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BALTIMORE, MD -- December 15, 2006 -- A drug commonly used to slow the loss of central ision has shown promise in stemming a common precursor of blindness in diabetics, which inoles the same central light-sensitie area of retina, Johns Hopkins Wilmer Eye Institute scientists report.

马里兰州,巴尔地摩,2006年12月15日讯据约翰霍普金斯Wilmer眼科研究所的科学家报道,一种目前被广泛用来延缓中心视觉丧失的药物有希望用来防治导致糖尿病患者致盲的视网膜早期病变,该病变也发生在视网膜中心的光敏区。

objectiveto study the effects of alcoholic extracts of averrhoa carambola l. root on blood glucose level and lipid peroxidation in stz-induced diabetic mice.methodsdiabetic model were induced by once intraperitoneal injection of stz.

目的研究阳桃根醇提物对链脲佐菌素(streptozocin, stz)致糖尿病模型小鼠的血糖及抗脂质过氧化反应的影响。

Full protection was achieved when protective cells were transferred 3-4 days before diabetogenic cells, whereas transfer 2 days before conferred only partial protection.

注射致糖尿病细胞前3-4天给大鼠给予保护性细胞能得到完全性的保护,而提前2天则只能获得部分性的保护。

Full protection was achieed when protectie cells were transferred 3-4 days before diabetogenic cells, whereas transfer 2 days before conferred only partial protection.

注射致糖尿病细胞前3-4天给大鼠给予保护性细胞能得到完全性的保护,而提前2天则只能获得部分性的保护。

Objective To construct retrovirus vectors carrying IL17 or siRNAIL17 genes with Thy1.1 gene and determine the infected ability of the retrovirus vectors to diabetogenic BDC2.5 T cells.

目的 构建含有Thy1.1细胞表面抗原(Thy1.1 cell surface antigen,Thy1.1)基因的携带IL17或siRNAIL17基因的逆转录病毒载体,并观察逆转录病毒对致糖尿病性BDC2.5 T细胞的转染能力。

Methods The IL17 cDNA and Thy1.1 fulllength cDNA were subcloned into MIT(MSCVIRESThy1.1) retrovirus vector, and the siRNAIL17, U6 promoter and Thy1.1 fulllength cDNA were also inserted into retrovirus vector of pMNDBANSHEE.The recombined vectors were transfected 293 packaging cells by DNA calcium phosphate coprecipitation. Virus supernatant which infected preactivated spleen cells from NOD/BDC mice was collected. After incubation, the IL17 expression in diabetogenic T cells was detected.

利用基因工程和细胞克隆技术分别将IL17的cDNA插入MSCVIRESThy1.1逆转录病毒载体,将Thy1.1、U6增强子(U6 promoter)基因和IL17的siRNA cDNA插入逆转录病毒载体pMNDBANSHEE,采用磷酸钙沉淀法将重组载体转染293包装细胞;收集病毒上清,转染预先活化的NOD/BDC小鼠脾细胞,测定致糖尿病性T细胞的IL17和siRNAIL17的表达。

The animal test results showed that Gymnemic acid could significantly decreased blood glucose level of the diabetic mice induced by alloxan by Gymnemic acid 100 mg/kg weight everyday.

通过动物实验,得出每日灌喂100mg/kg体重的匙羹藤酸提取物对于降低四氧嘧啶致糖尿病模型小鼠血糖具有显著性。

The results showed an increased mean jitter value, fiber density and abnormal percentage both in EDC and AT muscles in group 1 and II diabetic patients comparing to the normal controls. These findings suggest an impaired or immatured neuromuscular junctions and an evidence of reinnervation through axonal sprouting in the diabetic patients either with or without nerve conduction abnormalities. In conclusion, the changes of axonal degeneration and reinnervation are the main pathophysiological mechanism of diabetic neuropathy, and the SFEMG is more sensitive than routine nerve conduction study in the diagnosis of diabetic neuropathyKeyword Axonal degeneration , diabetes mellitus , neuropathy , single fiber electromyography

结果显示两组糖尿病病患的连续间值差异,肌纤维密度及不正常比率比对照组显著增加(t试验,依序p.01),在第一组糖尿病患中,伸指总肌的连续波间值差异比第二组高(p.05),而连续波间值差异与纤维密度之间也成线性相关的增加(伸指总肌,r=0.471,p.01;胫前肌,r=0.386,p.02),在伸指总肌测得的连续波间值差异上,第一组糖尿病患有75%不正常,第二组有33.3%不正常,而在胫前肌的连续波间值差异上,第一组糖尿病患有83.3%的不正常,第二组有75%不正常,在肌纤维密度的测定中,第一组糖尿病患的伸指总肌有27.8%不正常,胫前肌有58.3%不正常,第二组病患的伸指总肌有25%不正常,胫前肌有41.7%不正常,此结果表示糖尿病神经变造成的神经肌像交接处不稳定及有神经轴再生的重分布现象,因此也证实糖尿病神经病变的主要病理机转为神经的退化所致,而在诊断上单纤维肌电图检查的敏感度也比运动神经传导速度检查为高。

The blood glucose levels in many strain animal models were determined after oral administration, with the models of diabetes induced by alloxan, of hyperglycemic mice induced by epinephrine and glucose, and normal mice.

采用四氧嘧啶所致糖尿病模型、肾上腺素和葡萄糖引起的高血糖小鼠模型,以及正常小鼠口服给药,测定各模型小鼠的血糖水平;并对GXTF进行了急性毒性试验。

Both diabectic angiopathy and lipid soakage are presented in group DMCH.Conclusion It was confirmed that there was rather high rate of cholecysts stone forming in the rabbits with DM led by Alloxan,that the bile acid,phospholipid reduced and cholesterol increased in the

证实四氧嘧啶致糖尿病大耳白兔胆囊结石形成率甚高,胆囊胆汁酸分泌减少、磷脂减少和胆固醇增加形成成石胆汁,以及形成胆囊微血管病变是胆石形成的重要因素,为深入研究提供了有用的工具。

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