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101.
本文报告了2,4,6-三硝基甲苯(TNT)的代谢物,2-氨基-4,6-二硝基甲苯2和2,4-二氨基-6-硝基甲苯3的合成。以邻甲基苯甲酸为原料,经硝化(HNO_3-H_2SO_4)和Schmidt反应(NaN_3-H_2SO_4)得到2,用NaHS还原TNT的方法合成化合物3。 相似文献
102.
Microinjections of Leu-enkephalin into the dorsal vagal complex induced hypotension and bradycardia. Both naloxone, given at a dose conferring selectivity for μ receptors, and the S antagonist ICI 154,129 prevented the cardiovascular effects of Leu-enkephalin. Naloxone was also found to decrease the gain of the baroreflex. These results suggest that Leu-enkephalin is involved in cardiovascular regulation through activation of δ-, and possibly μ-, opioid receptors in the dorsal vagal complex. 相似文献
103.
本文报道给C57小鼠腹腔注射不同剂量1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)后,发现组3(MPTP35 mg/kg,每天一次,共7天)鼠肝匀浆、线粒体和微粒体的膜丙二醛含量明显增加,与对照组相比分别增加70.5%,67%和51.4%(P<0.01),而组1(MPTP 35mg/kg,每4小时一次,共3次)和组2(MPTP35mg/kg,每天一次,共4天)鼠肝丙二醛含量与对照组相近。结果表明MPTP有明显地促进鼠肝脂质过氧化的作用,并与其剂量有关。 相似文献
104.
105.
本文以兔呼吸频率、通气量和血气作为指标,观察到iv吗啡0.5~4.0mg/kg产生剂量依赖性呼吸抑制。icv匹鲁卡品2.5mg/kg能完全逆转这一抑制效应。icv 4—氨基吡啶(4—AP),1.5μg/kg兴奋呼吸,并使吗啡量效曲线右移。用利血平耗竭儿茶酚胺后,吗啡仍能抑制呼吸,4—AP可消除之。表明吗啡抑制呼吸与中枢胆碱能系统有关,且可能系它抑制Ach释放所致。 相似文献
106.
根据由精氨酸-甘氨酸-天冬氨酸组成的肽能抑制血小板聚集的机制,设计并合成了[5-(4-甲脒-苄基)-2,4-二氧代-咪唑烷-3-基]-乙酰基-L-天冬氨酰-L-缬氨酸(9)。生物试验结果表明:(9)抑制血小板聚集作用最强,其活性以IC_(50)值相比,强于类似物。 相似文献
107.
Benjamin Sadlack Ralf Kühn Hubert Schorle Klaus Rajewsky Werner Müller Ivan Horak 《European journal of immunology》1994,24(1):281-284
Interleukin (IL)-2 and IL-4 are considered as important regulators of growth and differentiation of lymphocytes. We report that in mice made deficient for both IL-2 and IL-4 by gene targeting all major T cell subsets and B cells were normal, indicating that IL-2 and IL-4 are not essential for development of the immune system. Paradoxically, proliferation of T cells was increased in both IL-2- and IL-4-deficient homozygous mice. 相似文献
108.
