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991.
Phase III controlled evaluation of glutamine for decreasing stomatitis in patients receiving fluorouracil (5-FU)-based chemotherapy. 总被引:2,自引:0,他引:2
S H Okuno C O Woodhouse C L Loprinzi J A Sloan B I LaVasseur D Clemens-Schutjer D Swan C Axvig L P Ebbert M R Tirona J C Michalak N Pierson 《American journal of clinical oncology》1999,22(3):258-261
Mucositis is a prominent dose-limiting toxicity associated with 5-FU-based chemotherapy. On the basis of preliminary data suggesting that the amino acid glutamine could alleviate this problem, the authors developed this trial. Patients scheduled to receive their first 5-FU-based chemotherapy regimen were selected for study. Following stratification, patients were randomized, in a double-blind manner, to receive oral glutamine or a placebo preparation in a prophylactic manner. Patients in both groups were given oral cryotherapy before chemotherapy and were evaluated for mucositis by standard physicians' evaluation and by a self-report instrument. Sixty-six patients were randomized to receive glutamine and 68 to receive the placebo preparation. There were no significant differences or substantial trends in the mucositis scores between the two study arms as measured by either the physicians or the patients. It was concluded that the dose and schedule of glutamine used in this clinical trial does not alleviate 5-FU-induced mucositis. 相似文献
992.
Paternal or Maternal Uniparental Disomy of Chromosome 16 Resulting in Homozygosity of a Mutant Allele Causes Fanconi Anemia 下载免费PDF全文
Frank X. Donovan Danielle C. Kimble Francis P. Lach Ursula Harper Aparna Kamat MaryPat Jones Erica M. Sanborn Rebecca Tryon John E. Wagner Margaret L. MacMillan Elaine A. Ostrander Arleen D. Auerbach Agata Smogorzewska Settara C. Chandrasekharappa 《Human mutation》2016,37(5):465-468
Fanconi anemia (FA) is a rare inherited disorder caused by pathogenic variants in one of 19 FANC genes. FA patients display congenital abnormalities, and develop bone marrow failure, and cancer susceptibility. We identified homozygous mutations in four FA patients and, in each case, only one parent carried the obligate mutant allele. FANCA and FANCP/SLX4 genes, both located on chromosome 16, were the affected recessive FA genes in three and one family respectively. Genotyping with short tandem repeat markers and SNP arrays revealed uniparental disomy (UPD) of the entire mutation‐carrying chromosome 16 in all four patients. One FANCA patient had paternal UPD, whereas FA in the other three patients resulted from maternal UPD. These are the first reported cases of UPD as a cause of FA. UPD indicates a reduced risk of having another child with FA in the family and has implications in prenatal diagnosis. 相似文献
993.
Cine dyscontractility index: A novel marker of mechanical dyssynchrony that predicts response to cardiac resynchronization therapy 下载免费PDF全文
Konrad Werys MS Joanna Petryka‐Mazurkiewicz MD PhD Łukasz Błaszczyk MS Jolanta Miśko MD PhD Mateusz Śpiewak MD PhD Łukasz A. Małek MD PhD Łukasz Mazurkiewicz MD PhD Barbara Miłosz‐Wieczorek MD Magdalena Marczak MD PhD Agata Kubik MS Agnieszka Dąbrowska Ewa Piątkowska‐Janko PhD Błażej Sawionek PhD Rohan Wijesurendra MD Stefan K. Piechnik PhD Piotr Bogorodzki PhD 《Journal of magnetic resonance imaging : JMRI》2016,44(6):1483-1492
994.
Aurélie Ernst David T.W. Jones Kendra K. Maass Agata Rode Katharina I. Deeg Billy Michael Chelliah Jebaraj Andrey Korshunov Volker Hovestadt Michael A. Tainsky Kristian W. Pajtler Sebastian Bender Sebastian Brabetz Susanne Gröbner Marcel Kool Frauke Devens Jennifer Edelmann Cindy Zhang Pedro Castelo‐Branco Uri Tabori David Malkin Karsten Rippe Stephan Stilgenbauer Stefan M. Pfister Marc Zapatka Peter Lichter 《International journal of cancer. Journal international du cancer》2016,138(12):2905-2914
Chromothripsis is a recently discovered form of genomic instability, characterized by tens to hundreds of clustered DNA rearrangements resulting from a single dramatic event. Telomere dysfunction has been suggested to play a role in the initiation of this phenomenon, which occurs in a large number of tumor entities. Here, we show that telomere attrition can indeed lead to catastrophic genomic events, and that telomere patterns differ between cells analyzed before and after such genomic catastrophes. Telomere length and telomere stabilization mechanisms diverge between samples with and without chromothripsis in a given tumor subtype. Longitudinal analyses of the evolution of chromothriptic patterns identify either stable patterns between matched primary and relapsed tumors, or loss of the chromothriptic clone in the relapsed specimen. The absence of additional chromothriptic events occurring between the initial tumor and the relapsed tumor sample points to telomere stabilization after the initial chromothriptic event which prevents further shattering of the genome. 相似文献
995.
