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A 37-d laying hen experiment was performed to determine the effect of Diamond V XPC(LS) (XPC(LS), Diamond V Mills, Cedar Rapids, IA) during a subclinical Eimeria maxima infection on intestinal health and productivity. Two hundred and sixteen 18-wk-old Brown Nick laying hens were allocated to 24 litter pens based on a weight class system (9 hens/pen). The trial was carried out as a 2 × 2 factorial design with XPC(LS) and E. maxima challenge as main factors. Birds were fed a corn/wheat-based mash prelayer diet from wk 18 to 20 (10.9 MJ/kg of AME and 13.7% CP) and a standard phase I layer diet from wk 20 to 24 (11.7 MJ/kg of AME and 15.3% CP) that were supplemented with XPC(LS) at the rate of 0 or 0.75 g/kg. Hens were orally inoculated on d 23 (22 wk of age) with either 1 mL of saline (not infected) or 10,000 sporulated E. maxima oocysts/bird in 1 mL of saline (infected). Effects of XPC(LS) on intestinal health were determined by E. maxima lesion scoring. Results of E. maxima lesions were analyzed by Fisher exact, whereas severity of lesions and production parameters were analyzed by ANOVA. Supplementation of XPC(LS) significantly reduced severity of E. maxima lesions (P < 0.05) from 1.1 to 0.8 in challenged hens. An overall significant effect of XPC(LS) supplementation was demonstrated on d 34 by decreasing the severity of lesions from 0.3 to 0.1. The E. maxima challenge decreased (P < 0.05) production performance between 7 and 14 d postchallenge by lowering egg weight from 50 to 47 g/egg and laying rate from 84 to 70% and increasing feed per dozen eggs (P < 0.01) from 1.60 to 2.06 kg. Results indicate that Diamond V XPC(LS) supplementation reduced intestinal damage caused by an E. maxima infection in laying hens.

Various products and prototypes were added to poultry diets during an aflatoxin challenge on growth and histological parameters. Male broiler chicks were randomly assigned to 8 treatment groups with 8 replicates/treatment and 3 birds/replicate. Treatments were as follows: 1) negative control containing no aflatoxin (NC); 2) positive control containing aflatoxin (PC); 3) 0.1% glucomannan mycotoxin standard industry ameliorator (STD); 4) 0.1% prototype A, a proprietary mixture of a Saccharomyces cerevisiae product and diatomaceous clay; 5) 0.2% prototype A; 6) 0.15% prototype B, a proprietary mixture of a S. cerevisiae product and diatomaceous clay (PB); 7) 0.0625% XPC (S. cerevisiae fermentation product); and 8) 0.125% XPC (XPC2). All treatments except NC contained 2,280 +/- 102 ng/g of aflatoxin and were fed for 28 d. Body weight and feed intake were measured weekly. Livers were collected on d 28, weighed, and used for histopathological evaluation. Beginning weights were similar across treatments, but BW were lower (P /= 0.05) different among the treatment groups. Liver weights relative to BW were higher (P /= 0.05) compared with NC. Overall, BW gain in treatment groups PB and XPC2 was not different from NC and that corresponded to protective effects against liver lesions. Benefits observed during an aflatoxin challenge when broilers were supplemented with XPC, a fermentation product that does not contain any adsorbents, may be attributed to something other than adsorption as a primary mechanism.

This study established a method for preserving chicken primordial germ cells (PGC) that enables long-term storage in liquid N. Gonads were harvested from stage 27 chick embryos and pooled in groups of 5, 10 (10E), or 20 embryos, contributing gonads to the cell suspension. The gonadal cells, including PGC, were then frozen in 1 of the following cryoprotectant treatments: 2.5% dimethyl sulfoxide (DMSO), 5% DMSO, 10% DMSO, 2.5% ethylene glycol (EG), 5% EG, 10% EG, and 0% cryoprotectant as a control. The cells were liberated and frozen in a biosecure cryopreservation straw at a rate of -1 degrees C/min until reaching -85 degrees C and were then plunged into liquid N (-196 degrees C), in which they were stored until analysis. Flow cytometry was used to analyze the PGC post-thaw. The PGC marker stage-specific embryonic antigen-1, which was detected with goat antimouse IgM fluorescein isothiocyanate, was used to label all PGC, and propidium iodide was used to detect cells with compromised cell membranes. There was an interaction effect for the number of viable PGC per individual embryo (P < or = 0.05). The highest level (183.6 +/- 28.4) of viable PGC per individual embryo was observed for 10% EG with 10E and was significantly higher (P < or = 0.05) than cryopreservation in 2.5% DMSO with 10E and 20 embryos, 2.5% EG with 10E, 5% EG with 10E, and all 0% cryoprotectant treatments. No statistical interaction (P > 0.05) was observed for the percentage of viable PGC. However, the highest percentage (80.6%) was observed at 10% EG with 10E. It was demonstrated that PGC were successfully frozen, and the most effective treatment was 10% EG with 10 embryos/straw.

Early posthatch satellite cell mitotic activity is an important aspect of muscle development. An understanding of the interplay between nutrition and satellite cell mitotic activity will lead to more efficient meat production. The objective of this study was to test the influence of the leucine metabolite, beta-hydroxy beta-methylbutyrate (HMB), and feed deprivation on muscle development in the early posthatch poult. Male Nicholas poults were placed on 1 of 4 treatments: immediately fed a starter diet with 0.1% HMB (IF-HMB), immediately fed a starter diet containing 0.1% Solka-Floc for a control (IF-No HMB), feed and water withheld for 48 h immediately posthatch and then fed the HMB diet (WF-HMB), and feed and water withheld for 48 h immediately posthatch and then fed the control starter diet (WF-No HMB). 5-bromo-2'-deoxyuridine (BrdU) was injected intra-abdominally into all poults to label mitotically active satellite cells. The pectoralis thoracicus was harvested 2 h after the BrdU injection. Immunohistochemistry for BrdU, Pax7, and laminin along with computer-based image analysis was used to study muscle development. IF-HMB poults had higher body weights (P < 0.01) at 48 h and 1 wk of age and had higher satellite cell mitotic activity at 48 h of age (P < 0.01) compared with the IF-No HMB and WF poults. Therefore, dietary supplementation of HMB may have an anabolic effect on early posthatch muscle.

Analysis of prospective follow-up data usually includes a Cox regression model. When a hazard rate ratio, obtained as the exponential of an estimated regression coefficient from the Cox model, is greater than 1.0, it consistently exceeds relative risk, and is exceeded by the odds ratio. The divergence of these distinct epidemiologic measures increases with the product of three factors: (1) the length of follow-up, (2) the average rate of the end point occurence over the follow-up period, and (3) the magnitude of risk, either above or below 1. Cornfield's rare disease assumption is basically the product of the first two of these factors. However, risks in excess of 2.5 have a powerful effect on the divergence of these measures, and this point has received less emphasis. Conversely, and as seen frequently in applications, relative risk, hazard rate ratio, and odds ratio numerically approximate one another with shorter follow-up, rarer end points, and risks closer to 1. Although the hazard rate ratio is not always distinguished from relative risk, it is commonly close to, and is always between, relative risk and the odds ratio. Consistent and accurate terminology would have us use hazard rate ratio with Cox regression and odds ratio with logistic regression. The term "relative risk" seems to be a default choice, regardless of the model being used. However, when relative risk is the object of the model chosen, as in a Poisson regression approximation of two binomial proportions or an equivalent weighted least squares, then for us, relative risk is the accurate terminology.