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Konjac powder has the effect of improving blood lipids in the general population, but there is no research on schizophrenic patients who are susceptible to dyslipidemia. The aim of our study is to evaluate the effects of konjac powder on blood lipid, glucose levels, body weight, and blood pressure in schizophrenia inpatients with dyslipidemia.After a two-week adaptation period, 76 people with schizophrenia were enrolled in a 30-day double-blind randomized controlled trial. The subjects in the experimental group were given a beverage containing konjac powder 30 minutes before each meal, whereas those in the control group were given a beverage containing resistant maltodextrin.The lipid profile, plasma glucose, blood pressure, and body weight were measured at baseline and at the end of 30-day treatment. Fiftynine subjects completed the study. There was a substantial decrease in total serum cholesterol in the experimental group, but an increase in the control group. Likewise, apolipoprotein B decreased in the experimental group but increased in the control group.We concluded that a diet supplemented with konjac powder may prevent the deterioration of dyslipidemia in people with schizophrenia, demonstrating its potential value in the treatment of metabolic disorders in schizophrenia as a new therapeutic method.

Lung cancer has very high mortality and glycyrrhizin was found to significantly inhibit the growth of lung cancer cells in vitro and tissues in mice. However, the detailed inhibitory role of glycyrrhizin in the growth of lung cancer is still unclear. In this study, we first found that glycyrrhizin inhibited the growth of lung tumor in PDX mice. And high level of HMGB1 promoted the migration and invasion of lung cancer cells, which was suppressed by glycyrrhizin. Moreover, glycyrrhizin reduced the activity of JAK/STAT signaling pathway, which is the upstream regulator of HMGB1. Therefore, this study revealed a potential mechanism by which glycyrrhizin can inhibit the progression of lung cancer.

Several studies have reported a significant role of high mobility group box protein 1 (HMGB1) in lung cancer. Nevertheless, there is a lack of knowledge regarding the expression of HMGB1 and its correlation with the clinicopathological features of lung cancer. In addition, the potential molecular mechanisms underlying the role of HMGB1 in lung cancer are still unknown. We therefore investigated the clinicopathological and prognostic significance as well as the potential role of HMGB1 in the development and progression of lung cancer. HMGB1 expression in the tumor tissues of the cohort correlated with clinicopathological features. Moreover, lung cell migration and invasion were significantly increased after treatment with HMGB1. The matrix metalloproteinase-2 (MMP-2) expression and activity were upregulated after treatment with HMGB1, while the upregulated expression of MMP-2 stimulated by HMGB1 in lung cancer cells was significantly reduced with the blockage of si-p65. These results indicated that HMGB1 expression was significantly associated with lung cancer progression. We also showed that HMGB1 promoted lung cancer invasion and metastasis by upregulating the expression and activity of MMP-2 in an NF-κB-dependent manner. Taken together, these data suggested that HMGB1 may be a potential prognosis and therapeutic marker for lung cancer.

Integrins play an important role in tumor metastasis induced by vascular endothelial growth factor (VEGF). However, in the case of gastric cancer, the precise role of VEGF in regulating integrin alphavbeta6 is unclear. In this study, we found that most of the alphavbeta6 integrin-positive gastric cancer tissues were also VEGF-positive. Furthermore, when gastric carcinoma cells were exposed to VEGF, expression of alphavbeta6 integrin was up-regulated and the extracellular signal-related kinase (ERK) pathway was activated. When integrin alphavbeta6 was blocked either with beta6 siRNA or anti-alphavbeta6 antibody, the migration of tumor cells normally induced by VEGF, as well as the activation of ERK, were markedly inhibited. Blocking the ERK signaling pathway significantly inhibited cell mobility. Taken together, the data suggest that VEGF is critical to the invasive process in human gastric cancer and that this occurs via up-regulation of integrin alphavbeta6 expression and activation of ERK.

Background There have been few investigations conducted on the epidemiology and risk factors of osteoporosis in patients with diabetes in China. The aim of this study was to disclose the percentage and the possible risk factors that influence bone mineral density (BMD) in this population. Methods One hundred thirty-one elderly male patients with type 2 diabetes (73.12 ± 5.54 years of age, diabetic duration 5.28 ± 3.56 years, HbA 1C 7.87% ± 1.82 %), >65 years of age were recruited. All subjects were submitted to dual-energy X-ray absorptiometry to evaluate the BMD at lumbar spine (LS), femoral neck (FN), and femoral trochanter (FT). Fasting blood samples were taken to check hormones and biochemical levels. Demographic data were also collected. Results In the different bone sites studied, the percentage of osteoporosis and osteopenia varied in this group of patients ranging from 29.0 to 31.3% and 29.0 to 33.6%, respectively. Weight, HbA 1C , body mass index, and testosterone were correlated with BMD at all the bone sites studied. Weight was the best predictor among the above parameters for BMD by linear regression analysis at LS and FN, whereas testosterone was the best predictor for BMD at FT. Conclusions In the different bone sites studied, the percentage of osteoporosis and osteopenia varied ranging from 29.0 to 31.3% and 29.0 to 33.6%, respectively. Weight was the best predictor for BMD at LS and FN and testosterone was the best predictor for BMD at FT. Poor glycemic control was correlated with osteoporosis.

Integrin alphavbeta6 is up-regulated in a variety of human carcinomas and plays a crucial role in tumor invasion and metastasis. However, the function of alphavbeta6 in pancreatic carcinoma and its potential role in gemcitabine resistance remain unknown.Small interfering RNA (siRNA) targeting alphavbeta6 was constructed and transfected into PANC-1 cells. Effects of alphavbeta6 knockdown on cell proliferation, invasion, cell cycle progression, apoptosis and chemosensitivity to gemcitabine were investigated.Expression of alphavbeta6 in PANC-1 cells was markedly suppressed by siRNA. Silencing of alphavbeta6 expression significantly inhibited cell proliferation and invasiveness, resulted in cell cycle arrest, and induced cell apoptosis. More importantly, alphavbeta6 knockdown enhanced chemosensitivity to gemcitabine and increased gemcitabine-induced caspase-mediated apoptosis.These findings suggest a novel mechanism by which alphavbeta6 contributes to pancreatic carcinoma progression. The combination of alphavbeta6 silencing and gemcitabine treatment may provide an effective therapeutic strategy for highly resistant pancreatic carcinoma.

Norcantharidin has been used as an efficacious anticancer drug in China for many years, but its true mechanism remains poorly understood. Intriguingly, in an in vitro series study of anticancer drugs, we found that norcantharidin can effectively inhibit epithelial tumor cells from expressing integrin alphavbeta6. Our previous studies have confirmed that integrin alphavbeta6 is closely relevant to malignant epithelial cell tumor biology behavior, and it can promote cancer cells to invade and metastasize through a special alphavbeta6-extracellular signal-related kinase (ERK) direct signaling pathway. In this study, we investigated the relationship between the norcantharidin anticancer mechanism and integrin alphavbeta6. After HT-29 colon cancer cells were treated with norcantharidin, cell apoptosis increased remarkably. The expression of alphavbeta6 and the amount of p-ERK decreased substantially; simultaneously, the linkage between alphavbeta6 and ERK was barely detectable. However, the expression of other integrins and the levels of mitogen-activated protein kinase hardly changed. On these grounds, we presumed that norcantharidin induced HT-29 colon cancer cell apoptosis through the alphavbeta6-ERK signaling pathway. This finding elicited a novel strategy for targeting the whole alphavbeta6-ERK signal pathway, rather than simply blocking the combining site of alphavbeta6-ERK in colon cancer treatment.