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71.
单不饱和脂肪酸对心血管的保护作用 总被引:7,自引:0,他引:7
单不饱和脂肪酸(MUFA)是脂肪酸的一种,其碳链上只有一个双键。研究发现MUFA能够正向调节血脂代谢,降低低密度脂蛋白胆固醇(LDL)的氧化敏感性,保护血管内皮和降低血液高凝状态。本文将从以上几个方面介绍MUFA对心血管的保护作用。 相似文献
72.
通过对4种不同弱酸制成的乳酸杆菌阴道泡腾片质量的比较,探讨生物泡腾制剂中酸对乳酸杆菌的影响. 相似文献
73.
Cytochrome P450 epoxygenases as EDHF synthase(s) 总被引:2,自引:0,他引:2
The metabolism of arachidonic acid by cytochrome P450 (CYP) epoxygenases generates epoxyeicosatrienoic acids (EETs) which affect numerous cellular process including Ca(2+) signaling and the activity of Ca(2+)-dependent K(+) channels. The expression of the CYP epoxygenase(s) that generate EETs in endothelial cells is not constitutive but is determined by a number of physical (fluid shear stress and cyclic stretch) and pharmacological stimuli which also affect responses attributed to an endothelium-derived hyperpolarizing factor (EDHF). This review summarizes the role played by EETs, and the enzymes that generate and metabolize them, in EDHF-mediated responses. 相似文献
74.
目的 探讨奥利司他(Orlistat,赛尼可)对肥胖糖耐量低减(IGT)患者的干预效果。方法 患者随机分两组奥利司他治疗组(50例)和对照组(51例),治疗为期1年,于治疗前后测量血脂、口服糖耐量试验(OGTT)、体重、身高等指标。结果1年后,治疗组上述指标明显改善(P<0.01),其恶化为糖尿病的发病率明显低于对照组(P<0.01)。结论 在肥胖IGT干预治疗中,奥利司他加饮食和运动治疗后可使体重减轻,改善糖耐量,明显减少糖尿病的发生。 相似文献
75.
76.
Ling Luo Junzhao Ye Congxiang Shao Yansong Lin Yanhong Sun Shiting Feng Wei Wang Bihui Zhong 《Nutrients》2022,14(10)
Whether the associations between serum vitamin D (VitD) and metabolic-associated fatty liver disease (MAFLD) vary with chronic hepatitis B (CHB) infection has not been well established. This study aims to investigate the relationships between serum VitD and metabolism, liver fat content (LFC) and fibrosis among MAFLD patients with and without CHB. Consecutive subjects (healthy controls: 360, CHB: 684, MAFLD: 521, CHB with MAFLD: 206) were prospectively enrolled between January 2015 and December 2021. Anthropometric, laboratory, imaging, and histological evaluations were conducted, with LFC measured via magnetic resonance imaging-based proton density fat fraction (MRI-PDFF). Serum VitD levels were lower in MAFLD patients than in healthy controls and patients with CHB alone or overlapping with MAFLD (24.4 ± 8.1 vs. 29.0 ± 9.5 vs. 27.4 ± 9.6 vs. 26.8 ± 8.4 ng/mL respectively; p < 0.001 in one-way ANOVA test). After adjusting for confounding factors, including season, hypersensitive C-reactive protein, insulin resistance, liver stiffness measurements, sun exposure, exercise and dietary intake, multivariate linear regression analysis revealed that VitD remained significantly negatively correlated with LFC in MAFLD patients (β = −0.38, p < 0.001), but not in CHB with MAFLD patients. Moreover, quantile regression models also demonstrated that lower VitD tertiles were inversely associated with the risk of insulin resistance and moderate–severe steatosis in the MAFLD group (p for trend <0.05) but not in the MAFLD with CHB group. VitD deficiency was associated with the severity of metabolic abnormalities and steatosis independent of lifestyle factors in MAFLD-alone subjects but not in MAFLD with CHB subjects. 相似文献
77.
大黄素、小檗碱对HepG2细胞胰岛素抵抗的预防作用研究 总被引:1,自引:0,他引:1
目的:研究大黄素、小檗碱对HepG2细胞产生胰岛素抵抗的预防作用及机制。方法:首先用MTT法筛选大黄素、小檗碱作用于HepG2细胞的实验浓度,然后用软脂酸诱导HepG2细胞,同时分别加入大黄素、小檗碱干预,并设正常组、对照组进行比较,通过葡萄糖氧化酶法、蒽酮法、RT-PCR法,观察大黄素、小檗碱对HepG2细胞上糖代谢及瘦素长型受体、短型受体mRNA表达水平的影响。结果:对照组成为具有胰岛素抵抗的HepG2细胞,且细胞上瘦素长型及短型受体mRNA的表达水平较正常纽显著下降(P〈0.01);而大黄素、小檗碱组培养液中葡萄糖含量、细胞内糖原含量以及细胞上瘦素长型及短型受体mRNA的表达水平较正常组无明显改变(P〉0.05)。结论:大黄素、小檗碱均能预防HepG2细胞产生胰岛素抵抗,这一作用与它们影响HepG2细胞上糖代谢及瘦素受体mRNA表达水平有关。 相似文献
78.
