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171.
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174.
Campylobacter fetus bacteremia is a rare human infection that occurs almost exclusively in the setting of advanced age, immunosuppression, human immunodeficiency virus infection, alcoholism, or recent gastrointestinal surgery. This report of C. fetus bacteremia in a 39-year-old immunocompetent traveler who ate raw beef identifies C. fetus as a potential emerging pathogen in normal hosts.Campylobacter fetus is a common pathogen of cattle, sheep, and other ungulates. Human C. fetus infection is associated with consumption of raw or undercooked meat, unpasteurized milk, and other uncooked foods.1 Although the Campylobacter genus is a common cause of gastrointestinal symptoms in humans, C. fetus bacteremia is very rare, occurring almost exclusively in the setting of advanced age, immunosuppression, human immunodeficiency virus (HIV) infection, alcoholism, or recent gastrointestinal surgery.2 We report a case of C. fetus bacteremia in an immunocompetent patient after travel to Ethiopia.A 39-year-old Ethiopian male presented with fever, hypotension, tachycardia, watery diarrhea, lower back and hip pain, nausea, and vomiting. His symptoms began 2 days after returning from a trip to Addis Ababa, Ethiopia, where he stayed within the city for 3 months to visit his family. He reported eating uncooked beef and raw honey during his trip. He did not take malarial prophylaxis because of the high elevation of the area. He reported consuming two to three alcoholic beverages a week, and his medical history was significant only for mild hepatic steatosis, treated latent tuberculosis infection 15 years before, and obstructive sleep apnea. His initial hospital treatment included intravenous fluid resuscitation as well as intravenous vancomycin and piperacillin/tazobactam. An abdominal computed tomography scan without contrast revealed a diffusely distended colon with multiple air–fluid levels. The patient was transitioned to oral ciprofloxacin and metronidazole as he clinically improved. Blood cultures were positive for C. fetus on day 3 of hospitalization. Because fluoroquinolone resistance in C. fetus can exceed 30%,3 antibiotic therapy was empirically changed to azithromycin, and the patient was discharged to complete a 14-day total antibiotic course. Other laboratory testing revealed three negative malaria smears, normal immunoglobulin levels, a negative serum HIV enzyme-linked immunosorbent assay, negative anti-Hepatitis C virus antibodies, and positive Hepatitis B surface antibodies.Reports on the incidence of C. fetus bacteremia vary. Of 183 episodes of Campylobacter bacteremia in 23 French hospitals between 2000 and 2004, 53% were caused by C. fetus.3 Other investigators have identified C. fetus less frequently; 19% of 71 Campylobacter bacteremia episodes were C. fetus in one Spanish teaching hospital over 23 years, and 8.6% of 394 Campylobacter bacteremia cases were C. fetus in an English report spanning 11 years.4,5 Although the Centers for Disease Control and Prevention Foodborne Outbreak Online Database (FOOD) reported only one confirmed case of C. fetus infection from 1998 to 2011, US cases may be underreported.6 Cases of C. fetus bacteremia are more likely to occur in patients with advanced age, comorbid illness, or immunodeficiency.3 Our case shows that systemic infection from this organism can occur in immunocompetent individuals and highlights the importance of pre-travel education on sanitary food practices.  相似文献   
175.
