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101.
粉防己碱舒张离体新西兰白兔阴茎海绵体平滑肌的机制研究 总被引:1,自引:0,他引:1
目的观察粉防己碱(tetrandrine,Tet)对阴茎海绵体平滑肌胞内钙释放和胞外钙内流的影响,初步探讨其舒张作用的机制。方法采用离体阴茎海绵体平滑肌肌条张力记录法,观察Tet对去氧肾上腺素(phenylephrine,PE)和氯化钾(KCI)诱导收缩的肌条的影响;采用无Ca~(2 )-复Ca~(2 )实验法,观察Tet对PE诱导的依赖细胞内钙和细胞外钙的肌条收缩反应的影响。结果Tet对PE或kcl诱导的肌条收缩均具有浓度依赖性的抑制作用。100μmol/L Tet可抑制20μmol/L PE引起的依赖细胞内钙和细胞外钙的肌条收缩(P<0.05);结论Tet可通过阻滞电压依赖性钙通道、受体依赖性钙通道和抑制细胞内钙库释放,从而介导其对海绵体平滑肌的舒张作用。 相似文献
102.
目的:研究PCO—Pin,Nic,Lem及RP对VMSC内[Ca~(2 )]_i的改变及其可能机制。方法:VSMC加入Fura-2 AM 2.5μmol·L~(-1)37℃下孵育50min,[Ca~(2 )]_i用荧光分光光度计检测。结果:4种PCO能较弱地抑制K~ 30 mmol·L~(-1)诱导的[Ca~(2 )]_i增加,但明显抑制ATP 0.1mmol·L~(-1)诱导的[Ca~(2 )]_i峰相及持续相增加,且呈剂量依赖性。格列苯脲完全阻断Pin,Lem及RP的作用,只部分抑制Nic的作用。无钙液中先给4种PCO,能显著抑制ATP诱导的[Ca~(2 )]_i峰相增加。结论:4种PCO均抑制ATP诱导的[Ca~(2 )]_i增加,此作用与减少细胞外钙内流及细胞内钙释放有关。 相似文献
103.
Stratum corneum architecture, metabolic activity and interactivity with subjacent cell layers 总被引:3,自引:0,他引:3
Peter M. Elias 《Experimental dermatology》1996,5(4):191-201
104.
J T Fujii 《The Journal of comparative neurology》1992,316(3):279-286
The avian Edinger Westphal nucleus, through the ciliary ganglion, controls accommodation, iris constriction, and blood flow through the choroid. In live brainstem slices, the nucleus is easily identifiable as an olive-shaped cluster of neurons dorsal to the oculomotor nerve and nucleus. Intracellular recordings from neurons in the nucleus identified two classes of responses to sustained (300 to 500 ms) injections of depolarizing current. One set of cells fired action potentials for the duration of the pulse while a second set of cells fired action potentials only transiently, during the first 50 to 100 ms, after which they remained silent regardless of the size of the depolarization. Intracellular recordings followed by injections of the fluorescent dye lucifer yellow revealed that repetitively firing cells were located in the lateral half of the nucleus while non-repetitively or transiently firing cells were located in the medial half. These locations correspond to different Edinger Westphal subdivisions which have distinct inputs and target populations. The varying firing patterns are discussed with reference to the known functions of the subdivisions in which they occur. Replacement of calcium by magnesium in the extracellular medium had no effect on the number of action potentials fired by non-repetitively firing cells, suggesting that a calcium-activated potassium current is not responsible for suppressing repetitive firing in these cells. In contrast, in repetitively firing cells removal of extracellular calcium increased the frequency of action potential discharge and decreased the amplitude of afterhyperpolarizations following single action potentials. Addition of cadmium to the bath medium had similar effects.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
105.
Jun Anabuki Masatoshi Hori Hiroshi Ozaki Iwao Kato Hideaki Karaki 《European journal of pharmacology》1990,190(3):373-379
The mechanism of the vasodilator effect of pinacidil was examined. Pinacidil (0.1–100 μM) inhibited the increases in cytosolic Ca2+ ([Ca2+]i) and muscle tension due to norepinephrine in rat aorta. In contrast, a Ca2+ channel blocker, verapamil, inhibited the norepinephrine-stimulated [Ca2+]i more strongly than the contraction. Higher concentrations of pinacidil (3–100 μM) inhibited the verapamil-insensitive portion of the contraction and [Ca2+]i. An inhibitor of ATP-sensitive K+ channels, glibenclamide, antagonized the inhibitory effect of low concentrations ( 10 pM) of pinacidol. Pinacidil did not change the contraction induced by Ca2+ in vascular smooth muscle permeabilized with Staphylococcus aureus -toxin. Norepinephrine (in the presence of GTP), 12-deoxyphorbol 13-isobutyrate (in the absence of GTP), and treatment with GTPγS potentiated the contraction of permeabilized smooth muscle induced by the addition of Ca2+. Pinacidil (100 μM) inhibited the potentiation due to GTPγS or noepinephrine but not to phorbol ester. These results suggest that pinacidil has dual effects on vascular smooth muscle contraction. At lower concentrations (>0.1 μM), it decreases [Ca2+]i, possibly by activating ATP-sensitive K+ channels. At higher concentrations (> 3 μM), it may additionally inhibit the receptor-mediated, GTP-binding protein-coupled phosphatidyl inositol turnover. 相似文献
106.
