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51.
Purpose: To determine whether the difference of resistive indexes (RIs) in spleen and kidney (DI-RISK) is a more specific ultrasonographic (US) marker of intrarenal parenchymal damage than intrarenal RI alone. Materials and Methods: The study was approved by the local ethics committee. All study participants provided informed consent. The authors defined standard values for renal RI, splenic RI, and DI-RISK in 152 healthy subjects; carotid intima media thickness (IMT) was assessed as a marker of systemic vascular disease. Next, the authors measured these US parameters and collected echocardiographic data in 290 patients with chronic kidney disease (stage 2-4) recruited between September 2008 and February 2011 to evaluate the DI-RISK across the spectrum of stages of kidney function. Correlation coefficients were calculated with the Spearman test, and multivariate linear regression was used to analyze independent predictors of renal RI, splenic RI, and DI-RISK. Results: Healthy subjects had a mean age of 34.3 years ± 8.7, and patients with chronic kidney disease had a mean age of 65.0 years ± 12.3 (P < .001). In healthy subjects, both renal and splenic RIs were associated with IMT (renal RI: r = 0.19, P = .022; splenic RI: r = 0.23, P = .005); there was no correlation between DI-RISK and IMT (r = -0.10, P = .215). Similarly, in patients with chronic kidney disease, renal and splenic RIs correlated with IMT (renal RI: r = 0.33, P < .001; splenic RI: r = 0.30, P = .001). DI-RISK was associated with the estimated glomerular filtration rate (eGFR; r = -0.19, P = .001) but not with IMT (r = 0.08, P = .174). At multivariate regression analysis, DI-RISK was independently associated with eGFR but not with extrarenal factors. Conclusion: In patients with chronic kidney disease, renal RIs do not selectively indicate organ damage, but also mirror systemic vascular disease. The authors introduced DI-RISK as a potential US marker that may more specifically reflect kidney damage. ? RSNA, 2012. 相似文献
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Heine GH Ortiz A Massy ZA Lindholm B Wiecek A Martínez-Castelao A Covic A Goldsmith D Süleymanlar G London GM Parati G Sicari R Zoccali C Fliser D;European Renal Cardiovascular Medicine 《Nature reviews. Nephrology》2012,8(6):362-369
Chronic microinflammation and its cellular hallmark, monocyte activation, contribute substantially to the tremendous burden of cardiovascular disease (CVD) in patients with chronic kidney diseases (CKD). Monocyte heterogeneity is widely acknowledged. Cell-surface expression of CD14 and CD16 defines three functionally and phenotypically distinct subsets of monocytes: classical (CD14(++)CD16(-)) monocytes, intermediate (CD14(++)CD16(+)) monocytes, and nonclassical (CD14(+)CD16(++)) monocytes. A growing body of circumstantial evidence suggests that intermediate monocytes, in particular, contribute to the development of atherosclerosis in the general population as well as in patients with CKD. Intermediate monocytes express a unique pattern of chemokine receptors that have been implicated in atherogenesis. Moreover, this subset of monocytes is predisposed to secrete proinflammatory cytokines. Findings from epidemiological studies indicate that numbers of intermediate monocytes increase with worsening renal function, and that high cell counts predict adverse outcomes in patients undergoing dialysis as well as in patients at early stages of CKD. Based on laboratory and clinical data, intermediate monocytes are a promising therapeutic target for CVD in patients with CKD. 相似文献
53.
