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排序方式: 共有4483条查询结果,搜索用时 62 毫秒
41.
氯菊酯可明显抑制Ca~(2+)—ATP酶活性,其抑制作用是可逆的,底物动力学分析表明为非竞争性抑制,介质的酸度可影响其抑制效应;氯氰菊酯对该酶活性无明显影响.氯菊酯和氯氰菊酯均能可逆性地抑制Ca~(2+),Mg~(2+)—ATP酶活性,但氯菊酯为反竞争性抑制.且有一定的pH依赖性,而氯氰菊酯为非竞争性抑制,其抑制率基本不受pH的影响,表明这两种杀虫剂在Ca~(2+) ,Mg~(2+)—ATP酶上有不同的结合位点. 相似文献
42.
K. Hatayama J. Kambayashi T. Kawasaki K. Morimoto T. Ohshiro T. Mori 《Thrombosis research》1986,41(6):761-770
The interrelationship between ATP-secretion, protein phosphorylation and intracellular Ca2+ concentration ([Ca2+]i) was studied in both 32P and quin 2 loaded human platelets stimulated by thrombin or thromboxane A2 analogue (STA2). In platelets stimulated by thrombin, the degree of 47,000 dalton polypeptides (P47) phosphorylation was observed in completely dose-related manner, regardless of the amount of [Ca2+]i. In the same condition, the degree of myosin light chain (P20) phosphorylation, however, was well correlated with ATP secretion and [Ca2+]i, when platelets were stimulated by lower dose of thrombin. The similar results were obtained in platelets stimulated by STA2. These findings suggested that P20, but not P47, phosphorylation in activated platelets is mediated by a rise of [Ca2+]i and is well correlated with the secretory reaction. It was unlikely that P47 phosphorylation plays any role in promoting platelet activation. 相似文献
43.
Ant nio F. Ambr sio Jo o O. Malva Ars lio P. Carvalho Caetana M. Carvalho 《European journal of pharmacology》1997,340(2-3):301-310
The effects of the adenosine A1 receptor agonist, N6-cyclopentyladenosine (CPA), on both the increase in intracellular free Ca2+ concentration ([Ca2+]i) and on the release of endogenous glutamate in rat hippocampal synaptosomes were studied. The inhibitory effect of CPA on the increase in [Ca2+]i stimulated with 4-aminopyridine was neutralized by the adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). The inhibitory effect of CPA was greater in synaptosomes from the CA1 subregion than in whole hippocampal synaptosomes. The inhibitory effects of both CPA and of the Ca2+ channel blockers, ω-conotoxin GVIA, ω-conotoxin MVIIC or ω-conotoxin GVIA plus ω-conotoxin MVIIC, were greater than those caused by the Ca2+ channel blockers. The release of endogenous glutamate was inhibited by 41% by CPA. The inhibition observed when CPA and ω-conotoxin GVIA or CPA and ω-conotoxin MVIIC were present was also greater than the inhibition by the Ca2+ channel blockers alone. The presence of both ω-conotoxin GVIA and ω-conotoxin MVIIC did not completely inhibit the release of glutamate, and CPA significantly enhanced this inhibition. The membrane potential and the accumulation of []tetraphenylphosphonium of polarized or depolarized synaptosomes was not affected by CPA, suggesting that adenosine did not increase potassium conductances. The present results suggest that, in hippocampal glutamatergic nerve terminals, adenosine A1 receptor activation partly inhibits P/Q- and other non-identified types of Ca2+ channels. 相似文献
44.
Youngnam Kang Takashi Okada Harunori Ohmori 《The European journal of neuroscience》1998,10(4):1363-1375
We report here on the ionic mechanisms underlying the depolarizing afterpotential (DAP) in neocortical pyramidal cells, with special interest in those underlying the burst afterdischarge. Injections of short depolarizing current pulses under whole-cell current clamp with a CsCl-based internal medium generated, in most pyramidal cells, a single action potential with a plateau phase (plateau-AP), followed by a slowly decaying DAP both in the absence and presence of TTX. Under voltage-clamp, the same cells displayed a slow tail current (tail-I) at the offset of depolarization. When intracellular free Ca2+ was chelated with 10 mm BAPTA or when extracellular Ca2+ was replaced with equimolar Ba2+, neither the slow DAP nor the slow tail-I was observed. Extracellular application of Co2+ or Cd2+ reduced Ca2+ currents and the slow tail-I. Cation substitution experiments revealed that the channel generating the slow tail-I was permeable to K+ and Cs+ more than to Na+ (PK≈PCs > PNa > PNMDG≈PTEA). The cationic slow tail-I was not reduced by applying antagonists of the metabotropic glutamate receptor (MCPG, 1 mm ) and the muscarinic receptor (atropine, 1–10 μm ). Thus, the slow DAP was produced by activation of the cationic channel whose gating is solely dependent on [Ca2+]i. An increase in [K+]o from 3 to 6 or 9 mm enhanced the slow DAP, and resulted in a generation of burst afterdischarges. An anticonvulsant, phenytoin (PT; 1–10 μm ) suppressed the slow DAP while enhancing the plateau-AP in the presence of TTX, most likely by blocking the cationic channel. 相似文献
45.
