Moderation-excess interactions of epigallocatechin gallate and CaCl2 modulate the gelation performance of egg white transparent gels.

In this study, the moderation-excess interaction of epigallocatechin gallate (EGCG) and calcium ions (Ca2+) to the gelation performance of transparent egg white protein (EWP) gel (EWG) was explored. The oxidation of EGCG introduced a yellowish-brown EWG, whereas the weakening of Ca2+ ionic bonds caused a notable reduction in the hardness of EWG, from 120.67 g to 73.57 g. Achieving the optimal EGCG-to-Ca2+ ratio in EWG conferred enhanced water-holding capacity to 86.98%, while an excess of EGCG attributed to the creation of a three-dimensional structure within the void "walls". The elevated presence of EGCG influenced the ionic bonds and hydrophobic interactions, thereby presenting a moderate-excess relationship with sulfhydryl and disulfide bonds, ß-sheet, and α-helical structures. Notably, EGCG reduced the digestibility of EWG to 50.06%, while concurrently fostering the creation of smaller particle sizes. This study provides a scientific basis for the controllable preparation and quality regulation of transparent EWG.

Inhibition of autophagy impairs free fatty acid-induced excessive lipid accumulation in hepatocellular carcinoma and hepatic cells.

Autophagy is a reparative life-sustaining process. Dysfunctions of autophagy play an important role in the progression of chronic liver diseases. The role of autophagy in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) is still controversial. This study aimed to analyse the roles and molecular mechanisms of autophagy in NAFLD. In hepatic L02 and liver cancer cells (HuH-7), nonalcoholic fatty liver (NAFL) cell model was induced by free fatty acids (FFA). The cytotoxic effect was measured by MTS assay. Lipid droplets were detected by immunofluorescence assay and flow cytometry. The autophagy-related genes were measured by Western blot analysis. The autophagy inhibitor 3-methyladenine (3-MA) was used to block the autophagy. FFA induced a significant increase in the intracellular content of lipid droplets, and the accumulation of fatty droplets was dose-dependent in L02 and HuH-7 cells. FFA (800 lM) had no cytotoxic effect on L02 and HuH-7 cells. The levels of LC3-II/LC3-I and BECN1 were increased, but the level of p62 was decreased in the NAFL cell models. The expression of these genes was dose-dependent in the NAFL cell models. Intracellular lipid accumulation was associated with the upregulation of LC3-II/LC3-I and BECN1 and the deregulation of p62 in the NAFL cell models. The autophagy inhibitor 3-MA suppressed the FFA-induced autophagy in the NAFL cell models. Furthermore, 3-MA treatment significantly alleviated the accumulation of lipid droplets in L02 and HuH-7 cells. Our results suggest that autophagy has a significant effect on lipid accumulation in the NAFL cell models. Inhibition of autophagy impairs FFA-induced excessive lipid accumulation in hepatocellular carcinoma and hepatic cells.

Estimating Economic Losses Caused by COVID-19 under Multiple Control Measure Scenarios with a Coupled Infectious Disease-Economic Model: A Case Study in Wuhan, China.

BACKGROUND: The outbreak of the COVID-19 epidemic has caused an unprecedented public health crisis and drastically impacted the economy. The relationship between different control measures and economic losses becomes a research hotspot. METHODS: In this study, the SEIR infectious disease model was revised and coupled with an economic model to quantify this nonlinear relationship in Wuhan. The control measures were parameterized into two factors: the effective number of daily contacts (people) (r); the average waiting time for quarantined patients (day) (g). RESULTS: The parameter r has a threshold value that if r is less than 5 (people), the number of COVID-19 infected patients is very close to 0. A "central valley" around r = 5~6 can be observed, indicating an optimal control measure to reduce economic losses. A lower value of parameter g is beneficial to stop COVID-19 spread with a lower economic cost. CONCLUSION: The simulation results demonstrate that implementing strict control measures as early as possible can stop the spread of COVID-19 with a minimal economic impact. The quantitative assessment method in this study can be applied in other COVID-19 pandemic areas or countries.

Correlation between PLCE1 rs2274223 variant and digestive tract cancer: A meta-analysis.

BACKGROUND: The relationship between phospholipase C ε-1 (PLCE1) rs2274223 variant and digestive tract cancer remains inconclusive despite extensive investigations. Therefore, we performed this meta-analysis to obtain a more credible conclusion. METHODS: PubMed, Medline, and Embase were systematic searched. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. RESULTS: A total of 27 studies were finally included. Pooled analyses suggested that PLCE1 rs2274223 variant was significantly correlated with the likelihood of esophageal cancer (dominant model: p < 0.001, OR = 0.77, 95% CI 0.72-0.83; recessive model: p < 0.001, OR = 1.28, 95% CI 1.12-1.45; additive model: p < 0.001, OR = 1.20, 95% CI 1.11-1.29; allele model: p < 0.001, OR = 0.80, 95% CI 0.74-0.88) and gastric cancer (recessive model: p = 0.001, OR = 1.27, 95% CI 1.10-1.47; allele model: p = 0.03, OR = 0.88, 95% CI 0.78-0.98) in overall population. Further subgroup analyses showed that the positive results were mainly driven by the East Asians. However, no positive results were detected in Caucasians and West Asians. CONCLUSION: Our findings indicated that the PLCE1 rs2274223 variant might serve as a promising genetic biomarker of esophageal and gastric cancer in East Asians.

