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Large polyethylene glycol (PEG) is a standard regimen for bowel preparation. However, elderly patients suffered from adverse events. This study was to compare the efficacy and safety of oral magnesium sulfate solution (MSS) vs standard PEG in elderly patients undergoing colonoscopy.Elderly patients aged 60-90 years, from two endoscopic centers, were enrolled in China. Patients were randomized to take a low dose of MSS or a standard PEG regime in a split-dose regime. The primary endpoint was the proportion of patients with adequate bowel preparation, which was defined as the total Boston Bowel Preparation Scale (BBPS) ≥6 and each segmental BBPS was ≥2. Secondary outcomes included adenoma detection rate (ADR), safety, adverse events, cecal intubation rate, willingness to repeat BP, and so on.1174 elderly patients were randomly allocated to the MSS group (Low dose of MSS was not inferior to the standard PEG regime in terms of bowel preparation quality for elderly patients. Low-dose MSS offered fewer adverse events and better tolerability. It is a preferable choice for the elderly to undergo bowel preparation for colonoscopy.NCT04948567.

Studies on average-risk individuals undergoing gastroscopy screening in China are scarce.To determine and compare the prevalence of lesions found by gastroscopy and the association between sex, age,Gastroscopy results were analysed for 60,519 individuals enrolled from January 2013 to December 2019.The median age was 49.84 years (SD, 9.47 years) for women and 48.90 years (SD, 8.82 years) for men, and the ratio of females to males was 35.10% (The prevalence of upper gastrointestinal endoscopic lesions is high in the asymptomatic population undergoing physical examination and is associated with sex, age, and

BACKGROUND: Current management of patients with atrial fibrillation (AF) is limited by low detection of AF, nonadherence to guidelines and lack of consideration of patient's preferences, thus highlighting the need for a holistic and integrated approach to AF management. The present study aims to determine whether a mHealth technology-supported AF integrated management strategy will reduce AF-related adverse events.METHODS/DESIGN: The mAFA II trial is a prospective, cluster randomized controlled trial. The 40 sites will be randomized to mAFA-integrated care intervention or usual care arms. Prior to randomization, study sites will be paired to be matched in size and the proportion of study eligible patients. All AF patients aged over 18 years old with CHA2 DS2 -VASc score ≥2 will be enrolled. Assuming a composite adverse event rate of 10% pre-intervention, reduced to 5% after intervention, we aim to recruit 3660 patients assuming a 10% loss to follow-up. The primary study endpoint is a composite of stroke/thromboembolism, all-cause death, and rehospitalization. Ancillary analyses would determine patient-related outcome measures, health economics and cost effectiveness, as well as an embedded qualitative study.DISCUSSION: The mAFA II trial will provide evidence for an integrated care approach to holistic AF care, supported by mobile health technology to improve screening, patient involvement and optimization of management. This article is protected by copyright. All rights reserved.

Purpose S100P has been shown to participate in processes of various human malignancies. In this study, we analyzed the tissue expression of S100P in gastric cancer and evaluated its significance. Methods We determined the S100P expression in 156 gastric cancer patients by quantitative RT-PCR. Tumor characteristics and overall survival (OS) for each patient were examined. In vitro experiments were conducted to examine whether ectopic expression of S100P modifies the proliferation and drug resistance of gastric cancer cells. Results Higher expression of S100P occurred in human gastric cancer tissues in comparison with normal controls. Highly expressed S100P in gastric cancer was correlated with TNM stage and prognosis. The 5-year survival rate was significantly lower in patients with high levels of S100P expression than in patients with low levels of expression. Ectopic expression of S100P was associated with an increase in tumor cell proliferation and drug resistance. Conclusion The expression of S100P in human gastric cancer tissues was upregulated in comparison with normal controls. By establishing an association between S100P expression and shortened OS, increase in proliferation and drug resistance, this study indicates that S100P may be a useful prognostic marker for gastric cancer patients.

Previous studies have shown that microRNA-31 (miR-31) functions as a tumor-suppressor in various types of cancer. In the present study we found that miR-31 was significantly downregulated in gastric cancer (GC) as determined by microRNA (miRNA) array screening analysis. Although aberrant expression of miR-31 has been found in different types of cancer, its pathophysiological effect and role in tumorigenesis still remain to be elucidated. In the present study, we detected miR-31 expression in both metastatic GC cell lines and tissues that are potentially highly metastatic by real-time polymerase chain reaction (PCR). Transwell and scratch healing assays were conducted to examine whether the ectopic expression of miR-31 could modify the invasion and migration abilities of GC cells in vitro. We found that miR-31 inhibited GC metastasis in a nude mouse xenograft model of GC. Luciferase reporter assays demonstrated that miR-31 could directly bind to the 3' untranslated region of RhoA and downregulate the expression of RhoA. Significant downregulation of miR-31 in 78 GC tissues and four GC cell lines was examined by real-time reverse transcription-PCR. Moreover, the decreased expression of miR-31 was demonstrated to be associated with lymph node metastasis, poor pT and pN stage, and invasion ability into lymphatic vessels as determined by the Mann-Whitney U test. We also found that miR-31 could inhibit cell invasion and migration abilities in vitro using the Transwell and scratch healing assays in BGC-823, SGC-7901, MGC-803 as well as AGS cells. Experiments in a nude mouse model revealed that miR-31 suppressed tumorigenicity in vivo. The luciferase activity assay and western blotting indicated that RhoA was the potential target of miR-31 in GC cells. Collectively, our results provide important evidence that the downregulation of miR-31 inhibited the invasion and migration abilities of GC cells through direct targeting of the tumor metastasis‑associated gene, RhoA. These findings suggest that miR-31 may be a promising therapeutic candidate in the treatment of GC metastasis.

