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991.
Dan Weng Robyn Marty-Roix Sandhya Ganesan Megan K. Proulx Gregory I. Vladimer William J. Kaiser Edward S. Mocarski Kimberly Pouliot Francis Ka-Ming Chan Michelle A. Kelliher Phillip A. Harris John Bertin Peter J. Gough Dmitry M. Shayakhmetov Jon D. Goguen Katherine A. Fitzgerald Neal Silverman Egil Lien 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(20):7391-7396
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Hypothalamic prolyl endopeptidase (PREP) regulates pancreatic insulin and glucagon secretion in mice
Jung Dae Kim Chitoku Toda Giuseppe D’Agostino Caroline J. Zeiss Ralph J. DiLeone John D. Elsworth Richard G. Kibbey Owen Chan Brandon K. Harvey Christopher T. Richie Mari Savolainen Timo My?h?nen Jin Kwon Jeong Sabrina Diano 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(32):11876-11881
Prolyl endopeptidase (PREP) has been implicated in neuronal functions. Here we report that hypothalamic PREP is predominantly expressed in the ventromedial nucleus (VMH), where it regulates glucose-induced neuronal activation. PREP knockdown mice (Prepgt/gt) exhibited glucose intolerance, decreased fasting insulin, increased fasting glucagon levels, and reduced glucose-induced insulin secretion compared with wild-type controls. Consistent with this, central infusion of a specific PREP inhibitor, , impaired glucose tolerance and decreased insulin levels in wild-type mice. Arguing further for a central mode of action of PREP, isolated pancreatic islets showed no difference in glucose-induced insulin release between Prepgt/gt and wild-type mice. Furthermore, hyperinsulinemic euglycemic clamp studies showed no difference between Prepgt/gt and wild-type control mice. Central PREP regulation of insulin and glucagon secretion appears to be mediated by the autonomic nervous system because Prepgt/gt mice have elevated sympathetic outflow and norepinephrine levels in the pancreas, and propranolol treatment reversed glucose intolerance in these mice. Finally, re-expression of PREP by bilateral VMH injection of adeno-associated virus–PREP reversed the glucose-intolerant phenotype of the Prepgt/gt mice. Taken together, our results unmask a previously unknown player in central regulation of glucose metabolism and pancreatic function.Prolyl endopeptidase (PREP; EC 3.4.21.26) is a highly conserved enzyme ( S170921). In humans and rodents it is highly expressed in the brain (2), including the cortex, striatum, hypothalamus, hippocampus, and amygdala (3–6). The physiological role of PREP remains elusive (7). Many studies have focused on the putative effect of PREP on neuropeptide levels because this enzyme could function to cleave virtually all neuropeptides shorter than 30 amino acids that contain an internal proline residue (8).However, much of our understanding of this enzyme is based on in vitro data. Because PREP’s putative targets regulate a large number of signaling pathways, PREP has the capacity to regulate a variety of cellular tasks.To gain a better understanding of the role of PREP in the hypothalamus, we analyzed the effect of PREP knockdown on hypothalamic mechanisms including glucose and energy metabolism. 相似文献
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Shih-Chieh Shao MS Kai-Cheng Chang MS Rong-Nan Chien MD Swu-Jane Lin PhD Ming-Jui Hung MD Yuk-Ying Chan MS Yea-Huei Kao Yang BPharm Edward Chia-Cheng Lai PhD 《Diabetes, obesity & metabolism》2020,22(1):128-134
Clinical trials have indicated that sodium-glucose co-transporter-2 (SGLT2) inhibitors have a favourable effect on serum alanine aminotransferase (ALT) levels in people with type 2 diabetes (T2D), but supporting evidence from real-world studies is lacking. We identified patients with T2D who initiated SGLT2 inhibitors during the period 2016 to 2017 from Chang Gung Research Database, which covers 1.3 million individuals from seven hospitals (6% of the Taiwan population). We classified patients by baseline ALT level and evaluated changes in ALT values from baseline to 1 year after initiation of SGLT2 inhibitors. We identified 11 690 new users of SGLT2 inhibitors with a mean (SD) age of 59.3 (11.8) years. The mean (SD) glycated haemoglobin and ALT levels were 8.9 (1.7)% and 34.7 (28.9) U/L at baseline, respectively. The mean change in ALT levels was −5.0 U/L (95% confidence interval [CI] –6.4, −3.5) 1 year after initiation of SGLT2 inhibitors. In patients with ALT levels ≤1× the upper limit of normal (ULN), the change in ALT levels was 1.6 U/L (95% CI –0.1, 3.4), while in those with ALT levels >1× ULN, the change in ALT levels was −26.5 U/L (95% CI –28.6, −24.3). The higher the baseline ALT level, the greater the decline after SGLT2 inhibitor treatment. Our findings suggest the initiation of SGLT2 inhibitors for T2D management could improve serum ALT levels in clinical practice, particularly in patients with especially high ALT levels. 相似文献
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Hoang Huong Thi Xuan Molassiotis Alex Chan Choi Wan Nguyen Thi Huong Liep Nguyen Van 《Sleep & breathing》2020,24(1):241-251
Sleep and Breathing - Although insomnia is common among cancer patients, its prevalence remains variable, and its risk factors and correlation with other cancer-related symptoms are not fully... 相似文献
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