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abnormal release
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  异常释放
     100% in MODS group. Conclusions The abnormal release of the TNF-α? IL-1β?
     结论 细胞因子TNF -α、IL - 1β、IL - 6、IL - 8、IL - 10的异常释放可能参与了危重病MODS的病理过程。
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     Conclusions The abnormal release of TNF-α,IL-1β,IL-6,IL-10 play an important role in the pathophysiology of MODS with elderly patients. To maintain the balance of cytokines may be a method of treatment in future.
     结论 细胞因子TNF -α、IL - 1β、IL - 6、IL - 10的异常释放参与了老年MODS的病理生理过程,选择不同时机以纠正细胞因子的失衡可能是今后的救治方向。
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     Findings of this serial studies strongly suggested that the uncontrollable "mediator disease" resuIted from ischemic-reperfusion damage, swelling and edema of visceraI tissues, the endothelial cell damage and abnormal release mediators might be of importance in the pathogenesis of early PB organ damage。
     缺血和再灌流损伤、脏器水肿、内皮细胞损伤及多种炎症介质的异常释放,导致难以控制的介质病,是脏器损害的重要因素;
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     Objective To study the effect of extracorporeal circulation on the abnormal release of proinflammatory and anti inflammatory cytokines, and explore their effect on systemic inflammatory response after operation.
     目的 研究体外循环术对致炎性细胞因子和抗炎性细胞因子异常释放的影响 ,并探讨其在术后炎症反应中的作用。
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     Hypothalamic Orphanin FQ Participates in Neuroendocrinologic Mechanism of Electroacupuncture Normalizing Abnormal Release of Pituitary LH in Ovariectomized Rats
     下丘脑孤啡肽参与电针调整去卵巢大鼠LH异常释放的神经内分泌机制
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  “abnormal release”译为未确定词的双语例句
     Objective To explore the neuroendocrinologic mechanism underlying the regulation effect of eletroacupuncture (EA), the mRNA and protein expression of OFQ ( Nociceptin/Orphanin FQ) and ORLl receptor ( opioid receptor-like receptor 1) in medial basal hypothalamus (MBH) was investigated following EA normalizing the abnormal release of pituitary LH (luteinizing hormone) in ovariectomized rats.
     目的 本文在去卵巢(OVX)大鼠模型上,观察下丘脑孤啡肽(Nociceptin/OrphaninFQ,OFQ)及孤儿受体(opiod receptor-like receptor 1,ORLl)是否参与电针对黄体生成素(luteinizing hormone,LH)超常释放的影响,进一步探讨电针作用的神经内分泌机制。
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     Some investigators regarded that PCOS may be related to abnormal release of GnRH, hyperandrogenism, hyperinsulinemia and insulin resistance.
     一般认为,高雄激素血症、胰岛素抵抗及高胰岛素血症可能是PCOS的发病机制。
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     GM1 did not influence the releases of NPY during cerebral ischemia suggesting that releases of NPY from there synaptsomes were not modulated by GM1.CR1505 was able to significantly inhibit the abnormal release of NPY during cerebral ischemia suggesting a coordinated interaction between NPY and CCK in brain ischemia.
     GM1不影响脑缺血时NPY的释放,表明含NPY的突触释放NPY时不受GM1的调节。
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     The results suggested that HIE caused an abnormal release of AVP into plasma and CSF. AVP in CSF played a role in the pathophysiology of HIE.
     结果提示:HIE时,使AVP异常分泌,血浆和脑脊液中AVP升高,脑脊液中AVP可能参与了HIE的病理生理发病机制;
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     Conclusion: The abnormal release of all five kinds of amino acids are involved in the pathophysiological process of cerebral ischemia. The significanly increased release of inhibitory amino acids promoted by L-NNA during global ischemia may be one of the protective mechanisms of this agent on brain ischemia. 
     结论:半球缺血时所有五种氨基酸的不正常释放都参与了脑缺血病理过程,L-NNA促进半球缺血时抑制性氨基酸的释放可能是其保护缺血大脑的机制之一。
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     NEW RELEASE
     新片推荐
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     The release of Windows.
     Windows.
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     On the abnormal employment
     试论非正规就业——兼谈我国妇女的非正规就业
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     Japanese is Abnormal?
     日本人都是反常的?
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     CLASSIFICATION OF ABNORMAL HIGH PRESSURE AND HYDROCARBON MIGRATION AFTER PRESSURE RELEASE
     异常高压分类及其释压后油气运聚过程
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  abnormal release
We hypothesized that some motor changes of the gut might be secondary to impaired neural input to smooth muscle or abnormal release of gut endocrine peptides.
      
Abnormal release of glutamate, which may trigger auras, and abnormal platelet behaviour, which constitutes a possible predisposing factor to MwA, are possible targets for MwA-specific prophylactic therapy.
      
Abnormal release of glutamate, that may trigger auras, and abnormal platelet behaviour, that constitute a possible predisposing factor to MwA, may be possible targets for MwA specific prophylactic therapy.
      
There is thus no reason to suspect any abnormal release of BB to the blood.
      
In addition, in CF patients, impaired neutrophil functions may contribute to an abnormal release of inflammatory mediators.
      


A2-hr manometry of decending-sigmoid colon was performed in 20 patients with IBS and 9 healthy volunteers. Neostigmine was administered following 1 hour of basal recording to determine the motor response. Plasma levels of gut hormones were investigated simutaneously. At basal state, constipation-predominant IBS(Cp-IBS) showed less frequent contractions in sigmoid colon(SC) and a lower percentage of contractile time(PCT) both in the sigmoid and in the decending colon(DC), whereas in diarrhea predominant type...

