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The adenine nucleotide translocation in mitochondria has previously been established as an exchange between exogenous and endogenous adenine nucleotides across the inner membrane. The specificity and the control of the exchange are examined with the following major results: The adenine nucleotide translocation is relatively specific for exogenous ADP and ATP, AMP being nearly inactive. Among other nucleotides tested, only dADP and dATP exchange with a noticeable activity. In the controlled state ADP exchanges 2–4 times faster than ATP. If simultaneously added, ADP and ATP compete for the exchange, with ADP being about tenfold more active than ATP. The specificity of the exit of adenine nucleotides in the exchange is similar to the specificity of the entrance with the difference that ADP and ATP are released with equal activity in proportion to their intramitochondrial content. AMP is released only after a slow conversion to ADP. Therefore the short time exchange is limited by the endogenous content of ADP plus ATP. The exchange is influenced by the metabolic state of the mitochondria. The ATP exchange is more variable than the ADP exchange. Two effects are elucidated: (a) the influence of the metabolic state on the relative content of AMP which inhibits both the ADP and ATP exchange (b) the coupling of the energy transfer system which inhibits only the ATP exchange. An example for case (a) is the inhibition of the ADP and ATP exchange by arsenate and an example for case (b) is the strong increase of the ATP exchange on uncoupling. The following effects are relevant to the mechanism of the control of the exchange by ATP. The stimulation of the ATP exchange by uncoupler has the same concentration dependence as the uncoupling of oxidative phosphorylation (Km [CCP] = 0.08 μM, where CCP = carbonyl‐cyanide‐phenylhydrazone). Oligomycin does not abolish the uncoupler effect on the ATP exchange. “Endogenous uncoupling” on aging of mitochondria also stimulates the ATP exchange. Valinomycin plus K+ only slightly stimulate the ATP exchange. Anaerobiosis stimulates the ATP exchange to a smaller extent than uncoupling.In competition with ADP the effects of energy transfer on ATP exchange are more strongly revealed. On uncoupling the more than tenfold preference for ADP is fully abolished. It is concluded that basically the exchange for ADP and ATP has equal specificity in forward and reverse reaction. In the controlled state a superimposed force makes the specificity asymmetric and inhibits the entrance of ATP. This control of the ATP exchange is concluded to be based on the anionic character of the adenine nucleotides. Thus the ATP4‐ex–ADP3‐in exchange is inhibited unless the charge difference is compensated for by an uncoupler stimulated H+ movement across the membrane. Furthermore an electric potential gradient appears to be effective in the controlled state which is abolished on uncoupling.

Abstract Catalyst layer structural changes in polymer electrolyte membrane fuel cells have significant impact on the cell performance and durability. In this study, ex-situ experiments are designed to investigate the effect of humidity and/or thermal cycles on the structural changes of catalyst layers. The relative humidity and temperature are controlled by an environmental chamber and the catalyst layer structure is characterized by scanning electron microscopy and optical microscopy. The experimental results indicate that crack growth and development, catalyst agglomerate detachment, and surface bulges are the main structural changes of the catalyst layers. Applying relative humidity and thermal cycling simultaneously causes the most significant crack growth, while applying thermal cycling alone causes no appreciable changes. This indicates that the absolute humidity is the key parameter for the crack growth. Through cyclic voltammetry analysis, it is shown that the electrochemical active surface area decreases from 64.1 m2 g−1 to 49.1 m2 g−1 after 500 combined relative humidity and thermal cycles. Analyses of electrochemical impedance spectroscopy show that the charge transfer resistance and ohmic resistance increase significantly after 500 combined relative humidity and thermal cycles, causing the cell performance degradation.

Climate change is already affecting the cardiorespiratory health of populations around the world, and these impacts are expected to increase. The present overview serves as a primer for respirologists who are concerned about how these profound environmental changes may affect their patients. The authors consider recent peer‐reviewed literature with a focus on climate interactions with air pollution. They do not discuss in detail cardiorespiratory health effects for which the potential link to climate change is poorly understood. For example, pneumonia and influenza, which affect >500 million people per year, are not addressed, although clear seasonal variation suggests climate‐related effects. Additionally, large global health impacts in low‐resource countries, including migration precipitated by environmental change, are omitted. The major cardiorespiratory health impacts addressed are due to heat, air pollution and wildfires, shifts in allergens and infectious diseases along with respiratory impacts from flooding. Personal and societal choices about carbon use and fossil energy infrastructure should be informed by their impacts on health, and respirologists can play an important role in this discussion.

Sustainable development goals (SDGs) adopted in 2015 are geared toward sustainable development through various pathways, one being reducing inequality as covered in SDG 10. Inequalities are a threat to health and wellbeing of populations and a planet Earth in which we live. This rapid review aims to identify key issues that are likely to exacerbate inequalities around the six SDGs directly related to One Health, which are SDG 3, 6, 11, 13, 14 and 15, and suggest some actions that may help to address them using inclusive governance taking into account the coronavirus disease of 2019 (COVID-19) pandemic. Informed by the literature on SDGs and using the “inclusive development concept” by Gupta and Vegelin, literature search was done in Google Scholar, PubMed Central, as well as, searching of references in the relevant articles identified using search terms from the six SDGs that are directly related to One Health. In the context of the SDGs, in order to achieve One Health through inclusive governance, and tackle inequalities, the following needs to be considered and addressed: increasing number of armed conflicts; ongoing COVID-19 pandemic; ensuring availability of water and sanitation facilities; improving city and urban areas planning to cope with climate change; improving governance arrangements for addressing climate change factoring gender and human rights; multisectoral planning for conservation of oceans, seas, and marine resources; balancing trade regulation of wildlife trade with conservation efforts; need for a research collaborative involving experts from environmental sciences, wildlife, agriculture and human health to study and develop scientific evidence on contribution of changes in land use practices to occurrence of zoonotic diseases; and need of a legislation for promoting animal welfare to protect public health. Also, inclusion of people with disabilities in the use of digital technologies is critical.

