An increased fraction of circulating miR-363 and miR-16 is particle bound in patients with chronic lymphocytic leukaemia as compared to normal subjects.

In vitro culture studies have shown that miR-363 is enriched in extracellular vesicles from chronic lymphocytic leukaemia cells. We wondered whether miR-363 was detectable in plasma, which is an essential precondition for further studies to assess its usefulness as a biomarker. Using samples from two clinical trials: one enrolling patients with advanced disease and the other asymptomatic patients with early stage disease, we determined plasma miR-363 levels and secondly investigated the distribution of this miRNA between plasma and particle bound fractions in patients and normal subjects.Advanced disease (n = 95) was associated with higher levels of miR-363 than early stage disease (n = 45) or normal subjects (n = 11) but there was no association with markers of prognosis. The distribution of specific miRNA between particle bound and plasma protein fractions was investigated using size exclusion chromatography on plasma from patients (n = 4) and normal subjects (n = 3). ~ 20% of total miR-16 and miR-363 is particle bound in patients while there was no detectable particle bound material in normal subjects. Our work demonstrates that miR-363 levels are raised in chronic lymphocytic leukaemia patients and raises the possibility that distribution of circulating miRNA between plasma fractions differs in health and disease

The efficacy of bentonite and zeolite in reducing aflatoxin B1 toxicity on production performance and intestinal and hepatic health of broiler chickens

This research aimed to assess the influences of bentonite (BN) and zeolite (ZE) on reducing toxic influences of aflatoxin B1 (AFB1) in broilers by examining growth performance, carcase characteristics, serum indices, ileum morphology, apparent nutrient digestibility, and liver AFB1 residues. In total, 360 11-d-old straight-run broilers (Ross 308) were randomly allocated into 6 dietary treatments, with 10 replications of 6 birds each, in a 20-d experiment. The treatments were as follows: standard basal diet (negative control, NC); NC + 0.25 mg/kg AFB1 (positive control, PC); NC + 0.4% BN; NC + 0.4% ZE; PC + 0.4% BN; PC + 0.4% ZE. Compared to the NC diet, feeding the PC diet decreased daily feed intake (DFI) during the grower and overall periods (p < .01), reduced daily weight gain (DWG) and production efficiency factor (PEF) and increased feed conversion ratio (FCR) during grower, finisher, and overall periods (p < .001), lowered breast meat yield (p < .01), diminished dressing percentage, serum concentrations of total protein (TP), albumin (ALB), glucose (GLU), total antioxidant capacity (T-AOC), and total superoxide dismutase (T-SOD), villus height (VH), villus surface area (VSA), apparent digestibility of crude protein (CP) and ether extract (EE), apparent metabolisable energy (AME), and nitrogen-corrected AME (AMEn) (p < .001), and raised proportional liver weight, serum activities of glutamic oxaloacetic transaminase (GOT) and glutamate pyruvate transaminase (GPT), and residues of AFB1 in the liver (p < .001). Compared to the PC diet, feeding the PC + 0.4% BN or PC + 0.4% ZE diets increased DWG and PEF and decreased FCR during finisher and overall periods, raised dressing percentage, serum levels of TP, GLU, T-AOC, and T-SOD, apparent CP digestibility, and reduced proportional liver weight and AFB1 residues in the liver (p < .001). Moreover, feeding the PC + 0.4% BN diet increased VH, VSA, apparent EE digestibility, AME, and AMEn, and decreased serum GOT and GPT activities when compared to the PC diet (p < .001). Whereas, feeding the PC + 0.4% ZE diet increased DFI during all experimental periods (p < .05) and DWG and PEF during the grower period (p < .001) as compared to the PC diet. To conclude, our findings demonstrate that dietary addition of 4 g/kg BN can deliver a better safeguard against the adverse influences of AFB1 in broiler chickens

Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity (vol 50, pg 26, 2017)

An amendment to this paper has been published and can be accessed via a link at the top of the paper