Lyngegrant3206

Globally, the widespread occurrence of disrespect and abuse (D&A) on maternity wards is well-documented. Using ethnography and cultural consensus analysis we explore how the practice of midwives hitting women who are in the second stage of labor (pushing) has become a locally accepted form of care in Tanzania if a baby's life appears to be at risk. This analysis interrogates the deep uncertainty of birth outcomes in this setting that may motivate abuse during this time. Seriously engaging with local discourses on abuse and care sheds light on hegemonic norms and power dynamics and is critical for improving maternity services.Purpose DNA damage contributes to the pathogenesis of age-related cataract (ARC) and is repaired through the nucleotide excision repair (NER) pathway, which includes ERCC6. Evidence has demonstrated that defective autophagy leads to lens organelle degradation and cataract. This study aimed to investigate the effects of ERCC6 on autophagy and determine its mechanisms in ARC.Methods The clinical case-control study comprised 30 patients with ARC and 30 age-matched controls who received transparent lens extraction. Transmission electron microscopy was used to assess the ultrastructure of autophagic vesicles in lens anterior capsule tissues and lens epithelial cell line (SRA01/04). Real-time polymerase chain reaction and western blot analyses were performed to measure relative gene expression levels. Gene expression levels and localization were assessed by immunofluorescence. A coimmunoprecipitation assay was used to investigate the relationship between CSB which encoded by ERCC6 and VCP. see more ERCC6-siRNA and let-7 c-5p mimic were used to alter the expression of ERCC6 and let-7 c-5p.Results Autophagy induction occurred in lens anterior capsule tissues of patients with ARC and in UVB-induced SRA01/04 cells, where the number of LC3B puncta was increased. Consistent with this result, the expression of beclin1 (BECN1) and LC3B, in addition to that of p62, was increased. Additionally, ERCC6 expression decreased, and silencing ERCC6 induced increases in the expression of BECN1, LC3B and p62. Moreover, CSB interacted with VCP, and let-7 c-5p induced dysregulation of autophagy by targeting ERCC6.Conclusion In ARC, Let-7 c-5p-mediated downregulation of ERCC6 might prevent the degradation of autophagic vacuoles. CSB binds to VCP, inducing autophagosomes to combine with lysosomes and be degraded.To date, there exists a debate on the effect of milk added to coffee infusions/beverages concerning the nutritional quality of coffee and the functional properties of its phenolic compounds. Yet, the full nutritional quality and functional properties of a coffee beverage without a significant negative impact on its sensorial profile are highly desired by the consumers. Negative/masking, positive, and neutral effects of milk on the antioxidant activity and bioavailability of coffee phenolics (particularly, chlorogenic acids) have been reported. Some potential factors including the type and amount of milk added, type of coffee beverage, the composition of both milk (protein and fat) and coffee (phenolic compounds), preparation method, assays used to measure antioxidant properties, and sampling size may account for the various reported findings. Interactions between phenolic compounds in coffee and milk proteins could account as the main responsible aspect for the reported masking/negative impact of milk on the antioxidant activity and bioaccessibility/bioavailability of coffee bioactives. However, considering the interactions between milk components and coffee phenolics, which result in the loss of their functionality, the role of milk fat globules and the milk fat globule membrane can also be crucial, but this has not been addressed in the literature so far.HighlightsIn most cases, milk is added to the coffee beverages in several various ways.Effect of milk on the nutritional/functional properties of coffee is controversial.Enough evidence suggests negative effects of milk addition on properties of coffee.Interactions of coffee phenolics and milk proteins could account as the main aspect.The role of milk fat globules and milk fat globule membrane may also be crucial.Isolation and utilization of proteins from seaweeds have been a novel trend in the world at present due to the increasing demand for healthy non-animal proteins. The attention of scientific community has been paid on the protein derived from seaweed Undaria pinnatifida due to their high nutritional quality and bioactivity. This article aims to provide an integrated overview on methods of extraction, isolation and purification of U. pinnatifida-derived proteins and composition, nutritional value and potential nutraceutical and food applications with an interest to stimulate further research to optimize the utilization. Potential food applications of U. pinnatifida derived proteins are nutritional components in human diet, food ingredients and additives, alternative meat and meat analogues and animal and fish feed. Excellent antioxidant, antihypertension, anticoagulant, anti-diabetes, antimicrobial and anti-cancer activities possessed by proteins of U. pinnatifida enable the use of these proteins in various nutraceutical applications. A number of studies have been carried out on antioxidant and antihypertensive activities of U. pinnatifida proteins, whereas other bioactivites are yet to be further studied. Hence, more research works are crucial to be done in order to facilitate and promote the emerging novel foods and nutraceuticals, using proteins from seaweed U. pinnatifida.Fucoxanthin is a marine xanthophyll found in edible brown algae, and a metabolite, fucoxanthinol (FxOH), possesses a potent apoptosis inducing effect in many cancer cells. Chloride intracellular channel 4 (CLIC4) is a member of the CLIC family that plays an important role in cancer development and apoptosis. However, the role of CLIC4 in FxOH-induced apoptosis is not well understood. In this study, we investigated whether CLIC4 affects the apoptotic properties of FxOH in human colorectal cancer (CRC) cells under FxOH treatment. Treating human CRC DLD-1 cells with 5.0 μmol/L FxOH significantly induced apoptosis. FxOH downregulated CLIC4, integrin β1, NHERF2 and pSmad2 (Ser465/467) by 0.6-, 0.7-, 0.7-, and 0.5-fold, respectively, compared with control cells without alteration of Rab35 expression. No colocalizing change was observed in CLIC4-related proteins in either control or FxOH-treated cells. CLIC4 knockdown suppressed cell growth and apoptosis. Interestingly, apoptosis induction by FxOH almost disappeared with CLIC4 knockdown.