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Objectives. We compared risk for several medical illnesses between immigrant and US-born older Mexican Americans to determine the relationship between functional health and years of US residency among immigrants.Methods. Cross-sectional, multistage probability sample data for 3050 Mexican Americans aged 65 years or older from 5 US southwestern states were analyzed. Self-rated health, medical illnesses, and functional measures were examined in multivariate regression models that included nativity and years of US residency as key predictors.Results. Self-rated health and medical illnesses of immigrant and US-born groups did not differ significantly. Immigrants with longer US residency had significantly higher cognitive functioning scores and fewer problems with functional activities after adjustment for predisposing and medical need factors.Conclusions. Among older Mexican Americans, immigrant health advantages over their US-born counterparts were not apparent. Immigrants had better health functioning with longer US residency that may derive from greater socioeconomic resources. Our findings suggest that the negative acculturation–health relationship found among younger immigrant adults may become a positive relationship in later life.More than 30 years ago, Teller and Clyburn reported more favorable birth outcomes in Bexar County, Texas, for Spanish-surnamed residents than for non-Latino White and African American residents.1 Despite the disadvantaged economic and social position of many Latinos, additional reports appeared of unexpected favorable birth and longevity outcomes for Latinos (primarily Mexican Americans) compared with other ethnic groups.25 These findings were considered paradoxical, since they ran contrary to the negative socioeconomic health gradient documented in the public health literature.6,7 The Latino health paradox contends that despite experiencing disproportionate exposure to risk factors for excess morbidity and mortality associated with low socioeconomic position, Latinos, primarily Mexican American immigrants, generally have more favorable health outcomes than Mexican Americans born in the United States, most other minorities, and nonminorities.8 The longer these healthy immigrants resided in the United States and acculturated, the more likely they were to report deterioration in health status indicators compared with recent immigrants.9The mental health researchers Rogler et al. referred to “acculturation as an exogenous force shaping the conditions for the rise to psychological distress.”10(p588) This phenomenon was later coined the “acculturative stress” hypothesis and widely used in mental health research of the Latino population. However, acculturative stress models have important limitations in health research because they confound the effects of cultural change on health behaviors with pathology. In addition, they are temporally unspecific and thus inconsistent with developmental models of health. We offer an alternative, the “acculturation–health” hypothesis, to emphasize that health outcomes are instead conditional on multiple life-course contingencies that vary in importance as determinants over one''s life span. The temporal relationships between acculturation and health can range from negative to positive during the lifespan of an individual. Although the negative effects of acculturation are commonly described in the literature, positive outcomes are observed as well and also require explanations.1115 Acculturative stress assumes a cumulative, linear, dose–response association of acculturation with health. An acculturation–health hypothesis accounts for transactions between endogenous (individual-level) and exogenous (external) factors that affect health differentially over the life course. These factors are systematically influenced by acculturation across multiple domains of life activity.The proposed acculturation–health model assumes that there are multiple points in the life course that are critical for improving health and lowering the risk of weathering effects seen in aging among minority groups.16 Carefully focused research could lead to timely and effective interventions that improve health outcomes across the life course. The assumption that a constant acculturation–health relationship is generally negative and leads to declines in health among Mexican Americans is limiting because it is overly deterministic and restricts opportunities for identifying determinants of long-range outcomes and life-course stages when they are most consequential. Although we can assume that living in a new society introduces behavioral, social, and environmental changes that may negatively influence health, there may be benefits as well, such as acquisition of new occupational skills, greater exposure to public health information, and use of preventive medicine. Nevertheless, it is unclear how these changes are expressed in the long run in the health of older Mexican Americans.Mexican Americans represent more than two-thirds of US Latinos and, perhaps accordingly, most previous studies have focused on the relationship between Mexican American acculturation (or various proxies of acculturation, such as language preference and years of US residency) and health.17 For younger Mexican Americans, most studies have reported negative relationships between acculturation and health11—for example, for birth outcomes18,19 and perinatal health behaviors,20,21 general health behaviors (e.g., nutrition and physical exercise),22 vascular disease risks (e.g., diabetes),23,24 and substance abuse and mental disorders.25,26 Several reports have shown positive associations between acculturation and higher use of preventive medical services, which may relate to the higher economic position of more acculturated and US-born Mexican Americans.2730 Among older adults, the prevalence of depression and dementia are reportedly lower among acculturated Mexican Americans.12,13 Furthermore, there is evidence that greater social assimilation, as evidenced by English-language acquisition and more years of education, are associated with lower disability rates and higher self-esteem.14,15,31These general findings have led scientists to hypothesize that immigrants are