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1.
The abdominal visceral fat content in obese SD rats induced by high fat diet for 10 weeks was significantly higher than that in control group [(26±6 vs 13±3)g,P<0.01] ,along with increased CRP mRNA expression in abdominal visceral fat (0.901±0.085 vs O. 402±0.036, P<0.01). As compared with normal control group, in the high fat group the concentrations of CRP in portal vein [(743.8±95.8 vs 558.3 ±118.3) mg/L, P<0.01] and peripheral vein[(596.3±38.9 vs 485.8±30.2) mg/L,P<0. 05] were higher. The concentration of CRP in portal vein was significantly higher than that in peripheral vein in high fat diet group(P<0.01) ,but this was not evident in control group. These results suggest that the increased CRP expression in visceral adipose tissue may partially account for the elevation of serum CRP in obesity.  相似文献   
2.
The abdominal visceral fat content in obese SD rats induced by high fat diet for 10 weeks was significantly higher than that in control group [(26±6 vs 13±3)g,P<0.01] ,along with increased CRP mRNA expression in abdominal visceral fat (0.901±0.085 vs O. 402±0.036, P<0.01). As compared with normal control group, in the high fat group the concentrations of CRP in portal vein [(743.8±95.8 vs 558.3 ±118.3) mg/L, P<0.01] and peripheral vein[(596.3±38.9 vs 485.8±30.2) mg/L,P<0. 05] were higher. The concentration of CRP in portal vein was significantly higher than that in peripheral vein in high fat diet group(P<0.01) ,but this was not evident in control group. These results suggest that the increased CRP expression in visceral adipose tissue may partially account for the elevation of serum CRP in obesity.  相似文献   
3.
The abdominal visceral fat content in obese SD rats induced by high fat diet for 10 weeks was significantly higher than that in control group [(26±6 vs 13±3)g,P<0.01] ,along with increased CRP mRNA expression in abdominal visceral fat (0.901±0.085 vs O. 402±0.036, P<0.01). As compared with normal control group, in the high fat group the concentrations of CRP in portal vein [(743.8±95.8 vs 558.3 ±118.3) mg/L, P<0.01] and peripheral vein[(596.3±38.9 vs 485.8±30.2) mg/L,P<0. 05] were higher. The concentration of CRP in portal vein was significantly higher than that in peripheral vein in high fat diet group(P<0.01) ,but this was not evident in control group. These results suggest that the increased CRP expression in visceral adipose tissue may partially account for the elevation of serum CRP in obesity.  相似文献   
4.
The abdominal visceral fat content in obese SD rats induced by high fat diet for 10 weeks was significantly higher than that in control group [(26±6 vs 13±3)g,P<0.01] ,along with increased CRP mRNA expression in abdominal visceral fat (0.901±0.085 vs O. 402±0.036, P<0.01). As compared with normal control group, in the high fat group the concentrations of CRP in portal vein [(743.8±95.8 vs 558.3 ±118.3) mg/L, P<0.01] and peripheral vein[(596.3±38.9 vs 485.8±30.2) mg/L,P<0. 05] were higher. The concentration of CRP in portal vein was significantly higher than that in peripheral vein in high fat diet group(P<0.01) ,but this was not evident in control group. These results suggest that the increased CRP expression in visceral adipose tissue may partially account for the elevation of serum CRP in obesity.  相似文献   
5.
Graves病(GD)是器官特异性自身免疫性甲状腺疾病,其主要发病机制是机体失去了对促甲状腺激素受体(TSHR)的免疫耐受,从而产生TSHR自身抗体。GD的确切发病机制还不完全清楚,但已明确遗传因素在GD发病中起重要作用。由于TSHR是GD发病的主要抗原,因此其基因可能是GD的易感基因,但目前该基因是否与GD的发病相关还存在争议。  相似文献   
6.
α-硫辛酸联合甲钴胺口服治疗糖尿病周围神经病变   总被引:1,自引:0,他引:1  
目的探讨α-硫辛酸联合甲钴胺治疗糖尿病周围神经病变(DPN)的临床疗效及安全性。方法选择DPN患者64例,采取分层随机、开放、对照的研究方法将患者分为试验组32例、对照组32例。患者常规给予饮食控制、胰岛素或口服降糖药将血糖控制在良好范围,维持原降压、调脂等综合治疗,对照组同时给予甲钴胺0.5mg、每日3次口服,试验组同时给予α-硫辛酸600mg、每日1次联合甲钴胺0.5mg、每日3次口服,疗程均为12周。分别在治疗前后记录两组患者的总症状评分(TSS)和神经传导速度(NCV),并观察有无药物不良反应。结果治疗后两组患者TSS评分和NCV均较治疗前有改善(P<0.05)。治疗后试验组的TSS评分低于对照组(P<0.05),治疗后试验组的正中神经运动传导速度、腓总神经运动和感觉传导速度与对照组比较差异有统计学意义(P<0.05)。治疗过程中两组均未见明显的药物不良反应。结论α-硫辛酸联合甲钴胺口服治疗DPN疗效优于单用甲钴胺,而且安全简便,依从性好,值得推广。  相似文献   
7.
