Influence of environmental temperature and electrolyte balance on the performance of quails (Coturnix Coturnix Coturnix)

High environmental temperatures have a negative effect on the production efficiency of poultry reared in hot climates. This study evaluated the efficiency of electrolyte supplementation under high environmental temperature conditions by manipulating water and feed electrolyte balance (EB) on the survival and performance of European quails. In experiment 1, a completely randomized experimental design was applied in a 4 x 2 factorial arrangement. Treatments consisted in four feed EB values (0, 120, 240, 360 mEq/kg), and two environmental temperatures (25 and 34 ºC). Feed electrolyte balance was manipulated by the addition of sodium bicarbonate and ammonium chloride. In experiment 2, birds were randomly distributed according to a 5 x 2 factorial arrangement. Treatments consisted in five BE values in the drinking water (0, 30, 60, 90, 120 mEq/L) and two environmental temperatures (25 and 34 °C). Only sodium bicarbonate was added to the water to obtain the different BE values. The experiments were carried out simultaneously in environmental chambers at constant temperatures with 20- to 37-d-old quails. Most evaluated parameters were influenced by temperature in both experiments. In experiment 1, EB affected water intake and intestinal length. In experiment 2, EB values influenced (p < 0.05) water intake and heart and liver relative weights. Electrolyte balance values of 120 mEq/kg of feed and of 30 mEq/L of drinking water are recommended to increase water intake of grower European quails reared under hot temperature.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)UFPB CCAUFPB CCHSAUnespUnes

Can asthma control be improved by understanding the patient's perspective?

Clinical trials show that asthma can be controlled in the majority of patients, but poorly controlled asthma still imposes a considerable burden. The level of asthma control achieved reflects the behaviour of both healthcare professionals and patients. A key challenge for healthcare professionals is to help patients to engage in self-management behaviours with optimal adherence to appropriate treatment. These issues are particularly relevant in primary care, where most asthma is managed. An international panel of experts invited by the International Primary Care Respiratory Group considered the evidence and discussed the implications for primary care practice

Antitumor activity of efrapeptins, alone or in combination with 2-deoxyglucose, in breast cancer in vitro and in vivo

Efrapeptins (EF), a family of fungal peptides, inhibit proteasomal enzymatic activities and the in vitro and in vivo growth of HT-29 cells. They are also known inhibitors of F1F0-ATPase, a mitochondrial enzyme that functions as an Hsp90 co-chaperone. We have previously shown that treatment of cancer cells with EF results in disruption of the Hsp90:F1F0-ATPase complex and inhibition of Hsp90 chaperone activity. The present study examines the effect of EF on breast cancer growth in vitro and in vivo. As a monotherapy, EF inhibited cell proliferation in vitro with an IC50 value ranging from 6 nM to 3.4 μM. Inhibition of Hsp90 chaperone function appeared to be the dominant mechanism of action and the factor determining cellular sensitivity to EF. In vitro inhibition of proteasome became prominent in the absence of adequate levels of Hsp90 and F1F0-ATPase as in the case of the relatively EF-resistant MDA-MB-231 cell line. In vivo, EF inhibited MCF-7 and MDA-MB-231 xenograft growth with a maximal inhibition of 60% after administration of 0.15 and 0.3 mg/kg EF, respectively. 2-Deoxyglucose (2DG), a known inhibitor of glycolysis, acted synergistically with EF in vitro and antagonistically in vivo. In vitro, the synergistic effect was attributed to a prolonged endoplasmic reticulum (ER) stress. In vivo, the antagonistic effect was ascribed to the downregulation of tumoral and/or stromal F1F0-ATPase by 2DG