Cellular prion protein (PrP(C)), a glycosyl-phosphatidylinositol-anchored membrane protein with unclear physiological function, was previous found to be upregulated in adriamycin (ADR)-resistant gastric carcinoma cell line SGC7901/ADR compared to its parental cell line SGC7901. Overexpression of PrP(C) in gastric cancer has certain effects on drug accumulation through upregulation of P-glycoprotein (P-gp), which is suggested to play an important role in determining the sensitivity of tumor cells to chemotherapy and is linked to activation of the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) pathway. In the present study, we further investigate the role of the PI3K/Akt pathway in PrP(C)-induced multidrug-resistance (MDR) in gastric cancer. Immunohistochemistry and confocal microscope detection suggest a positive correlation between PrP(C) and phosphorylated Akt (p-Akt) expression in gastric cancer. Using established stable PrP(C) transfectant cell lines, we demonstrated that the level of p-Akt was increased in PrP(C)-transfected cells. Inhibition of PrP(C) expression by RNA interference resulted in decreased p-Akt expression. Inhibition of the PI3K/Akt pathway by one of its specific inhibitors, LY294002, or by Akt small interfering RNA (siRNA) resulted in decreased multidrug resistance of SGC7901 cells, partly through downregulation of P-gp induced by PrP(C). Taken together, our results suggest that PrP(C)-induced MDR in gastric cancer is associated with activation of the PI3K/Akt pathway. Inhibition of PI3K/Akt by LY2940002 or Akt siRNA leads to inhibition of PrP(C)-induced drug resistance and P-gp upregulation in gastric cancer cells, indicating a possible novel mechanism by which PrP(C) regulates gastric cancer cell survival.

Cellular prion protein (PrP(C)), a copper-binding glycosyl-phosphatidylinositol (GPI)-anchored membrane protein that is expressed predominantly in neurons can be induced in ischemia/hypoxic brain tissues. It was also found to be overexpressed and conferred multidrug resistance, promoting cancer metastasis and inhibiting apoptosis in gastric cancer in our lab. In solid tumors, hypoxia can promote malignant progression and confer resistance to chemotherapy by altering gene expression. In present study, we investigated the molecular mechanisms and signaling pathway involved in the induction of the PrP(C) gene by hypoxia in cancer cell lines. PrP(C) was detected to be upregulated in several cancer cell lines at both mRNA and protein level, and then found to be induced by hypoxia in a time-dependent manner. After hypoxia treatment, gastric cancer MKN28 cells transfected with luciferase reporter constructs of the human PrP(C) promoter, which contained HSE, expressed higher luciferase activities (4.3-fold) than those cells transfected with the constructs containing no HSE. In addition, the upregulation of PrP(C) was reduced by MERK/ERK inhibitor (PD98059). siRNA knockdown of PrP(C) could make the cells more sensitive to hypoxia induced drug sensitivity. In conclusion, from these findings, we can propose that some transcriptional factors phosphorylated by ERK1/2, could in turn interact with HSE in the promoter of PrP(C) resulting in upregulation of PrP(C) in gastric cancer cell line MKN28 during hypoxia. Downregulation of PrP(C) makes gastric cancer cells more sensitive to hypoxia induced drug sensitivity. However, other mechanisms might also be responsible for hypoxia induced overexpression of PrP(C) in gastric cancer.

Cellular prion protein (PrP(C)), a glycosyl-phosphatidylinositol-anchored membrane protein with unclear physiological function, was previous found to be upregulated in adriamycin (ADR)-resistant gastric carcinoma cell line SGC7901/ADR compared to its parental cell line SGC7901. Overexpression of PrP(C) in gastric cancer has certain effects on drug accumulation through upregulation of P-glycoprotein (P-gp), which is suggested to play an important role in determining the sensitivity of tumor cells to chemotherapy and is linked to activation of the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) pathway. In the present study, we further investigate the role of the PI3K/Akt pathway in PrP(C)-induced multidrug-resistance (MDR) in gastric cancer. Immunohistochemistry and confocal microscope detection suggest a positive correlation between PrP(C) and phosphorylated Akt (p-Akt) expression in gastric cancer. Using established stable PrP(C) transfectant cell lines, we demonstrated that the level of p-Akt was increased in PrP(C)-transfected cells. Inhibition of PrP(C) expression by RNA interference resulted in decreased p-Akt expression. Inhibition of the PI3K/Akt pathway by one of its specific inhibitors, LY294002, or by Akt small interfering RNA (siRNA) resulted in decreased multidrug resistance of SGC7901 cells, partly through downregulation of P-gp induced by PrP(C). Taken together, our results suggest that PrP(C)-induced MDR in gastric cancer is associated with activation of the PI3K/Akt pathway. Inhibition of PI3K/Akt by LY2940002 or Akt siRNA leads to inhibition of PrP(C)-induced drug resistance and P-gp upregulation in gastric cancer cells, indicating a possible novel mechanism by which PrP(C) regulates gastric cancer cell survival.