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Different neoadjuvant therapy regimens are available for rectal cancer, but the relative effects are controversial. The aim of the present network meta-analysis (NMA) was to estimate the relative efficacy and safety of neoadjuvant therapies for resectable rectal cancer. MEDLINE, EMBASE and Cochrane Central Registry of Controlled Trials were searched for publications dated from 1946 up to June 2018. The present study included randomized clinical trials that compared treatments for resected rectal cancer Surgery alone, surgery preceded by neoadjuvant radiotherapy (RT), neoadjuvant chemotherapy (CT) or neoadjuvant chemoradiotherapy (CRT). Direct pairwise comparisons and NMA were conducted. A total of 23 randomized controlled trials were included in the present study. RT had an overall survival (OS) benefit when compared with surgery alone [HR (hazard ratio), 0.89; 95% confidence interval (CI), 0.82-0.97; quality of evidence, high]. All three neoadjuvant regimens were associated with lower local recurrence (LR) wstomotic leak between each treatment was observed in the NMA. In conclusion, RT decreased the LR and improved OS compared with surgery alone for resected rectal cancer. CRT was the best neoadjuvant therapy analyzed and CT was likely the second best for all outcomes based on SUCRA. However, these findings were limited by overall low quality of evidence. Copyright © Zhong et al.The utility of color Doppler echocardiography in the diagnosis and follow-up of Kawasaki disease (KD) with coronary artery lesions (CAL) was analyzed, and the clinical parameters associated with the disease were examined. The general data, the color Doppler echocardiography data and the biochemical indexes from 102 children with KD were analyzed. The patients were divided into a CAL group and a non-coronary artery lesion (NCAL) group based on the presence or absence of CAL. The risk factors for CAL in KD were screened by univariate and multivariate analyses. Among the 102 cases, CAL complications were identified in 47 cases (46.08%). Compared with the NCAL group, the CAL group showed significantly higher incidences of fever duration, increased levels of N-terminal pro B-type natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), C-reactive protein (CRP), intravenous immunoglobulin resistance, erythrocyte sedimentation rate (ESR), platelets, alanine aminotransferase and aspartate aminotransferase, and significantly lower serum albumin levels (P less then 0.05). According to the multivariate analysis, fever duration [odds ratio (OR)=2.014], NT-proBNP (OR=3.004), cTnI level (OR=2.638), ESR (OR=1.461) and CRP elevation (OR=1.094) were predictors of CAL in KD. During convalescence, the left and right coronary artery diameters in the CAL group significantly decreased (P less then 0.05). Color Doppler echocardiography can observe the condition of coronary artery disease in patients with KD in real time and predicts its outcomes, which may be helpful for early diagnosis and long-term follow-up. Fever duration, cTnI, NT-proBNP and ESR levels were correlated with coronary artery diameter, of which the comprehensive use may be more accurate in determining the occurrence of CAL in KD. Copyright © Xue et al.Hepatic ischemia/reperfusion (I/R) injury is a side effect of major liver surgery that is difficult to prevent. I/R injury induces metabolic strain on hepatocytes and limits the tolerable ischemia during liver resection, as well as preservation times during transplantation. Additionally, I/R injury induces apoptosis in hepatocytes. CD5-like (CD5L), an inducer of autophagy, is a soluble scavenger cysteine-rich protein that modulates hepatocyte apoptosis. The aim of the present study was to determine if pharmacologic CD5L was protective against hepatic ischemia-reperfusion injury. Hepatocytes were subjected to I/R culture conditions, and apoptosis and caspase family activity were measured after I/R to model hepatic injury. Treatment with recombinant CD5L significantly suppressed apoptosis and caspase activity through modulating cellular autophagy to maintain activation of the cluster of differentiation 36 (CD36)-dependent autophagy-related 7 (ATG7) signaling pathway. The regulation loop between CD5L and the autophagy signaling pathway was identified to be associated with the inhibition of oxidative stress. Treatment with CD5L significantly inhibited cellular oxidative stress, which was confirmed by silencing the CD36 receptor or the autophagy related protein ATG7 using small interfering RNA, which reversed the antiapoptotic and antioxidative effects of CD5L on hepatocytes under I/R conditions. The results of the present study suggested that CD5L-mediated attenuation of hepatic I/R injury occurs through the CD36-dependent ATG7 pathway, accompanied by the inhibition of oxidative stress, which is associated with enhanced autophagy. In conclusion, the present study identifies CD5L as a novel therapeutic agent for hepatic I/R injury. Copyright © Li et al.Deregulation of microRNAs (miRs) has been demonstrated to contribute to the development and malignant progression of nasopharyngeal carcinoma (NPC). Recently, miR-93 was reported to be significantly upregulated in NPC tissues and cell lines, and promote the proliferation, migration and invasion of NPC cells in vitro, as well as tumor growth in vivo. However, whether there is any clinical value of serum miR-93 expression in NPC still remains unclear. Therefore, the present study aimed to explore the clinical significance of serum miR-93 expression in NPC. A total of 85 serum samples from NPC patients and 30 from healthy controls were collected. Reverse transcription-quantitative polymerase chain reaction data demonstrated that the serum expression of miR-93 was significantly increased in NPC patients, when compared with those in healthy controls. Following receiving chemo-radiotherapy, the serum miR-93 levels were significantly decreased in NPC patients. Furthermore, the increased serum levels of miR-93 were significantly associated with advanced grade, clinical stage, lymph node metastasis, as well as worse 5-year overall survival of NPC patients. Furthermore, the serum miR-93 expression was demonstrated to be an independent factor for predicating the prognosis of NPC. SF2312 In vitro experiments demonstrated that knockdown of miR-93 caused a decrease in NPC cell proliferation, whereas overexpression of miR-93 promoted NPC cell proliferation. PDCD4 was then identified as a direct target of miR-93 in NPC cells. Overexpression of PDCD4 significantly eliminated the promoting effects of miR-93 overexpression on NPC cell proliferation. Taken together, these findings suggest that the serum miR-93 expression could be used as a predicator for the clinical outcome of NPC patients, and suggest that miR-93 may also become a potential therapeutic target for NPC treatment. Copyright © Sun et al.
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