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991.
新生儿重症监护病房中遗传代谢病的临床特点及分析 总被引:3,自引:0,他引:3
目的提高临床医生对重症监护病房新生儿期发生的遗传代谢病的认识,提高早期诊断率。方法对2005年5月-2006年2月NICU中新生儿早期原因不明的严重酸中毒、高血钾、猝死、窒息等进行尿气相色谱-质谱仪检测;同时部分检测血乳酸、丙酮酸、血氨等。结果7例早期新生儿分别于出生时15小时、2天、3天、4天、6天发病,诊断为先天性丙酮酸代谢障碍1例、同型半胱氨酸血症1例、有机酸血症2例、戊二酸尿症Ⅱ型1例、酪氨酸血症1例、先天性肾上腺皮质增生症1例。结论NICU应警惕早期新生儿遗传代谢病,可利用目前的技术力量提高诊断率。 相似文献
992.
Vacher C Mañanos EL Breton B Marmignon MH Saligaut C 《Journal of neuroendocrinology》2000,12(12):1219-1226
The two gonadotrophins follicle stimulating hormone (FSH) and luteinizing hormone (LH) have distinct temporal expression and release profiles in fish, but little is known regarding their neuroendocrine control, especially for FSH. The present experiments were performed on previtellogenic, mature and preovulatory female trout. The catecholamine synthesis inhibitor, alpha-methyl-p-tyrosine, increased plasma LH and FSH concentrations of mature fish. The dopamine agonist apomorphine decreased and the dopamine antagonist domperidone increased plasma LH concentration of preovulatory fish and delayed ovulation, but did not modify plasma FSH concentration. The dopamine D2 agonist bromocryptine inhibited LH release in cultured gonadotrophs from mature and preovulatory fish, but not from previtellogenic fish. Bromocryptine also significantly inhibited basal and salmon gonadotrophin releasing-hormone (sGnRH)-induced FSH release from cultured gonadotrophs of mature fish, but not of preovulatory fish, and increased FSH release from gonadotrophs of previtellogenic fish. The dopamine D1 agonist SKF 38393 had no observed effect on the release of FSH and LH, at any reproductive stage studied. The D1 agonist SKF 38393, the D2 agonist bromocriptine and sGnRH had no observed effects on cell contents of FSH and LH. Taken together, these data suggest that, at the level of the pituitary, dopamine inhibits LH release as vitellogenesis proceeds, via activation of dopamine D2 receptors. We demonstrate for the first time in fish a control of FSH release (a dopamine control), especially in mature fish which have low circulating concentrations of FSH. 相似文献
993.
994.
应用层次分析加权法评价医院质量 总被引:1,自引:0,他引:1
医院工作包括若干层次和若干指标,是难以完全用定量的方法精确地加以评定的,而层次分析法正是对非定量事物作定量分析的一种简便方法。本研究运用此法对某综合医院1993~2002年的工作进行了评价。 相似文献
995.
高效液相色谱法测定清肺抑火片中黄芩苷的含量 总被引:1,自引:0,他引:1
目的:探讨清肺抑火片的含量测定方法.方法:采用高效液相色谱法(HPLC法)测定清肺抑火片黄芩中黄芩苷的含量.色谱柱为Elite 0DS C18柱(250 mm×4.0 mm,5μm),流动相为甲醇-水-磷酸(45:55:0.2),流速为1 mL/min,检测波长为315 nm.结果:回归方程为Y=85.915 4 2 701.674 3X,r=0.999 3,平均回收率为97.93%,RSD为1.76%(n=6).结论:HPLC法简便、快速、可靠,可用于清肺抑火片的质量控制. 相似文献
996.
Xuejun J Yin Caroline C Dong Jane Y C Ma James M Antonini Jenny R Roberts Mark W Barger Joseph K H Ma 《Toxicological sciences》2005,88(1):73-81
Studies have shown that exposure to diesel exhaust particles (DEP) suppresses pulmonary host defense against bacterial infection. The present study was carried out to characterize whether DEP exposure exerts a sustained effect in which inhaled DEP increase the susceptibility of the lung to bacterial infection occurring at a later time. Brown Norway rats were exposed to filtered air or DEP by inhalation at a dose of 21.2 +/- 2.3 mg/m3, 4 h/day for 5 days, and intratracheally instilled with saline or 100,000 Listeria monocytogenes (Listeria) 7 days after the final DEP exposure. Bacterial growth and cellular responses to DEP and Listeria exposures were examined at 3 and 7 days post-infection. The results showed that inhaled DEP prolonged the growth of bacteria, administered 7 days post DEP exposure, in the lung as compared to the air-exposed controls. Pulmonary responses to Listeria infection were characterized by increased production of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-12, and IL-10 by alveolar macrophages (AM) and increased presence of T lymphocytes and their CD4+ and CD8+ subsets in lung draining lymph nodes that secreted elevated levels of IL-2, IL-6, IL-10, and interferon (IFN)-gamma. Diesel exhaust particles were found to inhibit Listeria-induced production of IL-1beta and TNF-alpha, which are responsible for the innate immunity, and IL-12, which initiates the development of T helper (Th)1 responses, but enhance Listeria-induced AM production of IL-10, which prolongs Listeria survival in these phagocytes. The dual action of DEP on AM production of IL-12 and IL-10 correlated with an inhibition of the development of bacteria-specific T lymphocytes by DEP. Cytokine production by lymphocytes from DEP- and Listeria-exposed rats showed a marked decrease in the production of IL-2, IL-10, and IFN-gamma compared to Listeria infection alone, suggesting either that DEP inhibit the production of cytokines by lymphocytes or that these lymphocytes contained T-cell subsets that are different from those of Listeria infection alone and less effective in mediating Th1 immune responses. This study demonstrates that inhaled DEP, after a 7-day resting period, increase the susceptibility of the lung to bacterial infection occurring at a later time by inhibiting macrophage immune function and suppressing the development of T-cell-mediated immune responses. The results support the epidemiological observations that exposure to DEP may be responsible for the pulmonary health effects on humans. 相似文献
997.
