factor 1, alpha Subunit</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020244" MajorTopicYN="N">Infarction, Middle Cerebral Artery</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein Serine-Threonine Kinases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015424" MajorTopicYN="N">Reperfusion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015427" MajorTopicYN="Y">Reperfusion Injury</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="eng"><AbstractText Label="OBJECTIVE:">To investigate the effects of salt-inducible kinase 2 (SIK2) on energy metabolism in rats with cerebral ischemia-reperfusion.<AbstractText Label="METHODS:">Adult SD male rats (240-260 g) were divided into 5 groups: sham group, ischemia group, reperfusion group, adenovirus no-load group, and SIK2 overexpression group with 5 animals in each group. The middle cerebral artery occlusion (MCAO) was induced with the modified Zea-Longa line thrombus method to establish the cerebral ischemia reperfusion model. Eight days before the MCAO, SIK2 overexpression was induced by injecting 7 μL adenovirus in the right ventricle, then MCAO was performed for 2 h, followed by reperfusion 24 h. HE staining was used to observe the pathological changes of cerebral tissue in rats; TTC staining was used to observe the volume of cerebral infarct. The levels of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) in rat brain tissue were detected by ELISA; the levels of SIK2 and hypoxia-inducible factor 1α (HIF-1α) in the rat brain tissues were detected by RT-qPCR and Western blotting.<AbstractText Label="RESULTS:">Compared with the sham group, SIK2 level was decreased in the ischemia group, and it was further declined in the reperfusion group ( <i>P</i><0.05). Compared with the sham group and ischemic group, the pathological injury in reperfusion group were more severe, and the infarct size was larger; compared with the reperfusion group and adenovirus no-load group, the pathological injury of the SIK2 overexpression group was milder, and the infarct size is less. Compared with the sharn group, HIF-1α was increased in both ischemia group and reperfusion group, especially in ischemia group (all <i>P</i><0.05); HIF-1α level in the SIK2 overexpression group was higher than that in the reperfusion group and adenovirus no-load group (all <i>P</i><0.05). ATP level in ischemia group and reperfusion group was lower than that in the sham group, and the reperfusion group decreased more significantly than the ischemia group ( <i>P</i><0.05); ADP content was increased in the ischemia and reperfusion group, and the ADP content in reperfusion group was significantly higher than that in the ischemia group ( <i>P</i><0.05). ATP level in the SIK2 overexpression group was higher than that in the reperfusion group and adenovirus no-load group (all <i>P</i><0.05), and ADP was decreased in the SIK2 overexpression group (all <i>P</i><0.05).<AbstractText Label="CONCLUSION:">SIK2 can up-regulate the ATP level and down-regulate the ADP level in rat brain tissue and alleviate cerebral ischemia-reperfusion injury by increase the level of HIF-1α. |
2,331,151 | Pediatric intracranial neurenteric cyst of the oculomotor nerve: a case-based review. | Neurenteric cysts (NECs) of the central nervous system (CNS) are uncommon congenital entities arising from embryonal elements. Intracranial NECs in the pediatric population are rare.</AbstractText>The authors describe the presentation, radiographic imaging, and pathologic findings of an 11-year-old boy with a right oculomotor nerve NEC. A literature review was performed to identify additional cases of pediatric intracranial NECs published in the English language, over the past 30 years (1990-2020). The authors discuss the presentation, investigations, management, and prognosis of this interesting entity.</AbstractText>We describe an 11-year-old boy who presented to neurosurgical attention with disconjugate gaze, anisocoria, and ptosis. Magnetic resonance imaging (MRI) demonstrated a lobulated, cystic, and peripherally enhancing mass involving the right oculomotor nerve. The patient underwent pterional craniotomy for drainage of the cyst and subtotal resection of the cyst wall. The tan-colored mass was displacing the basilar artery, compressing the cerebral peduncle, and adherent to the inferior surface of the tentorium. The lesion was within the oculomotor nerve and splitting the fibers, and the cystic contents were thick and mucinous. Histopathological examination of the specimen demonstrated a thin fibrous cyst wall with scattered inflammatory cells and lined by simple columnar epithelium containing mucin. The lining cells were immunoreactive with epithelial membrane antigen (EMA) and pan-keratin AE1/AE3. The diagnosis of a NEC was rendered. A comprehensive literature review of pediatric intracranial NECs yielded 46 additional lesions published in the literature, involving the skull base, posterior fossa, cerebral convexity, and cranial nerves. NECs present with local mass effect and less commonly, with aseptic meningitis or intracystic hemorrhage. Maximal safe GTR remains the mainstay management, although cyst drainage and marsupialization, cyst shunting, and fenestration of cystic contents into the ventricle or basal cisterns have been reported with variable success.</AbstractText>CNS NECs are rare congenital entities; although they occur less frequently in the intracranial components compared to the spine, their diagnosis and management should be considered for intracranial cystic lesions. Maximal safe GTR is the mainstay treatment and frequently yields favorable outcomes.</AbstractText>© 2021. This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.</CopyrightInformation> |
2,331,152 | Penetrating cardiac injury repaired under "intentional cardiac arrest" with adenosine triphosphate. | Repairing a cardiac injury with beating heart is sometimes difficult and is associated with increased risks of complications. Here we report a case of cardiac injury repaired with administration of adenosine triphosphate (ATP).</AbstractText>A 46-year-old man was stabbed in his chest with a knife and transferred to our hospital. He was hemodynamically unstable, and echocardiography showed pericardial effusion. Emergency thoracotomy revealed a full-thickness injury in the right ventricle next to the coronary artery. He went into cardiac arrest and was resuscitated with adrenaline administration. We tried to suture immediately, but it was difficult because of tachycardia. After administering 20 mg of ATP (80 mg in total over 15 min), bradycardia was induced that led to "intentional cardiac arrest" after which suturing was performed. He was discharged on the 13th day without complications.</AbstractText>Cases of penetrating cardiac injury repaired using ATP are rare. Administration of ATP may be a useful option while repairing cardiac injuries.</AbstractText>© 2021 The Authors. Acute Medicine & Surgery published by John Wiley & Sons Australia, Ltd on behalf of Japanese Association for Acute Medicine.</CopyrightInformation> |
2,331,153 | Ventricular pacemaker lead in the left hemithorax: Mechanisms and evidence-based management of a late-onset hazardous complication. | Late-onset migration of pacing leads in the left hemithorax is a rare but potentially life-threatening complication. Radiological examinations are required to detect any involvement of either left ventricle or lung parenchyma, prompting immediate surgical extraction in this setting. Identification of high-risk patients is mandatory to prevent this complex iatrogenic complication. |
2,331,154 | Major brain malformations: corpus callosum dysgenesis, agenesis of septum pellucidum and polymicrogyria in patients with BCORL1-related disorders. | BCORL1, a transcriptional co-repressor, has a role in cortical migration, neuronal differentiation, maturation, and cerebellar development. We describe BCORL1 as a new genetic cause for major brain malformations.</AbstractText>We report three patients from two unrelated families with neonatal onset intractable epilepsy and profound global developmental delay. Brain MRI of two siblings from the first family depicted hypoplastic corpus callosum and septal agenesis (ASP) in the older brother and unilateral perisylvian polymicrogyria (PMG) in the younger one. MRI of the patient from the second family demonstrated complete agenesis of corpus callosum (CC). Whole Exome Sequencing revealed a novel hemizygous variant in NM_021946.5 (BCORL1):c.796C>T (p.Pro266Ser) in the two siblings from the first family and the NM_021946.5 (BCORL1): c.3376G>A; p.Asp1126Asn variant in the patient from the second family, both variants inherited from healthy mothers. We reviewed the patients' charts and MRIs and compared the phenotype to the other published BCORL1-related cases. Brain malformations have not been previously described in association with the BCORL1 phenotype. We discuss the potential influence of BCORL1 on brain development.</AbstractText>We suggest that BCORL1 variants present with a spectrum of neurodevelopmental disorders and can lead to major brain malformations originating at different stages of fetal development. We suggest adding BCORL1 to the genetic causes of PMG, ASP, and CC dysgenesis.</AbstractText>© 2021. The Author(s), under exclusive licence to The Japan Society of Human Genetics.</CopyrightInformation> |
2,331,155 | Impact of sex differences on thrombin-induced hydrocephalus and white matter injury: the role of neutrophils. | Thrombin has been implicated in playing a role in hydrocephalus development following intraventricular hemorrhage (IVH). However, the mechanisms underlying the sex differences to the detrimental effects of thrombin post-IVH remain elusive.</AbstractText>Three-month old male and female Sprague-Dawley rats underwent unilateral intracerebroventricular (ICV) injections of 3U or 5U thrombin, or saline, to examine differences in thrombin-induced hydrocephalus and white matter injury. Mortality, and lateral ventricle volume and white matter injury were measured on magnetic resonance imaging evaluation at 24 h post-injection. In addition, male rats were pretreated with 17-β estradiol (E2, 5 mg/kg) or vehicle at 24 and 2 h prior to ICV injection of 3U thrombin. All rats were euthanized at 24 h post-injection for histology and immunohistochemistry.</AbstractText>ICV injection of 5U thrombin caused 100 and 0% mortality in female and male rats, respectively. 3U of thrombin resulted in significant ventricular dilation and white matter damage at 24 h in both male and female rats, but both were worse in females (p < 0.05). Furthermore, neutrophil infiltration into choroid plexus and periventricular white matter was enhanced in female rats and may play a critical role in the sex difference in brain injury. Pre-treating male rats with E2, increased thrombin (3U)-induced hydrocephalus, periventricular white matter injury and neutrophil infiltration into the choroid plexus and white matter.</AbstractText>ICV thrombin injection induced more severe ventricular dilation and white matter damage in female rats compared to males. Estrogen appears to contribute to this difference which may involve greater neutrophil infiltration in females. Understanding sex differences in thrombin-induced brain injury may shed light on future interventions for hemorrhagic stroke.</AbstractText>© 2021. The Author(s).</CopyrightInformation> |
2,331,156 | Impact of Venoarterial Extracorporeal Membrane Oxygenation Flow on Outcomes in Cardiogenic Shock. | Venoarterial extracorporeal membrane oxygenation (VA ECMO) is used to provide cardiopulmonary support in cardiogenic shock; however, high extracorporeal flow may increase left ventricular (LV) afterload leading to LV distention and intracardiac stasis. It is unclear how ECMO flow affects patient outcomes and complications related to ECMO. Retrospective review of patients at a single institution placed on VA ECMO from 2007 to 2018 was performed. Patients were divided into full flow (flow index > 2.2 L/min/m2) and partial flow (flow index < 2.2 L/min/m2) groups. In-hospital mortality and markers of end-organ perfusion were compared between groups balanced for risk factors using propensity score inverse probability of treatment weighting. ECMO-related complications such as LV distention, limb ischemia, and bleeding were recorded. There were 488 patients included, 405 (83%) in the partial flow group, and 83 (17%) in the full flow group. No major differences in age, gender, or comorbidities were found. There was no difference in in-hospital mortality between groups (51% vs. 55%, p = 0.59). At 72 hours post-ECMO initiation, there was no difference in the change in renal, hepatic function, or lactate from baseline nor in the rates of continuous venoveno hemofiltration initiation (p = 0.41). There was a trend towards the decreased incidence of LV distention requiring LV vent placement in the partial flow group (12% vs. 7%, p = 0.16). Compared with full flow VA ECMO, partial flow VA ECMO in carefully selected patients results in similar in-hospital mortality and provides similar end-organ perfusion for the treatment of refractory cardiogenic shock. |
