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71.
Pavlos Brikas DVM PhD Bogdan F. Kania DVM Jean Fioramonti PhD DSc Dr. Lionel Bueno PhD DSc 《Digestive diseases and sciences》1993,38(6):1079-1086
The effects of duodenal distension on forestomach and abomasal motility were investigated in conscious sheep chronically fitted with intraparietal electrodes, a duodenal cannula, and an intracerebroventricular cannula. Duodenal distensions with a balloon inflated with 40 ml (DD40) of water reduced the frequency of forestomach and abomasal contractions by 45 and 32%, respectively, while distension with 80 ml (DD80) induced a total inhibition. Methysergide, a mixed 5HT1-5HT2 antagonist administered intravenously (200 g/kg) or intracerebroventricularly (20 g/kg) suppressed the DD40-induced inhibition and reduced that induced by DD80. Sprioxatrine, a selective 5HT1A antagonist, intravenously (100 g/kg) or intracerebroventricularly (10 g/kg), suppressed the DD40 and DD80-induced inhibition, which was also attenuated by the 5HT2 antagonist ritanserin given intravenously (200 g/kg) or intracerebroventricularly (20 g/kg). Granisetron, a 5HT3 antagonist, injected intravenously (150 g/kg), abolished the effects of DD40 and DD80 while it had no antagonistic action on DD40 and DD80 when given intracerebroventricularly (15 g/kg). It is concluded that in sheep, duodenal distension inhibits forestomach and abomasal motility through 5HT1A and 5HT2 receptors at the level of the central nervous system and 5HT3 receptors located peripherally.This work was presented in part at the First United European Gastroenterology Week, September 25–30, 1992, Athens, Greece. 相似文献
72.
73.
Schinzel–Giedion syndrome in two Brazilian patients: Report of a novel mutation in SETBP1 and literature review of the clinical features 下载免费PDF全文
74.
Sant’ Anna B. G. Musolino N. R. C. Gadelha M. R. Marques C. Castro M. Elias P. C. L. Vilar L. Lyra R. Martins M. R. A. Quidute A. R. P. Abucham J. Nazato D. Garmes H. M. Fontana M. L. C. Boguszewski C. L. Bueno C. B. Czepielewski M. A. Portes E. S. Nunes-Nogueira V. S. Ribeiro-Oliveira A. Francisco R. P. V. Bronstein M. D. Glezer A. 《Pituitary》2020,23(2):120-128
Pituitary - To evaluate the maternal–fetal outcomes of CAB-induced pregnancies in patients with prolactinoma in a large cohort. The prevalence of tumor growth, miscarriage, preterm, low birth... 相似文献
75.
C. Baquero‐Montoya M.C. Gil‐Rodríguez M.E. Teresa‐Rodrigo M. Hernández‐Marcos G. Bueno‐Lozano I. Bueno‐Martínez S. Remeseiro R. Fernández‐Hernández M. Bassecourt‐Serra M. Rodríguez de Alba E. Queralt A. Losada B. Puisac F.J. Ramos J. Pié 《Clinical genetics》2014,85(5):446-451
The disorders caused by mutations in genes encoding subunits and accessory proteins of cohesin complex are collectively termed as cohesinopathies. The best known cohesinopathy is Cornelia de Lange Syndrome (CdLS), which is a multisystem developmental disorder characterized by facial dysmorphism, limb malformations, growth and cognitive impairment. Mutations in five genes, encoding subunits of the cohesin complex (SMC1A, SMC3, RAD21) and its regulators (NIPBL, HDAC8), are responsible for ~70% of CdLS cases. We describe a 16‐year‐old boy with facial dysmorphism, growth retardation, intellectual disability, hirsutism and small hands, who has a small Supernumerary Marker Chromosome (sSMC) present in mosaic form. sSMC is composed of two duplicated segments encompassing 17 genes including SMC1A gene, at the regions Xp11.22 and Xp11.21q11.1. Clinical comparison between our patient with a previously reported individual with a SMC1A duplication and four male carriers of similar sSMC reported in databases, suggest that they all share clinical features related to cohesinopathies. Although our patient does not have the classical CdLS craniofacial phenotype, he has pre and postnatal growth retardation, intellectual disability and mild musculoskeletal anomalies, features commonly seen in patients with cohesinopathies. 相似文献
76.
