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<正>The efficacy of platelet-rich plasma(PRP)to promote tissue regeneration has been largely confirmed in several clinical settings,such as in human maxillo-facial(Froum et al.,2002),heart(Vu et al.,2015)and orthopaedic surgery(Zhang and Wang,2010).Up to date,few studies are available regarding the topical use of platelet-rich plasma in models of 相似文献
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Balietti M Giorgetti B Fattoretti P Grossi Y Di Stefano G Casoli T Platano D Solazzi M Orlando F Aicardi G Bertoni-Freddari C 《Rejuvenation research》2008,11(3):631-640
Ketogenic diets (KDs) have beneficial effects on several diseases, such as epilepsy, mitochondriopathies, cancer, and neurodegeneration. However, little is known about their effects on aging individuals. In the present study, late-adult (19-month-old) rats were fed for 8 weeks with two medium chain triglycerides (MCT)-KDs, and the following morphologic parameters reflecting synaptic plasticity were evaluated in stratum moleculare of hippocampal CA1 region (SM CA1) and outer molecular layer of hippocampal dentate gyrus (OML DG): average area (S), numeric density (Nv(s)), and surface density (Sv) of synapses, and average volume (V), numeric density (Nv(m)), and volume density (Vv) of synaptic mitochondria. In SM CA1, MCT-KDs induced the early appearance of the morphologic patterns typical of old animals (higher S and V, and lower Nv(s) and Nv(m)). On the contrary, in OML DG, Sv and Vv of MCT-KDs-fed rats were higher (as a result of higher Nv(s) and Nv(m)) versus controls; these modifications are known to improve synaptic function and metabolic supply. The opposite effects of MCT-KDs might reflect the different susceptibility to aging processes: OML DG is less vulnerable than SM CA1, and the reactivation of ketone bodies uptake and catabolism might occur more efficiently in this region, allowing the exploitation of their peculiar metabolic properties. Present findings provide the first evidence that MCT-KDs may cause opposite morphologic modifications, being potentially harmful for SM CA1 and potentially advantageous for OML DG. This implies risks but also promising potentialities for their therapeutic use during aging. 相似文献
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Maria Angela Guzzardi Leanne Hodson Letizia Guiducci Elena Sanguinetti Pietro Di Cecco Tiziana Liistro Cristina Vassalle Silvia Pardini Lucia Giorgetti Piero A. Salvadori Silvia Burchielli Patricia Iozzo 《Diabetologia》2014,57(9):1937-1946
Aims/hypothesis
Cardiac steatosis and myocardial insulin resistance elevate the risk of cardiac complications in obesity and diabetes. We aimed to disentangle the effects of circulating glucose, insulin and NEFA on myocardial triacylglycerol (TG) content and myocardial glucose uptake.Methods
Twenty-two pigs were stratified according to four protocols: low NEFA?+?low insulin (nicotinic acid), high NEFA?+?low insulin (fasting) and high insulin?+?low NEFA?±?high glucose (hyperinsulinaemia–hyperglycaemia or hyperinsulinaemia–euglycaemia). Positron emission tomography, [U-13C]palmitate enrichment techniques and tissue biopsies were used to assess myocardial metabolism. Heart rate and rate–pressure product (RPP) were monitored.Results
Myocardial glucose extraction was increased by NEFA suppression and was similar in the hyperinsulinaemia–hypergylcaemia, hyperinsulinaemia–euglycaemia and nicotinic acid groups. Hyperglycaemia enhanced myocardial glucose uptake due to a mass action. Myocardial TG content was greatest in the fasting group, whereas hyperinsulinaemia had a mild effect. Heart rate and RPP increased in hyperinsulinaemia–euglycaemia, in which cardiac glycogen content was reduced. Heart rate correlated with myocardial TG and glycogen content.Conclusions/interpretation
Elevated NEFA levels represent a powerful, self-sufficient promoter of cardiac TG accumulation and are a downregulator of myocardial glucose uptake, indicating that the focus of treatment should be to ‘normalise’ adipose tissue function to lower the risk of cardiac TG accumulation and myocardial insulin resistance. The observation that hyperinsulinaemia and nicotinic acid led to myocardial fuel deprivation provides a potential explanation for the cardiovascular outcomes reported in recent intensive glucose-lowering and NEFA-lowering clinical trials. 相似文献27.
Montanari Eva Bonasoni Maria Paola Alessandrini Federica Frazzi Raffaele Mocchegiani Federico Busardò Francesco Paolo Giorgetti Raffaele Tagliabracci Adriano 《Forensic Toxicology》2019,37(2):507-516
Forensic Toxicology - 相似文献
28.
Alessia Gimelli Riccardo Liga Assuero Giorgetti Brunella Favilli Emilio Maria Pasanisi Paolo Marzullo 《Journal of nuclear cardiology》2016,23(4):728-736
Background
An interaction between coronary anatomy, myocardial perfusion, and left ventricular (LV) functional parameters in the development of mechanical LV dyssynchrony (LVD) has been suggested. This study examined the correlates of LVD in a large sample size of patients with known or suspected coronary artery disease (CAD) using cadmium-zinc-telluride camera.Methods
Six-hundred and fifty-seven consecutive patients who underwent myocardial perfusion imaging (MPI) and coronary angiography were included. Coronary stenosis >70% was considered significant. LV perfusion and functional parameters were computed from MPI images. The presence of significant LVD was evaluated by phase standard deviation and histogram bandwidth.Results
415/657 (63%) patients had significant CAD. LVD was present in 247 (38%) patients and was associated with the presence of a higher CAD burden (P < .001), more impaired measures of LV perfusion (P < .001), contractile function (P < .001), and larger LV volumes (P < .001). By multivariate analysis, the LV end-systolic volume index (P < .001) and ischemic burden (P < .001) were the strongest predictors of LVD independent of CAD extent and LV systolic dysfunction.Conclusions
LVD is frequent in patients undergoing MPI for suspected or known CAD. Its presence is independent of CAD burden and LV systolic dysfunction, but is dependent on the presence of myocardial perfusion abnormalities and LV end-systolic volume.29.
30.
Joel Jakobsson Maria Bjerke Carl Johan Ekman Carl Sellgren Anette GM Johansson Henrik Zetterberg Kaj Blennow Mikael Landén 《Neuropsychopharmacology》2014,39(10):2349-2356
Bipolar disorder (BD) is characterized by mood swings between manic and depressive states. The etiology and pathogenesis of BD is unclear, but many of the affected cognitive domains, as well as neuroanatomical abnormalities, resemble symptoms and signs of small vessel disease. In small vessel disease, cerebrospinal fluid (CSF) markers reflecting damages in different cell types and subcellular structures of the brain have been established. Hence, we hypothesized that CSF markers related to small vessel disease may also be applicable as biomarkers for BD. To investigate this hypothesis, we sampled CSF from 133 patients with BD and 86 healthy controls. The concentrations of neurofilament light chain (NF-L), myelin basic protein (MBP), S100B, and heart-type fatty acid binding protein (H-FABP) were measured in CSF and analyzed in relation to diagnosis, clinical characteristics, and ongoing medications. Hereby we found an elevation of the marker of subcortical axonal damage, NF-L, in bipolar subjects. We also identified positive associations between NF-L and treatment with atypical antipsychotics, MBP and lamotrigine, and H-FABP and lithium. These findings indicate axonal damage as an underlying neuropathological component of bipolar disorder, although the clinical value of elevated NF-L remains to be validated in follow-up studies. The associations between current medications and CSF brain injury markers might aid in the understanding of both therapeutic and adverse effects of these drugs. 相似文献