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831.
Lalloo DG; Trevett AJ; Black J; Mapao J; Saweri A; Naraqi S; Owens D; Kamiguti AS; Hutton RA; Theakston RD; Warrell DA 《QJM : monthly journal of the Association of Physicians》1996,89(1):25-35
Thirty-two patients with enzyme-immunoassay-proven death adder (Acanthophis
sp.) bites were studied in Port Moresby, Papua New Guinea. Eighteen were
envenomed; local signs were rare and none had incoagulable blood, but all
except one had signs of neurotoxicity. Five (27.7%) envenomed patients
required intubation and ventilation. One patient developed renal failure,
previously undescribed following death adder bites. Laboratory
investigations showed mild prolongation of prothrombin and partial
thromboplastin times in some patients. In vitro studies showed that the
venom contains anticoagulant activity, but does not cause fibrinogenolysis.
In contrast to taipan envenoming, neurotoxicity did not progress after
antivenom administration, and there was reversal of neurotoxicity, evident
within 6 h, in three severely envenomed patients treated less than 12 h
after the bite. One patient treated with antivenom and anticholinesterases
had the most dramatic response to treatment; the optimum management of
bites by this species may include prompt treatment with both antivenom and
anticholinesterases in addition to effective first aid.
相似文献
832.
833.
The role of epithelial Toll-like receptor signaling in the pathogenesis of intestinal inflammation 总被引:1,自引:0,他引:1
Emerging evidence suggests that the innate immune system, comprised of Toll-like receptors (TLRs) and their associated molecules, plays a pivotal role in the regulation of intestinal inflammation and in the response to invading pathogens. Although TLRs are thought to have predominantly beneficial effects in pathogen recognition and bacterial clearance by leukocytes, their dysregulation and unique signaling effects within intestinal epithelia in the setting of inflammation may have devastating consequences. For instance, activation of TLR4 in enterocytes leads to an inhibition of enterocyte migration and proliferation as well as the induction of enterocyte apoptosis-factors that would be expected to promote intestinal injury while inhibiting intestinal repair. TLR signaling has been shown to be abnormal in several intestinal inflammatory diseases, including Crohn's disease, ulcerative colitis, and necrotizing enterocolitis. This review serves to examine the evidence regarding the patterns of expression and signaling of TLRs in the intestinal mucosa at basal levels and during physiologic stressors to gain insights into the pathogenesis of intestinal inflammation. We conclude that the data reviewed suggest that epithelial TLR signaling-acting in concert with TLR signaling by leukocytes-participates in the development of intestinal inflammation. We further conclude that the evidence reviewed provides a rationale for the development of novel, epithelial-specific, TLR-based agents in the management of diseases of intestinal inflammation. 相似文献