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51.
52.
利用全细胞膜片钳技术 ,采用胶原酶B急性分离的大鼠心室肌细胞 ,研究了牛黄酸和二甲基 -氨氯吡咪对心肌细胞膜Na /Ca2 交换电流的影响。结果表明 ,10 μmol,2 0 μmol和 4 0 μmol的二甲基 -氨氯吡咪可使Ni2 敏感电流浓度依赖性地增加 ;膜电位为 5 0mV时分别增加 ( 2 7± 7) % ,( 12 1± 4 3 ) % ,和 ( 173± 68) % ;膜电位为 - 10 0mV时分别增加 ( 110±5 2 ) % ,( 2 2 1± 88) %和 ( 2 81± 80 ) %。牛黄酸对Na /Ca2 交换的内向和外向电流均无影响 相似文献
53.
Huang FY 《Maternal and child health journal》1997,1(2):69-80
Objectives: This study assesses the health insurance coverage of children of immigrants in the United States and variations among immigrant groups. Method: The study uses data from the March supplements of the 1994 and 1996 Current Population Survey to compare health insurance coverage of children who report foreign parentage. Separate logistic regressions are conducted to estimate the likelihood of being covered by any insurance, public insurance, and private insurance. Results: 27.3% of all children of immigrants are without health insurance, 34.1% are on public insurance, and 44.3% have private insurance. Foreign-born children who have not yet become U.S. citizens are the most likely to be without health insurance (38.0%). Many of these children are not covered because their parents are unable to find jobs that provide coverage and Medicaid fails to enroll as many of them as possible. Overall, the children's chances of being covered by any health insurance vary little according to when their parents came to this country. However, children of recent immigrants are more likely to rely on public health insurance (40.1% vs. 24.8%) and less likely to be covered through private sources (36.8% vs. 60.6%) than those of established immigrants. Among immigrant groups, children of Haitian (48.4%) and Korean (45.3%) immigrants are at the highest risks of being uninsured. Both children of the Dominican Republic (65.9%) and Laos (83.3%) report high rates of public insurance coverage. Conclusions: Greater disparity in health insurance coverage among children of immigrants is expected once the new welfare reform bills take effect. In particular, noncitizen children, children of recent immigrants, illegal immigrants, and Dominican Republican immigrants will be affected most. Efforts aimed at reducing the harm should target these vulnerable groups. 相似文献
54.
Hideo Tanaka Yoshizumi Habuchi Taku Yamamoto Manabu Nishio Junichiro Morikawa Manabu Yoshimura 《British journal of pharmacology》1997,122(2):321-329
- The effects of endothelin-1 (ET-1) on sinoatrial (SA) node preparations of the rabbit heart were studied by means of whole-cell clamp techniques.
- ET-1 at 1 nM slowed the spontaneous beating activity and rendered half of the cells quiescent. At a higher concentration of 10 nM, the slowing and cessation of spontaneous activity were accompanied by hyperpolarization.
- In voltage-clamp experiments, ET-1 decreased the basal L-type Ca2+ current (ICa(L)) dose-dependently with a half-maximal inhibitory concentration (EC50) of 0.42 nM and maximal inhibitory response (Emax) of 49.5%. The delayed rectifying K+ current (IK) was also reduced by 33.2±11.1% at 1 nM. In addition, an inwardly rectifying K+ current was activated by ET-1 at higher concentrations (EC50=4.8 nM). These ET-1-induced changes in membrane currents were abolished by BQ485 (0.3 μM), a highly selective ETA receptor antagonist.
- When ICa(L) was inhibited by ET-1 (1 nM), subsequent application of 10 μM ACh showed no additional decrease in ICa(L), suggesting the involvement of cyclic AMP in the effects of ET-1 on ICa(L). In contrast, 1 nM ET-1 further decreased ICa(L) in the presence of 10 μM ACh, suggesting that ET-1 activates some additional mechanism(s) which inhibit ICa(L). The ET-1-induced ICa(L) inhibition was abolished by protein kinase A inhibitory peptide (PKI, 20 μM) or H-89 (5 μM). However, the ICa(L) inhibition was not affected by methylene blue (10 μM), suggesting a minor role for cyclic GMP in the effect of ET-1 under basal conditions.
- ET-1 failed to inhibit ICa(L) when the pipette contained GDPβS (200 μM). However, incubation of the cells with pertussis toxin (PTX, 5 μg ml−1, >6 h) only reduced the ET-1-induced inhibition to 21.5±9.5%, whereas it abolished the inhibitory effect of ACh on ICa(L).
- Intracellular perfusion of 8-bromo cyclicAMP (8-Br cyclicAMP, 500 μM) attenuated, but did not abolish the inhibitory effect of ET-1 on ICa(L). This 8-Br cyclicAMP-resistant component (17.5±14.4%, n=20) was not affected by combined application of 8-Br cyclicAMP with 8-bromo cyclicGMP (500 μM), ryanodine (1 μM) or phorbol-12-myristate-13-acetate (TPA; 50 nM).