Caroline C Dong Xuejun J Yin Jane Y C Ma Lyndell Millecchia Mark W Barger Jenny R Roberts Xing-Dong Zhang James M Antonini Joseph K H Ma 《Toxicological sciences》2005,88(1):150-160
Exposure to diesel exhaust particles (DEP) during the sensitization process has been shown to increase antigen-specific IgE production and aggravate allergic airway inflammation in human and animal models. In this study, we evaluated the effect of short-term DEP exposure on ovalbumin (OVA)-mediated responses using a post-sensitization model. Brown Norway rats were first exposed to filtered air or DEP (20.6 +/- 2.7 mg/m3) for 4 h/day for five consecutive days. One day after the final air or DEP exposure (day 1), rats were sensitized with aerosolized OVA (40.5 +/- 6.3 mg/m3), and then again on days 8 and 15, challenged with OVA on day 29, and sacrificed on days 9 or 30, 24 h after the second OVA exposure or the final OVA challenge, respectively. Control animals received aerosolized saline instead of OVA. DEP were shown to elicit an adjuvant effect on the production of antigen-specific IgE and IgG on day 30. At both time points, no significant airway inflammatory responses and lung injury were found for DEP exposure alone. However, the OVA-induced inflammatory cell infiltration, acellular lactate dehydrogenase activity and albumin content in bronchoalveolar lavage (BAL) fluid, and numbers of T cells and their CD4+ and CD8+ subsets in lung-draining lymph nodes were markedly reduced by DEP on day 30 compared with the air-plus-OVA exposure group. The OVA-induced nitric oxide (NO) in the BAL fluid and production of NO, interleukin (IL)-10, and IL-12 by alveolar macrophages (AM) were also significantly lowered by DEP on day 30 as well as day 9. DEP or OVA alone decreased intracellular glutathione (GSH) in AM and lymphocytes on days 9 and 30. The combined DEP and OVA exposure resulted in further depletion of GSH in both cell types. These results show that short-term DEP exposure prior to sensitization had a delayed effect on enhancement of the sensitization in terms of allergen-specific IgE and IgG production, but caused an attenuation of the allergen-induced airway inflammatory responses. 相似文献
998.
Qiang Zhang Peng Ma Weiqun Wang Richard B Cole Guangdi Wang 《Drug metabolism and disposition》2005,33(4):508-517
Diarylpyrazoles are a group of 1,5-diphenylpyrazole analogs of which several have been found to exhibit antagonist properties toward the cannabinoid receptors. SR141716A [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide], the first reported antagonist, is a highly potent and selective CB1 receptor ligand that prevents or reverses CB1-mediated effects. Other analogs, such as AM251 [N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide] and AM281 [1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-4-morpholinyl-1H-pyrazole-3-carboxamide], have also shown high binding affinities to the central cannabinoid receptor and behave as antagonists/inverse agonists. There has been no report on the metabolism of any of the diarylpyrazoles, and it is unknown whether their metabolites retain any receptor binding properties. We report a study of the in vitro metabolisms of three diarylpyrazole analogs, SR141716A, AM251, and AM281, in rat liver microsomes. The metabolic profile was obtained using high-performance liquid chromatography with UV and mass spectrometry detectors. All identified metabolites are characterized by structural modifications on the terminal group of the 3-substituent. Thus, three pairs of isomeric metabolites were identified from the microsomal incubation of SR141716A; these metabolites are products of hydroxylation, hydroxylation followed by dehydration, and a combination of the two. For AM251, only four metabolic products were detected, with two resulting from monohydroxylation of the piperidine ring and the other two being products of dehydration of the first pair of metabolites. For AM281, in which the terminal group of the 3-substituent is a morpholine ring, dehydration of the first two metabolites yielded a single third metabolite due to only one possible position for the carbon-carbon double bond on the morpholinyl ring. 相似文献
999.
1000.
灯盏花素在家犬与家兔体内的药代动力学研究 总被引:5,自引:0,他引:5
目的:研究灯盏花素在家犬与家兔体内的药代动力学.方法:采用液-液萃取法制备血样供试品,HPLC法测定.结果:灯盏花素在家犬体内的过程符合双室模型,主要药动学参数为:A=56.93±23.14,B=1.61±1.11,α=0.2328±0.1321min-,β=0.0255±0.0187min-,T1/2α=2.98±1.42min,T1/2β=27.14±14.35min,K21=0.0312±0.0112min-,K10=0.1904±0.1319min-,K12=0.0367±0.0306min-1,CL=39.41±20.44ml·min-,AUC=3074±1055mg·min·L-;灯盏花素在家兔体内的过程符合双室模型,主要药动学参数为:A=2.64±1.12,B=0.28±0.12,α=0.1439±0.0681min-,β=0.0162±0.0456min-,t1/2α=4.82±1.65min,t1/2β=42.66±18.77min,K21=0.0285±0.0147min-,K10=0.0820±0.00378min-,K12=0.0496±0.0241min-,CL=337.05±156.48ml·min-1,AUC=356±114mg·min·L-1.结论:灯盏花素在家犬与家兔体内半衰期很短,其作用时间短,消除速度快. 相似文献