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91.
目的探讨表没食子儿茶素没食子酸酯(EGCG)对体外培养的人肝癌细胞系HepG2细胞跨内皮迁移的影响及其机制。方法采用癌细胞与内皮细胞的单层粘附实验检测HepG2细胞与内皮细胞的粘附;利用Transwell小室法分析HepG2细胞的跨内皮迁移;运用real time PCR检测LOX-1mRNA水平,Western Blot分析LOX-1蛋白的表达。结果 EGCG(5,10,20μM)能够浓度依赖性地抑制TNF-α(50ng·mL-1)所诱导的HepG2细胞与内皮细胞的粘附、HepG2细胞的跨内皮迁移以及LOX-1mRNA和蛋白表达的上调。LOX-1中和抗体TS20(10ng·mL-1)也能抑制TNF-α对HepG2细胞的这些效应。结论 EGCG通过减少LOX-1的表达能明显抑制TNF-α诱导的肝癌细胞与内皮细胞的粘附及跨内皮迁移。LOX-1可能作为一种粘附分子,参与介导肝癌细胞与内皮细胞的相互作用。 相似文献
92.
Toshihiro Kazawa Takashi Kawasaki Azusa Sakamoto Masaru Imamura Riuko Ohashi Shuying Jiang Toshiya Tanaka Hiroko Iwanari Takao Hamakubo Juro Sakai Tatsuhiko Kodama Makoto Naito 《Pathology international》2009,59(3):152-160
Liver X receptor (LXR) is a nuclear receptor that acts as a sterol sensor and metabolic regulator of cholesterol and lipid homeostasis. The foam cell transformation of macrophages (Mφ) is considered a critical process in atherosclerotic lesions. The relationship, however, of the foam cell transformation of Mφ and LXR is not fully understood. The purpose of the present study was to examine the expression of LXRα, retinoid X receptor (RXR)α, ATP-binding cassette transporter (ABCA1), and macrophage scavenger receptor A (MSR-A), and lipid accumulation in human monocyte-derived Mφ. The expression of LXRα, ABCA1, MSR-A in 7 day cultured granulocyte–macrophage colony-stimulating factor (GM-CSF)-induced Mφ (GM-Mφ) was significantly higher than that in 7 day cultured M-CSF-induced Mφ (M-Mφ). The expression levels of LXRα, ABCA1 and MSR-A protein decreased from 48 h to 5 days after the addition of lipopolysaccharide (LPS) in GM-Mφ, but only MSR-A protein decreased at 5 days after the addition of LPS in M-Mφ. Intracellular lipid accumulation was clearly observed when GM-Mφ was pre-stimulated with LPS for 48 h and incubated with oxidized LDL for an additional 5 days. These findings suggest that the inhibitory activity of LXRα, ABCA1 and MSR-A by LPS may be related to the transformation of Mφs, especially GM-Mφ into foam cells. 相似文献
93.
Elevated peroxidative glutathione redox status in atherosclerotic patients with increased thickness of carotid intima media 总被引:1,自引:0,他引:1
HUANG Yan-sheng WANG Li-xia SUN Lin WU Yu LU Jian-min ZHAO Shi-chao DAI Fu-min XU Bo-shi WANG Shu-ren 《中华医学杂志(英文版)》2009,122(23):2827-2832
Background Atherosclerosis is a chronic inflammatory disease. Accumulated evidences suggest a deep involvement of oxidative damage in the development of atherosclerosis, but little is discussed over the relationship between plasma glutathione redox status as the most important intrinsic antioxidant defensive mechanism and the atherosclerosis. Methods A total of 132 patients suspected with atherosclerosis were assigned to three groups by high frequency ultrasonic examination of the carotid artery. With the thickness of intima of the carotid artery as an index of degree of atherosclerosis progression, 56 were included in plaque-forming group (A), 42 in carotid artery intima-thickening group (B), and 34 in normal carotid artery intima-thickness group (C). All patients were subjected to the measurement of plasma glutathione (GSH) (reduced form GSH and oxidized form GSSG), nicotinamide adenine dinucleotide phosphate (NADP) (reduced form NADPH and oxidized form NADP^+), oxidized low density lipoprotein (oxLDL), and malondialdehyde (MDA) The GSH/GSSG and NADPH/NADP^+ redox potentials were calculated according to the Nernst equation, and their correlation with intima thickness and oxLDL was analyzed. Results With the thickening of artery intima (from group C to A), GSH concentration and the ratio of GSH/GSSG gradually reduced, and GSSG and GSH/GSSG redox potential gradually increased (more positive) (P 〈0.05). The NADPH and NADPH/NADP^+ redox status also showed similar but milder changes. The products of oxidative stress oxLDL and MDA increased significantly along with the thickening of artery intima (P 〈0.05). The analysis of the relationship between GSH/GSSG redox potential, intima thickness, and oxLDL showed positive correlations (P 〈0.05). The plasma GSH/GSSG redox status was positively correlated with the intima thickness of the carotid artery and the oxidized injury of LDL. The redox status shifted to oxidizing direction along with the intima thickening and plaque-forming. Conclusion Elevated peroxidative glutathione redox status was deeply implicated in atherosclerosis progressing, and it may be a sensitive and reliable index for monitoring oxidative status in atherosclerosis. 相似文献
94.