A variety of ecological processes influence diversity and species composition in natural communities. Most of these processes, whether abiotic or biotic, differentially filter individuals from birth to death, thereby altering species’ relative abundances. Nonrandom outcomes could accrue throughout ontogeny, or the processes that generate them could be particularly influential at certain stages. One long-standing paradigm in tropical forest ecology holds that patterns of relative abundance among mature trees are largely set by processes operating at the earliest life cycle stages. Several studies confirm filtering processes at some stages, but the longevity of large trees makes a rigorous comparison across size classes impossible without long-term demographic data. Here, we use one of the world’s longest-running, plot-based forest dynamics projects to compare nonrandom outcomes across stage classes. We considered a cohort of 7,977 individuals in 186 species that were alive in 1971 and monitored in 13 mortality censuses over 42 y to 2013. Nonrandom mortality with respect to species identity occurred more often in the smaller rather than the larger size classes. Furthermore, observed nonrandom mortality in the smaller size classes had a diversifying influence; species richness of the survivors was up to 30% greater than expected in the two smallest size classes, but not greater than expected in the larger size classes. These results highlight the importance of early life cycle stages in tropical forest community dynamics. More generally, they add to an accumulating body of evidence for the importance of early-stage nonrandom outcomes to community structure in marine and terrestrial environments.Processes that operate nonrandomly with respect to species identity contribute to the structure of natural communities (13). Evidence from diverse rain forests includes demographic transitions from seeds to seedlings (4, 5), at the seedling (6, 7) and sapling stages (8) and among large trees (912). Although the relative contributions of nonrandom processes at each life cycle stage to determining patterns of abundance and diversity in the mature canopy are unknown, one long-standing paradigm is that community assembly is mediated primarily by events occurring from seed dispersal through seedling germination and small-sapling establishment (1317). However, despite suggestive patterns (6, 7, 18, 19), evidence is lacking for the comparative strength of early-stage dynamics in determining canopy abundance and diversity.Numerous studies demonstrate significant interspecific variation in the susceptibility of tropical tree seedlings to postgermination hazards, including natural enemies (20, 21), adverse climatic or edaphic conditions (22), physical damage (23), and the crowding or shared-enemies effects of con- and heterospecific neighbors (24, 25). In other words, the per capita probability of seedling mortality is nonrandom because the probability of death is not the same for all individuals in a local community – it is dependent to some degree on species identity. In plant communities in which generation times are relatively short, experiments have demonstrated that nonrandom mortality through these early transitions can be sufficiently strong to affect the species composition of mature plants (2629). Such demonstrations are impossible in studies of a few decades or less in duration when generation times are long and even juveniles live for several decades or centuries, such as in many tropical forests. Even so, some hypotheses explicitly identify stressors that affect plants at the earliest life cycle stages (such as pests and pathogens, 13, 14, 30) as disproportionately influential. In addition, some empirical studies find a lack of support for nonrandom processes operating among larger stems (31, 32). Together these hypotheses and observations provide the rationale underpinning the considerable body of research on seed and seedling dynamics in tropical forests worldwide. However, no empirical or experimental assessment has been made of the relative contributions across life cycle stages from nonrandom mortality.Here, we evaluate the comparative contribution of early-stage dynamics using a multidecadal study of a tropical forest dynamics plot initiated by one of us (J.H.C.) in 1963 at a site in north Queensland, Australia. We considered a cohort of 7,977 individuals in 186 species that were alive on the plot in 1971, from tiny seedlings to large canopy trees, whose fates were monitored in 13 mortality censuses over 42 y to 2013. Individuals were assigned to one of six size classes (
Size class*N in 1971S in 1971S in 2013D in 2013 (% mortality)
SC1 (0-6.0-cm ht)1,46591241,421 (97.0)
SC2 (6.1–15.2-cm ht)1,275105471,156 (90.7)
SC3 (15.3–36.6-cm ht)1,29110677965 (74.7)
SC4 (36.7–182.9-cm ht)1,351124101639 (47.3)
SC5 (183.0-cm ht – 10-cm dbh)1,208135123330 (27.3)
SC6 (≥10.1-cm dbh)1,387122113357 (25.7)
Open in a separate windowS, number of species; N, number of stems alive in 1971; D, number of stems that died by 2013; dbh, diameter at breast height.*The original units of measurement on this plot were decimal inches and feet. Individuals < 3.2-inches girth have always been measured for height, to the nearest 0.1 ft. The upper height limits of size classes 1–4 are the metric equivalents of 0.2, 0.5, 1.2, and 6.0 ft.Our analyses proceeded in three stages. First, we determined the percentage, P, of species in each size class dying nonrandomly between 1971 and 13 progressively longer census periods to 2013. A species died nonrandomly within a given size class if the observed number of individuals dying over a census period was significantly different from the number of deaths expected under Monte Carlo simulations (10,000 runs) in which the probability of mortality was random with respect to species identity within the size class (i.e., “expected mortality”). Second, we determined for each census period and size class the effect of nonrandom mortality on the observed species richness of both the stems that survived (SS) and the stems that died (SD). From the simulations we generated means and 95% confidence limits for the expected numbers of survivors for each species in each size class in each census interval. We also calculated means and 95% confidence limits for the expected numbers of deaths for each species in each size class and census interval, as well as the means and 95% confidence limits for expected SS and SD. Third, we investigated frequency-dependent mortality as a potential mechanism explaining departures from expected species richness among observed survivors and the stems that died.  相似文献   
176.
