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2,330,100
[Therapeutic Tactics for Pediatric Hydrocephalus].
Since hydrocephalus is usually an exacerbating disease, we need to arrest the hydrocephalus by surgical treatments such as ventricular access devices, V-P shunts, and endoscopic third ventriculostomy(ETV)with or without choroid plexus cauterization. For a long time, V-P shunt has been the GOLD standard treatment for pediatric hydrocephalus. In recent years, although there are more and more reports on the usefulness of ETV ± CPC, its results are not completely superior to V-P shunt, and therefore, V-P shunt is expected to remain the gold standard treatment for pediatric hydrocephalus in the near future. Therefore, overcoming complications, such as shunt dysfunction and shunt infection, will continue to be important in V-P shunt. A recent clinical trial has shown that antibiotic-impregnated catheters are effective in preventing shunt infections, which is why the incidence of shunt infection is expected to decrease in the future. For pediatric hydrocephalus, it is important to establish and maintain a regular follow-up system, because shunt malfunction may occur even in the chronic postoperative period.
2,330,101
[Theory and Practice of Endoscopic Third Ventriculostomy].
Endoscopic third ventriculostomy(ETV)is a basic procedure for the surgical treatment of hydrocephalus. It buffers pulsatile pressure by creating an alternative route for the flow of cerebrospinal fluid and reduces trans-mantle pulsatile stress, thereby increasing compliance of the brain parenchyma. Blunt perforation of the third ventricular floor is done while avoiding injury to the foramen of Monro, the hypothalamus, the pituitary stalk, and some cisternal vessels. A major complication of ETV is arterial bleeding caused by injury to the basilar artery. Surgeons should wait with irrigation and opening the root into the ventricle to control the intra-ventricular pressure until packing the third ventricle with hematoma. Since ETV may close by gliosis or scarring of the inter-peduncular cistern, regular physical examinations and MRI should follow the procedure.
2,330,102
[Epidemiology of Idiopathic Normal Pressure Hydrocephalus and Hereditary Hydrocephalus].
Several cohort studies in Japan have revealed that the prevalence of idiopathic normal pressure hydrocephalus(iNPH)is around 1.6% among the elderly population(&#x2267; 50 years old). The incidence of iNPH from the Yamagata(Takahata)cohort was 1.2/ 1,000 person-years in the elderly population. Although the Japanese guidelines for iNPH clearly describe the definition of "possible iNPH with MRI support," it is still difficult to find out not only patients with iNPH but also individuals in its preclinical stage with radiological findings of asymptomatic ventriculomegaly with features of iNPH on MRI(AVIM)or asymptomatic ventricular enlargement(AVE). It is assumed that only less than 10% of patients with iNPH were referred to hospitals in Japan. Several genes associated with congenital hydrocephalus have been found, including ciliopathy-related genes that directly affect the ependymal cilia in ventricles. Loss of the copy number of <i>SFMBT1</i> was found to be a risk factor for iNPH. Knowledge about risk genes and their mechanisms in congenital and familial NPH may be a clue for the further understanding of the pathophysiology of iNPH.
2,330,103
[Anatomy of Ventricular System for Neuroendoscopic Surgery].
Minimally invasive endoscopes with excellent deep observation capabilities are effective means for surgery for intraventricular lesions. The ventricles have a complex three-dimensionally structure, and important structures around the ventricles may causes symptoms even with slight damage. Therefore, familiarity with the ventricular anatomy and protective manipulations are important. During endoscopic observations in actual surgery, the ventricular wall is entirely covered with the ependymal tissue, limiting the visibility of landmarks. Furthermore, when distorted by the tumor, the anatomical orientation may be lost, and identifying the lesion can be difficult. In this chapter, we describe the ventricular anatomy under endoscopic observation using actual photographs and illustrations based on anatomical landmarks, in order to safely perform intraventricular surgery.
2,330,104
[Locations and Functions of Water Selective Channels from the View-Points of Cerebrospinal Fluid Distribution].
Water not only exists in the ventricles and cisterns but is also contained in the cerebral parenchyma. Water movement in most tissues has been described to be mediated by water channels since the discovery of these channels(aquaporins: AQPs). As to the intracranial situation, AQP-1 is abundantly expressed in the epithelial cells of the choroid plexus. AQP-4 is also enriched in the ependyma, endfeet of astrocytes at the blood-brain barrier, and glia limitans. AQP-4 is involved in cerebrospinal fluid(CSF)absorption, while AQP-1 is involved in CSF production. Impairment of CSF absorption through AQP-4 is considered to be caused by an inflammatory mechanism and finally leads to the development of hydrocephalus. Recently, the glymphatic system was recognized as an intracranial lymphatic system and hypothesized to be involved in CSF absorption and waste removal into the CSF. Disturbances of this glymphatic system may induce Alzheimer's disease and idiopathic normal-pressure hydrocephalus. Although the mechanism of CSF production in the epithelial cells of the choroid plexus remains to be elucidated, the existence of glycolysis leading to the facilitation of AQP-1 expression is considered a key point in CSF production.
2,330,105
[Mechanisms of Cerebrospinal Fluid Production and Absorption and Ventricular Dilatation in Hydrocephalus].
The concept of cerebrospinal fluid(CSF)production and absorption changed significantly in the early 2010s from "third circulation theory" and "classical bulk flow theory" as follows. First, CSF is mainly produced from the interstitial fluid excreted from the brain; CSF produced by the choroid plexus is important in maintaining homeostasis of the brain. Next, CSF is not absorbed in the venous sinus via the arachnoid granules, but rather in the dural lymphatic vessels. Finally, the ventricles and subarachnoid spaces have several compensatory direct CSF pathways around the attachment of the choroid plexus other than the foramina of Luschka and Magendie. Because of the compensatory direct CSF pathways, the lateral ventricles and the basal cistern are enlarged simultaneously in idiopathic normal pressure hydrocephalus(iNPH). Due to the decrease in brain volume with aging, the average total intracranial CSF volume increases from approximately 150 mL at 20 years to approximately 350 mL at 70 years, and further increases by approximately 50-100 mL to above 400 mL in patients with iNPH. CSF movement is composed of a steady flow produced by the rhythmic wavy movement of motile cilia on the ventricular surface and the dynamic pulsatile flow produced by the pulsation of the cerebral arteries or brain, respiration, and head movement. In general, this pulsatile CSF flow decreases with aging but increases at the opening of the foramen of Magendie and causes the ventricles to expand in iNPH.
2,330,106
Case Report: Ventriculoperitoneal Shunting and Radiation Therapy Treatment in a Cat With a Suspected Choroid Plexus Tumor and Hypertensive Hydrocephalus.
A 14-year-old male neutered domestic short-hair cat was presented for a history of behavioral changes and episodes of urinary retention. Neurological examination was consistent with a multifocal intracranial neuroanatomical localization, with suspected right sided lateralisation and suspected raised intracranial pressure (ICP). Brain magnetic resonance imaging (MRI) revealed an intraventricular multilobulated well-defined T2W-hyperintense and T1W-isointense, markedly contrast enhancing mass lesion within the dorsal aspect of the III ventricle extending into the left lateral ventricle, causing hypertensive obstructive hydrocephalus. A ventriculoperitoneal shunt (VPS) was placed within the left lateral ventricle, followed by a radiation therapy (RT) course of 45 Gy total dose in 18 daily fractions. Six-months post-RT, computed tomography revealed mild reduction in mass size and resolution of the hydrocephalus. The patient was neurologically normal with no medical treatment. Raised ICP causes severe clinical signs, can lead to brain ischaemia and herniation, and significantly increases anesthetic risk during RT. Placement of a VPS in cats with hypertensive obstructive hydrocephalus may allow improvement of neurological signs due to raised ICP, and therefore making the patient a more stable candidate for anesthesia and radiation therapy.
2,330,107
Hematoma expansion caused by trapped cerebrospinal fluid in subacute phase intracerebral hemorrhage: A case report.
Although hematoma expansion (HE) is caused by active bleeding in patients with intracranial hemorrhage in most cases, cerebrospinal fluid (CSF) trapped in the hematoma cavity is not a well-known cause of HE.</AbstractText>We present a case of subcortical hemorrhage in an 80-year-old woman who experienced neurological deterioration in the subacute phase because of HE caused by CSF pooling in the hematoma cavity. The patient was transferred to our hospital from a previous hospital for surgical treatment because the consciousness disturbance was likely caused by the perihematomal edema that occurred 4 days after onset. Head computed tomography (CT) at admission to our hospital showed a blend sign, and a part of the low-density area of the hematoma was enlarged compared with the CT at admission to the previous hospital. Although the hematoma was located adjacent to the lateral ventricle, no intraventricular hemorrhage was observed. Emergent hematoma evacuation was performed, and intraoperative findings indicated that the enlarged hematoma cavity was caused by CSF pooling. The patient's postoperative course was uneventful. She was transferred to a rehabilitation hospital 16 days after admission to our hospital.</AbstractText>Hematomas adjacent to the ventricle and showing a blend sign can expand in the subacute phase because of the trapped CSF.</AbstractText>Copyright: &#xa9; 2022 Surgical Neurology International.</CopyrightInformation>
2,330,108
Surgical nuances in corpus callosotomy as a palliative epilepsy surgery.
Corpus callosotomy is a well-established palliative procedure in selected patients with drug resistant epilepsy (DRE). It has a beneficial role in ameliorating generalized seizures mainly drop attacks. Here, we present some technical tips for performing callosotomy depending on the anatomical basis, to minimize craniotomy size and guard against inadvertently entering the lateral ventricles.</AbstractText>This study was a retrospective review of patients who received corpus callosotomy at our institute as a palliative epilepsy surgery. We present our experience and surgical tips with the extraventricular technique of corpus callosotomy with comparison of surgery-related complications and operative time between extraventricular and conventional techniques in selected patients with DRE.</AbstractText>Our study included 34 patients. First group of patients included 14 patients who received conventional approach, while the extraventricular approach was done in 20 patients. Extraventricular approach showed significantly lower wound complications rate of 10% compared to 78% in intraventricular approach (P</i> &lt; 0.001). Mean operative time was significantly lower in extraventricular versus conventional technique with 52 min versus 94 min, respectively (P</i> &lt; 0.001). Planned extent of corpus callosotomy resection was achieved in all our patients using both approaches.</AbstractText>The cleft of the septum pellucidum offers a natural pursuit to section corpus callosum strictly midline and completely extraventricular in well selected patients of DRE candidate for callosotomy. Performing corpus callosotomy in extraventricular approach provided better patients outcomes regarding surgery and wound-related complications when compared to conventional approach.</AbstractText>Copyright: &#xa9; 2022 Surgical Neurology International.</CopyrightInformation>
2,330,109
Decision-Making and Management in a Patient With Coexistent Colloid Cyst and Pituitary Macroadenoma: A Case Report.
The coexistence of separate and distinct primary intracranial tumors is rare. Specifically, there are no previous reports of a colloid cyst coexisting with a pituitary macroadenoma. We present the case of a 40-year-old male with a colloid cyst associated with mild enlargement of the right lateral ventricle and a coexistent pituitary macroadenoma with compression of the optic apparatus. An endoscopic endonasal transsphenoidal surgery (EETS) for resection of the pituitary mass was performed first due to the patient's complaints of acute visual changes. He then underwent a right frontal craniotomy for resection of the colloid cyst one month later. The patient recovered without residual deficits in vision, and he did not require ventricular shunting after removal of the colloid cyst. We aimed to discuss our decision-making process and the management of these coexistent lesions.
2,330,110
Arterial Baroreflex Inhibits Muscle Metaboreflex Induced Increases in Effective Arterial Elastance: Implications for Ventricular-Vascular Coupling.
The ventricular-vascular relationship assesses the efficacy of energy transferred from the left ventricle to the systemic circulation and is quantified as the ratio of effective arterial elastance to maximal left ventricular elastance. This relationship is maintained during exercise via reflex increases in cardiovascular performance raising both arterial and ventricular elastance in parallel. These changes are, in part, due to reflexes engendered by activation of metabosensitive skeletal muscle afferents-termed the muscle metaboreflex. However, in heart failure, ventricular-vascular uncoupling is apparent and muscle metaboreflex activation worsens this relationship through enhanced systemic vasoconstriction markedly increasing effective arterial elastance which is unaccompanied by substantial increases in ventricular function. This enhanced arterial vasoconstriction is, in part, due to significant reductions in cardiac performance induced by heart failure causing over-stimulation of the metaboreflex due to under perfusion of active skeletal muscle, but also as a result of reduced baroreflex buffering of the muscle metaboreflex-induced peripheral sympatho-activation. To what extent the arterial baroreflex modifies the metaboreflex-induced changes in effective arterial elastance is unknown. We investigated in chronically instrumented conscious canines if removal of baroreflex input via sino-aortic baroreceptor denervation (SAD) would significantly enhance effective arterial elastance in normal animals and whether this would be amplified after induction of heart failure. We observed that effective arterial elastance (E<sub>a</sub>), was significantly increased during muscle metaboreflex activation after SAD (0.4 &#xb1; 0.1 mmHg/mL to 1.4 &#xb1; 0.3 mmHg/mL). In heart failure, metaboreflex activation caused exaggerated increases in E<sub>a</sub> and in this setting, SAD significantly increased the rise in E<sub>a</sub> elicited by muscle metaboreflex activation (1.3 &#xb1; 0.3 mmHg/mL to 2.3 &#xb1; 0.3 mmHg/mL). Thus, we conclude that the arterial baroreflex does buffer muscle metaboreflex induced increases in E<sub>a</sub> and this buffering likely has effects on the ventricular-vascular coupling.
2,330,111
A Single Model Deep Learning Approach for Alzheimer's Disease Diagnosis.
Early and accurate diagnosis of Alzheimer's disease (AD) and its prodromal period mild cognitive impairment (MCI) is essential for the delayed disease progression and the improved quality of patients' life. The emerging computer-aided diagnostic methods that combine deep learning with structural magnetic resonance imaging (sMRI) have achieved encouraging results, but some of them are limit of issues such as data leakage, overfitting, and unexplainable diagnosis. In this research, we propose a novel end-to-end deep learning approach for automated diagnosis of AD. This approach has the following differences from the current approaches: (1) Convolutional Neural Network (CNN) models of different structures and capacities are evaluated systemically and the most suitable model is adopted for AD diagnosis; (2) A data augmentation strategy named Two-stage Random RandAugment (TRRA) is proposed to alleviate the overfitting issue caused by limited training data and to improve the classification performance in AD diagnosis; (3) An explainable method of Grad-CAM++ is introduced to generate the visually explainable heatmaps to make our model more transparent. Our approach has been evaluated on two publicly accessible datasets for two classification tasks of AD vs. cognitively normal (CN) and progressive MCI (pMCI) vs. stable MCI (sMCI). The experimental results indicate that our approach outperforms the state-of-the-art approaches, including those using multi-model and three-dimensional (3D) CNN methods. The resultant heatmaps from our approach also highlight the lateral ventricle and some regions of cortex, which have been proved to be affected by AD.
2,330,112
Resolution of Primary or Recalcitrant Chiari-Associated Syringomyelia Requires Adequate Cerebrospinal Fluid Egress from the Fourth Ventricle.
Syringomyelia is often resistant to various treatment modalities.<sup>1</sup> Chiari I malformations are associated with syringomyelia in approximately 69% of operative cases.<sup>2</sup> Failure to resolve syringomyelia after Chiari decompression is common.<sup>3</sup> The pathophysiology of Chiari-associated syringomyelia has been well studied, with Oldfield emphasizing the water-hammer mechanism, with treatment limited to bony decompression and duraplasty.<sup>4</sup> On the other hand, capacious fourth ventricular drainage is thought to be essential for syrinx resolution. Persistence or progression of the syrinx after decompression is an indication for reoperation. Direct shunting of the syrinx is associated with high failure rates.<sup>1</sup><sup>,</sup><sup>5-7</sup> The technique of shunting the fourth ventricle has been applied successfully in the pediatric population.<sup>3</sup><sup>,</sup><sup>8-10</sup> We emphasize the need to ensure outflow from the fourth ventricle in Chiari decompressions associated with syringomyelia. In revisions to treat progressive syringomyelia after failed decompression, we undertake the following steps: 1) adequate lateral bony decompression,<sup>11-13</sup> 2) lysis of scar/adhesions around the cisterna magna, 3) opening the fourth ventricle outlet by releasing any web/adhesions, 4) insertion of a shunt from the fourth ventricle to the cervical subarachnoid space, and 5) bipolar coagulation of the lateral tonsillar pia to maintain patency of cerebrospinal fluid pathways.<sup>8</sup> We favor autologous fascia or pericranium for expansile duraplasty, as the use of nonautologous materials may cause excessive scarring.<sup>14-16</sup> In this video, we demonstrate these tenets in 3 cases of Chiari-associated syringomyelia, 2 revisions and 1 primary case, with excellent resolution of the syrinx (Video 1). The patients consented to surgery and publication of images.
2,330,113
Non-invasive in vivo MRI detects long-term microstructural brain alterations related to learning and memory impairments in a model of inflammation-induced white matter injury.<Pagination><StartPage>113884</StartPage><MedlinePgn>113884</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbr.2022.113884</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0166-4328(22)00152-8</ELocationID><Abstract><AbstractText>Magnetic resonance imaging (MRI) is currently under investigation as a non-invasive tool to monitor neurodevelopmental trajectories and predict risk of cognitive deficits following white matter injury (WMI) in very preterm infants. In the present study, we evaluated the capacity of multimodal MRI (high-resolution T2-weighted imaging and diffusion tensor imaging)to assess changes following WMI and their relationship to learning and memory performance in Wistar rats as it has been demonstrated for preterm infants. Multimodal MRI performed at P31-P32 shown that animals exposed to neonatal LPS could be classified into two groups: minimal and overt injury. Animals with overt injury had significantly enlarged ventricles, hippocampal atrophy, diffusivity changes in hippocampal white and gray matter, in the striatum and the cortex. Following neonatal LPS exposure, animals presented learning and memory impairments as shown at the fear conditioning test at P36-P38. The severity of learning and memory deficits was related to increased mean diffusivity in the hippocampal region. In conclusion, non-invasive multimodal MRI (volumetric and DTI) assessed and classified the extent of injury at long-term following neonatal LPS exposure. Microstructural changes in the hippocampus at DTI were associated to learning and memory impairments. This further highlights the utility of multimodal MRI as a non-invasive quantitative biomarker following perinatal inflammation.</AbstractText><CopyrightInformation>Copyright &#xa9; 2022 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pierre</LastName><ForeName>Wyston C</ForeName><Initials>WC</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada; Department of Pharmacology, Universit&#xe9; de Montr&#xe9;al, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Erjun</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada; Institute of Biomedical Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada; Montreal Heart Institute, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Londono</LastName><ForeName>Ir&#xe8;ne</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De Leener</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Computer Engineering and Software Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada; Institute of Biomedical Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lesage</LastName><ForeName>Fr&#xe9;d&#xe9;ric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Institute of Biomedical Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada; Montreal Heart Institute, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lodygensky</LastName><ForeName>Gregory A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada; Department of Pharmacology, Universit&#xe9; de Montr&#xe9;al, Montreal, QC, Canada; Montreal Heart Institute, Montreal, QC, Canada. Electronic address: ga.lodygensky@umontreal.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>136908</GrantID><Agency>CIHR</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>04</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Behav Brain Res</MedlineTA><NlmUniqueID>8004872</NlmUniqueID><ISSNLinking>0166-4328</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001930" MajorTopicYN="Y">Brain Injuries</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056324" MajorTopicYN="N">Diffusion Tensor Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007234" MajorTopicYN="N">Infant, Premature</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008569" MajorTopicYN="N">Memory Disorders</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066127" MajorTopicYN="Y">White Matter</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diffusion tensor imaging</Keyword><Keyword MajorTopicYN="N">Fear conditioning</Keyword><Keyword MajorTopicYN="N">In vivo high-field MRI</Keyword><Keyword MajorTopicYN="N">Lipopolysaccharides</Keyword><Keyword MajorTopicYN="N">Periventricular leukomalacia</Keyword><Keyword MajorTopicYN="N">T2-weigthed imaging</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>3</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>4</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>4</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>4</Month><Day>10</Day><Hour>20</Hour><Minute>24</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35398230</ArticleId><ArticleId IdType="doi">10.1016/j.bbr.2022.113884</ArticleId><ArticleId IdType="pii">S0166-4328(22)00152-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35398036</PMID><DateRevised><Year>2022</Year><Month>05</Month><Day>31</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1552-6259</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Apr</Month><Day>07</Day></PubDate></JournalIssue><Title>The Annals of thoracic surgery</Title><ISOAbbreviation>Ann Thorac Surg</ISOAbbreviation></Journal>Plasma Exosome Hemoglobin Released During Surgery Is Associated With Cardiac&#xa0;Injury in Animal Model.
Magnetic resonance imaging (MRI) is currently under investigation as a non-invasive tool to monitor neurodevelopmental trajectories and predict risk of cognitive deficits following white matter injury (WMI) in very preterm infants. In the present study, we evaluated the capacity of multimodal MRI (high-resolution T2-weighted imaging and diffusion tensor imaging)to assess changes following WMI and their relationship to learning and memory performance in Wistar rats as it has been demonstrated for preterm infants. Multimodal MRI performed at P31-P32 shown that animals exposed to neonatal LPS could be classified into two groups: minimal and overt injury. Animals with overt injury had significantly enlarged ventricles, hippocampal atrophy, diffusivity changes in hippocampal white and gray matter, in the striatum and the cortex. Following neonatal LPS exposure, animals presented learning and memory impairments as shown at the fear conditioning test at P36-P38. The severity of learning and memory deficits was related to increased mean diffusivity in the hippocampal region. In conclusion, non-invasive multimodal MRI (volumetric and DTI) assessed and classified the extent of injury at long-term following neonatal LPS exposure. Microstructural changes in the hippocampus at DTI were associated to learning and memory impairments. This further highlights the utility of multimodal MRI as a non-invasive quantitative biomarker following perinatal inflammation.<CopyrightInformation>Copyright &#xa9; 2022 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pierre</LastName><ForeName>Wyston C</ForeName><Initials>WC</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada; Department of Pharmacology, Universit&#xe9; de Montr&#xe9;al, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Erjun</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada; Institute of Biomedical Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada; Montreal Heart Institute, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Londono</LastName><ForeName>Ir&#xe8;ne</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>De Leener</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Computer Engineering and Software Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada; Institute of Biomedical Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lesage</LastName><ForeName>Fr&#xe9;d&#xe9;ric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Institute of Biomedical Engineering, &#xc9;cole Polytechnique de Montr&#xe9;al, Montreal, QC, Canada; Montreal Heart Institute, Montreal, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lodygensky</LastName><ForeName>Gregory A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>Departments of Pediatrics, Ophthalmology and Pharmacology, CHU Sainte-Justine Research Centre, Montreal, QC, Canada; Department of Pharmacology, Universit&#xe9; de Montr&#xe9;al, Montreal, QC, Canada; Montreal Heart Institute, Montreal, QC, Canada. Electronic address: ga.lodygensky@umontreal.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>136908</GrantID><Agency>CIHR</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>04</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Behav Brain Res</MedlineTA><NlmUniqueID>8004872</NlmUniqueID><ISSNLinking>0166-4328</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001930" MajorTopicYN="Y">Brain Injuries</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056324" MajorTopicYN="N">Diffusion Tensor Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007231" MajorTopicYN="N">Infant, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007234" MajorTopicYN="N">Infant, Premature</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008569" MajorTopicYN="N">Memory Disorders</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066127" MajorTopicYN="Y">White Matter</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Diffusion tensor imaging</Keyword><Keyword MajorTopicYN="N">Fear conditioning</Keyword><Keyword MajorTopicYN="N">In vivo high-field MRI</Keyword><Keyword MajorTopicYN="N">Lipopolysaccharides</Keyword><Keyword MajorTopicYN="N">Periventricular leukomalacia</Keyword><Keyword MajorTopicYN="N">T2-weigthed imaging</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>3</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>4</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>4</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>4</Month><Day>10</Day><Hour>20</Hour><Minute>24</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35398230</ArticleId><ArticleId IdType="doi">10.1016/j.bbr.2022.113884</ArticleId><ArticleId IdType="pii">S0166-4328(22)00152-8</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35398036</PMID><DateRevised><Year>2022</Year><Month>05</Month><Day>31</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1552-6259</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Apr</Month><Day>07</Day></PubDate></JournalIssue><Title>The Annals of thoracic surgery</Title><ISOAbbreviation>Ann Thorac Surg</ISOAbbreviation></Journal><ArticleTitle>Plasma Exosome Hemoglobin Released During Surgery Is Associated With Cardiac&#xa0;Injury in Animal Model.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0003-4975(22)00483-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.athoracsur.2022.02.084</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Patients with valvular heart disease require cardiopulmonary bypass and cardiac arrest. Here, we test the hypothesis that exosomal hemoglobin formed during cardiopulmonary bypass mediates acute cardiac injury in humans and in an animal model system.<AbstractText Label="METHODS" NlmCategory="METHODS">Plasma exosomes were collected from arterial blood at baseline and 30 minutes after aortic cross-clamp release in 20 patients with primary mitral regurgitation and 7 with aortic stenosis. These exosomes were injected into Sprague-Dawley rats and studied at multiple times up to 30 days. Tissue was examined by hematoxylin and eosin stain, immunohistochemistry, transmission electron microscopy, and brain natriuretic peptide.<AbstractText Label="RESULTS" NlmCategory="RESULTS">Troponin I levels increased from 36 &#xb1; 88 ng/L to 3622 &#xb1; 3054 ng/L and correlated with exosome hemoglobin content (Spearman r&#xa0;= 0.7136, &lt; .0001, n&#xa0;= 24). Injection of exosomes isolated 30 minutes after cross-clamp release into Sprague-Dawley rats resulted in cardiomyocyte myofibrillar loss at 3 days. Transmission electron microscopy demonstrated accumulation of electron dense particles of ferritin within cardiomyocytes, in the interstitial space, and within exosomes. At 21 days after injection, there was myofibrillar and myosin breakdown, interstitial fibrosis, elevated brain natriuretic peptide, and left ventricle diastolic dysfunction measured by echocardiography/Doppler. Pericardial fluid exosomal hemoglobin content is fourfold higher than simultaneous plasma exosome hemoglobin, suggesting a cardiac source of exosomal hemoglobin.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Red blood cell and cardiac-derived exosomal hemoglobin may be involved in myocardial injury during cardiopulmonary bypass in patients with valvular heart disease.
2,330,114
Pathogenesis of posthemorrhagic hydrocephalus of prematurity: New horizons.
Posthemorrhagic hydrocephalus of prematurity (PHHP) remains a vexing problem for patients, their families, and the healthcare system. The complexity of the pathogenesis of PHHP also presents a unique challenge within the fields of neonatology, neurology and neurosurgery. Here we focus on pathogenesis of PHHP and its impact on the development of CSF dynamics including choroid plexus, ependymal motile cilia and glymphatic system. PHHP is contrasted with infantile hydrocephalus from other etiologies, and with other types of posthemorrhagic hydrocephalus that occur later in life. The important concept that distinguishing ventricular volume from brain health and function is highlighted. The influence of the pathogenesis of PHHP on current interventions is reviewed, with particular emphasis on how the unique pathogenesis of PHHP contributes to the high rate of failure of current existing interventions. Finally, we discuss emerging interventions. A thorough understanding of the pathogenesis of PHHP is essential to developing effective non-surgical therapeutics to prevent the transformation from severe IVH to PHHP.
2,330,115
Reproducibility of Systolic Strain in Mice Using Cardiac Magnetic Resonance Feature Tracking of Black-Blood Cine Images.
Mouse models are widely utilized to enhance our understanding of cardiac disease. The goal of this study is to investigate the reproducibility of strain parameters that were measured in mice using cardiac magnetic resonance (CMR) feature-tracking (CMR42, Canada).</AbstractText>We retrospectively analyzed black-blood CMR datasets from thirteen C57BL/6 B6.SJL-CD45.1 mice (N&#xa0;=&#xa0;10 female, N&#xa0;=&#xa0;3 male) that were imaged previously. The circumferential, longitudinal, and radial (Ecc</sub>, Ell</sub>, and Err</sub>, respectively) parameters of strain were measured in the mid-ventricular region of the left ventricle. Intraobserver and interobserver reproducibility were assessed for both the end-systolic (ES) and peak strain.</AbstractText>The ES strain had larger intraclass correlation coefficient (ICC) values when compared to peak strain, for both the intraobserver and interobserver reproducibility studies. Specifically, the intraobserver study showed excellent reproducibility for all three ES strain parameters, namely, Ecc</sub> (ICC 0.95, 95% CI 0.83-0.98), Ell</sub> (ICC 0.90, 95% CI 0.59-0.97), and Err</sub> (ICC 0.92, 95% CI 0.73-0.97). This was also the case for the interobserver study, namely, Ecc</sub> (ICC 0.92, 95% CI 0.60-0.98), Ell</sub> (ICC 0.76, 95% CI 0.33-0.93), and Err</sub> (ICC 0.93, 95% CI 0.68-0.98). Additionally, the coefficient of variation values were all &lt;&#xa0;10%.</AbstractText>The results of this preliminary study showed excellent reproducibility for all ES strain parameters, with good to excellent reproducibility for the peak strain parameters. Moreover, all ES strain parameters had larger ICC values than the peak strain. In general, these results imply that feature-tracking with CMR42 software and black-blood cine images can be reliably used to assess strain patterns in mice.</AbstractText>&#xa9; 2022. The Author(s) under exclusive licence to Biomedical Engineering Society.</CopyrightInformation>
2,330,116
A Special Approach for Stereotactic Radiofrequency Thermocoagulation of Hypothalamic Hamartomas With Bilateral Attachments to the Hypothalamus: The Transthird Ventricular Approach to the Contralateral Attachment.
