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Foot Processes (foot + process)
Selected AbstractsUltrastructure of the ovary and oogenesis in six species of patellid limpets (Gastropoda: Patellogastropoda) from South AfricaINVERTEBRATE BIOLOGY, Issue 3 2000Alan N. Hodgson Abstract. The ultrastructural features of the ovary and oogenesis have been described in 6 species of patellid limpets from South Africa. The ovary is a complex organ that is divided radially into numerous compartments or lacunae by plate-like, blind-ended, hollow trabeculae that extend from the outer wall of the ovary to its central lumen. Trabeculae are composed of outer epithelial cells, intermittent smooth muscle bands, and extensive connective tissue. Oocytes arise within the walls of the trabeculae and progressively bulge outward into the ovarian lumen during growth while partially surrounded by squamous follicle cells. During early vitellogenesis, the follicle cells lift from the surface of the underlying oocytes and microvilli appear in the perivitelline space. Follicle cells restrict their contact with the oocytes to digitate foot processes that form desmosomes with the oolamina. When vitellogenesis is initiated, the trabecular epithelial cells hypertrophy and become proteosynthetically active. Yolk synthesis involves the direct incorporation of extraoocytic precursors from the lumen of the trabeculae (hemocoel) into yolk granules via receptor-mediated endocytosis. Lipid droplets arise de novo and Golgi complexes synthesize cortical granules that form a thin band beneath the oolamina. A fibrous jelly coat forms between the vitelline envelope and the overlying follicle cells in all species. [source] Blood,brain barrier breakdown in septic encephalopathy and brain tumours*JOURNAL OF ANATOMY, Issue 6 2002D. C. DaviesArticle first published online: 28 JUN 200 Abstract Septic encephalopathy is associated with breakdown of the blood,brain barrier and cerebral oedema. These features are also common properties of brain tumours. Perimicrovessel oedema, disruption of associated astrocyte end feet and neuronal injury occur in a porcine model of acute septic encephalopathy. The adrenergic system has been implicated in the inflammatory response to sepsis and may play a role in controlling blood,brain barrier permeability, since the ,2 -adrenoceptor agonist dopexamine inhibits perimicrovessel oedema formation whereas the ,1 -adrenoceptor agonist methoxamine provokes it. Electron microscopy revealed tight junction opening in high-grade astrocytoma microvessels. Expression of the tight junction protein occludin is reduced in these microvessels and this reduction is inversely correlated with the degree of cerebral oedema. Normal astrocytes secrete factors that induce barrier properties in endothelial cells, whereas high-grade astrocytomas secrete vascular endothelial growth factor, which stimulates angiogenesis, down regulates occludin and increases endothelial cell permeability. The water channel protein aquaporin-4 is normally expressed in astrocyte foot processes around cerebral microvessels. Its expression is massively up-regulated in high-grade astrocytoma and around metastatic adenocarcinoma. There is a significant correlation between aquaporin-4 expression and the degree of cerebral oedema, but it is not clear whether increased aquaporin-4 expression enhances oedema formation or clearance. These results suggest that the pathophysiology of brain oedema is multifactorial, but that there may be common processes operating regardless of the aetiology. [source] Role of aquaporins in endothelial water transportJOURNAL OF ANATOMY, Issue 5 2002A. S. Verkman The aquaporins (AQP) are a family of homologous water channels expressed in many epithelial and endothelial cell types involved in fluid transport. AQP1 protein is strongly expressed in most microvascular endothelia outside of the brain as well as in endothelial cells in cornea, intestinal lacteals, and other tissues. AQP4 is expressed in astroglial foot processes adjacent to endothelial cells in the central nervous system. Transgenic mice lacking aquaporins have been useful in defining their role in mammalian physiology. Mice lacking AQP1 manifest defective urinary concentrating ability, in part because of decreased water permeability in renal vasa recta microvessels. These mice also show a defect in dietary fat processing that may involve chylomicron absorption by intestinal lacteals. There is preliminary evidence that AQP1 might play a role in tumour angiogenesis and in renal microvessel structural adaptation. However AQP1 in most endothelial tissues does not appear to have a physiological function despite its role in osmotically driven water transport. For example mice lacking AQP1 have low alveolar capillary water permeability but unimpaired lung fluid absorption, as well as unimpaired saliva and tear secretion, aqueous fluid outflow, and pleural and peritoneal fluid transport. In the central nervous system mice lacking AQP4 are partially protected from brain oedema in water intoxication and ischaemic models of brain injury. Therefore although the role of aquaporins in epithelial fluid transport is in most cases well understood there remain many questions about the role of aquaporins in endothelial cell function. It is unclear why many leaky microvessels strongly express AQP1 without apparent functional significance. Improved understanding of aquaporin endothelial biology may lead to novel therapies for human disease, such as pharmacological modulation of tumour angiogenesis, renal fluid clearance and intestinal absorption. [source] Familial fibronectin glomerulopathy: analysis of chromosome 1q32 and uteroglobin gene loci in a large New Zealand familyNEPHROLOGY, Issue 5 2001Robert Walker SUMMARY: Recently, a