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Simeprevir added to peginterferon and ribavirin lessens time with fatigue,depressive symptoms and functional limitations in patients with chronic hepatitis C compared with peginterferon and ribavirin: results from 1161 patients in the QUEST‐1, QUEST‐2 and PROMISE studies
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J. Scott L. Gilles M. Fu E. Brohan C. Panter R. Arbuckle W. Jessner M. Beumont 《Journal of viral hepatitis》2015,22(8):639-650
The value of adding simeprevir (SMV) vs placebo (PBO) to peginterferon and ribavirin (PR) for treatment of chronic hepatitis C virus infection was examined using patient‐reported outcomes (PROs); further, concordance of PROs with virology endpoints and adverse events (AEs) was explored. Patients (n = 768 SMV/PR, n = 393 PBO/PR) rated fatigue (FSS), depressive symptoms (CES‐D) and functional impairment (WPAI: Hepatitis C Productivity, Daily Activity and Absenteeism) at baseline and throughout treatment in three randomised, double‐blind trials comparing the addition of SMV or PBO during initial 12 weeks of PR. PR was administered for 48 weeks (PBO group) and 24/48 weeks (SMV group) using a response‐guided therapy (RGT) approach. Mean PRO scores (except Absenteeism) worsened from baseline to Week 4 to the same extent in both groups but reverted after Week 24 for SMV/PR and only after Week 48 for PBO/PR. Accordingly, there was a significantly lower area under the curve (baseline–Week 60, AUC60) and fewer weeks with clinically important worsening of scores in the SMV/PR group at any time point. Incidences of patients with fatigue and anaemia AEs were similar in both groups, but FSS scores showed that clinically important increases in fatigue lasted a mean of 6.9 weeks longer with PBO/PR (P < 0.001). PRO score subgroup analysis indicated better outcomes for patients who met the criteria for RGT or achieved sustained virological response 12 weeks post‐treatment (SVR12); differences in mean PRO scores associated with fibrosis level were only observed with PBO/PR. Greater efficacy of SMV/PR enabled reduced treatment duration and reduced time with PR‐related AEs without adding to AE severity. 相似文献
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Xiaojie Wu Leyan Zhang Jiadi Zhou Luying Liu Qiang Fu Aili Fu Xiaoying Feng Rui Xin Hongrui Liu Yong Gao Jiangnan Xue 《Current problems in cancer》2019,43(1):18-26
Aim
Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is an immune inhibitory receptor which is expressed within most types of hematopoietic cells and negatively regulates immune responses. Recently, we found LAIR-1 expression to be present within tumors of nonhematopoietic lineages. However, the roles of LAIR-1 in hepatocellular carcinoma (HCC) have yet to be examined. The purpose of this study was to investigate the expression of LAIR-1 in HCC tissue and assess its clinical significance at this site.Materials and methods
Expression levels of LAIR-1 within HCC samples collected from 90 patients and compared with that of slides of normal liver tissue collected from 9 non-HCC patients were measured by immunohistochemistry using tissue microarrays. A semiquantitative score was assigned, as was based on staining intensity and percent of positive cells and a Spearman Rank correlation test was used to assess any potential significant correlations between LAIR-1 expression and clinicopathological factors. Overall survival analysis was performed using the Kaplan-Meier and Log Rank statistical test.Results
LAIR-1 expression was detected in cancer tissue and adjacent tumor tissue, but not in normal liver tissue. The percent of LAIR-1-positive expression in cancer tissue of HCC samples was 97.78% (88/90) while that in adjacent tumor tissue was 96.67% (87/90). Significantly greater expression levels of LAIR-1 were obtained from cancer tissue (Mean?±?SD?=?5.722?±?2.145) than that in adjacent tumor tissue (4.141?±?1.486). In addition, LAIR-1 expression was found to be significantly correlated with pathological grade of HCC, T stage, and age. Expression levels of LAIR-1 were related with worse overall survival rates of HCC patients, especially in HCC patients with hepatic cirrhosis.Conclusion
Results of this study show that LAIR-1 is expressed in HCC tissues and that high levels of LAIR-1 expression are associated with the poor cancer differentiation. In addition, overexpression of LAIR-1 was significantly associated with worse overall survival in the patients with HCC. These data suggest that LAIR-1 may be an independent predictor for clinical outcomes in patients with HCC. 相似文献9.
目的探讨高血压合并脑卒中患者的血浆同型半胱氨酸(Hcy)水平与其他危险因素对于脑卒中复发的影响。
方法分析徐州市中心医院心内科和徐州医科大学附属医院神经外科自2012年5月至2013年12月收治的1623例高血压脑卒中患者的基线资料,中位随访4.9年,根据随访事件中是否发生脑卒中分为复发组(312例)与未复发组(1311例)。Kaplan-Meier生存分析比较不同危险因素脑卒中复发率的差异,单因素与多因素Cox回归模型分析影响脑卒中复发的独立危险因素,以及危险因素之间的交互作用。
结果复发组年龄、空腹血糖、Lg Hcy的水平,以及糖尿病、房颤的患病率均高于未复发组(P<0.05)。Kaplan-Meier生存分析显示,糖尿病、房颤、年龄≥60岁、空腹血糖≥7.0 mmol/L、Hcy≥15 μmol/L的脑卒中复发率明显升高(Log-rank检验,P<0.05)。多因素Cox回归模型分析显示,高龄、Lg Hcy水平升高,以及房颤、糖尿病是脑卒中复发的独立危险因素。Lg Hcy分别与糖尿病、空腹血糖、年龄存在交互作用。
结论血浆Hcy水平升高既是高血压合并脑卒中患者卒中复发的独立危险因素,又通过与糖尿病、高龄、空腹血糖水平升高的交互作用显著增加脑卒中复发风险。 相似文献
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Xue Yao Yan Zhang Jian Hao Hui-Quan Duan Chen-Xi Zhao Chao Sun Bo Li Bao-You Fan Xu Wang Wen-Xiang Li Xuan-Hao Fu Yong Hu Chang Liu Xiao-Hong Kong Shi-Qing Feng 《中国神经再生研究》2019,(3)
Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury. 相似文献