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991.
Gang CHEN Shi-qi PAN Cong SHEN Shi-fen PAN Xiu-min ZHANG Qi-yang HE 《Acta pharmacologica Sinica》2014,35(4):463-475
Aim: To investigate the effects of puerarin (Pue), an isoflavone derived from Kudzu roots, on angiotensin II (Ang II)-induced hypertrophy of cardiomyocytes in vivo and in vitro.
Methods: C57BL/6J mice were infused with Ang II and treated with Pue (100 mg·kg-1·d-1, po) for 15 d. After the treatment, systolic blood pressure (SBP) and left ventricular wall thickness were assessed. The ratios of heart weight to body weight (HW/BW) and left ventricular weight to body weight (LVW/BW) were determined, and heart morphometry was assessed. Expression of fetal-type genes (ANP, BNP and β-MHC) in left ventricles was measured using semi-quantitative RT-PCR. Mouse primary cardiomyocytes were treated with Pue (50, 100, 200 μmol/L), then exposed to Ang II (1 μmol/L). ROS level was examined with flow cytometry, the binding activity of NF-κB was determined using EMSA. Western blot was used to measure the levels of ERK1/2, p38 and NF-κB pathway proteins. [3H]leucine incorporation was used to measure the rate of protein synthesis.
Results: Oral administration of Pue significantly suppressed Ang II-induced increases in the myocyte surface area, HW/BW, LVW/BW, SBP and left ventricular wall thickness. Furthermore, Pue significantly suppressed Ang II-induced increases in ANP, BNP and β-MHC expression in the left ventricles in vivo. Treatment of cardiomyocytes with Pue (50–500 μmol/L) did not affect the viability of cardiomyocytes in vitro. Pretreatment of cardiomyocytes with Pue dose-dependently inhibited Ang II-induced increases in ROS production, NF-κB binding activity, protein synthesis and cell breadth. Furthermore, pretreatment with Pue significantly suppressed Ang II-induced activation of ERK1/2, p38 and the NF-κB pathway proteins and the expression of ANP and β-MHC in cardiomyocytes. The positive drug valsartan exerted similar effects on Ang II-induced cardiac hypertrophy in vivo and in vitro.
Conclusion: Pue attenuates Ang II-induced cardiac hypertrophy by inhibiting activation of the redox-sensitive ERK1/2, p38 and the NF-κB pathways. 相似文献
Methods: C57BL/6J mice were infused with Ang II and treated with Pue (100 mg·kg-1·d-1, po) for 15 d. After the treatment, systolic blood pressure (SBP) and left ventricular wall thickness were assessed. The ratios of heart weight to body weight (HW/BW) and left ventricular weight to body weight (LVW/BW) were determined, and heart morphometry was assessed. Expression of fetal-type genes (ANP, BNP and β-MHC) in left ventricles was measured using semi-quantitative RT-PCR. Mouse primary cardiomyocytes were treated with Pue (50, 100, 200 μmol/L), then exposed to Ang II (1 μmol/L). ROS level was examined with flow cytometry, the binding activity of NF-κB was determined using EMSA. Western blot was used to measure the levels of ERK1/2, p38 and NF-κB pathway proteins. [3H]leucine incorporation was used to measure the rate of protein synthesis.
Results: Oral administration of Pue significantly suppressed Ang II-induced increases in the myocyte surface area, HW/BW, LVW/BW, SBP and left ventricular wall thickness. Furthermore, Pue significantly suppressed Ang II-induced increases in ANP, BNP and β-MHC expression in the left ventricles in vivo. Treatment of cardiomyocytes with Pue (50–500 μmol/L) did not affect the viability of cardiomyocytes in vitro. Pretreatment of cardiomyocytes with Pue dose-dependently inhibited Ang II-induced increases in ROS production, NF-κB binding activity, protein synthesis and cell breadth. Furthermore, pretreatment with Pue significantly suppressed Ang II-induced activation of ERK1/2, p38 and the NF-κB pathway proteins and the expression of ANP and β-MHC in cardiomyocytes. The positive drug valsartan exerted similar effects on Ang II-induced cardiac hypertrophy in vivo and in vitro.
Conclusion: Pue attenuates Ang II-induced cardiac hypertrophy by inhibiting activation of the redox-sensitive ERK1/2, p38 and the NF-κB pathways. 相似文献
992.
