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61.
小檗碱对大鼠再灌心律失常及钙调节的作用 总被引:8,自引:0,他引:8
小檗碱(Ber,10mg·kg-1)使缺血/再灌后VT发生率明显降低,持续时间明显缩短,无1例发生VF及死亡,与对照组比较差异有显著性。离体实验表明:小檗碱(30μmol·L-1),能抑制高钙条件下Ca2+内流,而增加低钙条件下的Ca2+内流。结果表明:小檗碱具有预防再灌心律失常作用;不同Ca2+浓度能够影响心肌45Ca内流;小檗碱对心肌Ca2+内流有双向调节作用,尤其在高Ca2+条件下,降低45Ca内流可能是其抗心律失常作用机制之一。 相似文献
62.
In a sample of 55 consecutive methadone maintenance admissions to our clinic, 42% were diagnosed with antisocial personality disorder (ASPD) using the National Institute of Mental Health Diagnostic Interview Schedule NIMH DIS. Individuals with ASPD exhibited greater risk for HIV infection as defined by more sexual contacts, needle use and equipment sharing. Data at 1 year follow-up were obtained on this group of patients. The objective was to compare the ASPD and non-ASPD groups with regards to demographics, drug abuse history, outcome and retention in treatment. There were no significant differences between the groups on any demographic or treatment outcome variables. Survival analysis indicated that there were no group differences in treatment retention. In conclusion, although there were no differences in treatment outcome between ASPD and non-ASPD groups it is possible that ASPD patients who drop out of treatment will be at higher risk for contracting and spreading HIV within the IV drug using population. These data also suggest that in this population the diagnosis of ASPD using primarily behavioral traits as measured in the NIMH-DIS-III, has little utility in predicting treatment outcome. 相似文献
63.
哈乐在良性前列腺增生伴急性尿潴留中的应用 总被引:5,自引:0,他引:5
目的 :探讨α1A肾上腺素能受体阻滞剂哈乐 (tamsulosin)对良性前列腺增生 (BPH)伴急性尿潴留病人的治疗作用。方法 :对 72例BPH伴急性尿潴留病人采用随机、对照研究 ,分为治疗组和对照组。病人均行保留导尿 ,口服抗生素治疗。治疗组加用哈乐 0 .4mg ,1次 /d ,连续服用 3次。 72h后拔除导尿管。 结果 :拔除导尿管后 4 4 % (32 / 72 )的病人能自行排尿。有效率治疗组为 6 1% (2 2 / 36 ) ,对照组为 2 8% (10 / 36 ) ,两组比较差异有显著性 (P <0 .0 1)。 结论 :对BPH伴急性尿潴留应用哈乐治疗 ,可提高早期拔除导尿管后病人自行排尿的成功率 ,且疗效与前列腺体积大小无关。 相似文献
64.
65.
The Effects of Na~+/Ca~(2+) exchange (NCX) on the Repolarization of Canine Ventricular Myocyte-Potential Arrhythmogenic Effect of NCX during a Mis-matched Repolarization and Relaxation Xiamen Zhongshan Hospital, Xiamen Medical College, Xiamen University@巩燕$Visiting scholar of cardiac arrhythmia research institute,university hospital of Oklahoma!U.S.A
@王焱
@BELA Szabo$Basic cardiac research laboratory,cardiac arrhythmia research institute,university hospital of Oklahoma!… 相似文献
66.
67.