2,331,157 | Prevalence of supratentorial anomalies assessed by magnetic resonance imaging in fetuses with open spina bifida. | To determine the prevalence of brain anomalies at the time of preoperative magnetic resonance imaging (MRI) assessment in fetuses eligible for prenatal open spina bifida (OSB) repair, and to explore the relationship between brain abnormalities and features of the spinal defect.</AbstractText>This was a retrospective cross-sectional study, conducted in three fetal medicine centers, of fetuses eligible for OSB fetal surgery repair between January 2009 and December 2019. MRI images obtained as part of the presurgical assessment were re-evaluated by two independent observers, blinded to perinatal results, to assess: (1) the type and area of the defect and its anatomical level; (2) the presence of any structural central nervous system (CNS) anomaly and abnormal ventricular wall; and (3) fetal head and brain biometry. Binary regression analyses were performed and data were adjusted for type of defect, upper level of the lesion (ULL), gestational age (GA) at MRI and fetal medicine center. Multiple logistic regression analysis was performed in order to identify lesion characteristics and brain anomalies associated with a higher risk of presence of abnormal corpus callosum (CC) and/or heterotopia.</AbstractText>Of 115 fetuses included, 91 had myelomeningocele and 24 had myeloschisis. Anatomical level of the lesion was thoracic in seven fetuses, L1-L2 in 13, L3-L5 in 68 and sacral in 27. Median GA at MRI was 24.7 (interquartile range, 23.0-25.7) weeks. Overall, 52.7% of cases had at least one additional brain anomaly. Specifically, abnormal CC was observed in 50.4% of cases and abnormality of the ventricular wall in 19.1%, of which 4.3% had nodular heterotopia. Factors associated independently with higher risk of abnormal CC and/or heterotopia were non-sacral ULL (odds ratio (OR), 0.51 (95% CI, 0.26-0.97); P = 0.043), larger ventricular width (per mm) (OR, 1.23 (95% CI, 1.07-1.43); P = 0.005) and presence of abnormal cavum septi pellucidi (OR, 3.76 (95% CI, 1.13-12.48); P = 0.031).</AbstractText>Half of the fetuses assessed for OSB repair had an abnormal CC and/or an abnormal ventricular wall prior to prenatal repair. The likelihood of brain abnormalities was increased in cases with a non-sacral lesion and wider lateral ventricles. These findings highlight the importance of a detailed preoperative CNS evaluation of fetuses with OSB. © 2021 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology.</AbstractText>© 2021 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology.</CopyrightInformation> |
2,331,158 | Prenatal diagnosis and outcome of fetuses with isolated agenesis of septum pellucidum: cohort study and meta-analysis. | To evaluate the postnatal outcome of children with a prenatal diagnosis of apparently isolated agenesis of the septum pellucidum (ASP).</AbstractText>A retrospective cohort study of cases of prenatally diagnosed ASP followed in two tertiary centers and a meta-analysis combining data from the cohort study with data from published studies identified in a systematic review were carried out. Only cases with apparently isolated ASP on antenatal ultrasound and/or magnetic resonance imaging and with available postnatal follow-up data were considered eligible for inclusion. The following outcomes were analyzed: incidence of chromosomal anomalies, agreement between antenatal and postnatal findings, overall incidence of septo-optic dysplasia (SOD) and incidence of major neurological disability (motor, language, coordination or behavioral disorder or epilepsy) in non-SOD children. The incidence of SOD in infants with apparently normal optic pathways on antenatal imaging was also evaluated.</AbstractText>Fifteen cases of isolated ASP, with median postnatal follow-up of 36 months (range, 12-60 months), were selected from the two centers. Six previously published studies met the inclusion criteria for the systematic review and a total of 78 cases were eligible for the analysis, including the 15 cases from our series. Genetic tests were carried out antenatally in 30 fetuses, of which two had an abnormal result (pooled proportion, 9.0% (95% CI, 1.8-20.7%); I2</sup>  = 0%). Additional or discordant imaging findings were noted postnatally in 9/70 (pooled proportion, 13.7% (95% CI, 3.5-29.0%); I2</sup>  = 63.9%) cases. Of all 78 neonates with available follow-up, SOD was diagnosed postnatally in 14 (pooled proportion, 19.4% (95% CI, 8.6-33.2%); I2</sup>  = 51.2%). In 60 cases, the optic pathways were considered to be normal on antenatal imaging, and six of these (pooled proportion, 9.1% (95% CI, 1.1-24.0%); I2</sup>  = 62.0%) were diagnosed postnatally with SOD. Of the 46 infants with available neurological follow-up who were not affected by SOD, a major neurological disability was diagnosed in three (pooled proportion, 6.5% (95% CI, 0.5-18.6%); I2</sup>  = 40.1%).</AbstractText>In the vast majority of cases with a prenatal diagnosis of apparently isolated ASP, the prognosis is favorable. However, an additional anomaly is detected after birth in about 14% of cases and has a negative impact on clinical outcome. Detailed antenatal assessment of the brain and optic pathways is strongly recommended in order to identify the presence of associated anomalies. Antenatal visualization of apparently normal optic pathways does not rule out SOD. © 2021 International Society of Ultrasound in Obstetrics and Gynecology.</AbstractText>© 2021 International Society of Ultrasound in Obstetrics and Gynecology.</CopyrightInformation> |
2,331,159 | Lipopolysaccharide Alters the m6A Epitranscriptomic Tagging of RNAs in Cardiac Tissue. | N6-methyladenosine (m<sup>6</sup>A) modification plays important roles in the pathology of a variety of diseases. However, the roles of m<sup>6</sup>A modification in sepsis-induced myocardial dysfunction are not well defined. Rats were divided into control and lipopolysaccharide (LPS)-induced sepsis group. Global m<sup>6</sup>A levels of left ventricle tissue were measured by LC-MS/MS, and transcriptome-wide m<sup>6</sup>A modifications were profiled using epitranscriptomic microarrays (mRNAs and lncRNAs). Bioinformatics analysis was conducted to understand the functional implications of m<sup>6</sup>A modifications during sepsis. Methylated lncRNAs and mRNAs were measured by m<sup>6</sup>A single-base site qPCR. The global m<sup>6</sup>A levels in left ventricle tissue were significantly decreased in the LPS group. While 27 transcripts (23 mRNAs and four lncRNAs) were hypermethylated, 46 transcripts (39 mRNAs and 7 lncRNAs) were hypomethylated in the LPS group. The mRNA expression of writers and readers was significantly decreased in the LPS group. The m<sup>6</sup>A modification of Clec1b, Stk38l and Tnfrsf26 was associated with platelet activation and apoptotic pathways. Moreover, the decrease in m<sup>6</sup>A modification of lncRNA XR_346,771 may be related to cation import in cardiac tissue. Our data provide novel information regarding changes to m<sup>6</sup>A modifications in cardiac tissue during sepsis, and m<sup>6</sup>A modifications might be promising therapeutic targets. |
2,331,160 | Therapeutic Hypothermia Reduces Peritoneal Dialysis Induced Myocardial Blood Flow Heterogeneity and Arrhythmia. | <b>Background:</b> Moderate therapeutic hypothermia (TH) is a well-recognized cardio-protective strategy. The instillation of fluid into the peritoneum provides an opportunity to deliver moderate hypothermia as primary prevention against cardiovascular events. We aimed to to investigate both cardiac perfusion consequences (overall blood flow and detailed assessment of perfusion heterogeneity) and subsequently simulate the associated arrhythmic risk for patients undergoing peritoneal dialysis (PD) induced TH. <b>Methods:</b> Patients underwent high resolution myocardial perfusion scanning using high resolution 256 slice CT scanning, at rest and with adenosine stress. The first visit using the patient's usual PD regimen, on the second visit the same regime was utilized but with cooled peritoneal dialysate at 32°C. Myocardial blood flow (MBF) was quantified from generated perfusion maps, reconstructed in 3D. MBF heterogeneity was assessed by fractal dimension (FD) measurement on the 3D left ventricular reconstruction. Arrhythmogenicity was quantified from a sophisticated computational simulation using a multi-scale human 3D ventricle wedge electrophysiological computational model. <b>Results:</b> We studied 7 PD patients, mean age of 60 ± 7 and mean vintage dialysis of 23.6 ± 17.6 months. There were no significant different in overall segmental MBF between normothermic condition (NT) and TH. MBF heterogeneity was significantly decreased (-14%, <i>p</i> = 0.03) at rest and after stress (-14%, <i>p</i> = 0.03) when cooling was applied. Computational simulation showed that TH allowed a normalization of action potential, QT duration and T wave. <b>Conclusion:</b> TH-PD results in moderate hypothermia leading to a reduction in perfusion heterogeneity and simulated risk of non-terminating malignant ventricular arrhythmias. |
2,331,161 | 3D Reconstruction of the Clarified Rat Hindbrain Choroid Plexus. | The choroid plexus (CP) acts as a regulated gate between blood and cerebrospinal fluid (CSF). Despite its simple histology (a monostratified cuboidal epithelium overlying a vascularized stroma), this organ has remarkably complex functions several of which involve local interaction with cells located around ventricle walls. Our knowledge of CP structural organization is mainly derived from resin casts, which capture the overall features but only allow reconstruction of the vascular pattern surface, unrelated to the overlying epithelium and only loosely related to ventricular location. Recently, CP single cell atlases are starting to emerge, providing insight on local heterogeneities and interactions. So far, however, few studies have described CP spatial organization at the mesoscale level, because of its fragile nature and deep location within the brain. Here, using an iDISCO-based clearing approach and light-sheet microscopy, we have reconstructed the normal rat hindbrain CP (hCP) macro- and microstructure, using markers for epithelium, arteries, microvasculature, and macrophages, and noted its association with 4th ventricle-related neurovascular structures. The hCP is organized in domains associated to a main vessel (fronds) which carry a variable number of villi; the latter are enclosed by epithelium and may be flat (leaf-like) or rolled up to variable extent. Arteries feeding the hCP emerge from the cerebellar surface, and branch into straight arterioles terminating as small capillary anastomotic networks, which run within a single villus and terminate attaching multiple times to a large tortuous capillary (LTC) which ends into a vein. Venous outflow mostly follows arterial pathways, except for the lateral horizontal segment (LHS) and the caudal sagittal segment. The structure of fronds and villi is related to the microvascular pattern at the hCP surface: when LTCs predominate, leaflike villi are more evident and bulge from the surface; different, corkscrew-like villi are observed in association to arterioles reaching close to the CP surface with spiraling capillaries surrounding them. Both leaf-like and corkscrew-like villi may reach the 4th ventricle floor, making contact points at their tip, where no gap is seen between CP epithelium and ependyma. Contacts usually involve several adjacent villi and may harbor epiplexus macrophages. At the junction between medial (MHS) and lateral (LHS) horizontal segment, arterial supply is connected to the temporal bone subarcuate fossa, and venous outflow drains to a ventral vein which exits through the cochlear nuclei at the Luschka foramen. These vascular connections stabilize the hCP overall structure within the 4th ventricle but make MHS-LHS joint particularly fragile and very easily damaged when removing the brain from the skull. Even in damaged samples, however, CP fronds (or isolated villi) often remain strongly attached to the dorsal cochlear nucleus (DCN) surface; in these fronds, contacts are still present and connecting "bridges" may be seen, suggesting the presence of real molecular contacts rather than mere appositions. |
