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101.
Objective To evaluate the bioequivalence between recombinant human growth hormone (rhGH) for reconstitution, and two dosages of liquid formulation of rhGH [ (151U) 5mg or (301U) lOmg per 3ml ]. Methods The study drugs were tested in a randomized, single-blind and three-period crossover studies in 24 healthy male subjects. The three drugs were administered by subcutaneous injection at a dose of O. 21U/kg body weight. A continuous somatostatin infusion was given in order to suppress the secretion of endogenous GH. The ve- nous blood samples were drawn at different time points to test the serum concentration of GH. The pharmacokinetic parameters were analyzed by statistical methods. Results 90% confidence intervals (CI) of AUC0-24h among three products were all within 80% - 125% interval ( 103. 4% - 116. 5%, 105. 7% - 119. 6% and 91.9% - 103. 7%, respectively), and the Cls of C,~ among three products were all within 70% - 143% interval (91.9% - 114. 0%, 103. 7% -127. 2% and 81.6% -97. 4%, respectively). There was no statisitical difference of tmax among all the three products. Conclusion These data demonstrate that there is bioequivalence between rhGH for reconstitution and two liquid formulations of rhGH. 相似文献
102.
103.
Ts. V. Serbenyuk I. E. Gurskaya A. D. Slyuta G. Ya. Roze P. Ya. Romanovskii 《Bulletin of experimental biology and medicine》1988,106(1):931-933
Department of Physiology of Man and Animals, Biological Faculty, M. V. Lomonosov Moscow University. (Presented by Academician of the Academy of Medical Sciences of the USSR I. P. Ashmarin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 7, pp. 17–19, July, 1988. 相似文献
104.
Administration of antiserum to thyrotropin-releasing hormone (TRH) into the lateral cerebral ventricle of mice significantly attenuated recovery from hyperglycemia induced by treatment with 2-deoxyglucose but had no effect on the plasma glucose of saline-treated mice. TRH, injected centrally together with the anti-TRH antibody, reversed the effect of the antiserum and blocked the development of hyperglycemia. These findings suggest that activation of TRH neurons in the central nervous system may be a physiological event influencing recovery from hyperglycemia. 相似文献
105.
Osteopenia and inhibited longitudinal growth in childhood are serious side effects during glucocorticoid therapy. The effects of glucocorticoids on bone have been confirmed in animal experiments. Long-term glucocorticoid administration to rats results in reduced body weights, reduced bone growth (length and cross-sectional area), and bone strength. Glucocorticoid treatment also resulted in a reduced bending stress, indicating reduced bone quality. Growth hormone, on the other hand, increased body weights, bone dimensions, and bone strength. The aim of the present study was to evaluate if growth hormone administration would have an anabolic effect on rat bone when given to animals also receiving a high dosage of glucocorticoid. Five groups of female rats, 3.5 months old, were treated as follows: (1) saline control; (2) glucocorticoid (prednisolone: Delcortol 5 mg/kg/day); (3) growth hormone (recombinant human growth hormone 5 mg/kg/day); (4) glucocorticoid and growth hormone; and (5) food restriction, consisting of restricted access to food to reduce their weight gain to match that of the glucocorticoid injected rats. After 80 days of hormone administration the animals were sacrificed. The right femur was removed and tested biomechanically in a three-point bending procedure. The left femur was used for determination of bone dimensions. Biomechanical parameters (ultimate load and ultimate stiffness) were then normalized to diaphyseal cross-sectional diameters of the femur, giving the values of ultimate bending stress and Young's modulus. Results: administration of both hormones simultaneously could not reverse the decrease in body weights, bone length, and diameters, or the decreased bone strength induced by glucocorticoid administration. In conclusion, growth hormone cannot prevent cortical osteopenia in female rats induced by a high dose of glucocorticoid with protracted effect. 相似文献
106.
目的研究经咽旁入路选择性的切除大鼠垂体前叶,以制备大鼠垂体前叶激素缺乏模型如生长激素(GH)缺乏模型。方法经腹侧咽旁入路,运用显微神经外科技术经基蝶骨底选择性地切除垂体前叶。然后采用竞争免疫沉淀法检测大鼠生长激素的含量,术后统计死亡率、成功率。结果切除垂体前叶后大鼠的死亡率为26.7%,成活率为73.3%,全切率为91%;成功制备大鼠模型的GH显著低于假手术组和对照组。结论运用显微外科技术可以成功的选择性的切除大鼠垂体前叶,制备出垂体前叶激素如生长激素缺乏的动物模型。 相似文献
107.
108.
目的:研究中药生精冲剂对大鼠精索静脉曲张的影响及疗效。方法:从80只SD雄性大鼠中随机抽出20只作为假手术组,余60只均建立精索静脉曲张病理模型后随机均分为模型组、生精冲剂组和克罗米芬组。造模后15d生精冲剂组和克罗米酚组分别给予生精冲剂4g/(kg·d)和克罗米芬20mg/(kg·d)灌胃,模型组和假手术组正常喂食。造模后45d放免法测定血清性激素(FSH、LH和T)及观察各组大鼠睾丸组织结构。结果:生精冲剂组大鼠光镜下睾丸组织结构优于模型组和克罗米芬组;血清FSH、LH生精冲剂组显著低于模型组和克罗米芬组(P〈0.05),而克罗米芬组显著高于其他3组。T在生精冲剂组、克罗米芬组和假手术组之间无显著差异,但均显著高于模型组(P〈0.05)。结论:中药生精冲剂对精索静脉曲张引起的睾丸损害有保护及修复作用,且可能优于克罗米芬。 相似文献
109.
110.
Howard B Moss Thomas L Hardie John P Dahl Wade Berrettini Ke Xu 《Neuropsychopharmacology》2007,61(8):974-978
BACKGROUND: Some studies have associated alcohol dependence (AD) with the human serotonin (5-HT)(1B) receptor (HTR1B). This investigation explored the functional responsivity of HTR1B in abstinent AD men using a sumatriptan challenge, while measuring genetic heterogeneity in the HTR1B promoter. METHODS: Abstinent AD men (n = 27) and abstinent men without any alcohol use disorder (n = 19) were administered 6 mg of sumatriptan succinate, subcutaneously. Plasma samples collected over the following 2 hours were assayed for growth hormone (GH) concentrations. His DNA was genotyped for the A-161T and T-261G polymorphisms of the HTR1B promoter and diplotypes determined. RESULTS: Integrated GH responses were predicted by interactions of AD and promoter diplotypes, as well as subject ethnicity. The final model accounted for nearly 35% of the variance in GH responses. Post hoc evaluation revealed that AD was associated with a blunting of GH secretion only among individuals with the most common HTR1B diplotype (TT/TT). CONCLUSIONS: A blunting of GH responses in abstinent AD men was observed only among those with the most common HTR1B promoter diplotype. Less common promoter diplotypes appeared protective. Controlling for genetic background is a useful augmentation of case-control pharmacological challenge strategies designed to elucidate the psychobiology of AD and other complex disorders. 相似文献