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941.
Masahiko Asami Jonas Lanz Stefan Stortecky Lorenz Räber Anna Franzone Dik Heg Lukas Hunziker Eva Roost George CM Siontis Marco Valgimigli Stephan Windecker Thomas Pilgrim 《JACC: Cardiovascular Interventions》2018,11(6):593-601
Objectives
This study sought to determine the impact of left ventricular diastolic dysfunction (LVDD) on clinical outcomes in patients undergoing transcatheter aortic valve replacement (TAVR).Background
Left ventricular (LV) hypertrophy in response to afterload increase promotes the development of LVDD and represents an early stage in the progression to valvular heart failure.Methods
In a consecutive cohort of 777 aortic stenosis patients undergoing TAVR, LVDD was categorized according to the latest guidelines. The primary endpoint was 1-year all-cause mortality.Results
There were 545 (70.1%) patients with LVDD. Ninety-eight (18.0%), 198 (36.3%), and 104 (19.1%) patients were classified as LVDD grades I, II, and III, respectively. In 145 (26.6%) patients, LVDD grade could not be determined because of only 1 or 2 discrepant variables. One-year all-cause mortality was higher in patients with LVDD grades I (16.3%; adjusted hazard ratio [HR]adj: 2.32; 95% confidence interval [CI]: 1.15 to 4.66), II (17.9%; HRadj: 2.58; 95% CI: 1.43 to 4.67), and III (27.6%; HRadj: 4.21; 95% CI: 2.25 to 7.86) than in those with normal diastolic function (6.9%). The difference in clinical outcome emerged within 30 days, was driven by cardiovascular death, and maintained in a sensitivity analysis of patients with normal systolic LV function. Furthermore, LVDD grades I (HRadj: 2.36; 95% CI: 1.17 to 4.74), II (HRadj: 2.58; 95% CI: 1.42 to 4.66), and III (HRadj: 4.41; 95% CI: 2.37 to 8.20) were independent predictors of 1-year mortality.Conclusions
Advancing stages of LVDD are associated with an incremental risk of all-cause mortality after TAVR, driven by cardiovascular death and taking effect as early as 30 days after the intervention. 相似文献942.
943.
944.
Oral iloprost in Raynaud's phenomenon secondary to systemic sclerosis: a multicentre, placebo-controlled, dose-comparison study 总被引:3,自引:2,他引:3
Black CM; Halkier-Sorensen L; Belch JJ; Ullman S; Madhok R; Smit AJ; Banga JD; Watson HR 《Rheumatology (Oxford, England)》1998,37(9):952-960
OBJECTIVE: To identify the optimal dose of oral iloprost on the basis of
efficacy and tolerability in patients with Raynaud's phenomenon secondary
to systemic sclerosis. DESIGN: Multicentre, randomized, parallel-group
comparison of two different doses of oral iloprost and placebo. SETTING:
European university hospitals. PATIENTS: A total of 103 patients with
Raynaud's phenomenon secondary to systemic sclerosis. INTERVENTION:
Patients received one of three treatments for 6 weeks: placebo, oral
iloprost 50 microg or oral iloprost 100 microg. Each treatment was taken
twice daily, giving total daily doses of iloprost of 100 and 200 microg.
MEASUREMENTS: The frequency, total daily duration and severity of Raynaud's
attacks were recorded in a specially designed patient diary; physician's
global assessment and adverse events were recorded at visits to the clinic.
Analysis was performed on an intention-to-treat population. RESULTS: A
total of 103 patients were recruited, 89 completed the assessments
throughout the treatment period and 82 completed an additional 6 weeks of
follow-up after treatment. Thirty-five patients received placebo, 33
received iloprost 50 microg and 35 received iloprost 100 microg. The mean
percentage reductions in the frequency, total daily duration and severity
of Raynaud's attacks were numerically greater in the iloprost groups at the
end of treatment and at the end of follow-up. At the end of treatment (6
weeks), there were significant treatment differences in the total daily
duration of attacks (P = 0.03), but not in the severity (P = 0.07) or the
frequency of attacks (P = 0.37). At the end of follow-up (12 weeks), there
were significant treatment differences in the total daily duration of
attacks (P = 0.001) and in the severity of attacks (P = 0.007), but not in
the frequency of attacks (P = 0.07). Percentages of patients improved at
the end of treatment as assessed by the physician were 44% placebo, 57%
iloprost 50 microg and 64% iloprost 100 microg (not significant).
Side-effects were reported by 80% of patients on placebo, 85% on oral
iloprost 50 microg and 97% on oral iloprost 100 microg. Premature
discontinuations of treatment in each group were 9, 30 and 51%,
respectively, with 6, 27 and 51% being due to adverse events. CONCLUSION:
The results on the daily duration of Raynaud's attacks suggest that both 50
and 100 microg oral iloprost twice daily may be effective in the treatment
of Raynaud's phenomenon secondary to systemic sclerosis. The 50 microg
iloprost dose was better tolerated in this patient group.