2,331,162 | Sonographic Findings of Left Ventricular Dysfunction to Predict Shock Type in Undifferentiated Hypotensive Patients: An Analysis From the Sonography in Hypotension and Cardiac Arrest in the Emergency Department (SHoC-ED) Study. | Introduction Patients that present to the emergency department (ED) with undifferentiated hypotension have a high mortality rate. Hypotension can be divided into four categories: obstructive, hypovolemic, distributive, and cardiogenic. While it is possible to have overlapping or concomitant shock states, being able to differentiate between cardiogenic shock and the other categories is important as it entails a different treatment regime and extra cautions. In this secondary analysis, we investigate if using focused cardiac ultrasonography (FOCUS) to determine left ventricular dysfunction (LVD) can serve as a reliable test for cardiogenic shock. Methods We prospectively collected FOCUS findings performed in 135 ED patients with undifferentiated hypotension as part of an international study. Patients with clearly identified etiologies for hypotension were excluded, along with other specific presumptive diagnoses. LVD was defined as the identification of a generally hypodynamic left ventricle in the setting of shock. FOCUS findings were collected using a standardized protocol and data collection form. All scans were performed by emergency physicians trained in ultrasound. Final shock type was defined as cardiogenic or noncardiogenic by independent specialist blinded chart review. Results In our findings, 135 patients had complete records for assessment of left ventricular function and additional follow-up data and so were included in this secondary analysis. The median age was 56 years and 53% of patients were male. Disease prevalence for cardiogenic shock was 12% and the mortality rate was 24%. The presence of LVD on FOCUS had a sensitivity of 62.50% (95% confidence interval 35.43% to 84.80%), specificity of 94.12% (88.26% to 97.60%), positive likelihood ratio (LR) 10.62 (4.71 to 23.95), negative LR 0.40 (0.21 to 0.75) and accuracy of 90.37% (84.10% to 94.77%) for detecting cardiogenic shock. Conclusion Detecting left ventricular dysfunction on FOCUS may be useful in the early identification of cardiogenic shock in otherwise undifferentiated hypotensive adult patients in the emergency department. |
2,331,163 | Effects of Multisession Anodal Electrical Stimulation of the Auditory Cortex on Temporary Noise-Induced Hearing Loss in the Rat. | The protective effect of the efferent system against acoustic trauma (AT) has been shown by several experimental approaches, including damage to one ear, sectioning of the olivocochlear bundle (OCB) in the floor of the IV ventricle, and knock-in mice overexpressing outer hair cell (OHC) cholinergic receptors, among others. Such effects have been related to changes in the regulation of the cholinergic efferent system and in cochlear amplification, which ultimately reverse upon protective hearing suppression. In addition to well-known circuits of the brainstem, the descending corticofugal pathway also regulates efferent neurons of the olivary complex. In this study, we applied our recently developed experimental paradigm of multiple sessions of electrical stimulation (ES) to activate the efferent system in combination with noise overstimulation. ABR thresholds increased 1 and 2 days after AT (8-16 kHz bandpass noise at 107 dB for 90 min) recovering at AT + 14 days. However, after multiple sessions of epidural anodal stimulation, no changes in thresholds were observed following AT. Although an inflammatory response was also observed 1 day after AT in both groups, the counts of reactive macrophages in both experimental conditions suggest decreased inflammation in the epidural stimulation group. Quantitative immunocytochemistry for choline acetyltransferase (ChAT) showed a significant decrease in the size and optical density of the efferent terminals 1 day after AT and a rebound at 14 days, suggesting depletion of the terminals followed by a long-term compensatory response. Such a synthesis recovery was significantly higher upon cortical stimulation. No significant correlation was found between ChAT optical density and size of the buttons in sham controls (SC) and ES/AT + 1day animals; however, significant negative correlations were shown in all other experimental conditions. Therefore, our comparative analysis suggests that cochleotopic cholinergic neurotransmission is also better preserved after multisession epidural stimulation. |
2,331,164 | Use of emerging technologies to enhance the treatment paradigm for spontaneous intraventricular hemorrhage. | The presence of intraventricular hemorrhage (IVH) portends a worse prognosis in patients presenting with spontaneous intracerebral hemorrhage (ICH). Intraventricular hemorrhage increases the rates of hydrocephalus, ventriculitis, and long-term shunt dependence. Over the past decade, novel medical devices and protocols have emerged to directly treat IVH. Presently, we review new technological adaptations to treating intraventricular hemorrhage in an effort to focus further innovation in treating this morbid neurosurgical pathology. We summarize current and historical treatments as well as innovations in IVH including novel procedural techniques, use of the Integra Surgiscope, use of the Artemis evacuator, use of BrainPath, novel catheter technology, large bore external ventricular drains, the IRRAflow, the CerebroFlo, and the future directions of the field. Technology and medical devices for both surgical and nonsurgical methods are advancing the treatment of IVH. With many promising new technologies on the horizon, prospects for improved clinical care for IVH and its etiologies remain hopeful. |
2,331,165 | Activation of CD200-CD200R1 Axis Attenuates Perioperative Neurocognitive Disorder Through Inhibition of Neuroinflammation in Mice. | Perioperative neurocognitive disorder (PND) is the mild cognitive impairment associated with surgery and anesthesia. It is a common surgical complication in the elderly. An important mechanism of PND is the surgically induced neuroinflammation. The interaction between the neuronal surface protein CD200 and its receptor in microglia, CD200R1, is an important regulatory pathway to control neuroinflammation. However, the potential role of the CD200-CD200R1 pathway in the acute period of PND has not been fully investigated. In this study, in a PND mouse model, we first measured the protein expression level of CD200, CD200R1, and the related pro- and anti-inflammatory cytokines in the hippocampus. Then, we investigated cognitive function, neuroinflammation and postsynaptic density protein 95 (PSD-95) expression after the injection of CD200-Fc (agonist), CD200R1-Fc (antagonist) or IgG1-Fc (vehicle) into lateral ventricle in PND models. Compared with the control group, the expression of CD200 was up-regulated at day 1 after surgery in PND models. The injection of the CD200-Fc into the lateral ventricle could mitigate primed neuroinflammation and cognitive decline, increase the expression of PSD-95 at day 1 after surgery in PND models. In conclusion, we have demonstrated that CD200-CD200R1 signaling was involved in the acute inflammatory process of PND, and activating CD200R1 can inhibit neuroinflammation and attenuate PND. Thus, the CD200-CD200R1 axis is a potential novel target for PND prevention and treatment. |
2,331,166 | Uncertainty estimation and explainability in deep learning-based age estimation of the human brain: Results from the German National Cohort MRI study. | Brain ageing is a complex neurobiological process associated with morphological changes that can be assessed on MRI scans. Recently, Deep learning (DL)-based approaches have been proposed for the prediction of chronological brain age from MR images yielding high accuracy. These approaches, however, usually do not address quantification of uncertainty and, therefore, intrinsic physiological variability. Considering uncertainty is essential for the interpretation of the difference between predicted and chronological age. In addition, DL-based models lack in explainability compared to classical approaches like voxel-based morphometry. In this study, we aim to address both, modeling uncertainty and providing visual explanations to explore physiological patterns in brain ageing. T1-weighted brain MRI datasets of 10691 participants of the German National Cohort Study, drawn from the general population, were included in this study (chronological age from 20 to 72 years). A regression model based on a 3D Convolutional Neural Network taking into account aleatoric noise was implemented for global as well as regional brain age estimation. We observed high overall accuracy of global brain age estimation with a mean absolute error of 3.2 ± 2.5 years and mean uncertainty of 2.9 ± 0.6 years. Regional brain age estimation revealed higher estimation accuracy and lower uncertainty in central compared to peripheral brain regions. Visual explanations illustrating the importance of brain sub-regions were generated using Grad-CAM: the derived saliency maps showed a high relevance of the lateral and third ventricles, the insular lobe as well as parts of the basal ganglia and the internal capsule. |
2,331,167 | Alterations of brain metrics in fetuses of women with polycystic ovary syndrome : a retrospective study based on fetal magnetic resonance imaging. | Maternal polycystic ovary syndrome (PCOS) has potential detrimental effects on the neurodevelopment of offspring. This study aimed to evaluate the brain metrics in fetuses of women with PCOS based on fetal magnetic resonance imaging (MRI).</AbstractText>This retrospective study included 60 pregnant women with PCOS (PCOS group) and 120 pregnant non-PCOS women (control group). Fetal MRI was performed followed an ultrasound and for numerous clinical indications including known or suspected fetal pathology, history of fetal abnormality in previous pregnancy or in a family member. Fetal brain biometry and apparent diffusion coefficient (ADC) value were analysed.</AbstractText>After adjusting for potential confounders, fetuses in the PCOS group showed the following characteristics compared to fetuses in the control group: (1) smaller cerebral fronto-occipital diameter (FOD), vermian height (VH) and anteroposterior diameter of the pons (APDP) (evident before 32 weeks; P = 0.042, P = 0.002 and P = 0.016, respectively); (2) larger left and right biparietal index (evident before 32 weeks; P = 0.048 and P = 0.025, respectively); (3) smaller left lateral ventricle (LV) (evident after 32 weeks; P = 0.005); (4) larger anteroposterior diameter of the vermis (APDV) and hippocampal infolding angle (HIA) (evident after 32 weeks; P = 0.003 and P < 0.001, respectively); (5) higher ADC value in frontal white matter (FWM) and in basal ganglia (BG) (evident before and after 32 weeks; all P < 0.05).</AbstractText>There exist a different pattern of brain metrics in PCOS offspring in utero.</AbstractText>© 2021. The Author(s).</CopyrightInformation> |
2,331,168 | A practical approach to prenatal diagnosis of malformations of cortical development. | Malformations of cortical development (MCD) can frequently be diagnosed at multi-disciplinary Fetal Neurology clinics with the aid of multiplanar neurosonography and MRI. The patients are usually referred following prenatal sonographic screening that raises the suspicion of a possible underlying MCD. These indirect findings include, but are not limited to, ventriculomegaly (lateral ventricles larger than 10 mm), asymmetric ventricles, commissural anomalies, absent cavum septum pellucidum, cerebellar vermian and/or hemispheric anomalies, abnormal head circumference (microcephaly or macrocephaly), multiple CNS malformations, and associated systemic defects. The aim of this paper is to suggest a practical approach to prenatal diagnosis of malformations of cortical development utilizing dedicated neurosonography and MRI, based on the current literature and our own experience. We suggest that an MCD should be suspected in utero when the following intracranial imaging signs are present: abnormal development of the Sylvian fissure; delayed achievement of cortical milestones, premature appearance of sulcation; irregular ventricular borders, abnormal cortical thickness (thick, thin); abnormal shape and orientation of the sulci and gyri; irregular, abnormal, asymmetric, and enlarged hemisphere; simplified cortex; non continuous cortex or cleft; and intraparenchymal echogenic nodules. Following the putative diagnosis of fetal MCD by neurosonography and MRI, when appropriate and possible (depending on gestational age), the imaging diagnosis is supplemented by genetic studies (CMA and trio whole exome sequencing). In some instances, no further studies are required during pregnancy due to the clear dire prognosis and then the genetic evaluation can be deferred after delivery or termination of pregnancy (in countries where allowed). |