蛋白酪氨酸激酶抑制剂对脑血管平滑肌细胞Ca~(2+)池操纵性Ca~(2+)内流的影响 总被引:1,自引:1,他引:1
目的 研究蛋白酪氨酸激酶和蛋白酪氨酸磷酸酶抑制剂对牛脑血管平滑肌细胞 (CSMC)Ca2 + 池操纵性Ca2 + 内流的影响。方法 采用培养的CSMC ,在生物荧光双波长影像分析系统用Fura 2 /Am荧光探针测定单个细胞内游离Ca2 + 浓度。结果 (1)蛋白酪氨酸激酶抑制剂 (genistein ,2 5 ,5 ,10 μmol·L-1)能浓度依赖性降低内皮素 1(ET 1,10 -7mol·L-1)刺激引起的CSMCCa2 + 内流 ,抑制率分别为5 6%± 2 .9%、2 5 6%± 3 9%、48 9%± 3 7% ;蛋白酪氨酸磷酸酶抑制剂 (vanadate ,2 ,4,8μmol·L-1)能浓度依赖性升高CPA刺激引起的CSMCCa2 + 内流 ,增加比率分别为8 2 %± 3 9%、18 8%± 4 9%、46 6%± 6 9% ;(2 ) genistein(2 5 ,5 ,10 μmol·L-1)能浓度依赖性降低ATP(10 μmol·L-1)刺激引起的CSMCCa2 + 内流 ,抑制率分别为 6 7%±2 6%、2 4 6%± 6 5 %、5 1 3 %± 6 9% ;vanadate (2 ,4,8μmol·L-1)能浓度依赖性升高ATP刺激引起的CSMCCa2 +内流 ,增加比率分别为 4 8%± 2 0 %、2 8 5 %± 4 6%、49 6%± 3 3 % ;(3 ) genistein (2 5 ,5 ,10 μmol·L-1)能浓度依赖性降低环匹阿尼酸 (Cyclopiazonicacid ,CPA ,10 μmol·L-1)刺激引起的CSMCCa2 + 内流 ,抑制率分别为 6 5 %± 3 0 %、2 2 5 %± 5 2 %、 相似文献
993.
火麻仁油对D-半乳糖致衰老小鼠学习记忆障碍的保护作用研究 总被引:1,自引:0,他引:1
目的:研究火麻仁油对D-半乳糖(D-gal)致衰老小鼠学习记忆能力的保护作用,并探讨其作用机制.方法:采用D-半乳糖诱导小鼠衰老模型,用跳台法、水迷宫法和Morris水迷宫法测定衰老小鼠学习记忆能力,检测小鼠脑组织丙二醛(MDA)含量和总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及大脑皮层和海马组织中乙酰胆碱(Ach)含量和乙酰胆碱酯酶(AchE)、胆碱乙酰化转移酶(ChAT)活性,观察脑组织组织形态学变化.结果:火麻仁油(3、6和12 mL/kg)能明显延长跳台实验的跳台潜伏期,缩短错误次数;缩短水迷宫实验达到时间和减少错误次数;缩短Morris水迷宫实验逃避潜伏期和第1次到达原平台时间,增加穿越原平台次数和逗留时间;能显著增加脑组织中T-AOC、SOD、GSH-Px活性和降低MDA含量,增加大脑皮层和海马组织中Ach含量和AchE、ChAT活性,减轻脑组织损伤.结论:火麻仁油可显著改善D-半乳糖致衰老小鼠学习记忆能力,其机制可能与其提高脑组织抗氧化和清除自由基能力,增强中枢胆碱能神经系统功能有关. 相似文献
994.
995.
HPLC法测定阿奇霉素胶囊的含量 总被引:1,自引:2,他引:1
目的建立阿奇霉素胶囊含量的HPLC法。方法采用Shim-pack VP-ODS(4.6 mm×150 mm,5 nm)(岛津柱),流动相为0.067 mol.L-1磷酸二氢铵溶液(三乙胺调pH至6.5)-乙腈(74∶26),检测波长200 nm,流速1 ml.min-1,柱温30℃。结果阿奇霉素在0.76~3.82 g.L-1范围内线性关系良好,r=0.999 9,方法的回收率为100.2%(n=3)。结论本法简便、准确、重现性好,结果可靠,可用于阿奇霉素的含量测定。 相似文献
996.
997.