A2-hr manometry of decending-sigmoid colon was performed in 20 patients with IBS and 9 healthy volunteers. Neostigmine was administered following 1 hour of basal recording to determine the motor response. Plasma levels of gut hormones were investigated simutaneously. At basal state, constipation-predominant IBS(Cp-IBS) showed less frequent contractions in sigmoid colon(SC) and a lower percentage of contractile time(PCT) both in the sigmoid and in the decending colon(DC), whereas in diarrhea predominant type (Dp-IBS)only the amplitude(AMP) of contractions in DC decreased. The motor index of SC was incrreased in Dp-IBS but decreased in Cp-IBS.Post-neostigmine motor response was different among the three groups. In Cp-IBS, the motor response of SC as well as DC was exaggerated in the initial 30 mins but attenuated in the late 30mins. Cp-IBS had higher basal plasma levels of VIP and NT, and higher SST following neostigmine stunlation. Dp-IBS showed higher basal plasma SP Ievel than that in the controls, and NT level was persistently lower than that in Cp-IBS. Our data suggest that decending-siginoid colonic motility and its response to cholinergic stimulation are altered but is heterogeneous in both types of IBS.Abnormal release of certain gut hormones may be involved in its mechanisms.

对20例肠易激综合征(IBS)和9例健康志愿者的降-乙状结肠动力进行检测,并观察其对胆碱能刺激(新斯的明)的反应),同时测定刺激前后血中胃肠激素水平。结果表明,便秘型的乙状结肠或降结肠收缩频率和时间多降低,尤以降结肠明显,对新斯的明刺激的反应性较低;腹泻型在基础状态下,乙状结肠的收缩频率、持续时间及幅度略高或近似于正常,且动力指数升高。刺激后乙状结肠和降结肠收缩的某些指标增长高峰前移。表明结肠的反应性增高。患者血中SP、VIP、SST和NT的水平与正常有异,可能与动力变化有关。

Abstract In this study, the effects of Monosialoganglioside GM1 and Cholecystokinin antagonist CR 1505 on release of neuropeptide Y(NPY)were observed in vivo and in vitro.Results show that the releases of NPY were significantly increased 1h after cerebral ischemia,then,decreased progressively.However,they were increased again 6h after cerebral ischemia.These results suggest that NPY may be involved in the pathophysiological processes of brain ischemia.GM1 did not influence the releases of NPY during cerebral...

Abstract In this study, the effects of Monosialoganglioside GM1 and Cholecystokinin antagonist CR 1505 on release of neuropeptide Y(NPY)were observed in vivo and in vitro.Results show that the releases of NPY were significantly increased 1h after cerebral ischemia,then,decreased progressively.However,they were increased again 6h after cerebral ischemia.These results suggest that NPY may be involved in the pathophysiological processes of brain ischemia.GM1 did not influence the releases of NPY during cerebral ischemia suggesting that releases of NPY from there synaptsomes were not modulated by GM1.CR1505 was able to significantly inhibit the abnormal release of NPY during cerebral ischemia suggesting a coordinated interaction between NPY and CCK in brain ischemia.The inhibition of NPY release may be one of the protective mechanism of CCK antagonist to ischemic brain.

本研究观察了神经节苷脂GM1和缩胆囊肽(CCK)拮抗剂CR1505对正常和脑缺血时神经肽Y(NPY)体内的体外释放的影响。结果表明,脑缺血1小时后,NPY释放明显增高,其后,逐步减小。而缺血6小时后是到释放再次增高。揭示NPY参与脑缺血的病理生理过程。GM1不影响脑缺血时NPY的释放,表明含NPY的突触释放NPY时不受GM1的调节。CR1505能明显抑制脑缺血时NPY的释放,表明脑缺血时CCK和NPY有协同的相互作用,抑制NPY释放是CCK拮抗剂保护缺血大脑的机制之一。

The pathogenesis of postburn organ damage as well as the effective measures for its prevention and treatment were studied. The present clinical prospective studies and animal experiments revealed or further confirmed that all the main organs could be damaged in the early stage following severe burns. Findings of this serial studies strongly suggested that the uncontrollable "mediator disease" resuIted from ischemic-reperfusion damage, swelling and edema of visceraI tissues, the endothelial cell damage and...

The pathogenesis of postburn organ damage as well as the effective measures for its prevention and treatment were studied. The present clinical prospective studies and animal experiments revealed or further confirmed that all the main organs could be damaged in the early stage following severe burns. Findings of this serial studies strongly suggested that the uncontrollable "mediator disease" resuIted from ischemic-reperfusion damage, swelling and edema of visceraI tissues, the endothelial cell damage and abnormal release mediators might be of importance in the pathogenesis of early PB organ damage。 Fast fluid infusion for delayed resuscitation, the use of the mediator antagonixtxanisodamine and gensinosides or escharectomy by one operation are effective in the prevention and treatment of organ damage in the early stage of severe burns。

通过系列的临床前瞻性研究与动物实验,发现并从多方面进一步证实了严重烧伤早期各主要脏器均可发生损害;缺血和再灌流损伤、脏器水肿、内皮细胞损伤及多种炎症介质的异常释放,导致难以控制的介质病,是脏器损害的重要因素;延迟复苏快速补液和使用介质拮抗剂山莨菪碱及人参皂甙或一次性切痂是防治严重烧伤早期脏器损害的有效方法。

 
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