2,331,169 | Transmantle and transvenous pressure gradients in cerebrospinal fluid disorders. | Hydrocephalus is the symptomatic endpoint of a variety of disease processes. Simple hydrodynamic models have failed to explain the entire spectrum of cerebrospinal fluid (CSF) disorders. Physical principles argue that for ventricles to expand, they must be driven by a force, Fishman's transmantle pressure gradient (TMPG). However, the literature to date, reviewed herein, is heterogenous and fails to consistently measure a TMPG. The venous system, like CSF, traverses the cerebral mantle, and thus analogous transparenchymal and transvenous pressure gradients have been described, reliant on the differential haemodynamics of the deep and superficial venous systems. Interpreting CSF disorders through these models provides new insights into the possible pathophysiological mechanisms underlying these diseases. However, until more sophisticated testing is performed, these models should remain heuristics. |
2,331,170 | CSF-space volumetric change following posterior fossa decompression in paediatric Chiari type-I malformation: a correlation with outcome. | We have previously reported inferior post-operative clinical outcomes in younger children with Chiari type-I malformation (CIM). We sought to quantify the CSF volumetric changes pre- and post-decompression, in a paediatric cohort, to determine whether cisternal volume change is associated with clinical outcomes.</AbstractText>In this retrospective clinical study, the CSF spaces of the posterior fossa (supracerebellar/quadrigeminal, prepontine, fourth ventricle, cisterna magna) were measured on magnetic resonance images pre- and post-operatively using a semi-automated method. Additionally, we describe a novel CSF space of the upper cervical canal incorporating the subarachnoid space from the foramen magnum to the inferior cortex of the C2 body, FM-C2 cistern. Morphometric measurements included the pB-C2 distance, clivoaxial angle, clival length, clival angle and Boogard's angle. Volumetric and morphometric data were correlated with clinical outcomes at 4-12 months post-operatively as measured by the Chicago Chiari Outcome Scale (CCOS).</AbstractText>Of 59 adequate clinical cases, 57 and 36 patients had acceptable imaging for morphometric and volumetric analysis respectively. All CSF spaces measured had a significant increase in volume post-operatively (p < 0.05). There was no correlation between the change in volume or post-operative CSF volumes and CCOS. The pre-operative volume of the FM-C2 was positively correlated with total CCOS (Wald [Formula: see text], [Formula: see text]) and was significantly smaller in the 0-6-year age group (2.38 ± 1.27 ml vs. 3.67 ± 1.56 ml, p = 0.014). No morphometric measurement changed significantly after surgery or demonstrated a relationship with CCOS.</AbstractText>Volumetric changes in the CSF cisterns of the posterior cranial fossa and upper cervical canal do not correlate with the age-related differences in clinical outcomes in paediatric CIM. The pre-operative volume of the FM-C2 cistern may have a role in predicting the likelihood of a beneficial post-operative outcome in paediatric CIM.</AbstractText>© 2021. Crown.</CopyrightInformation> |
2,331,171 | Multiple intracranial juvenile xanthogranuloma not a straightforward diagnosis (a case report). | Juvenile xanthogranuloma (JXG) rarely presents as multifocal intracranial disease in the paediatric population. Therefore, this case of extensive tumour burden, primarily within the lateral ventricles, presented a neurosurgical challenge on numerous fronts.</AbstractText>This is the case of a 9-year-old male presenting with a 2-year history of visual disturbances. Radiographic imaging demonstrated extensive intracranial masses involving both lateral ventricles, the straight sinus and right cerebellum. A staged tumour resection was planned, targeting the lesions within the right lateral ventricle initially. Complete resection was achieved during surgery. Post-operative morbidity showed a decline in the patient's functional status with respect to mobility and communication, Glasgow outcome scale 3. Extensive immunohistochemical analysis ultimately revealed a diagnosis of JXG. The patient is undergoing chemotherapy, with subsequent surgical resection being dependent on overall recovery.</AbstractText>JXG is the most common form of non-Langerhans histiocytosis and typically arises as a cutaneous disorder during early childhood. It is a rare cause of extensive intracranial tumour burden, with limited publications of this kind in the literature. This is even more atypical given the absence of any of the classic cutaneous morphology seen in JXG.</AbstractText>JXG involving the central nervous system is a rare encounter. Therefore, a clear algorithm for the management of a case of extensive intracranial tumours resulting from JXG has not been defined. This only amplifies the difficulty in treating these cases.</AbstractText>Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation> |
2,331,172 | Where the central canal begins: endoscopic in vivo description. | Although evidence and descriptions of the central canal (CC) along the medulla oblongata and the spinal cord have been provided by several anatomical and radiological studies, a clear picture and assessment of the opening of the CC, or apertura canalis centralis (ACC), into the fourth ventricle is lacking, due to its submillimetric size and hidden position in the calamus scriptorius.</AbstractText>The authors reviewed all of their cases in which patients underwent ventricular transaqueductal flexible endoscopic procedures and selected 44 cases in which an inspection of the region of the calamus scriptorius had been performed and was suitable for study inclusion. Patients were divided into different groups, based on the presence or absence of a chronic pathological process involving the fourth ventricle. In each case, the visual appearance of the opening of the CC of the ACC was classified as no evidence (A0), indirect evidence (A1), or clear evidence (A2). Morphometric measurements were inferred from surrounding structures and the size of surgical tools visible in the field.</AbstractText>The opening of the CC could be clearly observed in all cases (A1 4.5%, A2 95.5%). In normal cases, a lanceolate shape along the median sulcus was most frequently found, with an average size of 600 × 250 µm that became rounded and smaller in size in cases of hydrocephalus. The distance between the caudal margin of the ACC and the obex was about 1.8 mm in normal cases, 2.1 mm in cases of obstructive hydrocephalus, and 1 mm in cases of normal pressure hydrocephalus. The two wings of the area postrema, variable in size and shape, were sited just caudal to the opening.</AbstractText>A flexible scope inserted through the cerebral aqueduct can approach the hidden calamus scriptorius like a pen fits into an inkpot. With this privileged viewpoint, the authors provide for the first time, to their knowledge, a clear and novel vision of the opening of the CC in the fourth ventricle, along with the precise location of this tiny structure compared to other anatomical landmarks in the inferior triangle.</AbstractText> |
2,331,173 | Ventriculomegaly and postoperative lateral/third ventricular blood as predictors of cerebrospinal fluid diversion following posterior fossa tumor resection. | Postoperative hydrocephalus occurs in one-third of children after posterior fossa tumor resection. Although models to predict the need for CSF diversion after resection exist for preoperative variables, it is unknown which postoperative variables predict the need for CSF diversion. In this study, the authors sought to determine the clinical and radiographic predictors for CSF diversion in children following posterior fossa tumor resection.</AbstractText>This was a retrospective cohort study involving patients ≤ 18 years of age who underwent resection of a primary posterior fossa tumor between 2000 and 2018. The primary outcome was the need for CSF diversion 6 months after surgery. Candidate predictors for CSF diversion including age, race, sex, frontal occipital horn ratio (FOHR), tumor type, tumor volume and location, transependymal edema, papilledema, presence of postoperative intraventricular blood, and residual tumor were evaluated using a best subset selection method with logistic regression.</AbstractText>Of the 63 included patients, 26 (41.3%) had CSF diversion at 6 months. Patients who required CSF diversion had a higher median FOHR (0.5 vs 0.4) and a higher percentage of postoperative intraventricular blood (30.8% vs 2.7%) compared with those who did not. A 0.1-unit increase in FOHR or intraventricular blood was associated with increased odds of CSF diversion (OR 2.9 [95% CI 1.3-7.8], p = 0.02 and OR 20.2 [95% CI 2.9-423.1], p = 0.01, respectively) with an overfitting-corrected concordance index of 0.68 (95% CI 0.56-0.80).</AbstractText>The preoperative FOHR and postoperative intraventricular blood were significant predictors of the need for permanent CSF diversion within 6 months after posterior fossa tumor resection in children.</AbstractText> |
2,331,174 | Cardiac Involvement in Women With Pathogenic Dystrophin Gene Variants. | <b>Objective:</b> To determine the frequency and extent of cardiac involvement in female carriers of pathogenic variants in <i>DMD</i>, 53 women were examined through an observational, cross-sectional study. <b>Methods:</b> Genetically verified female carriers of pathogenic <i>DMD</i> variants were examined by cardiac magnetic resonance imaging (CMR) with late gadolinium enhancement, echocardiography, 24-h Holter monitoring, ECG, and blood concentrations of skeletal and cardiac muscle biomarkers. <b>Results:</b> Fifty-three female carriers of pathogenic <i>DMD</i> variants (mean age 49.6 years, 33 associated with DMD, and 20 with BMD) were included in the study. Sixty-two percent had cardiac dysfunction on echocardiography. On CMR, 49% had myocardial fibrosis, 35% had dilated left ventricles, and 10% had left ventricular hypertrophy. ECGs were abnormal in 72%, and abnormal Holter monitoring was found in 43%. Age did not correlate with myocardial fibrosis or cardiac dysfunction. Myocardial fibrosis was more frequent in carriers of pathogenic variants associated with DMD vs. BMD (61 vs. 28%, <i>p</i> = 0.02). <b>Conclusion:</b> This study shows that cardiac involvement, affecting both structure and function of the heart, is found in over 2/3 of women with a pathogenic <i>DMD</i> variant. The study supports early cardiac screening, including ECG, Holter, and cardiac imaging, in this group of carriers, so that symptoms related to pathogenic variants in <i>DMD</i> can be recognized, and relevant treatment can be initiated. Longitudinal studies are needed to assess morbidity and mortality related to single, pathogenic <i>DMD</i> variants in women. |
2,331,175 | Transmantle Pressure Computed from MR Imaging Measurements of Aqueduct Flow and Dimensions. | Measuring transmantle pressure, the instantaneous pressure difference between the lateral ventricles and the cranial subarachnoid space, by intracranial pressure sensors has limitations. The aim of this study was to compute transmantle pressure noninvasively with a novel nondimensional fluid mechanics model in volunteers and to identify differences related to age and aqueductal dimensions.</AbstractText>Brain MR images including cardiac-gated 2D phase-contrast MR imaging and fast-spoiled gradient recalled imaging were obtained in 77 volunteers ranging in age from 25-92 years of age. Transmantle pressure was computed during the cardiac cycle with a fluid mechanics model from the measured aqueductal flow rate, stroke volume, aqueductal length and cross-sectional area, and heart rate. Peak pressures during caudal and rostral aqueductal flow were tabulated. The computed transmantle pressure, aqueductal dimensions, and stroke volume were estimated, and the differences due to sex and age were calculated and tested for significance.</AbstractText>Peak transmantle pressure was calculated with the nondimensional averaged 14.4 (SD, 6.5) Pa during caudal flow and 6.9 (SD, 2.8) Pa during rostral flow. It did not differ significantly between men and women or correlate significantly with heart rate. Peak transmantle pressure increased with age and correlated with aqueductal dimensions and stroke volume.</AbstractText>The nondimensional fluid mechanics model for computing transmantle pressure detected changes in pressure related to age and aqueductal dimensions. This novel methodology can be easily used to investigate the clinical relevance of the transmantle pressure in normal pressure hydrocephalus, pediatric communicating hydrocephalus, and other CSF disorders.</AbstractText>© 2021 by American Journal of Neuroradiology.</CopyrightInformation> |
