Portrayal regarding 5Oglucosyltransferase involved in anthocyanin biosynthesis throughout Cyclamen purpurascens

2. © 2020 Suárez-Delgado et al.BACKGROUND Pediatric pineoblastomas are highly aggressive tumors that portend poor outcomes despite multimodal management. Controversy remains regarding optimal disease management. OBJECTIVE To evaluate patterns of care and optimal clinical management of pediatric pineoblastoma. METHODS A total of 211 pediatric (age 0-17 yr) histologically confirmed pineoblastoma patients diagnosed between 2004 and 2015 were queried from the National Cancer Database. Wilcoxon rank-sum statistics and chi-squared analyses were used to compare continuous and categorical variables, respectively. Univariable and multivariable Cox regressions were used to evaluate prognostic impact of covariates. Propensity-score matching was used to balance baseline characteristics. RESULTS Older patients (age ≥ 4 yr) experienced improved overall survival compared to younger patients (age  less then  4 yr) (hazard ratio [HR] = 0.41; 95% CI 0.25-0.66). Older patients (adjusted odds ratio [aOR] = 5.21; 95% CI 2.61-10.78) and those residing in high-income regions (aOR = 3.16; 95% CI 1.21-8.61) received radiotherapy more frequently. Radiotherapy was independently associated with improved survival in older (adjusted HR [aHR] = 0.31; 95% CI 0.12-0.87) but not younger (aHR = 0.64; 95% CI 0.20-1.90) patients. The benefits of radiotherapy were more pronounced in patients receiving surgery than in those not receiving surgery (aHR [surgical patients] = 0.23; 95% CI 0.08-0.65; aHR [nonsurgical patients] = 0.46; 95% CI 0.22-0.97). Older patients experienced improved outcomes associated with aggressive resection (P = .041); extent of resection was not associated with survival in younger patients (P = .880). CONCLUSION Aggressive tumor resection was associated with improved survival only in older pediatric patients. Radiotherapy was more effective in patients receiving surgery. Age-stratified approaches might allow for improved disease management of pediatric pineoblastoma. Copyright © 2020 by the Congress of Neurological Surgeons.Breast cancer (BC) poses a great threaten to women health. Numerous evidences suggest the important role of long non-coding RNAs (lncRNAs) in BC development. In the present study, we intended to investigate the role of ARAP1-AS1 in BC progression. First of all, the GEPIA data suggested that ARAP1-AS1 was highly-expressed in BRAC (breast invasive carcinoma) tissues compared to the normal breast tissues. Meanwhile, the expression ARAP1-AS1 was greatly upregulated in BC cell lines. ARAP1-AS1 knockdown led to repressed proliferation, strengthened apoptosis and blocked migration of BC cells. Moreover, ARAP1-AS1 could boost HDAC2 expression in BC through sponging miR-2110 via a ceRNA mechanism. Of note, the UCSC predicted that HDAC2 was a potential transcriptional regulator of PLIN1, an identified tumor suppressor in BC progression. Moreover, we explained that the repression of HDAC2 on PLIN1 was owing to its deacetylation on PLIN1 promoter. More importantly, depletion of PLIN1 attenuated the mitigation function of ARAP1-AS1 silence on the malignant phenotypes of BC cells. To sum up, ARAP1-AS1 serves a tumor-promoter in BC development through modulating miR-2110/HDAC2/PLIN1 axis, which may help to develop novel effective targets for BC treatment. Copyright 2020 The Author(s).BACKGROUND Previous studies have suggested that the association between APOE ɛ4 and dementia is moderated by physical activity (PA), but the results remain inconclusive and longitudinal data on cognitive decline is missing. In this study we examine whether there is a gene-environment interaction between APOE and PA on cognitive decline in older adults using 9-year follow-up data of three cohort studies. METHODS We followed 7176 participants from three longitudinal cohort studies Longitudinal Aging Study Amsterdam (LASA), InCHIANTI and Rotterdam Study for 9 years. PA was assessed with self-reported questionnaires and was categorized in low, moderate and high PA. Cognitive function was assessed with the Mini-Mental State Examination (MMSE) and cognitive decline was defined as a decrease of 3 points or more on the MMSE during 3 years follow-up. We fitted logistic regression models using Generalized Estimating Equations adjusting for age, sex, education, depressive symptoms and number of chronic disease. Interaction between APOE and PA was tested on multiplicative and additive scale. RESULTS Cohorts were similar in most aspects but InCHIANTI participants were on average older and had lower education. NVP-BHG712 price APOE ɛ4 carriers had higher odds of cognitive decline (OR=1.46, 95% CI (1.29-1.64)) while PA was not significantly associated with cognitive decline overall (Moderate PA OR 0.87(0.67-1.13); High PA OR 0.71(0.36-1.40)). There was no evidence for an interaction effect between PA and APOE ɛ4 in cognitive decline in older adults (APOE*Moderate PA p=0.83; APOE*High PA p=0.90). CONCLUSIONS Previous claims of a gene-environment interaction between APOE ɛ4 and PA in cognitive decline are not supported by our results. © The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America.Heat shock factor 1 (HSF1) is a powerful multifaceted oncogenic modifier that plays a role in maintaining the protein balance of cancer cells under various stresses. In recent studies, there have been reports of increased expression of HSF1 in colorectal cancer (CRC) cells, and the depletion of the HSF1 gene knockdown has inhibited colon cancer growth both in vivo and in vitro. Therefore, HSF1 is a promising target for colon cancer treatment and chemoprevention. In the present study, we found that Schizandrin A (Sch A) significantly inhibited the growth of CRC cell lines by inducing cell cycle arrest, apoptosis and death. Through HSE luciferase reporter assay and quantitative PCR (qPCR), we identified Sch A as a novel HSF1 inhibitor. In addition, Sch A could effectively inhibit the induction of HSF1 target proteins such as heat-shock protein (HSP) 70 (HSP70) and HSP27, whether in heat shock or normal temperature culture. In the Surface Plasmon Resonance (SPR) experiment, Sch A showed moderate affinity with HSF1, further confirming that Sch A might be a direct HSF1 inhibitor.