The general properties of the heat shock response in Pseudomonas aeruginosa were characterized. The transfer of cells from 30 to 45 degrees C repressed the synthesis of many cellular proteins and led to the enhanced production of 17 proteins. With antibodies raised against the Escherichia coli proteins, two polypeptides of P. aeruginosa with apparent molecular weights of 76,000 and 61,000 (76K and 61K proteins) were shown to be analogous to the DnaK and GroEL heat shock proteins of E. coli due to their immunologic cross-reactivity. The major sigma factor (sigma 87) of P. aeruginosa was shown to be a heat shock protein that was immunologically related to the sigma 70 of E. coli by using polyclonal antisera. A hybridoma was produced, and the monoclonal antibody MP-S-1 was specific for the sigma 87 and did not cross-react with sigma 70 of E. coli. A smaller 40K protein was immunoprecipitated with RNA polymerase antisera from cells that had been heat shocked. The 40K protein was also associated with RNA polymerase which had been purified from heat-shocked cells and may be the heat shock sigma factor of P. aeruginosa. Exposure to ethanol resulted in the production of seven new proteins, three of which appeared to be heat shock proteins.

The inhalation toxicity of an ethanol-gasoline mixture was investigated in rats. Groups of 15 male and 15 female rats were exposed by inhalation to 6130 ppm ethanol, 500 ppm gasoline or a mixture of 85% ethanol and 15% gasoline (by volume, 6130 ppm ethanol and 500 ppm gasoline), 6 h a day, 5 days per week for 4 weeks. Control rats of both genders received HEPA/charcoal-filtered room air. Ten males and ten females from each group were killed after 4 weeks of treatment and the remaining rats were exposed to filtered room air for an additional 4 weeks to determine the reversibility of toxic injuries. Female rats treated with the mixture showed growth suppression, which was reversed after 4 weeks of recovery. Increased kidney weight and elevated liver microsomal ethoxyresorufin-O-deethylase (EROD) activity, urinary ascorbic acid, hippuric acid and blood lymphocytes were observed and most of the effects were associated with gasoline exposure. Combined exposure to ethanol and gasoline appeared to exert an additive effect on growth suppression. Inflammation of the upper respiratory tract was observed only in the ethanol-gasoline mixture groups, and exposure to either ethanol and gasoline had no effect on the organ, suggesting that an irritating effect was produced when the two liquids were mixed. Morphology in the adrenal gland was characterized by vacuolation of the cortical area. Although histological changes were generally mild in male and female rats and were reversed after 4 weeks, the changes tended to be more severe in male rats. Brain biogenic amine levels were altered in ethanol- and gasoline-treated groups; their levels varied with respect to gender and brain region. Although no general interactions were observed in the brain neurotransmitters, gasoline appeared to suppress dopamine concentrations in the nucleus accumbens region co-exposed to ethanol. It was concluded that treatment with ethanol and gasoline, at the levels studied, produced mild, reversible biochemical hematological and histological effects, with some indications of interactions when they were co-administered.

Abstract Radiation damage in biological systems is initiated by free radicals and progresses with time through a variety of mechanisms. The time-scale and details of these mechanisms are briefly reviewed. Because of the variety of mechanisms of radio-biological damage, any single radio-protective or therapeutic agent can be only partially effective. The potential of and need for simultaneously using several radio-protective and therapeutic agents, including sulfhydryl compounds, superoxide dismutase, antioxidant proteins, and DNA repair enzymes, are examined, based on a priori considerations of the consequences of radiation exposure.

The role of peripherally and centrally acting acetaldehyde in ethanol‐induced conditioned taste aversion (CTA) was investigated using various enzyme manipulations. Cyanamide, an aldehyde dehydrogenase inhibitor (ALDH) elevates blood acetaldehyde levels in the presence of ethanol. Concurrent administration with 4‐methylpyrazole (4MP), an alcohol dehydrogenase inhibitor, prevents peripheral accumulation of acetaldehyde by cyanamide. Under both treatment conditions brain and liver ALDH activity is inhibited. Water‐deprived rats were pretreated 4 hr prior to fluid presentation with intraperitoneal injections of saline (S+S), 4‐methylpyrazole (4MP+S), cyanamide (S+C), or 4‐methylpyrazole + cyanamide (4MP+C). Subsequently, animals were presented with a novel saccharin solution followed immediately by intraperitoneal injection of one of three doses of ethanol (0.4, 0.8, or 1.2 g/kg) or saline vehicle on four occasions. Results suggested that animals pretreated with cyanamide (groups S+C and 4MP+C) drank significantly less saccharin after conditioning with a subthreshold dose of ethanol (0.4 g/kg) in comparison to groups S+S and 4MP+S. Moreover, at the conditioning dose of 1.2 g/kg, cyanamide‐treated animals demonstrated an attenuation of CTA compared to the other two groups. These effects cannot be attributed to elevated blood acetaldehyde levels since pretreatment with 4MP+C prevented peripheral acetaldehyde accumulation. A characteristic common to both cyanamide‐treated groups was the inhibition of brain ALDH. It is therefore suggested that brain ALDH may play a role in the mediation of ethanol‐induced CTAs. It is conceivable that ALDH plays this role by regulating the levels of acetaldehyde in brain.