Based on the meta-analysis, fish oil-supplemented parenteral nutrition was safe, improved clinical outcomes, and altered the fatty acid pattern as well as leukotriene synthesis. More laboratory parameters should be considered in future meta-analyses.

Background and objectives:Diarrhea is a common complication of enteral nutrition (EN), which affects recovery and prolongs the length of hospital stay (LOHS). To investigate the effect of fiber and probiotics in reducing diarrhea associated with EN in postoperative patients with gastric cancer (GC), the authors designed this prospective randomized-controlled trial.Methods and study design:This study included 120 patients with GC, and the patients were classified into 3 groups via random picking of envelopes: fiber-free nutrition formula (FF group, n = 40), fiber-enriched nutrition formula (FE group, n = 40), and fiber- and probiotic-enriched nutrition formula (FEP group, n = 40). All patients were given EN formulas for 7 consecutive days after surgery.Results:The number of diarrhea cases was higher in the FF group than in the FE group (P = .007). The FEP group had a lower number of diarrhea cases compared with the FE group (P = .003). Patients in the FE group had a significantly shorter first flatus time than the FF group (P = .002). However, no significant difference was observed between the FE group and FEP group (P = .30). Intestinal disorders were similar between the FE group and FF group (P = .38). The FEP group had a lower number of intestinal disorder cases than the FF group (P = .03). LOHS in the FE and FEP groups was shorter than that in the FF group (P = .004; P < .001). However, no significant difference was observed between the FE and FEP groups (P = .28). In addition, no significant difference was observed between the 3 groups in terms of total lymphocyte count, albumin, prealbumin, and transferrin levels on day 7 of enteral feeding.Conclusions:The combination of fiber and probiotics was significantly effective in treating diarrhea that is associated with EN in postoperative patients with GC.

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Endotoxin tolerance is defined as a reduced capacity of a cell to respond endotoxin (lipopolysaccharide, LPS) challenge after an initial encounter with endotoxin in advance. The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage induced by inflammatory reaction are significantly reduced in the state of endotoxin tolerance. The main characteristics of endotoxin tolerance are downregulation of inflammatory mediators such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), and C‐X‐C motif chemokine 10 (CXCL10) and upregulation of anti‐inflammatory cytokines such as IL‐10 and transforming growth factor β (TGF‐β). Therefore, endotoxin tolerance is often regarded as the regulatory mechanism of the host against excessive inflammation. Endotoxin tolerance is a complex pathophysiological process and involved in multiple cellular signal pathways, receptor alterations, and biological molecules. However, the exact mechanism remains elusive up to date. To better understand the underlying cellular and molecular mechanisms of endotoxin tolerance, it is crucial to investigate the comprehensive cellular signal pathways, signaling proteins, cell surface molecules, proinflammatory and anti‐inflammatory cytokines, and other mediators. Endotoxin tolerance plays an important role in reducing the mortality of sepsis, endotoxin shock, and other endotoxin‐related diseases. Recent reports indicated that endotoxin tolerance is also related to other diseases such as cystic fibrosis, acute coronary syndrome, liver ischemia‐reperfusion injury, and cancer. The aim of this review is to discuss the recent advances in endotoxin tolerance mainly based on the cellular and molecular mechanisms by outline the current state of the knowledge of the involvement of the toll‐like receptor 4 (TLR4) signaling pathways, negative regulate factor, microRNAs, apoptosis, chromatin modification, and gene reprogramming of immune cells in endotoxin tolerance. We hope to provide a new idea and scientific basis for the rational treatment of endotoxin‐related diseases such as endotoxemia, sepsis, and endotoxin shock clinically.

Tumor cells along with a small proportion of cancer stem cells exist in a stromal microenvironment consisting of vasculature, cancer-associated fibroblasts, immune cells and extracellular components. Recent epidemiological and clinical studies strongly support that vitamin D supplementation is associated with reduced cancer risk and favorable prognosis. Experimental results suggest that vitamin D not only suppresses cancer cells, but also regulates tumor microenvironment to facilitate tumor repression. In this review, we have outlined the current knowledge on epidemiological studies and clinical trials of vitamin D. Notably, we summarized and discussed the anticancer action of vitamin D in cancer cells, cancer stem cells and stroma cells in tumor microenvironment, providing a better understanding of the role of vitamin D in cancer. We presently re-propose vitamin D to be a novel and economical anticancer agent.