Disconnection surgery for the treatment of epileptic hypothalamic hamartomas (HHs) is strategically difficult in cases with complex-shaped HHs, especially with bilateral hypothalamic attachments, despite its effectiveness.</AbstractText>To evaluate the feasibility of a new approach for stereotactic radiofrequency thermocoagulation (SRT) using penetration of the third ventricle (SRT-TT) aiming to disconnect bilateral hypothalamic attachments in a single-staged, unilateral procedure.</AbstractText>Ninety patients (median age at surgery, 5.0 years) who had HHs with bilateral hypothalamic attachments and were followed for at least 1 year after their last SRT were retrospectively reviewed.</AbstractText>Thirty-three patients underwent SRT-TT as initial surgery. Of the 58 patients after mid-2013 when SRT-TT was introduced, 33 underwent SRT-TT and 12 (20.7%) required reoperation (ReSRT), whereas 20 of 57 patients (35.1%) without SRT-TT underwent reoperation. Reoperation was required in significantly fewer patients after mid-2013 (n = 12 of 58, 20.7%) than before mid-2013 (n = 15 of 32, 46.9%) ( P = .01). Final seizure freedoms were not different between before and after mid-2013 (gelastic seizure freedom, n = 30 [93.8%] vs n = 49 [84.5%] and other types of seizure freedom, n = 21 of 31 [67.7%] vs n = 32 of 38 [84.2%]). Persistent complications were less in SRT-TT than in ReSRT using the bilateral approach, but not significantly. However, hormonal replacement was required significantly more often in ReSRT using the bilateral approach (4 of 9, 44.4%) than in SRT-TT (3 of 32, 9.4%) ( P = .01).</AbstractText>SRT-TT enabled disconnection of bilateral attachments of HHs in a single-staged procedure, which reduced the additional invasiveness of reoperation. Moreover, SRT-TT reduced damage to the contralateral hypothalamus, with fewer endocrinological complications than the bilateral approach.</AbstractText>Copyright &#xa9; Congress of Neurological Surgeons 2022. All rights reserved.</CopyrightInformation>
2,330,117
The Presence of the Temporal Horn Exacerbates the Vulnerability of Hippocampus During Head Impacts.
Hippocampal injury is common in traumatic brain injury (TBI) patients, but the underlying pathogenesis remains elusive. In this study, we hypothesize that the presence of the adjacent fluid-containing temporal horn exacerbates the biomechanical vulnerability of the hippocampus. Two finite element models of the human head were used to investigate this hypothesis, one with and one without the temporal horn, and both including a detailed hippocampal subfield delineation. A fluid-structure interaction coupling approach was used to simulate the brain-ventricle interface, in which the intraventricular cerebrospinal fluid was represented by an arbitrary Lagrangian-Eulerian multi-material formation to account for its fluid behavior. By comparing the response of these two models under identical loadings, the model that included the temporal horn predicted increased magnitudes of strain and strain rate in the hippocampus with respect to its counterpart without the temporal horn. This specifically affected cornu ammonis (CA) 1 (CA1), CA2/3, hippocampal tail, subiculum, and the adjacent amygdala and ventral diencephalon. These computational results suggest that the presence of the temporal horn exacerbate the vulnerability of the hippocampus, highlighting the mechanobiological dependency of the hippocampus on the temporal horn.
2,330,118
High Periventricular T1 Relaxation Times Predict Gait Improvement After Spinal Tap in Patients with Idiopathic Normal Pressure Hydrocephalus.
The diagnosis of idiopathic normal pressure hydrocephalus (iNPH) can be challenging. Aim of this study was to use a&#xa0;novel T1 mapping method to enrich the diagnostic work-up of patients with suspected iNPH.</AbstractText>Using 3T magnetic resonance imaging (MRI) we prospectively evaluated rapid high-resolution T1&#xa0;mapping at 0.5&#x202f;mm resolution and 4&#x202f;s acquisition time in 15&#xa0;patients with suspected iNPH and 8&#xa0;age-matched, healthy controls. T1&#xa0;mapping in axial sections of the cerebrum, clinical and neuropsychological testing were performed prior to and after cerebrospinal fluid tap test (CSF-TT). T1&#xa0;relaxation times were measured in 5&#xa0;predefined periventricular regions.</AbstractText>All 15&#xa0;patients with suspected iNPH showed gait impairment, 13 (86.6%) showed signs of cognitive impairment and 8 (53.3%) patients had urinary incontinence. Gait improvement was noted in 12&#xa0;patients (80%) after CSF-TT. T1&#xa0;relaxation times in all periventricular regions were elevated in patients with iNPH compared to controls with the most pronounced differences in the anterior (1006&#x202f;&#xb1;&#x2009;93&#x202f;ms vs. 911&#x202f;&#xb1;&#x2009;77&#x202f;ms; p&#x202f;=&#x2009;0.023) and posterior horns (983&#x202f;&#xb1;&#x2009;103&#x202f;ms vs. 893&#x202f;&#xb1;&#x2009;68&#x202f;ms; p&#x202f;=&#x2009;0.037) of the lateral ventricles. Montreal cognitive assessment (MoCA) scores at baseline were negatively correlated with T1&#xa0;relaxation times (r&#x202f;&lt;&#x2009;-0.5, p&#x202f;&lt;&#x2009;0.02). Higher T1&#xa0;relaxation times were significantly correlated with an improvement of the 3&#x2011;m timed up and go test (r&#x202f;&gt;&#x2009;0.6 and p&#x202f;&lt;&#x2009;0.03) after CSF-TT.</AbstractText>In iNPH-patients, periventricular T1&#xa0;relaxation times are increased compared to age-matched controls and predict gait improvement after CSF-TT. T1&#xa0;mapping might enrich iNPH work-up and might be useful to indicate permanent shunting.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
2,330,119
Anatomical Limitation of Posterior Spinal Myelotomy for Intramedullary Hemorrhage Associated with Ependymoma or Cavernous Malformation of the High Cervical Spine.
Spinal intramedullary tumors such as ependymoma or vascular lesions such as cavernous malformation are often at risk of intramedullary hemorrhage. Surgical procedures involving the high cervical spinal cord are often challenging. This technical note included four patients who presented with acute, subacute, or gradual onset of spinal cord dysfunction associated with intramedullary hemorrhage at the C1 or C1/2 level of the high cervical spine. The mean age was 46.3 years (16-74 years). All patients underwent posterior spinal cord myelotomy of the posterior median sulcus or posterolateral sulcus. It was not to exceed the caudal opening of the fourth ventricle (foramen of Magendie) and was assumed to be as high as the caudal medulla oblongata. Total removal of the intramedullary ependymoma or cavernous malformation occurred in three of four cases, and the remaining case had subtotal removal of the ependymoma. None of the patients showed postoperative deterioration of the neurological condition. Pathological examination of all cases revealed intramedullary hemorrhage was associated with ependymoma or cavernous malformation. Posterior spinal myelotomy should be limited to the caudal opening of the fourth ventricle (foramen of Magendie), that is the caudal medulla oblongata, to avoid the significant deterioration after surgery.
2,330,120
MSC Transplantation Attenuates Inflammation, Prevents Endothelial Damage and Enhances the Angiogenic Potency of Endogenous MSCs in a Model of Pulmonary Arterial Hypertension.
Pulmonary arterial hypertension (PAH) is a progressive and fatal pulmonary vascular disease initiated by endothelial dysfunction. Mesenchymal stromal cells (MSCs) have been shown to ameliorate PAH in various rodent models; however, these models do not recapitulate all the histopathological alterations observed in human PAH. Broiler chickens (Gallus gallus</i>) can develop PAH spontaneously with neointimal and plexogenic arteriopathy strikingly similar to that in human patients. Herein, we examined the protective effects of MSC transplantation on the development of PAH in this avian model.</AbstractText>Mixed-sex broilers at 15 d of age were received 2&#xd7;106</sup> MSCs or PBS intravenously. One day later, birds were exposed to cool temperature with excessive salt in their drinking water to induce PAH. Cumulative morbidity from PAH and right-to-left ventricle ratio were recorded. Lung histologic features were evaluated for the presence of endothelial damage, endothelial proliferation and plexiform lesions. Expression of proinflammatory mediators and angiogenic factors in the lung was detected. Matrigel tube formation assay was performed to determine the angiogenic potential of endogenous MSCs.</AbstractText>MSC administration reduced cumulative PAH morbidity and attenuated endothelial damage, plexiform lesions and production of inflammatory mediators in the lungs. No significant difference in the expression of paracrine angiogenic factors including VEGF-A and TGF-&#x3b2; was determined between groups, suggesting that they are not essential for the beneficial effect of MSC transplantation. Interestingly, the endogenous MSCs from birds receiving MSC transplantation demonstrated endothelial differentiatial capacity in vitro whereas those from the mock birds did not.</AbstractText>Our results support the therapeutic use of MSC transplantation for PAH treatment and suggest that exogenous MSCs produce beneficial effects through modulating inflammation and endogenous MSC-mediated vascular repair.</AbstractText>&#xa9; 2022 Shao et al.</CopyrightInformation>
2,330,121
[Third ventricle width measured by transcranial ultrasound and its diagnostic value in patients with Alzheimer's disease].
<b>Objective:</b> To explore the diagnostic value of third ventricle width (TVW) measured by transcranial ultrasound (TCS) in the clinical diagnosis of Alzheimer's disease (AD) by analyzing and comparing the image characteristics of TVW in AD patients and healthy controls, and its correlation with cranial magnetic resonance medial temporal lobe atrophy (MTA) visual score and neuropsychological characteristics. <b>Methods:</b> TCS examination, MTA score and neuropsychological tests were performed in 39 confirmed AD and 41 normal controls from the Second Affiliated Hospital of Soochow University between January and July 2021. The correlation of TVW with MTA score and neuropsychological characteristics was analyzed and compared between the two groups. <b>Results:</b> A total of thirty-nine AD patients were enrolled, with 28 males and 11 females, aged (73&#xb1;9) years, including 18 mild, 20 moderate, and 1 severe AD patient. Meanwhile, 41 healthy controls were also included, with 24 males and 17 females, aged (69&#xb1;6) years old. TVW in AD patients was significantly wider than that in normal controls [0.76(0.66, 0.87) cm vs 0.50(0.44, 0.56) cm, <i>P</i>&lt;0.001]. In neuropsychological tests, compared with normal controls, AD patients showed impaired performances in several cognitive functions, and there were statistically significant differences in delayed memory [0(0, 0) vs 4.0(4.0, 5.0), <i>P</i>&lt;0.001], naming [2.0(1.0, 3.0) vs 3.0(2.0, 3.0), <i>P</i>&lt;0.001], executive function [2.0(2.0, 3.0) vs 3.0(2.5, 3.0), <i>P</i>&lt;0.001], language [0.0(0.0, 2.0) vs 3.0(2.0, 3.0), <i>P</i>&lt;0.001] and other aspects between AD patients and normal controls (all <i>P</i>&lt;0.05). TVW was negatively correlated with immediate memory (<i>r</i>=-0.339, <i>P</i>=0.035), delayed recall (<i>r</i>=-0.523, <i>P</i>&lt;0.001), attention and computing power (<i>r</i>=-0.409, <i>P</i>=0.045), visual space and executive function (<i>r</i>=-0.333, <i>P</i>=0.039), but positively correlated with the atrophy of the medial temporal lobe (<i>r</i>= 0.552, <i>P</i>&lt;0.001). <b>Conclusions:</b> TCS can be used to measure TVW in AD patients. When combined with MTA score and neuropsychological tests, it can provide a reliable objective basis for the clinical diagnosis of AD.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>S W</ForeName><Initials>SW</Initials><AffiliationInfo><Affiliation>Department of Neurology, the Second Affiliated Hospital of Soochow University, Suzhou 215004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xie</LastName><ForeName>W Y</ForeName><Initials>WY</Initials><AffiliationInfo><Affiliation>Department of Neurology, the Second Affiliated Hospital of Soochow University, Suzhou 215004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Y C</ForeName><Initials>YC</Initials><AffiliationInfo><Affiliation>Department of Ultrasound, the Second Affiliated Hospital of Soochow University, Suzhou 215004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>J T</ForeName><Initials>JT</Initials><AffiliationInfo><Affiliation>Department of Medical Imaging, the Second Affiliated Hospital of Soochow University, Suzhou 215004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>C F</ForeName><Initials>CF</Initials><AffiliationInfo><Affiliation>Department of Neurology, the Second Affiliated Hospital of Soochow University, Suzhou 215004, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>H</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neurology, the Second Affiliated Hospital of Soochow University, Suzhou 215004, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Yi Xue Za Zhi</MedlineTA><NlmUniqueID>7511141</NlmUniqueID><ISSNLinking>0376-2491</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="Y">Alzheimer Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001284" MajorTopicYN="N">Atrophy</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009483" MajorTopicYN="N">Neuropsychological Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020542" MajorTopicYN="Y">Third Ventricle</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>&#x76ee;&#x7684;&#xff1a;</b> &#x901a;&#x8fc7;&#x5206;&#x6790;&#x6bd4;&#x8f83;&#x963f;&#x5c14;&#x8328;&#x6d77;&#x9ed8;&#x75c5;&#xff08;AD&#xff09;&#x60a3;&#x8005;&#x4e0e;&#x5065;&#x5eb7;&#x5bf9;&#x7167;&#x8005;&#x7ecf;&#x9885;&#x8d85;&#x58f0;&#xff08;TCS&#xff09;&#x6d4b;&#x91cf;&#x7b2c;&#x4e09;&#x8111;&#x5ba4;&#x5bbd;&#x5ea6;&#xff08;TVW&#xff09;&#x56fe;&#x50cf;&#x7279;&#x70b9;&#x3001;&#x53ca;&#x5176;&#x4e0e;&#x5934;&#x9885;&#x78c1;&#x5171;&#x632f;&#x989e;&#x53f6;&#x5185;&#x4fa7;&#x840e;&#x7f29;&#xff08;MTA&#xff09;&#x89c6;&#x89c9;&#x8bc4;&#x5206;&#x3001;&#x795e;&#x7ecf;&#x5fc3;&#x7406;&#x5b66;&#x7279;&#x5f81;&#x7684;&#x76f8;&#x5173;&#x6027;&#xff0c;&#x63a2;&#x8ba8;TCS&#x6280;&#x672f;&#x5728;AD&#x4e34;&#x5e8a;&#x8bca;&#x65ad;&#x5e94;&#x7528;&#x4e2d;&#x7684;&#x4ef7;&#x503c;&#x3002; <b>&#x65b9;&#x6cd5;&#xff1a;</b> &#x7eb3;&#x5165;2021&#x5e74;1&#x2014;7&#x6708;&#x5728;&#x82cf;&#x5dde;&#x5927;&#x5b66;&#x9644;&#x5c5e;&#x7b2c;&#x4e8c;&#x533b;&#x9662;&#x795e;&#x7ecf;&#x5185;&#x79d1;&#x8bb0;&#x5fc6;&#x969c;&#x788d;&#x95e8;&#x8bca;&#x786e;&#x8bca;&#x7684;39&#x4f8b;AD&#x60a3;&#x8005;&#x53ca;41&#x540d;&#x5065;&#x5eb7;&#x5bf9;&#x7167;&#x8005;&#xff0c;&#x8fdb;&#x884c;TCS&#x68c0;&#x67e5;&#x3001;MTA&#x8bc4;&#x5206;&#x3001;&#x795e;&#x7ecf;&#x5fc3;&#x7406;&#x5b66;&#x6d4b;&#x8bd5;&#xff0c;&#x5206;&#x6790;&#x6bd4;&#x8f83;&#x4e24;&#x7ec4;TVW&#x5dee;&#x5f02;&#x3001;&#x53ca;&#x5176;&#x4e0e;MTA&#x8bc4;&#x5206;&#x3001;&#x795e;&#x7ecf;&#x5fc3;&#x7406;&#x5b66;&#x7279;&#x5f81;&#x4e4b;&#x95f4;&#x7684;&#x76f8;&#x5173;&#x6027;&#x3002; <b>&#x7ed3;&#x679c;&#xff1a;</b> 39&#x4f8b;AD&#x60a3;&#x8005;&#xff0c;&#x7537;28&#x4f8b;&#x3001;&#x5973;11&#x4f8b;&#xff0c;&#x5e74;&#x9f84;&#xff08;73&#xb1;9&#xff09;&#x5c81;&#xff0c;&#x8f7b;&#x5ea6;AD&#x60a3;&#x8005;18&#x4f8b;&#xff0c;&#x4e2d;&#x5ea6;AD&#x60a3;&#x8005;20&#x4f8b;&#xff0c;&#x91cd;&#x5ea6;AD&#x60a3;&#x8005;1&#x4f8b;&#xff1b;41&#x540d;&#x5065;&#x5eb7;&#x5bf9;&#x7167;&#x8005;&#xff0c;&#x7537;24&#x540d;&#x3001;&#x5973;17&#x540d;&#xff0c;&#x5e74;&#x9f84;&#xff08;69&#xb1;6&#xff09;&#x5c81;&#x3002;&#x4e0e;&#x5065;&#x5eb7;&#x5bf9;&#x7167;&#x7ec4;&#x76f8;&#x6bd4;&#xff0c;AD&#x7ec4;TVW&#x66f4;&#x5bbd;&#xff3b;0.76&#xff08;0.66&#xff0c;0.87&#xff09;cm&#x6bd4;0.50&#xff08;0.44&#xff0c;0.56&#xff09;cm&#xff0c;<i>P</i>&lt;0.001&#xff3d;&#x3002;&#x795e;&#x7ecf;&#x5fc3;&#x7406;&#x5b66;&#x6d4b;&#x8bd5;&#x4e2d;&#xff0c;AD&#x60a3;&#x8005;&#x591a;&#x4e2a;&#x8ba4;&#x77e5;&#x529f;&#x80fd;&#x9886;&#x57df;&#x53d7;&#x635f;&#xff0c;&#x5982;&#x5ef6;&#x8fdf;&#x8bb0;&#x5fc6;&#xff3b;0&#xff08;0&#xff0c;0&#xff09;&#x5206;&#x6bd4;4.0&#xff08;4.0&#xff0c;5.0&#xff09;&#x5206;&#xff0c;<i>P</i>&lt;0.001&#xff3d;&#x3001;&#x547d;&#x540d;&#xff3b;2.0&#xff08;1.0&#xff0c;3.0&#xff09;&#x5206;&#x6bd4;3.0&#xff08;2.0&#xff0c;3.0&#xff09;&#x5206;&#xff0c;<i>P</i>&lt;0.001&#xff3d;&#x3001;&#x6267;&#x884c;&#x529f;&#x80fd;&#xff3b;2.0&#xff08;2.0&#xff0c;3.0&#xff09;&#x5206;&#x6bd4;3.0&#xff08;2.5&#xff0c;3.0&#xff09;&#x5206;&#xff0c;<i>P</i>&lt;0.001&#xff3d;&#x3001;&#x8bed;&#x8a00;&#xff3b;0.0&#xff08;0.0&#xff0c;2.0&#xff09;&#x5206;&#x6bd4;3.0&#xff08;2.0&#xff0c;3.0&#xff09;&#x5206;&#xff0c;<i>P</i>&lt;0.001&#xff3d;&#x7b49;&#x65b9;&#x9762;&#x4e0e;&#x5065;&#x5eb7;&#x5bf9;&#x7167;&#x8005;&#x6bd4;&#x8f83;&#xff0c;&#x5dee;&#x5f02;&#x5747;&#x6709;&#x7edf;&#x8ba1;&#x5b66;&#x610f;&#x4e49;&#x3002;AD&#x7ec4;TVW&#x589e;&#x5bbd;&#x4e0e;&#x5373;&#x523b;&#x8bb0;&#x5fc6;&#xff08;<i>r</i>=-0.339&#xff0c;<i>P</i>=0.035&#xff09;&#x3001;&#x5ef6;&#x8fdf;&#x8bb0;&#x5fc6;&#xff08;<i>r</i>=-0.523&#xff0c;<i>P</i>&lt;0.001&#xff09;&#x3001;&#x6ce8;&#x610f;&#x529b;&#x4e0e;&#x8ba1;&#x7b97;&#x529b;&#xff08;<i>r</i>=-0.409&#xff0c;<i>P</i>=0.045&#xff09;&#x3001;&#x89c6;&#x7a7a;&#x95f4;&#x4e0e;&#x6267;&#x884c;&#x529f;&#x80fd;&#xff08;<i>r</i>=-0.333&#xff0c;<i>P</i>=0.039&#xff09;&#x7b49;&#x5747;&#x5448;&#x8d1f;&#x76f8;&#x5173;&#xff0c;&#x4e14;TVW&#x4e0e;MTA&#x8bc4;&#x5206;&#xff08;<i>r</i>= 0.552&#xff0c;<i>P</i>&lt;0.001&#xff09;&#x5448;&#x660e;&#x663e;&#x6b63;&#x76f8;&#x5173;&#x3002; <b>&#x7ed3;&#x8bba;&#xff1a;</b> &#x8fd0;&#x7528;TCS&#x6d4b;&#x91cf;AD&#x60a3;&#x8005;TVW&#xff0c;&#x5e76;&#x7ed3;&#x5408;MTA&#x8bc4;&#x5206;&#x3001;&#x795e;&#x7ecf;&#x5fc3;&#x7406;&#x5b66;&#x6d4b;&#x8bd5;&#xff0c;&#x53ef;&#x4e3a;AD&#x4e34;&#x5e8a;&#x8bca;&#x65ad;&#x63d0;&#x4f9b;&#x8f83;&#x4e3a;&#x53ef;&#x9760;&#x7684;&#x5ba2;&#x89c2;&#x4f9d;&#x636e;&#x3002;.
2,330,122
GnRH and the photoperiodic control of seasonal reproduction: Delegating the task to kisspeptin and RFRP-3.
Synchronization of mammalian breeding activity to the annual change of photoperiod and environmental conditions is of the utmost importance for individual survival and species perpetuation. Subsequent to the early 1960s, when the central role of melatonin in this adaptive process was demonstrated, our comprehension of the mechanisms through which light regulates gonadal activity has increased considerably. The current model for the photoperiodic neuroendocrine system points to pivotal roles for the melatonin-sensitive pars tuberalis (PT) and its seasonally-regulated production of thyroid-stimulating hormone (TSH), as well as for TSH-sensitive hypothalamic tanycytes, radial glia-like cells located in the basal part of the third ventricle. Tanycytes respond to TSH through increased expression of thyroid hormone (TH) deiodinase 2 (Dio2), which leads to heightened production of intrahypothalamic triiodothyronine (T3) during longer days of spring and summer. There is strong evidence that this local, long-day driven, increase in T3 links melatonin input at the PT to gonadotropin-releasing hormone (GnRH) output, to align breeding with the seasons. The mechanism(s) through which T3 impinges upon GnRH remain(s) unclear. However, two distinct neuronal populations of the medio-basal hypothalamus, which express the (Arg)(Phe)-amide peptides kisspeptin and RFamide-related peptide-3, appear to be well-positioned to relay this seasonal T3 message towards GnRH neurons. Here, we summarize our current understanding of the cellular, molecular and neuroendocrine players, which keep track of photoperiod and ultimately govern GnRH output and seasonal breeding.
2,330,123
Clinical efficacy and safety of neuroendoscopic surgery for severe thalamic hemorrhage with ventricle encroachment.
To summarize and analyze the clinical efficacy and safety of neuroendoscopic surgery (NES) in the treatment of patients for severe thalamic hemorrhage with ventricle encroachment (THVE). Eighty-three patients with severe THVE were treated in the Neurosurgery Department of Anqing Hospital Affiliated to Anhui Medical University from July 2019 to August 2021. Our study was approved by the ethics committee. The patients were randomly divided into NES group and extraventricular drainage (EVD) group. The hospital stay, Glasgow coma scale (GCS) scores on the 1st and 14th days postoperatively, the incidence of intracranial infections, and the clearance of postoperative hematomas were compared and analyzed between the two groups. The patients had follow-up evaluations 6&#xa0;months postoperatively. The prognosis was evaluated based on the activity of daily living (ADL) score. A head CT or MRI was obtained to determine whether there was hydrocephalus, cerebral infarction, or other related complications. Eighty-three patients were randomly divided into 41 cases of NES group and 42 cases of EVD group. The length of postoperative hospital stay was 17.42&#x2009;&#xb1;&#x2009;1.53&#xa0;days, the GCS scores were 6.56&#x2009;&#xb1;&#x2009;0.21, and 10.83&#x2009;&#xb1;&#x2009;0.36 on days 1 and 14, respectively; intracranial infections occurred in 3 patients (7.31%) and the hematoma clearance rate was 83.6&#x2009;&#xb1;&#x2009;5.18% in the NES group, all of which were significantly better than the EVD group (P&#x2009;&lt;&#x2009;0.05). After 6&#xa0;months of follow-up, 28 patients (68.29%) had a good prognosis, 5 patients (12.19%) died, and 4 patients (9.75%) had hydrocephalus in the NES group. In the EVD group, the prognosis was good in 15 patients (35.71%), 12 patients (28.57%) died, and 17 patients (40.47%) had hydrocephalus. The prognosis, mortality rate, and incidence of hydrocephalus in the NES group were significantly better than the EVD group (P&#x2009;&lt;&#x2009;0.05). Compared to traditional EVD, NES for severe THVE had a higher hematoma clearance rate, and fewer intracranial infections and patients with hydrocephalus, which together improve the clinical prognosis and is thus recommended for clinical use.
2,330,124
Xanthogranulomatous Colloid Cyst in a 13-Year-Old Boy: A Case Report and Surgical Implications.
Colloid cysts are relatively uncommon lesions in the pediatric population. The xanthogranulomatous (XG) variant is very rare with less than 30 reported cases.</AbstractText>In this report, the patient was a 13-year-old boy who presented with transient episodes of headache with blurring of vision. His MRI brain showed a T2 hyperintense well-defined cystic lesion, with an eccentrically located T2 hypointense partially enhancing nodule, at the foramen of Monro. He underwent middle frontal gyrus transcortical, transchoroidal gross total excision of the cyst. The histopathology of the lesion revealed an XG colloid cyst. The patient recovered well from the procedure and was relieved of the symptoms.</AbstractText>XG colloid cyst may present with altered radiological features compared to the normal variant. This can pose a diagnostic dilemma, and it is important to differentiate it from a craniopharyngioma or a parasitic cyst, as in our case. When considered preoperatively, surgeons should be conscious to review their surgical strategies. Stereotactic aspiration of the XG cyst should be avoided as contents are thicker and heterogeneous than the usual. The spillage of cyst contents should be prevented. Also, the XG cysts are likely to have a poor cyst-fornix or -choroid plexus interface due to inflammation limiting complete resection.</AbstractText>&#xa9; 2022 S. Karger AG, Basel.</CopyrightInformation>
2,330,125
Two-dimensional mapping of the ultrasonic attenuation and speed of sound in brain.
Brain is inhomogeneous due to its composition of different tissue types (gray and white matter), anatomical structures (e.g. thalamus and cerebellum), and cavities in the brain (ventricles). These inhomogeneities lead to spatial variations in the ultrasonic properties of the organ. The goal of this study is to characterize the spatial variation of the speed of ultrasound and frequency slope of attenuation in fixed sheep brain. 1-cm-thick slices of tissue from the coronal, sagittal and transverse cardinal planes were prepared from 12 brains. Ultrasonic measurements were performed using broadband transducers with center frequencies of 3.5, 5.0, 7.5 and 10&#xa0;MHz. By mechanically scanning the transducers over the specimens, two-dimensional maps of the speed of sound (SOS) and frequency slope of attenuation (FSA) were produced. Measured values for the spatial mean and standard deviation of FSA ranged between 0.59 and 0.81&#xa0;dB/cm&#xb7;MHz and 0.29-0.60&#xa0;dB/cm&#xb7;MHz, respectively, depending on the specimen and transducer frequency. Measured values for the spatial mean and standard deviation of SOS ranged from 1532-1541&#xa0;m/s and 10-14&#xa0;m/s, respectively. Detailed, two-dimensional maps of FSA and SOS were produced, representing the first such characterization of the spatial variation of the ultrasonic properties of normal mammalian brain.
2,330,126
Ventriculoperitoneal Shunt Failure Due to Distal Peritoneal Catheter Kinking.