- In summary, ET-1 exerts negative chronotropic effects on the SA node via ETA-receptors. ET-1 inhibits both ICa(L) and IK, and increases background K+ current. The inhibition of ICa(L) by ET-1 is mainly due to reduction of the cyclicAMP levels via PTX-sensitive G protein, but some other mechanism(s) also seems to be operative.
55.
The rationale and methodology behind the Australian Quality Assurance Project is described. The Project aimed to develop guidelines for treatment content based on three sources of information: research findings, current practice and expert opinion. The issue of the gap between research and practice is discussed, as well as the role of dissemination in altering clinician behaviour. 相似文献
56.
In sheep cardiac Purkinje fibers concentration-dependent inhibition of transient outward current (ito) by 4-aminopyridine (4-AP, 3-1000 mol/l) was recorded with the two-microelectrode voltage-clamp technique, and correlated effects on action potential duration measured at — 70 mV (APD-70) were investigatigated.Half-maximal inhibition of ito-amplitude occurred at 15 mol/l 4-AP. The drug exhibited no major effect on voltage-dependent control of inactivation but reduced the maximally available ito-current. At different activation frequencies (0.05 Hz, 0.25 Hz, 1 Hz) an equal amount of ito-current, measured as percentage of the respective control, was inhibited by 4-AP. The APD-70 was on the average increased by 4-AP (3–500 mol/l) in a concentration-dependont manner up to 151 % of control. The drug-induced prolongation, measured as percentage of the respective control, was independent of stimulation frequency (0.05 Hz, 0.25 Hz, 1 Hz). Prolongation of APD-70 was on the average more pronounced for short action potentials (APD-70<150 ms: 169 % of reference) than for longer ones (APD-70 150–300 ms: prolongation to 117 % of reference; 500 mol/l 4-AP; 0.25 Hz stimulation rate). Few long control signals (APD-70 >300 ms) were shortened by 4-AP. These results indicate that inhibition of ito-current by appropriate drugs will result in a reduction of inhomogeneity of action potential duration. 相似文献
57.
The effects of the phenylalkylamines verapamil, gallopamil, and devapamil on L-type calcium currents (ICa) were studied in ventricular myocytes from rat hearts using the whole-cell patch-clamp technique. In particular, the question was addressed, whether the pharmacological binding sites for these drugs were located at the inner and/or at the outer surface of the cell membrane. Therefore, tertiary verapamil, gallopamil, and devapamil and their corresponding quaternary derivatives were applied either from the outside or the inside of the cell membrane. Extracellular application of verapamil, gallopamil and devapamil (each at 3 M) reduced Ica to 16.1 ±8.6%, 11 ± 8.9 %, and 9.3 ± 6 % of control, respectively. Intracellular application of the same substances, via the patch pipette filled with 30 M of either verapamil, gallopamil, or devapamil, failed to depress ICa. The quaternary derivatives of the phenylalkylamines (30 M) were ineffective both when applied extracellularly or intracellularly. It is suggested that phenylalkylamines block ICa in ventricular myocytes by acting on a binding site of the calcium channel molecule located at the outer surface of the cell membrane. 相似文献
58.
目的观察正常及模拟“缺血”时胺碘酮对绵羊心室浦肯野纤维起搏离子流(If)的影响。方法双微电极电压钳制术,使膜电位过度极化以激活If。结果胺碘酮1×10-5mol/L在正常台氏液中显著降低浦肯野纤维If幅值;模拟“缺血”也使If幅值降低,在此基础上,胺碘酮使If幅值进一步减小,加剧了“缺血”对If离子流的抑制作用。结论提示胺碘酮能抑制心肌缺血时心室正常自律性活动。 相似文献
59.
60.
Piccolino M Vellani V Rakotobe LA Pignatelli A Barnes S McNaughton P 《The European journal of neuroscience》1999,11(11):4134-4138
At the first synaptic level of the vertebrate retina, photoreceptor light responses are transmitted to second order neurones through a chemical synapse based on a tonic release of neurotransmitter modulated by graded changes of presynaptic potential. The possibility that such synapses could work through a Ca2+-independent process had been proposed by previous authors, based on the persistence of transmission process in low Ca2+ media containing Co2+ or Ni2+ ions. Recently, we were able to explain these results within the framework of the classical calcium-hypothesis of synaptic transmission by taking into account the modifications of presynaptic surface potential brought about by changes of divalent cation concentrations. Here we report data showing how a surface-charge hypothesis could account for several apparently paradoxical effects of divalent cation manipulations such as: the enhancement of neurotransmitter release induced by low Ca2+ media; the transmission "unblocking" effect of Zn2+, Co2+ and Ni2+; and the reversal of transmission polarity induced by application of low Ca2+ media containing Cd2+ or Mg2+ ions. 相似文献