Aquaporin 4 expression increases in the rat hippocampus and cortex during trimethyltin-induced neurodegeneration

Trimethyltin (TMT) is a neurotoxicant know to produce significant and selective neuronal degeneration in the rodent CNS (for review, 1). Magnetic resonance imaging (MRI) investigation in TMT-treated rats has evidenced dilation of lateral ventricles, possibly correlated to alterations in blood brain barrier permeability .In order to explore the molecular mechanisms involved in the phenomenon we have investigated in the hippocampus and cortex of TMT-treated rats the expression of aquaporin 4 (AQP4), a glial water channel protein believed to play a role in brain oedematous conditions. AQP4 expression was tested both by real-time PCR and western blotting analysis in hippocampus and cortex homogenates. To confirm molecular results and visualize the AQP4 cell distribution double-label immunofluorescence for AQP4 and GFAP was performed. Real-time PCR and western blotting data show a significant upregulation of AQP4 starting from 14 days of TMT treatment both in the hippocampus and the cortex. Accordingly, the immunofluorescence shows an intense astrogliosis and AQP4 immunoreactivity diffusely pronounced in the hippocampal and cortex areas starting from 14 days after intoxication. In particular, AQP4 immunolabelling was localized in astrocytic end-feet encircling the blood vessels. The study of the Rhodamine B fluorescent tracer, intraperitoneally administered, also revealed an intense vascular reaction, characterized by hypertrophic vessels with abnormal course and dimensions in the brain of TMT-treated rats, indicating a vascular involvement in the TMT-induced neurodegenerative processes.. AQP4 over-expression and astrogliosis occurring in the brain of TMT-treated rats might putatively play a role in alterations of vascular permeability and brain oedema formation evidenced by MRI studies

Urinary lithogenic profile of patients with non-alcoholic fatty liver disease.

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Increased expression of Aquaporin 4 in the rat hippocampus and cortex during trimethyltin-induced neurodegeneration

Trimethyltin chloride (TMT) is a neurotoxicant producing neuronal degeneration and reactive astrogliosis in the mammalian central nervous system, especially the hippocampus. A previous magnetic resonance imaging investigation in TMT-treated rats evidenced dilation of lateral ventricles, also suggesting alterations in blood-brain barrier permeability and brain edema. Aquaporin 4 (AQP4), a glial water channel protein expressed mainly in the nervous system, is considered a specific marker of vascular permeability and thought to play an important role in brain edema (conditions). We studied AQP4 expression in the hippocampus and cerebral cortex of TMT-treated rats in order to explore the molecular mechanisms involved in brain edema occurring in these experimental conditions. Real-time PCR and western blotting data showed significant up-regulation of both AQP4 mRNA and protein levels starting 14 days after TMT treatment in the hippocampus and cortex. Parallel immunofluorescence studies indicated intense astrogliosis and AQP4 immunoreactivity diffusely pronounced in the hippocampal and cortex areas starting 14 days after TMT intoxication. In order to study the effects of TMT on vascular integrity, double-label immunofluorescence experiments for rat immunoglobulin G (IgG) and rat endothelial cell antigen-1 (RECA-1) or neuronal nuclei (NeuN) (endothelial and neuronal markers respectively) were performed. The results indicated, at 21 and 35 days after treatment, the presence of rat IgG in paravasal parenchyma and in some neuronal cells of the hippocampus and cortex. The extravasated IgG staining was temporally correlated with over-expression of neuronal vascular endothelial growth factor (VEGF) and the active phosphorylated form of its neuronal receptor (VEGFR-2P), suggesting that these factors may cooperate in mediating vascular leakage

Current and Novel Uses of Intestinal Ultrasound in Inflammatory Bowel Disease

Intestinal ultrasound (IUS) is a patient-centric, noninvasive, real-time, point-of-care tool with the capability to aid in diagnosis and monitoring of disease activity in both Crohn’s disease and ulcerative colitis without the need for bowel preparation. IUS can be used as a tool for precision monitoring of inflammatory bowel disease (IBD) treatment response. IUS as a cross-sectional imaging tool is as accurate as magnetic resonance enterography (MRE) for assessing the ileum and is more accurate than MRE for colonic assessment proximal to the rectum. Multiple simple ultrasound-based scoring systems have been internally validated with endoscopy in both Crohn’s disease and ulcerative colitis, and changes in IUS parameters can be seen as early as 2 weeks after treatment initiation. IUS also plays a unique role in IBD activity monitoring of patients in whom avoidance of invasive testing is paramount, such as children and pregnant patients. Novel uses go beyond monitoring activity, with potential use of elastography to measure bowel wall stiffness to detect fibrosis and bowel damage for enhanced decision-making. Ultimately, IUS is likely to expand in the United States, facilitated by accessible expert training, access to equipment, and the development of a reimbursement model. This article provides a comprehensive review of the current and novel uses of IUS in IBD

Aquaporin 4 (AQP4) expression and blood brain barrier damage in an experimental model of neurodegeneration induced by trimethyltin

Trimethyltin (TMT) is well know

Regolamento (CE) n. 593/2008 del Parlamento europeo e del Consiglio del 17 giugno 2008 sulla legge applicabile alle obbligazioni contrattuali (“Roma I”) - Commentario

Si tratta di un commentario articolo per articolo del regolamento (CE) n. 593/2008 sulla legge applicabile alle obbligazioni contrattuali, strumento che sostituisce, nei rapporti fra gli Stati membri della Comunità europea, la Convenzione di Roma del 19 giugno 1980