Multiple sclerosis (MS) is a common autoimmune neurodegenerative disease of unknown cause, which results in inflammation and plaques of demyelination in brain and eventual axonal degeneration. We report the novel presence of oxidized phosphatidylcholine [1-palmitoyl-2-(5'-oxo)valeryl-sn-glycero-3-phosphorylcholine (POVPC)], a lipid associated with inflammatory diseases such as atherosclerosis and lung disease, in the brain of MS patients. The OxPC epitope was detected by Western blotting with the E06 monoclonal antibody. E06-positive lipid was present in the highest amounts in MS plaques, which also showed evidence of low-molecular-weight (15-kDa) OxPC-modified protein. E06 reactivity did not change with post-mortem interval, and E06-positive lipids were largely absent from control tissue. We then used a second monoclonal antibody (AB1-2, which recognizes the E06/T15 idiotype and therefore detects the presence of antibody to OxPC) to show that MS brain samples were strongly positive for the 50-kDa antibody heavy chain. We also showed that isoelectric focussing of the oligoclonal IgG characteristic of MS revealed some immunoglobulin bands that Western blotted with the AB1-2 antibody. Spinal cords from mice induced to undergo experimental allergic encephalomyelitis (EAE) also showed strong AB1-2 reactivity by both immunocytochemistry and Western blot analysis. We therefore conclude that we can detect both OxPC and 15-kDa protein modified by OxPC and the antibody to the antibody to OxPC (antiidiotype) in pathological tissue and suggest that this could play a role in the progression of MS. 相似文献
95.
Lead, a ubiquitous and potent neurotoxicant causes oxidative stress which leads to numerous neurobehavioral and physiological alterations. The ability of lead to bind sulfhydryl groups or compete with calcium could be one of the reasons for its debilitating effects. In the present study, we addressed: i) if chelation therapy could circumvent the altered oxidative stress and prevent neuronal apoptosis in chronic lead-intoxicated rats, ii) whether chelation therapy could reverse biochemical and behavioral changes, and iii) if mono or combinational therapy with captopril (an antioxidant) and thiol chelating agents (DMSA/MiADMSA) is more effective than individual thiol chelator in lead-exposed rats. Results indicated that lead caused a significant increase in reactive oxygen species, nitric oxide, and intracellular free calcium levels along with altered behavioral abnormalities in locomotor activity, exploratory behavior, learning, and memory that were supported by changes in neurotransmitter levels. A fall in membrane potential, release of cytochrome c, and DNA damage indicated mitochondrial-dependent apoptosis. Most of these alterations showed significant recovery following combined therapy with captopril with MiADMSA and to a smaller extend with captopril + DMSA over monotherapy with these chelators. It could be concluded from our present results that co-administration of a potent antioxidant (like captopril) might be a better treatment protocol than monotherapy to counter lead-induced oxidative stress. The major highlight of the work is an interesting experimental evidence of the efficacy of combinational therapy using an antioxidant with a thiol chelator in reversing neurological dystrophy caused due to chronic lead exposure in rats. 相似文献
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98.
The Effect of Aggressive Versus Conventional Lipid-lowering Therapy on Markers of Inflammatory and Oxidative Stress 总被引:2,自引:0,他引:2
Mulder DJ van Haelst PL Wobbes MH Gans RO Zijlstra F May JF Smit AJ Tervaert JW van Doormaal JJ 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》2007,21(2):91-97
Purpose Recent trial results are in favor of aggressive lipid lowering using high dose statins in patients needing secondary prevention.
It is unclear whether these effects are solely due to more extensive lipid lowering or the result of the potentially anti-inflammatory
properties of statins. We aimed to determine whether aggressive compared with conventional statin therapy is more effective
in reducing systemic markers of inflammation and oxidative stress.
Materials and methods This was a multi-centre, double-blind, placebo-controlled trial. Patients with previous cardiovascular disease, who did not
achieve low density lipoprotein (LDL) cholesterol levels <2.6 mmol/l on conventional statin therapy (simvastatin 40 mg) were
randomized to continue with simvastatin 40 mg or to receive atorvastatin 40 mg for 8 weeks and thereafter atorvastatin 80 mg
for the final 8 weeks (aggressive treatment). Lipids, C-reactive protein, soluble cellular adhesion molecules, neopterin,
von Willebrand Factor, and antibodies against oxidized LDL were measured at baseline and after 16 weeks.
Results Lipid levels decreased significantly in the aggressive treatment group (LDL-C reduction 20.8%; P < 0.001), whereas a slight increase was observed in the conventional group (LDL-C increase 3.7%; P = 0.037). A significant reduction in antibodies against oxidized LDL was seen in the aggressive (13.4%; P < 0.001) and the conventional (26.8%; P < 0.001) group, but there was no difference between groups (P = 0.25). Furthermore, no significant differences in change in other biomarkers was observed between both groups.
Conclusions This study does not support the hypothesis that a more profound reduction in inflammatory and oxidative stress contributes
to the benefits of aggressive statin therapy. 相似文献
99.
A. V. Aseychev O. A. Azizova L. V. Shulenina A. P. Piryazev 《Bulletin of experimental biology and medicine》2009,147(3):312-318
The effect of oxidized fibrinogen on platelet-neutrophil complex formation was evaluated by studying the platelet aggregation
(changes in light transmission and turbidimetric assay). Activation of cells by thrombin (0.015 U/ml) in the presence of oxidized
fibrinogen was accompanied by the formation of larger intermolecular aggregates of platelets and leukocytes as compared to
those detected in experiments with non-oxidized fibrinogen. Addition of thrombin (0.2 U/ml) in the presence of oxidized fibrinogen
was followed by the formation of more stable complexes of platelets and leukocytes as compared to those revealed in experiments
with non-oxidized fibrinogen. An increase in the width of aggregation curves was most pronounced in the system of 10−4 M Fe2+ and 10−4 M H2O2 with oxidized fibrinogen. Our results indicate that oxidized fibrinogen contributes to the “floating” or suspension of platelet-leukocyte
complexes.
Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 147, No. 3, pp. 284–290, March, 2009 相似文献
100.