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71.
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失血性休克大鼠PKCα mRNA表达变化规律及对血管低反应性的调节作用 总被引:2,自引:0,他引:2
目的 观察PKCot在大鼠失血性休克血管平滑肌中mRNA表达变化规律,及其对失血性休克血管反应性和钙敏感性的调控作用.方法 采用PCR技术测定大鼠肠系膜上动脉不同休克时间点(休克即时、30 min、1 h、2 h、4 h)的PKCct mRNA表达;用离体血管环张力测定技术观察不同休克时间点的肠系膜上动脉一级分支的血管环反应性和钙敏感性变化,以及PKCa激动剂和抑制剂对休克2 h血管反应性、钙敏感性的影响.结果 ①失血性休克后大鼠血管反应性和钙敏感性早期增高、晚期降低,PKCot mRNA表达逐渐增高,于1 h达到峰值(P<0.01),4 h时仍处于较高水平(P<0.01).②PKCa激动剂和抑制剂可分别增高和降低休克2 h大鼠的血管反应性和钙敏感性.结论 PKCct在失血性休克血管反应性和钙敏感性调控中起重要作用,可能是休克血管功能的重要保护性分子. 相似文献
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近年来,多种肿瘤生物治疗方法已进行了较为系统的基础研究和临床应用,我们2005—01/2006—06应用香菇多糖联合化疗药物治疗40例癌性腹水病人,取得了较好的近期疗效,现总结报告如下。 相似文献
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腹部开发性刺伤后外口常有鲜血流出或大网膜及内脏从外口露出 ,病人比较紧张 ,立即就诊 ,临床医生采取一些临床检查和辅助检查 ,仍难以判断脏器伤情 ,尤其是具体脏器及损伤程度。采取何种治疗措施是临床急需解决的问题。本文总结 1989年 1月至 1999年2月我院收治的 2 8例腹部开放性刺伤病人 ,诊治情况如下。1 临床资料1·1 一般资料 全部 2 8例病人 ,男性 2 0例 ,女性 8例。年龄 16至 5 8岁 ,平均 2 9 5岁。伤后大网膜及肠管外露 12例 ,胃肠液外溢 3例 ,并失血性休克 4例。急诊剖腹后无内脏伤 3例 ,肠管伤 7例 ,肝损伤 1例 ,肠系膜伤 2例… 相似文献
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莲子心为睡莲科莲属植物莲Nelumbo nucifera Gaertn种子的幼叶及胚根收载于2000年版《中华人民共和国药典》Ⅰ部。莲子心味苦性寒,具有清心去热、固肾涩精的功效,用于心烦,目赤肿痛,遗精等症的治疗。临床报道其清心火、平肝火、泻胃火、降肺火,可治疗老年人心烦失眠、青年人心火亢盛的高血压。 相似文献
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Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats. 相似文献
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为解决泉州市三资石雕职业危害因素及其对工人健康影响,保障工人的身体健康,促进生产发展。根据泉州市卫生局、经委、建委颁发泉卫防(1992)字第026号文件《关于对市属三资企业石材加工,制鞋业职业危害调查的通知》要求,我站对三家市直三资石雕厂进行较全面的劳动卫生学调查,并作卫生学评价,现将调查结果报告如下:一、对象与方法 相似文献
80.
Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats. 相似文献