Heat stress (HS) causes oxidative stress, which compromises broiler performance and meat quality. The aim of this study was to determine whether dietary antioxidants could be used as an amelioration strategy. Seventy-two day-old-male Ross-308 chicks were exposed to either thermoneutral or cyclical heat stress conditions. Diets were either control commercial diet (CON), CON plus betaine (BET), or with a combination of betaine, selenized yeast, and vitamin E (BET + AOX). Heat stress increased the rectal temperature (p < 0.001), respiration rate (p < 0.001), decreased blood pCO2 (p = 0.002), and increased blood pH (p = 0.02), which indicated the HS broilers had respiratory alkalosis. Final body weight was decreased by HS (p < 0.001), whereas it was improved with BET (p = 0.05). Heat stress reduced cooking loss (p = 0.007) and no effect on drip loss, while BET decreased the drip loss (p = 0.01). Heat stress reduced the myofibril fragmentation index (p < 0.001) and increased thiobarbituric acid reactive substances (p < 0.001), while these were improved with the combination of BET + AOX (p = 0.003). In conclusion, BET overall improved growth rates and product quality in this small university study, whereas some additional benefits were provided by AOX on product quality in both TN and HS broilers.

Heat stress compromises efficient poultry production by impairing growth performance and increasing mortality. Mechanisms to dissipate excess heat divert energy from efficient production. This includes increased energy expenditure for respiration, oxidative stress and micronutrient absorption. The fortification of diets with particular feed additives has been known as one of the most important approaches to minimize the negative impacts of heat stress on broiler production. In this context, the promising functional feed additives appeared to be selenium and vitamins E and C. The fortification of broiler diets with these feed additives has been proven to enhance the function of vital organs, immune system response and growth performance of broilers under heat stress. The current review highlights recent successful experiences in the alleviation of heat stress symptoms in broilers using the above-mentioned additives. Selenium and vitamins E and C enhanced production performance in broiler chickens challenged with acute heat stress. The combination of these additives, by employing multiple mechanisms and through synergistic effects, improves heat stress symptoms more efficiently than their individual forms. Emerging literature reveals that selenium and vitamins E and C are involved in close interactions to protect proteins and lipids from oxidative damage and boost immune system function.

In a 2 × 2 factorial design, 60 male Ross-308 broilers were fed either a control or 1 g/kg betaine diet and housed under thermoneutral (TN) or heat stress (HS) conditions. Broilers were acclimated to diets for 1 week under TN (25 °C), then either kept at TN or HS, where the temperature increased 8 h/day at 33 °C and 16 h/day at 25 °C for up to 10 days. Respiration rate (RR) was measured at four time points, and on each of 1, 2, 3, 7 and 10 days of HS, 12 broilers were injected with 0.5 mg/kg of Evans Blue Dye (EBD) solution to quantify regional changes in tissue damage. Betaine was quantified in tissues, and ileal damage was assessed via morphometry and transepithelial resistance (TER). Heat stress elevated RR (p < 0.001) and resulted in reduced villous height (p = 0.009) and TER (p < 0.001), while dietary betaine lowered RR during HS (p < 0.001), increased betaine distribution into tissues, and improved ileal villous height (p < 0.001) and TER (p = 0.006). Heat stress increased EBD in the muscle and kidney of chickens fed the control diet but not in those receiving betaine. Overall, these data indicate that supplemented betaine is distributed to vital organs and the gastrointestinal tract, where it is associated with improved tolerance of HS. Furthermore, EBD markers help reveal the effects of HS on organs dysfunction.