2,331,176 | Oxidized/deamidated-ceruloplasmin dysregulates choroid plexus epithelial cells functionality and barrier properties via RGD-recognizing integrin binding. | Choroid plexus epithelial cells (CPEpiCs) determine the composition of cerebrospinal fluid (CSF) and constitute the blood-CSF barrier (BCSFB), functions that are altered in neurodegenerative diseases. In Parkinson's disease (PD) the pathological environment oxidizes and deamidates the ceruloplasmin, a CSF-resident ferroxidase, which undergoes a gain of RGD-recognizing integrin binding property, that may result in signal transduction. We investigated the effects that oxidized/deamidated ceruloplasmin (Cp-ox/de) may exert on CPEpiCs functions. Through RGD-recognizing integrins binding, Cp-ox/de mediates CPEpiCs adhesion and intracellular signaling, resulting in cell proliferation inhibition and alteration of the secretome profile in terms of proteins related to cell-extracellular matrix interaction. Oxidative conditions, comparable to those found in the CSF of PD patients, induced CPEpiCs barrier leakage, allowing Cp-ox/de to cross it, transducing integrins-mediated signal that further worsens BCSFB integrity. This mechanism might contribute to PD pathological processes altering CSF composition and aggravating the already compromised BCSFB function. |
2,331,177 | Verminous meningoencephalomyelitis in a red kangaroo associated with <i>Angiostrongylus cantonensis</i> infection. | <i>Angiostrongylus cantonensis</i> is a zoonotic parasitic helminth that normally resides in the pulmonary arteries and the right ventricle of rats (<i>Rattus</i> sp.), the definitive host, where it causes little disease. Humans, dogs, opossums, and various zoo animals are "accidental" hosts. Here we report verminous meningoencephalomyelitis caused by <i>A. cantonensis</i> in a 9-mo-old male red kangaroo (<i>Macropus rufus</i>). The kangaroo was first presented lethargic, recumbent, and hypothermic, with severe muscle wasting. Within 3 wk, he progressed to non-ambulatory paraparesis and died. Gross examination revealed multifocal areas of dark-brown discoloration, malacia, and cavitation in the brain and the spinal cord. Histologically, there were several sections of nematodes surrounded by extensive areas of rarefaction, hemorrhage, spongiosis, neuronal necrosis, and gliosis. Based on size, morphology, and organ location, the nematodes were identified as subadult males and females. Interestingly, an eosinophilic response was largely absent, and the inflammatory response was minimal. <i>A. cantonensis</i> infection had not been reported previously in a red kangaroo in Louisiana or Mississippi, to our knowledge. Our case reaffirms the widespread presence of the helminth in the southeastern United States and indicates that <i>A. cantonensis</i> should be considered as a differential in macropods with neurologic clinical signs in regions where <i>A. cantonensis</i> is now endemic. |
2,331,178 | Intraventricular mucin-producing glioblastoma arising in the septum pellucidum at the frontal horn of the lateral ventricle: A case report. | Glioblastoma (GBM) most commonly appears to be intraparenchymal tumor, and intraventricular GBMs are rarely reported. In previous reports, the sites of origin were not identified. Here, we report a rare case of intraventricular mucin-producing GBM in a 73-year-old woman who had a strongly enhancing tumor in the right anterior horn of the lateral ventricle. The tumor had previously been identified one and a half years ago as a small asymptomatic lesion attached to the septum pellucidum. It had been documented to gradually enlarge during subsequent follow-up examinations. The patient underwent a gross total resection of the tumor, and a soft and gelatinous mass was observed. The pathological diagnosis was compatible with GBM, and numerous tumor cells having cytoplasmic mucin vacuoles were observed. Genetic analysis revealed TP53 and NFKBIA deletions. The patient received postoperative concurrent chemotherapy with temozolomide and radiotherapy, followed by maintenance administration of temozolomide. A follow-up examination seven months later detected an asymptomatic local recurrent lesion, which was treated with gamma-knife therapy, followed by bevacizumab administration for six months. The patient has remained clinically well for five years following surgery. The origin of a rare tumor entity, intraventricular GBM, and the specific spatial and pathological findings in our case are discussed in this report. |
2,331,179 | Oculocerebrocutaneous Syndrome (Delleman Syndrome): A Case with a Novel Presentation of Orbital Involvement. | Oculocerebrocutaneous syndrome (OCCS), also known as Delleman syndrome (DS), is a rare congenital anomaly featuring focal skin defects, orbital anomalies, and central nervous system malformations. Diagnosis of Delleman syndrome is based on the triad of eye, central nervous system (CNS), and cutaneous defects and confirmed by magnetic resonance imaging. A 23-day-old girl was referred to our department for brain imaging. The infant had multiple cutaneous appendages on the right side of her face. There also was a fleshy mass measuring about 12 mm over her right eye. Brain MRI demonstrated the evidence of colpocephaly, agenesis of the corpus callosum, nodular subependymal heterotopias adjacent to the right lateral ventricle, aplasia of the cerebellar vermis, hypoplasia of the right cerebellar hemisphere, and widening of CSF space in the posterior fossa. There was also an exophytic skin lesion on her right cheek, measuring about 13 × 12 mm in size. In the orbital MRI, there was a mixed cystic solid mass measuring about 25 × 20 mm in her right orbital cavity. The orbital content was abnormal and suggestive of rudimentary orbit. Considering the findings, diagnosis of oculocerebrocutaneous syndrome (Delleman syndrome) was established for the patient. Because of the variations in orbital and CNS manifestations, all patients with clinical suspicion of DS should be assessed by brain and orbital MRI and managed by a pediatric neurologist and ophthalmologist. |
2,331,180 | Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury. | Our previous study has shown that the transcription factor Krüppel-like factor 7 (KLF7) promotes peripheral nerve regeneration and motor function recovery after spinal cord injury. KLF7 also participates in traumatic brain injury, but its regulatory mechanisms remain poorly understood. In the present study, an HT22 cell model of traumatic brain injury was established by stretch injury and oxygen-glucose deprivation. These cells were then transfected with an adeno-associated virus carrying KLF7 (AAV-KLF7). The results revealed that, after stretch injury and oxygen-glucose deprivation, KLF7 greatly reduced apoptosis, activated caspase-3 and lactate dehydrogenase, downregulated the expression of the apoptotic markers B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) and cleaved caspase-3, and increased the expression of βIII-tubulin and the antiapoptotic marker Bcl-2. Furthermore, KLF7 overexpression upregulated Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) phosphorylation in HT22 cells treated by stretch injury and oxygen-glucose deprivation. Immunoprecipitation assays revealed that KLF7 directly participated in the phosphorylation of STAT3. In addition, treatment with AG490, a selective inhibitor of JAK2/STAT3, weakened the protective effects of KLF7. A mouse controlled cortical impact model of traumatic brain injury was then established. At 30 minutes before modeling, AAV-KLF7 was injected into the ipsilateral lateral ventricle. The protein and mRNA levels of KLF7 in the hippocampus were increased at 1 day after injury and recovered to normal levels at 3 days after injury. KLF7 reduced ipsilateral hippocampal atrophy, decreased the injured cortex volume, downregulated Bax and cleaved caspase-3 expression, and increased the number of 5-bromo-2'-deoxyuridine-positive neurons and Bcl-2 protein expression. Moreover, KLF7 transfection greatly enhanced the phosphorylation of JAK2 and STAT3 in the ipsilateral hippocampus. These results suggest that KLF7 may protect hippocampal neurons after traumatic brain injury through activation of the JAK2/STAT3 signaling pathway. The study was approved by the Institutional Review Board of Mudanjiang Medical University, China (approval No. mdjyxy-2018-0012) on March 6, 2018. |
2,331,181 | Increased plasmin-mediated proteolysis of L1CAM in a mouse model of idiopathic normal pressure hydrocephalus. | Idiopathic normal pressure hydrocephalus (iNPH) is a common neurological disorder that is characterized by enlarged cerebral ventricles, gait difficulty, incontinence, and dementia. iNPH usually develops after the sixth decade of life in previously asymptomatic individuals. We recently reported that loss-of-function deletions in <i>CWH43</i> lead to the development of iNPH in a subgroup of patients, but how this occurs is poorly understood. Here, we show that deletions in <i>CWH43</i> decrease expression of the cell adhesion molecule, L1CAM, in the brains of <i>CWH43</i> mutant mice and in human HeLa cells harboring a <i>CWH43</i> deletion. Loss-of-function mutations in L1CAM are a common cause of severe neurodevelopmental defects that include congenital X-linked hydrocephalus. Mechanistically, we find that <i>CWH43</i> deletion leads to decreased N-glycosylation of L1CAM, decreased association of L1CAM with cell membrane lipid microdomains, increased L1CAM cleavage by plasmin, and increased shedding of cleaved L1CAM in the cerebrospinal fluid. <i>CWH43</i> deletion also decreased L1CAM nuclear translocation, suggesting decreased L1CAM intracellular signaling. Importantly, the increase in L1CAM cleavage occurred primarily in the ventricular and subventricular zones where brain <i>CWH43</i> is most highly expressed. Thus, <i>CWH43</i> deletions may contribute to adult-onset iNPH by selectively downregulating L1CAM in the ventricular and subventricular zone. |
2,331,182 | Cerebrospinal fluid cell count variability is a major confounding factor in external ventricular drain-associated infection surveillance diagnostics: a prospective observational study. | External ventricular drain (EVD)-related infections (EVDIs) are feared complications that are difficult to rapidly and correctly diagnose, which can lead to unnecessary treatment with broad-spectrum antibiotics. No readily available diagnostic parameters have been identified to reliably predict or identify EVDIs. Moreover, intraventricular hemorrhage is common and affect cerebrospinal fluid (CSF) cellularity. The relationship between leukocytes and erythrocytes is often used to identify suspected infection and triggers the use of antibiotics pending results of cultures, which may take days. Cell count based surveillance diagnostics assumes a homogeneous distribution of cells in the CSF. Given the intraventricular sedimentation of erythrocytes on computed tomography scans this assumption may be erroneous and could affect diagnostics.</AbstractText>To evaluate the consistency of cell counts in serially sampled CSF from EVDs, with and without patient repositioning, to assess the effect on infection diagnostics.</AbstractText>We performed a prospective single-center study where routine CSF sampling was followed by a second sample after 10 min, allocated around a standard patient repositioning, or not. Changes in absolute and pairwise cell counts and ratios were analyzed, including mixed regression models.</AbstractText>Data from 51 patients and 162 paired samples were analyzed. We observed substantial changes in CSF cellularity as the result of both resampling and repositioning, with repositioning found to be an independent predictor of bidirectional cellular change. Glucose and lactate levels were affected, however clinically non-significant. No positive CSF cultures were seen during the study. Thirty percent (30%) of patients changed suspected EVDI status, as defined by the cell component of local and national guidelines, when resampling after repositioning.</AbstractText>CSF cell counts are not consistent and are affected by patient movement suggesting a heterogeneity in the intraventricular space. The relationship between leukocytes and erythrocytes was less affected than absolute changes. Importantly, cell changes are found to increase with increased cellularity, often leading to changes in suspected EVDI status. Faster and more precise diagnostics are needed, and methods such as emerging next generation sequencing techniques my provide tools to more timely and accurately guide antibiotic treatment. Trial Registration NCT04736407, Clinicaltrials.gov, retrospectively registered 2nd February 2021.</AbstractText>© 2021. The Author(s).</CopyrightInformation> |