BACKGROUND Hydrocephalus is a common condition associated with high morbidity and mortality rates. Despite advancements in shunt systems and valve designs, complications associated with ventriculoperitoneal (VP) shunts are steadily recognized and reported in the literature. Here, we present an unusual case of VP shunt failure due to catheter kinking at the site of the slits in the distal peritoneal catheter. CASE REPORT A 30-year-old woman with type I Chiari malformation, prior suboccipital craniectomy, and shunted hydrocephalus with prior revisions presented with 2 months of progressive, low-pressure headaches. Shunt series X-rays demonstrated kinking of the distal peritoneal catheter. A computed tomography (CT) scan showed interval enlargement of her ventricles concerning for shunt failure, which prompted return to the operating room. During shunt revision, her valve was nonfunctioning with loss of resistance and her distal catheter was kinked at the most proximal peritoneal slit. Postoperative shunt series X-rays demonstrated an intact shunt system without kinking or discontinuity and a CT of her head showed interval decease in the caliber of her ventricles. CONCLUSIONS Distal peritoneal catheter kinking at the site of slits is an unusual complication of VP shunts and should be considered. Surgeons should add this possibility to the differential diagnosis of shunt malfunction when an imaging irregularity is identified in the peritoneal catheter.
2,330,127
Three-dimensional QCA-based vessel fractional flow reserve (vFFR) in Heart Team decision-making: a multicentre, retrospective, cohort study.<Pagination><StartPage>e054202</StartPage><MedlinePgn>e054202</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">e054202</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1136/bmjopen-2021-054202</ELocationID><Abstract><AbstractText Label="OBJECTIVES">To evaluate the feasibility of three-vessel three-dimensional (3D) quantitative coronary angiography (QCA)-based fractional flow reserve (FFR) computation in patients discussed within the Heart Team in whom the treatment decision was based on angiography alone, and to evaluate the concordance between 3D QCA-based vessel FFR (vFFR)-confirmed functional lesion significance and revascularisation strategy as proposed by the Heart Team.</AbstractText><AbstractText Label="DESIGN">Retrospective, cohort.</AbstractText><AbstractText Label="SETTING">3D QCA-based FFR indices have not yet been evaluated in the context of Heart Team decision-making; consecutive patients from six institutions were screened for eligibility and three-vessel vFFR was computed by blinded analysts.</AbstractText><AbstractText Label="PARTICIPANTS">Consecutive patients with chronic coronary syndrome or unstable angina referred for Heart Team consultation. Exclusion criteria involved: presentation with acute myocardial infarction (MI), significant valve disease, left ventricle ejection fraction &lt;30%, inadequate quality of angiogram precluding vFFR computation in all three epicardial coronary arteries (ie, absence of a minimum of two angiographic projections with views of at least 30&#xb0; apart, substantial foreshortening/overlap of the vessel, poor contrast medium injection, ostial lesions, chronic total occlusions).</AbstractText><AbstractText Label="PRIMARY AND SECONDARY OUTCOME MEASURES">Discordance between vFFR-confirmed lesion significance and revascularisation was assessed as the primary outcome measure. Rates of major adverse cardiac events (MACE) defined as cardiac death, MI and clinically driven revascularisation were reported.</AbstractText><AbstractText Label="RESULTS">Of a total of 1003 patients were screened for eligibility, 416 patients (age 65.6&#xb1;10.6, 71.2% male, 53% stable angina) were included. The most important reason for screening failure was insufficient quality of the angiogram (43%). Discordance between vFFR confirmed lesion significance and revascularisation was found in 124/416 patients (29.8%) corresponding to 149 vessels (46/149 vessels (30.9%) were reclassified as significant and 103/149 vessels (69.1%) as non-significant by vFFR). Over a median of 962 days, the cumulative incidence of MACE was 29.7% versus 18.5% in discordant versus concordant patients (p=0.031).</AbstractText><AbstractText Label="CONCLUSIONS">vFFR computation is feasible in around 40% of the patients referred for Heart Team discussion, a limitation that is mostly based on insufficient quality of the angiogram. Three vessel vFFR screening indicated discordance between vFFR confirmed lesion significance and revascularisation in 29.8% of the patients.</AbstractText><CopyrightInformation>&#xa9; Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tomaniak</LastName><ForeName>Mariusz</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0003-0966-3313</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>First Department of Cardiology, Medical University of Warsaw, Warsaw, Poland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Masdjedi</LastName><ForeName>Kaneshka</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Neleman</LastName><ForeName>Tara</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kucuk</LastName><ForeName>Ibrahim T</ForeName><Initials>IT</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vermaire</LastName><ForeName>Alise</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Zandvoort</LastName><ForeName>Laurens J C</ForeName><Initials>LJC</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Van Boven</LastName><ForeName>Nick</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>van Dalen</LastName><ForeName>Bas M</ForeName><Initials>BM</Initials><AffiliationInfo><Affiliation>Sint Franciscus Gasthuis &amp; Vlietland Hospital, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soei</LastName><ForeName>Loe Kie</ForeName><Initials>LK</Initials><AffiliationInfo><Affiliation>Sint Franciscus Gasthuis &amp; Vlietland Hospital, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>den Dekker</LastName><ForeName>Wijnand K</ForeName><Initials>WK</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kardys</LastName><ForeName>Isabella</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wilschut</LastName><ForeName>Jeroen M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Diletti</LastName><ForeName>Roberto</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zijlstra</LastName><ForeName>Felix</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Van Mieghem</LastName><ForeName>Nicolas M</ForeName><Initials>NM</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Daemen</LastName><ForeName>Joost</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-8628-1410</Identifier><AffiliationInfo><Affiliation>Department of Cardiology, Erasmus University Medical Center, Thorax Center, Rotterdam, the Netherlands j.daemen@erasmusmc.nl.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>04</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMJ Open</MedlineTA><NlmUniqueID>101552874</NlmUniqueID><ISSNLinking>2044-6055</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015331" MajorTopicYN="N">Cohort Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017023" MajorTopicYN="N">Coronary Angiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003331" MajorTopicYN="N">Coronary Vessels</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053805" MajorTopicYN="Y">Fractional Flow Reserve, Myocardial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012189" MajorTopicYN="N">Retrospective Studies</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cardiology</Keyword><Keyword MajorTopicYN="N">coronary heart disease</Keyword><Keyword MajorTopicYN="N">coronary intervention</Keyword><Keyword MajorTopicYN="N">ischaemic heart disease</Keyword></KeywordList><CoiStatement>Competing interests: MT acknowledges funding as the laureate of the European Society of Cardiology Research and Training Program in the form of the ESC 2018 Grant. KM received institutional grant support from Acist Medical. LJCvZ received institutional research grant support from Acist Medical. NMVM received research grant support from Edwards, Medtronic, Abbott, Boston Scientific, Pulse Cath, Acist Medical and Essential Medical. JD received institutional grant/research support from Abbott Vascular, Boston Scientific, Acist Medical, Medtronic and PulseCath, and consultancy and speaker fees from Acist medical, Boston Scientific, ReCor Medical, Medtronic and Pulse Cath. The remaining authors have nothing to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>4</Month><Day>5</Day><Hour>5</Hour><Minute>30</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>4</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35379622</ArticleId><ArticleId IdType="pmc">PMC8981358</ArticleId><ArticleId IdType="doi">10.1136/bmjopen-2021-054202</ArticleId><ArticleId IdType="pii">bmjopen-2021-054202</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Zimmermann FM, Ferrara A, Johnson NP, et al. . 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[Epub ahead of print: 14 Oct 2021].</Citation><ArticleIdList><ArticleId IdType="doi">10.4244/EIJ-D-21-00471</ArticleId><ArticleId IdType="pubmed">34647890</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35379474</PMID><DateRevised><Year>2022</Year><Month>04</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-685X</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>The Journal of thoracic and cardiovascular surgery</Title><ISOAbbreviation>J Thorac Cardiovasc Surg</ISOAbbreviation></Journal>A novel intrapericardial pulsatile device for individualized, biventricular circulatory support without direct blood contact.
To evaluate the feasibility of three-vessel three-dimensional (3D) quantitative coronary angiography (QCA)-based fractional flow reserve (FFR) computation in patients discussed within the Heart Team in whom the treatment decision was based on angiography alone, and to evaluate the concordance between 3D QCA-based vessel FFR (vFFR)-confirmed functional lesion significance and revascularisation strategy as proposed by the Heart Team.</AbstractText>Retrospective, cohort.</AbstractText>3D QCA-based FFR indices have not yet been evaluated in the context of Heart Team decision-making; consecutive patients from six institutions were screened for eligibility and three-vessel vFFR was computed by blinded analysts.</AbstractText>Consecutive patients with chronic coronary syndrome or unstable angina referred for Heart Team consultation. Exclusion criteria involved: presentation with acute myocardial infarction (MI), significant valve disease, left ventricle ejection fraction &lt;30%, inadequate quality of angiogram precluding vFFR computation in all three epicardial coronary arteries (ie, absence of a minimum of two angiographic projections with views of at least 30&#xb0; apart, substantial foreshortening/overlap of the vessel, poor contrast medium injection, ostial lesions, chronic total occlusions).</AbstractText>Discordance between vFFR-confirmed lesion significance and revascularisation was assessed as the primary outcome measure. Rates of major adverse cardiac events (MACE) defined as cardiac death, MI and clinically driven revascularisation were reported.</AbstractText>Of a total of 1003 patients were screened for eligibility, 416 patients (age 65.6&#xb1;10.6, 71.2% male, 53% stable angina) were included. The most important reason for screening failure was insufficient quality of the angiogram (43%). Discordance between vFFR confirmed lesion significance and revascularisation was found in 124/416 patients (29.8%) corresponding to 149 vessels (46/149 vessels (30.9%) were reclassified as significant and 103/149 vessels (69.1%) as non-significant by vFFR). Over a median of 962 days, the cumulative incidence of MACE was 29.7% versus 18.5% in discordant versus concordant patients (p=0.031).</AbstractText>vFFR computation is feasible in around 40% of the patients referred for Heart Team discussion, a limitation that is mostly based on insufficient quality of the angiogram. Three vessel vFFR screening indicated discordance between vFFR confirmed lesion significance and revascularisation in 29.8% of the patients.</AbstractText>&#xa9; Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation>
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Exposure to 5 cGy 28Si Particles Induces Long-Term Microglial Activation in the Striatum and Subventricular Zone and Concomitant Neurogenic Suppression.<Pagination><StartPage>28</StartPage><EndPage>39</EndPage><MedlinePgn>28-39</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1667/RADE-21-00021.1</ELocationID><Abstract><AbstractText>The proposed mission to Mars will expose astronauts to space radiation that is known to adversely affect cognition and tasks that rely on fine sensorimotor function. Space radiation has also been shown to affect the microglial and neurogenic responses in the central nervous system (CNS). We recently reported that a low dose of 5 cGy 600 MeV/n 28Si results in impaired cognition and skilled motor behavior in adult rats. Since these tasks rely at least in part on the proper functioning of the striatum, we examined striatal microglial cells in these same subjects. Using morphometric analysis, we found that 28Si exposure increased activated microglial cells in the striatum. The majority of these striatal Iba1+ microglia were ED1-, indicating that they were in an alternatively activated state, where microglia do not have phagocytic activity but may be releasing cytokines that could negatively impact neuronal function. In the other areas studied, Iba1+ microglial cells were increased in the subventricular zone (SVZ), but not in the dentate gyrus (DG). Additionally, we examined the relationship between the microglial response and neurogenesis. An analysis of new neurons in the DG revealed an increase in doublecortin-positive (DCX+) hilar ectopic granule cells (hEGC) which correlated with Iba1+ cells, suggesting that microglial cells contributed to this aberrant distribution which may adversely affect hippocampal function. Taken together, these results indicate that a single dose of 28Si radiation results in persistent cellular effects in the CNS that may impact astronauts both in the short and long-term following deep space missions.</AbstractText><CopyrightInformation>&#xa9;2022 by Radiation Research Society. All rights of reproduction in any form reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ton</LastName><ForeName>Son T</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laghi</LastName><ForeName>Julia R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsai</LastName><ForeName>Shih-Yen</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blackwell</LastName><ForeName>Ashley A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Department of Psychology, Northern Illinois University, DeKalb, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adamczyk</LastName><ForeName>Natalie S</ForeName><Initials>NS</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Osterlund Oltmanns</LastName><ForeName>Jenna R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Department of Psychology, Northern Illinois University, DeKalb, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Britten</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology, Eastern Virginia Medical School, Norfolk, Virginia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wallace</LastName><ForeName>Douglas G</ForeName><Initials>DG</Initials><AffiliationInfo><Affiliation>Department of Psychology, Northern Illinois University, DeKalb, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kartje</LastName><ForeName>Gwendolyn L</ForeName><Initials>GL</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular Pharmacology and Neuroscience, Loyola University Chicago Health Sciences Division, Maywood, Illinois.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Radiat Res</MedlineTA><NlmUniqueID>0401245</NlmUniqueID><ISSNLinking>0033-7587</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020547" MajorTopicYN="Y">Lateral Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017628" MajorTopicYN="Y">Microglia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055495" MajorTopicYN="N">Neurogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>3</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>4</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>4</Month><Day>4</Day><Hour>12</Hour><Minute>15</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35377458</ArticleId><ArticleId IdType="doi">10.1667/RADE-21-00021.1</ArticleId><ArticleId IdType="pii">479853</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35377356</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>06</Day></DateCompleted><DateRevised><Year>2022</Year><Month>05</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>181</Issue><PubDate><Year>2022</Year><Month>Mar</Month><Day>17</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension.
The proposed mission to Mars will expose astronauts to space radiation that is known to adversely affect cognition and tasks that rely on fine sensorimotor function. Space radiation has also been shown to affect the microglial and neurogenic responses in the central nervous system (CNS). We recently reported that a low dose of 5 cGy 600 MeV/n 28Si results in impaired cognition and skilled motor behavior in adult rats. Since these tasks rely at least in part on the proper functioning of the striatum, we examined striatal microglial cells in these same subjects. Using morphometric analysis, we found that 28Si exposure increased activated microglial cells in the striatum. The majority of these striatal Iba1+ microglia were ED1-, indicating that they were in an alternatively activated state, where microglia do not have phagocytic activity but may be releasing cytokines that could negatively impact neuronal function. In the other areas studied, Iba1+ microglial cells were increased in the subventricular zone (SVZ), but not in the dentate gyrus (DG). Additionally, we examined the relationship between the microglial response and neurogenesis. An analysis of new neurons in the DG revealed an increase in doublecortin-positive (DCX+) hilar ectopic granule cells (hEGC) which correlated with Iba1+ cells, suggesting that microglial cells contributed to this aberrant distribution which may adversely affect hippocampal function. Taken together, these results indicate that a single dose of 28Si radiation results in persistent cellular effects in the CNS that may impact astronauts both in the short and long-term following deep space missions.<CopyrightInformation>&#xa9;2022 by Radiation Research Society. All rights of reproduction in any form reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ton</LastName><ForeName>Son T</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laghi</LastName><ForeName>Julia R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsai</LastName><ForeName>Shih-Yen</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blackwell</LastName><ForeName>Ashley A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Department of Psychology, Northern Illinois University, DeKalb, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adamczyk</LastName><ForeName>Natalie S</ForeName><Initials>NS</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Osterlund Oltmanns</LastName><ForeName>Jenna R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Department of Psychology, Northern Illinois University, DeKalb, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Britten</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology, Eastern Virginia Medical School, Norfolk, Virginia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wallace</LastName><ForeName>Douglas G</ForeName><Initials>DG</Initials><AffiliationInfo><Affiliation>Department of Psychology, Northern Illinois University, DeKalb, Illinois.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kartje</LastName><ForeName>Gwendolyn L</ForeName><Initials>GL</Initials><AffiliationInfo><Affiliation>Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular Pharmacology and Neuroscience, Loyola University Chicago Health Sciences Division, Maywood, Illinois.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Radiat Res</MedlineTA><NlmUniqueID>0401245</NlmUniqueID><ISSNLinking>0033-7587</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020547" MajorTopicYN="Y">Lateral Ventricles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017628" MajorTopicYN="Y">Microglia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055495" MajorTopicYN="N">Neurogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>11</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>3</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>4</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>7</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>4</Month><Day>4</Day><Hour>12</Hour><Minute>15</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35377458</ArticleId><ArticleId IdType="doi">10.1667/RADE-21-00021.1</ArticleId><ArticleId IdType="pii">479853</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35377356</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>06</Day></DateCompleted><DateRevised><Year>2022</Year><Month>05</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>181</Issue><PubDate><Year>2022</Year><Month>Mar</Month><Day>17</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/58057</ELocationID><Abstract>The development of acute right heart failure (ARHF) in the context of chronic pulmonary hypertension (PH) is associated with poor short-term outcomes. The morphological and functional phenotyping of the right ventricle is of particular importance in the context of hemodynamic compromise in patients with ARHF. Here, we describe a method to induce ARHF in a previously described large animal model of chronic PH, and to phenotype, dynamically, right ventricular function using the gold standard method (i.e., pressure-volume PV loops) and with a non-invasive clinically available method (i.e., echocardiography). Chronic PH is first induced in pigs by left pulmonary artery ligation and right lower lobe embolism with biological glue once a week for 5 weeks. After 16 weeks, ARHF is induced by successive volume loading using saline followed by iterative pulmonary embolism until the ratio of the systolic pulmonary pressure over systemic pressure reaches 0.9 or until the systolic systemic pressure decreases below 90 mmHg. Hemodynamics are restored with dobutamine infusion (from 2.5 &#xb5;g/kg/min to 7.5 &#xb5;g/kg/min). PV-loops and echocardiography are performed during each condition. Each condition requires around 40 minutes for induction, hemodynamic stabilization and data acquisition. Out of 9 animals, 2 died immediately after pulmonary embolism and 7 completed the protocol, which illustrates the learning curve of the model. The model induced a 3-fold increase in mean pulmonary artery pressure. The PV-loop analysis showed that ventriculo-arterial coupling was preserved after volume loading, decreased after acute pulmonary embolism and was restored with dobutamine. Echocardiographic acquisitions allowed to quantify right ventricular parameters of morphology and function with good quality. We identified right ventricular ischemic lesions in the model. The model can be used to compare different treatments or to validate non-invasive parameters of right ventricular morphology and function in the context of ARHF.
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Differential transcriptomic landscapes of multiple organs from SARS-CoV-2 early infected rhesus macaques.
SARS-CoV-2 infection causes complicated clinical manifestations with variable multi-organ injuries, however, the underlying mechanism, in particular immune responses in different organs, remains elusive. In this study, comprehensive transcriptomic alterations of 14 tissues from rhesus macaque infected with SARS-CoV-2 were analyzed. Compared to normal controls, SARS-CoV-2 infection resulted in dysregulation of genes involving diverse functions in various examined tissues/organs, with drastic transcriptomic changes in cerebral cortex and right ventricle. Intriguingly, cerebral cortex exhibited a hyperinflammatory state evidenced by significant upregulation of inflammation response-related genes. Meanwhile, expressions of coagulation, angiogenesis and fibrosis factors were also up-regulated in cerebral cortex. Based on our findings, neuropilin 1 (NRP1), a receptor of SARS-CoV-2, was significantly elevated in cerebral cortex post infection, accompanied by active immune response releasing inflammatory factors and signal transmission among tissues, which enhanced infection of the central nervous system (CNS) in a positive feedback way, leading to viral encephalitis. Overall, our study depicts a multi-tissue/organ transcriptomic landscapes of rhesus macaque with early infection of SARS-CoV-2, and provides important insights into the mechanistic basis for COVID-19-associated clinical complications.
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Sensitivity analysis and inverse uncertainty quantification for the left ventricular passive mechanics.
Personalized computational cardiac models are considered to be a unique and powerful tool in modern cardiology, integrating the knowledge of physiology, pathology and fundamental laws of mechanics in one framework. They have the potential to improve risk prediction in cardiac patients and assist in the development of new treatments. However, in order to use these models for clinical decision support, it is important that both the impact of model parameter perturbations on the predicted quantities of interest as well as the uncertainty of parameter estimation are properly quantified, where the first task is a priori in nature (meaning independent of any specific clinical data), while the second task is carried out a posteriori (meaning after specific clinical data have been obtained). The present study addresses these challenges for a widely used constitutive law of passive myocardium (the Holzapfel-Ogden model), using global sensitivity analysis (SA) to address the first challenge, and inverse-uncertainty quantification (I-UQ) for the second challenge. The SA is carried out on a range of different input parameters to a left ventricle (LV) model, making use of computationally efficient Gaussian process (GP) surrogate models in place of the numerical forward simulator. The results of the SA are then used to inform a low-order reparametrization of the constitutive law for passive myocardium under consideration. The quality of this parameterization in the context of an inverse problem having observed noisy experimental data is then quantified with an I-UQ study, which again makes use of GP surrogate models. The I-UQ is carried out in a Bayesian manner using Markov Chain Monte Carlo, which allows for full uncertainty quantification of the material parameter estimates. Our study reveals insights into the relation between SA and I-UQ, elucidates the dependence of parameter sensitivity and estimation uncertainty on external factors, like LV cavity pressure, and sheds new light on cardio-mechanic model formulation, with particular focus on the Holzapfel-Ogden myocardial model.
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Photon versus proton whole ventricular radiotherapy for non-germinomatous germ cell tumors: A report from the Children's Oncology Group.
To determine if proton therapy reduces doses to cranial organs at risk (OARs) as compared to photon therapy in children with non-germinomatous germ cell tumors (NGGCT) receiving whole ventricular radiotherapy (WVRT).</AbstractText>Dosimetric data for patients with NGGCT prospectively enrolled in stratum 1 of the Children's Oncology Group study ACNS1123 who received 30.6&#xa0;Gy WVRT were compared. Target segmentation was standardized using a contouring atlas. Doses to cranial OARs were compared between proton and photon treatments. Clinically relevant dose-volume parameters that were analyzed included mean dose and dose to 40% of the OAR volume (D40).</AbstractText>Mean and D40 doses to the supratentorial brain, cerebellum, and bilateral temporal, parietal, and frontal lobes were statistically significantly lower amongst proton-treated patients, as compared to photon-treated patients. In a subgroup analysis of patients uniformly treated with a 3-mm planning target volume, patients who received proton therapy continued to have statistically significantly lower doses to brain OARs.</AbstractText>Children treated with proton therapy for WVRT had lower doses to normal brain structures, when compared to those treated with photon therapy. Proton therapy should be considered for patients receiving WVRT for NGGCT.</AbstractText>&#xa9; 2022 Wiley Periodicals LLC.</CopyrightInformation>
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Independent distribution between tauopathy secondary to subacute sclerotic panencephalitis and measles virus: An immunohistochemical analysis in autopsy cases including cases treated with aggressive antiviral therapies.
Subacute sclerotic panencephalitis (SSPE) is a refractory neurological disorder after exposure to measles virus. Recently, SSPE cases have been treated with antiviral therapies, but data on the efficacy are inconclusive. Abnormal tau accumulation has been reported in the brain tissue of SSPE cases, but there are few reports in which this is amply discussed. Five autopsied cases diagnosed as definite SSPE were included in this study. The subject age or disease duration ranged from 7.6 to 40.9&#x2009;years old or from 0.5 to 20.8&#x2009;years, respectively. Cases 3 and 4 had been treated with antiviral therapies. All evaluated cases showed marked brain atrophy with cerebral ventricle dilatation; additionally, marked demyelination with fibrillary gliosis were observed in the cerebral white matter. The brainstem, cerebellum, and spinal cord were relatively preserved. Immunoreactivity (IR) against measles virus was seen in the brainstem tegmentum, neocortex, and/or limbic cortex of the untreated cases but was rarely seen in the two treated cases. Activated microglia were broadly observed from the cerebrum to the spinal cord and had no meaningful difference among cases. Neurofibrillary tangles characterized by a combination of 3- and 4-repeat tau were observed mainly in the oculomotor nuclei, locus coeruleus, and limbic cortex. IR against phosphorylated tau was seen mainly in the cingulate gyrus, oculomotor nuclei, and pontine tegmentum, and tended to be observed frequently in cases with long disease durations but also tended to decrease along with neuronal loss, as in Case 5, which had the longest disease duration. Since the distribution of phosphorylated tau was independent from that of measles virus, the tauopathy following SSPE was inferred to be the result of diffuse brain inflammation triggered by measles rather than a direct result of measles virus. Moreover, antiviral therapies seemed to suppress measles virus but not the progression of tauopathy.
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Hydrocephalus-Associated Hyponatremia: A Review.
Hydrocephalus is the pathological accumulation of cerebrospinal fluid within the ventricles of the brain. Hydrocephalus may be broadly divided into three categories: congenital, acquired, or other. Hyponatremia, serum sodium level &lt;135 meq/ml, may be caused by dilution (e.g. syndrome of inappropriate antidiuretic hormone (SIADH)), depletion (e.g. cerebral salt wasting (CSW)), or delusion (e.g. psychogenic water intake) etiologies.&#xa0;This review discusses "hydrocephalus-associated hyponatremia" as a clinical entity, distinct from SIADH and CSW. Some experts believe that in hydrocephalus patients, increased pressure on the hypothalamus leads to the release of antidiuretic hormone (ADH),&#xa0;which in turn causes hyponatremia.&#xa0;The true etiology of hyponatremia is critical to diagnose, as it will determine the treatment.&#xa0;So while both SIADH and CSW may result in hyponatremia, the former is treated with fluid restriction, while the latter requires fluid repletion; treating SIADH as CSW, and vice versa, will exacerbate the hyponatremia. The etiology and severity of hyponatremia will determine the management. For hydrocephalus-associated hyponatremia, treating the underlying problem (i.e. hydrocephalus) is the mainstay of therapy.&#xa0;Theoretically, treatment of hydrocephalus-related hyponatremia with CSF-diversion procedures should relieve the pressure on the hypothalamus, mitigating ADH production, which in turn will decrease sodium excretion and ameliorate the hyponatremia.
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Selective Depletion of Adult GFAP-Expressing Tanycytes Leads to Hypogonadotropic Hypogonadism in Males.
In adult mammals, neural stem cells are localized in three neurogenic regions, the subventricular zone of the lateral ventricle (SVZ), the subgranular zone of the dentate gyrus of the hippocampus (SGZ) and the hypothalamus. In the SVZ and the SGZ, neural stem/progenitor cells (NSPCs) express the glial fibrillary acidic protein (GFAP) and selective depletion of these NSPCs drastically decreases cell proliferation <i>in vitro</i> and <i>in vivo</i>. In the hypothalamus, GFAP is expressed by &#x3b1;-tanycytes, which are specialized radial glia-like cells in the wall of the third ventricle also recognized as NSPCs. To explore the role of these hypothalamic GFAP-positive tanycytes, we used transgenic mice expressing herpes simplex virus thymidine kinase (HSV-Tk) under the control of the mouse <i>Gfap</i> promoter and a 4-week intracerebroventricular infusion of the antiviral agent ganciclovir (GCV) which kills dividing cells expressing Tk. While GCV significantly reduced the number and growth of hypothalamus-derived neurospheres from adult transgenic mice <i>in vitro</i>, it causes hypogonadotropic hypogonadism <i>in vivo.</i> The selective death of dividing tanycytes expressing GFAP indeed results in a marked decrease in testosterone levels and testicular weight, as well as vacuolization of the seminiferous tubules and loss of spermatogenesis. Additionally, GCV-treated GFAP-Tk mice show impaired sexual behavior, but no alteration in food intake or body weight. Our results also show that the selective depletion of GFAP-expressing tanycytes leads to a sharp decrease in the number of gonadotropin-releasing hormone (GnRH)-immunoreactive neurons and a blunted LH secretion. Overall, our data show that GFAP-expressing tanycytes play a central role in the regulation of male reproductive function.
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Tetramethylpyrazine Improves Monocrotaline-Induced Pulmonary Hypertension through the ROS/iNOS/PKG-1 Axis.
Tetramethylpyrazine (TMP), a potent anti-free radical and anti-inflammations substance, has been demonstrated to possess a direct vessel relaxation property. This study aimed to evaluate the effect of TMP treatment in pulmonary hypertension (PH) and test the hypothesis that TMP prevents or reverses the process of PH.</AbstractText>Rats (n</i>&#x2009;=&#x2009;36) injected with 50&#x2009;mg/kg of monocrotaline (MCT) subcutaneously 4 weeks to develop PH were then randomized to TMP (5&#x2009;mg/kg per day) for another 4 weeks. Hemodynamics was evaluated via the right ventricle. Pulmonary vessels structural remodeling and inflammation were examined by histologic and transmission electron microscopy observation. The expression of inducible nitric oxide synthase (iNOS) and cGMP-dependent protein kinases 1 (PKG-1) was detected by immunohistochemical staining and Western blot. Generation of reactive oxygen species (ROS) and antioxidation species was measured by biochemical analyses.</AbstractText>MCT increased PH and right ventricle hypertrophy. TMP alleviated pulmonary arterial pressure elevation, leukocyte infiltration, and structural remodeling of pulmonary arterials induced by MCT successfully. TMP treatment significantly increased the PKG-1 expression and suppressed the iNOS expression. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT) was significantly higher than control group, while malondialdehyde (MDA) levels were lower compared with MCT group.</AbstractText>TMP can suppress established MCT-induced PH through the ROS/iNOS/PKG axis. The underlying mechanisms may be associated with its anti-inflammatory, antioxidant, and antiproliferative properties in pulmonary arterial.</AbstractText>Copyright &#xa9; 2022 Dong-Peng Yang et al.</CopyrightInformation>
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Long-Term Impact of Arteriovenous Fistula Ligation on Cardiac Structure and Function in Kidney Transplant Recipients: A 5-Year Follow-Up Observational Cohort Study.
