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991.
生物可降解肋骨骨折内固定材料-蚕丝纤维增强纯聚己内酯的体内降解实验研究 总被引:2,自引:0,他引:2
目的对纯聚己内酯(PCL)和蚕丝纤维增强PCL多孔复合材料进行体内降解实验研究,观察其降解速度变化及组织反应情况,为临床应用于多发性肋骨骨折固定材料提供实验依据。方法将纯PCL和蚕丝纤维增强PCL植入兔背部脊柱两侧皮下和肌肉之间,于2、4、8、12、16、24周取材,分别测试2种材料的生物吸收率、组织学观察(HE染色)和扫描电镜观察。结果蚕丝纤维增强PCL在体内植入过程中生物吸收率大于纯PCL,材料内部结构断裂融合降解明显,未见材料周围组织变性、坏死或异常增生现象。结论蚕丝纤维增强PCL多孔复合材料植入体内后具有合适的降解速度,异物反应小,是具有良好应用价值的新型肋骨骨折内固定材料。 相似文献
992.
壳聚糖在过氧化氢存在下的氧化降解 总被引:28,自引:1,他引:27
主要研究了壳聚糖在H_2O_2存在下的氧化降解反应,分别讨论不同的pH值、H_2O_2浓度、温度和反应时间对降解反应影响。实验结果表明用H_2O_2使壳聚糖降解是制备低分子量可溶性壳聚糖的一种有效和简便的方法。 相似文献
993.
The utilization time for a parenteral prodrug solution with a bioavailable fraction of unity was defined as the time during which the total of the prodrug concentration and the drug concentration equals or exceeds 90% of the initial prodrug concentration. This utilization time was calculated as a function of pH, buffer, and temperature using the experimentally determined rate expressions for bacampicillin and talampicillin. The results were compared to the shelf life of ampicillin solutions under identical storage conditions. First-order rate constants were determined for conversion of the prodrugs to ampicillin (k
c), for -lactam degradation of the prodrugs (k
nc), for the overall loss of prodrugs (k
sum), and for -lactam degradation of ampicillin (k
h) in aqueous solutions at 25.0 to 60.0°C, µ = 0.5, in the pH range 0.90 to 8.4. Loss of bacampicillin proceeded primarily by degradation at pH levels below 4 but was due predominantly to conversion at pH levels above 5. Loss of talampicillin was due primarily to conversion throughout the entire pH range. While the prodrug utilization times were approximately twice the shelf life of ampicillin in acidic solutions, ampicillin was significantly better in neutral solutions. The results illustrate the potential for increased prodrug storage periods when utilization time is defined on the basis of the bioactivity rather than on the prodrug concentration alone. 相似文献
994.
Degradation of microcystin-RR by UV radiation in the presence of hydrogen peroxide. 总被引:11,自引:0,他引:11
Experiments were conducted to investigate the degradation of microcystin-RR in order to assess the effectiveness and feasibility of the combined UV/H(2)O(2) catalytic system for purification of water polluted by microcystins. The operating parameters such as hydrogen peroxide dosage, pH value, UV light intensity, initial concentration of microcystin-RR and reaction time were evaluated, respectively. The degradation efficiency increased nonlinearly with increasing UV light intensity and hydrogen peroxide dosage, respectively. There existed an optimal hydrogen peroxide dosage, beyond which the reagent exhibited an inhibitory effect, for degrading microcystin-RR. The degradation process could be fitted by both of the pseudo-first-order and second-order kinetics well and primarily followed a mechanism of both direct photolysis and hydroxyl radical oxidation. Compared with the treatment using UV radiation and hydrogen peroxide individually, the combined UV/H(2)O(2) system could significantly enhance the degradation efficiency due to the synergetic effect between UV radiation and hydrogen peroxide oxidation. The observed rate constants decreased and the corresponding half-lives prolonged as the concentrations of microcystin-RR increased. The combined UV/H(2)O(2) process provides an effective technology for the removal of microcystins from drinking water supplies. 相似文献
995.
Effects of Ro 31-8220 on smooth muscle cell proliferation induced by fibrinogen degradation products
目的:研究纤维蛋白原降解产物的致有丝分裂原活性及一种新型PKC抑制剂Ro318220(Ro)的作用.方法:大鼠主动脉平滑肌细胞增殖采用结晶紫染色法测定.结果:纤维蛋白原降解产物促进大鼠主动脉平滑肌细胞的增殖,Ro(001-1μmol·L-1)剂量依赖地抑制增殖.结论:Ro抑制纤维蛋白原降解产物诱导的平滑肌细胞的增殖. 相似文献
996.