Xiao-Yun Li Pei-Xuan Ji Xi-Xi Ni Yu-Xin Chen Li Sheng Min Lian Can-Jie Guo Jing Hua 《World journal of hepatology》2022,14(7):1365
BACKGROUNDLipid metabolism disorder and inflammatory-immune activation are vital triggers in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Various studies have shown that PPAR-γ exerts potent anti-inflammatory and immunomodulatory properties. However, little is known about the regulation of PPAR-γ activity in modulating cell crosstalk in NAFLD.AIMTo investigate whether the regulation of PPAR-γ activity in lipid-laden hepatocytes affects macrophage polarization and inflammation.METHODSPrimary hepatocytes were isolated from wild-type C57BL6/J mice or hepatocyte-specific PPAR-γ knockout mice and incubated with free fatty acids (FFAs). Macrophages were incubated with conditioned medium (CM) from lipid-laden hepatocytes with or without a PPAR-γ agonist. Wild-type C57BL/6J mice were fed a high-fat (HF) diet and administered rosiglitazone.RESULTSPrimary hepatocytes exhibited significant lipid deposition and increased ROS production after incubation with FFAs. CM from lipid-laden hepatocytes promoted macrophage polarization to the M1 type and activation of the TLR4/NF-κB pathway. A PPAR-γ agonist ameliorated oxidative stress and NLRP3 inflammasome activation in lipid-laden hepatocytes and subsequently prevented M1 macrophage polarization. Hepatocyte-specific PPAR-γ deficiency aggravated oxidative stress and NLRP3 inflammasome activation in lipid-laden hepatocytes, which further promoted M1 macrophage polarization. Rosiglitazone administration improved oxidative stress and NLRP3 inflammasome activation in HF diet-induced NAFLD mice in vivo.CONCLUSIONUpregulation of PPAR-γ activity in hepatocytes alleviated NAFLD by modulating the crosstalk between hepatocytes and macrophages via the reactive oxygen species-NLRP3-IL-1β pathway. 相似文献
79.
目的观察参七散对2型糖尿病(T2DM)患者血游离脂肪酸(FFA)的影响。方法将169例T2DM患者随机分为治疗组89例,对照组80例。治疗组给予口服参七散5g/次,每日3次;对照组给予非诺贝特胶囊200mg/次,每日1次。两组均给药8周为1个疗程。治疗前后测定患者糖化血红蛋白(HbA1c)、空腹血糖(FBG)、餐后2小时血糖(2hPG)、甘油三酯(TG)、FFA的含量,同时记录体重指数(BMI)。结果治疗组治疗后HbA1c、FBG、2hPG及BMI与治疗前比较,差异均有统计学意义(P<0.05或P<0.01);两组患者治疗后血清FFA及TG水平与治疗前比较,差异均有统计学意义(P<0.05),但治疗后两组患者血清FFA及TG水平差异无统计学意义(P>0.05)。结论参七散能有效降低糖尿病患者的TG、FFA及血糖水平。 相似文献
80.
柱前衍生HPLC法测定鸦胆子油中的脂肪酸含量 总被引:8,自引:0,他引:8
目的建立HPLC法测定鸦胆子油中的脂肪酸的方法。方法以2,4′-二溴苯乙酮为衍生化试剂,18-冠-6醚为相转移催化剂,采用KromasilC8(250mm×4mm,5μm)反相柱,波长254nm,以乙腈-水(80∶20)为流动相等度洗脱,柱温室温,体积流量为1.3mL/min,正十七烷酸为内标,一次基线分离5种脂肪酸。结果亚油酸的线性范围为0.022~0.330μg,软脂酸的线性范围为0.014~0.213μg,油酸线性范围为0.028~0.416μg,硬脂酸的线性范围为0.012~0.177μg。平均回收率分别为99.2%、97.2%、101.8%、97.8%,RSD分别为1.2%、1.5%、0.4%、2.3%。结论该方法重现性好,定量准确,可作为鸦胆子油中脂肪酸的定量方法。 相似文献