相似文献
945.
自进行第1例脐血干细胞移植以来,各国科研机构相继开展对于脐血干细胞的研究,脐血库也纷纷建立.随着再生医学的发展,众多国内外学者在尝试进行非肝源性细胞向肝细胞分化方面的研究,并已经证实脐血干细胞在特定的微环境下可以在体内和体外转化为肝样细胞,为脐血干细胞在肝脏疾病中的应用奠定了基础.本文就脐血干细胞向肝细胞转化的最新研究进展作一综述. 相似文献
946.
报告1例苯巴比妥治疗Gilbert综合征致固定性药疹的少见病例,并复习了相关文献.固定性药疹是药物过敏反应中皮肤损害的常见疹型, 但由苯巴比妥所致者较少见.对苯巴比妥过敏的部分患者可有磺胺、去痛片过敏史;某些复方制剂含有苯巴比妥,故使用苯巴比妥前应仔细了解有无磺胺、去痛片过敏史,对复方制剂必须清楚其组成成分,防止苯巴比妥引起不良反应. 相似文献
947.
Chao NJ; Schriber JR; Grimes K; Long GD; Negrin RS; Raimondi CM; Horning SJ; Brown SL; Miller L; Blume KG 《Blood》1993,81(8):2031-2035
Hematopoietic growth factors have been used to accelerate engraftment after bone marrow transplantation and to "mobilize" peripheral blood progenitor cells (PBPC). We report on the data in 85 consecutive patients with Hodgkin's disease who were treated in a single institution using different methods to obtain PB progenitor cells. Use of granulocyte colony-stimulating factor for mobilization resulted in a significantly accelerated time to recovery of granulocytes (10 days v 12 days, P < .01) when compared with "nonmobilized" PBPC recipients. Similarly, use of mobilized PBPC resulted in a significantly accelerated time to platelet engraftment (13 days v 30 days, P < .001) when compared with "nonmobilized" recipients. Moreover, there was a statistically significant difference in total costs in favor of the group receiving "mobilized" PBPC. 相似文献
948.
949.
Prostaglandins of the E series (PGE) inhibit proliferation of normal bone marrow granulocyte/macrophage progenitors (CFU-GM). Circulating CFU-GM are known to differ from marrow CFU-GM in many characteristics, and in the present study, we compared the effect of PGE1 on circulating and bone marrow progenitors in normals and in patients with chronic myelogenous leukemia (CML). PGE1 caused a dose-dependent inhibition of normal marrow CFU-GM. Circulating CFU-GM were inhibited only at concentrations of 10(-5) mol/L or greater, and progenitor proliferation was, in fact, significantly stimulated at PGE1 concentrations between 10(-8) and 10(-6) mol/L. Bone marrow CFU-GM from patients with CML were inhibited in a manner similar to that of normal bone marrow. Circulating cells from patients with CML were, however, less sensitive to PGE1 inhibition than CML bone marrow cells and demonstrated a pattern intermediate between normal circulating and normal marrow progenitors. These studies suggest that peripheral blood and bone marrow contain different progenitor cell populations. 相似文献
950.
N Arber EK Han A Sgambato GA Piazza TM Delohery M Begemann CM Weghorst NH Kim R Pamukcu DJ Ahnen JC Reed IB Weinstein PR Holt 《Gastroenterology》1997,113(6):1892-1900
BACKGROUND & AIMS: Mutations of c-K-ras occur commonly in colonic neoplasms. The aim of this study was to determine how c-K-ras mutations alter the responses to the chemopreventive agent sulindac. METHODS: The parental rat intestinal cell line IEC-18 and c-K-ras-transformed derivatives were treated with sulindac sulfide. Cell cycle distribution was determined by flow-cytometric analysis (fluorescence-activated cell sorter), apoptosis by DNA fragmentation (laddering), flow cytometry, and microscopy, and changes in gene expression by immunoblotting. RESULTS: Sulindac sulfide inhibited cell growth and induced apoptosis in a time- and dose-dependent manner more rapidly in and at lower concentrations in parental cells than ras-transformed cells. Expression of the sulindac sulfide arrested cells in G0/G1, but cells entered apoptosis throughout the cell cycle. Proapoptotic protein Bak was relatively high in untreated parental cells and increased markedly after sulindac sulfide but was low in untreated ras-transformed cells and did not increase after sulindac sulfide. Expression of other Bcl-2 family members was unchanged after sulindac sulfide. However, sulindac sulfide reduced levels of cyclin D1 protein and cyclin E- and cyclin D1- associated kinase activity. CONCLUSIONS: c-K-ras-transformed enterocytes are relatively resistant to sulindac sulfide-induced growth inhibition and apoptosis, which may result from specific reduction of bak expression. (Gastroenterology 1997 Dec;113(6):1892-900) 相似文献