目的研究胰腺星形细胞(PSCs)是否表达糖化终末产物受体(RAGE),并探讨糖化终末产物(AGEs)对RAGE表达的调节作用。方法分离培养SD大鼠PSCs,采用半定量逆转录聚合酶链反应(RT-PCR)和免疫细胞化学检测静息和活化的PSCs RAGE在mRNA和蛋白水平的表达,同时用RT-PCR检测AGEs刺激后RAGE表达的变化。结果静息和活化的PSCs均表达RAGE,且活化后表达水平提高;AGEs能上调RAGE的表达。结论静息和活化的PSCs均表达RAGE,活化的PSCs RAGE表达上调,提示PSCs是AGEs作用的靶细胞。  相似文献   
8.
目的构建pcDNA3.1/人TSH受体(human thyroid-stimulating hormone receptor,hTSHR)基因真核表达载体(已完成),将该真核表达载体在CHO细胞(中国仓鼠卵巢细胞)中表达,并筛选获得稳定表达细胞株。方法通过脂质体介导,用重组质粒pcDNA3.1-hTSHR转染CHO细胞,以G 418筛选稳定表达细胞株,挑取单克隆,扩大培养并传代;取P5代细胞,抽提基因组DNA及蛋白分别用PCR及Western blot方法鉴定被转染CHO细胞hTSHR的表达情况。结果得到阳性单克隆5个,传代培养。P5代细胞PCR扩增产物为约530 bp特异性条带,大小与预期相符,未见非特异性条带。Western印记法结果表明被转染CHO传代细胞有hTSHR蛋白表达。结论pcDNA3.1-hTSHR真核表达载体可以在CHO细胞中稳定表达,成功构建稳定表达细胞株。为测定自身免疫性甲状腺疾病患者血清TSHR奠定了基础。  相似文献   
9.
高脂喂养大鼠内脏脂肪组织C反应蛋白的表达   总被引:1,自引:1,他引:0  
高脂饲料喂养10周的SD肥胖大鼠腹部内脏脂肪含量明显高于对照组[(26±6 vs 13±3)g,P<0.01],高脂组大鼠腹部内脏脂肪中C反应蛋白(CRP)mRNA水平较对照组高(0.901±0.085 vs 0.402+0.036,P<0.01),高脂组门静脉[(743.8±95.8 vs 558.3±118.3)ms/L,P<0.01]和外周静脉血清CRP浓度[(596.3±38.9 vs 485.8±30.2)mg/L,P<0.05]均高于对照组.高脂组门静脉血清CRP浓度显著高于外周静脉(P<0.01),但对照组差异无统计学意义.提示腹部内脏脂肪产生的CRP可能是肥胖者循环CRP的重要来源之一.  相似文献   
10.
目的研究体外模拟低氧对小鼠3T3-L1脂肪细胞脂连蛋白(ADPN)表达的影响。方法体外培养小鼠3T3-L1前脂肪细胞,将其诱导分化成为成熟的脂肪细胞,油红O染色鉴定脂肪细胞分化程度和脂质积聚情况。氯化钴(CoCl2)化学模拟脂肪细胞低氧环境,采用实时PCR(Real-TimePCR)检测低氧诱导因子-1α(HIF-1α)和ADPNmRNA的表达,蛋白质印迹法(Westernblotting)检测低氧诱导因子-1α(HIF-1α)的蛋白表达;酶联免疫吸附测定(ELISA)分析细胞培养上清液中ADPN蛋白的分泌水平。结果在CoCl,诱导3T3-L1脂肪细胞低氧的条件下,细胞内HIF-1αmRNA和蛋白的表达水平均显著上调;细胞内ADPNmRNA表达和细胞培养上清液中ADPN蛋白的分泌水平均显著下降;HIF-1αmRNA与ADPNmRNA的表达水平呈显著负相关(r=-0.854,P〈0.001)。结论CoCl2诱导低氧能够下调3T3-L1脂肪细胞ADPN的表达,该作用可能与脂肪细胞代谢功能障碍和胰岛素抵抗有关。  相似文献   
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