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6%) and gene expression in colon polyps (fold change -4.0) compared to AOM/DSS. AOM/DSS+D3G non-polyp tissue gene expression clustered with the healthy control tissue with only four genes modified (secreted phosphoprotein 1 and CXC motif chemokine ligands 2, 5, and 10). AOM/DSS+BL downregulated programmed death ligand-1 protein expression in colon tissue (-54.7%) and gene expression by 2.8-fold compared to the AOM/DSS control. In fecal samples, gallic and protocatechuic acids and epicatechin were found, and concentration of most amino acids was lower and unsaturated fatty acids were higher for AOM/DSS+BL and AOM/DSS+D3G. BL and D3G-rich extracts showed anti-inflammatory and pro-immune response effects while BL additionally prevented growth of neoplasia. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email journals.permissions@oup.com.INTRODUCTION Plasmodium falciparum infected erythrocytes bind to specific endothelial cell receptors via members of PfEMP1 family exported onto the erythrocyte surface. These interactions are mediated by different types of cysteine-rich inter-domain region (CIDR) domains found in the N-terminal region of all PfEMP1. CIDRα1 domains bind EPCR, CIDRα2-6 domains bind CD36 whilst the receptor specificity of CIDRβ/γ/δ domains is unknown. METHODS Here, we investigated the level of IgG targeting the different types of PfEMP1 CIDR during the first year of life. We used plasma collected longitudinally from children of pregnant women who had been followed closely through pregnancy. RESULTS Antibodies to CIDRα1 domains were more frequent in cord blood compared to antibodies to CIDRα2-6 domains. Higher IgG levels to EPCR-binding CIDRα1 variants positively correlated with the timing of first infections. Antibodies to all PfEMP1 types declined at similar rates to the point of disappearance over the first six months of life. At 12 months, children had acquired antibody to all types of CIDR domains, mostly in children with documented P. falciparum infections. CONCLUSION These observations agree with the notion that the timing and phenotype of first P. falciparum infections in life are influenced by the immune status of the mother. © The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail journals.permissions@oup.com.BACKGROUND Interindividual variability in 24-hour energy expenditure (24EE) during energy-balance conditions is mainly determined by differences in body composition and demographic factors. Previous studies suggested that 24EE might also be influenced by sympathetic nervous system activity via catecholamine (norepinephrine, epinephrine) secretion. Therefore, we analyzed the association between catecholamines and energy expenditure in 202 individuals from a heterogeneous population of mixed ethnicities. METHODS Participants (n = 202, 33% female, 14% black, 32% white, 41% Native American, 11% Hispanic, age 36.9 ± 10.3 y [mean ± SD], percentage body fat 30.3 ± 9.4) resided in a whole-room calorimeter over 24 hours during carefully controlled energy-balance conditions to measure 24EE and its components sleeping metabolic rate (SMR), awake-fed thermogenesis (AFT), and spontaneous physical activity (SPA). Urine samples were collected, and 24-h urinary epinephrine and norepinephrine excretion rates were assessed by high-performance liquid chromatography. Ivacaftor RESULTS Both catecholamines were associated with 24EE and SMR (norepinephrine +27 and +19 kcal/d per 10 μg/24h; epinephrine +18 and +10 kcal/d per 1 μg/24h) in separate analyses after adjustment for age, sex, ethnicity, fat mass, fat-free mass, calorimeter room, temperature, and physical activity. In a multivariate model including both norepinephrine and epinephrine, only norepinephrine was independently associated with both 24EE and SMR (both P  less then  .008), whereas epinephrine became insignificant. Neither epinephrine nor norepinephrine were associated with adjusted AFT (both P = .37) but epinephrine was associated with adjusted SPA (+0.5% per 1 μg/24h). CONCLUSIONS Our data provide compelling evidence that sympathetic nervous system activity, mediated via norepinephrine, is a determinant of human energy expenditure during nonstressed, eucaloric conditions. Published by Oxford University Press on behalf of the Endocrine Society 2020.Withaferin A (WA) is a promising phytochemical exhibiting in vitro and in vivo anticancer activity against prostate and other cancers but the mechanism of its action is not fully understood. In this study, we performed RNA-seq analysis using 22Rv1 human prostate cancer cell line to identify mechanistic targets of WA. Kyoto Encyclopedia of Genes and Genomes pathway analysis of the differentially expressed genes showed most significant enrichment of genes associated with metabolism. These results were validated using LNCaP and 22Rv1 human prostate cancer cells and Hi-Myc transgenic mice as models. The intracellular levels of acetyl-CoA, total free fatty acids, and neutral lipids were decreased significantly following WA treatment in both cells, which was accompanied by downregulation of mRNA (confirmed by quantitative reverse transcription-polymerase chain reaction) and protein levels of key fatty acid synthesis enzymes, including ATP citrate lyase (ACLY), acetyl-CoA carboxylase 1 (ACC1), fatty acid synthase (FASN), and carnitine palmitoyltransferase 1A (CPT1A). Ectopic expression of c-Myc, but not constitutively active Akt, conferred a marked protection against WA-mediated suppression of ACC1 and FASN protein expression, and clonogenic cell survival. WA was a superior inhibitor of cell proliferation and fatty acid synthesis in comparison with known modulators of fatty acid metabolism including cerulenin and etomoxir. Intraperitoneal WA administration to Hi-Myc transgenic mice (0.1 mg/mouse, three times/week for 5 weeks) also resulted in a significant decrease in circulating levels of total free fatty acids and phospholipids, and expression of ACLY, ACC1, FASN, and CPT1A proteins in the prostate in vivo. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email journals.permissions@oup.com.