Comparisons between short-peptide formula and intact-protein formula for early enteral nutrition initiation in patients with acute gastrointestinal injury: a single-center retrospective cohort study.

Background: Early enteral nutrition (EN) in critically ill patients is important and most of them have suffered acute gastrointestinal injury (AGI). In this study, we investigated the influence of short-peptide EN formula and intact-protein EN formula on the prognosis of patients with AGI grades I-II to provide some guidance. Methods: A retrospective cohort study was performed. The primary outcomes were the percentage of EN calories (25 kcal/kg/d) and protein (1.2 g/kg/d) on the 3rd and 7th days of intensive care unit (ICU) admission, EN percent elevation in calories and protein on days 3-7, and the incidence of gastric retention and diarrhea after EN administration. Secondary outcomes included ICU and 28-day mortality, length of ICU stay, total hospitalization cost, and ventilator-free days. Univariate and multivariate Cox regression analysis was used to identify factors associated with gastric retention and diarrhea. And we used Kaplan-Meier survival curves to compare 28-day mortality rates between the two groups. Results: There were no statistically significant differences in ICU and 28-day mortality, ICU length of stay, total hospitalization cost, or ventilator-free days in the short-peptide formula group compared with the intact-protein formula group. Kaplan-Meier survival curves of 28-day mortality also showed no statistically significant difference. The EN percent elevation in calories and protein on days 3-7 in the short-peptide formula group was significantly higher than the intact-protein formula group (48% vs. 38%, P=0.03 and 37% vs. 38%, P=0.04, respectively). For gastrointestinal (GI) adverse events, the incidence of gastric retention (15.5% vs. 29.8%, P=0.03) and diarrhea (8.5% vs. 19.8%, P=0.04) were lower in the short-peptide group. In the multivariate-adjusted model, the use of short-peptide formula was the only independent variable of reduction in gastric retention and diarrhea [HR =0.469 (95% CI: 0.239-0.922), P=0.028; and HR =0.394 (95% CI: 0.161-0.965), P=0.041, respectively]. Conclusions: Short-peptide formula is more easily tolerated by patients in the acute phase of AGI and can quickly achieve nutritional goals by EN provision, making it the preferred formula for the initiation of EN in the acute phase of AGI.

ROS-Triggered Autophagy Is Involved in PFOS-Induced Apoptosis of Human Embryo Liver L-02 Cells.

The liver is the primary target organ for perfluorooctane sulphonate (PFOS), a recently discovered persistent organic pollutant. However, the mechanisms mediating hepatotoxicity remain unclear. Herein, we explored the relationship between reactive oxygen species (ROS) and autophagy and apoptosis induced by PFOS in L-02 cells, which are incubated with different concentrations of PFOS (0, 50, 100, 150, 200, or 250 µmol/L) for 24 or 48 hrs at 37°C. The results indicated that PFOS exposure decreased cell activities, enhanced ROS levels in a concentration-dependent manner, decreased mitochondrial membrane potential (MMP), and induced autophagy and apoptosis. Compared with the control, 200 µmol/L PFOS increased ROS levels; enhanced the expression of Bax, cleaved-caspase-3, and LC3-II; induced autophagy; decreased MMP; and lowered Bcl-2, p62, and Bcl-2/Bax ratio. The antioxidant N-acetyl cysteine (NAC) protected MMP against PFOS-induced changes and diminished apoptosis and autophagy. Compared with 200 µmol/L PFOS treatment, NAC pretreatment reversed the increase in ROS, Bax, and cleaved-caspase-3 protein caused by PFOS, lowered the apoptosis rate increased by PFOS, and increased the levels of MMP and Bcl-2/Bax ratio decreased by PFOS. The autophagy inhibitor 3-methyladenine and chloroquine decreased apoptosis and cleaved-caspase-3 protein level and increased the Bcl-2/Bax ratio. In summary, our results suggest that ROS-triggered autophagy is involved in PFOS-induced apoptosis in L-02 cells.

LncRNA SNHG6 promotes breast cancer progression and epithelial-mesenchymal transition via miR-543/LAMC1 axis.

PURPOSE: Breast cancer (BC) is the most prevalent cancer in women with an estimated incidence of 10% and the leading cause of mortality due to its heterogenous property and high metastasis rate. Development of novel therapy is very necessary and requires an understanding of molecular mechanisms. We investigated the function of SNHG6/miR-543/LAMC1 axis in BC. METHODS: Human BC tissues were obtained from diagnosed patients. BC cell lines and normal breast cells were used. QRT-PCR and Western blotting were employed to measure expression levels of SNHG6, miR-543, LAMC1, EMT-related proteins, and PI3K/AKT pathway. Dual-luciferase assay was performed to validate interactions of SNHG6/miR-543 and miR-543/LAMC1. Colony formation assay, flow cytometry, scratch wound healing assay, and transwell assay were utilized to assess the proliferation, apoptosis, migration, and invasion of BC cells. Nude mouse xenograft model was used the evaluate the function of SNHG6/miR-543 in tumor growth in vivo. RESULTS: SNHG6 and LAMC1 were elevated, but miR-543 was reduced in BC tissues and cells. SNHG6 interacted directly with miR-543, while miR-543 targeted LAMC1. Knockdown of SNHG6 suppressed BC cell proliferation, migration, invasion, EMT, and PI3K/AKT pathway, but promoted cell apoptosis, while miR-543 inhibitor or overexpression of LAMC1 reversed those effects. Overexpression of LAMC1 also blocked the effects of miR-543 on BC cell proliferation, migration, invasion, and EMT. Knockdown of SNHG6 restrained BC growth in vivo, while miR-543 inhibitor inhibited that suppression. CONCLUSION: SNHG6 promoted EMT and BC cell proliferation and migration by acting as a miR-543 sponge and disinhibiting LAMC1/PI3K/AKT pathway. SNHG6/miR-543/LAMC1 axis could serve as candidates for the development of therapeutic strategies for BC.

Effect of the tyrosinase inhibitor (S)-N-trans-feruloyloctopamine from garlic skin on tyrosinase gene expression and melanine accumulation in melanoma cells.

In our searching for novel tyrosinase inhibitors from natural sources, (S)-N-trans-feruloyloctopamine isolated from garlic skin was found to be a potential mushroom tyrosinase inhibitor. Here, we examined the effects of the potential tyrosinase inhibitor in B16F10 cells on intracellular melanin contents, cytotoxicity, and the signaling mechanism involved in the expression of tyrosinase. The results showed the inhibitor displayed little or no cytotoxicity at all concentrations examined and decreased the relative melanin contents in a dose-dependent manner in the α-MSH-stimulated B16F10 cells. Real-time PCR and Western blot analysis showed that it inhibits melanogenesis signaling by down-regulates mRNA and protein expression levels of tyrosinase, which leads to a lower melanin contents. These results suggested that (S)-N-trans-feruloyloctopamine was an ideal tyrosinase inhibitor, and could be used in food and medical industry.