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881.
This study describes Australian media portrayal of mental illnesses, focusing on depression. A random sample of 1,123 items was selected for analysis from a pool of 13,389 nonfictional media items about mental illness collected between March 2000 and February 2001. Depression was portrayed more frequently than other mental illnesses. Items about depression, eating disorders, and substance use disorders most commonly described policies or programs, whereas items about schizophrenia most frequently portrayed individuals or symptoms and treatment. A minority of items about depression presented information about symptoms, causes, treatment, or prognosis. Although such information was generally accurate, a proportion of items conveyed misleading messages. There is therefore scope for increasing the level of accurate information provided about depression in the Australian media. © 2005 Wiley Periodicals, Inc. J Comm Psychol 33: 283–297, 2005.  相似文献   
882.
Outpatient high-dose chemotherapy and autologous stem cell transplantation (ASCT) has been shown to be feasible in terms of physical morbidity and mortality outcomes, but few data exist on the psychosocial impact of delivering such aggressive therapy in this manner. The purpose of this observational study was to compare effects of inpatient (n = 20) and outpatient (n = 21) modes of care on physical status, psychological well-being, quality of life, personal finances and caregiver burden. Most patients were treated according to their preference for inpatient or outpatient care. Those choosing outpatient care were screened for eligibility according to established criteria for ambulatory management. Measures were taken at baseline, then at days 4-6, 12-16 and 30 post ASCT. Results showed that overall, the psychological, physical, social and financial outcomes of the outpatient ASCT group were comparable, to or better than inpatients. Factors that seem to be important for successful outpatient management are previous experience with cancer treatment, a satisfying quality of life, physical well-being, patient's preference for a particular mode of care and physical proximity to the treatment centre. The study results suggest that outpatient ASCT is an efficient, effective and acceptable form of care for motivated patients and caregivers who have the physical and psychological capability and desire to receive cancer treatment in this manner.  相似文献   
883.
PURPOSE: To evaluate the efficacy of the aromatase inhibitor letrozole in preselected estrogen receptor (ER)-positive relapsed epithelial ovarian cancer patients and to identify markers that predict endocrine-sensitive disease. EXPERIMENTAL DESIGN: This was a phase II study of letrozole 2.5 mg daily until clinical or marker evidence of disease progression in previously treated ER-positive ovarian cancer patients with a rising CA125 that had progressed according to Rustin's criteria. The primary end point was response according to CA125 and response evaluation criteria in solid tumors (RECIST) criteria. Marker expression was measured by semiquantitative immunohistochemistry in sections from the primary tumor. RESULTS: Of 42 patients evaluable for CA125 response, 7 (17%) had a response (decrease of >50%), and 11 (26%) patients had not progressed (doubling of CA125) following 6 months on treatment. The median time taken to achieve the CA125 nadir was 13 weeks (range 10-36). Of 33 patients evaluable for radiological response, 3 (9%) had a partial remission, and 14 (42%) had stable disease at 12 weeks. Eleven patients (26%) had a PFS of >6 months. Subgroup analysis according to ER revealed CA125 response rates of 0% (immunoscore, 150-199), 12% (200-249), and 33% (250-300); P = 0.028, chi(2) for trend. Expression levels of HER2, insulin-like growth factor binding protein 5, trefoil factor 1, and vimentin were associated with CA125 changes on treatment. CONCLUSIONS: This is the first study of a hormonal agent in a preselected group of ER-positive ovarian cancer patients. A signature of predictive markers, including low HER2 expression, predicts response.  相似文献   
884.
