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The discovery of an inducible isoform of cyclooxygenase (COX-2) requires a refinement of the theory that inhibition of cyclooxygenase
activity is responsible for both therapeutic and side-effects of nonsteroidal anti-inflammatory drugs (NSAIDs). Pharmacological
results with developmental compounds suggest that COX-2 is the relevant target for the therapeutic (i.e. anti-inflammatory)
effects of NSAIDs, whereas gastric and renal side-effects are related to inhibition of constitutive COX-1. However a role
of COX-1 in inflammation cannot be excluded. Furthermore, more research effort is needed to investigate the functional relevance
of COX-2 in normal tissue. 相似文献
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Seong‐II BIN Shing‐Sheng WU Xiaofeng ZENG Alan MOORE Nicole FRANK 《International journal of rheumatic diseases》2007,10(3):190-197
Aim: The aim of the current study was to assess the efficacy, safety, and tolerability of lumiracoxib 200 mg once daily (o.d.) in relieving osteoarthritis (OA) knee pain in patients in China, Taiwan, and South Korea. Methods: Patients of either sex (aged ≥ 18 years) with symptomatic, primary OA of the knee for ≥ 3 months were eligible for inclusion if they had OA pain intensity of ≥ 40 mm (100 mm visual analogue scale [VAS]) in the target knee joint during the previous 24 h. Patients were required to undergo regular non‐steroidal anti‐inflammatory drug therapy for ≥ 6 weeks. After 3–7 days of screening, patients were randomized (1 : 1) to receive either lumiracoxib 200 mg o.d. or celecoxib 200 mg o.d. The primary efficacy comparison between the study groups was overall OA pain intensity (VAS) in the target knee after 6 weeks of treatment. Results: The mean overall OA pain intensity (VAS) in the target knee after 6 weeks decreased from 60.6 mm to 35.7 mm and 60.5 mm to 36.1 mm in the lumiracoxib and celecoxib groups, respectively. Both study groups showed similar results in terms of improvement in both patient's and physician's global assessment of disease activity and functional health status. The percentage of adverse events (AEs) in the lumiracoxib and celecoxib groups (40.3% and 37.9%, respectively) was similar, as was the proportion of treatment‐related AEs (21.0% and 18.2%, respectively). Conclusions: Lumiracoxib 200 mg o.d. provided effective and well‐tolerated pain relief similar to that achieved with celecoxib 200 mg o.d. in knee OA patients. 相似文献
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2005~2007年我国非甾体抗炎药市场应用分析 总被引:1,自引:0,他引:1
目的:以骨骼肌肉系统使用非甾体抗炎药物为例,分析该类药物在2005~2007年的销售数量、销售金额及生产厂家风云榜。方法:采用药物分类累加的方法统计2005~2007年非甾体抗炎药的销售数量和金额排序,并对前10位药品销售数量和金额对比,及前10位厂家对比。结果:双氯芬酸稳居销售榜首,美洛昔康、布洛芬等药物位居其后。结论:新一代的非甾体抗炎药已经占据主要市场,各类药物各有特色,但是仍需注意其消化系统及心血管系统的不良反应。 相似文献
7.
Do NSAIDs affect the progression of osteoarthritis? 总被引:6,自引:0,他引:6
Ding C 《Inflammation》2002,26(3):139-142
NSAIDs are widely used to alleviate the symptoms of OA. It remains controversial as to what effects these agents have on the progression of OA. In vitro studies showed several types of NSAIDs (e.g., sodium salicylate, indomethacin) inhibited the synthesis of cartilage matrix component, but some types of NSAIDs (e.g., aceclofenac, meloxicam, nimesulide) increased the matrix component synthesis and protected the chondrocytes against apoptosis, while others (e.g., piroxicam) had no effects. Studies in animal models verified that NSAIDs had favourable or detrimental action on OA progression, even the same NSAID (e.g., naproxen, tiaprofenic acid) had reverse effects on articular cartilage in different studies. Preliminary clinical trials revealed some NSAIDs such as indomethacin had a negative influence on joint structure, other NSAIDs such as diclofenac and naproxen had no acceleration of radiographic damage to OA within 2-years of treatment. So far, there are no convincing data to show the widely used NSAIDs and recommended selective COX-2 inhibitor have favourable effects on cartilage. Therefore, it is necessary and valuable to clarify the effects of these NSAIDs on cartilage in patients with OA using validated non-invasive methods such as MRI. 相似文献
8.
