Li J.,Shandong UniversityShandong |
Han T.,Shandong University |
Xu L.,Taian Central Hospital |
Luan X.,Taian Central Hospital
Przeglad Gastroenterologiczny | Year: 2015
Introduction: A number of studies have shown that diabetes mellitus is implicated in susceptibility to several cancers. However, the relationship between diabetes and cholangiocarcinoma remain unclear. Aim: To quantitatively assess the relationship between diabetes and incidence of cholangiocarcinoma in cohort and case-control studies. Material and methods: A literature search was performed for entries from 1996 to 2014 using the PubMed and EMBASE databases. Studies were included if they reported odds ratios (OR) and corresponding 95% CI of cholangiocarcinoma with respect to diabetes mellitus. Results: Twenty studies met the inclusion criteria, which included fifteen case-control studies and five cohort studies from Asia (n = 11), the United States (n = 5), and Europe (n = 4). Compared with individuals without diabetes, the pooled OR of cholangiocarcinoma was 1.74 (95% CI: 1.62-1.87, p = 0.568 for heterogeneity) for patients with diabetes, ICC (summary RR, 1.93; 95% CI: 1.65-2.25; p = 0.037 for heterogeneity), and ECC (summary RR, 1.66; 95% CI: 1.39-1.98; p = 0.001 for heterogeneity). The funnel plot revealed no evidence for publication bias concerning diabetes and the risk of CC (including ICC and ECC). Conclusions: The findings from this meta-analysis suggest that diabetes may increase the risk of cholangiocarcinoma. This relationship needs to be confirmed by further follow-up studies. © 2015, Termedia Publishing House Ltd. All rights reserved.
Long M.,Arizona Cancer Center |
Long M.,Chongqing Medical University |
Tao S.,Arizona Cancer Center |
De La Vega M.R.,Arizona Cancer Center |
And 6 more authors.
Cancer Prevention Research | Year: 2015
The progressive nature of colorectal cancer and poor prognosis associated with the metastatic phase of the disease create an urgent need for the development of more efficacious strategies targeting colorectal carcinogenesis. Cumulative evidence suggests that the redox-sensitive transcription factor Nrf2 (nuclear factor-E2-related factor 2), a master regulator of the cellular antioxidant defence, represents a promising molecular target for colorectal cancer chemoprevention. Recently, we have identified cinnamon, the ground bark of Cinnamomum aromaticum (cassia cinnamon) and Cinnamomum verum (Ceylon cinnamon), as a rich dietary source of the Nrf2 inducer cinnamaldehyde (CA) eliciting the Nrf2-regulated antioxidant response in human epithelial colon cells, conferring cytoprotection against electrophilic and genotoxic insult. Here, we have explored the molecular mechanism underlying CA-induced Nrf2 activation in colorectal epithelial cells and have examined the chemopreventive potential of CA in a murine colorectal cancer model comparing Nrf2+/+ with Nrf2-/- mice. In HCT116 cells, CA caused a Keap1-C151-dependent increase in Nrf2 protein half-life via blockage of ubiquitination with upregulation of cytoprotective Nrf2 target genes and elevation of cellular glutathione. After optimizing colorectal Nrf2 activation and target gene expression by dietary CA-supplementation regimens, we demonstrated that CA suppresses AOM/DSS-induced inflammatory colon carcinogenesis with modulation of molecular markers of colorectal carcinogenesis. Dietary suppression of colorectal cancer using CA supplementation was achieved in Nrf2+/+ but not in Nrf2-/- mice confirming the Nrf2 dependence of CA-induced chemopreventive effects. Taken together, our data suggest feasibility of colorectal cancer suppression by dietary CA, an FDA-approved food additive derived from the third most consumed spice in the world. ©2015 AACR.
Yang Y.,Saarland University |
Shrestha Y.R.,ETH Zurich |
Li W.,Changsha University |
Guo J.,Shandong UniversityShandong
Lecture Notes in Computer Science (including subseries Lecture Notes in Artificial Intelligence and Lecture Notes in Bioinformatics) | Year: 2016
In the k-Vertex-Disjoint Paths problem, we are given a graph G and k terminal pairs of vertices, and are asked whether there is a set of k vertex-disjoint paths linking these terminal pairs, respectively. In the k-Path problem, we are given a graph and are asked whether there is a path of length k. It is known that both problems are NP-hard even in split graphs, which are the graphs whose vertices can be partitioned into a clique and an independent set. We study kernelization for the two problems in split graphs. In particular, we derive a 4k vertex-kernel for the k-Vertex-Disjoint Paths problem and a 3/2k2+ ½k vertex-kernel for the k-Path problem. © Springer International Publishing Switzerland 2016.
Xu C.,Qingdao University |
Yin X.,Shandong UniversityShandong |
Sun X.,Qingdao University |
Xing J.,Qingdao University |
Sun Y.,Qingdao University
International Journal of Clinical and Experimental Medicine | Year: 2016
Baicalein is a medicinal herb and has various biological activities. Our present work aimed to evaluate the protective effect of baicalein on sepsis-associated encephalopathy (SAE) and further probe the potential mechanisms. SAE model was prepared using cecal ligation and puncture in mice. Animals were treated with saline or baicalein by doses of 10, 20 and 40 mg/kg for seven consecutive days. Neuronal function was assessed with the Open Field tests, Morris Water Maze task and Y Maze tests. The serum ammonia levels were measured after SAE. Besides, malondialdehyde (MDA) contents and the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and inducible nitric oxide synthase (iNOS) activities were also detected using respective commercial kits. Detection of NO production was conducted using Griess reagent. No significance was found in Open Field test. However, the cognitive deficits were remarkably improved in SAE-induced mice after baicalein treatment based on the results of Morris Water Maze and Y Maze tests. Meanwhile, baicalein didn’t alter the serum ammonia levels in SAE-induced mice. But baicalein significantly suppressed oxidative stress, the protein levels of iNOS and NO production while the protein expressions of BDNF was found to be markedly enhanced in mice with SAE after baicalein treatment. It was concluded that baicalein reversed cognitive deficits in a mouse model of SAE via suppressing oxidative stress and iNOS-mediated NO production and activating BDNF/TrkB signaling. © 2016, E-Century Publishing Corporation. All rights reserved.
Qiu G.-Z.,Shandong UniversityShandong |
Tian W.,Linyi Oncosurgical HospitalShandong |
Fu H.-T.,Shandong UniversityShandong |
Li C.-P.,Eye Institute of XuzhouJiangsu |
Liu B.,Tongji University
Biochemical and Biophysical Research Communications | Year: 2016
Microvascular dysfunction is an important characteristic of diabetic retinopathy. Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes. In this study, we investigated the role of lncRNA-MEG3 in diabetes-related microvascular dysfunction. We show that MEG3 expression level is significantly down-regulated in the retinas of STZ-induced diabetic mice, and endothelial cells upon high glucose and oxidative stress. MEG3 knockdown aggravates retinal vessel dysfunction in vivo, as shown by serious capillary degeneration, and increased microvascular leakage and inflammation. MEG3 knockdown also regulates retinal endothelial cell proliferation, migration, and tube formation in vitro. The role of MEG3 in endothelial cell function is mainly mediated by the activation of PI3k/Akt signaling. MEG3 up-regulation may serve as a therapeutic strategy for treating diabetes-related microvascular complications. © 2016 Elsevier Inc. All rights reserved.