The objective of this study was to evaluate the effect of nisin in combination with different types of packaging on the survival of Listeria monocytogenes in ready-to-eat low-fat turkey bologna. Bologna was inoculated with L. monocytogenes exposed to 1 of 6 treatments: 3 packaging treatments (100% CO2, air, vacuum), each with and without nisin. Bologna was refrigerated and sampled 9 times over 42 d. Nisin reduced initial L. monocytogenes populations by 1.5 to 2 log cycles and 100% CO2 packaging prevented outgrowth throughout 42 d of storage, whereas non-CO2 packaging displayed a 2-log increase in population during storage. Nisin (500 IU/mL) combined with 100% CO2 was effective in reducing Listeria and preventing outgrowth on bologna over 42 d of refrigerated storage.
Hesham Taher Naas(3-2013)

The neurotransmitter(s) that generate the inhibitory junctional potential (IJP) in the circular muscle of hamster distal colon and their mechanisms have not been elucidated. The aim of the present study, therefore, was to determine the contributing roles of the non-adrenergic, non-cholinergic (NANC) inhibitory transmitter(s) including nitric oxide (NO), adenosine 5′-triphosphate (ATP) and vasoactive intestinal polypeptide (VIP) in the generation of IJP in the hamster distal colon. For this purpose, the effects of the corresponding blockers of these putative NANC inhibitory mediators have been investigated using microelectrode technique. arabic 8 English 62
M. Draid(12-2006)

The imprinted expression of the IGF2 and H19 genes is controlled by the imprinting control region 1 (ICR1) located at chromosome 11p15.5. This methylation-sensitive chromatin insulator works by binding the zincfinger protein CTCF in a parent-specific manner. DNA methylation defects involving the ICR1 H19/IGF2 domain result in two growth disorders with opposite phenotypes: an overgrowth disorder, the Beckwith– Wiedemann syndrome (maternal ICR1 gain of methylation in 10% of BWS cases) and a growth retardation disorder, the Silver–Russell syndrome (paternal ICR1 loss of methylation in 60% of SRS cases). Although a few deletions removing part of ICR1 have been described in some familial BWS cases, little information is available regarding the mechanism of ICR1 DNA methylation defects. We investigated the CTCF gene and the ICR1 domain in 21 BWS patients with ICR1 gain of methylation and 16 SRS patients with ICR1 loss of methylation. We identified four constitutional ICR1 genetic defects in BWS patients, including a familial case. Three of those defects are newly identified imprinting defects consisting of small deletions and a single mutation, which do not involve one of the CTCF binding sites. Moreover, two of those defects affect OCT-binding sequences which are suggested to maintain the unmethylated state of the maternal allele. A single-nucleotide variation was identified in a SRS patient. Our data extends the spectrum of constitutive genetic ICR1 abnormalities and suggests that extensive and accurate analysis of ICR1 is required for appropriate genetic counseling in BWS patients with ICR1 gain of methylation.
Demars, J., Mansur Ennuri Moftah Shmela, S. Rossignol, J. Okabe, I. Netchine, S. Azzi, S. Cabrol, C. Le Caignec, A. David , Y. Le Bouc, A. El-Osta , C. Gicquel(9-2010)