The long-term effects of arteriovenous fistula (AVF) ligation on cardiovascular structure following kidney transplantation remain uncertain. A prospective randomized, controlled trial (RCT) examined the effect of AVF ligation at 6 months on cardiovascular magnetic resonance imaging (CMR)-derived parameters in 27 kidney transplant recipients compared with 27 controls. A mean decrease in left ventricular mass (LVM) of 22.1 g (95% CI, 15.0 to 29.1) was observed compared with an increase of 1.2 g (95% CI, -4.8 to 7.2) in the control group (P</i>&lt;0.001). We conducted a long-term follow-up observational cohort study in the treated cohort to determine the evolution of CMR-derived parameters compared with those documented at 6 months post-AVF ligation.</AbstractText>We performed CMR at long-term follow-up in the AVF ligation observational cohort from our original RCT published in 2019. Results were compared with CMR at 6 months postintervention. The coprimary end point was the change in CMR-derived LVM and LVM index at long-term follow-up from imaging at 6 months postindex procedure.</AbstractText>At a median of 5.1 years (interquartile range, 4.7-5.5 years), 17 patients in the AVF ligation group were studied with repeat CMR with a median duration to follow-up imaging of 5.1 years (IQR, 4.7-5.5 years). Statistically significant further reductions in LVM (-17.6&#xb1;23.0 g, P</i>=0.006) and LVM index (-10.0&#xb1;13.0 g/m2</sup>, P</i>=0.006) were documented.</AbstractText>The benefit of AVF ligation on LVM and LVM index regression appears to persist long term. This has the potential to lead to a significant reduction in cardiovascular mortality.</AbstractText>Copyright &#xa9; 2021 by the American Society of Nephrology.</CopyrightInformation>
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Surgical Resection of a Third Ventricle Nongerminomatous Germ Cell Tumor: Two-Dimensional Operative Video.
Surgical resection of a pineal tumor growing into the third ventricle is difficult owing to the complex neurovascular structures, and nongerminomatous germ cell tumor is the most common malignant tumor in pediatric patients. Removing the tumor efficiently with minimal blood loss while protecting the surrounding neurovascular structure is challenging. We present a surgical case of a 9-year-old patient with a third ventricle nongerminomatous germ cell tumor (Video). Mass effect of the tumor or acute hydrocephalus is the possible reason for the coma. In this case, the reason of coma may be mass effect of the tumor, not the acute hydrocephalus. Informed consent was obtained from the patient's guardian. Intraoperatively we used a modified right head-up park bench position and a linear incision. The right occipital bone flap was designed to cross the superior sagittal sinus and transverse sinus. The primary surgical approach was the occipital transtentorial approach; an alternative was the supracerebellar infratentorial approach. After cutting the tentorium, a spatula was applied to retract the cerebellum and incised tentorium, with no extra brain retraction on the occipital lobe to minimize visual disturbance. The quadrigeminal cistern was opened, and the tumor was yellowish with heterogeneous consistency. Instead of rushing into the tumor debulking, we paid more attention to devascularization of the tumor from bilateral posterior medial choroidal arteries as much as possible. After debulking using an ultrasound aspirator, the tumor was removed in a piecemeal fashion, and the surgical field was inspected using an endoscope for any residue.
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Energetic demands of lactation produce an increase in the expression of growth hormone secretagogue receptor in the hypothalamus and ventral tegmental area of the rat despite a reduction in circulating ghrelin.
Lactating rats show changes in the secretion of hormones and brain signals that promote hyperphagia and facilitate the production of milk. Little is known, however, about the role of ghrelin in the mechanisms sustaining lactational hyperphagia. Here, we used Wistar female rats that underwent surgery to sever the galactophores to prevent milk delivery (GC rats) and decrease the energetic drain of milk delivery. We compared plasma acyl-ghrelin concentrations and growth hormone secretagogue receptor (GHSR) mRNA expression in different brain regions of GC rats with those of sham operated lactating and nonlactating rats. Additional lactating and nonlactating rats were implanted with cannulae aimed at the lateral ventricles and were used to compare feeding responses to central ghrelin or GHSR antagonist infusions to those of nonlactating rats receiving similar infusions on day 14-16 postpartum (pp). Results show lower plasma acyl-ghrelin concentrations on day 15&#x2009;pp sham operated lactating rats compared to GC or nonlactating rats. These changes occur in association with increased GHSR mRNA expression in the hypothalamic arcuate nucleus (ARC) and ventral tegmental area (VTA) of sham operated lactating rats. Despite lactational hyperphagia, infusions of ghrelin (0.25 or 1&#xa0;&#x3bc;g) resulted in similar increases in food intake in lactating and nonlactating rats. In addition, infusions of the GHSR antagonist JMV3002 (4&#xa0;&#x3bc;g in 1&#xa0;&#x3bc;l of vehicle) produced greater suppression of food intake in lactating rats than in nonlactating rats. These data suggest that, despite lower plasma ghrelin, the energetic drain of lactation increases sensitivity to the orexigenic effects of ghrelin in brain regions important for food intake and energy balance, and these events are associated with lactational hyperphagia.
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Automaticity in ventricular myocyte cell pairs with ephaptic and gap junction coupling.<Pagination><StartPage>033123</StartPage><MedlinePgn>033123</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">033123</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1063/5.0085291</ELocationID><Abstract><AbstractText>Spontaneous electrical activity, or automaticity, in the heart is required for normal physiological function. However, irregular automaticity, in particular, originating from the ventricles, can trigger life-threatening cardiac arrhythmias. Thus, understanding mechanisms of automaticity and synchronization is critical. Recent work has proposed that excitable cells coupled via a shared narrow extracellular cleft can mediate coupling, i.e., ephaptic coupling, that promotes automaticity in cell pairs. However, the dynamics of these coupled cells incorporating both ephaptic and gap junction coupling has not been explored. Here, we show that automaticity and synchronization robustly emerges via a Hopf bifurcation from either (i) increasing the fraction of inward rectifying potassium channels (carrying the I<sub>K1</sub> current) at the junctional membrane or (ii) by decreasing the cleft volume. Furthermore, we explore how heterogeneity in the fraction of potassium channels between coupled cells can produce automaticity of both cells or neither cell, or more rarely in only one cell (i.e., automaticity without synchronization). Interestingly, gap junction coupling generally has minor effects, with only slight changes in regions of parameter space of automaticity. This work provides insight into potentially new mechanisms that promote spontaneous activity and, thus, triggers for arrhythmias in ventricular tissue.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ly</LastName><ForeName>Cheng</ForeName><Initials>C</Initials><Identifier Source="ORCID">0000000332798240</Identifier><AffiliationInfo><Affiliation>Department of Statistical Sciences and Operations Research, Virginia Commonwealth University, 1015 Floyd Avenue, Richmond, Virginia 23284, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weinberg</LastName><ForeName>Seth H</ForeName><Initials>SH</Initials><Identifier Source="ORCID">0000000311700419</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Ohio State University, 333 W 10th Avenue, Columbus, Ohio 43210, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL138003</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Chaos</MedlineTA><NlmUniqueID>100971574</NlmUniqueID><ISSNLinking>1054-1500</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017629" MajorTopicYN="Y">Gap Junctions</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008955" MajorTopicYN="Y">Models, Cardiovascular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>4</Month><Day>2</Day><Hour>5</Hour><Minute>20</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35364829</ArticleId><ArticleId IdType="pmc">PMC8934194</ArticleId><ArticleId IdType="doi">10.1063/5.0085291</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Luo C.-H. and Rudy Y., &#x201c;A model of the ventricular cardiac action potential. 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Spontaneous electrical activity, or automaticity, in the heart is required for normal physiological function. However, irregular automaticity, in particular, originating from the ventricles, can trigger life-threatening cardiac arrhythmias. Thus, understanding mechanisms of automaticity and synchronization is critical. Recent work has proposed that excitable cells coupled via a shared narrow extracellular cleft can mediate coupling, i.e., ephaptic coupling, that promotes automaticity in cell pairs. However, the dynamics of these coupled cells incorporating both ephaptic and gap junction coupling has not been explored. Here, we show that automaticity and synchronization robustly emerges via a Hopf bifurcation from either (i) increasing the fraction of inward rectifying potassium channels (carrying the I<sub>K1</sub> current) at the junctional membrane or (ii) by decreasing the cleft volume. Furthermore, we explore how heterogeneity in the fraction of potassium channels between coupled cells can produce automaticity of both cells or neither cell, or more rarely in only one cell (i.e., automaticity without synchronization). Interestingly, gap junction coupling generally has minor effects, with only slight changes in regions of parameter space of automaticity. 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S. and Casadei B., &#x201c;Mechanisms of atrial fibrillation,&#x201d; Heart 105, 1860&#x2013;1867 (2019). 10.1136/heartjnl-2018-314267</Citation><ArticleIdList><ArticleId IdType="doi">10.1136/heartjnl-2018-314267</ArticleId><ArticleId IdType="pubmed">31444267</ArticleId></ArticleIdList></Reference><Reference><Citation>Vermij S. H., Abriel H., and van Veen T. A., &#x201c;Refining the molecular organization of the cardiac intercalated disc,&#x201d; Cardiovasc. Res. 113, 259&#x2013;275 (2017). 10.1093/cvr/cvw259</Citation><ArticleIdList><ArticleId IdType="doi">10.1093/cvr/cvw259</ArticleId><ArticleId IdType="pubmed">28069669</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">35605083</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK580614</ArticleId><ArticleId IdType="doi">10.36255/exon-publications-epilepsy-anatomical-basis</ArticleId></ArticleIdList><Book><Publisher><PublisherName>Exon Publications</PublisherName><PublisherLocation>Brisbane (AU)</PublisherLocation></Publisher><BookTitle book="cod9780645332049">Epilepsy</BookTitle><PubDate><Year>2022</Year><Month>04</Month><Day>02</Day></PubDate><AuthorList Type="editors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Czuczwar</LastName><ForeName>Stanislaw J.</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Pathophysiology, Medical University of Lublin, Lublin, Poland</Affiliation></AffiliationInfo></Author></AuthorList><Isbn>9780645332049</Isbn><ELocationID EIdType="doi">10.36255/exon-publications-epilepsy</ELocationID><Medium>Internet</Medium></Book><LocationLabel Type="chapter">Chapter 2</LocationLabel><ArticleTitle book="cod9780645332049" part="Ch2">The Anatomical Basis of Seizures</ArticleTitle><Language>eng</Language><AuthorList Type="authors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Chauhan</LastName><ForeName>Pradip</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Anatomy, All India Institute of Medical Sciences, Rajkot, Gujarat, India</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Philip</LastName><ForeName>Shalom Elsy</ForeName><Initials>SE</Initials><AffiliationInfo><Affiliation>Department of Anatomy, All India Institute of Medical Sciences, Rajkot, Gujarat, India</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chauhan</LastName><ForeName>Girish</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Oral Pathology, Government Dental College, Jamanagar, Gujarat, India</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mehra</LastName><ForeName>Simmi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Anatomy, All India Institute of Medical Sciences, Rajkot, Gujarat, India</Affiliation></AffiliationInfo></Author></AuthorList><PublicationType UI="D016454">Review</PublicationType><Abstract>Paroxysmal alteration of neurological function caused by an excessive hypersynchronous neuronal discharge in the brain is known as seizure. Non-epileptic seizure is short-lived while epilepsy is a neurological condition characterized by two or more provoked seizures. The hippocampus, amygdala, frontal cortex, temporal cortex, and olfactory cortex are the common areas involved in seizures. According to the &#x2018;dormant basket cell&#x2019; theory, loss of excitatory input from the dentate mossy cells makes inhibitory basket cells dormant while according to the &#x2018;mossy fiber&#x2019; theory, mossy fibers induce the formation of excitatory circuits resulting in hyperexcitability. Amygdala is present at the anterior end of the inferior horn of the lateral ventricle; basolateral part plays an important role in temporal lobe epilepsy. The thalamus is an ovoid mass of grey matter; midline nuclei of the thalamus is involved in memory function and arousal, while it plays a crucial role in controlling seizures. Dendrites are short post-synaptic neural processes; in pathological conditions dendrites can cause hyperexcitability in neuronal circuits and lead to decreased seizure thresholds and progressive epileptogenesis. Regions specialized for learning/memory are most prone to seizures, particularly, the neocortical regions and the hippocampus.
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Boosting phase-contrast MRI performance in idiopathic normal pressure hydrocephalus diagnostics by means of machine learning approach.
Phase-contrast MRI allows detailed measurements of various parameters of CSF motion. This examination is technically demanding and machine dependent. The literature on this topic is ambiguous. Machine learning (ML) approaches have already been successfully utilized in medical research, but none have yet been applied to enhance the results of CSF flowmetry. The aim of this study was to evaluate the possible contribution of ML algorithms in enhancing the utilization and results of MRI flowmetry in idiopathic normal pressure hydrocephalus (iNPH) diagnostics.</AbstractText>The study cohort consisted of 30 iNPH patients and 15 healthy controls examined on one MRI machine. All major phase-contrast parameters were inspected: peak positive, peak negative, and average velocities; peak amplitude; positive, negative, and average flow rates; and aqueductal area. The authors applied ML algorithms to 85 complex features calculated from a phase-contrast study.</AbstractText>The most distinctive parameters with p &lt; 0.005 were the peak negative velocity, peak amplitude, and negative flow. From the ML algorithms, the Adaptive Boosting classifier showed the highest specificity and best discrimination potential overall, with 80.4% &#xb1; 2.9% accuracy, 72.0% &#xb1; 5.6% sensitivity, 84.7% &#xb1; 3.8% specificity, and 0.812 &#xb1; 0.047 area under the receiver operating characteristic curve (AUC). The highest sensitivity was 85.7% &#xb1; 5.6%, reached by the Gaussian Naive Bayes model, and the best AUC was 0.854 &#xb1; 0.028 by the Extra Trees classifier.</AbstractText>Feature extraction algorithms combined with ML approaches simplify the utilization of phase-contrast MRI. The highest-performing ML algorithm was Adaptive Boosting, which showed good calibration and discrimination on the testing data, with 80.4% accuracy, 72.0% sensitivity, 84.7% specificity, and 0.812 AUC. Phase-contrast MRI boosted by the ML approach can help to determine shunt-responsive iNPH patients.</AbstractText>
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Alobar holoprosencephaly with cebocephaly in a neonate: A rare case report from Northern Tanzania.
Holoprosencephaly is a rare brain malformation consisting of impaired midline cleavage of the embryonic forebrain presenting with variable features of craniofacial dysmorphism. It affects 1 in 10,000 live births occurring more in females than males. We present a case of alobar HPE and aim to raise awareness on the importance of early prenatal detection and counselling.</AbstractText>We present a case of 3200-gram female baby, born by spontaneous vaginal delivery with APGAR scores of 5 and 6 in the first and fifth minute of life respectively. On admission, the baby was lethargic, had central and peripheral cyanosis, hypothermic with temperature of 32.1&#xa0;&#xb0;C, respiratory rate of 65 breaths/min, heart rate of 135 beats/min and oxygen saturation of 94% with an oropharyngeal airway and on oxygen support via a face mask. She had microcephaly, hypotelorism, and a small nose with a single imperforate nostril. She was diagnosed to have alobar holoprosencephaly with cebocephaly. A computed tomography scan of the brain revealed a cephalohematoma in the vertex and an intranasal soft tissue density lesion blocking the entrance measuring approximately 10&#xa0;&#xd7;&#xa0;8.5&#xa0;mm. Absence of the corpus callosum and septum pellucidum with a resulting monoventricle formed from the lateral ventricles, the fusion of the thalami and a sizeable arachnoid cyst involving the left cerebellar hemisphere were evident. She was started on IV antibiotics and IV fluids. Non-invasive airway management was opted for by the ENT team based on the condition of the baby. She succumbed to death 6&#xa0;days post admission due to severe respiratory failure.</AbstractText>The types of HPE are alobar, semi lobar, lobar and interhemispheric variants. Alobar HPE is the most severe form and is incompatible with life. Clinical presentation entails facial dysmorphism with features of hypotelorism, microcephaly and a blind ended nostril. Alobar and semilobar HPE can reliably be diagnosed with ultrasound during the first and second trimesters of pregnancy. Absence of choroid plexus and fused cortex are pathognomonic characteristic on ultrasound and CT scan respectively.</AbstractText>Alobar holoprosencephaly is a rare brain malformation which is incompatible with life. Prenatal ultrasound screening of the foetus brain is essential and reliable in making a diagnosis. Absence of the "butterfly" sign in the foetal brain ultrasonography should raise a high index of suspicion for brain malformation with unfavourable outcome. Legal medical termination of pregnancy may serve as an early intervention.</AbstractText>Copyright &#xa9; 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation>
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The auto segmentation for cardiac structures using a dual-input deep learning network based on vision saliency and transformer.
Accurate segmentation of cardiac structures on coronary CT angiography (CCTA) images is crucial for the morphological analysis, measurement, and functional evaluation. In this study, we achieve accurate automatic segmentation of cardiac structures on CCTA image by adopting an innovative deep learning method based on visual attention mechanism and transformer network, and its practical application value is discussed.</AbstractText>We developed a dual-input deep learning network based on visual saliency and transformer (VST), which consists of self-attention mechanism for cardiac structures segmentation. Sixty patients' CCTA subjects were randomly selected as a development set, which were manual marked by an experienced technician. The proposed vision attention and transformer mode was trained on the patients CCTA images, with a manual contour-derived binary mask used as the learning-based target. We also used the deep supervision strategy by adding auxiliary losses. The loss function of our model was the sum of the Dice loss and cross-entropy loss. To quantitatively evaluate the segmentation results, we calculated the Dice similarity coefficient (DSC) and Hausdorff distance (HD). Meanwhile, we compare the volume of automatic segmentation and manual segmentation to analyze whether there is statistical difference.</AbstractText>Fivefold cross-validation was used to benchmark the segmentation method. The results showed the left ventricular myocardium (LVM, DSC&#xa0;=&#xa0;0.87), the left ventricular (LV, DSC&#xa0;=&#xa0;0.94), the left atrial (LA, DSC&#xa0;=&#xa0;0.90), the right ventricular (RV, DSC&#xa0;=&#xa0;0.92), the right atrial (RA, DSC&#xa0;=&#xa0;0.91), and the aortic (AO, DSC&#xa0;=&#xa0;0.96). The average DSC was 0.92, and HD was 7.2 &#xb1; 2.1&#xa0;mm. In volume comparison, except LVM and LA (p&#xa0;&lt;&#xa0;0.05), there was no significant statistical difference in other structures. Proposed method for structural segmentation fit well with the true profile of the cardiac substructure, and the model prediction results closed to the manual annotation.</AbstractText>The adoption of the dual-input and transformer architecture based on visual saliency has high sensitivity and specificity to cardiac structures segmentation, which can obviously improve the accuracy of automatic substructure segmentation. This is of gr.</AbstractText>&#xa9; 2022 The Authors. Journal of Applied Clinical Medical Physics published by Wiley Periodicals, LLC on behalf of The American Association of Physicists in Medicine.</CopyrightInformation>
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Echinacoside alleviates sevoflurane-induced cognitive dysfunction by activating FOXO1-mediated autophagy.
The current study aimed to examine the effects of echinacoside on cognitive impairment in mice after exposure to sevoflurane. To examine the role of FOXO1, si-FOXO1 and si-con were injected into the hippocampus through the left lateral cerebral ventricles. Sevoflurane-induced mice had serious cognitive dysfunction. However, pretreatment with echinacoside alleviated the cognitive dysfunction, as measured by a shortened escape latency time, and increased platform crossing times, the percentage of distance in the target quadrant and Y-maze spontaneous alternations. In addition, we found that echinacoside elevated FOXO1 expression in the hippocampus; increased the expression of autophagy-related proteins including Beclin 1, ATG5, ATG7, and LC3; and reduced P62 expression. Silencing of FOXO1 aggravated the cognitive deficits and reduced expression of the autophagy-related markers, whereas the effects of si-FOXO1 on memory were abrogated by echinacoside. Echinacoside attenuated the cognitive impairment in sevoflurane-induced mice through FOXO1-mediated autophagy.
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Aging-Related Alterations of Glymphatic Transport in Rat: <i>In vivo</i> Magnetic Resonance Imaging and Kinetic Study.
Impaired glymphatic waste clearance function during brain aging leads to the accumulation of metabolic waste and neurotoxic proteins (e.g., amyloid-&#x3b2;, tau) which contribute to neurological disorders. However, how the age-related glymphatic dysfunction exerts its effects on different cerebral regions and affects brain waste clearance remain unclear.</AbstractText>We investigated alterations of glymphatic transport in the aged rat brain using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and advanced kinetic modeling. Healthy young (3-4 months) and aged (18-20 months) male rats (n</i> = 12/group) underwent the identical MRI protocol, including T2-weighted imaging and 3D T1-weighted imaging with intracisternal administration of contrast agent (Gd-DTPA). Model-derived parameters of infusion rate and clearance rate, characterizing the kinetics of cerebrospinal fluid (CSF) tracer transport via the glymphatic system, were evaluated in multiple representative brain regions. Changes in the CSF-filled cerebral ventricles were measured using contrast-induced time signal curves (TSCs) in conjunction with structural imaging.</AbstractText>Compared to the young brain, an overall impairment of glymphatic transport function was detected in the aged brain, evidenced by the decrease in both infusion and clearance rates throughout the brain. Enlarged ventricles in parallel with reduced efficiency in CSF transport through the ventricular regions were present in the aged brain. While the age-related glymphatic dysfunction was widespread, our kinetic quantification demonstrated that its impact differed considerably among cerebral regions with the most severe effect found in olfactory bulb, indicating the heterogeneous and regional preferential alterations of glymphatic function.</AbstractText>The robust suppression of glymphatic activity in the olfactory bulb, which serves as one of major efflux routes for brain waste clearance, may underlie, in part, age-related neurodegenerative diseases associated with neurotoxic substance accumulation. Our data provide new insight into the cerebral regional vulnerability to brain functional change with aging.</AbstractText>Copyright &#xa9; 2022 Li, Ding, Zhang, Davoodi-Bojd, Chopp, Li, Zhang and Jiang.</CopyrightInformation>
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Cellular distribution of C-C motif chemokine ligand 2 like immunoreactivities in frontal cortex and corpus callosum of normal and lipopolysaccharide treated animal.
C-C motif chemokine ligand 2 (CCL2) is reported to be involved in the pathogenesis of various neurological and/or psychiatric diseases. Tissue or cellular expression of CCL2, in normal or pathological condition, may play an essential role in recruiting monocytes or macrophages into targeted organs, and be involved in a certain pathogenic mechanism. However, few studies focused on tissue and cellular distribution of the CCL2 peptide in brain grey and white matters (GM, WM), and the changes of the GM and WM cellular CCL2 level in septic or endotoxic encephalopathy was not explored. Hence, the CCL2 cellular distribution in the front brain cortex and the corpus callosum (CC) was investigated in the present work by using immunofluorescent staining.</AbstractText>(1) CCL2 like immunoreactivity (CCL2-ir) in the CC is evidently higher than the cortex. When the measurement includes ependymal layer attached to the CC, CCL2-ir intensity is significantly higher than cortex. (2) Structures in perivascular areas, most of them are GFAP positive, contribute major CCL2-ir positive profiles in both GM and WM, but apparently more in the CC, where they are bilaterally distributed in the lateral CC between the cingulate cortex and ventricles. (3) The neuron-like CCL2-ir positive cells in cortex are significantly more than in the CC, and that number is significantly increased in the cortex following systemic lipopolysaccharide (LPS), but not in the CC. (4) In addition to CCL2-ir positive perivascular rings, more CCL2-ir filled cashew shape elements are observed, probably inside of microvasculature, especially in the CC following systemic LPS. (5) Few macrophage/microglia marker-Iba-1 and CCL2-ir co-labeled structures especially the soma is found in normal cortex and CC; the co-localizations are significantly augmented following systemic LPS, and co-labeled amoeba like somata are presented. (6) CCL2-ir and astrocyte marker GFAP or Iba-1 double labeled structures are also observed within the ependymal layer. No accumulation of neutrophils was detected.</AbstractText>There exist differences in the cellular distribution of the CCL2 peptide in frontal cortex GM and subcortical WM-CC, in both the physiological condition and experimental endotoxemia. Which might cause different pathological change in the GM and WM.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
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"The only thing I wonder is when I will have surgery again": everyday life for children with right ventricle outflow tract anomalies during assessment for heart surgery.
Children with right ventricle outflow tract anomalies require repeated heart surgeries, thereby needing regular preoperative assessments throughout their lifetime. This situation puts a heavy burden on these children. Thus, the aim of this study was to explore how children diagnosed with right ventricle outflow tract anomalies experience their heart disease and their everyday life during the preoperative assessment and after the decision on whether to perform a new cardiac surgery.</AbstractText>Individual interviews were conducted with nine children between 9 to 17 years of age on three occasions from 2014 to 2016. In total there were 27 interviews which all were analyzed with thematic analysis.</AbstractText>The analysis yielded three themes and eight subthemes. The theme Me and my heart disease</i> concerns children's experiences of the heart disease. Almost all described symptoms and how they adapt in their everyday life. The theme Being me</i> concerns the children's sense of self, where their heart disease was not prominent. The theme Being placed in someone else's hands</i> describes how the assessment was more of a safety net at least until the decision of heart surgery.</AbstractText>The children's symptoms, their experiences during the assessment, their future surgeries and how the heart disease affects their everyday life could be better understood as elements of their adaptation to the heart disease. In order to achieve individualized support based on the child's experiences and to ensure that these children are involved in their own care a child-centered approach is recommended.</AbstractText>
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Superficial siderosis and nonobstructive hydrocephalus due to subependymoma in the ventricle: An illustrative case report.
Intraventricular tumors can generally result in obstructive hydrocephalus as they grow. Rarely, however, some intraventricular tumors develop superficial siderosis (SS) and trigger hydrocephalus, even though the tumor has hardly grown. Here, we present an illustrative case of SS and nonocclusive hydrocephalus caused by subependymoma of the lateral ventricles.</AbstractText>A 78-year-old man with an intraventricular tumor diagnosed 7 years ago had been suffering from gait disturbance for 2 years. He also developed cognitive impairment. Intraventricular tumors showed little growth on annual magnetic resonance imaging (MRI). MRI T2-star weighted images (T2*WI) captured small intratumoral hemorrhages from the beginning of the follow-up. Three years before, at the same time as the onset of ventricular enlargement, T2*WI revealed low intensity in the whole tumor and cerebral surface. Subsequent follow-up revealed that this hemosiderin deposition had spread to the brain stem and cerebellar surface, and the ventricles had expanded further. Cerebrospinal fluid (CSF) examination revealed xanthochromia. The tumor was completely removed en bloc</i>. Histopathological findings were consistent with those of subependymoma. Although CSF findings improved, SS and hydrocephalus did not improve. Therefore, the patient underwent a lumboperitoneal shunt for CSF diversion after tumor resection.</AbstractText>Some intraventricular tumors cause SS and nonobstructive hydrocephalus due to microbleeding, even in the absence of tumor growth. T2*WI and, if necessary, timely CSF examination can allow identification of presymptomatic SS. This follow-up strategy may provide a favorable course by facilitating early intervention in patients with intraventricular lesions, not just subependymomas.</AbstractText>Copyright: &#xa9; 2021 Surgical Neurology International.</CopyrightInformation>
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Strategies for the Long-Term Preservation of Site for Future Implantation of Cardiac Implantable Electronic Devices (CIEDs): Two Decades of Experience.
Introduction Implantation of cardiac implantable electronic devices (CIEDs) is an art of science. As the volume of implantation has increased worldwide, so has the rate of complications. Infection, fibrosis, lead and device erosion, lead displacement, right ventricle perforation, lead fracture, and insulation break are the common complications in the implantation process. This exposes the patient for reopening and threatens the implantation for further complication due to infection, fibrosis of veins, failure to retrieve the implanted wire, and failure to re-implant the device on the same site. We slightly changed our implantation technique to preserve the implantation site for future implantation and reduce the rate of complication in the index implantation. Methods This randomized control trial was conducted from January 2016 to September 2019 at Hayatabad Medical Complex Peshawar, Pakistan. A consecutive sampling technique was used to obtain a sample size of&#xa0;602 patients keeping a 95% confidence interval and a 5% margin error. We adopted a strategy to take prick, for implantation of devices, inside the pocket, which reduces the number of sutures, hastens the procedure, prevents erosion, and minimizes the chance of subclavian crush syndrome and insulation break. We also selected the minimum possible length of leads. This will possibly decrease the chances of cumbersome fibrosis around the lead and device and will make future implantation convenient. Results There was a total of 602 procedures in the study period. About 253 (42%) procedures were done in the newly adopted strategy and 349 (58%) were performed in the conventional way. Our complication rate grossly reduces in the novel way of implantation in which we took our prick inside the pocket. Conclusion A slight modification in the implantation of CIEDs not only prevents the rate of complication in the index implantation but will also possibly preserve the site for future implantation.
