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The finding of elevated intracellular levels of adenosine deaminase (ADA) in some patients with acute lymphoblastic leukemia has led to attempts to control this disease with the adenosine deaminase inhibitor 2'-deoxycoformycin (dCF). Because of clinical reports indicating its relative freedom from myelotoxicity, we have tested the effects of this drug on erythroid, granulocytic, and T-lymphocyte colony formation by normal marrow and peripheral blood cells. While clinically the drug has been found to be active at serum concentrations of approximately 10 microM, we have tested it at concentrations up to and including 1 mM. It was found that both erythroid and granulocytic colony growth was completely unaffected by 1 mM dCF, a concentration at least 2 magnitudes higher than that necessary to totally ablate intracellular ADA levels. T-lymphocyte colony growth was unaffected by 100 microM dCF, but at 1 mM some inhibition was observed. These findings therefore indicate that dCF, while able to cause leukemic cell lysis in vivo, has no inhibitory effect on the proliferative capacity of normal hematopoietic cells. 相似文献
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JV Lodhia S Appiah P Tcherveniakov P Krysiak 《Annals of the Royal College of Surgeons of England》2015,97(2):e27-e29
Iatrogenic injury accounts for the second most common cause of acquired diaphragmatic hernias after penetrating trauma. An increased incidence of these hernias has been observed with the widespread use of laparoscopic surgery. We present the case of a 65-year-old woman who initially underwent sigmoid resection for an adenocarcinoma and a subsequent liver resection for metastasis. She was noted to have a left lower lobe pulmonary nodule on surveillance computed tomography, for which she underwent a mini-thoracotomy for a planned resection. At the time of surgery, the pulmonary nodule was discovered to be a diaphragmatic hernia, most probably of iatrogenic origin. We discuss the difficulty in diagnosis given her history and the location of such a lesion. 相似文献
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The third international meeting on genetic disorders in the RAS/MAPK pathway: Towards a therapeutic approach 下载免费PDF全文
Bruce Korf Reza Ahmadian Judith Allanson Yoko Aoki Annette Bakker Emma Burkitt Wright Brian Denger Ype Elgersma Bruce D. Gelb Karen W. Gripp Bronwyn Kerr Maria Kontaridis Conxi Lazaro Corinne Linardic Reymundo Lozano Calum A. MacRae Ludwine Messiaen Sonia Mulero‐Navarro Benjamin Neel Scott Plotkin Katherine A. Rauen Amy Roberts Alcino J. Silva Sitta G. Sittampalam Chao Zhang Lisa Schoyer 《American journal of medical genetics. Part A》2015,167(8):1741-1746
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Hermine A van Duyvenvoorde Julian C Lui Sarina G Kant Wilma Oostdijk Antoinet CJ Gijsbers Mari?tte JV Hoffer Marcel Karperien Marie JE Walenkamp Cees Noordam Paul G Voorhoeve Verónica Mericq Alberto M Pereira Hedi L Claahsen-van de Grinten Sandy A van Gool Martijn H Breuning Monique Losekoot Jeffrey Baron Claudia AL Ruivenkamp Jan M Wit 《European journal of human genetics : EJHG》2014,22(5):602-609
Height is a highly heritable and classic polygenic trait. Recent genome-wide association studies (GWAS) have revealed that at least 180 genetic variants influence adult height. However, these variants explain only about 10% of the phenotypic variation in height. Genetic analysis of short individuals can lead to the discovery of novel rare gene defects with a large effect on growth. In an effort to identify novel genes associated with short stature, genome-wide analysis for copy number variants (CNVs), using single-nucleotide polymorphism arrays, in 162 patients (149 families) with short stature was performed. Segregation analysis was performed if possible, and genes in CNVs were compared with information from GWAS, gene expression in rodents'' growth plates and published information. CNVs were detected in 40 families. In six families, a known cause of short stature was found (SHOX deletion or duplication, IGF1R deletion), in two combined with a de novo potentially pathogenic CNV. Thirty-three families had one or more potentially pathogenic CNVs (n=40). In 24 of these families, segregation analysis could be performed, identifying three de novo CNVs and nine CNVs segregating with short stature. Four were located near loci associated with height in GWAS (ADAMTS17, TULP4, PRKG2/BMP3 and PAPPA). Besides six CNVs known to be causative for short stature, 40 CNVs with possible pathogenicity were identified. Segregation studies and bioinformatics analysis suggested various potential candidate genes. 相似文献
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Yamile Haito-Chavez Joanna K. Law Thomas Kratt Alberto Arezzo Mauro Verra Mario Morino Reem Z. Sharaiha Jan-Werner Poley Michel Kahaleh Christopher C. Thompson Michele B. Ryan Neel Choksi B. Joseph Elmunzer Sonia Gosain Eric M. Goldberg Rani J. Modayil Stavros N. Stavropoulos Drew B. Schembre Christopher J. DiMaio Vinay Chandrasekhara Muhammad K. Hasan Shyam Varadarajulu Robert Hawes Victoria Gomez Timothy A. Woodward Sergio Rubel-Cohen Fernando Fluxa Frank P. Vleggaar Venkata S. Akshintala Gottumukkala S. Raju Mouen A. Khashab 《Gastrointestinal endoscopy》2014
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Christopher E. Dandoy Stella M. Davies Kwang Woo Ahn Yizeng He Anders E. Kolb John Levine Stephanie Bo-Subait Hisham Abdel-Azim Neel Bhatt Joseph Chewing Shahinaz Gadalla Nicholas Gloude Robert Hayashi Nahal R. Lalefar Jason Law Margaret MacMillan Tracy OBrien Timothy Prestidge Akshay Sharma Peter Shaw Lena Winestone Mary Eapen 《Haematologica》2021,106(7):1839
With limited data comparing hematopoietic cell transplant outcomes between myeloablative total body irradiation (TBI) containing and non-TBI regimens in children with de novo acute myeloid leukemia, the aim of this study was to compare transplant-outcomes between these regimens. Cox regression models were used to compare transplant-outcomes after TBI and non-TBI regimens in 624 children transplanted between 2008 and 2016. Thirty two percent (n=199) received TBI regimens whereas 68% (n=425) received non-TBI regimens. Five-year non-relapse mortality was higher with TBI regimens (22% vs. 11%, P<0.0001) but relapse was lower (23% vs. 37%, P<0.0001) compared to non-TBI regimens. Consequently, overall (62% vs. 60%, P=1.00) and leukemia-free survival (55% vs. 52%, P=0.42) did not differ between treatment groups. Grade 2-3 acute graft versus host disease was higher with TBI regimens (56% vs. 27%, P<0.0001) but not chronic graft versus host disease. The 3-year incidence of gonadal or growth hormone deficiency was higher with TBI regimens (24% vs. 8%, P<0.001) but there were no differences in late pulmonary, cardiac or renal impairment. In the absence of a survival advantage, the choice of TBI or non-TBI regimen merits careful consideration with the data favoring non-TBI regimens to limit the burden of morbidity associated with endocrine dysfunction. 相似文献