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Zhambalova BA Azizova OA Lopukhin YM 《Bulletin of experimental biology and medicine》2002,133(5):448-449
Fibrinogen intensified luminol-dependent chemiluminescence of blood leukocytes stimulated with opsonized zymosan. It is hypothesized that fibrinogen stimulates and prolongs functional activity of leukocytes during inflammation. 相似文献
95.
T. I. Torkhovskaya E. S. Fortinskaya É. M. Khalilov S. S. Markin T. I. Borkunova Yu. M. Lopukhin 《Bulletin of experimental biology and medicine》1992,113(5):645-648
Research Institute of Physicochemical Medicine, Ministry of Health, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 113, No. 5, pp. 481–483, May, 1992. 相似文献
96.
Azizova OA Piryazev AP Nikitina NA Savchenkova AP Lopukhin YM 《Bulletin of experimental biology and medicine》2002,134(2):137-138
Using the method of peroxide-induced chemiluminescence we showed that incubation of the whole blood with oxidized LDL or oxidized blood plasma increased plasma hemoglobin concentration, which linearly depended on the degree of LDL oxidation. Similar effects were observed in erythrocyte suspension. Hemolytic activity of oxidized plasma 3-4-fold surpassed that of LDL isolated by ultracentrifugation. LDL capacity to oxidation in the presence of Cu2+ increased by 50% and osmotic hemolysis of erythrocytes increased by 53% in coronary patients in comparison with healthy donors. These results indicate that oxidized LDL induce erythrocyte hemolysis. 相似文献
97.
RA Botham M Franco AL Reeder A Lopukhin K Shiota S Yamada PF Nichol 《Journal of pediatric surgery》2012,47(7):1369-1379
PurposeDuodenal atresia in humans has been hypothesized to arise from a failure of the duodenal lumen to recanalize after formation of an endodermal plug. Recently, mutations in the fibroblast growth factor receptor 2 gene (Fgfr2IIIb) have been shown to cause atretic defects of the duodenum in mice. However, work in rats suggests that murine species do not form an endodermal plug during normal duodenal development. These lines of data led us to hypothesize that mice are able to form a duodenal atresia in the absence of an endodermal plug. To test this hypothesis, we examined duodenal development in wild-type and Fgfr2IIIb?/? embryos.MethodsParaffin sections were generated for H&;E, E-cadherin, or terminal deoxynucleotidyl transferase-mediated X-dUTP nick end labeling staining from Fgfr2IIIb?/? and wild-type embryos between embryonic days (E) 10.5 and E14.5. Sections were photographed and reconstructed into 3-dimensional display using Adobe Photoshop and Amira Visage software.ResultsNormal mouse duodenum does not form an endodermal plug, although a plug does form in the pyloric region of the stomach at E14.5. Fgfr2IIIb?/? embryos experience significant apoptosis in the duodenal region at E10.5, followed by the disappearance of the endoderm in the atretic precursor by E11.5. Thereafter, the mesoderm of the atretic precursor involutes over the next 2 days in the absence of further apoptosis. Interestingly, an endodermal plug was not observed at any point during the formation of a duodenal atresia.ConclusionsThese results suggest that duodenal atresia in the Fgfr2IIIb?/? model does not arise from persistence of an epithelial plug. Rather it appears to result from the loss of the endoderm because of apoptosis very early in development. 相似文献