Neferine inhibits growth and migration of gastrointestinal stromal tumor cell line GIST-T1 by up-regulation of miR-449a.

BACKGROUND: Gastrointestinal stromal tumor (GIST) threatens the health of middle-aged and older people with high recurrence rate and low survival rate. In this study, Neferin (Nef) was hoped to control growth and migration of GIST cell line GIST-T1. METHODS: Cell viability, proliferation, apoptosis, and migration were determined by cell counting kit-8 (CCK-8) assay, bromodeoxyuridine (BrdU) assay, Annexin V-FITC/PI double staining method, and Transwell assay, respectively. The expression level of miR-449a was determined by qRT-PCR. Cell transfection was conducted to alter the expression level of miR-449a. Protein expression levels of key factors involved in cell cycle, cell apoptosis, cell migration, PI3K/AKT pathway and Notch pathways were analyzed by western boltting. RESULTS: Nef significantly inhibited GIST-T1 cell viability, proliferation, migration, but promoted cell apoptosis. The expression level of miR-449a was up-regulated in GIST-T1 cells after Nef treatment. Suppression of miR-449a reversed the Nef-induced GIST-T1 cell proliferation and migration inhibition, as well as cell apoptosis. Importantly, Nef inactivated PI3K/AKT and Notch pathways in GIST-T1 cells by up-regulating miR-449a. Inhibitors of PI3K/AKT and Notch pathways notably reversed the effects of Nef + miR-449a inhibitor on GIST-T1 cell proliferation, apoptosis and migration. Besides, Nef also suppressed human gastric cancer SGC7901 cell migration and induced cell apoptosis. CONCLUSION: Nef suppressed growth and migration of GIST-T1 cells possibly via up-regulation of miR-449a and then inactivation of PI3K/AKT and Notch pathways.

LncRNA-AK012226 Is Involved in Fat Accumulation in db/db Mice Fatty Liver and Non-alcoholic Fatty Liver Disease Cell Model.

Instances of obesity and related metabolic abnormalities are increasing across the world. Non-alcoholic fatty liver disease (NAFLD) is a common disorder in obese people and is becoming the leading cause of hepatocellular carcinoma. Recently, long non-coding RNAs (lncRNAs) have been proven to play remarkable roles in numerous biological processes and human diseases, including NAFLD. However, the function of lncRNA in NAFLD pathogenesis remains largely unknown. The aim of this study was to explore the lncRNA expression profile in NAFLD mice and to identify novel lncRNAs involved in the pathogenesis of NAFLD. We performed microarray analysis to compare the expression profiles of lncRNAs and mRNAs in the liver of diabetic db/db mice with NAFLD and normal mice. A total of 3360 lncRNAs (2048 up-regulated and 1312 down-regulated) and 2685 mRNAs (1195 up-regulated and 1490 down-regulated) were found to be differentially expressed between the NAFLD and control groups. Real-time PCR validation of five differentially expressed lncRNAs in the liver samples was consistent with the microarray results. Besides, the up-regulated lncRNA, AK012226, was also significantly increased in an NCTC1469 NAFLD cellular model. Thus, the up-regulated lncRNA, AK012226, was chosen for subsequent studies. A co-expression network of AK012226-mRNAs was constructed and bioinformatic analysis of these co-expressed mRNAs indicated that they were enriched in the PPAR signaling pathway. Furthermore, Nile red staining and flow cytometry analysis revealed that knockdown of AK012226 by siRNA significantly reduced the lipid accumulation in the NCTC1469 cells treated with free fatty acids. In conclusion, the present study identifies the dysregulated lncRNAs and mRNAs involved in NAFLD, and in particular, a novel lncRNA, AK012226, was identified to be associated with lipid accumulation in NAFLD.

Poly[aqua-[µ(3)-N'-(carboxy-meth-yl)ethyl-ene-diamine-N,N,N'-triacetato]samarium(III)].

In the title coordination polymer, [Sm(C(10)H(13)N(2)O(8))(H(2)O)](n), each samarium(III) centre is nine-coordinated by six O and two N atoms from three N'-(carboxy-meth-yl)ethyl-enediamine-N,N,N'-triacetate ligands and one O atom of a water mol-ecule, forming polymeric chains running parallel to the a axis. The packing is governed by inter-molecular O-H⋯O hydrogen-bonding inter-actions.