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1.
Type 1 diabetes can lead to several well-described complications such as retinopathy, nephropathy and peripheral neuropathy. Evidence is accumulating that it is also associated with gradually developing end-organ damage in the central nervous system. This relatively unknown complication can be referred to as ‘diabetic encephalopathy’ and is characterised by electrophysiological and neuroradiological changes, such as delayed latencies of evoked potentials, modest cerebral atrophy and (periventricular) white matter lesions. Furthermore, individuals with type 1 diabetes may show performance deficits in a wide range of cognitive domains. The exact mechanisms underlying this diabetic encephalopathy are only partially known. Chronic metabolic and vascular changes appear to play an important role. Interestingly, the differences in the ‘cognitive profile’ between type 1 and type 2 diabetes also suggest a critical role for disturbances of insulin action in the central nervous system.  相似文献
2.
T细胞介导的1型糖尿病小鼠模型的建立及机制研究   总被引:3,自引:0,他引:3  
邹晓蕾  曹瑜  袁思佑  向明 《中国药师》2006,9(10):883-886
目的:建立T细胞介导的1型糖尿病(IDDM)小鼠模型。方法:BALB/c小鼠小剂量连续多次ip链脲佐菌素(STZ)制备1型糖尿病模型,4周后处死取脾制备脾细胞悬液建立T淋巴细胞系,并将不同数量T淋巴细胞过继转移到经不同方式预处理的BALB/c小鼠体内。符合高血糖诊断标准后处死动物,观察胰腺病理变化,检测脾淋巴细胞增殖反应。结果:2次ip小剂量STZ联合3×106T细胞过继转移,或采用2次ip环磷酰胺联合2次ip STZ和1.5×106T细胞过继转移,均可建立1型糖尿病动物模型。血糖分别于T细胞过继转移后第20和第13天显著升高(P<0.05),脾淋巴细胞增殖能力明显增强(P< 0.05),胰腺见大量淋巴细胞浸润和严重胰岛β细胞破坏。结论:BALB/c小鼠一次性过继转移IDDM发病T淋巴细胞可成功复制1型糖尿病模型。  相似文献
3.
1型糖尿病患者外周血白细胞端粒长度的变化及其意义   总被引:2,自引:0,他引:2  
目的 探讨1型糖尿病(T1DM)患者外周血白细胞端粒长度的变化及意义.方法 T1DM患者(T1DM组)20例,健康对照组20例,提取外周血白细胞DNA,纯度检测合格后用地高辛标记的探针行Southern杂交,经图像分析系统扫描和软件分析后测得端粒长度.结果 T1DM组外周血白细胞端粒长度较对照组明显缩短(P< 0.01).结论 T1DM患者外周血白细胞端粒长度的缩短可能与自身免疫密切相关,提示端粒可能在T1DM的发病中起重要作用.  相似文献
4.
5.
Acetaminophen normalizes glucose homeostasis in mouse models for diabetes   总被引:1,自引:0,他引:1  
Loss of pancreatic beta cell insulin secretion is the most important element in the progression of type 1 and type 2 diabetes. Since oxidative stress is involved in the progressive loss of beta cell function, we evaluated the potential for the over-the-counter analgesic drug and antioxidant, acetaminophen (APAP), to intervene in the diabetogenic process. We used mouse models for type 1 diabetes (streptozotocin) and type 2 diabetes (high-fat diet) to examine the ability of APAP to intervene in the progression of diabetes. In C57BL/6J mice, streptozotocin caused a dosage dependent increase in fasting blood glucose (FBG), from 100 to >600mg/dl. Daily APAP (20mg/kg BW, gastric gavage), significantly prevented and partially reversed the increase in FBG levels produced by streptozotocin. After 10 weeks on a high-fat diet, mice developed fasting hyperinsulemia and impaired glucose tolerance compared to animals fed a control diet. APAP largely prevented these changes in insulin and glucose tolerance. Furthermore, APAP prevented most of the increase in body fat in mice fed the high-fat diet. One protective mechanism for APAP is suggested by studies using isolated liver mitochondria, where low micromolar concentrations abolished the production of reactive oxygen that might otherwise contribute to the destruction of pancreatic beta-cells. These findings suggest that administration of APAP to mice, in a dosage used safely by humans, reduces the production of mitochondrial reactive oxygen and concomitantly prevents the development of type 1 and type 2 diabetes in established animal models.  相似文献
6.