本实验以铁骨晶(多肽钙),进口脱脂奶粉,活性钙冲剂,贝壳钙为钙源添加于大鼠正常饲料中。观察结果表明:上述4组钙的吸收率分别为64.4%,69.1%,59.9%,51.6%;钙的储留率分别为89.8%,93.3%,85.2%,79.0%;钙的存留率分别为43.6%,49.0%,32.4%,26.8%;股骨指数分别为7.02×10(-3),6.43×10(-3),6.84×10(-3)。6.88×10(-3);折断力(牛顿)分别为60.54±12.55,46.81±9.32,43.26±16.62,38.24±10.79。同时以铁骨晶为钙源对70例(5~6岁)儿童进行了血清Ca,Fe,Zn,Hb及生长发育的检测。铁骨晶组的身高,体重,胸围分别比对照组增加。铁骨晶组血清Ca,Fe,Zn,Hb也均有较好的改善。这表明铁骨晶具有较好的促进钙吸收利用作用,同时能增加骨强度作用。 相似文献
107.
Summary— The regulation and role of the intracellular Ca2+ pools were studied in rat peritoneal mast cells. Cytosolic free calcium concentration ([Ca2+ ]i) was monitored in fura-2 loaded mast cells. In the presence of Ca2+ and K+, compound 48/80 induced a biphasic increase in [Ca2+ ]i composed of a fast transient phase and an apparent sustained phase. The sustained phase was partially inhibited by the addition of Mn2+ . DTPA, a cell-impermeant chelator of Mn2+ , reversed this inhibition, suggesting that a quenching of fura-2 fluorescence occurs in the extracellular medium. In the absence of extracellular Ca2+ , the transient phase, but not the sustained one, could be preserved, provided that mast cells were depolarized. The transient phase was completely abolished by thapsigargin, a microsomal Ca2+ -ATPase inhibitor. Maximum histamine release induced by either compound 48/80 or antigen was obtained in the absence of added Ca2+ only when mast cells were depolarized. These histamine releases were inhibited by low doses (< 30 nM) of thapsigargin. Thapsigargin at higher doses induced histamine release which was unaffected by changing the plasma membrane potential, but was completely dependent on extracellular Ca2+ , showing that a Ca2+ influx is required for thapsigargin-induced exocytosis. Together, these results suggest that the mobilization of Ca2+ from thapsigargin sensitive-intracellular pools induced by compound 48/80 or antigen is sufficient to trigger histamine release. The modulation of these pools by the plasma membrane potential suggest their localization is close to the plasma membrane. 相似文献
108.
109.
Tetsumori Yamashima Takaomi C. Saido Masatoshi Takita Atsuo Miyazawa Jun Yamano Atsuo Miyakawa Hisashi Nishijyo Junkoh Yamashita Seiichi Kawashima Taketoshi Ono Tohru Yoshioka 《The European journal of neuroscience》1996,8(9):1932-1944
To clarify the mechanism of postischaemic delayed cornu Ammonis (CA)-1 neuronal death, we studied correlations among calpain activation and its subcellular localization, the immunoreactivity of phosphatidylinositol 4,5-bisphosphate (PIP2) and Ca2+ mobilization in the monkey hippocampus by two independent experimental approaches: in vivo transient brain ischaemia and in vitro hypoxia-hypoglycaemia of hippocampal acute slices. The CA-1 sector undergoing 20 min of ischaemia in vivo showed microscopically a small number of neuronal deaths on day 1 and almost global neuronal loss on day 5 after ischaemia. Immediately after ischaemia, CA-1 neurons ultrastructurally showed vacuolation and/or disruption of the lysosomes. Western blotting using antibodies against inactivated or activated μ-calpain demonstrated μ-calpain activation specifically in the CA-1 sector immediately after ischaemia. This finding was confirmed in the perikarya of CA-1 neurons by immunohistochemistry. CA-1 neurons on day 1 showed sustained activation of μ-calpain, and increased immunostaining for inactivated and activated forms of μ- and m-calpains and for PIP2. Activated μ-calpain and PIP2 were found to be localized at the vacuolated lysosomal membrane or endoplasmic reticulum and mitochondrial membrane respectively, by immunoelectron microscopy. Calcium imaging data using hippocampal acute slices showed that hypoxia-hypoglycaemia in vitro provoked intense Ca2+ mobilization with increased PIP2 immunostaining specifically in CA-1 neurons. These data suggest that transient brain ischaemia increases intracellular Ca2+ and PIP2 breakdown, which will activate calpain proteolytic activity. Therefore, we suggest that activated calpain at the lysosomal membrane, with the possible release of biodegrading enzyme, will cause postischaemic CA-1 neuronal death. 相似文献
110.
Michael Nelson† Gillian F. Hague† Cyrus Cooper‡ Valda W. Bunker§ 《Journal of human nutrition and dietetics》1988,1(2):115-127
Epidemiological studies of calcium and osteoporosis have been hampered by the lack of a suitable tool for assessing calcium intake. This report describes a new frequency and amount questionnaire for measuring present and past calcium intake in the elderly. The validity of the questionnaire was tested against two commonly used standards of dietary assessment, five-day duplicate diets and seven-day weighed dietary inventories. The resulting correlation coefficients were, respectively, r = 0.76 and r = 0.69, while that for repeatability was r = 0.84. Furthermore, the questionnaire categorized subjects into thirds of the distribution of intake with almost no gross misclassification. It is suggested that the present findings may be extended to the majority of normal, healthy elderly subjects, implying wide application for the questionnaire in the assessment of calcium intake in the elderly. 相似文献