Effect of high dietary levels of α-tocopherol acetate on immune response of light and heavy weight male broiler breeders

Abstract

The objective of this study was to investigate the effect of overdosing dietary α-tocopherol acetate (α-TOH) on immune response of heavy weight roosters. A total of 60 roosters (Ross 308) of light (LW, n = 30) and heavy weight (HW, n = 30) were kept in individual cages. Roosters were randomly allotted to ten treatment groups in a 2 × 5 factorial design. Each group received a basal diet supplemented with graded levels of α-TOH (0, 100, 200, 300, 400 mg/kg diet) for 10 weeks (from 25 to 35 week of age). Blood samples were collected at the fifth and tenth weeks of the experiment. Afterwards, humoral immune system function was evaluated by sheep red blood cell (SRBC) hemagglutination assay (HA) (at 35 weeks of age) and hemagglutination inhibition (HI) tests including antibody response to Newcastle disease viruses (NDV) and avian influenza viruses (AIV) (at 30 and 35 weeks of age). Cell-mediated immune response was evaluated by the cutaneous basophil hypersensitivity (CBH) test. A positive linear relationship was observed between incremental levels of dietary α-TOH and both humoral and cell-mediated immunity (P ≤ 0.05), with the highest immune parameters recorded for dietary supplementation of 400 mg/kg α-TOH (P ≤ 0.05). The results showed that CBH was significantly higher in LW roosters in comparison with HW roosters (P ≤ 0.05). However, the interaction of BW and α-TOH doses did not have any significant effect on immune responses (P ≥ 0.05). In conclusion, dietary supplementation of α-TOH at higher levels (four times more than the strain nutrients recommendation) had beneficial effects on the immune response of both HW and LW male broiler breeders.

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Rectal cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up

Ann Oncol 2017; 28: iv22–iv40 (doi:10.1093/annonc/mdx224)

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Management of infusion reactions to systemic anticancer therapy: ESMO Clinical Practice Guidelines

Ann Oncol 2017; 28: iv100–iv118 (doi:10.1093/annonc/mdx216)

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Activity and safety of crizotinib in patients with advanced clear-cell sarcoma with MET alterations: European Organization for Research and Treatment of Cancer phase II trial 90101 ‘CREATE’

Ann Oncol 2017; 28: 3000–3008 (doi: 10.1093/annonc/mdx527)

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Cervical cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up

Ann Oncol 2017; 28: iv72–iv83 (doi:10.1093/annonc/mdx220)

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De-escalating and escalating treatments for early-stage breast cancer: the St. Gallen International Expert Consensus Conference on the Primary Therapy of Early Breast Cancer 2017

Ann Oncol 2017; 28: 1700–1712 (doi: 10.1093/annonc/mdx308)

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Pronounced maternal parent-of-origin bias for type-1 NF1 microdeletions

Abstract

Neurofibromatosis type 1 (NF1) is caused, in 4.7–11% of cases, by large deletions encompassing the NF1 gene and its flanking regions within 17q11.2. Different types of large NF1 deletion occur which are distinguishable by their breakpoint location and underlying mutational mechanism. Most common are the type-1 NF1 deletions of 1.4 Mb which exhibit recurrent breakpoints caused by nonallelic homologous recombination (NAHR), also termed unequal crossover. Here, we analyzed 37 unrelated families of patients with de novo type-1 NF1 deletions by means of short tandem repeat (STR) profiling to determine the parental origin of the deletions. We observed that 33 of the 37 type-1 deletions were of maternal origin (89.2% of cases; p < 0.0001). Analysis of the patients' siblings indicated that, in 14 informative cases, ten (71.4%) deletions resulted from interchromosomal unequal crossover during meiosis I. Our findings indicate a strong maternal parent-of-origin bias for type-1 NF1 deletions. A similarly pronounced maternal transmission bias has been reported for recurrent copy number variants (CNVs) within 16p11.2 associated with autism, but not so far for any other NAHR-mediated pathogenic CNVs. Region-specific genomic features are likely to be responsible for the maternal bias in the origin of both the 16p11.2 CNVs and type-1 NF1 deletions.

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