Type 2 diabetes has been suggested as an independent risk factor for the development of hepatocellular carcinoma (HCC). However, the role of Type 2 diabetes on the development of HCC in the presence of chronic hepatitis B (CHB) remains inconclusive. We conducted this hospital-based case-control study to evaluate the roles of Type 2 diabetes in HCC development in patients with CHB. From January 2004 to December 2008, a total of 6,275 eligible consecutive patients with chronic hepatitis B virus (HBV) infection were recruited. A total of 1,105 of them were patients with HBV-related HCC and 5,170 patients were CHB but without HCC. We used multivariate logistic regression models to investigate the association between Type 2 diabetes and HCC risk. The prevalence of Type 2 diabetes is higher among HCC patients without cirrhosis than among those with cirrhosis (12.1% vs. 6.7%, p 5 0.003). Type 2 diabetes was associated with a significantly high risk of HCC in female patients after adjusting for age, family history of HCC, city of residence, hepatitis B e antigen and cirrhosis with an odds ratio (95% confidence interval, CI) of 1.9 (1.1-3.4). Restricted analyses among female patients without cirrhosis indicated that Type 2 diabetes was strongly associated with HCC risk with adjusted odds ratio (95% CI) of 5.6 (2.2-14.1). In conclusion, Type 2 diabetes is independently associated with the increased risk of HCC in female CHB patients. Female CHB patients with Type 2 diabetes are of a high HCC risk population and should be considered for HCC close surveillance program.Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, with 55% occurring in China alone. 1,2 In China, nearly 80% of HCC cases have been linked to hepatitis B virus (HBV) infection and approximately 60-90% of these develop in patients with cirrhosis. 3,4 Other potential risk factors, such as diabetes mellitus, alcohol abuse and obesity, may also play a role in the development of HCC. 5 A number of cohort and case-control studies have investigated the relationship between diabetes mellitus and HCC risk. [6][7][8][9][10][11][12][13][14][15] Type 2 diabetes has been suggested as an independent risk factor for the development of HCC. However, the role of Type 2 diabetes in the development of HCC in the presence of chronic hepatitis B (CHB) has not been well documented. First, only a few cohort studies have followed a population with chronic HBV infection. In addition, most of the case-control studies used a normal population or cancers other than HCC as controls, and chronic HBV infection status was not well matched between cases and controls. 16 Second, none of these studies followed a cohort of patients with CHB or matched cirrhosis status between cases and controls with CHB. The majority of HBV-related HCC develops in patients with cirrhosis, 17 in which the prevalence of Type 2 diabetes is higher than in the general population, and in CHB patients without cirrhosis. 18 So, these studies may also inappropriately estimate the role of Type 2...

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BackgroundStudies have observed an association between the ABO blood group and risk of certain malignancies. However, no studies of the association with hepatocellular carcinoma (HCC) risk are available. We conducted this hospital-based case-control study to examine the association with HCC in patients with chronic hepatitis B (CHB).MethodsFrom January 2004 to December 2008, a total of 6275 consecutive eligible patients with chronic hepatitis B virus (HBV) infection were recruited. 1105 of them were patients with HBV-related HCC and 5,170 patients were CHB without HCC. Multivariate logistic regression models were used to investigate the association between the ABO blood group and HCC risk.ResultsCompared with subjects with blood type O, the adjusted odds ratio (AOR) for the association of those with blood type A and HCC risk was 1.39 [95% confidence interval (CI), 1.05–1.83] after adjusting for age, sex, type 2 diabetes, cirrhosis, hepatitis B e antigen, and HBV DNA. The associations were only statistically significant [AOR (95%CI) = 1.56(1.14–2.13)] for men, for being hepatitis B e antigen positive [AOR (95%CI) = 4.92(2.83–8.57)], for those with cirrhosis [AOR (95%CI), 1.57(1.12–2.20)], and for those with HBV DNA≤105copies/mL [AOR (95%CI), 1.58(1.04–2.42)]. Stratified analysis by sex indicated that compared with those with blood type O, those with blood type B also had a significantly high risk of HCC among men, whereas, those with blood type AB or B had a low risk of HCC among women.ConclusionsThe ABO blood type was associated with the risk of HCC in Chinese patients with CHB. The association was gender-related.

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The urban transit system in a real city usually has two major components: a sparse express (e.g. rail) network and a dense local (e.g. bus) network. The two networks intersect and interweave with each other throughout the city to furnish various route options for serving transit patrons with distinct ODs. The optimal design problem of this bimodal transit system, however, has not been well explored in the literature, partly due to the difficulty of modeling the patrons' complex route choice behavior in the bimodal networks. In light of this, we formulate parsimonious continuum models for minimizing the total cost of the patrons and the transit agency for an intersecting bimodal transit network in a grid city, where the perpendicular local and express lines intersect at transfer stops. Seven distinct route types are identified in this network, which represent realistic intra-and inter-modal route options. A lower-level assignment problem between these routes is embedded in the upper-level network design optimization problem. We develop an efficient method to find near-optimal designs of the intersecting network. Numerical results unveil a number of insightful findings, e.g., that sizable cost savings are observed for the intersecting bimodal design as compared to the single-mode designs for moderate to high demand levels, and that only moderate benefits are observed as compared to the trunk-feeder designs under certain operating conditions. We also show that the conventional practice of designing the local and express networks separately would greatly undermine the benefit of the bimodal system.

This study aimed to investigate the effects of polysaccharide from Angelica and Astragalus (AAP) on carbon tetrachloride (CCl4) induced liver damage in mice. A total of 120 Kunming mice were randomly distributed among 6 groups comprising (i) the normal control mice, (ii) the CCl4 treatment group, (iii) the bifendate treatment group, (iv) the AAP treatment group, (v) the Angelica sinensis polysaccharide (ASP) treatment group, and (vi) the Astragalus membranaceus polysaccharide (AMP) treatment group. AAP, ASP and AMP were administered to mice treated with CCl4. The activities of alanine transaminase (ALT) and aspartate transaminase (AST) in the serum, and superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver tissues were quantified, as well as the liver index. Hepatic histological changes were observed by staining liver sections with hematoxylin and eosin. Our results show that bifendate, AAP, ASP, and AMP significantly decreased the activities of MDA, AST, and ALT, and enhanced the activity of SOD in CCl4-treated mice. Bifendate, AAP, ASP, and AMP consistently ameliorated the liver injuries induced with CCl4. Notably, the hepatoprotective effect of AAP was stronger than that of bifendate, ASP, or AMP. In addition, AAP alleviated liver inflammation and decreased the liver indexes of mice induced with CCl4. These effects were at least partly due to the antioxidant properties of AAP in scavenging free radicals to ameliorate oxidative stress and to inhibit lipid peroxidation.

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