舒血宁治疗脑衰弱综合征的双盲对照研究 总被引:1,自引:0,他引:1
143例脑衰弱综合征患者随机分成舒血宁组和对照组,进行双盲的前瞻性研究。通过脑衰弱量表,打洞试验,连线实验的回查,结果表明:应用舒血宁治疗脑衰弱综合征,整体疗效明显优于对照组,脑衰弱量表的总评分显著优于对照组,而且对脑衰弱量表各个症状都有显著改善,易激惹,烦恼两项症状降分幅度较大,打洞、连线试验表明舒血宁治疗后患者的注意力、记忆力都有明显的改善,而且没有发现明显副作用。作者认为舒血宁治疗脑衰弱综合征有显著的作用,作为一种治疗脑血管疾患伴发精神症状和早期预防脑血管痴呆的新药是可行的。 相似文献
46.
内皮超极化因子(EDHF)是由内皮释放的NO和PGI_2以外的另一种舒张因子,它通过使平滑肌细胞膜超极化而舒张血管,是内皮依赖性血管松驰的第3种重要机制。EDHF可能是花生四烯酸的细胞色素P450代谢产物EET-s,乙酰胆碱、缓激肽等激动剂作用于内皮细胞,使细胞内游离钙浓度升高,合成和(或)释放EDHF,作用于平滑肌细胞膜,激活钙依赖性钾通道,使细胞膜超极化,抑制电压依赖性钙通道的开放,引起血管松弛。在大血管中NO-cGMP松弛机制可能占主导地位,并且抑制EDHF生成;而在阻力小血管,EDHF则可能是引起血管松弛的主要因素。 相似文献
47.
Summary A single glass micropipette voltage clamp technique with intracellular dialysis was used to study the effects of the trapidil derivatives AR 12–456 and AR 12–463 on Ca channel currents carried by Bat+ in isolated ventricular cells from mice hearts. Inspite of a more potent inhibition of the cAMP phosphodiesterase from heart (Bartel et al. 1985) a reversible Ca channel blocking action of both compounds could be observed. The concentration of half maximal block was calculated to about 50 mol/l for both derivatives tested. Neither a shift in the current-voltage relationships nor a significant change in the potential for half maximal activation was found. The maximal Ba2+ -conductance was reduced. The steady state inactivation was shifted towards more negative potentials by application of 100 mol/l AR 12–463. The decay of the Ba currents was accelerated in the range of the applied test potentials between –20 and +20 mV. It is concluded that the new trapidil derivatives with more potent inhibitory action on cardiac phosphodiesterase than trapidil can block myocardial Ca channels.
Send offprint requests to B. Nilius 相似文献
48.
Functional topography of discrete domains of human CD38 总被引:6,自引:0,他引:6
Ausiello CM Urbani F Lande R la Sala A Di Carlo B Baj G Surico N Hilgers J Deaglio S Funaro A Malavasi F 《Tissue antigens》2000,56(6):539-547
49.
The dependence of twitch relaxation on sodium ions and on internal Ca2+ stores in voltage clamped frog atrial fibres 总被引:5,自引:0,他引:5
Marie-Jeanne Roulet K. G. Mongo G. Vassort Renée Ventura-Clapier 《Pflügers Archiv : European journal of physiology》1979,379(3):259-268
Frog heart relaxation was analyzed under voltage clamp conditions as the tension decay observed after the membrane potential had been returned to its resting value. The tension decayed exponentially with a time constant of 188±3.8 ms SEM. The relaxation rate decreased with the external Na concentration. It fell to about one tenth in a Na-free solution. Increasing the intracellular Na-content by an application of veratrine also decreased the relaxation rate. Thus relaxation seems dependent on the Na gradient. The relaxation rate decreased within one second upon switching from a high to a low Na-containing solution. The relaxation rate reached a minimum before rising slightly to a new steady state value. This rebound may reflect the partial recovery of the Na gradient since a fast variation in [Na]i follows alteration of [Na]o. Mn and La ions also slowed relaxation. In a Na-free solution, adrenaline accelerated tension decay, an effect not noticeable in frog heart contained in Ringer solution. Other cAMP-promoting agents, such as dibutyryl-cAMP and aminophylline, also increased relaxation rate.It is concluded that in frog myocardium, part of the decrease of the intracellular Ca2+-concentration which occurs during each cardiac cycle could be dependent on a Na–Ca exchange mechanism. The relative importance of this mechanism, versus internal Ca sequestration, in the relaxation of tension may well be greater in contractile tissues whose cells have a large surface/volume ratio. 相似文献
50.
Gianfranco Liguri Cristina Cecchi Stefania Latorraca Alessandro Pieri Sandro Sorbi Donatella Degl'Innocenti Giampietro Ramponi 《Neuroscience letters》1996,210(3):153-156
Acylphosphatase (ATPase), an enzyme that modulates the activity of Ca2+-ATPase by hydrolysing its phosphorylated moiety, has been found to be significantly higher in cultured skin fibroblasts from donors affected by early onset familial Alzheimer's disease (EOFAD) with PS-1 and PS-2 gene mutations. Of the two known isoenzymes of acylphosphatase, only the erythrocyte one accounts for the total increase in activity. No relevant alteration was observed in phosphotyrosine phosphatase activity (PTPase), in Ca2+-ATPase and Na+,K+-ATPase activities of the same cells as compared to age-matched controls. This finding could suggest a possible explanation for the calcium-dependent biochemical alterations previously described in Alzheimer's disease fibroblasts. 相似文献