MicroRNA-205 suppresses the invasion and epithelial-mesenchymal transition of human gastric cancer cells.

Distant metastasis is the predominant pattern of gastric cancer (GC) recurrence, and is the most common cause of cancer­associated mortality. Accumulating evidence has suggested that aberrant activation of epithelial­mesenchymal transition has a crucial role in the genesis, invasion and metastasis of various types of cancer, including GC. Using Cell Counting kit­8 and Transwell assays, the effects of microRNA (miR)­205 on the proliferation, migration and invasion of NCI­H87 GC cells were determined, and the potential underlying mechanisms were explored. The results of the present study demonstrated that miR­205, which has been reported to function as a tumor suppressor in various types of cancer, significantly suppressed the migration and invasion of GC cells, which may be correlated with its suppressive effects on EMT. Upon transfection with miR­205, the epithelial marker CDH1 (E­cadherin) was upregulated, and the mesenchymal markers CDH2 (N­cadherin) and vimentin were suppressed. Furthermore, zinc­finger E­box­binding homeobox factor­1 (ZEB1) was identified as a putative target gene of miR­205 in GC, which may be associated with its suppressive effects. The results of the present study may provide novel diagnostic and therapeutic options for the treatment of human GC.

PGC-1α may associated with the anti-obesity effect of taurine on rats induced by arcuate nucleus lesion.

OBJECTIVE: To observe the effect of taurine treatment in rats with monosodium glutamate (MSG)-induced obesity. METHODS: Rats with MSG-induced obesity were administered taurine for five weeks. The Lee's index, food intake, blood pressure, body temperature, body mass index (BMI), fat weight, and triglyceride (TG), low density lipoprotein (LDL), and high density lipoprotein (HDL) levels were compared. The PGC-1α expression levels in white and brown adipose were measured using reverse transcription polymerase chain reaction and western blotting, and pathological changes in the arcuate nucleus and liver were examined. RESULTS: Compared with the model group, BMI, TG, and LDL in the high and low taurine dose groups were significantly lower, while HDL was higher. Body temperature in the taurine treatment groups was higher, and blood pressure was lower. The weight of brown fat in the taurine treatment groups was significantly higher than in the model group, while the white fat weight was significantly lower. Compared with the control group, the PGC-1α levels in white and brown adipose were higher in the taurine treatment groups and more significantly up-regulated in brown adipose. DISCUSSION: This study suggests that taurine prevents obesity in MSG-treated rats and may be closely associated with energy metabolism.

BDNF levels in adipose tissue and hypothalamus were reduced in mice with MSG-induced obesity.

OBJECTIVES: To observe the expression of brain-derived neurotrophic factor (BDNF) in hypothalamic and adipose tissue in mice with monosodium glutamate (MSG)-induced obesity. METHODS: The effects of hypothalamic lesions, specifically arcuate nucleus (ARC) lesions, induced by MSG injection were studied in male ICR mice at the neonatal stage. The following parameters were compared: body weight, body length, Lee's index, food intake, body temperature, fat weight, and levels of total cholesterol (CHOL), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and blood glucose (GLU). The BDNF expression levels in hypothalamic and adipose tissue were measured using western blotting. Results Compared with the control group, the model group body had significantly higher weight, Lee's index, food intake, fat weight, CHOL, TG, LDL, HDL, and GLU levels. BDNF expression levels in hypothalamic and adipose tissue were markedly down-regulated in the model group. DISCUSSION: BDNF may be closely associated with MSG-induced hypothalamic obesity.

Modified glasgow prognostic score predicting high conversion ratio in opioid switching from oral oxycodone to transdermal fentanyl in patients with cancer pain.

The aim of this study was to identify predictive factors for higher conversion ratio in opioid switching from oral oxycodone to transdermal fentanyl (TDF) in patients with cancer pain. The participants of this study were 156 hospitalized cancer patients who underwent opioid switching from oral oxycodone to TDF at the Affiliated Hospital of Binzhou Medical University between January 1st, 2010 and March 31st, 2014. Patient characteristics, modified Glasgow Prognostic Score (mGPS), daily oxycodone dose, and reasons for opioid switching were retrospectively collected. The effect of variables on the conversion ratio was analyzed by multiple regression analysis to identify the predictive factors for higher conversion ratio in opioid switching from oral oxycodone to TDF. The results showed that the mGPS (odds ratio [OR], 2.358; 95% CI 1.379-4.031; P = 0.002), the reason for opioid switching (OR, 0.497; 95% CI, 0.298-0.828; P = 0.007) and equivalent oral morphine dose (OR, 1.700; 95% CI, 1.008-2.867; P = 0.046) were found to be significant predictors requiring higher conversion ratio in opioid switching. This study indicates that higher mGPS, poor pain control before switching and higher equivalent oral morphine dose are significant predictors of a need for higher conversion ratio in opioid switching from oral oxycodone to TDF. These results could contribute to the establishment of evidence-based medicine in cancer pain relief.