Kilpeläinen TO Lakka TA Laaksonen DE Mager U Salopuro T Kubaszek A Todorova B Laukkanen O Lindström J Eriksson JG Hämäläinen H Aunola S Ilanne-Parikka P Keinänen-Kiukaanniemi S Tuomilehto J Laakso M Uusitupa M;Finnish Diabetes Prevention Study Group 《Metabolism: clinical and experimental》2008,57(3):428-436
Single nucleotide polymorphisms (SNPs) in the ADRB2, ADRB3, TNF, IL6, IGF1R, LIPC, LEPR, and GHRL genes were associated with the conversion from impaired glucose tolerance (IGT) to type 2 diabetes mellitus (T2D) in the Finnish Diabetes Prevention Study (DPS). In this study, we determined whether polymorphisms in these genes modified the effect of changes in physical activity (PA) on the risk of T2D in the DPS. Moreover, we assessed whether the polymorphisms modified the effect of changes in PA on changes in measures of body fat, serum lipids, and blood pressure during the first year of the follow-up of the DPS. Overweight subjects with IGT (n = 487) were followed for an average of 4.1 years, and PA was assessed annually with a questionnaire. The interactions of the polymorphisms with changes in total and moderate-to-vigorous PA on the conversion to T2D during the 4.1-year follow-up were assessed using Cox regression with adjustments for the other components of the intervention (dietary changes, weight reduction). Univariate analysis of variance was used to assess interactions on changes in continuous variables during the first year of the follow-up. No interaction between the polymorphisms and PA on the conversion to T2D was found. The Leu72Met (rs696217) polymorphism in GHRL modified the effect of moderate-to-vigorous PA on changes in weight and waist circumference, the -501A/C (rs26802) polymorphism in GHRL modified the effect of total and moderate-to-vigorous PA on change in high-density lipoprotein cholesterol, and the Lys109Arg (rs1137100) polymorphism in LEPR modified the effect of total PA on change in blood pressure. In conclusion, genetic variation may modify the magnitude of the beneficial effects of PA on characteristics of the metabolic syndrome in persons with IGT. 相似文献
996.
Wilson DN Schluenzen F Harms JM Starosta AL Connell SR Fucini P 《Proceedings of the National Academy of Sciences of the United States of America》2008,105(36):13339-13344
The oxazolidinones represent the first new class of antibiotics to enter into clinical usage within the past 30 years, but their binding site and mechanism of action has not been fully characterized. We have determined the crystal structure of the oxazolidinone linezolid bound to the Deinococcus radiodurans 50S ribosomal subunit. Linezolid binds in the A site pocket at the peptidyltransferase center of the ribosome overlapping the aminoacyl moiety of an A-site bound tRNA as well as many clinically important antibiotics. Binding of linezolid stabilizes a distinct conformation of the universally conserved 23S rRNA nucleotide U2585 that would be nonproductive for peptide bond formation. In conjunction with available biochemical data, we present a model whereby oxazolidinones impart their inhibitory effect by perturbing the correct positioning of tRNAs on the ribosome. 相似文献
997.
998.
999.
Wojciech Ambrosius Justyna Rosinska Slawomir Michalak Maria Lukasik Radoslaw Kazmierski Wojciech Kozubski 《Neurologia i neurochirurgia polska》2018,52(2):263-266
The role of the thyroid gland in ischemic stroke pathology is not well understood. As thyroid hormones modulate the extracellular matrix, we explored the possible link between them and secreted protein acidic and rich in cysteine like 1 (SC1) – one of the extracellular matrix molecules.In the 81 patients with acute ischemic stroke, serum SC1 levels were much higher compared with 30 control subjects: 4.47 vs 2.43 ng/mL (p < 0.001). Serum levels of free thyroxine (fT4) were higher in stroke subjects compared to those of controls (p = 0.03). In stroke patients, TSH concentration was lower than in the control group (p = 0.03). SC1 levels positively correlated with fT4 levels (p = 0.02) and negatively with TSH (p = 0.03) in stroke patients.Our results confirmed the association between thyroid hormones and SC1 – extracellular matrix protein. 相似文献
1000.