The efficacy of Na-butyrate encapsulated in palm fat on performance of broilers infected with necrotic enteritis with gene expression analysis.

AIM: To study the efficacy of Na-butyrate encapsulated in palm fat on performance of broiler chickens experimentally infected with necrotic enteritis (NE) with the determination of its protective effect against the changes in the gene expression profiles and deoxyribonucleic acid (DNA) fragmentation. MATERIALS AND METHODS: A total of 800 one-day-old male Arbor Acres Plus broiler chickens were randomly allocated into four groups for 5 weeks. Na-butyrate was supplemented at dosages of 1 kg/ton for starter diet, 0.5 kg/ton for grower diet, and 0.25 kg/ton for finisher diet (presence or absence). Birds of groups 1 and 2 were inoculated by crop gavages with 4×10(8) CFU/ml/bird of Clostridium perfringens in phosphate buffered saline for 4 successive days, from 14 to 17 days of age to produce NE. RESULTS: Addition of Na-butyrate, encapsulated in palm fat, to ration of experimentally infected broilers with NE resulted in increased final body weight, at 35 days of age, reduced total feed consumption, improved feed conversion ratio, reduced cumulative mortality, and increased production number. There were increased intestinal diameter, intestinal length, and significantly increased the weight of bursa of Fabricius(BF) with higher hemagglutination inhibition titers against Newcastle disease (ND) vaccination versus untreated infected and untreated negative control birds. The results showed increased expression levels of alpha-toxin and glyceraldehyde-3-phosphate dehydrogenase in the bursa tissues of broilers infected with C. perfringens. However, the expression levels of these genes in broilers treated with Na-butyrate were similar to the non-infected control group. Supplementation of broilers with Na-butyrate increased the expression level of insulin-like growth factor-1 (IGF-1) and decreased the DNA fragmentation induced by C. perfringens. CONCLUSION: Na-butyrate significantly improved chicken broiler body weights, increased relative weights of BF, increased antibody titers against ND vaccination, numerically lowered mortality due to C. perfringens infection, increased the expression level of IGF-1, and decreased the DNA fragmentation induced by C. perfringens. Obtained results point out the effectiveness of Na-butyrate encapsulated in palm fat in improving the production performance variables, immune response, and intestinal morphology in experimentally induced NE as well as in non-infected chicken broilers.

Cone beam CT evaluation of the presence of anatomic accessory canals in the jaws.

OBJECTIVES: To assess the prevalence, location and anatomical course of accessory canals of the jaws using cone beam CT. METHODS: A retrospective analysis of 4200 successive cone beam CT scans, for patients of both genders and ages ranging from 7 to 88 years, was performed. They were exposed at the School of Dentistry, University of Michigan, Ann Arbor, MI. After applying the exclusion criteria (the presence of severe ridge resorption, pre-existing implants, a previously reported history of craniofacial malformations or syndromes, a previous history of trauma or surgery, inadequate image quality and subsequent scans from the same individuals), 4051 scans were ultimately included in this study. RESULTS: Of the 4051 scans (2306 females and 1745 males) that qualified for inclusion in this study, accessory canals were identified in 1737 cases (42.9%; 1004 females and 733 males). 532 scans were in the maxilla (13.1%; 296 females and 236 males) and 1205 in the mandible (29.8%; 708 females and 497 males). CONCLUSIONS: A network of accessory canals bringing into communication the inner and outer cortical plates of the jaws was identified. In light of these findings, clinicians should carefully assess for the presence of accessory canals prior to any surgical intervention to decrease the risk for complications.

Reducing conditions significantly attenuate the neuroprotective efficacy of competitive, but not other NMDA receptor antagonists in vitro.

Inappropriate activation of NMDA receptors during a period of cerebral ischaemia is a crucial event in the pathway leading to neuronal degeneration. However, significant research has failed to deliver a clinically active NMDA receptor antagonist, and competitive NMDA antagonists are ineffective in many experimental models of ischaemia. The NMDA receptor itself has a number of modulatory sites which may affect receptor function under ischaemic conditions. Using rat organotypic hippocampal slice cultures we have investigated whether the redox modulatory site affects the neuroprotective efficacy of NMDA receptor antagonists against excitotoxicity and experimental ischaemia (OGD). NMDA toxicity was significantly enhanced in cultures pretreated with a reducing agent. The noncompetitive antagonist MK-801 and a glycine-site blocker were equally neuroprotective in both normal and reduced conditions, but there was a significant rightward shift in the dose-response curves of the competitive antagonists APV and CPP and the uncompetitive antagonist memantine. OGD produced neuronal damage predominantly in the CA1 region, which was prevented by MK-801 and memantine, but not by APV or CPP. Inclusion of an oxidizing agent during the period of OGD had no effect alone, but significantly enhanced the neuroprotective potency of the competitive antagonists. These data clearly demonstrate that chemical reduction of the redox modulatory site of the NMDA receptor decreases the ability of competitive antagonists to block NMDA receptor-mediated neuronal damage, and that the reducing conditions which occur during simulated ischaemia are sufficient to produce a similar effect. This may have important implications for the design of future neuroprotective agents.