Individuals with type 1 diabetes show mild performance deficits in a range of neuropsychological tests compared to healthy controls, but the mechanisms underlying this cognitive deterioration are still poorly understood. Basically, two diabetes-related mechanisms can be postulated: recurrent severe hypoglycaemia and/or chronic hyperglycaemia. Intensive insulin therapy in type 1 diabetes, resulting in a durable improvement of glycaemic control, has been shown to lower the risk of long-term microvascular and macrovascular complications. The down side of striving for strict glycaemic control is the considerably elevated risk of severe hypoglycaemia, sometimes leading to seizure or coma. While retrospective studies in adult patients with type 1 diabetes have suggested an association between a history of recurrent severe hypoglycaemia and a modest or even severe degree of cognitive impairment, large prospective studies have failed to confirm this association. Only fairly recently, better appreciation of the possible deleterious effects of chronic hyperglycaemia on brain function and structure is emerging. In addition, it can be hypothesized that hyperglycaemia associated microvascular changes in the brain are responsible for the cognitive decline in patients with type 1 diabetes. This review presents various pathophysiological considerations concerning the cognitive decline in patients with type 1 diabetes.  相似文献
7.
目的:探讨人工虫草(蝙蝠蛾拟青霉人工发酵菌丝培养物,PHC)对小鼠1型糖尿病的降糖作用及机制。方法:采用少量多次腹腔注射STZ的方法建立1型糖尿病模型,观察药物对胰腺组织、血糖、肝脏SOD、LPO含量、血清IL-2和IL-10分泌以及小鼠脾T淋巴细胞增殖的影响。结果:低剂量PHC能明显降低糖尿病高血糖,升高血清SOD活力,降低LPO含量,且明显降低IL-2水平,抑制脾T淋巴细胞增殖反应。结论:低剂量PHC对STZ所致小鼠1型糖尿病有明显降糖作用,降糖机制与抑制T细胞应答或细胞因子对胰岛β细胞的破坏,以及清除自由基有关。  相似文献
8.
目的:观察骨疏康对1型糖尿病骨质疏松大鼠体外培养破骨细胞的影响。方法:雌性Wistar大鼠60只,2.5~3月龄,按照体重随机分为正常组(n=24)和1型糖尿病组(n=36)两大组,正常组又分为正常对照组(n=8)、正常假手术组(n=8)和正常双侧卵巢切除组(n=8);1型糖尿病组又分为糖尿病对照组(n=12)、糖尿病假手术组(n=12)和糖尿病双侧卵巢切除组(n=12)。单剂量腹腔注射链脲菌素(柠檬酸钠缓冲液制成2%溶液) 60 mg·kg-1制备1型糖尿病大鼠模型;无菌条件下切除大鼠双侧卵巢制备骨质疏松模型。在造模后第0,2,4,8周末时用sRANKL和巨噬细胞集落刺激因子(M-CSF)诱导大鼠骨髓进行体外破骨细胞培养,并观察骨疏康(20μg·mL-1)的影响。结果:糖尿病对照组破骨细胞明显高于对照组(P<0.01),糖尿病双侧卵巢切除组破骨细胞明显高于对照组(P<0.01),糖尿病骨质疏松组破骨细胞明显高于糖尿病对照组和正常双侧卵巢切除组(P<0.01)。经20μg·mL-1骨疏康干预后,各组破骨细胞数均明显减少(P<0.01)。结论:骨疏康明显抑制1型糖尿病骨质疏松大鼠体外培养的破骨细胞生成。  相似文献
9.
1型糖尿病患者T细胞亚群和共刺激分子的表达及其意义   总被引:1,自引:0,他引:1  
目的:动态观察1型糖尿病患外周血T淋巴细胞亚群及CD28、CD80等共刺激分子的表达,探讨其在1型糖尿病发病中的作用。方法:应用免疫荧光标记技术和流式细胞仪,检测17例正常对照组及37例1型糖尿病患外周血T细胞亚群、CD28、CD80、人类白细胞抗原(HLA-DR)分子的表达,并进行随访。结果:(1)1型糖尿病组外周血CD4^ 、CD4^ CD28^ T细胞的百分率增加,CD8^ 、CD8^ CD28^ T细胞显降低,CD28、CD80、HLA-DR的表达也增加,与正常组比,差异均有显性。(2)经胰岛素治疗6个月后随访,T细胞亚群的失衡、共刺激分子的异常表达得到不同程度的改善,但CD4^ CD28^ 、CD8^ CD28^ T细胞、HLA-DR表达仍未恢复正常。结论:共刺激分子CD28、CD80及HLA-DR的异常表达、T细胞亚群的异常激活、增殖在1型糖尿病的发生、发展中起着重要的作用,监测其变化,为临床上免疫调节治疗,提供了理论依据。  相似文献
10.
口服干扰素-α延缓NOD小鼠1型糖尿病发生   总被引:1,自引:0,他引:1  
目的 研究干扰素 (IFN) -α对 NOD小鼠 1型糖尿病的预防作用。方法  6周龄 NOD雌鼠 1周 3次灌胃 IFN-α 10 0 U ,共 32周 ,观测胰岛炎和糖尿病发病。结果  IFN-α能明显降低 NOD小鼠糖尿病的发生和胰岛炎的严重程度。结论 口服 IFN-α能预防 NOD鼠糖尿病  相似文献
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