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Objective. Molar-Incisor Hypomineralization (MIH) is a common developmental enamel defect characterized by demarcated opacities in permanent molars and incisors. Its etiology still remains unclear. The aim of this retrospective cohort study was to assess if the socioeconomic environment of the child is associated with MIH. Materials and methods. The study was located in two rural towns and three urban cities in Finland. A total of 818 children, between 7–13 years old, were examined for MIH using the evaluation criteria in line with those of the European Academy of Paediatric Dentistry, but excluding opacities smaller than 2 mm in diameter. The mothers filled in a questionnaire which included questions related to the family’s way of living (e.g. area of residency, farming, day care attendance) and socioeconomic status (family income, number of mother’s school years, level of maternal education). Results. The prevalence of MIH in the study population was 17.1%. Family income, urban residency and day care attendance were associated with MIH in the univariate analysis. In the multivariate analysis using binary logistic regression, only urban residency during a child’s first 2 years of life remained associated with MIH. The prevalence of MIH in urban areas was 21.3% and in rural areas 11.5% (OR = 2.18, CI = 1.35–3.53, p = 0.001). Conclusions. The prevalence of MIH was related to urban residency and could not be explained by any other factor included in the study.  相似文献   
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Both fragile X mental retardation protein (FMRP) and brain-derived neurotrophic factor (BDNF) are implicated in the maturation of neurons and in the higher cognitive functions. We have investigated whether FMRP and BDNF are reciprocally regulated in neurons. Exposure of cultured hippocampal neurons to BDNF, but not to NT-3, reduced FMR1 mRNA levels to 84.8% of control at 4 h and the levels were back to baseline by 24 h or 4 days. Furthermore, expression of FMR1 mRNA was reduced (82.4% of control) in vivo in the hippocampus of transgenic mice overexpressing TrkB receptors, and a small but significant (5.1%) decrease was also detected in FMRP protein levels. In contrast, the expression patterns of BDNF and TrkB mRNAs were not altered in FMRP-deficient mice compared to wild-type mice. Our data provide evidence that BDNF via TrkB signaling decreases FMRP expression and suggest a role for FMRP in BDNF-induced synaptic plasticity.  相似文献   
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Clinical studies suggest that maternal smoking during pregnancy can reduce the crown size of the child's teeth. Delayed dental age compared with chronological age has also been reported in children whose parents smoke. Among the main components of tobacco smoke are nonhalogenated polycyclic aromatic hydrocarbons (PAHs), many of which are highly toxic. Humans are exposed to PAH compounds mainly via tobacco smoke and diet. The aim of our study was to investigate the effect of PAHs on tooth formation and the function of tooth-forming cells. We exposed mouse (NMRI) E18 mandibular first and second molar explants to 7,12-dimethylbenz[a]anthracene (DMBA), a toxic PAH compound, in organ culture for 7 or 12 days. DMBA concentrations used were 0.1, 0.5, 1, and 2 microM. The mesiodistal width of each first molar (12-day culture) was measured in stereomicroscopic images, and the teeth were analysed histologically. DMBA exposure significantly reduced the mesiodistal width of the first molars. DMBA impaired or delayed amelogenesis and dentinogenesis in both molars at the lowest concentration of 0.1 microM. DMBA affected enamel formation more severely than dentin formation and occasionally prevented amelogenesis completely. Elongation and polarization of ameloblasts were impaired, and blood vessel architecture of the dental papilla (future pulp) was altered. Cusps were thin and sharp. In line with the finding that maternal smoking during pregnancy has an adverse effect on child's tooth development, this study shows the toxic influence of PAHs on tooth development in vitro.  相似文献   
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OBJECTIVES: The aim of the study was to compare the health-related quality of life (HRQoL) of patients undergoing coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA) before the interventions and 6 and 12 months afterward, and to compare their HRQoL also with that of the general population. METHODS: The sample (n = 615) consisted of consecutive coronary artery disease patients treated with elective CABG (n=432) or PTCA (n=183). The baseline data before the treatments were collected by structured interview, the follow-up data mainly by mailed self-administered questionnaires. HRQoL was measured by the 15D. For comparisons, the groups were standardized for differences in socioeconomic and clinical characteristics with a regression analysis. RESULTS: At baseline, the average 15D scores of the patient groups were 0.752 (95 percent confidence interval [CI], 0.743-0.761) in CABG and 0.730 (95 percent CI, 0.716-0.744) in PTCA. After standardization, the difference between the groups was statistically significant but not clinically important. These scores were significantly worse (statistically and clinically) than the score of 0.883 (95 percent CI, 0.871-0.879) in the general population sample matched with the gender and age distribution of the patients. By 6 months, the CABG and PTCA patients had experienced a statistically significant and clinically important improvement to 0.858 (95 percent CI, 0.844-0.872) and 0.824 (95 percent CI, 0.806-0.842), respectively. No significant change took place in either group from 6 to 12 months. CONCLUSIONS: Both CABG and PTCA produces an approximately similar, clinically important improvement in HRQoL in 1-year follow-up.  相似文献   
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OBJECTIVE: Increased numbers of mast cells (MCs) are present in ruptured coronary plaques, suggesting to play a role in acute coronary syndromes. We evaluated the distribution densities of MCs, macrophages and T cells in carotid plaques and correlated these findings to stroke risk factors as well as history of stroke or TIA. METHODS AND RESULTS: Seventy-eight carotid samples from 75 patients (16 plaques from asymptomatic patients and 62 from patients with recent ischemic symptoms) undergoing carotid endarterectomy with an internal carotid stenosis >70% that were immunostained and quantified for MCs, macrophages and T cells. The MC distribution density showed positive correlation with the degree of carotid stenosis (p = 0.012), serum levels of total cholesterol (p = 0.021), LDL cholesterol (p = 0.013) and triglycerides (p = 0.005), and an inverse correlation with serum HDL cholesterol levels (p = 0.001). The average MC density (p = 0.023), but not the macrophage (p = 0.58) or T cell (p = 0.74) density, was higher in the symptomatic than in the asymptomatic patients. In a comparison of plaques ipsilateral and contralateral to the thromboembolic event, the densities of the three types of inflammatory cells were similar. CONCLUSIONS: Increased MC distribution density is associated with an atherogenic serum lipid profile, high-grade carotid artery stenosis and symptomatic carotid artery disease. These findings suggest a potential involvement of MCs in the pathophysiology of carotid artery stenosis.  相似文献   
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