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xing2007金蟲(chóng) (初入文壇)
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The processes involved in mammalian reproduction, from ovulation through to birth, clearly involve large-scale tissue remodelling, with some close analogies to in fl ammatory processes. One such process is the rupture of the ovarian follicle on ovulation. Human follicular fl uid has been found to contain heparan sulphate with unusually strong anticoagulant activity, due to a high content of 3-O-sulphated glucosamine [49]. Indeed, mice lacking the 3-O- sulfotransferase enzyme were found to have normal haemostasis but exhibited reproductive abnormalities [50]. Protracted labour is one of the major reasons for emergency caesarean section. Through clinical observations that women who were undergoing low molecular heparin treatment for thrombophilia had shorter labour time and experimental fi ndings that low molecular weight heparin increases myometrial contractility and induces increased synthesis of interleukin 8 in cervical fi broblasts [51], a non-anticoagulant heparin is now in Phase I clinical trial for the prevention and treatment of protracted labour [52]. The mechanism by which heparin acts in this indication is unclear. Human cervical ripening and cervical dilation is known to be a proinflammatory event [53,54] and heparin may have an effect on this process. Thrombosis is often associated with aggressive cancers such as pancreatic cancer and there are numerous clinical trials investigating the effect of heparin and low molecular weight heparin on the morbidity and mortality rate of cancer patients. Meta-analysis has shown that heparin therapies do improve survival rate for this group of patients. In addition, there is evidence to show that apart from acting as an antithrombotic, heparin may also possess antineoplastic properties. In cell based and animal models, Mellor et al.[55] demonstrated that non-anticoagulant heparin signi fi cantly inhibits the migration of breast cancer cells and that anticoagulant heparin can reduce migration and metastatic spread of cancer cells. The anti-metastatic effect may be due to its ability to inhibit the binding of growth factor on cell surface, leading to inhibition of angiogenesis. Heparin can also inhibit the adhesion by acting on L- and P-selectin [56] |
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2樓2010-08-22 07:49:03
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