Binzhou Medical College

About: Binzhou Medical College is a education organization based out in Yantai, China. It is known for research contribution in the topics: Apoptosis & Cancer. The organization has 959 authors who have published 619 publications receiving 7642 citations.

Catheter Aspiration With Recanalization for Budd-Chiari Syndrome With Inferior Vena Cava Thrombosis.

Abstract: PURPOSE To assess the safety and clinical effectiveness of catheter aspiration with recanalization in patients with Budd-Chiari syndrome (BCS) and inferior vena cava (IVC) thrombosis. MATERIALS AND METHODS Between January 2010 and December 2017, 33 patients with BCS and IVC thrombosis were treated by catheter aspiration with IVC recanalization in our center. A 12 F angled-tip guiding catheter was used for the aspiration of thrombi in the IVC. Recanalization was conducted following thrombi aspiration. Rates of technical success, clinical success and long-term patency were calculated. RESULTS Catheter aspiration with IVC recanalization was technically successful in all patients. After aspiration, no thrombi were detectable by IVC venography in 21 patients, while residual mural thrombi were found in 12 patients. IVC balloon dilation was performed in 18 patients, while stent insertion was performed in 15 patients. We also achieved clinical success in all patients. Symptomatic and asymptomatic pulmonary embolism were found in 1 patient each, respectively. The cumulative 1-, 3-, and 5-year patency rates were 93.6%, 93.6%, and 83.2%, respectively. All patients remained alive during the follow-up. CONCLUSIONS Catheter aspiration with recanalization is a safe and efficacious approach to treating patients with BCS and IVC thrombosis.

MicroRNA-1323 downregulation promotes migration and invasion of breast cancer cells by targeting tumour protein D52.

Abstract: Breast cancer (BC) is one of the most common malignancies globally in women, with high mortality rate as a result of tumour metastasis. MicroRNAs play vital roles in the occurrence and development of human cancer. This study aimed to investigate the biological roles of miR-1323 in BC. The expression levels of miR-1323 were detected by quantitative real-time PCR assay. The effect of miR-1323 on BC cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Wound healing analysis and Matrigel Transwell assay were conducted to evaluate miR-1323-mediated BC cell migration and invasion. A luciferase reporter assay was used to test the target of miR-1323. We found that miR-1323 levels were downregulated in BC tissues and serums. Low-miR-1323 levels were associated with lymph node metastasis and advanced clinical stage. Tumour protein D52 (TPD52) was identified as a direct target of miR-1323. Low expression of miR-1323 contributed to the overexpression of TPD52 leading to enhanced BC progression. Our findings suggest that silencing of miR-1323 enhances BC development by regulating TPD52 expression, suggesting that miR-1323 and TPD52 may serve as potential therapeutic targets for BC treatment.

The extract of concentrated growth factor enhances osteogenic activity of osteoblast through PI3K/AKT pathway and promotes bone regeneration in vivo.

Abstract: Background Concentrated growth factor (CGF) is a third-generation platelet concentrate product; the major source of growth factors in CGF is its extract; however, there are few studies on the overall effects of the extract of CGF (CGF-e). The aim of this study was to investigate the effect and mechanism of CGF-e on MC3T3-E1 cells in vitro and to explore the effect of combination of CGF-e and bone collagen (Bio-Oss Collagen, Geistlich, Switzerland) for bone formation in cranial defect model of rats in vivo. Methods The cell proliferation, ALP activity, mineral deposition, osteogenic-related gene, and protein expression were evaluated in vitro; the newly formed bone was evaluated by histological and immunohistochemical analysis through critical-sized cranial defect rat model in vivo. Results The cell proliferation, ALP activity, mineral deposition, osteogenic-related gene, and protein expression of CGF-e group were significantly increased compared with the control group. In addition, there was significantly more newly formed bone in the CGF-e + bone collagen group, compared to the blank control group and bone collagen only group. Conclusions CGF-e activated the PI3K/AKT signaling pathway to enhance osteogenic differentiation and mineralization of MC3T3-E1 cells and promoted the bone formation of rat cranial defect model.

PERK in POMC neurons connects celastrol with metabolism

Abstract: ER stress and activation of the unfolded protein response in the periphery as well as the central nervous system have been linked to various metabolic abnormalities. Chemically lowering protein kinase R-like ER kinase (PERK) activity within the hypothalamus leads to decreased food intake and body weight. However, the cell populations required in this response remain undefined. In the current study, we investigated the effects of proopiomelanocortin-specific (POMC-specific) PERK deficiency on energy balance and glucose metabolism. Male mice deficient for PERK in POMC neurons exhibited improvements in energy balance on a high-fat diet, showing decreased food intake and body weight, independent of changes in glucose and insulin tolerances. The plant-based inhibitor of PERK, celastrol, increases leptin sensitivity, resulting in decreased food intake and body weight in a murine model of diet-induced obesity (DIO). Our data extend these observations by demonstrating that celastrol-induced improvements in leptin sensitivity and energy balance were attenuated in mice with PERK deficiency in POMC neurons. Altogether, these data suggest that POMC-specific PERK deficiency in male mice confers protection against DIO, possibly providing a new therapeutic target for the treatment of diabetes and metabolic syndrome.

The protective effects of calcitonin gene-related peptide on gastric mucosa injury of gastric ischemia reperfusion in rats.

Abstract: Gastric mucosa is one of the most vulnerable tissues in human and animal. However, little is known about the effects of calcitonin gene-related peptide (CGRP) on gastric mucosa injuries induced by gastric ischemia reperfusion. The purpose of the present study was to investigate the protective effects and mechanism of CGRP on gastric mucosa injury after gastric ischemia reperfusion in rats. Thirty-six healthy Wistar rats were randomly divided into CGRP-treated, sham-operated, and control groups. Twelve rats were involved in each group. These groups were further divided into 24-h and 48-h subgroups. Gastric ischemia reperfusion injury (GI-RI) rat model was established by a 30-min celiac artery occlusion by an artery clamp, followed by 24 h or 48 h of reperfusion. CGRP (1 μg/ml) at the dose of 3 μg/kg was given intraperiloneally (IP) at the beginning of reperfusion for rats in CGRP-treated group. Saline as vehicle (3 ml/kg body weight), IP, was administered at the beginning of reperfusion for rats in control...