Background:Gastrointestinal complications and malnutrition are common problems that affect postoperative rehabilitation and survival of patients with esophageal cancer. Evidence has shown that probiotics have a positive effect on improving gastrointestinal complications and nutritional status of patients with esophageal cancer after surgery, but there is a lack of prospective studies on this topic. We designed this prospective randomized controlled trial to evaluate the effects of probiotics on gastrointestinal complications and nutritional status in patients with postoperative esophageal cancer.Methods:This is a prospective, randomized, double-blind, placebo-controlled trial. It was approved by the Clinical Research Ethics Committee of our hospital. 192 patients will be randomly divided into probiotics group and the placebo group in a 1:1 ratio. After operation, probiotics and placebo will be given orally for 8 weeks. The indexes of nutritional status and incidence of digestive tract complications will be recorded and the data will be analyzed by SPSS 18.0 software.Discussion:This study will evaluate the effect of probiotics on gastrointestinal complications and nutritional status of postoperative patients with esophageal cancer. The results of this study will provide clinical basis for the use of probiotics in postoperative treatment of esophageal cancer.Trial registration:OSF Registration number: D DOI 10.17605/OSF.IO/QHW86 相似文献
Introduction: Malnutrition increases the risk of cancer treatment-related complications. Nutritional intervention is beneficial for the outcomes of outpatients with cancer. This study investigated the impacts of nutrition consultation and care on energy intake and weight change in inpatients receiving cancer treatment.
Methods: We conducted a longitudinal study, enrolling 3221 inpatients with head and neck, lung, hepatobiliary, upper gastrointestinal, colorectal, breast, or gynecological cancer who received at least two nutrition consultations between April 2010 and July 2015. In every consultation, a dietitian calculated the total energy requirement and the actual energy intake was assessed using a 24-h dietary recall.
Results: Patients with head and neck cancer lost the most weight (1.16?kg/mo). For every consultation, a 0.03-kg weight gain per month was observed (P?=?0.001). The average energy consumption percentage (% estimated energy requirement) at the third consultation was 87.0%. After controlling for potential covariates, the energy consumption percentages at the third, fourth, fifth–seventh, eighth, and subsequent consultations were significantly higher than those at the first consultation (P?<?0.05).
Conclusion: For oncology inpatients, routine screening and at least three active nutrition consultations with dietitians effectively improved energy intake and preserved body weight. 相似文献
A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca2+ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca2+ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation. 相似文献