somehow healthier than US-born Mexican Americans and non-Latino Whites and that with longer US residency, acculturation erodes immigrants'' health.9,32 The negative aspects of the acculturation–health relationship dominate current thinking about Mexican American health, especially regarding acculturation-related changes in risk behaviors such as diet, exercise, and substance abuse.33 However, if the association between acculturation and health is conditional and predicated on various endogenous and exogenous life-course factors, recent work among older adults may better inform us about the long-term acculturation–health relationship.Our first aim was to examine whether the “healthy immigrant” phenomenon persists among older Mexican Americans by comparing the rates of several medical conditions between US-born and immigrant groups. Second, we sought to determine if functional health was negatively associated with longer exposure to the host country within a representative sample of immigrant Mexican Americans. On the basis of previous work,1214,31 we expected that the health status of US-born and immigrant older Mexican Americans would not differ. Third, we sought to examine if longer US residency would be associated with better functional health among older Mexican American immigrants. We expected that increased wealth, access to healthcare and services would facilitate or mediate better health functioning.6,34,35 Finally, in examining the health of older Mexican Americans, we aimed to compare the acculturative stress hypothesis and the acculturation–health hypothesis for a better understanding of their utility for the study of health.  相似文献   
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Huntington’s disease (HD) is caused by an expansion of the CAG repeat in the huntingtin gene leading to preferential neurodegeneration of the striatum. Disease-modifying treatments are not yet available to HD patients and their development would be facilitated by translatable pharmacodynamic biomarkers. Multi-modal magnetic resonance imaging (MRI) and plasma cytokines have been suggested as disease onset/progression biomarkers, but their ability to detect treatment efficacy is understudied. This study used the R6/2 mouse model of HD to assess if structural neuroimaging and biofluid assays can detect treatment response using as a prototype the small molecule p75NTR ligand LM11A-31, shown previously to reduce HD phenotypes in these mice. LM11A-31 alleviated volume reductions in multiple brain regions, including striatum, of vehicle-treated R6/2 mice relative to wild-types (WTs), as assessed with in vivo MRI. LM11A-31 also normalized changes in diffusion tensor imaging (DTI) metrics and diminished increases in certain plasma cytokine levels, including tumor necrosis factor-alpha and interleukin-6, in R6/2 mice. Finally, R6/2-vehicle mice had increased urinary levels of the p75NTR extracellular domain (ecd), a cleavage product released with pro-apoptotic ligand binding that detects the progression of other neurodegenerative diseases; LM11A-31 reduced this increase. These results are the first to show that urinary p75NTR-ecd levels are elevated in an HD mouse model and can be used to detect therapeutic effects. These data also indicate that multi-modal MRI and plasma cytokine levels may be effective pharmacodynamic biomarkers and that using combinations of these markers would be a viable and powerful option for clinical trials.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13311-021-01023-8.Key Words: Magnetic resonance imaging, Neurotrophin, p75NTR, Cytokine, Biomarker  相似文献   
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The spontaneous and simultaneous rupture of both quadriceps tendons is uncommon and has rarely been reported in the literature. The current case involves a 43-year-old man with end-stage renal disease requiring hemodialysis for the past 20 years. The patient experienced bilateral knee pain and swelling and was unable to bear weight. Physical examination revealed bilateral quadriceps tendon defect above the patella and loss of active extension. Although plain radiographs of both knees showed no fracture or widening of the joint space, an inferiorly positioned patella was observed. Ultrasonography of the knees revealed a quadriceps tendon defect at the upper edge of each patella, while MR imaging revealed a tear in each quadriceps tendon from the superior poles of the patella. The patient then underwent surgical correction wherein the tendons were repaired using sutures passed through drill holes in the patella. The knees were immobilized with splints for 4 wk before starting physiotherapy. The patient subsequently regained full functional activity within 1 year.  相似文献   
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Objective: Asthma is a chronic inflammatory disease associated with increased cardiovascular events. This study assesses the presence of inflammation and the vascular reactivity of pulmonary arteries in patients with acute asthma. Methods: Rings of human pulmonary arteries obtained from non-asthmatic and asthmatic patients were set up in organ bath for vascular tone monitoring. Reactivity was induced by vasoconstrictor and vasodilator agents. Protein expression of inflammatory markers was detected by western blot. Prostanoid releases and cyclic adenosine monophosphate (cAMP) levels were quantified using specific enzymatic kits. Results: Protein expression of cluster of differentiation 68, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and cyclooxygenase-2 was significantly increased in arteries obtained from asthmatic patients. These effects were accompanied by an alteration of vasodilatation induced by iloprost and treprostinil, a decrease in cAMP levels and an increase in prostaglandin (PG) E2 and PGI2 synthesis. The use of forskolin (50 µmol/L) has restored the vasodilatation and cAMP release. No difference was observed between the two groups in reactivity induced by norepinephrine, angiotensin II, PGE2, KCl, sodium nitroprusside, and acetylcholine. Conclusion: Acute asthma causes inflammation of pulmonary arteries and decreases vasodilation induced by PGI2 analogs through the impairment of cAMP pathway.  相似文献   
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