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91.
Mai Uchida Joseph Biederman John D. E. Gabrieli Jamie Micco Carlo de Los Angeles Ariel Brown Tara Kenworthy Elana Kagan Susan Whitfield-Gabrieli 《Social cognitive and affective neuroscience》2015,10(12):1738-1748
This study investigated the neural basis of individual variation in emotion regulation, specifically the ability to reappraise negative stimuli so as to down-regulate negative affect. Brain functions in young adults were measured with functional Magnetic Resonance Imaging during three conditions: (i) attending to neutral pictures; (ii) attending to negative pictures and (iii) reappraising negative pictures. Resting-state functional connectivity was measured with amygdala and dorsolateral prefrontal cortical (DLPFC) seed regions frequently associated with emotion regulation. Participants reported more negative affect after attending to negative than neutral pictures, and less negative affect following reappraisal. Both attending to negative vs neutral pictures and reappraising vs attending to negative pictures yielded widespread activations that were significantly right-lateralized for attending to negative pictures and left-lateralized for reappraising negative pictures. Across participants, more successful reappraisal correlated with less trait anxiety and more positive daily emotion, greater activation in medial and lateral prefrontal regions, and lesser resting-state functional connectivity between (a) right amygdala and both medial prefrontal and posterior cingulate cortices, and (b) bilateral DLPFC and posterior visual cortices. The ability to regulate emotion, a source of resilience or of risk for distress, appears to vary in relation to differences in intrinsic functional brain architecture. 相似文献
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93.
Variations in the morphology of pancreas are not very common. We observed a rare variant of the uncinate process of the pancreas that extended in the mesentery of the small intestine. After its origin from the lower part of the head of the pancreas, the mesenteric process (MP) passed over the third part of the duodenum to enter the mesentery of the jejunum and ileum and extended up to the level of the pelvic brim. The branches of the superior mesenteric vessels were embedded in the extended MP of the pancreas. This aberrant extension of the pancreas was drained by a narrow duct, which joined the main pancreatic duct inside the head. We did not observe a separate uncinate process arising from the head. On histology normal acini and endocrine cells were observed in the extension. This variant is important as symptoms of pancreatic disease from such extensions may be confused with other commonly encountered acute or chronic abdominal conditions. 相似文献
94.
Teoh G Tai YT Urashima M Shirahama S Matsuzaki M Chauhan D Treon SP Raje N Hideshima T Shima Y Anderson KC 《Blood》2000,95(3):1039-1046
It has been reported that the activation of multiple myeloma (MM) cells by CD40 induces proliferation, growth arrest, and apoptosis. To determine whether the biologic sequelae of CD40 activation in MM cells depends on p53 function, we identified temperature-sensitive p53 mutations in the RPMI 8226 (tsp53E285K) and the HS Sultan (tsp53Y163H) MM cell lines. These cells were then used as a model system of inducible wtp53-like function because wild-type-like p53 is induced at permissive (30 degrees C) but not at restrictive (37 degrees C) temperatures. Using p21-luciferase reporter assays, we confirmed that CD40 induces p53 transactivation in RPMI 8226 and HS Sultan cells cultured under permissive, but not restrictive, conditions. Furthermore, CD40 activation of these MM cells under permissive, but not restrictive, temperatures increased the expression of p53 and p21 mRNA and protein. Importantly, CD40 activation induced the proliferation of RPMI 8226 and HS Sultan cells at restrictive temperatures and growth arrest and increased subG1 phase cells at permissive temperatures. These data confirmed that CD40 activation might have distinct biologic sequelae in MM cells, depending on their p53 status. 相似文献
95.
96.