García-González MA Lanas A Savelkoul PH Santolaria S Benito R Crusius JB Peña AS 《Clinical and experimental immunology》2003,134(3):525-531
Cytokine genes taking part in the immunological response to Helicobacter pylori infection are good candidates to study for genetic predisposition to duodenal ulcer disease (DU). Among cytokines, interleukin (IL)-1beta and its natural specific inhibitor, the interleukin-1 receptor antagonist, are cytokines that play a key role in regulating gastric acid secretion and modulating the immune response in the gastrointestinal mucosa. We aimed to investigate whether polymorphisms in the IL-1B and IL-1RN genes are involved in the susceptibility to duodenal ulcer. DNA from 131 unrelated Spanish Caucasian patients with DU and 105 ethnically matched healthy controls was typed for the IL-1B-511, IL-1B-31, and IL-1B + 3954 gene polymorphisms, and the VNTR polymorphism in intron 2 of the IL-1RN gene by polymerase chain reaction (PCR)-based methods and TaqMan assays. H. pylori status and non-steroidal anti-inflammatory drugs (NSAIDs) use was determined in all patients and controls. Logistic regression analysis identified H. pylori infection (OR: 9.74; 95%CI = 3.53-26.89) and NSAIDs use (OR: 8.82; 95%CI = 3.51-22.17) as independent risk factors for DU. In addition, the simultaneous carriage of IL-1RN*2, IL-1B-511*C, IL-1B-31*T and IL-1B + 3954*C alleles was a genetic risk factor for DU in patients with H. pylori infection (OR: 3.22; 95%CI = 1.09-9.47). No significant differences in IL-1RN and IL-1B genotypes were found when patients were categorized according to gender, age of onset, smoking habit, NSAIDs use, type of complication and positive family history. Our results provide further evidence that host genetic factors play a key role in the pathogenesis of duodenal ulcer. 相似文献
9.
The three types (groups I, II and III) of stable extracellular 14 kDa phospholipase A2 enzymes differ in their primary amino acid sequences and their properties. It may thus be possible to design low-molecular weight inhibitors targeted to the secretory form of mammalian PLA2. this enzyme has been implicated in inflammatory disorders. We have studied the inhibition of four distinct PLA2 enzymes by a range of NSAIDs, using3H-oleate release from prelabelled membranes ofE. coli for assay. The enzymes used were cobra venom PLA2 (Naja naja, a group I enzyme), bee venom PLA2 (Apis mellifera, group III), recombinant human synovial PLA2 (group II) and rat peritoneal PLA2 (group II). Under the conditions of the3H-oleateE. coli assay, 1 mM concentrations of aspirin, sodium salicylate, paracetamol (acetaminophen), oxphenbutazone, ibuprofen, flurbiprofen and nabumetone failed to inhibit significantly any of the four enzymes. However, indomethacin inhibited all four enzymes, although effects were greatest on the two group II enzymes (rat peritoneal and human synovial PLA2). Approximate IC50 values were 28 and 35 M, respectively. Inhibition by indomethacin was not time dependent and was greater at micromolar rather than millimolar levels of calcium. We conclude that indomethacin but not the other tested classes of NSAID inhibits the group II PLA2 enzyme in a selective manner and suggest that this may be relevant both to its clinical spectrum and to the design of novel pharmaceutical leads. 相似文献
10.
G. Verbruggen MD. E. M. Veys A. M. Malfait L. Schatteman N. Wieme J. Nimmegeers M. G. Gerin C. Broddelez 《Clinical rheumatology》1990,9(1):32-41
Summary
The effect of niflumic acid on hyaluronic acid and proteoglycan metabolism of human cartilage cells was investigated in vitro. Cartilage cells were obtained from five different donors. Niflumic acid levels used in the test systems ranged from 0 to 22 gr/ml and were comparable to serum concentrations in humans after oral intake. Niflumic acid increased the synthesis rates of proteoglycan in some batches of isolated and monolayer-cultured chondrocytes. The effect on hyaluronate synthesis was less pronounced. The fact that this increase in the synthesis of proteoglycan was restricted to some of the donors whereas isolated cells or tissue samples from other individuals remained unaffected illustrates the heterogeneity of different human donors. Depression of proteoglycan synthesis in the presence of the drug was never observed. 相似文献