SUMMARY BackgroundHelicobacter pylori infection is a worldwide threat to human health with recurrence rates that vary widely. The precise correlation between H. pylori recurrence and socioeconomic development has not been determined.

81.2% mild); jaundice was observed in 62 patients. Preoperative radiologic imaging was done in 43 patients (CT scan in 7.1%, MRI in 31.3%). There were 70 transcystic and 42 transductal choledochoscopies with a median IQR operative time of 77.5 (110e65) vs. 122.5 (140e94) minutes, p < 0.001. T-tubes were placed only in 13 (11.5%) patients. Complete clearance of the bile duct was achieved in 91.1% leading to a conversion rate of 2.7%; in 6.2% of cases additional postoperative ERCP was performed. Readmission and ERCP for missed stones was needed in 3.6% of all cases. The overall postoperative complication rate reached 6.3%. The median IQR overall hospital stay was 9 (14e7) days. Conclusions: One-stage surgical approach is rational in the management of patients with a high risk of CBD stones.

Kearns-Sayre syndrome (KSS) is a disorder caused by mutations in mitochondrial DNA. Here, we report an unusual case of Kearns-Sayre syndrome accompanied by hypopituitarism (deficiencies in reproductive and growth hormones). A 20-year-old male presented with growth retardation for the last 8 years, as well as the following findings: short stature, delayed puberty, myasthenia, an extraocular movement deficit, drooping eyelids, pectus carinatum and scoliosis. Cerebral enhanced magnetic resonance imaging revealed dysplasias of the pituitary, white matter and cerebellum. Laboratory work-up showed subnormal testosterone and growth hormone levels, a subnormal testicular volume, sensorineural deafness, pigmentary retinopathy, complete right bundle branch block and left anterior bundle branch block. Pathological examination revealed ragged red muscle fibres. Thus, this rare case involved the coexistence of Kearns-Sayre syndrome and hypopituitarism in a patient. Administration of coenzyme Q10 for the KSS and hormone replacement therapy for the endocrinopathies were performed for treatment of this patient.

Introductions: Hepatocellular carcinoma (HCC) is a common cancer with poor prognosis. The multikinase inhibitor sorafenib is the only clinically proved systematic treatment for HCC. However, few patients respond to sorafenib. Hypoxic microenvironments contribute to sorafenib resistance. LB-100, a serine/threonine protein phosphatase 2A (PP2A) inhibitor was previously found to be a chemosensitizer in HCC. We aimed to test whether LB-100 could sensitize HCC to the effects of sorafenib. Methods: Cell viability was evaluated by using Cell Counting Kit-8. Cell apoptosis assay were performed with Annexin V-FITC Detection Kit. Relative protein expression changes were assessed by immunoblotting. PP2A activity was assessed by using a Ser/Thr phosphatase assay kit. HCC xenograft mouse model was

Copyright: Zeng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Gastrointestinal stromal tumor (GIST) is the most common sarcoma, often resulting from a KIT or platelet-derived growth factor receptor alpha (PDGFRA) mutation. The lineage transcription factor ETV1 is expressed similarly in GISTs regardless of malignant potential. Although the related transcription factor ETV4 has been associated with metastasis and tumor progression in other cancers, its role in GIST is unknown. In this study, we found that ETV4 levels were high in a subset of human GISTs and correlated with high mitotic rate. Through Gene Set Enrichment Analysis in selected human GISTs, we identified a relationship between ETV4 levels and β-catenin signaling, especially in advanced GISTs. GIST specimens with high ETV4 levels overexpressed cell cycle regulating genes and had aberrant activation of the canonical Wnt pathway. In human GIST cell lines, ETV4 RNA interference suppressed cell cycle genes and Wnt/β-catenin signaling. ETV4 knockdown also reduced tumor cell proliferation, invasion, and tumor growth in vivo. Conversely, ETV4 overexpression increased cyclin D1 expression and Wnt/β-catenin signaling. Moreover, we determined that ETV4 knockdown destabilized nuclear β-catenin and increased its degradation via COP1, an E3 ligase involved in both ETV4 and β-catenin turnover. Aberrant accumulation of ETV4 and nuclear β-catenin was found in patient derived xenografts created from metastatic GISTs that became resistant to tyrosine kinase inhibitors. Collectively, our findings highlight the significance of ETV4 expression in GIST and identify ETV4 as a biomarker in human GISTs.