2,331,183 | Left ventricular inflow obstruction due to a coronary arteriovenous fistula: a paediatric case report.<Pagination><StartPage>389</StartPage><MedlinePgn>389</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">389</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12872-021-02190-4</ELocationID><Abstract><AbstractText Label="BACKGROUND">We report a rare case of left ventricular inflow obstruction from a branch of the left circumflex coronary artery to the right atrium caused by a coronary arteriovenous fistula (CAVF) in a young Japanese male child.</AbstractText><AbstractText Label="CASE PRESENTATION">The patient was diagnosed with CAVF following a heart murmur shortly after birth. The left-to-right shunt caused right ventricular volume overload and pulmonary congestion. An emergency surgical intervention was performed for the CAVF on day 6 after birth. However, by 5 years of age, his left ventricular inflow obstruction worsened. We found an abnormal blood vessel originating from the proximal part of a branch of the left circumflex coronary artery, circling the outside of the mitral valve annulus along the medial side of the coronary sinus. As the child gets older, the blood inflow into the left ventricle might get restricted further, resulting in left-sided heart failure.</AbstractText><AbstractText Label="CONCLUSION">Our findings suggest that even after CAVF closure surgery, it is essential to monitor for complications caused by progressive dilatation of a persistent CAVF.</AbstractText><CopyrightInformation>© 2021. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chida-Nagai</LastName><ForeName>Ayako</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamazawa</LastName><ForeName>Hirokuni</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsujioka</LastName><ForeName>Takao</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Taniguchi</LastName><ForeName>Kota</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sasaki</LastName><ForeName>Osamu</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Izumi</LastName><ForeName>Gaku</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kato</LastName><ForeName>Nobuyasu</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular and Thoracic Surgery, Hokkaido University Hospital, Sapporo, Hokkaido, 060-8648, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takeda</LastName><ForeName>Atsuhito</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0001-9913-5834</Identifier><AffiliationInfo><Affiliation>Department of Paediatrics, Hokkaido University Hospital, Kita 14, Nishi 5, Kita-Ku, Sapporo, Hokkaido, 060-8648, Japan. a-takeda@med.hokudai.ac.jp.</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>2021</Year><Month>08</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Cardiovasc Disord</MedlineTA><NlmUniqueID>100968539</NlmUniqueID><ISSNLinking>1471-2261</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000367" MajorTopicYN="N">Age Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001164" MajorTopicYN="N">Arteriovenous Fistula</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054326" MajorTopicYN="N">Coronary Sinus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003330" MajorTopicYN="N">Coronary Vessel Anomalies</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004108" MajorTopicYN="N">Dilatation, Pathologic</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="Y">Heart Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006940" MajorTopicYN="N">Hyperemia</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018476" MajorTopicYN="N">Hypokinesia</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008943" MajorTopicYN="N">Mitral Valve</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011667" MajorTopicYN="N">Pulmonary Veins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018487" MajorTopicYN="N">Ventricular Dysfunction, Left</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Case report</Keyword><Keyword MajorTopicYN="N">Congenital heart disease</Keyword><Keyword MajorTopicYN="N">Coronary atrioventricular fistula</Keyword><Keyword MajorTopicYN="N">Left ventricular inflow obstruction</Keyword></KeywordList><CoiStatement>The authors declare that they have no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>12</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>7</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2021</Year><Month>8</Month><Day>12</Day><Hour>5</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2021</Year><Month>8</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2021</Year><Month>12</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">34380423</ArticleId><ArticleId IdType="pmc">PMC8359319</ArticleId><ArticleId IdType="doi">10.1186/s12872-021-02190-4</ArticleId><ArticleId IdType="pii">10.1186/s12872-021-02190-4</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Loukas M, Germain AS, Gabriel A, John A, Tubbs RS, Spicer D. 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Circ Cardiovasc Imaging. 2017;10:e006979. doi: 10.1161/CIRCIMAGING.117.006979.</Citation><ArticleIdList><ArticleId IdType="doi">10.1161/CIRCIMAGING.117.006979</ArticleId><ArticleId IdType="pmc">PMC5812349</ArticleId><ArticleId IdType="pubmed">29138232</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">34380377</PMID><DateRevised><Year>2021</Year><Month>08</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1563-5279</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2021</Year><Month>Aug</Month><Day>11</Day></PubDate></JournalIssue><Title>The International journal of neuroscience</Title><ISOAbbreviation>Int J Neurosci</ISOAbbreviation></Journal>Ghrelin improves cognition via activation of the cAMP- CREB signalling pathway in depressed male C57BL/6J mice. | <b>Background:</b> Depression leads to a cognitive decline and decreases in ghrelin are observed in depression. Ghrelin affects the level of Brain-derived nerve growth factor (BDNF) through the cAMP-CREB signalling pathway, and lower BDNF levels lead to cognitive decline. Therefore, it is reasonable to assume that in depression, lower ghrelin causes a decrease in BDNF levels and cognitive decline though the cAMP- CREB signalling pathway.<b>Methods:</b> A total of 120 C57BL/6J male mice were randomly divided into six groups of 20 mice: non-depression groups (sham group, ghrelin group, and ghrelin + (D-lys3)-GHRP-6 group) and depression groups (depression group, depression + ghrelin group and depression + ghrelin + (D-lys3)-GHRP group). A depression mouse model was established by injecting normal saline, ghrelin or ghrelin + (D-lys3) -GHRP-6 into the lateral ventricle of each group. Cognition, hippocampal long-term potentiation (LTP), ghrelin mRNA and protein level, BDNF level and CREB level in the hippocampus were detected.Results: <b>In the depression mouse model groups, all comparison indexes (cognition and hippocampal levels of LTP, ghrelin mRNA and proteins, and BDNF and CREB) had significant negative changes. In the mice with depression, ghrelin or ghrelin + (D-lys3)-GHRP-6 was injected, and all the comparison indicators showed significant positive changes. Supplementation of ghrelin+(D-lys3))-GHRP-6 resulted in more significant positive changes in all comparison indexes than those of ghrelin alone.</b><b>Conclusions:</b> In the depression model, lower ghrelin causes hippocampal BDNF to decrease and results in cognitive decline via the cAMP-CREB signalling pathway. |
2,331,184 | Mapping dependencies of BOLD signal change to end-tidal CO<sub>2</sub>: Linear and nonlinear modeling, and effect of physiological noise correction. | Disentangling physiological noise and signal of interest is a major issue when evaluating BOLD-signal changes in response to breath holding. Currently-adopted approaches for retrospective noise correction are general-purpose, and have non-negligible effects in studies on hypercapnic challenges.</AbstractText>We provide a novel approach to the analysis of specific and non-specific BOLD-signal changes related to end-tidal CO2</sub> (PET</sub>CO2</sub>) in breath-hold fMRI studies. Multiple-order nonlinear predictors for PET</sub>CO2</sub> model a region-dependent nonlinear input-output relationship hypothesized in literature and possibly playing a crucial role in disentangling noise. We explore Retrospective Image-based Correction (RETROICOR) effects on the estimated BOLD response, applying our analysis both with and without RETROICOR and analyzing the linear and non-linear correlation between PET</sub>CO2</sub> and RETROICOR regressors.</AbstractText>The RETROICOR model of noise related to respiratory activity correlated with PET</sub>CO2</sub> both linearly and non-linearly. The correction affected the shape of the estimated BOLD response to hypercapnia but allowed to discard spurious activity in ventricles and white matter. Activation clusters were best detected using non-linear components in the BOLD response model.</AbstractText>We evaluated the side-effects of standard physiological noise correction procedure, tailoring our analysis on challenging understudied brainstem and subcortical regions. Our novel approach allowed to characterize delays and non-linearities in BOLD response.</AbstractText>RETROICOR successfully avoided false positives, still broadly affecting the estimated non-linear BOLD responses. Non-linearities in the model better explained CO2</sub>-related BOLD signal fluctuations. The necessity to modify the standard procedure for physiological-noise correction in breath-hold studies was addressed, stating its crucial importance.</AbstractText>Copyright © 2021 Elsevier B.V. All rights reserved.</CopyrightInformation> |
2,331,185 | Lateral Ventricular Meningiomas: Clinical Features, Radiological Findings and Long-Term Outcomes. | Lateral ventricle meningioma (LVM) is a rare type of intracranial meningioma, which has been rarely studied. It has different clinical features, imaging features, and long-term results from other locations. This study investigated the epidemiology, clinical characteristics and prognosis of LVM and comprehensively describes its characteristics.</AbstractText>This article analyzes the LVMs that were diagnosed pathologically in West China hospital between January 1, 2009 and July 1 2020. Demographic information, imaging characteristics and prognostic factors are discussed. Data analysis was performed using SPSS 23.0 and R version 3.5.3.</AbstractText>We collected 7202 meningiomas and 195 LVMs (136 females; median age, 46 years; range, 5-81 years) were included in this study. Gross total resection was completed in 189 patients. The OS rate was 93.8%, and the recurrence rate was 5.2%. Multivariate regression analysis showed that sex (P = 0.01) and tumor size (P = 0.018) were related to WHO grade. Postoperative KPS (P = 0.003) was associated with OS. WHO grade (P = 0.025), extent of tumor resection (P < 0.001), and hospital day (P=0.028) were associated with recurrence.</AbstractText>LVMs require long-term follow-up, individualized treatment, and follow-up strategies to be formulated according to the relevant risk factors.</AbstractText>© 2021 Teng et al.</CopyrightInformation> |
2,331,186 | Effect of aspirin in takotsubo syndrome: protocol of a systematic review and meta-analysis. | Takotsubo syndrome (TTS) is a sudden reversible weakening of the left ventricle function induced by severe stress and resembles many features as acute coronary syndrome. Even though many guidelines had been published about TTS, there is no consensus regarding the long-term treatment. Aspirin is one of the most common prescribed medicines at discharge for patients with the intention to reduce thrombus events and improve the overall prognosis. However, existing studies yielded conflicting results concerning its effects. This study aims to evaluate the impact of long-term maintenance treatment of aspirin in TTS and provides insights in clinical management.</AbstractText>After searching through electronic databases (PubMed, Embase, Cochrane Library, Web of Science, National Library of Medicine Gateway, CNKI, Wanfang and VIP), grey literatures, conference abstract and trial registries for clinical studies investigating the impact of aspirin on patients with TTS, a systemic review and meta-analysis will be conducted. The search will be limited from inception of each database to 1 August 2020. The outcomes including all-cause death, TTS recurrence, stroke, transient ischaemic attack or myocardial infarction at 30-day and 5-year follow-up will be examined. Risk of bias will be assessed by Newcastle-Ottawa quality assessment scale for observational studies and Cochrane Effective Practice and Organization of Care evaluation tool for interventional studies. Grading of Recommendations Assessment, Development and Evaluations method will be applied to assess the quality of evidence. If available, the effects of aspirin on the above outcomes for patients with TTS will be evaluated using random-effect modelling with relative risk at 95% CIs. Subgroup analysis and sensitivity analysis will also be performed when possible.</AbstractText>Ethics approval was not required due to the retrospective nature of the study. Results of the review will be published in a peer-reviewed journal.</AbstractText>CRD42020212729.</AbstractText>© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation> |
