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排序方式: 共有713条查询结果,搜索用时 15 毫秒
91.
U PODDAR Y CHAWLA RK DHIMAN K VAIPHEI RK VASISHTA JB DILAWARI 《Journal of gastroenterology and hepatology》1998,13(1):109-111
Ascites may be associated with fulminant hepatic failure (FHF), but spontaneous bacterial peritonitis (SBP) is an extremely rare complication. We report on two patients with FHF who developed SBP. One patient died and the other recovered. 相似文献
92.
93.
In vitro and in vivo selectin-blocking activities of sulfated lipids and sulfated sialyl compounds 总被引:2,自引:0,他引:2
Mulligan MS; Warner RL; Lowe JB; Smith PL; Suzuki Y; Miyasaka M; Yamaguchi S; Ohta Y; Tsukada Y; Kiso M; Hasegawa A; Ward PA 《International immunology》1998,10(5):569-575
There is accumulating evidence that sulfated lipids, sulfated
oligosaccharides and other sulfated compounds are reactive with selectins
in a manner that interferes with selectin interactions with their natural
ligands. In the report we describe the ability of sulfated lipids
(sulfatides and gangliosides) and multimeric forms of sulfated sialic acid
to block binding of P- and E-selectin-Ig to neutrophils. The in vivo
ability of these compounds to block lung injury in rats following i.v.
infusion of purified cobra venom factor (CVF), which induces injury that is
L- and P-selectin dependent, was also determined as well as effects on
recruitment of neutrophils, as measured by lung myeloperoxidase. There was
a significant correlation between the ability of sulfated lipids and sialyl
compounds to interfere in vitro with P-selectin-Ig binding to neutrophils
and to protect against P-selectin-dependent acute lung injury induced by
CVF. The biological effects of these sulfated compounds were also
associated with diminished accumulation of neutrophils. The protective
effects of these compounds may be linked to their ability to interfere with
P- selectin binding to counter-receptors on neutrophils.
相似文献
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B.S. Anand A. Mahmood N.K. Ganguly M.M. Rehani J.B. Dilawari R.C. Mahajan 《Transactions of the Royal Society of Tropical Medicine and Hygiene》1982,76(5):616-619
It is well established that Giardia infection causes malabsorption. However, the precise mechanism of such a malabsorptipn is not known. To investigate this, transport studies, using the tissue accumulation technique, were carried out in mice infected with G. lamblia obtained from human stools. There was a significant fall in the transport of D-glucose, L-alanine and glycine in the infected animals compared with the controls. Kinetics of the D-glucose and glycine transport system were examined by measuring the tissue uptake in the presence of different concentrations of the substrate. For glucose, the affinity constant (Km) for the transport site was the same (4·37mM) in normal and infected animals but the maximal transport rate (V max) was considerably reduced in infected animals (158·7 μ moles/hr/g tissue) compared with (357·1 μ moles/hr/g tissue) in controls. Results with glycine were similar; the Km was similar in control and infected animals (5·7 mM) whereas the V max was reduced in infected animals (27·02 μ moles/hr/g tissue) compared with controls (45·5 μ moles/hr/g tissue).Analysis of the intestinal enzymes showed a significant decrease in the levels of brush border sucrase, lactase and alkaline phosphatase in infected animals; the cellular enzymes, LDH, GOT and GPT remained unaffected.The observed aberrations in the transport functions and brush border enzymes suggest that G. lamblia causes malabsorption by damaging the epithelial membrane of the enterocyte. 相似文献
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