Recapitulation of the forward nuclear auxin response pathway in yeast     
Edith Pierre-Jerome  Seunghee S. Jang  Kyle A. Havens  Jennifer L. Nemhauser  Eric Klavins 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(26):9407-9412
  相似文献   
177.
Respiratory syncytial virus‐ and human metapneumovirus‐associated emergency department and hospital burden in adults     
Kyle Widmer  Marie R. Griffin  Yuwei Zhu  John V. Williams  H. Keipp Talbot 《Influenza and other respiratory viruses》2014,8(3):347-352
  相似文献   
178.
A multisite controlled study of risk factors in pediatric psychogenic nonepileptic seizures     
Sigita Plioplys  Julia Doss  Prabha Siddarth  Brenda Bursch  Tatiana Falcone  Marcy Forgey  Kyle Hinman  W. Curt LaFrance Jr  Rebecca Laptook  Richard J. Shaw  Deborah M. Weisbrot  Matthew D. Willis  Rochelle Caplan 《Epilepsia》2014,55(11):1739-1747
  相似文献   
179.
Rates of hospitalizations for respiratory syncytial virus, human metapneumovirus, and influenza virus in older adults     
Widmer K  Zhu Y  Williams JV  Griffin MR  Edwards KM  Talbot HK 《The Journal of infectious diseases》2012,206(1):56-62
  相似文献   
180.
Evaluation of cytochrome P450-derived eicosanoids in humans with stable atherosclerotic cardiovascular disease     
Theken KN  Schuck RN  Edin ML  Tran B  Ellis K  Bass A  Lih FB  Tomer KB  Poloyac SM  Wu MC  Hinderliter AL  Zeldin DC  Stouffer GA  Lee CR 《Atherosclerosis》2012,222(2):530-536
ObjectivePreclinical and genetic epidemiologic studies suggest that modulating cytochrome P450 (CYP)-mediated arachidonic acid metabolism may have therapeutic utility in the management of coronary artery disease (CAD). However, predictors of inter-individual variation in CYP-derived eicosanoid metabolites in CAD patients have not been evaluated to date. Therefore, the primary objective was to identify clinical factors that influence CYP epoxygenase, soluble epoxide hydrolase (sEH), and CYP ω-hydroxylase metabolism in patients with established CAD.MethodsPlasma levels of epoxyeicosatrienoic acids (EETs), dihydroxyeicosatrienoic acids (DHETs), and 20-hydroxyeicosatetraenoic acid (20-HETE) were quantified by HPLC–MS/MS in a population of patients with stable, angiographically confirmed CAD (N = 82) and healthy volunteers from the local community (N = 36). Predictors of CYP epoxygenase, sEH, and CYP ω-hydroxylase metabolic function were evaluated by regression.ResultsObesity was significantly associated with low plasma EET levels and 14,15-EET:14,15-DHET ratios. Age, diabetes, and cigarette smoking also were significantly associated with CYP epoxygenase and sEH metabolic activity, while only renin-angiotensin system inhibitor use was associated with CYP ω-hydroxylase metabolic activity. Compared to healthy volunteers, both obese and non-obese CAD patients had significantly higher plasma EETs (P < 0.01) and epoxide:diol ratios (P < 0.01), whereas no difference in 20-HETE levels was observed (P = NS).ConclusionsCollectively, these findings suggest that CYP-mediated eicosanoid metabolism is dysregulated in certain subsets of CAD patients, and demonstrate that biomarkers of CYP epoxygenase and sEH, but not CYP ω-hydroxylase, metabolism are altered in stable CAD patients relative to healthy individuals. Future studies are necessary to determine the therapeutic utility of modulating these pathways in patients with CAD.  相似文献   
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