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101.
Luis Velázquez-Pérez DSc Roberto Rodriguez-Labrada PhD Yasmani González-Garcés BSc Eduardo Arrufat-Pie MD Reidenis Torres-Vega BSc Jacqueline Medrano-Montero PhD Beatriz Ramirez-Bautista MD Yaimeé Vazquez-Mojena MSc Georg Auburger MD Fay Horak PhD Ulf Ziemann PhD Christopher M. Gomez PhD 《Movement disorders》2021,36(2):471-480
102.
Alexey A. Shadrin PhD Sören Mucha PhD David Ellinghaus PhD Mary B. Makarious BSc Cornelis Blauwendraat PhD Ashwin A.K. Sreelatha MSc Antonio Heras-Garvin PhD Jinhui Ding PhD Monia Hammer PhD Alexandra Foubert-Samier MD Wassilios G. Meissner MD Olivier Rascol PhD Anne Pavy-Le Traon MD Oleksandr Frei PhD Kevin S. O'Connell PhD Shahram Bahrami PhD Stefan Schreiber MD Wolfgang Lieb MD Martina Müller-Nurasyid PhD Ulf Schminke MD Georg Homuth PhD Carsten O. Schmidt PhD Markus M. Nöthen MD Per Hoffmann PhD Christian Gieger PhD Gregor Wenning MD for the European Multiple System Atrophy Study Group J. Raphael Gibbs PhD Andre Franke PhD John Hardy PhD Nadia Stefanova PhD Thomas Gasser MD Andrew Singleton PhD Henry Houlden MD Sonja W. Scholz MD Ole A. Andreassen PhD Manu Sharma PhD 《Movement disorders》2021,36(2):449-459
103.
Shirley K. Knauer Britta Unruhe Sarah Karczewski Rouven Hecht Verena Fetz Carolin Bier Sandra Friedl Barbara Wollenberg Ralph Pries Negusse Habtemichael Ulf‐Rüdiger Heinrich Roland H. Stauber 《Human mutation》2013,34(2):395-404
Survivin (BIRC5) is an acknowledged cancer therapy‐resistance factor and overexpressed in head and neck squamous cell carcinomas (HNSCC). Driven by its nuclear export signal (NES), Survivin shuttles between the nucleus and the cytoplasm, and is detectable in both cellular compartments in tumor biopsies. Although predominantly nuclear Survivin is considered a favorable prognostic disease marker for HNSCC patients, the underlying molecular mechanisms are not resolved. Hence, we performed immunohistochemical and mutational analyses using laser capture microdissection on HNSCC biopsies from patients displaying high levels of nuclear Survivin. We found somatic BIRC5 mutations, c.278T>C (p.Phe93Ser), c.292C>T (p.Leu98Phe), and c.288A>G (silent), in tumor cells, but not in corresponding normal tissues. Comprehensive functional characterization of the Survivin mutants by ectopic expression and microinjection experiments revealed that p.Phe93Ser, but not p.Leu98Phe inactivated Survivin's NES, resulted in a predominantly nuclear protein, and attenuated Survivin's dual cytoprotective activity against chemoradiation‐induced apoptosis. Notably, in xenotransplantation studies, HNSCC cells containing the p.Phe93Ser mutation responded significantly better to cisplatin‐based chemotherapy. Collectively, our results underline the disease relevance of Survivin's nucleocytoplasmic transport, and provide first evidence that genetic inactivation of Survivin's NES may account for predominantly nuclear Survivin and increased therapy response in cancer patients. 相似文献
104.