2,331,187 | Clinical value and role of microRNA-29c-3p in sepsis-induced inflammation and cardiac dysfunction. | The goal of this study was to investigate the diagnostic value of miR-29c-3p in sepsis and its role in sepsis-induced inflammatory response and cardiac dysfunction.</AbstractText>Serum level of miR-29c-3p was detected by qRT-PCR. The ROC curve was used to evaluate the diagnostic value of miR-29c-3p for Sepsis. The cecal ligation and puncture method (CLP) was used to establish a rat sepsis model. To assess cardiac function, left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and maximum rate of rise/fall of left ventricle pressure (± dp/dtmax</sub>) in different experimental groups were detected, and the serum cardiac troponin I (cTnI), creative kinase isoenzyme MB (CK-MB) were measured by ELISA. Meanwhile, TNF-α, IL-1β, and IL-6 were detected by ELISA to assess the level of inflammatory response in animals.</AbstractText>miR-29c-3p level was upregulated in sepsis patients. ROC curve revealed that miR-29c-3p had the ability to distinguish sepsis patients from healthy controls. Cardiac dysfunction and inflammation were observed in sepsis rat, which were characterized by the decrease of LVSP and + dp/dtmax</sub>, the increase of LVEDP, - dp/dtmax</sub>, cTnI, CK-MB, TNF-α, IL-1β, IL-6. All effects were reversed by the injection of miR-29c-3p antagomir. Logistics regression analysis manifested miR-29c-3p is an independent factor in the occurrence of cardiac dysfunction in sepsis patients.</AbstractText>miR-29c-3p has potential as a biomarker for the diagnosis of sepsis, and inhibition of miR-29c-3p expression in animal models reduced sepsis-induced cardiac dysfunction and inflammatory response.</AbstractText>© 2021. The Author(s).</CopyrightInformation> |
2,331,188 | Ischemic heart failure mortality is not predicted by cardiac insulin resistance but by diabetes per se and coronary flow reserve: A retrospective dynamic cardiac <sup>18</sup>F-FDG PET study.<Pagination><StartPage>154862</StartPage><MedlinePgn>154862</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.metabol.2021.154862</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0026-0495(21)00162-1</ELocationID><Abstract><AbstractText Label="BACKGROUND & AIMS">The connection between peripheral insulin resistance (IR) and coronary artery disease is well-established. Both are major risk factors for the development of ischemic cardiomyopathy potentially leading to heart failure (HF). Whether cardiac IR also impacts overall survival and morbidity is still debated. We therefore aimed to test if cardiac IR predicts mortality and major cardiovascular events (MACE) in patients with HF scheduled for cardiac viability testing before revascularization.</AbstractText><AbstractText Label="METHODS">This retrospective study included 131 patients with a clinical diagnosis of ischemic HF (114 (87%) male, 33 (25%) with diabetes) referred to a viability Rubidium-82 (perfusion) and dynamic <sup>18</sup>F-Fluorodeoxyglucose (metabolism) positron emission tomography combined with computed tomography prior to a potential revascularization procedure. Cardiac IR was assessed by myocardial glucose uptake (MGU) in a remote (non-scarred) area of the left ventricle during a hyperinsulinemic-euglycemic clamp (1mIE/kg/min).</AbstractText><AbstractText Label="RESULTS">MGU correlated with skeletal muscle glucose uptake (p < 0.001) and whole-body glucose uptake (M-value) (p < 0.001), whereas no association was observed for individuals with diabetes. MGU did not predict the risk of death or MACE. However, both overt diabetes and reduced coronary flow reserve predicted overall survival.</AbstractText><AbstractText Label="CONCLUSION">Even though diabetes and related small-vessel disease is associated with increased mortality, cardiac IR per se does not predict cardiovascular morbidity and mortality.</AbstractText><CopyrightInformation>Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Luong</LastName><ForeName>Thien Vinh</ForeName><Initials>TV</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Palle Juul-Jensens Boulevard 165, 8200 Aarhus N, Denmark; Steno Diabetes Center Aarhus, Aarhus University Hospital, Hedeager 3, 8200 Aarhus N, Denmark. Electronic address: thiluo@clin.au.dk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pedersen</LastName><ForeName>Mette Glavind Bülow</ForeName><Initials>MGB</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Aarhus, Aarhus University Hospital, Hedeager 3, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kjærulff</LastName><ForeName>Mette Louise Blouner Gram</ForeName><Initials>MLBG</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Palle Juul-Jensens Boulevard 165, 8200 Aarhus N, Denmark; Steno Diabetes Center Aarhus, Aarhus University Hospital, Hedeager 3, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Madsen</LastName><ForeName>Simon</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Palle Juul-Jensens Boulevard 165, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lauritsen</LastName><ForeName>Katrine Meyer</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Aarhus, Aarhus University Hospital, Hedeager 3, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tolbod</LastName><ForeName>Lars Poulsen</ForeName><Initials>LP</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Palle Juul-Jensens Boulevard 165, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Søndergaard</LastName><ForeName>Esben</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Steno Diabetes Center Aarhus, Aarhus University Hospital, Hedeager 3, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gormsen</LastName><ForeName>Lars Christian</ForeName><Initials>LC</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Palle Juul-Jensens Boulevard 165, 8200 Aarhus N, Denmark.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2021</Year><Month>08</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Metabolism</MedlineTA><NlmUniqueID>0375267</NlmUniqueID><ISSNLinking>0026-0495</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0Z5B2CJX4D</RegistryNumber><NameOfSubstance UI="D019788">Fluorodeoxyglucose F18</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003326" MajorTopicYN="Y">Coronary Circulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003924" MajorTopicYN="N">Diabetes Mellitus, Type 2</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019788" MajorTopicYN="N">Fluorodeoxyglucose F18</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017202" MajorTopicYN="N">Myocardial Ischemia</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="N">Positron-Emission Tomography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Heart failure</Keyword><Keyword MajorTopicYN="N">Insulin resistance</Keyword><Keyword MajorTopicYN="N">Myocardial glucose uptake</Keyword><Keyword MajorTopicYN="N">Positron emission tomography</Keyword><Keyword MajorTopicYN="N">Prognosis</Keyword></KeywordList><CoiStatement>Declaration of competing interest All authors declare no conflict of interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>4</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2021</Year><Month>7</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2021</Year><Month>7</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2021</Year><Month>8</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2021</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2021</Year><Month>8</Month><Day>10</Day><Hour>20</Hour><Minute>10</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">34375646</ArticleId><ArticleId IdType="doi">10.1016/j.metabol.2021.154862</ArticleId><ArticleId IdType="pii">S0026-0495(21)00162-1</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">34374979</PMID><DateRevised><Year>2021</Year><Month>08</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1019-5149</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2021</Year><Month>Feb</Month><Day>09</Day></PubDate></JournalIssue><Title>Turkish neurosurgery</Title><ISOAbbreviation>Turk Neurosurg</ISOAbbreviation></Journal>Endoport-assisted Neuroendoscopic Techniques Used in the Resection of Intraventricular Lesions. | <AbstractText Label="BACKGROUND & AIMS">The connection between peripheral insulin resistance (IR) and coronary artery disease is well-established. Both are major risk factors for the development of ischemic cardiomyopathy potentially leading to heart failure (HF). Whether cardiac IR also impacts overall survival and morbidity is still debated. We therefore aimed to test if cardiac IR predicts mortality and major cardiovascular events (MACE) in patients with HF scheduled for cardiac viability testing before revascularization.</AbstractText>This retrospective study included 131 patients with a clinical diagnosis of ischemic HF (114 (87%) male, 33 (25%) with diabetes) referred to a viability Rubidium-82 (perfusion) and dynamic 18</sup>F-Fluorodeoxyglucose (metabolism) positron emission tomography combined with computed tomography prior to a potential revascularization procedure. Cardiac IR was assessed by myocardial glucose uptake (MGU) in a remote (non-scarred) area of the left ventricle during a hyperinsulinemic-euglycemic clamp (1mIE/kg/min).</AbstractText>MGU correlated with skeletal muscle glucose uptake (p < 0.001) and whole-body glucose uptake (M-value) (p < 0.001), whereas no association was observed for individuals with diabetes. MGU did not predict the risk of death or MACE. However, both overt diabetes and reduced coronary flow reserve predicted overall survival.</AbstractText>Even though diabetes and related small-vessel disease is associated with increased mortality, cardiac IR per se does not predict cardiovascular morbidity and mortality.</AbstractText>Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
2,331,189 | HMGB1-RAGE Pathway Contributes to the Abnormal Migration of Endogenous Subventricular Zone Neural Progenitors in an Experimental Model of Focal Microgyria. | Abnormal migration of subventricular zone (SVZ)-derived neural progenitor cells (SDNPs) is involved in the pathological and epileptic processes of focal cortical dysplasias (FCDs), but the underlying mechanisms are not clear. Recent studies indicated that high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) are widely expressed in epileptic specimens of FCDs, which suggests that the HMGB1-RAGE pathway is involved in the pathological and/or epileptic processes of FCDs. The present study used Nestin-GFP<sup>tg/+</sup> transgenic mice, and we established a model of freezing lesion (FL), as described in our previous report. A "migrating stream" composed of GFP-Nestin<sup>+</sup> SDNPs was derived from the SVZ region and migrated to the cortical FL area. We found that translocated HMGB1 and RAGE were expressed in cortical lesion in a clustered distribution pattern, which was especially obvious in the early stage of FL compared to the sham group. Notably, the number of GFP-Nestin<sup>+</sup> SDNPs within the "migrating stream" was significantly decreased when the HMGB1-RAGE pathway was blocked by a RAGE antagonist or deletion of the RAGE gene. The absence of RAGE also decreased the activity of pentylenetetrazol-induced cortical epileptiform discharge. In summary, this study provided experimental evidence that the levels of extranuclear HMGB1 and its receptor RAGE were increased in cortical lesion in the early stage of the FL model. Activation of the HMGB1-RAGE pathway may contribute to the abnormal migration of SDNPs and the hyperexcitability of cortical lesion in the FL model. |
2,331,190 | Aging reduces kisspeptin receptor (GPR54) expression levels in the hypothalamus and extra-hypothalamic brain regions. | Aging leads to the diminished pulsatile secretion of hypothalamic gonadotropin-releasing hormone (GnRH). Kisspeptin (Kp), the upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis, regulates GnRH synthesis and release through its cognate receptor, G-protein coupled receptor 54 (GPR54). In turn, GnRH regulates GPR54 expression. GnRH administration into the third ventricle has been shown to induce neurogenesis in different brain regions in old age. However, aging-associated changes in hypothalamic and extra-hypothalamic GPR54 expression were unclear. Therefore, the expression levels of GPR54 were evaluated in various brain regions of adult (age, 3-4 months) and old (age, 20-24 months) male Wistar rats in the present study. In the hypothalamus, mRNA and protein levels of Kp and GPR54 were identified to be significantly decreased in old age. Furthermore, <i>GnRH1</i> expression in the hypothalamus was analyzed to observe the functional consequence of a reduced Kp-GPR54 system in the hypothalamus. It was found that hypothalamic <i>GnRH1</i> levels were significantly decreased in old age. As GnRH regulates GPR54 levels, GPR54 was examined in extra-hypothalamic regions. GPR54 levels were found to be significantly decreased in the hippocampus and medulla and pons in old-age rats when compared to adult rats. Notably, GPR54 expression was observed in the frontal lobe, cortex, midbrain and cerebellum of adult and old-age rats; however, the difference between the two groups was not statistically significant. To the best of our knowledge, this is the first study that provides the quantitative distribution of GPR54 in different brain regions during aging. Thus, the reduced levels of Kp and its receptor, GPR54 in the hypothalamus could be cumulatively responsible for reduced levels of GnRH observed in old age. |