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Right Tegmental Hemorrhage with Urinary Retention: A Case Report.
The upper brainstem tegmentum is dense and complex, making it difficult to localize functions to specific subregions. In particular, the precise location and possible laterality of subregions supporting basic functions like consciousness and urinary continence remain unclear. Here, we describe a patient who presented with a right pontine tegmental syndrome caused by intraparenchymal hemorrhage. Despite hemorrhage extension into the fourth ventricle and expansion of both hemorrhage and edema into a large region of the caudal midbrain and right-sided pontine tegmentum, this patient did not lose consciousness. Instead, he developed new and total urinary retention, with residual bladder volumes of more than 1,000 mL. We conclude that injury to the right pontine tegmentum is sufficient to disrupt the micturition reflex pathway.
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Sirt1 Protects Subventricular Zone-Derived Neural Stem Cells from DNA Double-Strand Breaks and Contributes to Olfactory Function Maintenance in Aging Mice.
DNA damage is assumed to accumulate in stem cells over time and their ability to withstand this damage and maintain tissue homeostasis is the key determinant of aging. Nonetheless, relatively few studies have investigated whether DNA damage does indeed accumulate in stem cells and whether this contributes to stem cell aging and functional decline. Here, we found that, compared with young mice, DNA double-strand breaks (DSBs) are reduced in the subventricular zone (SVZ)-derived neural stem cells (NSCs) of aged mice, which was achieved partly through the adaptive upregulation of Sirt1 expression and non-homologous end joining (NHEJ)-mediated DNA repair. Sirt1 deficiency abolished this effect, leading to stem cell exhaustion, olfactory memory decline, and accelerated aging. The reduced DSBs and the upregulation of Sirt1 expression in SVZ-derived NSCs with age may represent a compensatory mechanism that evolved to protect stem cells from excessive DNA damage, as well as mitigate memory loss and other stresses during aging.
2,330,151
Pineal germinoma in a young adult: A case report.
Intracranial germinomas (GN) are rare cancers that primarily affect children, making them rarer still in adults. Standard treatment for this neoplasm includes neoadjuvant chemotherapy (NC) followed by radiotherapy (RT) or RT at a higher dose and larger field. These recommendations are based on studies focused mostly on children; it is currently unclear whether this treatment is applicable to adults.</AbstractText>We present a case of a 23-year-old adult male with no underlying pathologies, drug allergies, or family history of cancer, who presented for medical evaluation with blurred vision, diplopia, forgetfulness, and weight loss starting 3-4&#xa0;months before the evaluation. Clinical examination indicated Parinaud's Syndrome. Magnetic resonance imaging (MRI) and computed tomography (CT) revealed a pineal tumor with ependymal dissemination in both lateral ventricles, which was causing obstructive hydrocephalus. The patient had surgery consisting of ventriculostomy, Holter shunt insertion, cisternal ventricular intubation, and cisterna magna anastomosis to improve ventricular drainage. Pathology confirmed pineal germinoma. Cerebrospinal fluid cytology and MRI of the axis were negative. Four cycles of NC were given to the patient (carboplatin, etoposide, and ifosfamide), with reduced dosage. Once a partial volumetric response was confirmed, whole-ventricular radiotherapy (WVR) was initiated with a total tumor bed dose of 45&#x2009;Gy over 25 sessions in 5&#x2009;weeks. Optimum clinical results were observed, and no short-term (&lt;90&#x2009;day) radiation toxicity was observed. The patient was able to resume his normal activities soon after treatment. Follow-ups over 2&#x2009;years post-surgery indicated continued control of the lesion and absence of symptoms except for mild diplopia.</AbstractText>Although this is a case report, these data suggest that a reduced NC course and WVR may effectively treat adult GN. This protocol likely decreases the risk of undesirable NC and RT secondary effects, while providing excellent local control; however, using a narrower RT field is not recommended.</AbstractText>&#xa9; 2022 The Authors. Cancer Reports published by Wiley Periodicals LLC.</CopyrightInformation>
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Ionic currents underlying different patterns of electrical activity in working cardiac myocytes of mammals and non-mammalian vertebrates.
The orderly contraction of the vertebrate heart is determined by generation and propagation of cardiac action potentials (APs). APs are generated by the integrated activity of time- and voltage-dependent ionic channels which carry inward Na<sup>+</sup> and Ca<sup>2+</sup> currents, and outward K<sup>+</sup> currents. This review compares atrial and ventricular APs and underlying ion currents between different taxa of vertebrates. We have collected literature data and attempted to find common electrophysiological features for two or more vertebrate groups, show differences between taxa and cardiac chambers, and indicate gaps in the existing data. Although electrical excitability of the heart in all vertebrates is based on the same superfamily of channels, there is a vast variability of AP waveforms between atrial and ventricular myocytes, between different species of the same vertebrate class and between endothermic and ectothermic animals. The wide variability of AP shapes is related to species-specific differences in animal size, heart rate, stage of ontogenetic development, excitation-contraction coupling, temperature and oxygen availability. Some of the differences between taxa are related to evolutionary development of genomes, which appear e.g. in the expression of different Na<sup>+</sup> and K<sup>+</sup> channel orthologues in cardiomyocytes of vertebrates. There is a wonderful variability of AP shapes and underlying ion currents with which electrical excitability of vertebrate heart can be generated depending on the intrinsic and extrinsic conditions of animal body. This multitude of ionic mechanisms provides excellent material for studying how the function of the vertebrate heart can adapt or acclimate to prevailing physiological and environmental conditions.
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Simultaneous multislice steady-state free precession myocardial perfusion with full left ventricular coverage and high resolution at 1.5 T.
To implement and evaluate a simultaneous multi-slice balanced SSFP (SMS-bSSFP) perfusion sequence and compressed sensing reconstruction for cardiac MR perfusion imaging with full left ventricular (LV) coverage (nine slices/heartbeat) and high spatial resolution (1.4&#x2009;&#xd7;&#x2009;1.4&#x2009;mm2</sup> ) at 1.5T.</AbstractText>A preliminary study was performed to evaluate the performance of blipped controlled aliasing in parallel imaging (CAIPI) and RF-CAIPI with gradient-controlled local Larmor adjustment (GC-LOLA) in the presence of fat. A nine-slice SMS-bSSFP sequence using RF-CAIPI with GC-LOLA with high spatial resolution (1.4&#x2009;&#xd7;&#x2009;1.4&#x2009;mm2</sup> ) and a conventional three-slice sequence with conventional spatial resolution (1.9&#x2009;&#xd7;&#x2009;1.9&#x2009;mm2</sup> ) were then acquired in 10 patients under rest conditions. Qualitative assessment was performed to assess image quality and perceived signal-to-noise ratio (SNR) on a 4-point scale (0: poor image quality/low SNR; 3: excellent image quality/high SNR), and the number of myocardial segments with diagnostic image quality was recorded. Quantitative measurements of myocardial sharpness and upslope index were performed.</AbstractText>Fat signal leakage was significantly higher for blipped CAIPI than for RF-CAIPI with GC-LOLA (7.9% vs. 1.2%, p&#xa0;=&#x2009;0.010). All 10 SMS-bSSFP perfusion datasets resulted in 16/16 diagnostic myocardial segments. There were no significant differences between the SMS and conventional acquisitions in terms of image quality (2.6&#xa0;&#xb1;&#x2009;0.6 vs. 2.7&#xa0;&#xb1;&#x2009;0.2, p&#xa0;=&#x2009;0.8) or perceived SNR (2.8&#xa0;&#xb1;&#x2009;0.3 vs. 2.7&#xa0;&#xb1;&#x2009;0.3, p&#xa0;=&#x2009;0.3). Inter-reader variability was good for both image quality (ICC&#xa0;=&#xa0;0.84) and perceived SNR (ICC&#xa0;=&#xa0;0.70). Myocardial sharpness was improved using the SMS sequence compared to the conventional sequence (0.37&#x2009;&#xb1;&#x2009;0.08 vs 0.32&#x2009;&#xb1;&#x2009;0.05, p&#xa0;&lt;&#x2009;0.001). There was no significant difference between measurements of upslope index for the SMS and conventional sequences (0.11&#x2009;&#xb1;&#x2009;0.04 vs. 0.11&#x2009;&#xb1;&#x2009;0.03, p&#xa0;=&#x2009;0.84).</AbstractText>SMS-bSSFP with multiband factor 3 and compressed sensing reconstruction enables cardiac MR perfusion imaging with three-fold increased spatial coverage and improved myocardial sharpness compared to a conventional sequence, without compromising perceived SNR, image quality, upslope index or number of diagnostic segments.</AbstractText>&#xa9; 2022 The Authors. Magnetic Resonance in Medicine published by Wiley Periodicals LLC on behalf of International Society for Magnetic Resonance in Medicine.</CopyrightInformation>
2,330,154
Successful treatment of hypodipsic/adipsic hypernatremia in a cat with lobar holoprosencephaly using oral desmopressin.
A 2-year-old female spayed domestic shorthair cat was presented with a history of collapse, possible hypodipsia/adipsia, severe dehydration and hypernatremia. MRI of the brain revealed a failure of separation of the cerebral hemispheres as characterized by an absence of the rostral part of the corpus callosum, fornix and septum pellucidum and the presence of a single fused lateral ventricle. A diagnosis of hypodipsic/adipsic hypernatremia with lobar holoprosencephaly was made. Dietary management of the cat's condition was attempted by increasing oral water intake, but the cat's hypernatremia and azotemia persisted. Plasma arginine vasopressin (AVP) analysis revealed a low concentration of circulating AVP (2.3&#x2009;pg/ml), prompting therapy with oral desmopressin in addition to the dietary management. This combined therapy decreased water consumption of the cat from 200&#x2009;ml/day (85&#x2009;ml/kg/day) to 100&#x2009;ml/day (30&#x2009;ml/kg/day), normalized plasma sodium concentration and resolved the azotemia.</AbstractText>To our knowledge, this is the second case report of an MRI diagnosis of lobar holoprosencephaly with hypodipsic/adipsic hypernatremia in a cat and the first case report of the successful management of this condition using oral desmopressin. This case report emphasizes that holoprosencephaly should be suspected in cats presented with hypodipsic/adipsic hypernatremia and highlights the utility of MRI in establishing the diagnosis. Measurements of plasma osmolality and AVP concentration corroborate the pathophysiology and support the use of oral desmopressin in addition to dietary management to resolve the hypernatremia.</AbstractText>&#xa9; The Author(s) 2022.</CopyrightInformation>
2,330,155
Characteristic and Management of Symptomatic Septum Pellucidum Cyst in Extreme Elderly Patient: Case Report and Literature Review.
Septum pellucidum cyst is rare and is defined as a fluid-filled space between the lateral ventricles; it has a width of 10 mm or more. In this case report, a surgical patient of symptomatic septum pellucidum cyst (SPC) in extreme age is described. To the best our knowledge, this is the first report of an extremely aged patient with symptomatic SPC that was successfully treated using a flexible neuroendoscope. An 85-year-old male complained of gradually worsening gait disturbance, dementia, and urinary incontinence without headache and was admitted to our hospital. MRI revealed a huge cyst between the lateral ventricles as well as ventricle dilatation with periventricular hyperintensity in T2-weighted image. The patient was diagnosed with symptomatic hydrocephalus with SPC and underwent neuroendoscopic fenestration of the cyst with the use of a flexible endoscope without cerebrospinal fluid shunt placement. Immediately after the surgery, the patient's gait disturbance and dementia were dramatically improved. In extremely aged patients, SPC tended to develop with idiopathic normal pressure hydrocephalus-like symptoms, including gait disturbance without increasing intracranial pressure, sensorimotor disturbances, and psychological disorders. Neuroendoscopic cyst fenestration with the use of a flexible scope for SPC is a less-invasive procedure and should be considered even for extreme elderly symptomatic patients.
2,330,156
In vivo Correlation Tensor MRI reveals microscopic kurtosis in the human brain on a clinical 3T scanner.
Diffusion MRI (dMRI) has become one of the most important imaging modalities for noninvasively probing tissue microstructure. Diffusional Kurtosis MRI (DKI) quantifies the degree of non-Gaussian diffusion, which in turn has been shown to increase sensitivity towards, e.g., disease and orientation mapping in neural tissue. However, the specificity of DKI is limited as different sources can contribute to the total intravoxel diffusional kurtosis, including: variance in diffusion tensor magnitudes (K<sub>iso</sub>), variance due to diffusion anisotropy (K<sub>aniso</sub>), and microscopic kurtosis (&#x3bc;K) related to restricted diffusion, microstructural disorder, and/or exchange. Interestingly, &#x3bc;K is typically ignored in diffusion MRI signal modelling as it is assumed to be negligible in neural tissues. However, recently, Correlation Tensor MRI (CTI) based on Double-Diffusion-Encoding (DDE) was introduced for kurtosis source separation, revealing non negligible &#x3bc;K in preclinical imaging. Here, we implemented CTI for the first time on a clinical 3T scanner and investigated the sources of total kurtosis in healthy subjects. A robust framework for kurtosis source separation in humans is introduced, followed by estimation of &#x3bc;K (and the other kurtosis sources) in the healthy brain. Using this clinical CTI approach, we find that &#x3bc;K significantly contributes to total diffusional kurtosis both in grey and white matter tissue but, as expected, not in the ventricles. The first &#x3bc;K maps of the human brain are presented, revealing that the spatial distribution of &#x3bc;K provides a unique source of contrast, appearing different from isotropic and anisotropic kurtosis counterparts. Moreover, group average templates of these kurtosis sources have been generated for the first time, which corroborated our findings at the underlying individual-level maps. We further show that the common practice of ignoring &#x3bc;K and assuming the multiple Gaussian component approximation for kurtosis source estimation introduces significant bias in the estimation of other kurtosis sources and, perhaps even worse, compromises their interpretation. Finally, a twofold acceleration of CTI is discussed in the context of potential future clinical applications. We conclude that CTI has much potential for future in vivo microstructural characterizations in healthy and pathological tissue.
2,330,157
Boron Delivery to Brain Cells via Cerebrospinal Fluid (CSF) Circulation for BNCT in a Rat Melanoma Model.
Recently, exploitation of cerebrospinal fluid (CSF) circulation has become increasingly recognized as a feasible strategy to solve the challenges involved in drug delivery for treating brain tumors. Boron neutron capture therapy (BNCT) also faces challenges associated with the development of an efficient delivery system for boron, especially to brain tumors. Our laboratory has been developing a system for boron delivery to brain cells using CSF, which we call the "boron CSF administration method". In our previous study, we found that boron was efficiently delivered to the brain cells of normal rats in the form of small amounts of L-p-boronophenylalanine (BPA) using the CSF administration method. In the study described here, we carried out experiments with brain tumor model rats to demonstrate the usefulness of the CSF administration method for BNCT. We first investigated the boron concentration of the brain cells every 60 min after BPA administration into the lateral ventricle of normal rats. Second, we measured and compared the boron concentration in the melanoma model rats after administering boron via either the CSF administration method or the intravenous (IV) administration method, with estimation of the T/N ratio. Our results revealed that boron injected by the CSF administration method was excreted quickly from normal cells, resulting in a high T/N ratio compared to that of IV administration. In addition, the CSF administration method resulted in high boron accumulation in tumor cells. In conclusion, we found that using our developed CSF administration method results in more selective delivery of boron to the brain tumor compared with the IV administration method.
2,330,158
Microelectromechanical Systems Based on Magnetic Polymer Films.
Microelectromechanical systems (MEMS) have been increasingly used worldwide in a wide range of applications, including high tech, energy, medicine or environmental applications. Magnetic polymer composite films have been used extensively in the development of the micropumps and valves, which are critical components of the microelectromechanical systems. Based on the literature survey, several polymers and magnetic micro and nanopowders can be identified and, depending on their nature, ratio, processing route and the design of the device, their performances can be tuned from simple valves and pumps to biomimetic devices, such as, for instance, hearth ventricles. In many such devices, polymer magnetic films are used, the disposal of the magnetic component being either embedded into the polymer or coated on the polymer. One or more actuation zones can be used and the flow rate can be mono-directional or bi-directional depending on the design. In this paper, we review the main advances in the development of these magnetic polymer films and derived MEMS: microvalve, micropump, micromixer, microsensor, drug delivery micro-systems, magnetic labeling and separation microsystems, etc. It is important to mention that these MEMS are continuously improving from the point of view of performances, energy consumption and actuation mechanism and a clear tendency in developing personalized treatment. Due to the improved energy efficiency of special materials, wearable devices are developed and be suitable for medical applications.
2,330,159
Comparative Analysis of Myocardial Viability Multimodality Imaging in Patients with Previous Myocardial Infarction and Symptomatic Heart Failure.<ELocationID EIdType="pii" ValidYN="Y">368</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/medicina58030368</ELocationID><Abstract><AbstractText>Background and Objectives: To compare the accuracy of multimodality imaging (myocardial perfusion imaging with single-photon emission computed tomography (SPECT MPI), 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET), and cardiovascular magnetic resonance (CMR) in the evaluation of left ventricle (LV) myocardial viability for the patients with the myocardial infarction (MI) and symptomatic heart failure (HF). Materials and Methods: 31 consecutive patients were included in the study prospectively, with a history of previous myocardial infarction, symptomatic HF (NYHA) functional class II or above, reduced ejection fraction (EF) &#x2264; 40%. All patients had confirmed atherosclerotic coronary artery disease (CAD), but conflicting opinions regarding the need for percutaneous intervention due to the suspected myocardial scar tissue. All patients underwent transthoracic echocardiography (TTE), SPECT MPI, 18F-FDG PET, and CMR with late gadolinium enhancement (LGE) examinations. Quantification of myocardial viability was assessed in a 17-segment model. All segments that were described as non-viable (score 4) by CMR LGE and PET were compared. The difference of score between CMR and PET we named reversibility score. According to this reversibility score, patients were divided into two groups: Group 1, reversibility score &gt; 10 (viable myocardium with a chance of functional recovery after revascularization); Group 2, reversibility score &#x2264; 10 (less viable myocardium when revascularisation remains questionable). Results: 527 segments were compared in total. A significant difference in scores 1, 2, 3 group, and score 4 group was revealed between different modalities. CMR identified &#x201c;non-viable&#x201d; myocardium in 28.1% of segments across all groups, significantly different than SPECT in 11.8% PET in 6.5% Group 1 (viable myocardium group) patients had significantly higher physical tolerance (6 MWT (m) 3892 &#xb1; 94.5 vs. 301.4 &#xb1; 48.2), less dilated LV (LVEDD (mm) (TTE) 53.2 &#xb1; 7.9 vs. 63.4 &#xb1; 8.9; MM (g) (TTE) 239.5 &#xb1; 85.9 vs. 276.3 &#xb1; 62.7; LVEDD (mm) (CMR) 61.7 &#xb1; 8.1 vs. 69.0 &#xb1; 6.1; LVEDDi (mm/m2) (CMR) 29.8 &#xb1; 3.7 vs. 35.2 &#xb1; 3.1), significantly better parameters of the right heart (RV diameter (mm) (TTE) 33.4 &#xb1; 6.9 vs. 38.5 &#xb1; 5.0; TAPSE (mm) (TTE) 18.7 &#xb1; 2.0 vs. 15.2 &#xb1; 2.0), better LV SENC function (LV GLS (CMR) &#x2212;14.3 &#xb1; 2.1 vs. 11.4 &#xb1; 2.9; LV GCS (CMR) &#x2212;17.2 &#xb1; 4.6 vs. 12.7 &#xb1; 2.6), smaller size of involved myocardium (infarct size (%) (CMR) 24.5 &#xb1; 9.6 vs. 34.8 &#xb1; 11.1). Good correlations were found with several variables (LVEDD (CMR), LV EF (CMR), LV GCS (CMR)) with a coefficient of determination (R2) of 0.72. According to the cut-off values (LVEDV (CMR) &gt; 330 mL, infarct size (CMR) &gt; 26%, and LV GCS (CMR) &lt; &#x2212;15.8), we performed prediction of non-viable myocardium (reversibility score &lt; 10) with the overall percentage of 80.6 (Nagelkerke R2 0.57). Conclusions: LGE CMR reveals a significantly higher number of scars, and the FDG PET appears to be more optimistic in the functional recovery prediction. Moreover, using exact imaging parameters (LVEDV (CMR) &gt; 330 mL, infarct size (CMR) &gt; 26% and LV GCS (CMR) &lt; &#x2212;15.8) may increase sensitivity and specificity of LGE CMR for evaluation of non-viable myocardium and lead to a better clinical solution (revascularization vs. medical treatment) even when viability is low in LGE CMR, and FDG PET is not performed.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kazakauskaite</LastName><ForeName>Egle</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0002-0482-9372</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vajauskas</LastName><ForeName>Donatas</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-3769-3520</Identifier><AffiliationInfo><Affiliation>Radiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Unikaite</LastName><ForeName>Ruta</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jonauskiene</LastName><ForeName>Ieva</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Virbickiene</LastName><ForeName>Agneta</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-8451-9963</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zaliaduonyte</LastName><ForeName>Diana</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-8797-999X</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lapinskas</LastName><ForeName>Tomas</ForeName><Initials>T</Initials><Identifier Source="ORCID">0000-0001-7726-6948</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jurkevicius</LastName><ForeName>Renaldas</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Medicina (Kaunas)</MedlineTA><NlmUniqueID>9425208</NlmUniqueID><ISSNLinking>1010-660X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003287">Contrast Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019275">Radiopharmaceuticals</NameOfSubstance></Chemical><Chemical><RegistryNumber>AU0V1LM3JT</RegistryNumber><NameOfSubstance UI="D005682">Gadolinium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003287" MajorTopicYN="N">Contrast Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005682" MajorTopicYN="N">Gadolinium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="Y">Myocardial Infarction</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019275" MajorTopicYN="N">Radiopharmaceuticals</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">18F-fluorodeoxyglucose positron emission tomography</Keyword><Keyword MajorTopicYN="N">SENC imaging</Keyword><Keyword MajorTopicYN="N">late gadolinium enhancement</Keyword><Keyword MajorTopicYN="N">myocardial viability</Keyword><Keyword MajorTopicYN="N">reversibility score</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>2</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>2</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>3</Month><Day>26</Day><Hour>1</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>3</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>3</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35334543</ArticleId><ArticleId IdType="pmc">PMC8955633</ArticleId><ArticleId IdType="doi">10.3390/medicina58030368</ArticleId><ArticleId IdType="pii">medicina58030368</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Braunwald E., Kloner R.A. 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Part 2: inferior peduncular, rhomboid, and supraolivary.
Background and Objectives: To compare the accuracy of multimodality imaging (myocardial perfusion imaging with single-photon emission computed tomography (SPECT MPI), 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET), and cardiovascular magnetic resonance (CMR) in the evaluation of left ventricle (LV) myocardial viability for the patients with the myocardial infarction (MI) and symptomatic heart failure (HF). Materials and Methods: 31 consecutive patients were included in the study prospectively, with a history of previous myocardial infarction, symptomatic HF (NYHA) functional class II or above, reduced ejection fraction (EF) &#x2264; 40%. All patients had confirmed atherosclerotic coronary artery disease (CAD), but conflicting opinions regarding the need for percutaneous intervention due to the suspected myocardial scar tissue. All patients underwent transthoracic echocardiography (TTE), SPECT MPI, 18F-FDG PET, and CMR with late gadolinium enhancement (LGE) examinations. Quantification of myocardial viability was assessed in a 17-segment model. All segments that were described as non-viable (score 4) by CMR LGE and PET were compared. The difference of score between CMR and PET we named reversibility score. According to this reversibility score, patients were divided into two groups: Group 1, reversibility score &gt; 10 (viable myocardium with a chance of functional recovery after revascularization); Group 2, reversibility score &#x2264; 10 (less viable myocardium when revascularisation remains questionable). Results: 527 segments were compared in total. A significant difference in scores 1, 2, 3 group, and score 4 group was revealed between different modalities. CMR identified &#x201c;non-viable&#x201d; myocardium in 28.1% of segments across all groups, significantly different than SPECT in 11.8% PET in 6.5% Group 1 (viable myocardium group) patients had significantly higher physical tolerance (6 MWT (m) 3892 &#xb1; 94.5 vs. 301.4 &#xb1; 48.2), less dilated LV (LVEDD (mm) (TTE) 53.2 &#xb1; 7.9 vs. 63.4 &#xb1; 8.9; MM (g) (TTE) 239.5 &#xb1; 85.9 vs. 276.3 &#xb1; 62.7; LVEDD (mm) (CMR) 61.7 &#xb1; 8.1 vs. 69.0 &#xb1; 6.1; LVEDDi (mm/m2) (CMR) 29.8 &#xb1; 3.7 vs. 35.2 &#xb1; 3.1), significantly better parameters of the right heart (RV diameter (mm) (TTE) 33.4 &#xb1; 6.9 vs. 38.5 &#xb1; 5.0; TAPSE (mm) (TTE) 18.7 &#xb1; 2.0 vs. 15.2 &#xb1; 2.0), better LV SENC function (LV GLS (CMR) &#x2212;14.3 &#xb1; 2.1 vs. 11.4 &#xb1; 2.9; LV GCS (CMR) &#x2212;17.2 &#xb1; 4.6 vs. 12.7 &#xb1; 2.6), smaller size of involved myocardium (infarct size (%) (CMR) 24.5 &#xb1; 9.6 vs. 34.8 &#xb1; 11.1). Good correlations were found with several variables (LVEDD (CMR), LV EF (CMR), LV GCS (CMR)) with a coefficient of determination (R2) of 0.72. According to the cut-off values (LVEDV (CMR) &gt; 330 mL, infarct size (CMR) &gt; 26%, and LV GCS (CMR) &lt; &#x2212;15.8), we performed prediction of non-viable myocardium (reversibility score &lt; 10) with the overall percentage of 80.6 (Nagelkerke R2 0.57). Conclusions: LGE CMR reveals a significantly higher number of scars, and the FDG PET appears to be more optimistic in the functional recovery prediction. Moreover, using exact imaging parameters (LVEDV (CMR) &gt; 330 mL, infarct size (CMR) &gt; 26% and LV GCS (CMR) &lt; &#x2212;15.8) may increase sensitivity and specificity of LGE CMR for evaluation of non-viable myocardium and lead to a better clinical solution (revascularization vs. medical treatment) even when viability is low in LGE CMR, and FDG PET is not performed.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kazakauskaite</LastName><ForeName>Egle</ForeName><Initials>E</Initials><Identifier Source="ORCID">0000-0002-0482-9372</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vajauskas</LastName><ForeName>Donatas</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-3769-3520</Identifier><AffiliationInfo><Affiliation>Radiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Unikaite</LastName><ForeName>Ruta</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jonauskiene</LastName><ForeName>Ieva</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Virbickiene</LastName><ForeName>Agneta</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-8451-9963</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zaliaduonyte</LastName><ForeName>Diana</ForeName><Initials>D</Initials><Identifier Source="ORCID">0000-0002-8797-999X</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lapinskas</LastName><ForeName>Tomas</ForeName><Initials>T</Initials><Identifier Source="ORCID">0000-0001-7726-6948</Identifier><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jurkevicius</LastName><ForeName>Renaldas</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Cardiology Clinic, Medical Academy, University of Health Sciences, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Kaunas Region Society of Cardiology, 44307 Kaunas, Lithuania.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Medicina (Kaunas)</MedlineTA><NlmUniqueID>9425208</NlmUniqueID><ISSNLinking>1010-660X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003287">Contrast Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019275">Radiopharmaceuticals</NameOfSubstance></Chemical><Chemical><RegistryNumber>AU0V1LM3JT</RegistryNumber><NameOfSubstance UI="D005682">Gadolinium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D003287" MajorTopicYN="N">Contrast Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005682" MajorTopicYN="N">Gadolinium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="Y">Myocardial Infarction</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019275" MajorTopicYN="N">Radiopharmaceuticals</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">18F-fluorodeoxyglucose positron emission tomography</Keyword><Keyword MajorTopicYN="N">SENC imaging</Keyword><Keyword MajorTopicYN="N">late gadolinium enhancement</Keyword><Keyword MajorTopicYN="N">myocardial viability</Keyword><Keyword MajorTopicYN="N">reversibility score</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2022</Year><Month>1</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2022</Year><Month>2</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>2</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>3</Month><Day>26</Day><Hour>1</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>3</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Imaging. 2009;29:99&#x2013;105. doi: 10.1002/jmri.21612.</Citation><ArticleIdList><ArticleId IdType="doi">10.1002/jmri.21612</ArticleId><ArticleId IdType="pubmed">19097105</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">35334460</PMID><DateRevised><Year>2022</Year><Month>03</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1933-0693</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2022</Year><Month>Mar</Month><Day>25</Day></PubDate></JournalIssue><Title>Journal of neurosurgery</Title><ISOAbbreviation>J Neurosurg</ISOAbbreviation></Journal><ArticleTitle>A taxonomy for brainstem cavernous malformations: subtypes of pontine lesions. Part 2: inferior peduncular, rhomboid, and supraolivary.</ArticleTitle><Pagination><StartPage>1</StartPage><EndPage>14</EndPage><MedlinePgn>1-14</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3171/2022.1.JNS212691</ELocationID><ELocationID EIdType="pii" ValidYN="Y">2022.1.JNS212691</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Part 2 of this 2-part series on pontine cavernomas presents the taxonomy for subtypes 4-6: inferior peduncular (IP) (subtype 4), rhomboid (5), and supraolivary (6). (Subtypes 1-3 are presented in Part 1.) The authors have proposed a novel taxonomy for pontine cavernous malformations based on clinical presentation (syndromes) and anatomical location (MRI findings).<AbstractText Label="METHODS" NlmCategory="METHODS">The details of taxonomy development are described fully in Part 1 of this series. In brief, pontine lesions (323 of 601 [53.7%] total lesions) were subtyped on the basis of predominant surface presentation identified on preoperative MRI. Neurological outcomes were assessed according to the modified Rankin Scale, with score &#x2264; 2 defined as favorable.<AbstractText Label="RESULTS" NlmCategory="RESULTS">The 323 pontine brainstem cavernous malformations were classified into 6 distinct subtypes: basilar (6 [1.9%]), peritrigeminal (53 [16.4%]), middle peduncular (100 [31.0%]), IP (47 [14.6%]), rhomboid (80 [24.8%]), and supraolivary (37 [11.5%]). Subtypes 4-6 are the subject of the current report. IP lesions are located in the inferolateral pons and are associated with acute vestibular syndrome. Rhomboid lesions present to the fourth ventricle floor and are associated with disconjugate eye movements. Larger lesions may cause ipsilateral facial weakness. Supraolivary lesions present to the surface at the ventral pontine underbelly. Ipsilateral abducens palsy is a strong localizing sign for this subtype. A single surgical approach and strategy were preferred for subtypes 4-6: for IP cavernomas, the suboccipital craniotomy and telovelar approach predominated; for rhomboid lesions, the suboccipital craniotomy and transventricular approach were preferred; and for supraolivary malformations, the far lateral craniotomy and transpontomedullary sulcus approach were preferred. Favorable outcomes were observed in 132 of 150 (88%) patients with follow-up. There were no significant differences in outcomes between subtypes.<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">The neurological symptoms and signs associated with a hemorrhagic pontine subtype can help define that subtype clinically with key localizing signs. The proposed taxonomy for pontine cavernous malformation subtypes 4-6 meaningfully guides surgical strategy and may improve patient outcomes.
