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Laura Tonon Gaetano Bergamaschi Claudia Dellavecchia Vittorio Rosti Claudia Lucotti Lucia Malabarba Annunziata Novella Elena Vercesi Francesco Frassoni & Mario Cazzola 《British journal of haematology》1998,102(4):996-1003
We studied X-chromosome inactivation patterns in blood cells from normal females in three age groups: neonates (umbilical cord blood), 25–32 years old (young women group) and >75 years old (elderly women). Using PCR, the differential allele methylation status was evaluated on active and inactive X chromosomes at the human androgen receptor (HUMARA) and phosphoglycerate kinase (PGK) loci. A cleavage ratio (CR) 3.0 was adopted as a cut-off to discriminate between balanced and unbalanced X-chromosome inactivation. In adult women this analysis was also performed on hair bulbs. The frequency of skewed X-inactivation in polymorphonuclear (PMN) cells increased with age: CR 3.0 was found in 3/36 cord blood samples, 5/30 young women and 14/31 elderly women. Mathematical analysis of patterns found in neonates indicated that X-chromosome inactivation probably occurs when the total number of haemopoietic stem cell precursors is 14–16. The inactivation patterns found in T lymphocytes were significantly related to those observed in PMNs in both young ( P < 0.001) and elderly women ( P < 0.01). However, the use of T lymphocytes as a control tissue for distinguishing between skewed inactivation and clonal proliferation proved to be reliable in young females, but not in elderly women, where overestimation of the frequency of clonal myelopoiesis may appear. 相似文献
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Remodeling of myocyte gap junctions in arrhythmogenic right ventricular cardiomyopathy due to a deletion in plakoglobin (Naxos disease). 总被引:8,自引:0,他引:8
Starr R Kaplan Joseph J Gard Nikos Protonotarios Adalena Tsatsopoulou Chara Spiliopoulou Aris Anastasakis Catherine Prost Squarcioni William J McKenna Gaetano Thiene Cristina Basso Nicole Brousse Guy Fontaine Jeffrey E Saffitz 《Heart rhythm》2004,1(1):3-11
OBJECTIVES: We tested the hypothesis that defective interactions between adhesion junctions and the cytoskeleton caused by the plakoglobin mutation in Naxos disease lead to remodeling of gap junctions and altered expression of the major gap junction protein, connexin43. BACKGROUND: Naxos disease, a recessive form of arrhythmogenic right ventricular cardiomyopathy, is associated with a high incidence of arrhythmias and sudden cardiac death. Naxos disease is caused by a mutation in plakoglobin, a protein that links cell-cell adhesion molecules to the cytoskeleton. METHODS: Myocardial expression of connexin43 and other intercellular junction proteins was characterized in 4 patients with Naxos disease. Immunohistochemistry was performed in all 4 patients, and immunoblotting and electron microscopy were performed in 1 patient who died in childhood before overt arrhythmogenic right ventricular cardiomyopathy had developed. RESULTS: Connexin43 expression at intercellular junctions was reduced significantly in both right and left ventricles in all patients with Naxos disease. Electron microscopy revealed smaller and fewer gap junctions interconnecting ventricular myocytes. Mutant plakoglobin was expressed but failed to localize normally at intercellular junctions. Localization of N-cadherin, alpha- and beta-catenins, plakophilin-2, desmoplakin-1, and desmocollin-2 at intercalated disks appeared normal. CONCLUSIONS: Remodeling of gap junctions occurs early in Naxos disease, presumably because of abnormal linkage between mechanical junctions and the cytoskeleton. Gap junction remodeling may produce a coupling defect which, combined with the subsequent development of pathologic changes in myocardium, could contribute to a highly arrhythmogenic substrate and enhance the risk of sudden death in Naxos disease. 相似文献
86.