Pr Gyllfors 《The clinical respiratory journal》2007,1(1):56-57
Introduction: Inflammation in the airways in connection to asthma is complex and the mechanisms underlying the associated clinical symptoms involve the interaction of many different kinds of cells and mediators, giving rise to different phenotypes. Objective: The objective of the present thesis was to investigate the molecular and cellular mechanisms that result in two of these phenotypes, i.e. aspirin‐intolerant asthma (AIA) and allergic asthma. The main focus was on leukotrienes. Materials and Methods: (i) Thirty‐three subjects with diagnosed AIA were challenged with celecoxib, a selective inhibitor of cyclooxygenase (COX)‐2. (ii) With the ultimate objective of finding a marker that could be used to identify patients with leukotriene‐associated asthma, the capacity to produce leukotrienes and the responsiveness to inhaled leukotrienes were determined in 20 subjects with mild asthma and in 10 healthy control individuals. (iii) Eight individuals with mild allergic asthma were challenged repeatedly with low doses of allergen in an experimental model aimed at mimicking the natural exposure to allergen. Exhaled nitric oxide was measured throughout the study. (iv) Thirteen patients with allergic asthma were subjected to bronchial challenges with methacholine and leukotriene D4 (LTD4) prior to and after administration of 500‐µg fluticasone twice daily for 2 weeks, and their levels of exhaled nitric oxide and urinary leukotriene E4 (LTE4) were determined. Results: (i) Both escalating doses from 5–100 mg (administered in a blinded, placebo‐controlled study) and an open‐label challenge with 200 + 200 mg celecoxib were tolerated well by AIA individuals. (ii) Neither group exhibited a correlation between the formation of leukotriene B4 by their whole blood in response to ex vivo stimulation or urinary levels of LTE4 and airway responsiveness to LTD4. (iii) The level of nitric oxide in the air that they exhaled rose significantly. At the same time, these subjects did not report any symptoms of asthma, did not require rescue by bronchodilator medication, and did not display any change in the calibre of their airways. (iv) Inhalation of glucocorticoid attenuated the responsiveness to methacholine and reduced the level of exhaled nitric oxide, but neither the responsiveness to LTD4 nor urinary excretion of LTE4 was affected. Conclusions: (i) This finding indicates that the intolerance reaction leading to broncho‐constriction in patients with AIA is caused by inhibition of COX‐1 and, furthermore, provides a scientific basis for administration of selective inhibitors of COX‐2 to alleviate prostaglandin‐mediated pain and inflammation in these patients. (ii) In further attempts to predict which asthmatic patients will respond well to anti‐leukotriene treatment, investigations on the capacity for leukotriene synthesis, responsiveness to these agents and expression of their specific receptors in the lungs are being performed. (iii) Monitoring of exhaled nitric oxide on a daily basis may allow for early detection of exacerbation in subjects with allergic asthma. (iv) Neither the release nor the actions of leukotrienes appear to be sensitive to inhaled glucocorticoids, strengthening the rationale for using a combination of glucocorticosteroids and anti‐leukotrienes to treat allergic asthma. 相似文献
109.
Leukotriene B4 (LTB4) and the protein kinase C activator, 4-beta-phorbol dibutyrate (PDBu), both induced a pronounced and concentration-dependent stimulation of hydrogen peroxide (H2O2) generation by purified guinea pig peritoneal eosinophils in the concentration range 1 nM-1 microM. The LTB4 response was inhibited competitively by the specific LTB4 receptor antagonist, U-75302, with a KB of 25 nM, while the concentration-response curves for both stimuli were shifted rightwards (3.8-fold and 2.8-fold for LTB4 and PDBu, respectively) by the competitive protein kinase C inhibitor, 1-O-hexadecyl-2-O-methylglycerol at a concentration of 300 microM. LTB4 appears, therefore, to induce respiratory burst in eosinophils via a receptor-mediated mechanism involving protein kinase C. 相似文献
110.
Memantine (1-amino-3,5-dimethyladamantan) was tested as an antagonist of N-methyl-d-aspartate (NMDA) receptors on cultured superior collicular and hippocampal neurones using the patch clamp technique and its actions were compared to those of Mg2+ ions, ketamine, dextrorphan, dextromethorphan, phencyclidine and dizocilpine (MK-801). Memantine (2–33 μM) concentration-dependently antagonized responses to NMDA 100 μM with an IC50 of 2.92 ± 0.05 μM. In contrast, current responses to (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (l-AMPA 50–100 μM) and γ-amino butyric acid (GABA 10 μM) were unaffected by Memantine 8 μM. Memantine 8 μM caused a non-parallel shift of the NMDA concentration-response curve to the right in a manner indicative of uncompetitive open channel block. The effects of memantine were similar to ketamine in that both antagonists were weakly use- and strongly voltage-dependent. In contrast, MK-801, phencyclidine and dextrorphan showed much slower kinetics that was reflected in their marked use- and weaker voltage-dependency. The antagonistic effects of memantine were not reversed by increasing concentrations of glycine (0.1–100 μM) ruling out the possibility of an interaction of memantine with the strychnine-insensitive glycine modulatory site associated with the NMDA receptor-channel complex. Memantine (1–100 μM) also selectively antagonized responses to NMDA (40 μM) in the cortical wedge preparation with IC50 of 12.9 ± 1.5 μM. 相似文献