Ascending central canal dilation and progressive ependymal disruption in a contusion model of rodent chronic spinal cord injury

<p>Abstract</p> <p>Background</p> <p>Chronic spinal cord injury (SCI) can lead to an insidious decline in motor and sensory function in individuals even years after the initial injury and is accompanied by a slow and progressive cytoarchitectural destruction. At present, no pathological mechanisms satisfactorily explain the ongoing degeneration.</p> <p>Methods</p> <p>Adult female Sprague-Dawley rats were anesthetized laminectomized at T10 and received spinal cord contusion injuries with a force of 250 kilodynes using an Infinite Horizon Impactor. Animals were randomly distributed into 5 groups and killed 1 (n = 4), 28 (n = 4), 120 (n = 4), 450 (n = 5), or 540 (n = 5) days after injury. Morphometric and immunohistochemical studies were then performed on 1 mm block sections, 6 mm cranial and 6 mm caudal to the lesion epicenter. The SPSS 11.5 t test was used to determine differences between quantitative measures.</p> <p>Results</p> <p>Here, we document the first report of an ascending central canal dilation and progressive ependymal disruption cranial to the epicenter of injury in a contusion model of chronic SCI, which was characterized by extensive dural fibrosis and intraparenchymal cystic cavitation. Expansion of the central canal lumen beyond a critical diameter corresponded with ependymal cell ciliary loss, an empirically predictable thinning of the ependymal region, and a decrease in cell proliferation in the ependymal region. Large, aneurysmal dilations of the central canal were accompanied by disruptions in the ependymal layer, periependymal edema and gliosis, and destruction of the adjacent neuropil.</p> <p>Conclusion</p> <p>Cells of the ependymal region play an important role in CSF homeostasis, cellular signaling and wound repair in the spinal cord. The possible effects of this ascending pathology on ependymal function are discussed. Our studies suggest central canal dilation and ependymal region disruption as steps in the pathogenesis of chronic SCI, identify central canal dilation as a marker of chronic SCI and provide novel targets for therapeutic intervention.</p

Mutations in DCHS1 Cause Mitral Valve Prolapse

SUMMARY Mitral valve prolapse (MVP) is a common cardiac valve disease that affects nearly 1 in 40 individuals1–3. It can manifest as mitral regurgitation and is the leading indication for mitral valve surgery4,5. Despite a clear heritable component, the genetic etiology leading to non-syndromic MVP has remained elusive. Four affected individuals from a large multigenerational family segregating non-syndromic MVP underwent capture sequencing of the linked interval on chromosome 11. We report a missense mutation in the DCHS1 gene, the human homologue of the Drosophila cell polarity gene dachsous (ds) that segregates with MVP in the family. Morpholino knockdown of the zebrafish homolog dachsous1b resulted in a cardiac atrioventricular canal defect that could be rescued by wild-type human DCHS1, but not by DCHS1 mRNA with the familial mutation. Further genetic studies identified two additional families in which a second deleterious DCHS1 mutation segregates with MVP. Both DCHS1 mutations reduce protein stability as demonstrated in zebrafish, cultured cells, and, notably, in mitral valve interstitial cells (MVICs) obtained during mitral valve repair surgery of a proband. Dchs1+/− mice had prolapse of thickened mitral leaflets, which could be traced back to developmental errors in valve morphogenesis. DCHS1 deficiency in MVP patient MVICs as well as in Dchs1+/− mouse MVICs result in altered migration and cellular patterning, supporting these processes as etiological underpinnings for the disease. Understanding the role of DCHS1 in mitral valve development and MVP pathogenesis holds potential for therapeutic insights for this very common disease

Etude retrospective des pathologies mentales infantiles au centre hospitalier universitaire de Lome, Togo.

Objective: Objective was to determine clinical and epidemiological aspects of the psychiatric pathology in children at the teaching hospital of Lomé (Togo) Method: it has been a retrospective study of children aged from 0 to 19 years visited for psychiatric disorders from January 1994 to December 2004. Results: 30.28% (325) were aged of 0 to 19 years and sex-ratio respectively of 1.3 and 1.2. Eldest represented 34% and youngest children 32%. Motive for visit were behavioral disorders (31%) and learning difficulties (23%) among children, behavioral disorders (40%), somatic disorders (22.2%) and sleep disorders (17.7%) among adolescents. Diagnosis were  psychological development disorders (30%), emotional and behavioral disorders (25%) among children, depression (40%) and the psychotic disorders (30%) among adolescents. The associated factors were separated or divorced parents, loss of a parent and unsettled interfamilial relations.Conclusion: Emotional, psychotic and anxiety disorders are the main mental disorders among children in Lomé. Prevention by precocious psychosocial pathology tracking by formed professionals is a strategy to develop.Objectif : l’objectif a été de déterminer les aspects épidémio-cliniques des maladies mentales affectant l’enfant au CHU de LoméMéthodes : il s’est agi d’une étude rétrospective incluant les sujets de 0 à 19 ans, suivis pour trouble mental de janvier 1994 à décembre 2004Résultats : 325 (30,28%) étaient âgés de 0 à 19 ans, avec une sex-ratio respective de 1,3 et 1,2 chez les enfants et chez les adolescents. La position d’aîné a représenté 34% et celle de benjamin 32%. Les motifs de consultation ont été les troubles du comportement (31%) et les difficultés scolaires (23%) chez l’enfant, tandis que les troubles du comportement (40%), les troubles somatiques (22,2%) et du sommeil (17,7%) ont été les plus retrouvés chez l’adolescent. Les principaux diagnostics ont été les troubles du développement psychologique (30%) et les troubles émotionnels et du comportement (25%) chez l’enfant, la dépression (40%) et les troubles psychotiques (30%) chez l’adolescent. Les facteurs associés ont été la séparation ou le divorce des parents, la perte d’un parent et les relations intra-familiales perturbées.Conclusion : Les troubles affectifs, psychotiques et anxio-névrotiques sont les principales maladies mentales de l’enfant et de l’adolescent. La prévention grâce à un dépistage précoce des pathologiespsychosociales par des professionnels formés est une stratégie à développer.

Manifestations cliniques et facteurs declenchants de la depression a Lome, Togo

Objectives: Objectives of this study have been to determine clinic particularities of the reactive depression in the Togolese context and to identify factors associated.Patients and methods: It has been a retrospective study on five years realized into the clinique depsychiatrie et de psychologie médicale of Chu- Campus of Lomé. Have been included in the study processed patients in the course of the periodResults: reactive depression has represented 47.22% of depressive disorder. Patients aged from 20 to 49 years have represented 88.23%, women 67.06%. Affective factors (62.35%) and socio-economic factors(37.65%) have constituted the main releases. Multiple somatic symptoms have been in the forefront, while attempts of suicides were feebly observed.Conclusions: there is clinic sameness between reactive depression in Lomé and cases described in the literature