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1.
Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other. 相似文献
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低血钾致单纯性ST段下垂型下移1例 总被引:3,自引:0,他引:3
何晓明 《临床心血管病杂志》2003,19(2):119-120
患者 ,女 ,5 1岁。因间歇性肢体麻木 3周 ,伴胸闷憋气加重 1天来院就诊。既往有高血压病史 1年 ,近半年口服吲达帕胺片 (商品名 :寿比山 ) 2 .5mgqd。体检 :血压 110 /70mmHg (1mmHg =0 .133kPa) ,心率 70次 /min ,律齐 ,无病理性杂音。实验室检查 :血K+2 .77mmol/L ,Na+134.1mmol/L ,Cl-94 .8mmol/L。临床诊断 :低钾血症。心电图 (图1A)示 :窦性心律 ,心率 73次 /min ,P R间期 0 .16sSTⅡ ,Ⅲ ,aVF ,V3,V5,V6 下垂型下移 >0 .10mV ,STV4 下移 0 .15mV ,TⅡ ,aVF ,V2~ 6… 相似文献
4.
Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other. 相似文献
5.
目的:研究乙酰葛根素对于大鼠局灶性脑缺血再灌注损伤的脑组织与血清NO和iNOS的影响。方法:使用MCAO(大脑中动脉内拴线阻断法)测定大鼠局灶性缺血再灌注损伤模型,并观察脑组织与血清NO、血清iNOS的水平变化。结果:在小鼠脑缺血1h,再灌注24 h后,其血清NO以及iNOS水平上升显著;再灌注48h后,给予250、50、10 mg.kg~(-1)的乙酰葛根素以及葛根素组的小鼠血清NO、iNOS含量呈现出明显下降的趋势,P0.05,差异具有统计学意义。结论:将乙酰葛根素应用于治疗大鼠局灶性脑缺血再灌注损伤的过程中,能通过降低NO毒性起到保护脑组织的作用,从而减轻脑缺血再灌注损伤症状。 相似文献
6.
目的:评价阴道镜直视下活检诊断CINII的准确性,分析影响漏诊CINII以上病变(简称CINII~+)的相关因素,并探讨P16~(INK4a)蛋白表达在预测漏诊CINII~+中的价值。方法:回顾分析2013年12月至2015年7月在南京医科大学第一附属医院宫颈病中心阴道镜直视下宫颈活检诊断为CINII,且在短期内行LEEP的148例患者。研究患者手术前后病理诊断,同时对患者年龄、初次TCT结果、高危型HPV负荷量、阴道镜下病变累及宫颈象限数、转化区类型、阴道镜图像表现以及CINII组织中P16~(INK4a)蛋白表达等与漏诊CINII~+的关系进行单因素及多因素分析。结果:(1)阴道镜直视下活检诊断的148例CINII中,71例(49.97%)漏诊CINII~+,其中1例宫颈鳞癌IA1期,1例宫颈鳞癌IB1期。单因素分析显示,患者年龄、初次TCT结果、高危型HPV负荷量、阴道镜下病变累及象限数、转化区类型、阴道镜图像特征与CINII~+病变漏诊无明显相关性(P0.05),CINII组织中P16~(INK4a)蛋白表达与CINII~+病变漏诊明显相关(P0.05)。多因素分析显示,P16~(INK4a)蛋白阳性表达是影响阴道镜直视下活检诊断CINII漏诊CINII~+的危险因素(OR=9.846,95%CI为2.165~44.787;P=0.003)。(2)21例(14.19%)P16~(INK4a)蛋白呈阴性表达,127例(85.81%)呈阳性表达。P16~(INK4a)蛋白表达阴性组中漏诊CINII~+3例(14.29%),P16~(INK4a)蛋白表达阳性组中漏诊CINII~+68例(53.54%),两组比较差异有统计学意义(P0.05)。P16~(INK4a)阳性表达预测漏诊CINII~+的敏感性95.77%,特异性为23.38%,阴性预测值为85.71%,阳性预测值为53.54%。结论:阴道镜直视下活检诊断的CINII中存在CINII~+的漏诊,而CINII并P16~(INK4a)蛋白阳性表达是影响CINII~+漏诊的危险因素,对P16~(INK4a)蛋白表达阳性的CINII患者的临床干预存在其合理性。针对CINII的个体化管理,需综合考虑患者的年龄、P16~(INK4a)蛋白表达、对生育功能保护的需求及随访的依从性。 相似文献
7.
患者 ,男 ,4 7岁 ,因持续发热、咽痛、一过性皮疹、四肢大关节疼痛 30天于 1998年 5月 2 8日入院。患者30天前出现发热 (T37.8~ 38.5℃ )、咽痛、头痛、全身疲乏不适 ,自服安必仙胶囊、克感敏 3天 ,无效 ,且咽痛更甚。又静滴青霉素钠 80 0万U2天 ,咽痛减轻 ,但发热不退 ,且出现四肢大关节肿痛、麻木。继续静滴青霉素钠 4天 ,咽痛、关节痛仍反复发作 ,体温呈弛张热(T38~ 4 0℃ ) ,且关节肿痛随体温升高而加剧。发病第 9天 ,双腕、双膝、双髋关节周围皮肤出现环形红斑样皮疹 (如红墨水涂抹 ) ,持续 2天 ,皮疹逐渐消退 ,但发热、咽痛、关节… 相似文献
8.
目的:探讨使用Trivex静脉旋切系统行深筋膜下小腿交通支静脉旋切治疗下肢静脉性溃疡的可行性和临床疗效。方法:本组24例(28条肢体)下肢静脉性溃疡患者常规行大小隐静脉高位结扎后激光或射频腔内闭合浅静脉主干,使用Trivex静脉旋切系统行深筋膜下小腿交通支静脉旋切和浅筋膜下曲张静脉旋切。结果:术后全组患者症状均有明显改善,溃疡均在8~28d基本愈合(平均14.5d)。结论:Trivex静脉旋切系统治疗下肢静脉性溃疡创伤小,结合激光和射频治疗闭合浅静脉主干,疗效确切,值得推广: 相似文献
9.
Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other. 相似文献
10.
目的 观察分析青霉素钠治疗急性痛风性关节炎的疗效和机理。方法 报道39例确诊的急性痛风性关节炎的青霉素钠治疗。结果 显效12例,有效率19例,无效8例,总有效率79.5%。结论 青霉素钠是治疗急性痛风性关节炎的有效药物。其药理作用与青霉素的代谢产物抑制了炎症介质的产生和释放有关。 相似文献