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11.
本文对8名受试者在0.25~0.27MPa下进行三种氧剂量暴露后的肺呼吸功能和X线胸片跟踪观察,目的在于验证整体实验功能结果对本室以往肺表面活性物质(PS)物理特性测定结果的符合性。结果表明,氧暴露剂量达到1060UPTD(肺型氧中毒剂量单位)时,对呼吸道粘膜、肺泡内皮细胞可产生一定程度影响,导致FEV1、FEV,%、MMF、V10(呼气流速)显著改变(P<0.05或P<O.01),但在停止暴露后4—12h内上述指标完全恢复。以上与本室以往PS物理特性测定结果相一致。本义肺活量降低程度较Wright(1972)报道的小,X线胸片无异常;因此,间断用氧要达到连续用氧的等效剂量,应对Wright计量法进行一些修正。 相似文献
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本组老年脑出血发病率57%,明显高于中、青年组脑出血。首要病因是高血压病,社会环境变迁是老年脑出血的重要因素。CT扫描特点为①型别:壳核出血最多(35.4%)、其次为丘脑(29%)、脑叶(21.4%)、其它型别均低于5%;②血肿量:小量出血最多(68.8%)。预后特点是存活率较高87.2%、死亡率仅12.8%。 相似文献
14.
目的探讨呼吸障碍患者低通气时出现心律失常的发生情况,及不同类型的睡眠障碍诱发心律失常的临床特点。方法654例患者在多导睡眠图(PSG)监测的同时,观察心电图的动态变化,并对睡眠呼吸障碍时发生心律失常的临床特点进行分析。结果睡眠障碍组发生心律失常的情况显著增加,在OSAS类型睡眠障碍时尤为显著。结论睡眠呼吸暂停越严重,心律失常的发生率越高;此时是否有必要单纯应用抗心律失常药物需要临床研究进一步探讨。 相似文献
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Effect of Histamine Receptor Blocking on Human Antibody-dependent Cell-mediated Cytotoxicity 总被引:1,自引:0,他引:1
I. LÁNG K. TÖRÖK P. GERGELY K. NÉKÁM GY. PETRÁNYI 《Scandinavian journal of immunology》1981,13(4):361-366
The effect of H1 and H2 receptor-blocking agents on antibody-dependent cell-mediated cytotoxicity (ADCC) was studied. The H1 receptor-blocker clemastinum and the H2 receptor blocker cimetidine dose-dependently inhibited the antibody-dependent cytotoxic activity of normal human peripheral blood mononuclear cells on chicken erythrocytes. The inhibition cannot be explained either by a direct toxic effect on effector cells or by blocking of Fc receptors. The possible involvement of histamine receptor-bearing effector cells in human ADCC is suggested. 相似文献
17.
Mouse antibodies were prepared to human amniotic fluid fibronectin by means of somatic cell hybrids. Comparison of immunological reactivity of antibodies with amniotic and plasma fibronectin revealed that the two molecules had very similar patterns of antigenic determinants. Antibodies from one cell population, however, bound belier to amniotic fluid fibronectin, indicating that there is a difference in the molecular structure of fibronectins isolated from the two sources. 相似文献
18.
John C. Anthes Robert W. Bryant Mark W. Musch Kwokei NG Marvin I. Siegel 《Inflammation》1986,10(2):145-156
The human promyelocytic leukemia cell line HL60 can be differentiated to mature granulocytes upon exposure to DMSO (1.3%, 6 days). The ability of these cells to metabolize arachidonic acid via the 5-lipoxygenase pathway to form 5-HETE, LTB4, and 5,12-diHETEs, has been previously documented. However, the production of peptidoleukotrienes by DMSO-differentiated HL60 cells has not been previously reported. Arachidonic acid metabolites produced via 5-lipoxygenase were identified by reverse-phase, high-performance liquid chromatography, immunoreactivity specific for peptidoleukotriene, glutamyl transpeptidase transformation, characteristic UV spectra, and GC mass spectra. Leukotriene synthesis in the DMSO-differentiated HL60 cell is maximal at 5 min when stimulated with the calcium ioniphore, A23187 (1M), in the presence of calcium. These cells produce 12.94±1.8 ng/106 cells of LTC4 and 3.8±0.4 ng/106 cells of LTB4. LTC4 and LTB4 are also synthesized in the undifferentiated cell when stimulated with 1M A23187 and 1 mM Ca2+, but in much smaller quantities, i.e., 1.91±0.42 ng/106 cells of LTC4 and 0.41 ng±0.06/106 cells of LTB4. The synthetic chemotactic peptide, f-Met-Leu-Phe, also elicits formation of LTC4 and LTB4 in a dose-dependent manner in the presence of exogenously added calcium. Maximal stimulation of DMSO-differentiated cells with f-Met-Leu-Phe produces 2.5±0.2 ng of LTC4 and 1.45±0.2 ng of LTB4 per 106 cells. The observation that DMSO-differentiated HL60 cells produce LTC4, as well as other 5-lipoxygenase products, increases the utility of this cell line for unraveling the regulation of leukotriene biosynthesis by granulocytes. 相似文献
19.
软骨组织工程中力学因素的影响及应用 总被引:1,自引:0,他引:1
力学因素是软骨组织工程中的重要影响因素之一。近年来的研究表明,力学作用可以刺激细胞因子及激素的分泌,改变三维支架上培养的软骨细胞的新陈代谢,从而促进软骨组织的生长与重建。目前已经有诸多关于体外构建软骨组织的报道,但对于其中的力学因素的影响(包括力学因素对软骨细胞增殖的促进及力学刺激的传导机制等)还没有完全认识。就以上几方面做一综述,并简单介绍生物反应器在软骨组织工程中的应用。 相似文献
20.
Predominance of null mutations in ataxia-telangiectasia 总被引:15,自引:4,他引:15
Gilad S; Khosravi R; Shkedy D; Uziel T; Ziv Y; Savitsky K; Rotman G; Smith S; Chessa L; Jorgensen TJ; Harnik R; Frydman M; Sanal O; Portnoi S; Goldwicz Z; Jaspers NG; Gatti RA; Lenoir G; Lavin MF; Tatsumi K; Wegner RD; Shiloh Y; Bar-Shira A 《Human molecular genetics》1996,5(4):433-439
Ataxia-telangiectasia (A-T) is an autosomal recessive disorder involving
cerebellar degeneration, immunodeficiency, chromosomal instability,
radiosensitivity and cancer predisposition. The responsible gene, ATM, was
recently identified by positional cloning and found to encode a putative
350 kDa protein with a Pl 3-kinase-like domain, presumably involved in
mediating cell cycle arrest in response to radiation-induced DNA damage.
The nature and location of A-T mutations should provide insight into the
function of the ATM protein and the molecular basis of this pleiotropic
disease. Of 44 A-T mutations identified by us to date, 39 (89%) are
expected to inactivate the ATM protein by truncating it, by abolishing
correct initiation or termination of translation, or by deleting large
segments. Additional mutations are four smaller in-frame deletions and
insertions, and one substitution of a highly conserved amino acid at the Pl
3-kinase domain. The emerging profile of mutations causing A-T is thus
dominated by those expected to completely inactivate the ATM protein. ATM
mutations with milder effects may result in phenotypes related, but not
identical, to A-T.
相似文献