This study was conducted to evaluate potential hormonal mechanisms associated with the stress response, thermoregulation, and metabolic changes of broiler chickens exposed to high environmental temperature. Nine hundred 1-day-old male broiler chicks (Ross 708) were placed in floor pens and raised to 24 d. At 24 d, chicks were randomly assigned to 1 of 2 treatments, heat stress ( HS ) or no HS, and allocated into battery cages in 8 batteries (10 birds per cage, 2 cages per battery). On day 31, blood was collected prior to HS and analyzed using an iSTAT analyzer. Half of the batteries were then moved into 2 rooms with an elevated ambient temperature (35°C) for 8 h. The remaining batteries stayed in the thermoneutral rooms with an ambient temperature of 22°C. Beginning at 5 h after the initiation of HS, blood was collected and analyzed using an iSTAT analyzer, birds were euthanized, and hypothalamus and pituitary samples were collected (16 birds per treatment), flash frozen, and stored at −80°C until RNA extraction. Reverse transcription-quantitative PCR was used to compare mRNA levels of key corticotropic and thyrotrophic genes in the hypothalamus and pituitary. Levels of mRNA for each target gene were normalized to PGK1 (pituitary) and GAPDH (hypothalamus) mRNA. Differences were determined using mixed model ANOVA. HS decreased ( P < 0.05) feed intake, BW, bicarbonate, potassium, CO 2 , and triiodothyronine, while it increased mortality, glucose, pH, plasma thyroxine, and corticosterone. Expression of pituitary corticotropin-releasing hormone receptor 1 was downregulated ( P < 0.001), while corticotropin-releasing hormone receptor 2 mRNA levels were higher ( P = 0.001) in HS birds. HS increased expression of thyroid hormone receptor β ( P = 0.01) (2.8-fold) and thyroid stimulating hormone β ( P = 0.009) (1.4-fold). HS did not affect levels of mRNA of genes evaluated in the hypothalamus. Results showed that HS significantly affected both the thyrotropic and corticotropic axes. Understanding the role and regulation of these pathways during HS will allow researchers to better evaluate management strategies to combat HS.

D a v i d O l s o n , L i n d a F a r l e y , A l e x P a t r i c k , D i c k W a t l i n g , M a r i k a T u i w a w a V i l i k e s a M a s i b a l a v u , L e m e k i L e n o a , A l i v e r e t i B o g i v a , I n g r i d Q a u q a u J a m e s A t h e r t o n , A k a n i s i C a g i n i t o b a , M o a l a T o k o t a ' a , S u n i l P r a s a d W a i s e a N a i s i l i s i l i , A l i p a t e R a i k a b u l a , K i n i k o t o M a i l a u t o k a C r a i g M o r l e y and T h o m a s A l l n u t t Abstract Fiji's National Biodiversity Strategy and Action Plan encourages refinements to conservation priorities based on analyses of new information. Here we propose a network of Priority Forests for Conservation based on a synthesis of new studies and data that have become available since legislation of the Action Plan in 2001.For selection of Priority Forests we considered minimum-area requirements for some native species, representation goals for Fiji's habitats and species assemblages, key ecological processes and the practical realities of conservation areas in Fiji. Forty Priority Forests that cover 23% of Fiji's total land area and 58% of Fiji's remaining native forest were identified. The analysis confirms the majority of conservation priority areas previously identified, recommends several new areas, and supports the Government of Fiji's policy goal of protecting 40% of remaining natural forests to achieve the goals of the National Biodiversity Strategy and Action Plan and sustain ecosystem services for Fijian communities and economies.

During the normal embryonic-to-neonatal development, the chicken liver is subjected to intense lipid burden from high rates of yolk-lipid oxidation and also from the accumulation of the yolk-derived and newly synthesized lipids from carbohydrates. High rates of hepatic lipid oxidation and lipogenesis are also central features of non-alcoholic fatty liver disease (NAFLD) in both rodents and humans, but is associated with impaired insulin signaling, dysfunctional mitochondrial energetics and oxidative stress. However, these adverse effects are not apparent in the liver of embryonic and neonatal chicken, despite lipid burden. Utilizing comprehensive metabolic profiling, we identify that steady induction of hepatic mitochondrial tricarboxylic acid (TCA) cycle and lipogenesis are central features of embryonic-to-neonatal transition. More importantly, the induction of TCA cycle and lipogenesis occurred together with the downregulation of hepatic β-oxidation and ketogenesis in the neonatal chicken. This synergistic remodeling of hepatic metabolic networks blunted inflammatory onset, prevented accumulation of lipotoxic intermediates (ceramides and diacylglycerols) and reduced reactive oxygen species production during embryonic-to-neonatal development. This dynamic remodeling of hepatic mitochondrial oxidative flux and lipogenesis aids in the healthy embryonic-to-neonatal transition in chicken. This natural physiological system could help identify mechanisms regulating mitochondrial function and lipogenesis, with potential implications towards treatment of NAFLD.

On Pacific islands non-native rats and mongooses threaten many native species. In Fiji we compared visitation rates of rats and mongooses at bait stations and measured biomass of leaf-litter invertebrates to assess the relative predation pressure from these species in forest areas at different distances from the forest edge. Forest areas over 5 km from the forest edge had significantly fewer baits encountered by rats or mongooses than did natural forest areas nearer agricultural and urban habitats. Remote forest areas may function as a last refuge for island species threatened by predation from non-native rats and mongooses. The biomass of leaf-litter invertebrates in remote forest areas was higher indicating a refuge effect for some taxa targeted by rats and mongooses. Protection of the few remaining large blocks of natural forests on Pacific islands may be the most cost-effective approach for conserving many island endemics threatened by rats and mongooses. Logging roads can compromise this refuge effect by acting as dispersal routes for rats into natural forests.

Hypoxia dilates airways in vivo and reduces active tension of airway smooth muscle in vitro. To determine whether hypoxia impairs Ca2+ entry through voltage-dependent channels (VDC), we tested the ability of dihydropyridines to modulate hypoxia-induced relaxation of KCl- and carbamyl choline (carbachol)-contracted porcine bronchi. Carbachol- or KCl-contracted bronchial rings were exposed to progressive hypoxia in the presence or absence of 1 microM BAY K 8644 (an L-type-channel agonist). In separate experiments, rings were contracted with carbachol or KCl, treated with nifedipine (a VDC antagonist), and finally exposed to hypoxia. BAY K 8644 prevented hypoxia-induced relaxation in KCl-contracted bronchi. Nifedipine (10(-5) M) totally relaxed KCl- contracted bronchi. Carbachol-contracted bronchi were only partially relaxed by nifedipine but were completely relaxed when the O2 concentration of the gas was reduced from 95 to 0%. These data indicate that hypoxia can reduce airway smooth muscle tone by limiting entry of Ca2+ through a dihydropyridine-sensitive pathway, but that other mechanisms also contribute to hypoxia-induced relaxation of carbachol-contracted bronchi.