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5-aminolevulinic acid and sodium fluorescein in IV ventricle ependymoma surgery: preliminary experience comparing the two techniques.
The aim of this study is to compare the use of 5-aminolevulinic acid (5-ALA) and sodium fluorescein (SF) in IV ventricular ependymoma (IVEP) surgical resection.</AbstractText>In this retrospective study, six patients with IVEP were enrolled. Gender ratio 2:1 male to female, with mean age 38.9&#xa0;years old. A 5-ALA oral dose of 20&#xa0;mg/kg and a SF intravenous dose of 2&#xa0;mg/kg were administered. Telo-velar approach, operative microscope, and intraoperative monitoring were used in all the operations. We retrospectively compared the two fluorescence techniques at four steps during the surgical procedure: step 1: exposure of the tumor; step 2: dissection of the lesion from the cerebellum; step 3: assessment of the tumor borders and differentiation from normal tissue at the base of implants; and step 4: evaluation of possible residual tissue in the surgical cavity.</AbstractText>At the first step, the ependymomas resulted well delineated by both fluorescent agents. In this step, 5-ALA was particularly helpful in the case of recurrent ependymoma. At step 2, 5-ALA provided a better identification of the ependymoma boundaries and distinction from cerebellum hemispheres than SF. In steps 3 and 4, SF was really helpful to detect tumor tissue.</AbstractText>According to our experience, fluorescence-guided surgery of IVEP with 5-ALA and SF is useful to maximize surgical resection with less risk of brainstem injury. Both fluorescence techniques are helpful in different steps of IVEP resection. However, further studies are needed to confirm our preliminary data.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
2,330,161
Efficacy and Safety of a Krabbe Disease Gene Therapy.
Krabbe disease is a lysosomal storage disease caused by mutations in the gene that encodes galactosylceramidase, in which galactosylsphingosine (psychosine) accumulation drives demyelination in the central and peripheral nervous systems, ultimately progressing to death in early childhood. Gene therapy, alone or in combination with transplant, has been developed for almost two decades in mouse models, with increasing therapeutic benefit paralleling the improvement of next-generation adeno-associated virus (AAV) vectors. This effort has recently shown remarkable efficacy in the canine model of the disease by two different groups that used either systemic or cerebrospinal fluid (CSF) administration of AAVrh10 or AAV9. Building on our experience developing CSF-delivered, AAV-based drug products for a variety of neurodegenerative disorders, we conducted efficacy, pharmacology, and safety studies of AAVhu68 delivered to the CSF in two relevant natural Krabbe animal models, and in nonhuman primates. In newborn Twitcher mice, the highest dose (1&#x2009;&#xd7;&#x2009;10<sup>11</sup> genome copies [GC]) of AAVhu68.hGALC injected into the lateral ventricle led to a median survival of 130 days compared to 40.5 days in vehicle-treated mice. When this dose was administered intravenously, the median survival was 49 days. A single intracisterna magna injection of AAVhu68.cGALC at 3&#x2009;&#xd7;&#x2009;10<sup>13</sup> GC into presymptomatic Krabbe dogs increased survival for up to 85 weeks compared to 12 weeks in controls. It prevented psychosine accumulation in the CSF, preserved peripheral nerve myelination, ambulation, and decreased brain neuroinflammation and demyelination, although some regions remained abnormal. In a Good Laboratory Practice-compliant toxicology study, we administered the clinical candidate into the cisterna magna of 18 juvenile rhesus macaques at 3 doses that displayed efficacy in mice. We observed no dose-limiting toxicity and sporadic minimal degeneration of dorsal root ganglia (DRG) neurons. Our studies demonstrate the efficacy, scalability, and safety of a single cisterna magna AAVhu68 administration to treat Krabbe disease. ClinicalTrials.Gov ID: NCT04771416.
2,330,162
Subcortical segmentation of the fetal brain in 3D ultrasound using deep learning.
The quantification of subcortical volume development from 3D fetal ultrasound can provide important diagnostic information during pregnancy monitoring. However, manual segmentation of subcortical structures in ultrasound volumes is time-consuming and challenging due to low soft tissue contrast, speckle and shadowing artifacts. For this reason, we developed a convolutional neural network (CNN) for the automated segmentation of the choroid plexus (CP), lateral posterior ventricle horns (LPVH), cavum septum pellucidum et vergae (CSPV), and cerebellum (CB) from 3D ultrasound. As ground-truth labels are scarce and expensive to obtain, we applied few-shot learning, in which only a small number of manual annotations (n = 9) are used to train a CNN. We compared training a CNN with only a few individually annotated volumes versus many weakly labelled volumes obtained from atlas-based segmentations. This showed that segmentation performance close to intra-observer variability can be obtained with only a handful of manual annotations. Finally, the trained models were applied to a large number (n = 278) of ultrasound image volumes of a diverse, healthy population, obtaining novel US-specific growth curves of the respective structures during the second trimester of gestation.
2,330,163
Neurological Presentation of Giant Pituitary Tumour Apoplexy: Case Report and Literature Review of a Rare but Life-Threatening Condition.
Background: Giant pituitary adenomas are benign intracranial tumours with a diameter &#x2265;4 cm. Even if hormonally non-functional, they may still cause local extension, leading to symptoms that include mostly gland dysfunction, mass effects, and, much less frequently, apoplexy due to haemorrhage or infarction. Neurological presentation of giant pituitary tumour apoplexy is even more rare and has not been systematically reviewed. Case Presentation: An 81-year-old woman was admitted to the Emergency Department because of acute onset headache, bilateral visual deficit, and altered consciousness. Computed tomography showed a giant mass lesion (&gt;5.5 cm diameter) expanding upward to the suprasellar cistern, optic chiasm, and third ventricle, over-running the sphenoid sinus, and with lateral invasion of the cavernous sinus. Laboratory investigations revealed central adrenal and hypothyroidism insufficiency, while magnetic resonance imaging confirmed a voluminous suprasellar tumour (~6 cm diameter), with signs of pituitary tumour apoplexy. Neurological manifestations and gland-related deficits improved after hormonal replacement therapy with a high dose of intravenous hydrocortisone, followed by oral hydrocortisone and levo-thyroxine. The patient declined surgical treatment and follow-up visit. Conclusions: Giant pituitary tumour apoplexy is a rare but potentially life-threatening condition. Prompt diagnosis and multidisciplinary management may allow a remarkable clinical improvement, as seen in this case.
2,330,164
Sex-Dependent Protective Effect of Combined Application of Solubilized Ubiquinol and Selenium on Monocrotaline-Induced Pulmonary Hypertension in Wistar Rats.
Ubiquinol exhibits anti-inflammatory and antioxidant properties. Selenium is a part of a number of antioxidant enzymes. The monocrotaline inducible model of pulmonary hypertension used in this study includes pathological links that may act as an application for the use of ubiquinol with high bioavailability and selenium metabolic products. On day 1, male and female rats were subcutaneously injected with a water-alcohol solution of monocrotaline or only water-alcohol solution. On days 7 and 14, some animals were intravenously injected with either ubiquinol's vehicle or solubilized ubiquinol, or orally with selenium powder daily, starting from day 7, or received both ubiquinol + selenium. Magnetic resonance imaging of the lungs was performed on day 20. Hemodynamic parameters and morphometry were measured on day 22. An increased right ventricle systolic pressure in relation to control was demonstrated in all groups of animals of both sexes, except the group of males receiving the combination of ubiquinol + selenium. The relative mass of the right ventricle did not differ from the control in all groups of males and females receiving either ubiquinol alone or the combination. Magnetic resonance imaging revealed impaired perfusion in almost all animals examined, but pulmonary fibrosis developed in only half of the animals in the ubiquinol group. Intravenous administration of ubiquinol has a protective effect on monocrotaline-induced pulmonary hypertension development resulting in reduced right ventricle hypertrophy, and lung mass. Ubiquinol + selenium administration resulted in a less severe increase in the right ventricle systolic pressure in male rats but not in females 3 weeks after the start of the experiment. This sex-dependent effect was not observed in the influence of ubiquinol alone.
2,330,165
[Relationship between white matter lesions and theresponse of cerebral spinal fluid tap test and clinical features in the patients with idiopathic normal pressure hydrocephalus].
<b>Objective:</b> To explore the relationship between white matter lesions and clinical features and response of cerebral spinal fluid (CSF) tap test in patients with idiopathic normal pressure hydrocephalus(iNPH). <b>Methods:</b> Possible iNPH patients were enrolled from outpatients and inpatients in Peking Union Medical College Hospital between 2014 and 2019. All patients underwent detailed neuropsychological and walking assessments, CSF tap test, as well as head magnetic resonance imaging. The Fazekas score of white matter lesions, the fractional anisotropy (FA)and mean diffusivity (MD) values of regions of interest by means ofdiffusion tensor imaging (DTI) were compared between CSF tap test positive and negative response groups. The correlation between DTI parameters and clinical characteristics was analyzed. <b>Results:</b> Forty-three patients (29 male and 14 female, age range: 52-79 years] wererecruited.Compared with the negative group, patients in the positive group tended to have higher Fazekas score of periventricular white matter(<i>U</i>=108.00, <i>P</i>=0.03), higher MD value of the region near anterior horn of left lateral ventricles[(1.14&#xb1;0.27)&#xd7;10<sup>-9</sup>mm<sup>2</sup>/s vs (0.85&#xb1;0.08) &#xd7;10<sup>-9</sup>mm<sup>2</sup>/s, <i>P</i>=0.003], lower FA value of the region near anterior horn of the right lateral ventricles[(0.20&#xb1;0.07)vs(0.27&#xb1;0.09), <i>P</i>=0.058], and higher MD value near the posterior horn of right lateral ventricle [(1.17&#xb1;0.34)&#xd7;10<sup>-9</sup>mm<sup>2</sup>/s vs (0.95&#xb1;0.01)&#xd7;10<sup>-9</sup>mm<sup>2</sup>/s, <i>P</i>=0.003]. FA and MD were significantly correlated with motor function, cognitive and functional scores, and iNPH grading scale (iNPHGS) scores(all <i>P</i>&lt;0.05). <b>Conclusions:</b> The white matter lesions might be one of the pathogeneses of lNPH and apathological changewhich can be reversed by CSF drainage. More white matter lesions should not be the contraindication of CSF drainage surgery.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>C Y</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>J J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>X Y</ForeName><Initials>XY</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dong</LastName><ForeName>L L</ForeName><Initials>LL</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>D</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mao</LastName><ForeName>C H</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hou</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Radiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>F</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Radiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>L Y</ForeName><Initials>LY</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gao</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><GrantList CompleteYN="Y"><Grant><GrantID>2020YFA0804500, 2016YFC1306300</GrantID><Agency>National Key Research and Development Program of China</Agency><Country/></Grant><Grant><GrantID>81550021</GrantID><Agency>National Science Foundation of China</Agency><Country/></Grant><Grant><GrantID>2016-12 M-1-004</GrantID><Agency>CAMS Innovation fund for Medical Sciences</Agency><Country/></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Zhonghua Yi Xue Za Zhi</MedlineTA><NlmUniqueID>7511141</NlmUniqueID><ISSNLinking>0376-2491</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016880" MajorTopicYN="N">Anisotropy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056324" MajorTopicYN="N">Diffusion Tensor Imaging</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006850" MajorTopicYN="Y">Hydrocephalus, Normal Pressure</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066127" MajorTopicYN="Y">White Matter</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="chi"><b>&#x76ee;&#x7684;&#xff1a;</b> &#x63a2;&#x6c42;&#x7279;&#x53d1;&#x6027;&#x6b63;&#x5e38;&#x538b;&#x529b;&#x8111;&#x79ef;&#x6c34;&#xff08;iNPH&#xff09;&#x60a3;&#x8005;&#x7684;&#x8111;&#x767d;&#x8d28;&#x75c5;&#x53d8;&#x4e0e;&#x8111;&#x810a;&#x6db2;&#x653e;&#x6db2;&#x8bd5;&#x9a8c;&#x7ed3;&#x679c;&#x53ca;&#x4e34;&#x5e8a;&#x7279;&#x5f81;&#x7684;&#x5173;&#x7cfb;&#x3002; <b>&#x65b9;&#x6cd5;&#xff1a;</b> &#x56de;&#x987e;&#x6027;&#x5206;&#x6790;2014&#x5e74;&#x81f3;2019&#x5e74;&#x5317;&#x4eac;&#x534f;&#x548c;&#x533b;&#x9662;&#x795e;&#x7ecf;&#x79d1;&#x95e8;&#x8bca;&#x5c31;&#x8bca;&#x548c;&#x75c5;&#x623f;&#x4f4f;&#x9662;&#x7684;iNPH&#x60a3;&#x8005;&#x3002;&#x6240;&#x6709;&#x60a3;&#x8005;&#x90fd;&#x7ecf;&#x8fc7;&#x8be6;&#x7ec6;&#x7684;&#x795e;&#x7ecf;&#x5fc3;&#x7406;&#x5b66;&#x53ca;&#x884c;&#x8d70;&#x80fd;&#x529b;&#x7684;&#x8bc4;&#x4f30;&#xff0c;&#x5934;&#x78c1;&#x5171;&#x632f;&#x68c0;&#x67e5;&#x548c;&#x8111;&#x810a;&#x6db2;&#x653e;&#x6db2;&#x8bd5;&#x9a8c;&#x3002;&#x5e94;&#x7528;Fazekas&#x8bc4;&#x5206;&#x4ee5;&#x53ca;&#x5f25;&#x6563;&#x5f20;&#x91cf;&#x6280;&#x672f;&#xff0c;&#x6bd4;&#x8f83;&#x8111;&#x810a;&#x6db2;&#x653e;&#x6db2;&#x8bd5;&#x9a8c;&#x9633;&#x6027;&#x548c;&#x9634;&#x6027;&#x7ec4;&#x60a3;&#x8005;&#x7684;&#x8111;&#x767d;&#x8d28;&#x75c5;&#x53d8;&#x7684;&#x4e0d;&#x540c;&#x3002;&#x5206;&#x6790;&#x611f;&#x5174;&#x8da3;&#x533a;&#x7684;&#x5f25;&#x6563;&#x5f20;&#x91cf;&#x6210;&#x50cf;&#x6280;&#x672f;&#x76f8;&#x5173;&#x53c2;&#x6570;&#x5404;&#x5411;&#x5f02;&#x6027;&#x5206;&#x6570;&#xff08;FA&#xff09;&#x3001;&#x5e73;&#x5747;&#x6269;&#x6563;&#x7387;&#xff08;MD&#xff09;&#x4e0e;iNPH&#x60a3;&#x8005;&#x4e34;&#x5e8a;&#x7279;&#x5f81;&#x7684;&#x76f8;&#x5173;&#x6027;&#x3002; <b>&#x7ed3;&#x679c;&#xff1a;</b> 43&#x4f8b;iNPH&#x60a3;&#x8005;&#xff08;&#x7537;&#x2236;&#x5973;&#x4e3a;29&#x2236;14&#xff0c;&#x5e74;&#x9f84;52~79&#x5c81;&#xff09;&#x88ab;&#x7eb3;&#x5165;&#x672c;&#x7814;&#x7a76;&#x3002;&#x8111;&#x810a;&#x6db2;&#x653e;&#x6db2;&#x8bd5;&#x9a8c;&#x7ed3;&#x679c;&#x9633;&#x6027;&#x7ec4;&#x548c;&#x9634;&#x6027;&#x7ec4;&#x60a3;&#x8005;&#x76f8;&#x6bd4;&#xff0c;&#x503e;&#x5411;&#x4e8e;&#x6709;&#x66f4;&#x9ad8;&#x7684;&#x4fa7;&#x8111;&#x5ba4;&#x5468;&#x56f4;&#x767d;&#x8d28;Fazekas&#x8bc4;&#x5206;&#xff3b;2.5&#xff08;1.0&#xff0c;3.0&#xff09;&#x5206;&#x6bd4;1.0&#xff08;1.0&#xff0c;2.0&#xff09;&#x5206;<i>U</i>=108.00&#xff0c;<i>P</i>=0.033&#xff3d;&#xff0c;&#x66f4;&#x9ad8;&#x7684;&#x5de6;&#x4fa7;&#x4fa7;&#x8111;&#x5ba4;&#x540e;&#x89d2;&#x65c1;MD&#x503c;&#xff3b;&#xff08;1.14&#xb1;0.27&#xff09;&#xd7;10<sup>-9</sup> mm<sup>2</sup>/s &#x6bd4;&#xff08;0.85&#xb1;0.08&#xff09;&#xd7;10<sup>-9</sup> mm<sup>2</sup>/s&#xff0c;<i>P</i>=0.003&#xff3d;&#xff0c;&#x66f4;&#x4f4e;&#x7684;&#x53f3;&#x4fa7;&#x4fa7;&#x8111;&#x5ba4;&#x524d;&#x89d2;&#x65c1;FA&#x503c;&#xff3b;&#xff08;0.20&#xb1;0.07&#xff09;&#x6bd4;&#xff08;0.27&#xb1;0.09&#xff09;&#xff0c;<i>P</i>=0.058&#xff3d;&#xff0c;&#x66f4;&#x9ad8;&#x7684;&#x53f3;&#x4fa7;&#x4fa7;&#x8111;&#x5ba4;&#x540e;&#x89d2;&#x65c1;MD&#x503c;&#xff3b;&#xff08;1.17&#xb1;0.34&#xff09;&#xd7;10<sup>-9</sup> mm<sup>2</sup>/s&#x6bd4;&#xff08;0.95&#xb1;0.01&#xff09;&#xd7;10<sup>-9</sup> mm<sup>2</sup>/s&#xff0c;<i>P</i>=0.003&#xff3d;&#x3002;&#x53cc;&#x4fa7;&#x4fa7;&#x8111;&#x5ba4;&#x524d;&#x89d2;&#x65c1;&#x767d;&#x8d28;FA&#x3001;MD&#x503c;&#x4e0e;&#x8fd0;&#x52a8;&#x529f;&#x80fd;&#x3001;&#x8ba4;&#x77e5;&#x53ca;&#x529f;&#x80fd;&#x8bc4;&#x5206;&#x3001;&#x7279;&#x53d1;&#x6027;&#x6b63;&#x5e38;&#x538b;&#x529b;&#x8111;&#x79ef;&#x6c34;&#x8bc4;&#x5206;&#xff08;iNPHGS&#x8bc4;&#x5206;&#xff09;&#x5747;&#x76f8;&#x5173;&#xff08;&#x5747;<i>P</i>&lt;0.05&#xff09;&#x3002; <b>&#x7ed3;&#x8bba;&#xff1a;</b> &#x8111;&#x767d;&#x8d28;&#x75c5;&#x53d8;&#x53ef;&#x80fd;&#x662f;iNPH&#x4e34;&#x5e8a;&#x75c7;&#x72b6;&#x7684;&#x53d1;&#x75c5;&#x673a;&#x5236;&#x4e4b;&#x4e00;&#xff0c;&#x662f;&#x901a;&#x8fc7;&#x5f15;&#x6d41;&#x624b;&#x672f;&#x53ef;&#x4ee5;&#x9006;&#x8f6c;&#x7684;&#x75c5;&#x7406;&#x53d8;&#x5316;&#xff0c;&#x8f83;&#x591a;&#x7684;&#x8111;&#x767d;&#x8d28;&#x75c5;&#x53d8;&#x4e0d;&#x5e94;&#x662f;&#x5f15;&#x6d41;&#x624b;&#x672f;&#x7684;&#x6392;&#x9664;&#x6307;&#x5f81;&#x3002;.
2,330,166
Clinicoradiologic Correlation in 22 Egyptian Children With Megalencephalic Leukoencephalopathy With Subcortical Cysts.
Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a rare genetic form of cerebral white matter disease whose clinicoradiologic correlation has not been completely understood. In this study, we investigated the association between clinical and brain magnetic resonance imaging (MRI) features in 22 Egyptian children (median age 7 years) with MLC. Gross motor function was assessed using the Gross Motor Function Classification System, and evaluation of brain MRI followed a consistent scoring system. Each parameter of extensive cerebral white matter T2 hyperintensity, moderate-to-severe wide ventricle/enlarged subarachnoid space, and greater than 2 temporal subcortical cysts was significantly associated (<i>P&#x2009;</i>&lt;&#x2009;.05) with worse Gross Motor Function Classification System score, language abnormality, and ataxia. Having &gt;2 parietal subcortical cysts was significantly related to a worse Gross Motor Function Classification System score (<i>P</i> = .04). The current study indicates that patients with MLC manifest signification association between certain brain MRI abnormalities and neurologic features, but this should be confirmed in larger studies.
2,330,167
Non-enhancing intraventricular tumours in adults.
Intraventricular tumours are relatively uncommon among all brain tumours, and non-enhancing lesions, mostly subependymoma, are even less frequently reported. Select cases of subependymoma can show variable contrast enhancement as well. Gross total surgical resection is recommended for treating these lesions, with no significant role of adjuvant chemotherapy or radiotherapy.
2,330,168
Periostin-related progression of different types of experimental pulmonary hypertension: A role for M2 macrophage and FGF-2 signalling.
Remodelling of pulmonary arteries (PA) contributes to the progression of pulmonary hypertension (PH). Periostin, a matricellular protein, has been reported to be involved in the development of PH. We examined the role of periostin in the pathogenesis of PH using different types of experimental PH.</AbstractText>PH was induced by vascular endothelial growth factor receptor antagonist (Sugen5416) plus hypoxic exposure (SuHx) and venous injection of monocrotaline-pyrrole (MCT-P) in wild-type (WT) and periostin-/-</sup> mice. Pulmonary haemodynamics, PA remodelling, expression of chemokines and fibroblast growth factor (FGF)-2, accumulation of macrophages to small PA and the right ventricle (RV) were examined in PH-induced WT and periostin-/-</sup> mice. Additionally, the role of periostin in the migration of macrophages, human PA smooth muscle (HPASMCs) and endothelial cells (HPMVECs) was investigated.</AbstractText>In PH induced by SuHx and MCT-P, PH and accumulation of M2 macrophage to small PA were attenuated in periostin-/-</sup> mice. PA remodelling post-SuHx treatment was also mild in periostin-/-</sup> mice compared to WT mice. Expression of macrophage-associated chemokines and FGF-2 in lung tissue, and accumulation of CD68-positive cells in the RV were less in SuHx periostin-/-</sup> than in SuHx WT mice. Periostin secretion in HPASMCs and HPMVECs was enhanced by transforming growth factor-&#x3b2;. Periostin also augmented macrophage, HPASMCs and HPMVECs migration. Separately, serum periostin levels were significantly elevated in patients with PH compared to healthy controls.</AbstractText>Periostin is involved in the development of different types of experimental PH, and may also contribute to the pathogenesis of human PH.</AbstractText>&#xa9; 2022 The Authors. Respirology published by John Wiley &amp; Sons Australia, Ltd on behalf of Asian Pacific Society of Respirology.</CopyrightInformation>
2,330,169
Cerebrospinal fluid production by the choroid plexus: a century of barrier research revisited.
Cerebrospinal fluid (CSF) envelops the brain and fills the central ventricles. This fluid is continuously replenished by net fluid extraction from the vasculature by the secretory action of the choroid plexus epithelium residing in each of the four ventricles. We have known about these processes for more than a century, and yet the molecular mechanisms supporting this fluid secretion remain unresolved. The choroid plexus epithelium secretes its fluid in the absence of a trans-epithelial osmotic gradient, and, in addition, has an inherent ability to secrete CSF against an osmotic gradient. This paradoxical feature is shared with other 'leaky' epithelia. The assumptions underlying the classical standing gradient hypothesis await experimental support and appear to not suffice as an explanation of CSF secretion. Here, we suggest that the elusive local hyperosmotic compartment resides within the membrane transport proteins themselves. In this manner, the battery of plasma membrane transporters expressed in choroid plexus are proposed to sustain the choroidal CSF secretion independently of the prevailing bulk&#xa0;osmotic gradient.
2,330,170
Cerebral corridor creator for resection of trigone ventricular tumors: Two case reports.
Resection of deep intracranial tumors requires significant brain retraction, which frequently causes brain damage. In particular, tumor in the trigone of the lateral ventricular presents a surgical challenge due to its inaccessible location and intricate adjacent relationships with essential structures such as the optic radiation (OR) fibers. New brain retraction systems have been developed to minimize retraction-associated injury. To date, there is little evidence supporting the superiority of any retraction system in preserving the white matter tract integrity. This report illustrates the initial surgical excision in two patients using a new retraction system termed the cerebral corridor creator (CCC) and demonstrates its advantage in protecting OR fibers.</AbstractText>We report two patients with nonspecific symptoms, who had trigone ventricular lesions that involved the neighboring OR identified on preoperative diffusion tensor imaging (DTI). Both patients underwent successful surgical excision using the CCC. Total tumor removal was achieved without additional neurological deficit. DTI showed that the OR fibers were preserved along the surgical field. Preoperative symptoms were alleviated immediately after surgery. Clinical outcomes were improved according to the Glasgow-Outcome-Scale and Activity-of-Daily-Living Scale assessments.</AbstractText>In the two cases, the CCC was a safe and useful tool for creating access to the deep trigonal area while preserving the white matter tract integrity. The CCC is thus a promising alternative brain retractor.</AbstractText>&#xa9;The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.</CopyrightInformation>
2,330,171
Melatonin in ventricular and subarachnoid cerebrospinal fluid: Its function in the neural glymphatic network and biological significance for neurocognitive health.
The central nervous system (CNS) is endowed with a specialized cerebrospinal fluid (CSF)/lymph network which removes toxic molecules and metabolic by-products from the neural parenchyma; collectively, this has been named the glymphatic system. It allows CSF located in the subarachnoid space which surrounds the CNS to enter the depths of the brain and spinal cord by means of Virchow-Robin perivascular and perivenous spaces. CSF in the periarterial spaces is transferred across the astrocytic end feet which line these spaces aided by AQ4 channels; in the interstitium, the fluid moves via convection through the parenchyma to be eventually discharged into the perivenous spaces. As it passes through the neural tissue, the interstitial fluid flushes metabolic by-products and extracellular toxins and debris into the CSF of the perivenous spaces. The fluid then moves to the surface of the CNS where the contaminants are absorbed into true lymphatic vessels in the dura mater from where it is shunted out of the cranial vault to the cervical lymph nodes. Pineal melatonin released directly into the CSF causes the concentration of this molecule to be much higher in the CSF of the third ventricle than in the blood. After the ventricular melatonin enters the subarachnoid and Virchow-Robin spaces it is taken into the neural tissue where it functions as a potent antioxidant and anti-inflammatory agent. Experimental evidence indicates that it removes pathogenic toxins, e.g., amyloid-&#x3b2; and others, from the brain to protect against neurocognitive decline. Melatonin levels drop markedly during aging, coincident with the development of several neurodegenerative diseases and the accumulation of the associated neurotoxins.