Jose Rodriguez Wendy Jacques-Berg Coral Sanfeliu Ambrish J. Patel 《Brain research》1992,590(1-2):109-117
The possible involvement of ionotropic and metabotropic quisqualate (QA) receptors in neuronal plasticity was studied in cultured glutamtergic cerebellar or hippocampal cells in terms of the specific activity of phosphate-activated glutaminase, an enzyme important in the synthesis of the putative neurotransmitter pool of glutamate. When cerebellar of hippocampal neurons were treated with QA, it elevated the specific activity of glutaminase in a dose-dependent manner. The half-maximal effect was obtained at about 0.1 μM, the maximum increase was at about 1 μM, but levels higher than 10 μM QA produced progressive reduction in glutaminase activity. In contrast, QA had little effects on the activities of lactate dehydrogenase and aspartate aminotransferase and the amount of protein, indicating that the increase in glutaminase was relatively specific. The QA-mediated increase in glutaminase was mimicked by the ionotropic QA receptor agonist -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA; EC50, about 0.5 μM), but not by the metabotropic QA receptor agonist trans-(±)-1-aino-cyclopentyl-1,3,dicarboxyalte (t-ACPD; up to 0.5 mM). The specific ionotropic QA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) inhibited QA- and AMPA-mediated increases in glutaminase activity in a dose-dependent manner, whereas other glutamate receptor antagonists,
-2-amino-5-phosphonovalerate, γ-
-glutamyl aminomethyl sulphonic acid and γ-
-glutamyl diethyl ester were ineffective. The elevation of neurotransmitter enzyme was Ca2+-dependent. The increase in Ca2+ influx essentially through the activation of L-type voltage-operated Ca2+ channels, and not the mobilization of internal Ca2+ stores, was responsible for these QA receptor-mediated long-term plastic changes in hippocampal and cerebellar neurons. 相似文献
68.
Voltage-Gated calcium channels and nonvoltage-gated calcium uptake pathways in the rat incisor odontoblast plasma membrane 总被引:4,自引:1,他引:3
Odontoblasts participate actively in the transport and accumulation of Ca2+ ions to the mineralization front during dentinogenesis. These cells are known to carry membrane-bound ATP-driven pumps and
Na+/Ca2+ antiports for Ca2+ extrusion, but little is known about Ca2+ influx mechanisms into these cells. It has been shown that the administration of Ca2+ channel blockers in vivo strongly impairs Ca2+ uptake in the mineral phase during dentinogenesis in the rat; the present in vitro study is aimed at further elucidating
odontoblast Ca2+ uptake mechanisms. Dissected rat incisor odontoblasts exhibited a pronounced fluorescence when incubated with a fluorescently-labeled
(STBodipy) dihydropyridine, which is specific for voltage-gated Ca2+ channels of the L-type, and this binding was competitively abolished by nifedipine. As assayed by fluorescence spectrometry,
odontoblast Ca2+ uptake was enhanced by the agonistic dihydropyridine BAYK-8644 (5 μM) as well as by plasma membrane depolarization in a high
K+ (120 mM) medium. The Ca2+ uptake after depolarization was impaired by nifedipine (5 μM). When treated with the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA; 10 μM), a nonvoltage-gated uptake of 45Ca2+ was identified. This uptake was not influenced by nifedipine (20 μM) but was impaired by lanthanum ions (200 μM). A nonvoltage-gated
uptake of Mn2+ into CPA-treated cells could be traced using the fura-2 quenching technique. This CPA-induced Ca2+ flux was not caused by an alteration of the plasma membrane potential, as assayed with di-8-ANEPPS. The results demonstrate
that Ca2+ flux into dentinogenically active odontoblasts occurs through voltage-gated Ca2+ channels of the L-type and by nonvoltage-gated, agonist-sensitive Ca2+ uptake pathways.
Received: 6 November 1995 / Accepted: 21 February 1996 相似文献
69.
A. Saija P. Princi R. De Pasquale G. Costa G. B. De Sarro 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1992,88(1):151-157
Summary The genetically epileptic-prone rat (GEPR) is a valuable model for the study of gene-linked abnormalities involved in epilepsy. In comparison with normal Sprague-Dawley controls, we found, in GEPRs, a marked depression in local cerebral glucose utilization, widespread throughout the brain. This depression was accompanied by a significant increase of blood-brain barrier permeability and a reduction in regional blood volume. Finally GEPRs showed lower plasma levels of total triiodothyronine than normal controls. One can speculate that alterations in cerebral metabolism and microvascular regulation and thyroid hormone imbalance may be gene-linked factors involved in seizure susceptibility. 相似文献
70.
Tang Jian汤健 Wang Yu王瑜 Zkang Chenhui张晨晖 E. Costa Institute of Cardiovascular Research Beijing Medical University 《北京大学学报(医学版)》1994,(Z1)
THECLONINGOFNa ̄+/Ca ̄(2+)EXCHANGERGENEANDITSEXPRESSIONINBRAINISCHEMIATangJian汤健,WangYu王瑜,ZkangChenhui张晨晖,E.CostaInstituteofCar... 相似文献