Timo Speer Heinrich V Groesdonk Beate Zapf Vanessa Buescher Miriam Beyse Laura Duerr Stella Gewert Patrizia Krauss Aaron Poppleton Stefan Wagenpfeil Danilo Fliser Hans-Joachim Schaefers Matthias Klingele 《Critical care (London, England)》2015,19(1)
IntroductionSeveral scoring systems have been developed to predict postoperative mortality and complications in patients undergoing cardiac surgery. However, these computer-based calculations are time- and cost-intensive. A simple but highly predictive test for postoperative risk would be of clinical benefit with respect to increasingly scarce hospital resources. We therefore assessed the predictive power of fibroblast growth factor 23 (FGF23) measurement compared with an established scoring system.MethodsWe conducted a prospective interdisciplinary observational study at the Saarland University Medical Centre that included 859 patients undergoing elective cardiac surgery between January 2010 and March 2011 with a median follow-up after discharge of 822 days. We compared a single preoperative measurement of FGF23 as a prognostic tool with the 18 parameters comprising EuroSCORE II with respect to postoperative mortality, acute kidney injury, non-occlusive mesenteric ischemia, clinical course and long-term outcome.ResultsPreoperative FGF23 levels were highly predictive of postoperative outcome and complications. The predictive value of FGF23 for mortality in the receiver operating characteristic curve was greater than the EuroSCORE II (area under the curve: 0.800 versus 0.725). Moreover, preoperative FGF23 independently predicted postoperative acute kidney injury and non-occlusive mesenteric ischemia comparably to the EuroSCORE II. Finally, FGF23 was found to be an independent predictor of clinical course parameters, including duration of surgery, ventilation time and length of stay.ConclusionsIn patients undergoing elective cardiac surgery, a simple preoperative FGF23 measurement is a powerful indicator of surgical mortality, postoperative complications and long-term outcome. Its utility compares to the widely used EuroSCORE II.
Electronic supplementary material
The online version of this article (doi:10.1186/s13054-015-0925-6) contains supplementary material, which is available to authorized users. 相似文献54.
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Philipp Kümpers Alexander Lukasz Sascha David Rüdiger Horn Carsten Hafer Robert Faulhaber-Walter Danilo Fliser Hermann Haller Jan T Kielstein 《Critical care (London, England)》2008,12(6):R147
Introduction
The endothelial specific angiopoietin (Ang)-Tie2 ligand-receptor system has been identified as a non-redundant mediator of endothelial activation in experimental sepsis. Binding of circulating Ang-1 to the Tie2 receptor protects the vasculature from inflammation and leakage, whereas binding of Ang-2 antagonises Tie2 signalling and disrupts endothelial barrier function. Here, we examine whether circulating Ang-1 and/or Ang-2 independently predict mortality in a cohort of critically ill medical patients. 相似文献57.
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N. Shushakova J. K. Park J. Menne D. Fliser 《European journal of clinical investigation》2009,39(9):755-760
Background Recent studies in mice experimental models with acute ischaemic injury revealed that erythropoietin (EPO) has numerous tissue-protective effects in the heart, brain and kidneys. We therefore explored the tissue-protective properties of chronic EPO treatment in an experimental model of the db/db mouse with diabetic heart injury.
Material and methods We randomly treated 11 db/db mice with placebo (saline), 0·4 μg of the continuous erythropoietin receptor activator (CERA) per week ( n = 11) or 1·2 μg CERA per week ( n = 11) for 14 weeks, and analysed cardiac tissue. The lower CERA dose was a non-haematologically effective dose, whereas the second increased the haematocrit.
Results Compared with mice in the placebo group, CERA-treated mice had a reduction in TGF-β1 and collagen I expression in cardiac tissue ( P < 0·01 vs. higher dose CERA). In addition, an increased expression of the pro-survival intracellular pathway p-AKT was observed ( P < 0·05 vs. higher dose CERA). The values for the lower C.E.R.A had an intermediate nonsignificant effect. Furthermore, we were able to show that atrial natriuretic peptide (ANP) expression was increased in both CERA groups.
Conclusions Chronic treatment with CERA protects cardiac tissue in diabetic animals, i.e. it inhibits molecular pathways of cardiac fibrosis, and the effects are dose-dependent. 相似文献
Material and methods We randomly treated 11 db/db mice with placebo (saline), 0·4 μg of the continuous erythropoietin receptor activator (CERA) per week ( n = 11) or 1·2 μg CERA per week ( n = 11) for 14 weeks, and analysed cardiac tissue. The lower CERA dose was a non-haematologically effective dose, whereas the second increased the haematocrit.
Results Compared with mice in the placebo group, CERA-treated mice had a reduction in TGF-β
Conclusions Chronic treatment with CERA protects cardiac tissue in diabetic animals, i.e. it inhibits molecular pathways of cardiac fibrosis, and the effects are dose-dependent. 相似文献
60.
Philipp Kümpers Carsten Hafer Alexander Lukasz Ralf Lichtinghagen Korbinian Brand Danilo Fliser Robert Faulhaber-Walter Jan T Kielstein 《Critical care (London, England)》2010,14(1):R9