2,330,172
Novel finding of lissencephaly and severe osteopenia in a Chinese patient with SATB2-associated syndrome and a brief review of literature.
SATB2-associated syndrome (SAS) is a rare disorder characterized by developmental delay, behavioral problems, and craniofacial anomalies in particular dental and palatal abnormalities. We describe the clinical course, genetic and autopsy findings in a Chinese boy with global developmental delay, hypotonia, epilepsy, recurrent fractures and osteopenia. Brain magnetic resonance imaging showed pachygyria, white matter hypoplasia and hypogenesis of the corpus callosum. Whole-exome sequencing identified a novel heterozygous missense variant c.1555G&gt;A p.(Glu519Lys) in the SATB2 gene. Unfortunately, he died at 26&#x2009;months of bronchiolitis and pneumonia. Autopsy revealed pachygyria which was more severe anteriorly, dilated lateral and third ventricles and partial agenesis of the corpus callosum. Histology showed features compatible with two-layered lissencephaly. The bone showed disordered lamination and bone matrix. Although SATB2 has been shown to be involved in the regulation of neuronal migration in the developing brain, lissencephaly has not been reported so far. This could represent a more severe phenotype of SAS.
2,330,173
Multi&#x2011;omics analysis of right ventricles in rat models of pulmonary arterial hypertension: Consideration of mitochondrial biogenesis by chrysin.
In pulmonary arterial hypertension (PAH), right ventricular failure is accompanied by metabolic alterations in cardiomyocytes, which may be due to mitochondrial dysfunction and decreased energy production. Chrysin (CH) is a phytochemical with pharmacological activity that is involved in the regulation of mitochondrial biogenesis. The present study investigated the role of CH in the right ventricle (RV) by analyzing the cardiac transcriptome and metabolome of a SU5416(a vascular endothelial growth factor receptor blocker, /hypoxia (Su/Hx) rat model of PAH. RNA&#x2011;sequencing of the RV transcriptome between Su/Hx, Su/Hx with CH (Su/Hx&#xa0;+&#xa0;CH) and control groups, extracellular matrix (ECM) organization and ECM&#x2011;receptor interaction&#x2011;associated genes were upregulated in the RV of Su/Hx but not Su/Hx&#xa0;+&#xa0;CH rats. Furthermore, expression of mitochondrial function&#x2011;, energy production&#x2011;, oxidative phosphorylation&#x2011; and tricarboxylic acid (TCA) cycle&#x2011;associated genes was decreased in the RV of Su/Hx rats; this was reverse by CH. Metabolomic profiling analysis of Su/Hx and Su/Hx&#xa0;+&#xa0;CH rats showed no significant changes in glycolysis, TCA cycle, glutathione, NADH or NADPH. By contrast, in the RV of Su/Hx rats, decreased adenylate energy charge was partially reversed by CH administration, suggesting that CH was involved in the improvement of mitochondrial biogenesis. Reverse transcription&#x2011;quantitative PCR analysis revealed that expression of peroxisome proliferator&#x2011;activated receptor &#x3b3;, a master regulator of fatty acid metabolism and mitochondrial biogenesis, was increased in the RV of Su/Hx&#xa0;+&#xa0;CH rats. CH ameliorated cardiac abnormality, including cardiac fibrosis, RV hypertrophy and PH. The present study suggested that CH altered patterns of gene expression and levels of mitochondrial metabolites in cardiomyocytes, thus improving RV dysfunction in a Su/Hx PAH rat model.
2,330,174
Infantile Choroid Plexus Papilloma with Multiple Peritumoral Cysts.
Infantile choroid plexus papilloma (CPP) associated with multiple peritumoral cysts is a rare variant of CPP, and clinical course and optimal management are largely unknown. A 9-month-old boy presented with a large solid tumor in the left lateral ventricle associated with multiple peritumoral cysts, arachnoid cysts, and hydrocephalus containing xanthochromic fluid with high protein content. Shrinkage of these cysts and resolution of hydrocephalus were achieved after total resection of the hypervascular solid part of the tumor. Histological examination confirmed the solid part of the tumor as CPP and showed that the wall of the peritumoral cysts consisted of reactive gliosis without neoplastic cells. Follow-up magnetic resonance imaging 12 months after surgery revealed that these cysts remained stable. CPP with nonenhancing peritumoral cysts can be managed by resection of only the solid part of the tumor without permanent cerebrospinal fluid diversion.
2,330,175
Parasagittal dural space and cerebrospinal fluid (CSF) flow across the lifespan in healthy adults.
Recent studies have suggested alternative cerebrospinal fluid (CSF) clearance pathways for brain parenchymal metabolic waste products. One fundamental but relatively under-explored component of these pathways is the anatomic region surrounding the superior sagittal sinus, which has been shown to have relevance to trans-arachnoid molecular passage. This so-called parasagittal dural (PSD) space may play a physiologically significant role as a distal intracranial component of the human glymphatic circuit, yet fundamental gaps persist in our knowledge of how this space changes with normal aging and intracranial bulk fluid transport.</AbstractText>We re-parameterized MRI methods to assess CSF circulation in humans using high resolution imaging of the PSD space and phase contrast measures of flow through the cerebral aqueduct to test the hypotheses that volumetric measures of PSD space (1) are directly related to CSF flow (mL/s) through the cerebral aqueduct, and (2) increase with age. Multi-modal 3-Tesla MRI was applied in healthy participants (n&#x2009;=&#x2009;62; age range&#x2009;=&#x2009;20-83&#xa0;years) across the adult lifespan whereby phase contrast assessments of CSF flow through the aqueduct were paired with non-contrasted T1</sub>-weighted and T2</sub>-weighted MRI for PSD volumetry. PSD volume was extracted using a recently validated neural networks algorithm. Non-parametric regression models were applied to evaluate how PSD volume related to tissue volume and age cross-sectionally, and separately how PSD volume related to CSF flow (significance criteria: two-sided p&#x2009;&lt;&#x2009;0.05).</AbstractText>A significant PSD volume enlargement in relation to normal aging (p&#x2009;&lt;&#x2009;0.001, Spearman's-[Formula: see text]&#xa0;=&#xa0;0.6), CSF volume (p&#x2009;&lt;&#x2009;0.001, Spearman's-[Formula: see text]&#xa0;=&#xa0;0.6) and maximum CSF flow through the aqueduct of Sylvius (anterograde and retrograde, p&#x2009;&lt;&#x2009;0.001) were observed. The elevation in PSD volume was not significantly related to gray or white matter tissue volumes. Findings are consistent with PSD volume increasing with age and bulk CSF flow.</AbstractText>Findings highlight the feasibility of quantifying PSD volume non-invasively in vivo in humans using machine learning and non-contrast MRI. Additionally, findings demonstrate that PSD volume increases with age and relates to CSF volume and bi-directional flow. Values reported should provide useful normative ranges for how PSD volume adjusts with age, which will serve as a necessary pre-requisite for comparisons to persons with neurodegenerative disorders.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
2,330,176
Effects of selective orexin receptor-2 and cannabinoid receptor-1 antagonists on the response of medial prefrontal cortex neurons to tramadol.
Tramadol is widely used to control pain in various diseases, but the relevant mechanisms are less known despite the severe risks of abuse. The medial prefrontal cortex&#xa0;(mPFC) is one of the critical centers of the reward system. Studies have shown that orexins and endocannabinoids are likely to play an important role in addiction. In this study, the effect of orexin receptor-2 (OX2R) and endocannabinoid receptor-1 (CB1R) blockade on the neuronal activity of mPFC was investigated in response to tramadol in male rats. Tramadol was injected intraperitoneally, and its effects on the firing of mPFC pyramidal neurons were investigated using in vivo extracellular single-unit recording. Tramadol affected the pyramidal neuronal activity of the mPFC. AM251 (18&#xa0;nmol/4 &#x3bc;l), as a selective CB1R antagonist, and TCS-OX2-29 (50&#xa0;nmol/4 &#x3bc;l), as a selective OX2R antagonist, individually or simultaneously were microinjected into the&#xa0;lateral ventricle of the brain&#xa0;(intracerebroventricular, ICV). The results showed that the ratio of neurons with the excitatory/inhibitory or no responses was significantly changed by tramadol (p&#xa0;&lt;&#xa0;.05). These changes were prevented by blockade of CB1Rs alone or blockade of OX2Rs and CB1Rs simultaneously (p&#xa0;&lt;&#xa0;.05). However, blockade of these receptors in the vehicle group had no significant effect on neuronal activity. The findings of this study indicate the potential role of orexin and endocannabinoid systems in mediating the effects of tramadol in mPFC and the possible interaction between the two systems via OX2 and CB1 receptors. However, further studies are needed to identify these effects by examining intracellular signaling.
2,330,177
Effects of acute ischemia and hypoxia in young and adult calsequestrin (CSQ2) knock-out and wild-type mice.<Pagination><StartPage>1789</StartPage><EndPage>1801</EndPage><MedlinePgn>1789-1801</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11010-022-04407-2</ELocationID><Abstract><AbstractText>Calsequestrin (CSQ2) is the main Ca<sup>2+</sup>-binding protein in the sarcoplasmic reticulum of the mammalian heart. In order to understand the function of calsequestrin better, we compared two age groups (young: 4-5&#xa0;months of age versus adult: 18&#xa0;months of age) of CSQ2 knock-out mice (CSQ2(-/-)) and littermate wild-type mice (CSQ2(+/+)). Using echocardiography, in adult mice, the basal left ventricular ejection fraction and the spontaneous beating rate were lower in CSQ2(-/-) compared to CSQ2(+/+). The increase in ejection fraction by &#x3b2;-adrenergic stimulation (intraperitoneal injection of isoproterenol) was lower in adult CSQ2(-/-) versus adult CSQ2(+/+). After hypoxia in vitro (isolated atrial preparations) by gassing the organ bath buffer with 95% N<sub>2</sub>, force of contraction in electrically driven left atria increased to lower values in young CSQ2(-/-) than in young CSQ2(+/+). In addition, after global ischemia and reperfusion (buffer-perfused hearts according to Langendorff; 20-min ischemia and 15-min reperfusion), the rate of tension development was higher in young CSQ2(-/-) compared to young CSQ2(+/+). Finally, we evaluated signs of inflammation (immune cells, autoantibodies, and fibrosis). However, whereas no immunological alterations were found between all investigated groups, pronounced fibrosis was found in the ventricles of adult CSQ2(-/-) compared to all other groups. We suggest that in young mice, CSQ2 is important for cardiac performance especially in isolated cardiac preparations under conditions of impaired oxygen supply, but with differences between atrium and ventricle. Lack of CSQ2 leads age dependently to fibrosis and depressed cardiac performance in echocardiographic studies.</AbstractText><CopyrightInformation>&#xa9; 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Neumann</LastName><ForeName>Joachim</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany. Joachim.neumann@medizin.uni-halle.de.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institut f&#xfc;r Pharmakologie und Toxikologie, Martin-Luther-Universit&#xe4;t Halle-Wittenberg, Medizinische Fakult&#xe4;t, Magdeburger Str. 4, 06112, Halle, Germany. Joachim.neumann@medizin.uni-halle.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>B&#xf6;dicker</LastName><ForeName>Konrad</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buchwalow</LastName><ForeName>Igor B</ForeName><Initials>IB</Initials><AffiliationInfo><Affiliation>Institute for Hematopathology, 22547, Hamburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmidbaur</LastName><ForeName>Constanze</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramos</LastName><ForeName>Gustavo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Comprehensive Heart Failure Center, University Hospital W&#xfc;rzburg, 97080, W&#xfc;rzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frantz</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Comprehensive Heart Failure Center, University Hospital W&#xfc;rzburg, 97080, W&#xfc;rzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hofmann</LastName><ForeName>Ulrich</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Comprehensive Heart Failure Center, University Hospital W&#xfc;rzburg, 97080, W&#xfc;rzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gergs</LastName><ForeName>Ulrich</ForeName><Initials>U</Initials><Identifier Source="ORCID">0000-0001-6986-485X</Identifier><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Mol Cell Biochem</MedlineTA><NlmUniqueID>0364456</NlmUniqueID><ISSNLinking>0300-8177</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002155">Calsequestrin</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="Y">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002155" MajorTopicYN="Y">Calsequestrin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005355" MajorTopicYN="N">Fibrosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006325" MajorTopicYN="N">Heart Atria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008322" MajorTopicYN="N">Mammals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012519" MajorTopicYN="N">Sarcoplasmic Reticulum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aging</Keyword><Keyword MajorTopicYN="N">Calsequestrin</Keyword><Keyword MajorTopicYN="N">Hypertrophy</Keyword><Keyword MajorTopicYN="N">Hypoxia</Keyword><Keyword MajorTopicYN="N">Ischemia</Keyword></KeywordList><CoiStatement>The authors declare that they have no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>10</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>3</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>5</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>3</Month><Day>21</Day><Hour>17</Hour><Minute>18</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35312907</ArticleId><ArticleId IdType="pmc">PMC9068673</ArticleId><ArticleId IdType="doi">10.1007/s11010-022-04407-2</ArticleId><ArticleId IdType="pii">10.1007/s11010-022-04407-2</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Kornyeyev D, Petrosky AD, Zepeda B, et al. 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Autoimmunity. 2008;41:372&#x2013;376. doi: 10.1080/08916930801931142.</Citation><ArticleIdList><ArticleId IdType="doi">10.1080/08916930801931142</ArticleId><ArticleId IdType="pubmed">18568642</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35311828</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>181</Issue><PubDate><Year>2022</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats.<ELocationID EIdType="doi" ValidYN="Y">10.3791/63502</ELocationID><Abstract><AbstractText>Pulmonary hypertension due to left heart disease (PH-LHD) is the most common form of PH, yet its pathophysiology is poorly characterized than pulmonary arterial hypertension (PAH). As a result, approved therapeutic interventions for the treatment or prevention of PH-LHD are missing. Medications used to treat PH in PAH patients are not recommended for treatment of PH-LHD, as reduced pulmonary vascular resistance (PVR) and increased pulmonary blood flow in the presence of increased left-sided filling pressures may cause left heart decompensation and pulmonary edema. New strategies need to be developed to reverse PH in LHD patients. In contrast to PAH, PH-LHD develops due to increased mechanical load caused by congestion of blood into the lung circulation during left heart failure. Clinically, mechanical unloading of the left ventricle (LV) by aortic valve replacement in aortic stenosis patients or by implantation of LV assist devices in end-stage heart failure patients normalizes not only pulmonary arterial and right ventricular (RV) pressures but also PVR, thus providing indirect evidence for reverse remodeling in the pulmonary vasculature. Using an established rat model of PH-LHD due to left heart failure triggered by pressure overload with subsequent development of PH, a model is developed to study the molecular and cellular mechanisms of this physiological reverse remodeling process. Specifically, an aortic debanding surgery was performed, which resulted in reverse remodeling of the LV myocardium and its unloading. In parallel, complete normalization of RV systolic pressure and significant but incomplete reversal of RV hypertrophy was detectable. This model may present a valuable tool to study the mechanisms of physiological reverse remodeling in the pulmonary circulation and the RV, aiming to develop therapeutic strategies for treating PH-LHD and other forms of PH.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sang</LastName><ForeName>Pengchao</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic and Vascular Surgery, German Heart Center Berlin (DHZB); Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kucherenko</LastName><ForeName>Mariya M</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic and Vascular Surgery, German Heart Center Berlin (DHZB); Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin; mariya.kucherenko@charite.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Juquan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qiuhua</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simmons</LastName><ForeName>Szandor</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Kuebler</LastName><ForeName>Wolfgang M</ForeName><Initials>WM</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Knosalla</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic and Vascular Surgery, German Heart Center Berlin (DHZB); DZHK (German Centre for Cardiovascular Research), Partner Site Berlin; Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Vis Exp</MedlineTA><NlmUniqueID>101313252</NlmUniqueID><ISSNLinking>1940-087X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006976" MajorTopicYN="Y">Hypertension, Pulmonary</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011651" MajorTopicYN="N">Pulmonary Artery</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011652" MajorTopicYN="N">Pulmonary Circulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066253" MajorTopicYN="N">Vascular Remodeling</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>3</Month><Day>21</Day><Hour>12</Hour><Minute>17</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35311828</ArticleId><ArticleId IdType="doi">10.3791/63502</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35311818</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>181</Issue><PubDate><Year>2022</Year><Month>Mar</Month><Day>04</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal>Modified Technique for the Use of Neonatal Murine Hearts in the Langendorff Preparation.
Calsequestrin (CSQ2) is the main Ca<sup>2+</sup>-binding protein in the sarcoplasmic reticulum of the mammalian heart. In order to understand the function of calsequestrin better, we compared two age groups (young: 4-5&#xa0;months of age versus adult: 18&#xa0;months of age) of CSQ2 knock-out mice (CSQ2(-/-)) and littermate wild-type mice (CSQ2(+/+)). Using echocardiography, in adult mice, the basal left ventricular ejection fraction and the spontaneous beating rate were lower in CSQ2(-/-) compared to CSQ2(+/+). The increase in ejection fraction by &#x3b2;-adrenergic stimulation (intraperitoneal injection of isoproterenol) was lower in adult CSQ2(-/-) versus adult CSQ2(+/+). After hypoxia in vitro (isolated atrial preparations) by gassing the organ bath buffer with 95% N<sub>2</sub>, force of contraction in electrically driven left atria increased to lower values in young CSQ2(-/-) than in young CSQ2(+/+). In addition, after global ischemia and reperfusion (buffer-perfused hearts according to Langendorff; 20-min ischemia and 15-min reperfusion), the rate of tension development was higher in young CSQ2(-/-) compared to young CSQ2(+/+). Finally, we evaluated signs of inflammation (immune cells, autoantibodies, and fibrosis). However, whereas no immunological alterations were found between all investigated groups, pronounced fibrosis was found in the ventricles of adult CSQ2(-/-) compared to all other groups. We suggest that in young mice, CSQ2 is important for cardiac performance especially in isolated cardiac preparations under conditions of impaired oxygen supply, but with differences between atrium and ventricle. Lack of CSQ2 leads age dependently to fibrosis and depressed cardiac performance in echocardiographic studies.<CopyrightInformation>&#xa9; 2022. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Neumann</LastName><ForeName>Joachim</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany. Joachim.neumann@medizin.uni-halle.de.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institut f&#xfc;r Pharmakologie und Toxikologie, Martin-Luther-Universit&#xe4;t Halle-Wittenberg, Medizinische Fakult&#xe4;t, Magdeburger Str. 4, 06112, Halle, Germany. Joachim.neumann@medizin.uni-halle.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>B&#xf6;dicker</LastName><ForeName>Konrad</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buchwalow</LastName><ForeName>Igor B</ForeName><Initials>IB</Initials><AffiliationInfo><Affiliation>Institute for Hematopathology, 22547, Hamburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmidbaur</LastName><ForeName>Constanze</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramos</LastName><ForeName>Gustavo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Comprehensive Heart Failure Center, University Hospital W&#xfc;rzburg, 97080, W&#xfc;rzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frantz</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Comprehensive Heart Failure Center, University Hospital W&#xfc;rzburg, 97080, W&#xfc;rzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hofmann</LastName><ForeName>Ulrich</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Comprehensive Heart Failure Center, University Hospital W&#xfc;rzburg, 97080, W&#xfc;rzburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gergs</LastName><ForeName>Ulrich</ForeName><Initials>U</Initials><Identifier Source="ORCID">0000-0001-6986-485X</Identifier><AffiliationInfo><Affiliation>Institute for Pharmacology and Toxicology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06097, Halle, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Mol Cell Biochem</MedlineTA><NlmUniqueID>0364456</NlmUniqueID><ISSNLinking>0300-8177</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002155">Calsequestrin</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="Y">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002155" MajorTopicYN="Y">Calsequestrin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005355" MajorTopicYN="N">Fibrosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006325" MajorTopicYN="N">Heart Atria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008322" MajorTopicYN="N">Mammals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012519" MajorTopicYN="N">Sarcoplasmic Reticulum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aging</Keyword><Keyword MajorTopicYN="N">Calsequestrin</Keyword><Keyword MajorTopicYN="N">Hypertrophy</Keyword><Keyword MajorTopicYN="N">Hypoxia</Keyword><Keyword MajorTopicYN="N">Ischemia</Keyword></KeywordList><CoiStatement>The authors declare that they have no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2021</Year><Month>10</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2022</Year><Month>3</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Autoimmunity. 2008;41:372&#x2013;376. doi: 10.1080/08916930801931142.</Citation><ArticleIdList><ArticleId IdType="doi">10.1080/08916930801931142</ArticleId><ArticleId IdType="pubmed">18568642</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35311828</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>181</Issue><PubDate><Year>2022</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/63502</ELocationID><Abstract>Pulmonary hypertension due to left heart disease (PH-LHD) is the most common form of PH, yet its pathophysiology is poorly characterized than pulmonary arterial hypertension (PAH). As a result, approved therapeutic interventions for the treatment or prevention of PH-LHD are missing. Medications used to treat PH in PAH patients are not recommended for treatment of PH-LHD, as reduced pulmonary vascular resistance (PVR) and increased pulmonary blood flow in the presence of increased left-sided filling pressures may cause left heart decompensation and pulmonary edema. New strategies need to be developed to reverse PH in LHD patients. In contrast to PAH, PH-LHD develops due to increased mechanical load caused by congestion of blood into the lung circulation during left heart failure. Clinically, mechanical unloading of the left ventricle (LV) by aortic valve replacement in aortic stenosis patients or by implantation of LV assist devices in end-stage heart failure patients normalizes not only pulmonary arterial and right ventricular (RV) pressures but also PVR, thus providing indirect evidence for reverse remodeling in the pulmonary vasculature. Using an established rat model of PH-LHD due to left heart failure triggered by pressure overload with subsequent development of PH, a model is developed to study the molecular and cellular mechanisms of this physiological reverse remodeling process. Specifically, an aortic debanding surgery was performed, which resulted in reverse remodeling of the LV myocardium and its unloading. In parallel, complete normalization of RV systolic pressure and significant but incomplete reversal of RV hypertrophy was detectable. This model may present a valuable tool to study the mechanisms of physiological reverse remodeling in the pulmonary circulation and the RV, aiming to develop therapeutic strategies for treating PH-LHD and other forms of PH.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sang</LastName><ForeName>Pengchao</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic and Vascular Surgery, German Heart Center Berlin (DHZB); Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kucherenko</LastName><ForeName>Mariya M</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic and Vascular Surgery, German Heart Center Berlin (DHZB); Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin; mariya.kucherenko@charite.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Juquan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qiuhua</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simmons</LastName><ForeName>Szandor</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Kuebler</LastName><ForeName>Wolfgang M</ForeName><Initials>WM</Initials><AffiliationInfo><Affiliation>Institute of Physiology, Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health; DZHK (German Centre for Cardiovascular Research), Partner Site Berlin.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Knosalla</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Cardiothoracic and Vascular Surgery, German Heart Center Berlin (DHZB); DZHK (German Centre for Cardiovascular Research), Partner Site Berlin; Charit&#xe9; - Universit&#xe4;tsmedizin Berlin, corporate member of Freie Universit&#xe4;t Berlin, Humboldt-Universit&#xe4;t zu Berlin, and Berlin Institute of Health.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2022</Year><Month>03</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Vis Exp</MedlineTA><NlmUniqueID>101313252</NlmUniqueID><ISSNLinking>1940-087X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="Y">Heart Failure</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006976" MajorTopicYN="Y">Hypertension, Pulmonary</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011651" MajorTopicYN="N">Pulmonary Artery</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011652" MajorTopicYN="N">Pulmonary Circulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066253" MajorTopicYN="N">Vascular Remodeling</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2022</Year><Month>3</Month><Day>21</Day><Hour>12</Hour><Minute>17</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2022</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2022</Year><Month>4</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">35311828</ArticleId><ArticleId IdType="doi">10.3791/63502</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Automated"><PMID Version="1">35311818</PMID><DateCompleted><Year>2022</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2022</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>181</Issue><PubDate><Year>2022</Year><Month>Mar</Month><Day>04</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>Modified Technique for the Use of Neonatal Murine Hearts in the Langendorff Preparation.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.3791/63349</ELocationID><Abstract>The use of the ex-vivo retrograde perfused heart has long been a cornerstone of ischemia-reperfusion investigation since its development by Oskar Langendorff over a century ago. Although this technique has been applied to mice over the last 25 years, its use in this species has been limited to adult animals. Development of a successful method to consistently cannulate the neonatal murine aorta would allow for the systematic study of the isolated retrograde perfused heart during a critical period of cardiac development in a genetically modifiable and low-cost species. Modification of the Langendorff preparation enables cannulation and establishment of reperfusion in the neonatal murine heart while minimizing ischemic time. Optimization requires a two-person technique to permit successful cannulation of the newborn mouse aorta using a dissecting microscope and a modified commercially available needle. The use of this approach will reliably establish retrograde perfusion within 3 min. Because the fragility of the neonatal mouse heart and ventricular cavity size prevents direct measurement of intraventricular pressure generated using a balloon, use of a force transducer connected by a suture to the apex of the left ventricle to quantify longitudinal contractile tension is necessary. This method allows investigators to successfully establish an isolated constant-flow retrograde-perfused newborn murine heart preparation, permitting the study of developmental cardiac biology in an ex-vivo manner. Importantly, this model will be a powerful tool to investigate the physiological and pharmacological responses to ischemia-reperfusion in the neonatal heart.
2,330,178
Shared CSF Biomarker Profile in Idiopathic Normal Pressure Hydrocephalus and Subcortical Small Vessel Disease.
In this study, we examine similarities and differences between 52 patients with idiopathic normal pressure hydrocephalus (iNPH) and 17 patients with subcortical small vessel disease (SSVD), in comparison to 28 healthy controls (HCs) by a panel of cerebrospinal fluid (CSF) biomarkers.</AbstractText>We analyzed soluble amyloid precursor protein alpha (sAPP&#x3b1;) and beta (sAPP&#x3b2;), A&#x3b2; isoforms -38, -40, and -42, neurofilament light protein (NFL), glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), matrix metalloproteinases (MMP -1, -2, -3, -9, and -10), and tissue inhibitors of metalloproteinase 1 (TIMP1). Radiological signs of white matter damage were scored using the age-related white matter changes (ARWMC) scale.</AbstractText>All amyloid fragments were reduced in iNPH and SSVD (p</i> &lt; 0.05), although more in iNPH than in SSVD in comparison to HC. iNPH and SSVD showed comparable elevations of NFL, MBP, and GFAP (p</i> &lt; 0.05). MMPs were similar in all three groups except for MMP-10, which was increased in iNPH and SSVD. Patients with iNPH had larger ventricles and fewer WMCs than patients with SSVD.</AbstractText>The results indicate that patients with iNPH and SSVD share common features of subcortical neuronal degeneration, demyelination, and astroglial response. The reduction in all APP-derived proteins characterizing iNPH patients is also present, indicating that SSVD encompasses similar pathophysiological phenomena as iNPH.</AbstractText>Copyright &#xa9; 2022 Jeppsson, Bjerke, Hellstr&#xf6;m, Blennow, Zetterberg, Kettunen, Wikkels&#xf8;, Wallin and Tullberg.</CopyrightInformation>
2,330,179
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) and Precocious Puberty With a Third Ventricle Arachnoid Cyst.
Arachnoid cyst (AC) is a rare defect of the central nervous system that accounts for 1% of all intracranial lesions, of which only 1% of reported cases are located in the third ventricle. Endocrine manifestations associated with AC include precocious puberty, growth hormone deficiency, and hypothalamic dysfunction. We report a child who presented with a visual field defect, hyponatremia, and precocious puberty related to a third ventricle AC.&#xa0;Hyponatremia as a complication of AC is rare. A literature review revealed two case reports of Syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with suprasellar AC. The pathophysiology of SIADH in AC is not well understood. Hyponatremia may worsen following endoscopic fenestration of the AC secondary to changes in intracranial pressure. In conclusion, hyponatremia with AC should be recognized during the preoperative and postoperative periods and may require treatment with hypertonic saline in addition to fluid restriction.
2,330,180
Age- and Hypertension-Related Changes in NOS/NO/sGC-Derived Vasoactive Control of Rat Thoracic Aortae.