PURPOSE: To test the hypothesis that common sequence variants of cell cycle control genes may affect lung cancer predisposition. EXPERIMENTAL DESIGN: We explored lung cancer risk associations of 11 polymorphisms in seven cell cycle genes in a large case-control study including 1,518 Caucasian lung cancer patients and 1,518 controls. RESULTS: When individuals with variant-containing genotypes were compared with homozygous wild-type carriers, a significantly increased lung cancer risk was identified for polymorphisms in p53 intron 6 [rs1625895; odds ratio (OR), 1.29; 95% confidence interval (95% CI), 1.08-1.55] and in p27 5' untranslated region (UTR; rs34330; OR, 1.27; 95% CI, 1.01-1.60). Compared with homozygous wild-types, the homozygous variant genotypes of STK15 F31I and CCND1 G870A were associated with a significantly altered lung cancer risk with ORs of 0.58 (95% CI, 0.37-0.90) and 1.26 (95% CI, 1.03-1.53), respectively. To assess the cumulative effects of all the investigated polymorphisms on lung carcinogenesis, we conducted a combined analysis and found that compared with low-risk individuals with few adverse alleles, individuals with more adverse alleles had an increased risk in a significant dose-dependent manner (P(trend) = 0.041). This pattern was more evident in ever smokers (P(trend) = 0.037), heavy smokers (P(trend) = 0.020), and older subjects (P(trend) = 0.011). Higher-order gene-gene interactions were evaluated using the classification and regression tree analysis, which indicated that STK15 F31I and p53 intron 6 polymorphisms might be associated with lung carcinogenesis in never/light-smokers and heavy smokers, respectively. CONCLUSIONS: Our results suggest that cell cycle gene polymorphisms and smoking may function collectively to modulate the risk of lung cancer.  相似文献   
885.
BACKGROUND: Reducing the nicotine content of cigarettes to make them non-addictive has been widely discussed as a potential strategy for tobacco regulation. A major concern with nicotine reduction is that smokers will compensate for reduced nicotine by smoking more cigarettes and/or smoking more intensively, thereby increasing their exposure to tobacco smoke toxins. This study examined whether gradual reduction in nicotine exposure increases exposure to tobacco smoke toxins. METHODS: This 10-week longitudinal study of 20 healthy smokers involved smoking their usual brand followed by different types of research cigarettes with progressively lower nicotine content, each smoked for 1 week. Subjects were followed for 4 weeks after returning to smoking their usual brand (or quitting). Smoking behaviors, chemical biomarkers of tobacco smoke exposure, and cardiovascular effect biomarkers were measured. FINDINGS: Intake of nicotine declined progressively as the nicotine content of cigarettes was reduced, with little evidence of compensation. Cigarette consumption and markers of exposure to carbon monoxide and polycyclic aromatic hydrocarbons, as well as cardiovascular biomarkers remained stable, whereas urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol excretion decreased. Twenty-five percent of participants had spontaneously quit smoking 4 weeks after completing the research cigarette taper. IMPLICATIONS: Our findings with reduced nicotine content cigarettes differ from those of commercial low yields for which compensatory smoking for lower nicotine delivery is substantial. Our data suggest that the degree of nicotine dependence of smokers can be lowered without increasing their exposure to tobacco smoke toxins. Gradual reduction of nicotine content of cigarettes seems to be feasible and should be further evaluated as a national tobacco regulatory strategy.  相似文献   
886.
A hallmark of calcium-triggered synaptic transmission is the cooperative relationship between calcium and the amount of transmitter released. This relationship is thought to be important for improving the efficiency of synaptic vesicle exocytosis. Although it is generally held that cooperativity arises from the interaction of multiple calcium ions with a single calcium-sensing molecule, the precise molecular basis of this phenomenon is not known. The SNARE proteins are known to be critical for synaptic vesicle exocytosis. We therefore tested for a contribution of SNARE proteins to cooperativity by genetically reducing the levels of syntaxin IA and neuronal-synaptobrevin in Drosophila. Surprisingly, we found that reducing these SNARE proteins also reduced Ca(2+) cooperativity. Thus, SNARE proteins are important for determining the cooperative relationship between calcium and synaptic transmission.  相似文献   
887.