Ashish Correa Achint Patel Kinsuk Chauhan Harshil Shah Aparna Saha Mihir Dave Priti Poojary Abhishek Mishra Narender Annapureddy Shaman Dalal Ioannis Konstantinidis Renu Nimma Shiv Kumar Agarwal Lili Chan Girish Nadkarni Sean Pinney 《Journal of cardiac failure》2018,24(7):442-450
Background
Dialysis-requiring acute kidney injury (D-AKI) is a serious complication in hospitalized heart failure (HF) patients. However, data on national trends are lacking after 2002.Methods
We used the Nationwide Inpatient Sample (2002–2013) to identify HF hospitalizations with and without D-AKI. We analyzed trends in incidence, in-hospital mortality, length of stay (LoS), and cost. We calculated adjusted odds ratios (aORs) for predictors of D-AKI and for outcomes including in-hospital mortality and adverse discharge (discharge to skilled nursing facilities, nursing homes, etc).Results
We identified 11,205,743 HF hospitalizations. Across 2002–2013, the incidence of D-AKI doubled from 0.51% to 1.09%. We found male sex, younger age, African-American and Hispanic race, and various comorbidities and procedures, such as sepsis and mechanical ventilation, to be independent predictors of D-AKI in HF hospitalizations. D-AKI was associated with higher odds of in-hospital mortality (aOR 2.49, 95% confidence interval [CI] 2.36–2.63; P?<?.01) and adverse discharge (aOR 2.04, 95% CI 1.95–2.13; P?<?.01). In-hospital mortality and attributable risk of mortality due to D-AKI decreased across 2002–2013. LoS and cost also decreased across this period.Conclusions
The incidence of D-AKI in HF hospitalizations doubled across 2002–2013. Despite declining in-hospital mortality, LoS, and cost, D-AKI was associated with worse outcomes. 相似文献97.
98.
Kevan C. Herold Sahar Usmani-Brown Tara Ghazi Jasmin Lebastchi Craig A. Beam Melena D. Bellin Michel Ledizet Jay M. Sosenko Jeffrey P. Krischer Jerry P. Palmer the Type Diabetes TrialNet Study Group 《The Journal of clinical investigation》2015,125(3):1163-1173
Role of the funding source: Funding from the NIH was used for support of the participating clinical centers and the coordinating center. The funding source did not participate in the collection or the analysis of the data.BACKGROUND. The β cell killing that characterizes type 1 diabetes (T1D) is thought to begin years before patients present clinically with metabolic decompensation; however, this primary pathologic process of the disease has not been measured.METHODS. Here, we measured β cell death with an assay that detects β cell–derived unmethylated insulin (INS) DNA. Using this assay, we performed an observational study of 50 participants from 2 cohorts at risk for developing T1D from the TrialNet Pathway to Prevention study and of 4 subjects who received islet autotransplants.RESULTS. In at-risk subjects, those who progressed to T1D had average levels of unmethylated INS DNA that were elevated modestly compared with those of healthy control subjects. In at-risk individuals that progressed to T1D, the observed increases in unmethylated INS DNA were associated with decreases in insulin secretion, indicating that the changes in unmethylated INS DNA are indicative of β cell killing. Subjects at high risk for T1D had levels of unmethylated INS DNA that were higher than those of healthy controls and higher than the levels of unmethylated INS DNA in the at-risk progressor and at-risk nonprogressor groups followed for 4 years. Evaluation of insulin secretory kinetics also distinguished high-risk subjects who progressed to overt disease from those who did not.CONCLUSION. We conclude that a blood test that measures unmethylated INS DNA serves as a marker of active β cell killing as the result of T1D-associated autoimmunity. Together, the data support the concept that β cell killing occurs sporadically during the years prior to diagnosis of T1D and is more intense in the peridiagnosis period.TRIAL REGISTRATION. Clinicaltrials.gov .FUNDING. Funding was from the NIH, the Juvenile Diabetes Research Foundation, and the American Diabetes Association. NCT00097292相似文献
99.
Dinesh Singh Chauhan Yadavalli Guruprasad 《Journal of maxillofacial and oral surgery》2015,14(1):42-46
Goldenhar syndrome, a variant of hemifacial microsomia, is a well-known developmental anomaly of maxillofacial skeleton that is apparent at birth. The first and second branchial arch involvement during early embryonic development results in a wide spectrum of anomalies that may include macrostomia and lateral facial clefts. Though clefts of the orofacial region are among the most common congenital facial defects, the occurrence of lateral facial clefts (Tessier 7 cleft) in conditions such as the Goldenhar syndrome, is very rare (<5%). The lateral facial cleft, which results because of improper development of the perioral muscles of the face, gives an appearance of macrostomia giving rise to potential psychological, aesthetic and feeding problems. This clinical report describes the closure of a Tessier 7 cleft and the use of distraction osteogenesis to treat mandibular asymmetry in an 11-year-old female patient with Goldenhar’s syndrome. 相似文献