This study was aimed at examining the role of the NOS/NO/sGC signaling pathway in the vasoactive control of the thoracic aorta (TA) from the early to late ontogenetic stages (7 weeks, 20 weeks, and 52 weeks old) of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Systolic blood pressure (SBP) and heart rate (HR) were significantly increased in SHRs compared to age-matched WKYs, which was associated with left heart ventricle hypertrophy in all age groups of rats. The plasma urea level was increased in 20-week-old and 52-week-old SHRs compared with WKYs without increasing creatinine and uric acid. The total cholesterol levels were lower in 20-week-old and 52-week-old SHRs than in WKYs, but triglycerides were higher in 7-week-old SHRs. The fructosamine level was increased in 52-week-old SHRs compared with age-matched WKYs and unchanged in other age groups. Superoxide production was increased only in 7-week-old SHRs compared to age-matched WKYs. The endothelium-dependent relaxation (EDR) of the TA deteriorated in both rat strains during aging; however, endothelial dysfunction already occurred in 20-week-old SHRs and was even more enhanced in 52-week-old rats. Our results also demonstrated increased activity of NOS in 52-week-old WKYs. Moreover, 7-week-old and 52-week-old WKY rats displayed an enhanced residual EDR after L-NMMA (NOS inhibitor) incubation compared with 20-week-old rats. Our results showed that in 7-week-old SHRs, the residual EDR after L-NMMA incubation was increased compared to that in other age groups. The activity of NOS in the TA was comparable in 7-week-old and 20-week-old SHRs, but it was reduced in 52-week-old SHRs compared to younger SHRs and 52-week-old WKYs. Thus, it seems that, in contrast to SHRs, the NOS/NO system in WKYs is probably able to respond to age-related pathologies to maintain endothelial functions and thus optimal BP levels even in later periods of life.
2,330,181
Cerebellar morphometric and spectroscopic biomarkers for Machado-Joseph Disease.
Machado-Joseph disease (MJD) or Spinocerebellar ataxia type 3 (SCA3) is the most common form of dominant SCA worldwide. Magnetic Resonance Imaging (MRI) and Proton Magnetic Resonance Spectroscopy (<sup>1</sup>H-MRS) provide promising non-invasive diagnostic and follow-up tools, also serving to evaluate therapies efficacy. However, pre-clinical studies showing relationship between MRI-MRS based biomarkers and functional performance are missing, which hampers an efficient clinical translation of therapeutics. This study assessed motor behaviour, neurochemical profiles, and morphometry of the cerebellum of MJD transgenic mice and patients aiming at establishing magnetic-resonance-based biomarkers. <sup>1</sup>H-MRS and structural MRI measurements of MJD transgenic mice were performed with a 9.4&#xa0;Tesla scanner, correlated with motor performance on rotarod and compared with data collected from human patients. We found decreased cerebellar white and grey matter and enlargement of the fourth ventricle in both MJD mice and human patients as compared to controls. N-acetylaspartate (NAA), NAA&#x2009;+&#x2009;N-acetylaspartylglutamate (NAA&#x2009;+&#x2009;NAAG), Glutamate, and Taurine, were significantly decreased in MJD mouse cerebellum regardless of age, whereas myo-Inositol (Ins) was increased at early time-points. Lower neurochemical ratios levels (NAA/Ins and NAA/total Choline), previously correlated with worse clinical status in SCAs, were also observed in MJD mice cerebella. NAA, NAA&#x2009;+&#x2009;NAAG, Glutamate, and Taurine were also positively correlated with MJD mice motor performance. Importantly, these <sup>1</sup>H-MRS results were largely analogous to those found for MJD in human studies and in our pilot data in human patients. We have established a magnetic resonance-based biomarker approach to monitor novel therapies in preclinical studies and human clinical trials.
2,330,182
Radiologic and clinical outcome of isolated fourth ventricle following post-hemorrhagic hydrocephalus in children.
Few studies report radiologic and clinical outcome of post-hemorrhagic isolated fourth ventricle (IFV) with focus on surgical versus conservative management in neonates and children. Our aim is to investigate differences in radiological and clinical findings of IFV between patients who had surgical intervention versus patients who were treated conservatively.</AbstractText>A retrospective analysis of patients diagnosed with IFV was performed. Data included demographics, clinical exam findings, surgical history, and imaging findings (dilated FV extent, supratentorial ventricle dilation, brainstem and cerebellar deformity, tectal plate elevation, basal cistern and cerebellar hemisphere effacement, posterior fossa upward/downward herniation).</AbstractText>Sixty-four (30 females) patients were included. Prematurity was 94% with 90% being&#x2009;&lt;&#x2009;28&#xa0;weeks of gestation. Mean age at first ventricular shunt was 3.6 (range 1-19); at diagnosis of IFV, post-lateral ventricular shunting was 26.2 (1-173) months. Conservatively treated patients were 87.5% versus 12.5% treated with FV shunt/endoscopic fenestration. Severe FV dilation (41%), severe deformity of brainstem (39%) and cerebellum (47%) were noted at initial diagnosis and stable findings (34%, 47%, and 52%, respectively) were seen at last follow-up imaging. FV dilation (p&#x2009;=&#x2009;0.0001) and upward herniation (p&#x2009;=&#x2009;0.01) showed significant differences between surgery versus conservative management. No other radiologic or clinical outcome parameters were different between two groups.</AbstractText>Only radiologic outcome results showed stable or normal FV dilation and stable or decreased upward herniation in the surgically treated group.</AbstractText>&#xa9; 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</CopyrightInformation>
2,330,183
Measuring the Area of the Interventricular Septum in the 4-Chamber View: A New Technique to Evaluate the Fetus at Risk for Septal Hypertrophy.
One of the problems for the clinician who desires to measure the interventricular septum (IVS) in a high-risk fetus is to know where to make the measurement. The purpose of this study was to use speckle-tracking analysis to measure the IVS area, 24-segment widths, and length at end-diastole (ED) and end-systole (ES) in normal fetuses.</AbstractText>From the 4-chamber view, speckle-tracking analysis was performed at ED and ES on the IVS in 200 normal fetuses. The following were computed and regressed against gestational age (GA) and fetal biometric (FB) measurements: area, length, and the 24-segment transverse widths from the apex to the crux. The 24-segment width/length ratio was also measured. The speckle-tracking measurements of the ED area and length were compared using a point-to-point measurement tool available on all ultrasound machines.</AbstractText>The ED and ES areas, lengths, and 24-segment widths increased with GA and FB. The ED and ES areas were virtually identical. The 24-segment width/length ratio decreased from the apex to the crux of the septum. There was no significant difference in the measurement of the ED area and the length between speckle-tracking and the point-to-point measurements.</AbstractText>Measurement of the area and length of the IVS are simple to obtain and provide a new diagnostic tool to evaluate the fetus at risk for IVS hypertrophy which may be observed in fetuses of mothers with pregestational and gestational diabetes.</AbstractText>&#xa9; 2022 American Institute of Ultrasound in Medicine.</CopyrightInformation>
2,330,184
Assessment of the prevalence and associated risk factors of pediatric hydrocephalus in diagnostic centers in Addis Ababa, Ethiopia.
Hydrocephalus (HCP) is a common disorder of cerebral spinal fluid (CSF) physiology resulting in abnormal expansion of the cerebral ventricles. Infants commonly present with progressive macrocephaly whereas children older than 2&#x2009;years generally present with signs and symptoms of intracranial hypertension. Neither qualitatively nor quantitatively are there adequate data to determine the prevalence and incidence of HCP in the developing world. HCP is a treatable condition that when left untreated, has fatal consequences.</AbstractText>The objective of this study was to assess the prevalence of pediatric HCP and associated risk factors in diagnostic centers in Addis Ababa, Ethiopia.</AbstractText>This study was conducted using a cross-sectional facility-based study design over a two-time period, i.e. a 2-year retrospective data collection from January 2018 to January 2020 included 1101 patients and a prospective data collection from May 2019 to February 2020 included 99 patients. Children aged 5&#x2009;years and below who came to the selected diagnostic centers for MRI/CT examination were studied. The collected data were analyzed using binary logistic regression.</AbstractText>The retrospective study included 639(58%) males and 462 (42%) females. The mean age calculated was 22.3&#x2009;months. Infants aged younger than 24&#x2009;months 753 (68.4%) were significantly associated with HCP development (P&#x2009;&lt;&#x2009;0.05). In the retrospective study, HCP etiologies; Aqueductal stenosis (17.9%), Neural Tube defects (NTDs) (35.7%), post-infectious (10.1%) were identified. In the prospective study, the gender and age distribution was 57(57.6%) males, 42 (42.4%) females, 60.6% infants aged younger than 24&#x2009;months with a mean age of 24.9&#x2009;months. Inadequate consumption of folic acid and development of HCP was found to be statistically significant (P&#x2009;&lt;&#x2009;0.05). In the prospective study, HCP etiologies; Aqueductal stenosis (26.1%), Neural Tube defects (26.08%), and post-infectious (8.69%) were identified. The 3 years prevalence of HCP calculated in both studies was 22% (223 per 1000 live births).</AbstractText>The results of this study suggest that the high prevalence of HCP was due to the high prevalence of aqueductal stenosis and neural tube defects; with a small contribution of post-infectious causes. The majority of infants who present with HCP were aged younger than 24&#x2009;months.</AbstractText>&#xa9; 2022. The Author(s).</CopyrightInformation>
2,330,185
Why don't ventricles dilate in pseudotumor cerebri? A circuit model of the cerebral windkessel.
Pseudotumor cerebri is a disorder of intracranial dynamics characterized by elevated intracranial pressure (ICP) and chronic cerebral venous hypertension without structural abnormalities. A perplexing feature of pseudotumor is the absence of the ventriculomegaly found in obstructive hydrocephalus, although both diseases are associated with increased resistance to cerebrospinal fluid (CSF) resorption. Traditionally, the pathophysiology of ventricular dilation and obstructive hydrocephalus has been attributed to the backup of CSF due to impaired absorption, and it is unclear why backup of CSF with resulting ventriculomegaly would not occur in pseudotumor. In this study, the authors used an electrical circuit model to simulate the cerebral windkessel effect and explain the presence of ventriculomegaly in obstructive hydrocephalus but not in pseudotumor cerebri.</AbstractText>The cerebral windkessel is a band-stop filter that dampens the arterial blood pressure pulse in the cranium. The authors used a tank circuit with parallel inductance and capacitance to model the windkessel. The authors distinguished the smooth flow of blood and CSF and the pulsatile flow of blood and CSF by using direct current (DC) and alternating current (AC) sources, respectively. The authors measured the dampening notch from ABP to ICP as the band-stop filter of the windkessel.</AbstractText>In obstructive hydrocephalus, loss of CSF pathway volume impaired the flow of AC power in the cranium and caused windkessel impairment, to which ventriculomegaly is an adaptation. In pseudotumor, venous hypertension affected DC power flow in the capillaries but did not affect AC power or the windkessel, therefore obviating the need for adaptive ventriculomegaly.</AbstractText>In pseudotumor, the CSF spaces are unaffected and the windkessel remains effective. Therefore, ventricles remain normal in size. In hydrocephalus, the windkessel, which depends on the flow of AC power in patent CSF spaces, is impaired, and the ventricles dilate as an adaptive process to restore CSF pathway volume. The windkessel model explains both ventriculomegaly in obstructive hydrocephalus and the lack of ventriculomegaly in pseudotumor. This model provides a novel understanding of the pathophysiology of disorders of CSF dynamics and has significant implications in clinical management.</AbstractText>
2,330,186
Action of the Nrf2/ARE signaling pathway on oxidative stress in choroid plexus epithelial cells following lanthanum chloride treatment.
Lanthanum (La) can damage the blood brain barrier when it enters the brain tissue, causing learning and memory dysfunction. Currently, few studies have focused on La-induced oxidative stress in choroid plexus epithelial cells, which can severely impair the normal function of the blood-cerebrospinal fluid barrier (BCSFB) and ultimately cause central nervous system dysfunction. The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element(ARE) signaling pathway is one of the major antioxidant systems and is vital in protecting cells against oxidative injury in rodents. In this study, Z310 cells were employed to construct BCSFB in vitro and treated with lanthanum chloride (LaCl<sub>3</sub>); meanwhile, 40&#xa0;&#x3bc;mol/L tert-butylhydroquinone and the corresponding concentration of LaCl<sub>3</sub> was used as the intervention groups. The results showed that LaCl<sub>3</sub> treatment markedly decreased Z310 cell viability, increased the necrosis rate, and then reduced the transepithelial electrical resistance value of BCSFB in vitro; reactive oxygen species levels gradually increased, catalase and glutathione peroxidase activities decreased; furthermore, Nrf2 was significantly downregulated, and the expression of Nrf2 downstream genes such as heme oxygenase1, NADP(H): dehydrogenase quinone1, glutathione thiotransferase etc. noticeably decreased; in addition, interleukin-1&#x3b2; and tumour necrosis factor-&#x3b1; associated with Nrf2 activation noticeably increased. However, tert-butylhydroquinone could activate the Nrf2/AER signaling pathway and attenuate the Z310 cell oxidative damage induced by LaCl<sub>3</sub>. Thus, the Nrf2/ARE signaling pathway is probably involved in weakening the BCSFB in vitro that is created by La-induced oxidative stress. Tert-butylhydroquinone can activate this pathway to reverse severe oxidative damage, which significantly strengthen the function of BCSFB.
2,330,187
Impact of intraventricular septal fiber orientation on cardiac electromechanical function.
Cardiac fiber direction is an important factor determining the propagation of electrical activity, as well as the development of mechanical force. In this article, we imaged the ventricles of several species with special attention to the intraventricular septum to determine the functional consequences of septal fiber organization. First, we identified a dual-layer organization of the fiber orientation in the intraventricular septum of ex vivo sheep hearts using diffusion tensor imaging at high field MRI. To expand the scope of the results, we investigated the presence of a similar fiber organization in five mammalian species (rat, canine, pig, sheep, and human) and highlighted the continuity of the layer with the moderator band in large mammalian species. We implemented the measured septal fiber fields in three-dimensional electromechanical computer models to assess the impact of the fiber orientation. The downward fibers produced a diamond activation pattern superficially in the right ventricle. Electromechanically, there was very little change in pressure volume loops although the stress distribution was altered. In conclusion, we clarified that the right ventricular septum has a downwardly directed superficial layer in larger mammalian species, which can have modest effects on stress distribution.<b>NEW &amp; NOTEWORTHY</b> A dual-layer organization of the fiber orientation in the intraventricular septum was identified in ex vivo hearts of large mammals. The RV septum has a downwardly directed superficial layer that is continuous with the moderator band. Electrically, it produced a diamond activation pattern. Electromechanically, little change in pressure volume loops were noticed but stress distribution was altered. Fiber distribution derived from diffusion tensor imaging should be considered for an accurate strain and stress analysis.
2,330,188
Brain Network Connectivity and Executive Function in Children with Infantile Hydrocephalus.
<b><i>Introduction:</i></b> Infantile hydrocephalus (HCP) is a condition in which there is an abnormal buildup of cerebrospinal fluid in the ventricles within the first few months of life, which puts pressure on surrounding brain tissues. Compression of the developing brain increases the risk of secondary brain injury and cognitive disabilities. <b><i>Methods:</i></b> In this study, we used diffusion-weighted imaging and resting-state functional magnetic resonance imaging to investigate the effects of ventricle dilatation on structural and functional brain networks in children with shunted infantile HCP and examined how these brain changes may impact executive function. <b><i>Results:</i></b> We found that children with HCP have altered structural and functional connectivity between and within large-scale networks. Moreover, hyperconnectivity between the ventral attention and default mode network in children with HCP correlated with reduced executive function scores. Compared with typically developing age-matched control participants, our patient population also had lower fractional anisotropy in posterior white matter. <b><i>Discussion:</i></b> Overall, these findings suggest that infantile HCP has long-term effects on brain network connectivity, white matter development, and executive function in children at school age. Future work will examine the relationship between ventricular volumes before shunt placement in infancy and brain network development throughout childhood.
2,330,189
Bayesian optimisation for efficient parameter inference in a cardiac mechanics model of the left ventricle.
We consider parameter inference in cardio-mechanic models of the left ventricle, in particular the one based on the Holtzapfel-Ogden (HO) constitutive law, using clinical in vivo data. The equations underlying these models do not admit closed form solutions and hence need to be solved numerically. These numerical procedures are computationally expensive making computational run times associated with numerical optimisation or sampling excessive for the uptake of the models in the clinical practice. To address this issue, we adopt the framework of Bayesian optimisation (BO), which is an efficient statistical technique of global optimisation. BO seeks the optimum of an unknown black-box function by sequentially training a statistical surrogate-model and using it to select the next query point by leveraging the associated exploration-exploitation trade-off. To guarantee that the estimates based on the in vivo data are realistic also for high-pressures, unobservable in vivo, we include a penalty term based on a previously published empirical law developed using ex vivo data. Two case studies based on real data demonstrate that the proposed BO procedure outperforms the state-of-the-art inference algorithm for the HO constitutive law.
2,330,190
A U-snake based deep learning network for right ventricle segmentation.
Ventricular segmentation is of great importance for the heart condition monitoring. However, manual segmentation is time-consuming, cumbersome, and subjective. Many segmentation methods perform poorly due to the complex structure and uncertain shape of the right ventricle, so we combine deep learning to achieve automatic segmentation.</AbstractText>This paper proposed a method named U-Snake network which is based on the improvement of deep snake together with level set to segment the right ventricular in the MR images. U-snake aggregates the information of each receptive field which is learned by circular convolution of multiple dilation rates. At the same time, we also added dice loss functions and transferred the result of U-Snake to the level set so as to further enhance the effect of small object segmentation. Our method is tested on the test 1 and test 2 datasets in the right ventricular segmentation challenge (RVSC), which shows the effectiveness.</AbstractText>The experiment showed that we have obtained good result in the RVSC. The highest segmentation accuracy on the right ventricular test set 2 reached a dice coefficient of 0.911, and the segmentation speed reached 5 fps.</AbstractText>Our method, a new deep learning network named U-snake, has surpassed the previous excellent ventricular segmentation method based on mathematical theory and other classical deep learning methods, such as Residual U-net, Inception CNN, and Dilated CNN. However, it can only be used as an auxiliary tool instead of replacing the work of human beings.</AbstractText>&#xa9; 2022 American Association of Physicists in Medicine.</CopyrightInformation>
2,330,191
Systemic hypertonic saline enhances glymphatic spinal cord delivery of lumbar intrathecal morphine.
The blood-brain barrier significantly limits effective drug delivery to central nervous system (CNS) targets. The recently characterized glymphatic system offers a perivascular highway for intrathecally (i.t.) administered drugs to reach deep brain structures. Although periarterial cerebrospinal fluid (CSF) influx and concomitant brain drug delivery can be enhanced by pharmacological or hyperosmotic interventions, their effects on drug delivery to the spinal cord, an important target for many drugs, have not been addressed. Hence, we studied in rats whether enhancement of periarterial flow by systemic hypertonic solution might be utilized to enhance spinal delivery and efficacy of i.t. morphine. We also studied whether the hyperosmolar intervention affects brain or cerebrospinal fluid drug concentrations after systemic administration. Periarterial CSF influx was enhanced by intraperitoneal injection of hypertonic saline (HTS, 5.8%, 20&#xa0;ml/kg, 40&#xa0;mOsm/kg). The antinociceptive effects of morphine were characterized, using tail flick, hot plate and paw pressure tests. Drug concentrations in serum, tissue and microdialysis samples were determined by liquid chromatography-tandem mass spectrometry. Compared with isotonic solution, HTS increased concentrations of spinal i.t. administered morphine by 240% at the administration level (T13-L1) at 60&#xa0;min and increased the antinociceptive effect of morphine in tail flick, hot plate, and paw pressure tests. HTS also independently increased hot plate and paw pressure latencies but had no effect in the tail flick test. HTS transiently increased the penetration of intravenous morphine into the lateral ventricle, but not into the hippocampus. In conclusion, acute systemic hyperosmolality is a promising intervention for enhanced spinal delivery of i.t. administered morphine. The relevance of this intervention should be expanded to other i.t. drugs and brought to clinical trials.
2,330,192
Brain Volumes and Abnormalities in Adults Born Preterm at Very Low Birth Weight.
To assess radiographic brain abnormalities and investigate volumetric differences in adults born preterm at very low birth weight (&lt;1500&#xa0;g), using siblings as controls.</AbstractText>We recruited 79 adult same-sex sibling pairs with one born preterm at very low birth weight and the sibling at term. We acquired 3-T brain magnetic resonance imaging from 78 preterm participants and 72 siblings. A neuroradiologist, masked to participants' prematurity status, reviewed the images for parenchymal and structural abnormalities, and FreeSurfer software 6.0 was used to conduct volumetric analyses. Data were analyzed by linear mixed models.</AbstractText>We found more structural abnormalities in very low birth weight participants than in siblings (37% vs 13%). The most common finding was periventricular leukomalacia, present in 15% of very low birth weight participants and in 3% of siblings. The very low birth weight group had smaller absolute brain volumes (-0.4 SD) and, after adjusting for estimated intracranial volume, less gray matter (-0.2 SD), larger ventricles (1.5 SD), smaller thalami (-0.6 SD), caudate nuclei (-0.4 SD), right hippocampus (-0.4 SD), and left pallidum (-0.3 SD). We saw no volume differences in total white matter (-0.04 SD; 95% CI, -0.13 to 0.09).</AbstractText>Preterm very low birth weight adults had a higher prevalence of brain abnormalities than their term-born siblings. They also had smaller absolute brain volumes, less gray but not white matter, and smaller volumes in several gray matter structures.</AbstractText>Copyright &#xa9; 2022 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
2,330,193
Automatic Brain Midline Surface Delineation on 3D CT Images With Intracranial Hemorrhage.
Brain midline delineation plays an important role in guiding intracranial hemorrhage surgery, which still remains a challenging task since hemorrhage shifts the normal brain configuration. Most previous studies detected brain midline on 2D plane and did not handle hemorrhage cases well. We propose a novel and efficient hemisphere-segmentation framework (HSF) for 3D brain midline surface delineation. Specifically, we formulate the brain midline delineation as a 3D hemisphere segmentation task, and employ an edge detector and a smooth regularization loss to generate the midline surface. We also introduce a distance-weighted map to keep the attention on the midline. Furthermore, we adopt rectification learning to handle various head poses. Finally, considering the complex situation of ventricle break-in for hemorrhages in bilateral intraventricular (B-IVH) cases, we identify those cases via a classification model and design a midline correction strategy to locally adjust the midline. To our best knowledge, it is the first study focusing on delineating the brain midline surface on 3D CT images of hemorrhage patients and handling the situation of ventricle break-in. Extensive validation on our large in-house datasets (519 patients) and the public CQ500 dataset (491 patients), demonstrates that our method outperforms state-of-the-art methods on brain midline delineation.
2,330,194
Choroid plexus function in neurological homeostasis and disorders: The awakening of the circadian clocks and orexins.
As research regarding the role of circadian rhythms, sleep, and the orexinergic system in neurodegenerative diseases is growing, it is surprising that the choroid plexus (CP) remains underappreciated in this realm. Despite its extensive role in the regulation of circadian rhythms and orexinergic signalling, as well as acting as the primary conduit between cerebrospinal fluid (CSF) and the circulatory system, providing a mechanism by which toxic waste molecules can be removed from the brain, the CP has been largely unexplored in neurodegeneration. In this review, we explore the role of the CP in maintaining brain homeostasis and circadian rhythms, regulating CSF dynamics, and how these functions change across the lifespan, from development to senescence. In addition, we examine the relationship between the CP, orexinergic signalling, and the glymphatic system, highlighting gaps in the literature and areas that require immediate exploration. Finally, we assess current knowledge, including possible therapeutic strategies, regarding the role of the CP in neurological disorders, such as traumatic brain injury, migraine, Alzheimer's disease, and multiple sclerosis.
2,330,195
The expansion and severity of chronic MS lesions follows a periventricular gradient.
Expansion of chronic lesions in multiple sclerosis (MS) patients and recently described cerebrospinal fluid (CSF)-related gradient of tissue damage are linked to microglial activation. The aim of this study was to investigate whether lesion expansion is associated with proximity to ventricular CSF spaces.</AbstractText>Pre- and post-gadolinium three-dimensional (3D)-T1, 3D FLAIR and diffusion tensor images were acquired from 36 relapsing-remitting MS (RRMS) patients. Lesional activity was analysed between baseline and 48&#x2009;months at different distances from the CSF using successive 1&#x2009;mm thick concentric bands radiating from the ventricles.</AbstractText>Voxel-based analysis of the rate of lesion expansion demonstrated a clear periventricular gradient decreasing away from the ventricles. This was particularly apparent when lesions of equal diameter were analysed. Periventricular lesional tissue showed higher degree of tissue destruction at baseline that significantly increased during follow-up in bands close to CSF. This longitudinal change was proportional to degree of lesion expansion. Lesion-wise analysis revealed a gradual, centrifugal decrease in the proportion of expanding lesions from the immediate periventricular zone.</AbstractText>Our data suggest that chronic white matter lesions in close proximity to the ventricles are more destructive, show a higher degree of expansion at the lesion border and accelerated tissue loss in the lesion core.</AbstractText>
2,330,196
Hepatoma Derived Growth Factor Enhances Oligodendrocyte Genesis from Subventricular Zone Precursor Cells.
Oligodendrocytes, the myelinating cells of the central nervous system (CNS), perform vital functions in neural protection and communication, as well as cognition. Enhanced production of oligodendrocytes has been identified as a therapeutic approach for neurodegenerative and neurodevelopmental disorders. In the postnatal brain, oligodendrocytes are generated from the neural stem and precursor cells (NPCs) in the subventricular zone (SVZ) and parenchymal oligodendrocyte precursor cells (OPCs). Here, we demonstrate exogenous Hepatoma Derived Growth Factor (HDGF) enhances oligodendrocyte genesis from murine postnatal SVZ NPCs in vitro without affecting neurogenesis or astrogliogenesis. We further show that this is achieved by increasing proliferation of both NPCs and OPCs, as well as OPC differentiation into oligodendrocytes. In vivo results demonstrate that intracerebroventricular infusion of HDGF leads to increased oligodendrocyte genesis from SVZ NPCs, as well as OPC proliferation. Our results demonstrate a novel role for HDGF in regulating SVZ precursor cell proliferation and oligodendrocyte differentiation.
2,330,197
Feasibility of Fetal Proximal Lateral Cerebral Ventricle Measurement.
Measuring the posterior horn of the lateral ventricle in the fetus during ultrasound scans may be challenging. We aimed to examine this measurement feasibility, in relation to gestational age.</AbstractText>A cross-sectional study was conducted, including nonanomalous fetuses, in which both lateral ventricles measured less than 10&#x2009;mm during anomaly scans. The measurements were performed according to the International Society of Ultrasound in Obstetrics and Gynecology guidelines. Success rate of measuring both ventricles was assessed at different gestational ages. Association between lateral ventricle width with contralateral ventricle width, gender, gestational age, and fetal head position were assessed.</AbstractText>A total of 156 cases were recruited. The lateral ventricle distal to the probe was measured in all cases. In 10 cases proximal lateral ventricle could not be adequately measured (failed proximal ventricle measurement group). In 146 scans both ventricle measurements were available. All 10 cases of failed proximal ventricle measurement were in third trimester (30-38&#x2009;weeks). Success rate of measurement of both ventricles was 100%, 96.2%, 71.4%, and 37.5% for gestational week 14-29, 30-32, 33-35, and 36-38, respectively (P&#x2009;&lt;.001). Proximal lateral ventricle width was strongly associated with the distal ventricle width (B&#xa0;=&#xa0;0.422, 95% confidence interval 0.29, 0.555, P&#x2009;&lt;.001), but not with head position, fetal gender, or gestational age.</AbstractText>Measurement of the proximal lateral ventricle is feasible in most cases, even during late third trimester scans. Efforts should be made to visualize both ventricles in every evaluation of the fetal brain.</AbstractText>&#xa9; 2022 American Institute of Ultrasound in Medicine.</CopyrightInformation>
2,330,198
Remote cerebellar hemorrhage after the evacuation of a subdural hematoma: a case report.
Remote intracranial hemorrhage is postoperative bleeding that occurs away from the surgical site. Remote cerebellar hemorrhage (RCH) is a cerebellar hemorrhage that may occur in 0.04-0.8% of cases after supratentorial and spinal procedures. We report a case of a 73-year-old male who developed signs of increased intracranial pressure two days after the evacuation of a subdural hematoma. Brain computed tomography showed RCH with the "zebra sign" and triventricular hydrocephalus that indicated the placement of external ventricle drain in emergency. Therefore, surgeons must pay special attention to this rare postoperative complication because it can be devastating in terms of patient outcome especially due to its possible complications requiring surgical treatment.
2,330,199
Leptomeningeal and subependymal seeding of diffuse intrinsic pontine glioma: a case report.
DIPG (diffuse intrinsic pontine glioma) is a deadly cancerous tumor of the brainstem that spreads across the pons. The tumor's infiltrative nature, as well as the tumor's critical pathway and nuclei compression, contributes to the tumor's extremely poor prognosis and limited existing therapeutic options. A previous study revealed that in 40 patients with brainstem glioma, 13 (33%) patients had leptomeningeal spreading. In this paper, we reported a 7-year-old female patient who presented with a history of decreased consciousness and weakness of the right limb. Her magnetic resonance imaging (MRI) revealed a pontine mass. She was given 35 fractions of 54&#xa0;Gy whole-brain radiotherapy. The post-radiotherapy MRI evaluation showed multiple nodules in periventricular region, and was suggestive of leptomeningeal and subependymal seeding of the pontine glioma in the lateral ventricles. This case report elucidated the leptomeningeal seeding in a pediatric patient with diffuse intrinsic pontine glioma.