This study investigated how chain length affects fermentation properties of fructooligosaccharides (FOSs) and inulin (IN). Chain lengths of FOSs and IN vary from an average degree of polymerization (DP) of 3 to greater than 20. Three samples classified as FOSs (samples A, B, and C) and 3 samples classified as IN (samples D, E, and F) were fermented via an in vitro batch method with human fecal inoculum as the source of microbes. Samples were removed at 0, 4, 8, 12, and 24 hours for total short-chain fatty acid (SCFA), acetate, propionate, and butyrate measurement via gas chromatography. Sample chain length did not affect SCFA concentrations in a predictable manner. Sample E (90%-94% DP > 10, 6%-10% DP = 1-2), a mixture of long-chain IN and short-chain FOS, produced significantly more total SCFA and acetate than the other samples. Sample F (DP > 20), the longest-chain IN, produced the lowest concentration of butyrate at 24 hours. The rate of FOS fermentation was higher than IN fermentation during 0 to 4 hours for all SCFAs, and the rate of IN fermentation was higher than FOS fermentation during 12 to 24 hours for all SCFAs. Chain length affects in vitro fermentability, with short chains being rapidly fermented and long chains being steadily fermented. Clinical studies should follow this work to verify if these differences exist in vivo.  相似文献   
888.
Role of genetic factors in the pathogenesis of osteoporosis   总被引:22,自引:0,他引:22  
Osteoporosis is a common disease with a strong genetic component characterised by low bone mass, microarchitectural deterioration of bone tissue and an increased risk of fracture. Twin and family studies have shown that genetic factors play an important role in regulating bone mineral density and other determinants of osteoporotic fracture risk, such as ultrasound properties of bone, skeletal geometry and bone turnover. Osteoporosis is a polygenic disorder, determined by the effects of several genes, each with relatively modest effects on bone mass and other determinants of fracture risk. It is only on rare occasions that osteoporosis occurs as the result of mutations in a single gene. Linkage studies in man and experimental animals have defined multiple loci which regulate bone mass but the genes responsible for these effects remain to be defined. Population-based studies and case-control studies have similarly identified polymorphisms in several candidate genes that have been associated with bone mass or osteoporotic fracture, including the vitamin D receptor, oestrogen receptor and collagen type IalphaI gene. The individual contribution of these genes to the pathogenesis of osteoporosis is small however, reflected by the fact that the relationship between individual candidate genes and osteoporosis has been inconsistent in different studies. An important aim of future work will be to define how the genes which regulate bone mass, bone turnover and other aspects of bone metabolism interact with each other and with environmental variables to cause osteoporosis in individual patients. If that aim can be achieved then there is every prospect that preventative therapy could be targeted to those at greatest risk of the osteoporosis, before fractures have occurred.  相似文献   
889.
The high sensitivity and sharp frequency discrimination of hearing depend on mechanical amplification in the cochlea. To explore the basis of this active process, we examined the pharmacological sensitivity of spontaneous otoacoustic emissions (SOAEs) in a lizard, the Tokay gecko. In a quiet environment, each ear produced a complex but stable pattern of emissions. These SOAEs were reversibly modulated by drugs that affect mammalian otoacoustic emissions, the salicylates and the aminoglycoside antibiotics. The effect of a single i.p. injection of sodium salicylate depended on the initial power of the emissions: ears with strong control SOAEs displayed suppression at all frequencies, whereas those with weak control emissions showed enhancement. Repeated oral administration of acetylsalicylic acid reduced all emissions. Single i.p. doses of gentamicin or kanamycin suppressed SOAEs below 2.6 kHz, while modulating those above 2.6 kHz in either of two ways. For ears whose emission power at 2.6-5.2 kHz encompassed more than half of the total, individual emissions displayed facilitation as great as 35-fold. For the remaining ears, emissions dropped to as little as one-sixth of their initial values. The similarity of the responses of reptilian and mammalian cochleas to pharmacological intervention provides further evidence for a common mechanism of cochlear amplification.  相似文献   
890.
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