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11.
Inflammation and dephosphorylation of the tight junction protein occludin in an experimental model of multiple sclerosis 总被引:3,自引:0,他引:3
Morgan L Shah B Rivers LE Barden L Groom AJ Chung R Higazi D Desmond H Smith T Staddon JM 《Neuroscience》2007,147(3):664-673
Multiple sclerosis (MS) is a disease of the CNS in which inflammation, demyelination and neurodegeneration contribute to its initiation and progression. A frequently employed model of MS is experimental autoimmune encephalomyelitis (EAE). Here, to gain new insights into the disease process, an analysis of proteins in extracts of lumbar spinal cord from naïve and EAE rats was undertaken. The data mainly confirm that inflammation and blood–brain barrier (BBB) breakdown are the major hallmarks of disease in this model. Given their importance in the BBB, junctional proteins were further investigated. Occludin, a protein localizing to tight junctions in brain endothelial cells, showed strikingly increased migration in EAE when analyzed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE). This increased migration was mimicked by in vitro phosphatase treatment, implying its dephosphorylation in EAE. Occludin dephosphorylation coincided with the onset of inflammation, slightly preceding visible signs of disease, and was just prior to apparent changes in BBB permeability. These findings suggest occludin is a target for signaling processes in EAE, perhaps regulating the response of the BBB to the inflammatory environment as seen in MS. 相似文献
12.
Using protein chromatography, we purified and identified human prothrombin from human plasma as antiangiogenic. Prothrombin significantly inhibited endothelial cell tube formation in vitro at 10 microg/ml. Importantly, it also inhibited bFGF-induced angiogenesis in Matrigel-plug assays performed in mice. The proteolytic activity of thrombin appeared to be critical for the antiangiogenic activity of prothrombin. For example, thrombin exhibited inhibitory effects on endothelial cell tube formation in vitro at 10 U/ml. Addition of lepirudin, a specific inhibitor of thrombin, completely blocked prothrombin's and thrombin's antiangiogenic effects in vitro. We also assessed the importance of thrombin receptors in angiogenesis. Using small peptides that activate different protease-activated receptors (PARs), we showed that activation of PAR-1 led to inhibition of endothelial cell tube formation in vitro and bFGF-induced angiogenesis in vivo. Collectively, our data suggest that thrombin's proteolytic activity can be antiangiogenic. 相似文献
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Guadalupe Garcia-Tsao Fa-Yauh Lee Gertrude E. Barden Richard Cartun A. Brian West 《Gastroenterology》1995,108(6):1835-1841
Cirrhotic patients are predisposed to develop spontaneous bacteremias and/or peritonitis, mainly caused by enteric bacteria. The aim of this study was to investigate if bacterial translocation, which is the passage of bacteria from the intestinal lumen to regional lymph nodes and/or the systemic circulation, is increased in a rat model of cirrhosis. Rats were studied after 12–16 weeks of CCl4 inhalation, when samples of mesenteric lymph nodes, blood, liver, and spleen for standard bacteriologic cultures and a fragment of colon and liver for histology were obtained. Immunostaining of the cecum was performed using a polyclonal anti-Escherichia coli antibody. A significantly greater proportion of rats with cirrhosis and ascites (5 of 9; 56%) had positive mesenteric lymph node cultures compared with cirrhotics without ascites (0 of 9) and normal controls (0 of 12) (P < 0.01). In one cirrhotic rat, E. coli was isolated from both mesenteric lymph nodes and ascites. Rats with cirrhosis and ascites had significantly greater cecal submucosal edema and inflammation than rats with no ascites and controls. Immunoreactivity with E. coli was present in the cecal wall in 3 of 5 animals with E. coli translocation to mesenteric lymph nodes. In cirrhotic rats, bacterial translocation is increased after the development of ascites and may be a major factor in the development of spontaneous infections in cirrhosis. 相似文献
14.
Barschak AG Sitta A Deon M Barden AT Dutra-Filho CS Wajner M Vargas CR 《Metabolic brain disease》2008,23(1):71-80
Maple Syrup Urine Disease (MSUD) is an autossomal recessive metabolic disorder caused by a deficiency of branched-chain α-keto
acid dehydrogenase complex activity leading to accumulation of the branched-chain amino acids leucine, isoleucine and valine
and their corresponding branched-chain α-keto acids. Affected patients usually present hypoglycemia, ketoacidosis, convulsions,
poor feeding, coma, psychomotor delay and mental retardation. Considering that the pathophysiology of MSUD is still poorly
understood, in this study we evaluated some parameters of oxidative stress, namely thiobarbituric acid-reactive substances
(TBARS), total antioxidant reactivity (TAR) and total antioxidant status (TAS) in plasma from treated MSUD patients presenting
high and low plasma leucine levels. We verified a significant increase of TBARS (lipid peroxidation) and a decrease of TAR
(capacity to rapidly react with free radicals) in plasma from treated MSUD patients with low and with high plasma levels of
leucine compared to the control group. It was also verified that TAS (quantity of tissue antioxidants) was not altered in
plasma from treated MSUD patients with low and high blood leucine levels. Finally, we found no correlation between leucine,
valine and isoleucine levels with the various parameters of oxidative stress. These results are indicative that increased
lipid oxidative damage and decreased antioxidant defenses occur in plasma of MSUD patients and that the accumulating branched-chain
amino acids are probably not directly associated to oxidative stress in this disorder. 相似文献
15.
A nosocomial outbreak of Branhamella catarrhalis confirmed by restriction endonuclease analysis 总被引:13,自引:0,他引:13
T F Patterson J E Patterson B L Masecar G E Barden W J Hierholzer M J Zervos 《The Journal of infectious diseases》1988,157(5):996-1001
An outbreak of respiratory illness due to Branhamella catarrhalis occurred in the intermediate care unit of a Veterans Administration hospital and involved patients and staff members. Four patients had pneumonia and four had bronchitis. Infected patients were placed in a cohort separated from noninfected patients and were treated. Pharyngeal culture was used to survey prevalence in staff and all other patients on the unit; three of 18 staff members and two of 19 asymptomatic patients were positive for B. catarrhalis. A case-control study showed that respiratory therapy, steroid use, and location within the unit were significant risk factors for B. catarrhalis infection or colonization. Strains from five patients and two staff members had identical bacterial restriction endonuclease digestion patterns with three different enzymes; these patterns were distinct from those of control strains. This study is the first to document an outbreak of B. catarrhalis infection confirmed with a typing system and thus establishes B. catarrhalis as a nosocomial pathogen. 相似文献
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Granulocyte-colony stimulating factor in COVID-19: Is it stimulating more than just the bone marrow?
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