newly recognized familial glomerulopathy with predominant fibronectin deposits has been reported. This is the first report of a family with this condition in Australasia and spans two generations over a 30-year period, with the histologically confirmed glomerulopathy present in the father and five out of eight siblings. The clinical presentations have ranged from asymptomatic proteinuria, pregnancy-associated proteinuria and the nephrotic syndrome to hypertension and proteinuria with progressive renal failure. The time-course from presentation to renal failure was over a 20 years. Histology demonstrated global and diffuse thickening of capillary loops, but no cellular proliferation. Immunofluorescence demonstrated granular positivity for IgM in the capillary loops only. Electron microscopy demonstrated massive electron-dense subendothelial granular deposits with occasional small fibrils and unremarkable epithelial cell foot processes. Immunohistochemical staining was strongly positive for fibronectin and negative for type I or type IV collagen and transforming growth factor , in all biopsies. Genetic studies of familial fibronectin glomerulopathy have recently highlighted two genetic loci. Firstly, a large five-generation pedigree has been described with linkage of fibronectin glomerulopathy to chromosome 1q32. Secondly, fibronectin glomerulopathy has been reported in uteroglobin gene knockout mice. In our studies, DNA sequence analysis of the uteroglobin gene showed that it was normal in all family members, and a DNA polymorphism in the uteroglobin gene did not co-segregate with the disease. In addition, DNA microsatellite markers at the 1q32 locus did not co-segregate with the disease in our family. We presume that the underlying abnormality involves as yet undefined glomerular extracellular matrix regulation and is inherited as an autosomal dominant condition. These data favour genetic heterogeneity for the aetiology of fibronectin glomerulopathy. [source] Electron-microscopic examination of effects of yokukansan, a traditional Japanese medicine, on degeneration of cerebral cells in thiamine-deficient ratsNEUROPATHOLOGY, Issue 5 2010Seiichi Iizuka We previously demonstrated that yokukansan ameliorated not only learning disturbance but also behavioral and psychological symptoms of dementia-like behaviors (anxiety, aggressiveness) and neurological symptoms (opisthotonus) induced in rats by dietary thiamine deficiency (TD). In the present study, the effects of yokukansan on degeneration of cerebral cells were further examined electron-microscopically during pre-symptomatic and symptomatic stages in TD rats. In the pre-symptomatic TD stage, which appeared as increase in aggressive behaviors on the 21st and 28th days of TD diet-feeding, severe edematous degeneration of astrocytes was detected by electron microscopy, although the changes were not observed by light microscopy. In the symptomatic TD stage (the 34th day) characterized by development of neurological symptoms, severe sponge-like degeneration and multiple hemorrhages in the parenchyma were obvious by light microscopy. The electron-microscopic examination showed degeneration in neurons, oligodendroglias, and myelin sheaths in addition to astrocytes. TD rats, which exhibited multiple hemorrhages light microscopically, showed severe edematous changes and hypertrophy of the foot processes of astrocytes surrounding blood vessels. Administration of yokukansan ameliorated not only the TD-induced aggressive behavior and neurological symptoms but also degeneration of the cerebral cells. These results suggest that the inhibitory effect of yokukansan on degeneration in various brain cells might be closely related to the amelioration of aggression and neurological symptoms in TD rats. [source] Intrathecal pathogenic anti,aquaporin-4 antibodies in early neuromyelitis optica,ANNALS OF NEUROLOGY, Issue 5 2009Jeffrey L. Bennett MD Objective The serum of most neuromyelitis optica (NMO) patients contains autoantibodies (NMO-IgGs) directed against the aquaporin-4 (AQP4) water channel located on astrocyte foot processes in the perivessel and subpial areas of the brain. Our objectives were to determine the source of central nervous system (CNS) NMO-IgGs and their role in disease pathogenesis. Methods Fluorescence-activated cell sorting and single-cell reverse transcriptase polymerase chain reaction were used to identify overrepresented plasma cell immunoglobulin (Ig) sequences in the cerebrospinal fluid (CSF) of an NMO patient after a first clinical attack. Monoclonal recombinant antibodies (rAbs) were generated from the paired heavy and light chain sequences and tested for target specificity and Fc effector function. The effect of CSF rAbs on CNS immunopathology was investigated by delivering single rAbs to rats with experimental autoimmune encephalomyelitis (EAE). Results Repertoire analysis revealed a dynamic, clonally expanded plasma cell population with features of an antigen-targeted response. Using multiple independent assays, 6 of 11 rAbs generated from CSF plasma cell clones specifically bound to AQP4. AQP4-specific rAbs recognized conformational epitopes and mediated both AQP4-directed antibody-dependent cellular cytotoxicity and complement-mediated lysis. When administered to rats with EAE, an AQP4-specific NMO CSF rAb induced NMO immunopathology: perivascular astrocyte depletion, myelinolysis, and complement and Ig deposition. Interpretation Molecular characterization of the CSF plasma cell repertoire in an early NMO patient demonstrates that AQP4-specfic Ig is synthesized intrathecally at disease onset and directly contributes to CNS pathology. AQP4 is now the first confirmed antigenic target in human demyelinating disease. Ann Neurol 2009;66:617,629 [source] | |||||||||||||