It is known that pig offspring born from pregnant pigs exposed to elevated ambient temperatures during gestation have altered phenotypes, possibly due to placental insufficiency and impaired fetal growth. Therefore, the objective of this study was to quantify the effect of maternal heat exposure during early-mid gestation, when pig placentae grow heavily, on placental and fetal development. Fifteen pregnant pigs were allocated to thermoneutral (TN; 20 °C; n = 7) or cyclic elevated temperature conditions (ET; 28 to 33 °C; n = 8) from d40 to d60 of gestation. Following euthanasia of the pigs on d60, placental and fetal morphometry and biochemistry were measured. Compared to TN fetuses, ET fetuses had increased (P = 0.041) placental weights and a lower (P = 0.013) placental efficiency (fetal/placental weight), although fetal weights were not significantly different. Fetuses from ET pigs had reduced (P = 0.032) M. longissimus fibre number density and a thicker (P = 0.017) placental epithelial layer compared to their TN counterparts. Elevated temperatures decreased (P = 0.026) placental mRNA expression of a glucose transporter (GLUT-3) and increased (P = 0.037) placental IGF-2 mRNA expression. In conclusion, controlled elevated temperatures between d40 to d60 of gestation reduced pig placental efficiency, resulting in compensatory growth of the placentae to maintain fetal development. Placental insufficiency during early-mid gestation may have implications for fetal development, possibly causing a long-term phenotypic change of the progeny.

Heat stress (HS) impairs growth performance and has a severe impact on lipid and protein metabolism, leading to serious adverse effects on meat quality. Forty-eight day-old-male Ross-308 chicks were assigned to two temperature conditions, thermoneutral or cyclical HS, and fed with either a control diet (CON) or the CON plus betaine (BET). Heat stress increased rectal temperature (p < 0.001), respiration rate (p < 0.001) and increased blood pH (p = 0.017), indicating that HS caused respiratory alkalosis. Heat stress reduced body weight during the final stage of growing period (p = 0.005), while BET improved it (p = 0.023). Heat stress tended to reduce breast muscle water content and drip loss (p = 0.089 and p = 0.082), while both were improved with BET (p = 0.008 and p = 0.001). Heat stress tended to reduce the myofibril fragmentation index (p = 0.081) whereas it increased with BET (p = 0.017). Heat stress increased thiobarbituric acid reactive substances (p = 0.017), while BET improved it (p = 0.008). Meat tenderness was not affected by HS, but was improved with BET (p < 0.001). In conclusion, BET improved growth performance over the latter stages of the growing period, and improved product quality of broiler chickens when chickens exposed to HS.

A custom integrated circuit ("αRAM") capable of detecting the α particles emitted in the decay of radon and its progeny has been designed, fabricated and successfully tested. The αRAM has been incorporated in a complete radon monitor using electrostatic concentration of radon progeny. The monitor can detect hazardous levels of radon within hours.

A passive direct-reading radon monitor utilizing a custom α particle detecting MOS integrated circuit and electrostatic radon progeny concentrator has been designed, built and successfully tested. Radon concentrations at the threshold generally considered hazardous can be detected within hours. This monitor appears suitable for low-cost, high-volume production.

Placental insufficiency is a known consequence of maternal heat stress during gestation in farm animals. The molecular regulation of placentae during the stress response is little known in pigs. This study aims to identify differential gene expression in pig placentae caused by maternal heat exposure during early to mid-gestation. RNA sequencing (RNA-seq) was performed on female placental samples from pregnant pigs exposed to thermoneutral control (CON; constant 20 °C; n = 5) or cyclic heat stress (HS; cyclic 28 to 33 °C; n = 5) conditions between d40 and d60 of gestation. On d60 of gestation, placental efficiency (fetal/placental weight) was decreased (p = 0.023) by maternal HS. A total of 169 genes were differentially expressed (FDR ≤ 0.1) between CON and HS placentae of female fetuses, of which 35 genes were upregulated and 134 genes were downregulated by maternal HS. The current data revealed transport activity (FDR = 0.027), glycoprotein biosynthetic process (FDR = 0.044), and carbohydrate metabolic process (FDR = 0.049) among the terms enriched by the downregulated genes (HS vs. CON). In addition, solute carrier (SLC)-mediated transmembrane transport (FDR = 0.008) and glycosaminoglycan biosynthesis (FDR = 0.027), which modulates placental stroma synthesis, were identified among the pathways enriched by the downregulated genes. These findings provide evidence that heat-stress induced placental inefficiency may be underpinned by altered expression of genes associated with placental nutrient transport capacity and metabolism. A further understanding of the molecular mechanism contributes to the identification of placental gene signatures of summer infertility in pigs.