苦参碱对纤维蛋白纤维蛋白原降解产物诱导血管细胞损伤、增殖及腹腔巨噬细胞释放IL-1的影响 总被引:6,自引:0,他引:6
目的:研究苦参碱(Mat)对纤维蛋白纤维蛋白原降解产物(FFDP)作用的影响。方法:大鼠主动脉内皮细胞损伤以乳酸脱氢酶释放测定;大鼠主动脉平滑肌细胞增殖采用结晶紫染色法测定;白细胞介素1活性采用小鼠胸腺细胞增殖法测定。结果:FFDP能促进大鼠主动脉内皮细胞释放乳酸脱氢酶,诱导大鼠主动脉平滑肌细胞增殖,并促使小鼠腹腔巨噬细胞分泌IL1增加。结论:Mat可抑制FFDP的作用。对动脉粥样硬化的防治可能有一定意义。 相似文献
997.
998.
目的 研究溴甲纳曲酮在水溶液中的降解动力学特征,考察溴甲纳曲酮的降解影响因素,为其制剂的研究提供必要的实验结果和数据。方法 通过经典恒温实验,应用HPLC测定溴甲纳曲酮在不同温度、pH值、光照和Fe3+浓度条件下的降解动力学参数,用阿仑尼乌斯公式预测其有效期和活化能。结果 溴甲纳曲酮在水溶液中的降解反应级数为n=1,其水溶液最稳定的pH值在3.51左右;随着温度升高,溴甲纳曲酮降解速率增加,在常温水溶液中的有效期t0.9=145 d;Fe3+和光照能促进溴甲纳曲酮的降解。结论 溴甲纳曲酮在水溶液中的降解属近似一级动力学过程,降解速率与温度成正相关,pH对溴甲纳曲酮的降解有一定的影响,Fe3+和光照对溴甲纳曲酮的降解速率影响较明显。为制剂的研发提供了必要的实验结果和数据。 相似文献
999.
1000.
Heterogeneous Loss of Connexin43 Protein in Ischemic Dog Hearts 总被引:10,自引:0,他引:10
XIAO-DI HUANG M.D. GEORGE E. SANDUSKY Ph .D. DOUGLES P. ZIPES M.D. 《Journal of cardiovascular electrophysiology》1999,10(1):79-91
Heterogeneous Loss of Connexin43 Protein in Ischemic Dog Hearts. Introduction: Ischemia causes cell decoupling in the myocardium. Prolonged ischemia activates proteases and causes degradation of structural proteins as well as gap junctions. There is little information about the degradation of gap junction protein during the early time period after acute ischemia. The purpose of the present study was to investigate connexin43 (Cx43) protein degradation and distribution patterns in (he canine left ventricular wall during 1 to 6 hours of ischemia. Methods and Results: Ischemia of canine left ventricular myocardium was induced by ligation of the left anterior descending coronary artery. Following a period of in situ ischemia of up to 6 hours, samples were harvested, and standard paraffin slides were prepared for Cx43 and wheat germ agglutinin double labeling. Cx43 distribution was visualized by confocal microscopy. In controls, homogeneous distribution of Cx43 staining was determined. Ischemia caused a loss of Cx43 with a heterogeneous pattern by mixing foci of infarcted cells among normal cardiac myocytes. To determine if the changes were induced by heterogeneous reduction in the blood supply, an in vitro ischemic model was studied to induce more homogeneous ischemia. Western blot analysis of these in vitro ischemic tissue samples revealed a reduction of Cx43 protein concentration with a 50% decay time of 4.8 hours. Cx43 dephosphorylation was detected after 1 hour of in vitro ischemia. Heterogeneous loss of Cx43 was found in the in vitro ischemic tissue. There were no. significant changes in Cx43 staining density during the first hour of ischemia at a time when dephospharylation of the protein was observed. After 1 hour of ischemia, Cx43 was reduced at intercalated disk areas, and. after 6 hours, most Cx43 disappeared at intercalated disk areas, while small amounts of Cx43 remained at side-to-side junctions. Conclusion: Cx43 undergoes both distribution and concentration changes following acute cardiac Ischemia. The loss of Cx43 protein is heterogeneous. Cx43 dephosphorylation occurred within 1 hour following ischemia. 相似文献