Studies on the environmental consequences of stress are relevant for economic and animal welfare reasons. We recently reported that long-term heat stressors (31 ± 1°C and 36 ± 1°C for 10 h/d) applied to broiler chickens (Gallus gallus domesticus) from d 35 to 42 of life increased serum corticosterone concentrations, decreased performance variables and the macrophage oxidative burst, and produced mild, multifocal acute enteritis. Being cognizant of the relevance of acute heat stress on tropical and subtropical poultry production, we designed the current experiment to analyze, from a neuroimmune perspective, the effects of an acute heat stress (31 ± 1°C for 10 h on d 35 of life) on serum corticosterone, performance variables, intestinal histology, and peritoneal macrophage activity in chickens. We demonstrated that the acute heat stress increased serum corticosterone concentrations and mortality and decreased food intake, BW gain, and feed conversion (P < 0.05). We did not find changes in the relative weights of the spleen, thymus, and bursa of Fabricius (P > 0.05). Increases in the basal and the Staphylococcus aureus-induced macrophage oxidative bursts and a decrease in the percentage of macrophages performing phagocytosis were also observed. Finally, mild, multifocal acute enteritis, characterized by the increased presence of lymphocytes and plasmocytes within the lamina propria of the jejunum, was also observed. We found that the stress-induced hypothalamic-pituitary-adrenal axis activation was responsible for the negative effects observed on chicken performance and immune function as well as for the changes in the intestinal mucosa. The data presented here corroborate with those presented in other studies in the field of neuroimmunomodulation and open new avenues for the improvement of broiler chicken welfare and production performance.
Rationale: Major coronary vessels derive from the proepicardium, the cellular progenitor of the epicardium, coronary endothelium, and coronary smooth muscle cells (CoSMCs Key Words: retinoic acid Ⅲ heart development Ⅲ coronary Ⅲ smooth muscle Ⅲ endothelium C oronary morphogenesis has been receiving intense scrutiny because of its usefulness as a model to understand vascular development and as a source of cues for regenerative therapies. Coronary vessel morphogenesis is linked to the development of epicardium and proepicardium, a transient embryonic structure located between the sinus venosus and the liver primordium. 1,2 Avian embryos have been instrumental to our knowledge on coronary development. Lineagetracing studies indicate that the proepicardium contains precursors of the epicardium, coronary endothelial cells (CoEs) and coronary smooth muscle cells (CoSMCs). [2][3][4][5] Proepicardial and primitive epicardial cells undergo epithelial-to-mesenchymal transformation (EMT), 2,6 supplying mesenchymal cells to the outer surface of the heart. These epicardially derived cells occupy positions along the subepicardial space, where they will differentiate into coronary vessel cell types. 7 Around Hamburger-Hamilton stage (HH)26, highly migratory, epicardially derived cells leave the subepicardium to invade the myocardium, thus disseminating part of CoE progenitors throughout the cardiac muscle. 8,9 Coronary vessels are formed from primary subepicardial and intramyocardial endothelial plexuses. Subepicardial/intramyocardial coronary vessel morphogenesis display one of the most striking and least understood features of coronary development, ie, the pronounced delay between CoE/CoSMC differentiation. Already at stage HH24, precursors in subepicardium differentiate into CoEs and form endothelial tubes under the influence of myocardially secreted cytokines, such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor. 10,11 In contrast, full CoSMC differentiation is only apparent after HH31 to HH32, concomitant with connection of CoE network to the aorta, stabilization of directional blood flow, and the onset of shear stress on coronary endothelium. 11 Curiously, CoSMC differentiation is Original
The data suggest that the presence of a double deletion genotypes of the GSTM1 and GSTT1 genes is associated with hypertriglyceridemia and low HDL-cholesterol levels in humans. These novel findings may provide a new unexplored link between lipid metabolism and GST homeostasis.
Carriers of TXNIP genetic variants presented higher TXNIP expression, early signs of glucose homeostasis derangement and increased susceptibility to chronic metabolic conditions such as diabetes and hypertension. Our data suggest that genetic variation in the TXNIP gene may act as a "common ground" modulator of both traits: diabetes and hypertension.
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