2,331,191 | Subclinical cardiac impairment relates to traditional pulmonary function test parameters and lung volume as derived from whole-body MRI in a population-based cohort study. | To evaluate the relationship of cardiac function, including time-volume-curves, with lung volumes derived from pulmonary function tests (PFT) and MRI in subjects without cardiovascular diseases. 216 subjects underwent whole-body MRI and spirometry as part of the KORA-FF4 cohort study. Lung volumes derived semi-automatically using an in-house algorithm. Forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and residual volume were measured. Cardiac parameters derived from Cine-SSFP-sequence using cvi42, while left ventricle (LV) time-volume-curves were evaluated using pyHeart. Linear regression analyses assessed the relationships of cardiac parameters with PFT and MRI-based lung volumes. Mean age was 56.3 ± 9.2 years (57% males). LV and right ventricular (RV) end-diastolic-, end-systolic-, stroke volume, LV peak ejection- and early/late diastolic filling rate were associated with FEV1, FVC, and residual volume (excluding late diastolic filling rate with FEV1, LV end-systolic/stroke volume and RV end-diastolic/end-systolic volumes with residual volume). In contrast, LV end-diastolic volume (ß = - 0.14, p = 0.01), early diastolic filling rate (ß = - 0.11, p = 0.04), and LV/RV stroke volume (ß = - 0.14, p = 0.01; ß = - 0.11, p = 0.01) were inversely associated with MRI-based lung volume. Subclinical cardiac impairment was associated with reduced FEV1, FVC, and residual volume. Cardiac parameters decreased with increasing MRI-based lung volume contrasting the results of PFT. |
2,331,192 | Strain Estimation of the Murine Right Ventricle Using High-Frequency Speckle-Tracking Ultrasound. | Right ventricular (RV) strain measurements from ultrasound via speckle-tracking techniques are being used more frequently as a non-invasive diagnostic tool for a variety of cardiopulmonary pathologies. However, despite the clinical utility of ultrasound RV strain measurements, quantification of RV strain in rodents remains difficult owing to unique image artifacts and non-standardized methodologies. We demonstrate here a simple approach for measuring RV strain in both mice and rats using high-frequency ultrasound and automated speckle tracking. Our results show estimated peak RV free-wall longitudinal strain values (mean ± standard error of the mean) in mice (n = 15) and rats (n = 5) of, respectively, -10.38% ± 0.4% and -4.85% ± 0.42%. We further estimated the 2-D Green-Lagrange strain within the RV free wall, with longitudinal components estimated at -5.7% ± 0.48% in mice and -2.1% ± 0.28% in rats. These methods and data may provide a foundation for future work aimed at evaluating murine RV strain levels in different disease models. |
2,331,193 | Physical activity is important for cardiovascular health and cardiorespiratory fitness in patients with psoriasis. | Patients with psoriasis have a level of physical activity below that recommended for cardiovascular health, which is significantly limited by disease severity and other psoriasis-specific barriers. We hypothesized that physical activity is important for cardiovascular health in patients with psoriasis and that its objective measurement could have clinical utility.</AbstractText>To explore whether physical activity influences the risk of cardiovascular disease (CVD) in patients with psoriasis.</AbstractText>In total, 242 patients with chronic plaque psoriasis were recruited. History, examination and physical activity were assessed and arteriography, the noninvasive measurement of arterial function, was performed for each participant.</AbstractText>We observed a significant relationship between volume of physical activity and the likelihood of future CVD as measured by pulse wave velocity (PWV; P < 0.02). We identified a significant relationship between the diastolic reflection area (DRA) and health-promoting levels of physical activity (P < 0.001), in addition to a significant correlation between DRA and the likelihood of future CVD (P < 0.001). The DRA is a complex, dimensionless variable that describes the intensity of diastolic wave reflection and the duration of diastole, which are key determinants of the blood supply to the left ventricle. Our data suggest that DRA may represent a surrogate marker for cardiorespiratory fitness.</AbstractText>Our study describes a significant relationship between exercise, cardiorespiratory fitness and PWV, a preclinical indicator of future CVD risk, in patients with psoriasis. The DRA offers a noninvasive, objective measurement of exercise adherence, which could have clinical utility in the future.</AbstractText>© 2021 The Authors. Clinical and Experimental Dermatology published by John Wiley & Sons Ltd on behalf of British Association of Dermatologists.</CopyrightInformation> |
2,331,194 | A High-Fidelity 3D Micromechanical Model of Ventricular Myocardium. | Pulmonary arterial hypertension (PAH) imposes a pressure overload on the right ventricle (RV), leading to myofiber hypertrophy and remodeling of the extracellular collagen fiber network. While the macroscopic behavior of healthy and post-PAH RV free wall (RVFW) tissue has been studied previously, the mechanical microenvironment that drives remodeling events in the myofibers and the extracellular matrix (ECM) remains largely unexplored. We hypothesize that multiscale computational modeling of the heart, linking cellular-scale events to tissue-scale behavior, can improve our understanding of cardiac remodeling and better identify therapeutic targets. We have developed a high-fidelity microanatomically realistic model of ventricular myocardium, combining confocal microscopy techniques, soft tissue mechanics, and finite element modeling. We match our microanatomical model to the tissue-scale mechanical response of previous studies on biaxial properties of RVFW and examine the local myofiber-ECM interactions to study fiber-specific mechanics at the scale of individual myofibers. Through this approach, we determine that the interactions occurring at the tissue scale can be accounted for by accurately representing the geometry of the myofiber-collagen arrangement at the micro scale. Ultimately, models such as these can be used to link cellular-level adaptations with organ-level adaptations to lead to the development of patient-specific treatments for PAH. |
2,331,195 | A proof of concept treatment planning study of gated proton radiotherapy for cardiac soft tissue sarcoma. | Few studies on radiotherapy of cardiac targets exist, and none using a gating method according to cardiac movement. This study aimed to evaluate the dose-volume advantage of using cardiac-respiratory double gating (CRDG) in terms of target location with additional ECG signals in comparison to respiratory single gating (RSG) for proton radiotherapy of targets in the heart.</AbstractText>Cardiac motion was modeled using a cardiac-gated four-dimensional computed tomography scan obtained at the end-expiration. Plans with the prescription dose of 50 Gy (RSG and CRDG plans at diastole and systole phases) were compared in terms of clinically relevant dose-volume criteria for various target sizes and seven cardiac subsites. Potential dose sparing by utilizing CRDG over RSG was quantified in terms of surrounding organ at risk (OAR) doses while the dose coverage to the targets was fully ensured.</AbstractText>The average mean dose reductions were 28 ± 10% when gated at diastole and 21 ± 12% at systole in heart and 30 ± 17% at diastole and 8 ± 9% at systole in left ventricle compared to respiratory single gating. The diastole phase was optimal for gated treatments for all target locations except right ventricle and interventricular septum. The right ventricle target was best treated at the systole phase. However, an optimal gating phase for the interventricular septum target could not be determined.</AbstractText>We have studied the dose-volume benefits of CRDG for each cardiac subsite, and demonstrated that CRDG may spare organs at risk better than RSG.</AbstractText>© 2021 Published by Elsevier B.V. on behalf of European Society of Radiotherapy & Oncology.</CopyrightInformation> |
2,331,196 | Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling. | Pressure overload and heart failure are among the leading causes of cardiovascular morbidity and mortality. Accumulating evidence suggests that inflammatory cell activation and release of inflammatory mediators are of vital importance during the pathogenesis of these cardiac diseases. Yet, the roles of innate immune cells and subsequent inflammatory events in these processes remain poorly understood. Here, we outline the possible underlying mechanisms of innate immune cell participation, including mast cells, macrophages, monocytes, neutrophils, dendritic cells, eosinophils, and natural killer T cells in these pathological processes. Although these cells accumulate in the atrium or ventricles at different time points after pressure overload, their cardioprotective or cardiodestructive activities differ from each other. Among them, mast cells, neutrophils, and dendritic cells exert detrimental function in experimental models, whereas eosinophils and natural killer T cells display cardioprotective activities. Depending on their subsets, macrophages and monocytes may exacerbate cardiodysfunction or negatively regulate cardiac hypertrophy and remodeling. Pressure overload stimulates the secretion of cytokines, chemokines, and growth factors from innate immune cells and even resident cardiomyocytes that together assist innate immune cell infiltration into injured heart. These infiltrates are involved in pro-hypertrophic events and cardiac fibroblast activation. Immune regulation of cardiac innate immune cells becomes a promising therapeutic approach in experimental cardiac disease treatment, highlighting the significance of their clinical evaluation in humans. |
2,331,197 | Rare Case of Tension Pneumocephalus in Thoracic Trauma. | Tension pneumocephalus is the presence of air within the cranial vault compressing the ventricles and the brain parenchyma. High altitudes can exacerbate this problem, especially when a dural defect exists and air is forced into the cranial cavity with no way to escape. This case demonstrates a rare presentation of thoracic trauma causing tension pneumocephalus due to emergent air evacuation. |
2,331,198 | Utility of Constructive Interference in Steady-State Sequence in Detecting Thin Pituitary Stalk in Pituitary Stalk Interruption Syndrome. | Pituitary stalk interruption syndrome (PSIS) is a rare congenital anomaly, causing hypothalamic-pituitary malfunction. It is characterized by hypoplastic anterior pituitary, absent or thin infundibulum, and absent or ectopic posterior pituitary. Its early recognition is important in disease management. MRI plays a pivotal role in early diagnosis. We report a case of a 13-year-old male child, presenting with stunting of growth and discrepancy between chronological and bone age of four years. A subsequent MRI revealed a small anterior pituitary, hypoplastic pituitary stalk, and an absence of visualization of the bright pituitary gland signal in the sella. The posterior pituitary gland was present ectopically in the midline along the floor of the third ventricle near the median eminence. |
2,331,199 | Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1. | This study investigated the effects of reynoutrin on the improvement of ischemic heart failure (IHF) and its possible mechanism in rats. The rat heart failure model was established by permanently ligating the left anterior descending coronary artery (LAD) and administering different doses of reynoutrin. Cardiac function, inflammatory factors releasing, oxidative stress, cardiomyocytes apoptosis, and myocardial fibrosis were evaluated. Western blotting was used to determine protein expression levels of S100 calcium-binding protein A1 (S100A1), matrix metallopeptidase 2(MMP2), MMP9, phosphorylated (p-) p65, and transforming growth factor -β1 (TGF-β1) in myocardial tissue of the left ventricle. Results showed that reynoutrin significantly improved cardiac function, suppressed the release of inflammatory factors, reduced oxidative stress, inhibited cardiomyocytes apoptosis, and attenuated myocardial fibrosis in rats with IHF. In rat myocardial tissue, permanent LAD-ligation resulted in a significant down-regulation in S100A1 expression, whereas reynoutrin significantly up-regulated S100A1 protein expression while down-regulating MMP2, MMP9, p-p65, and TGF-β1 expressions. However, when S100A1 was knocked down in myocardial tissue, the above-mentioned positive effects of reynoutrin were significantly reversed. Reynoutrin is a potential natural drug for the treatment of IHF, and its mechanism of action involves the up-regulation of S100A1 expression, thereby inhibiting expressions of MMPs and the transcriptional activity of nuclear factor kappa-B. |
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