Sun K Wernstedt Asterholm I Kusminski CM Bueno AC Wang ZV Pollard JW Brekken RA Scherer PE 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(15):5874-5879
Obese fat pads are frequently undervascularized and hypoxic, leading to increased fibrosis, inflammation, and ultimately insulin resistance. We hypothesized that VEGF-A-induced stimulation of angiogenesis enables sustained and sufficient oxygen and nutrient exchange during fat mass expansion, thereby improving adipose tissue function. Using a doxycycline (Dox)-inducible adipocyte-specific VEGF-A overexpression model, we demonstrate that the local up-regulation of VEGF-A in adipocytes improves vascularization and causes a "browning" of white adipose tissue (AT), with massive up-regulation of UCP1 and PGC1α. This is associated with an increase in energy expenditure and resistance to high fat diet-mediated metabolic insults. Similarly, inhibition of VEGF-A-induced activation of VEGFR2 during the early phase of high fat diet-induced weight gain, causes aggravated systemic insulin resistance. However, the same VEGF-A-VEGFR2 blockade in ob/ob mice leads to a reduced body-weight gain, an improvement in insulin sensitivity, a decrease in inflammatory factors, and increased incidence of adipocyte death. The consequences of modulation of angiogenic activity are therefore context dependent. Proangiogenic activity during adipose tissue expansion is beneficial, associated with potent protective effects on metabolism, whereas antiangiogenic action in the context of preexisting adipose tissue dysfunction leads to improvements in metabolism, an effect likely mediated by the ablation of dysfunctional proinflammatory adipocytes. 相似文献
77.
78.
Barba P Sampol A Calbacho M Gonzalez J Serrano J Martínez-Sánchez P Fernández P García-Boyero R Bueno J Ribera JM 《American journal of hematology》2012,87(6):631-634
The present study reports the Spanish PETHEMA group experience in 31 heavily pretreated relapsed/refractory acute lymphoblastic leukemia (ALL) and lymphoma (LL) patients treated with clofarabine-based regimens. The complete remission (CR) rate was 31% (median CR duration of 3 months [range 2–28]) and the overall survival probability at 1 year was 10% (95%CI 4–16%). Responses were seen in B and T lineage diseases and in patients with adverse cytogenetics. Hematological and infectious grade >3 toxicities were found in 100 and 67% of the patients, respectively, with 7 (23%) treatment-related deaths. Other organ toxicities were infrequent. Clofarabine-based chemotherapy regimens might induce CRs in ALL and LL patients, but hematological toxicity and infections may limit their use in heavily pretreated patients. 相似文献
79.
Daniela Teixeira Joaquim Soares de Almeida Bruna Visniauskas Guiomar Nascimento Gomes Aparecida Emiko Hirata Valquiria Bueno 《Clinics (S?o Paulo, Brazil)》2013,68(6):858-864
OBJECTIVES:
Myeloid-derived suppressor cells contribute to the immunosuppressive microenvironment during tumor development and limit the efficacy of cancer immunotherapy. Identifying myeloid-derived suppressor cells and associated factors is the first step in creating strategies to reverse the suppressive effects of these cells on the immune system.METHODS:
To induce lung cancer, we administered 2 doses of urethane to BALB/c mice and observed these animals for 120 days. After this period, we evaluated the percentage of myeloid-derived suppressor cells in the blood, lung and bone marrow. The expression of alpha-smooth muscle actin, transforming growth factor-β, Toll-like receptor 2, Toll-like receptor 4, and interleukin-6 was also determined in the lung tissue.RESULTS:
Myeloid-derived suppressor cells were increased in all evaluated tissues after lung cancer development in association with increased Toll-like receptor 4 expression and decreased interleukin-6 expression in the lung. We observed alpha-smooth muscle actin and transforming growth factor-β expression in lung nodules.CONCLUSIONS:
We believe that the early diagnosis of cancer through determining the blood levels of myeloid-derived suppressor cells followed by the depletion of these cells should be further investigated as a possible approach for cancer treatment. 相似文献80.
Elizabete Bagordakis Lívia Máris Ribeiro Paranaiba Luciano Abreu Brito Sibele Nascimento de Aquino Ana Camila Messetti Hercílio Martelli‐Junior Mario Sergio Oliveira Swerts Edgard Graner Maria Rita Passos‐Bueno Ricardo D. Coletta DDS MS PhD 《American journal of medical genetics. Part A》2013,161(5):1177-1180