Rabbit Anti-Human SYN1 (Phospho-Ser605) polyclonal antibody

Background & aims: The sterile newborn digestive tract is rapidly colonized after birth and feeding type could influence this process. Infant formulas try to mimic the bifidogenic effect of human milk using prebiotic supplementation. The aim of this study was to demonstrate the efficacy, safety and tolerance of a 0.8 g/dL Orafti (R) Synergy1 (oligofructose-enriched inulin) supplemented infant formula during the first 4 months of life. Methods: In a double-blind, randomized, placebo-controlled and parallel trial, formula fed healthy term newborns were randomized to receive a control (controls) or SYN1 supplemented infant formula (SYN1). Breastfed newborns (BF) were also followed for comparison. Anthropometry, water balance, blood parameters, adverse events, stool frequency and characteristics and faecal microbiota were assessed. Results: A total of 252 formula fed infants were randomized at birth (n = 124 controls, n = 128 SYN1) and 131 BF infants were recruited; after 4 months 68 controls, 63 SYN1 and 57 BF completed the study. SYN1 infants showed a microbiota composition closer to that of BF infants, with a trend towards higher Bifidobacterium cell counts, softer stools and a higher deposition frequency compared to controls. There were no differences between formulas in anthropometry and relevant adverse events, water balance or blood parameters. Conclusion: A 0.8 g/dL SYN1-supplemented infant formula during the first 4 months of life is safe and effective, promoting a gut microbiota closer to that of breastfeeding. This clinical trial was registered at Clinicaltrials.gov as Study on Fermentable Carbohydrates in Healthy Infants (number NCT00808756). (C) 2013 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Diabetic cardiac autonomic neuropathy (DCAN) is one of the severe syndromes in diabetics. The neuropathy at superior cervical ganglia (SCG) is one of the important causes for leading to cardiac dysfunction upon diabetes. Previous studies reveal the deficiency of synapsin I (Syn1) in sciatic, retinal and hippocampal neurons in diabetes rodent model. However, the expression pattern of Syn1 in SCG of diabetic rat is poorly understood. In our study, we observed the presence of differential expression of two transcript isoforms of Syn1 in SCG. Isoform a (the longer one) was lower expressed while isoform b (the shorter one) was normally expressed in diabetic rats compared to control. Furthermore, we also explored the epigenetic landscape of H3K4me3, H3K9me3 and H3K36me3 on Syn1 and found that the enrichment of H3K4me3 and RNA pol II at the terminal exons was significantly different in SCG of diabetic and normal rats. In addition, the genomic H3K4me3 level of SCG abnormally increases in diabetic rats. Thus, we concluded that diabetes may impact on the distribution of H3K4me3, which can further regulate the transcriptional preference of Syn1 variants.