Elisa Postrach Rosa Aspalter Ulf Elbelt Michael Koller Rita Longin J?rg-Dieter Schulzke Luzia Valentini 《Journal of medical Internet research》2013,15(10)
Background
The Internet is widely available and commonly used for health information; therefore, Web-based weight loss programs could provide support to large parts of the population in self-guided weight loss. Previous studies showed that Web-based weight loss interventions can be effective, depending on the quality of the program. The most effective program tools are visual progress charts or tools for the self-monitoring of weight, diet, and exercises. KiloCoach, a commercial program currently available in German-speaking countries, incorporates these features. A previous investigation showed that the program effectively supports users in losing weight.Objective
We investigated weight loss dynamics stratified by weight loss success after 6-month use of KiloCoach. Furthermore, we analyzed possible associations between intensity of program use and weight loss. The results are intended for tailoring user recommendations for weight-loss Internet platforms.Methods
Datasets of KiloCoach users (January 1, 2008 to December 31, 2011) who actively used the platform for 6 months or more were assigned to this retrospective analysis. Users (N=479) were 42.2% men, mean age of 44.0 years (SD 11.7), with a mean body mass index (BMI) of 31.7 kg/m2 (SD 3.2). Based on the weight loss achieved after 6 months, 3 success groups were generated. The unsuccessful group lost <5%, the moderate success group lost 5%-9.9%, and the high success group lost ≥10% of their baseline body weight. At baseline, the unsuccessful (n=261, 54.5%), moderate success (n=133, 27.8%), and high success (n=85, 17.8%) groups were similar in age, weight, BMI, and gender distribution.Results
After 6 months, the unsuccessful group lost 1.2% (SD 2.4), the moderate success group lost 7.4% (SD 1.5), and the high success group lost 14.2% (SD 3.8) of their initial weight (P<.001). Multivariate regression showed that early weight loss (weeks 3-4), the total number of dietary protocols, and the total number of weight entries were independent predictors for 6-month weight reduction (all P<.001) explaining 52% of the variance in weight reduction. Sensitivity analysis by baseline carried forward method confirmed all independent predictors of 6-month weight loss and reduced the model fit by only 11%. The high success group lost weight faster and maintained weight loss more efficiently than the other groups (P<.001). Early weight loss was associated with weight maintenance after 1 year and 2 years (both P<.001). Weight dynamics did not differ between men and women over 6 months when adjusted for baseline and usage parameters (P=.91). The percentage of male long-term users was unusually high (42.2%).Conclusions
Our results suggest that early weight loss and close program adherence (ie, 5 dietary protocols per week and weekly entering of current weight), especially in the early phase of program usage, can improve weight loss outcome. 相似文献105.
106.
Ulf C. Schneider Katrin Bohlmann Peter Vajkoczy Hans-Beatus Straub 《Acta neurochirurgica》2015,157(4):721-728
107.
108.
109.
Yuan XM Li W Dalen H Lotem J Kama R Sachs L Brunk UT 《Proceedings of the National Academy of Sciences of the United States of America》2002,99(9):6286-6291
The tumor suppressor wild-type p53 can induce apoptosis. M1-t-p53 myeloid leukemic cells have a temperature-sensitive p53 protein that changes its conformation to wild-type p53 after transfer from 37 degrees C to 32 degrees C. We have now found that these cells showed an early lysosomal rupture after transfer to 32 degrees C. Mitochondrial damage, including decreased membrane potential and release of cytochrome c, and the appearance of apoptotic cells occurred later. Lysosomal rupture, mitochondrial damage, and apoptosis were all inhibited by the cytokine IL-6. Some other compounds can also inhibit apoptosis induced by p53. The protease inhibitor N-tosyl-l-phenylalanine chloromethyl ketone inhibited the decrease in mitochondrial membrane potential and cytochrome c release, the Ca(2+)-ATPase inhibitor thapsigargin inhibited only cytochrome c release, and the antioxidant butylated hydroxyanisole inhibited only the decrease in mitochondrial membrane potential. In contrast to IL-6, these other compounds that inhibited some of the later occurring mitochondrial damage did not inhibit the earlier p53-induced lysosomal damage. The results indicate that apoptosis is induced by p53 through a lysosomal-mitochondrial pathway that is initiated by lysosomal destabilization, and that this pathway can be dissected by using different apoptosis inhibitors. These findings on the induction of p53-induced lysosomal destabilization can also help to formulate new therapies for diseases with apoptotic disorders. 相似文献
110.