目的 探讨H2受体拮抗剂法莫替丁在预防奥氮平引起的体质量增加中的疗效.方法 选择40例符合中国精神障碍分类与诊断标准的首发精神分裂症患者,随机分为奥氮平合用法莫替丁组和奥氮平合用安慰剂组,均治疗观察8周.于治疗前和治疗后2周、4周、8周测身高、体质量,计算体重指数(BMI)及8周内体质量增加超过自身基线体质量7%的患者比例.采用阳性症状评定量表(SAPS)和阴性症状评定量表(SANS)评定疗效.结果 两组患者的体质量、BMI:治疗后各时点均有增加,与治疗前比较差异有统计学意义(P<0.05).奥氮平加法莫替丁组和奥氮平组治疗8周末体质量分别增加了3.7 kg,BMI各增加了2.5 kg/cm2和2.6 kg/cm2.治疗后各时点,两组患者的体质量、BMI增加程度比较差异无统计学意义(P>0.05).治疗8周末,体质量增加超过基线体质量7%的患者比例两组差异无统计学意义(P>0.05).治疗8周末,SAPS、SANS评分显著下降(P<0.05);SAPS与SANS分值与基线的差值无组间差异(P>0.05).结论 合用H2-拮抗剂法莫替丁不能减轻奥氮平引起的体质量增加. 相似文献
998.
Jian LI Ying-zi HE Wen LI Yun-zhen SHEN Yu-ru LI Yun-feng WANG 《Acta pharmacologica Sinica》2010,31(4):509-514
Aim:
To develop a novel non-viral vector with high transfection efficiency and low cytotoxicity.Methods:
Poly (ethylene glycol)-distearoylphosphatidylethanolamine (PEG-DSPE) was incorporated into polymer-lipid hybrid nanoparticles (PLN) to construct a PEG-DSPE modified long circulating PLN (L-PLN). The L-PLN was prepared by the emulsifying-solvent evaporation method, L-PLN and L-PLN/DNA complexes were characterized. Both HEK293 and MDA-MB-231 cells transfected by L-PLN/DNA complexes were observed under a fluorescence microscope. The transfection efficiency of the complexes to HEK293 cells was further evaluated by flow cytometry.Results:
The GFP fluorescence intensity in HEK293 cells transfected by the L-PLN/DNA complexes (N/P=10) was about 37.2%, which was higher than those transfected by PLN alone or commercial LipofectamineTM 2000. The L-PLN exhibited minimal toxicity at a low N/P ratio compared with other vectors.Conclusion:
L-PLN as a novel gene delivery system, has higher transfection efficiency and acceptable cytotoxicity compared to the corresponding PLN, which is beneficial for the development of non-viral gene transfer vectors and may offer an alternative strategy for the future gene therapy. 相似文献999.
目的探讨在激素常规治疗基础上联合宁血汤治疗重度儿童原发性免疫性血小板减少症(ITP)的临床疗效。方法将本院收治的50例重度ITP患儿随机分为治疗组和对照组,2组均给予西医常规治疗,治疗组患儿在此基础上给予自制宁血汤口服,每日1剂。比较治疗1月后2组的总有效率、止血时间、血小板计数恢复正常时间、住院时间等。结果治疗组总有效率为88.0%,对照组为72.0%,2组比较差异有统计意义(P<0.05)。治疗组止血时间、血小板计数恢复正常时间、住院时间等指标均短于对照组(P<0.05)。随访1年,治疗组1例因上呼吸道感染复发,症状较轻,经抗感染及口服宁血汤后血小板自行上升至正常;对照组5例因上呼吸道感染复发,3例较轻,经抗感染及口服宁血汤后血小板自行上升至正常,2例因血小板<30×109/L住院。结论激素常规联合宁血汤治疗能够显著提高ITP患儿的临床疗效,缩短激素用药时间,减少不良反应,显著降低复发率。 相似文献
1000.
c-Jun和CBP在槲皮素抑制前列腺癌中的作用 总被引:3,自引:0,他引:3
目的探讨槲皮素抑制前列腺癌的作用机制。方法应用蛋白印迹技术检查槲皮素(quercetin)对雄激素受体(androgen receptor,AR)的辅调节因子c-Jun和cAMP应答元件结合蛋白的结合蛋白[cAMP response element binding protein (CREB)-binding protein,CBP]蛋白表达的影响;利用细胞转染技术检测c-Jun和CBP对AR功能的影响; 免疫沉淀技术检验c-Jun与AR的蛋白-蛋白相互作用。结果槲皮素能够明显诱导c-Jun的高表达, 高表达的c-Jun能够抑制AR的功能。槲皮素对CBP的蛋白表达水平无明显影响,而增加CBP的表达并不能逆转槲皮素对AR功能的抑制作用。免疫沉淀结果表明,c-Jun与AR存在蛋白-蛋白相互作用。结论槲皮素抑制前列腺癌的机制可能是通过c-Jun与AR的蛋白相互作用,而不是通过c-Jun竞争结合AR的辅激活因子CBP来实现的。 相似文献