Ultraviolet radiation and laying pullets

1. Responses to ultraviolet (UV) radiation were studied in two trials. In one trial, sexually mature pullets, that had been maintained on an 8L:16D regimen from 2 d of age, were exposed sequentially, for periods of 9 to 12 d, to a further 8 h of very dim visible light (VDV), to 8 h of UV radiation and, finally, to an extra 8 h of normal light (conventional 16L:8D). Individual ovipositions were recorded during the last 48 h of each treatment. In the second trial, sexually mature pullets which had been allowed to 'free-run' for 14 d under continuous normal illumination (LL), were given, in addition to the normal light, a 12-h period of UV radiation commencing at midday or midnight for a further 15 d. During the final 48 h oviposition times were recorded and 4 food intakes for each 12-h period were determined. 2. In trial 1, mean oviposition time under VDV and UV supplementation was not significantly different from that under the 8L:16D regimen. Transfer to a 16L:8D regimen altered mean time of oviposition by about 4 h. In trial 2, eggs continued to be laid almost at random in all groups. 3. Food intake was suppressed during the 12-h period of UV supplementation compared with that when the birds were not receiving UV. 4. It is concluded that the addition of 8 h of UV radiation (at the intensity used in these studies) to 8 h of normal light does not cause a phase shift in the timing of the 'open-period' for pre-ovulatory luteinising hormone release which determines the time of oviposition. Furthermore, the insertion of 12-h periods of UV into continuous illumination does not entrain egg laying. 5. The suppressing effect of UV on food intake but lack of influence on the timing of the ovulatory cycle suggests that UV (at the intensity used in this study) acts principally at the retinal level and, as a result, stimulates only behavioural responses in laying birds.     

Yield Effects of Barley yellow dwarf virus in Soft Red Winter Wheat

ABSTRACT Three cultivars of soft red winter wheat were evaluated to determine the relationship between the incidence and time of infection by Barley yellow dwarf virus (BYDV) and yield. Wheat was planted in 1995, 1996, and 1997 in a split-plot design with six replicates at sites in Indiana and Illinois. Yield plots were infested with different amounts of viruliferous aphids, and the incidence of BYDV in each plot was measured. In a 2-year study in Illinois with cv. Clark and the PAV-IL isolate of BYDV, yields were assessed following aphid infestation in fall, early spring, and late spring. Early spring infections resulted in larger yield reductions than late spring infections in both years and larger than fall infections in one year. Regression analyses to relate incidence of infection and yield with data from fall and early spring infections provided R(2) values of 0.89 and 0.51 for the 1996 to 1997 and 1997 to 1998 seasons, respectively. An additional study at the same site in the 1996 to 1997 season compared the yield responses of cvs. Clark, Y88-3e, and PT8935b. Increases in the incidence of BYDV correlated with decreases in yield, with R(2) values of 0.80, 0.78, and 0.90 for the three cultivars, respectively. Estimated yield losses in both studies and all cultivars ranged from 27 to 45 kg/ha or 0.34 to 0.55% for each percent increase in virus infection. In a third study over a 2-year period in Indiana with the same three wheat genot ypes and a second BYDV isolate (PAV-P), BYDV treatments resulted in significant reductions in yield, but yield loss and the incidence of BYDV were not linearly correlated. Given the differences in yield reductions caused by the two BYDV isolates, PAV-P may be an attenuated strain of BYDV and may cross-protect plants from naturally occurring strains of the virus.     

Measuring the benefits of disease control: Relationship between herd structure,productivity and health

Summary The influence of calving percentage and mortality levels on heard structures is studied. Standard herd structures with set levels of mortality are calculated for comparison with field data. Herd structures from field surveys in Zambia are studied in order to determine how these can be used to gain more information about herd input and output dynamics. Methods of calculating off-take and the problems relating to making such calculations are discussed.

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Resumen Se estudió la influencia de los niveles de nacimientos y mortalidad en la estructura del hato. Se calcularon estructuras de hatos estandar, con niveles preconcebidos de mortalidad, para compararlos con datos de campo. Se estudiaron las estructuras de hatos en Zambia datos adquiridos en el campo, para determinar cómo éstos pueden utilizarse para obtener mayor información acerca de la dinámica costo-beneficio. Se discuten los métodos para calcular las ganancias y los problemas relacionados con estos cálculos.

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Résumé L'influence du niveau des intrants et des extrants (taux de vêlage et mortalité) sur la structure des troupeaux est étudiée. Des compositions standards avec des taux de mortalité pré-établis sont calculées pour permettre la comparaison avec les données recueillies sur le terrain. A partir d'enquêtes conduites en Zambie, la structure des troupeaux est étudiée en vue de déterminer comment ces résultats peuvent être utilisés pour accro?tre les données relatives à la dynamique des ressources et des emplois pour un troupeau donné. Les méthodes de calcul du taux d'exploitation et les problèmes relatifs à l'élaboration de ces calculs sont discutés.

     

Cytotoxic Effects of Loperamide Hydrochloride on Canine Cancer Cells

Loperamide is a peripheral opiate agonist that can cause apoptosis and G2/M arrest in human cancer cell lines and may sensitize cells to chemotherapy. The objectives of this study were to investigate the effects of loperamide on viability, apoptosis and cell cycle kinetics in canine cancer cells and to establish whether the drug sensitizes cells to doxorubicin. Cell viability was assessed using Alamar Blue. Cell death and cell cycle were studied using flow cytometry with 7-Aminoactinomycin-D (7-AAD) and propidium iodide (PI), respectively. Loperamide decreased cell viability in a dose-dependent fashion and was most effective against canine osteosarcoma cells. In all cell lines, it induced a dose and time dependent apoptosis and resulted in accumulation in G0/G1. When co-incubated with doxorubicin, loperamide induced a synergistic cell kill in canine carcinoma cells. Investigation is warranted into the role of loperamide in the treatment of canine cancer.