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991.
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993.
Novel orthobunyavirus in Cattle, Europe, 2011 总被引:4,自引:0,他引:4
Hoffmann B Scheuch M Höper D Jungblut R Holsteg M Schirrmeier H Eschbaumer M Goller KV Wernike K Fischer M Breithaupt A Mettenleiter TC Beer M 《Emerging infectious diseases》2012,18(3):469-472
In 2011, an unidentified disease in cattle was reported in Germany and the Netherlands. Clinical signs included fever, decreased milk production, and diarrhea. Metagenomic analysis identified a novel orthobunyavirus, which subsequently was isolated from blood of affected animals. Surveillance was initiated to test malformed newborn animals in the affected region. 相似文献
994.
995.
Meyer Kerstin Maria Klink Thomas Ugurel Selma Bröcker Eva-Bettina 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2012,250(3):463-464
Graefe's Archive for Clinical and Experimental Ophthalmology - 相似文献
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997.
Mangano A Gonzalez E Dhanda R Catano G Bamshad M Bock A Duggirala R Williams K Mummidi S Clark RA Ahuja SS Dolan MJ Bologna R Sen L Ahuja SK 《The Journal of infectious diseases》2001,183(11):1574-1585
If CC chemokine receptor 5 (CCR5)-dependent mechanisms at the time of initial virus exposure are important determinants of virus entry and disease outcome, then the polymorphisms in CCR5 that influence risk of transmission and disease progression should be similar; this hypothesis was tested in a cohort of 649 Argentinean children exposed perinatally to human immunodeficiency virus type 1 (HIV-1). Two lines of evidence support this hypothesis. First, CCR5 haplotype pairs associated with enhanced risk of transmission were the chief predictors of a faster disease course. Second, some of the haplotype pairs associated with altered rates of transmission and disease progression in children were similar to those that we previously found influenced outcome in European American adults. This concordance suggests that CCR5 haplotypes may serve as genetic rheostats that influence events occurring shortly after initial virus exposure, dictating not only virus entry but, by extension, also the extent of early viral replication. 相似文献
998.
K. W. Bock A. -B. Kobusch G. Fischer 《Journal of cancer research and clinical oncology》1989,115(3):285-289
Summary UDP-glucuronosyltransferase (UDPGT) was studied immunohistochemically in hepatic foci and nodules of N-nitrosomorpholine-treated mice. Serial sections were stained for glucose-6-phosphatase (G6Pase). It was found that a high percentage of G6Pase-negative liver foci and nodules were also UDPGT-negative (34%). In addition, G6Pase-negative foci without altered UDPGT phenotype (30%) and UDPGT-negative foci without altered G6Pase phenotype (8%) were detected. G6Pase-positive foci were also present (24%). Interestingly, most G6Pasepositive foci were UDPGT-positive (16%). Some G6Pase-positive lesions without altered UDPGT phenotype were also found (8%). The major phenotype observed in rat hepatocarcinogenesis models (UDPGT-positive/G6Pase-negative foci) was not detectable in the mouse model. These results demonstrate heterogeneous alterations of UDPGTs in mouse hepatic foci. They furthermore suggest marked differences between the mouse and the rat in the regulation of UDPGTs in similarly induced rat hepatic foci.Abbreviations UDPGT
UDP-glucuronosyltransferase
- G6Pase
glucose-6-phosphatase
Dedicated to Professor Dr. med. Dr. med. h.c. Herbert Remmer on the occasion of his 70th birthday 相似文献
999.
1000.
Kuhlmann CR Scharbrodt W Schaefer CA Most AK Backenköhler U Neumann T Tillmanns H Waldecker B Erdogan A Wiecha J 《Journal of molecular and cellular cardiology》2005,38(2):315-322
The inward rectifier K+ current (K(ir)) determines the resting membrane potential of endothelial cells. Basic fibroblast growth factor (bFGF) has been shown to activate K(ir) and acts as angiogenic factor and vasodilator. In contrast, nicotine has been demonstrated to reduce endothelium-dependent vasorelaxation by increasing radical formation. Aim of the present study was to investigate whether nicotine modulates K(ir) and if this plays a role in bFGF-mediated proliferation, migration and nitric oxide (NO)-formation of endothelial cells. Using the patch-clamp technique in cultured endothelial cells of human umbilical cord veins (HUVEC), we found characteristic K(ir), which were blocked by extracellular barium (100 micromol/l). Perfusion with nicotine (1 nmol/l-10 micromol/l) revealed a dose-dependent reduction of K(ir). The simultaneous perfusion with bFGF (50 ng/ml) and nicotine (10 micromol/l) still significantly reduced K(ir) (n = 8; P < 0.01). Cell counts revealed that bFGF-mediated proliferation of HUVEC was significantly inhibited when using 1-10 micromol/l nicotine (n = 8, P < 0.01). The bFGF-induced endothelial cell migration--examined using the "Fences-Migration-Assay"--was significantly reduced by 10 mumol/l nicotine (n = 12; P < 0.05). NO-production was examined using a cGMP-Radioimmunoassay. The significant bFGF-induced increase of cGMP-levels was reduced by nicotine (n = 10; P < 0.05). Our data indicate that the modulation of K(ir) seems to be an essential pathway in the antagonistic effects of nicotine on bFGF-mediated endothelial cell growth, migration and NO-formation. 相似文献