Giallauria F Palomba S Maresca L Vuolo L Tafuri D Lombardi G Colao A Vigorito C Francesco O 《Clinical endocrinology》2008,69(5):792-798
Background Polycystic ovary syndrome (PCOS) is a common female reproductive‐age endocrine disease predominantly characterized by chronic anovulation, hyperandrogenism, insulin‐resistance and low‐grade inflammatory status. Exercise training (ET) favourably modulates cardiopulmonary function and insulin‐sensitivity markers in PCOS women. The present study investigated the effects of ET on autonomic function and inflammatory pattern in PCOS women. Study design Prospective baseline uncontrolled clinical study. Methods One‐hundred and eighty five PCOS women referred to our department were screened for the inclusion into the study protocol from March 2004 to July 2007. One‐hundred and twenty four PCOS women met the criteria for the inclusion into the study protocol and were subdivided into two groups each composed of 62 patients: PCOS‐T (trained) group underwent 3‐month ET program, whereas PCOS‐UnT (untrained) group did not. At baseline and at 3‐month follow‐up, hormonal and metabolic profile, cardiopulmonary parameters, autonomic function (as expressed by heart rate recovery, HRR) and inflammatory pattern [as expressed by C‐reactive protein (CRP) and white blood cells (WBCs) count] were evaluated. Results PCOS‐T showed a significant (P < 0·05) improvement in maximal oxygen consumption (VO2max) and in post‐exercise HRR, and a significant (P < 0·001) decrease in CRP and WBCs; whereas no statistically significant changes of the same parameters were observed in PCOS‐UnT. Multiple linear regression analysis showed that 3‐month HRR is linearly related to the inclusion in training group (β = 0·316, P < 0·001), VO2max (β = 0·151, P = 0·032) and the ratio between glucose and insulin area under curve (AUC) (β = 0·207, P = 0·003), and inversely related to body mass index (β = –0·146, P = 0·046), insulin AUC (β = –0·152, P = 0·032), CRP (β = –0·165, P < 0·021), and WBCs count (β = –0·175, P = 0·039). Conclusions Exercise training improves autonomic function and inflammatory pattern in PCOS women. 相似文献
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Elisabetta Lazzarini Jan D. H. Jongbloed Kalliopi Pilichou Gaetano Thiene Cristina Basso Hennie Bikker Bart Charbon Morris Swertz Paul A. van der Zwaag 《Human mutation》2015,36(4):403-410
Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac disease characterized by myocardial atrophy, fibro‐fatty replacement, and a high risk of ventricular arrhythmias that lead to sudden death. In 2009, genetic data from 57 publications were collected in the arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) Genetic Variants Database (freeware available at http://www.arvcdatabase.info ), which comprised 481 variants in eight ACM‐associated genes. In recent years, deep genetic sequencing has increased our knowledge of the genetics of ACM, revealing a large spectrum of nucleotide variations for which pathogenicity needs to be assessed. As of April 20, 2014, we have updated the ARVD/C database into the ARVD/C database to contain more than 1,400 variants in 12 ACM‐related genes (PKP2, DSP, DSC2, DSG2, JUP, TGFB3, TMEM43, LMNA, DES, TTN, PLN, CTNNA3) as reported in more than 160 references. Of these, only 411 nucleotide variants have been reported as pathogenic, whereas the significance of the other approximately 1,000 variants is still unknown. This comprehensive collection of ACM genetic data represents a valuable source of information on the spectrum of ACM‐associated genes and aims to facilitate the interpretation of genetic data and genetic counseling. 相似文献
88.
Learning by counting blood platelets in population studies: survey and perspective a long way after Bizzozero 下载免费PDF全文
B. Izzi M. Bonaccio G. de Gaetano C. Cerletti 《Journal of thrombosis and haemostasis》2018,16(9):1711-1721
Summary
Platelet count represents a useful tool in clinical practice to discriminate individuals at higher risk of bleeding. Less obvious is the role of platelet count variability within the normal range of distribution in shaping the individual's disease risk profile. Epidemiological studies have shown that platelet count in the adult general population is associated with a number of health outcomes related to hemostasis and thrombosis. However, recent studies are suggesting a possible role of this platelet index also as an independent risk factor. In this review of adult population studies, we will first focus on known genetic and non‐genetic determinants of platelet number variability. Next, we will evaluate platelet count as a marker and/or a predictor of disease risk and its interaction with other risk factors. We will then discuss the role of platelet count variability within the normal distribution range as a contribution to disease and mortality risk. The possibility of considering platelet count as a simple, inexpensive indicator of increased risk of disease and death in general populations could open new opportunities to investigate novel platelet pathophysiological roles as well as therapeutic opportunities. Future studies should also consider platelet count, not only platelet function, as a modulator of disease and mortality risk.89.
Paola Forti Fabiola Maioli Elisabetta Magni Letizia Ragazzoni Roberto Piperno Marco Zoli Maura Coveri Gaetano Procaccianti 《Archives of physical medicine and rehabilitation》2018,99(3):477-483
Objective
To investigate whether oldest-old age (≥85y) is an independent predictor of exclusion from stroke rehabilitation.Design
Retrospective cohort study.Setting
Stroke unit (SU) of a tertiary hospital.Participants
Elderly patients (N=1055; aged 65–74y, n=230; aged 75–84y, n=432; aged ≥85y, n=393) who, between 2009 and 2012, were admitted to the SU with acute stroke and evaluated by a multiprofessional team for access to rehabilitation. The study excluded patients for whom rehabilitation was unnecessary or inappropriate.Interventions
Not applicable.Main Outcome Measures
Access to an early mobilization (EM) protocol during SU stay and subsequent access to postacute rehabilitation after SU discharge. Analyses were adjusted for prestroke and stroke-related characteristics.Results
32.2% of patients were excluded from EM. Multivariable-adjusted odds ratios (ORs) of EM exclusion were 1.30 (95% confidence interval [CI], .76–2.21) for ages 75 to 84 years and 2.07 (95% CI, 1.19–3.59) for ages ≥85 years compared with ages 65 to 74 years. Of 656 patients admitted to EM and who, at SU discharge, had not yet fully recovered their prestroke functional status, 18.4% were excluded from postacute rehabilitation. For patients able to walk unassisted at SU discharge, the probability of exclusion did not change across age groups. For patients unable to walk unassisted at SU discharge, ORs of exclusion from postacute rehabilitation were 3.74 (95% CI, 1.26–11.13) for ages 75 to 84 years and 9.15 (95% CI, 3.05–27.46) for ages ≥85 years compared with ages 65 to 74 years.Conclusions
Oldest-old age is an independent predictor of exclusion from stroke rehabilitation. 相似文献90.