Concomitant reactivity of the m-Terphenylindium dihydroxide [2,6-Mes2C6H3In(OH)2]4 toward carbon dioxide and ethylene glycol

The stepwise reaction of [2,6-Mes₂C₆H₃In(OH)₂]₄ with carbon dioxide and ethylene glycol proceeded with the formation of (2,6-Mes₂C₆H₃In)₄(CO₃)₂(OH)₄(H₂O)₂ (1) and (2,6-Mes₂C₆H₃In)₄(OCH₂CH₂O)₂(OH)₄ (2), respectively, and eventually produced (2,6-Mes₂C₆H₃In)₄(CO₃)₂(OCH₂CH₂OH)₂(OH)₂ (3). Attempts to liberate ethylene carbonate upon heating of 3 were unsuccessful.

PPARγ ligands, 15-deoxy-Δ12,14-prostaglandin J2 and rosiglitazone regulate human cultured airway smooth muscle proliferation through different mechanisms

1. The influence of two peroxisome proliferator-activated receptor γ (PPARγ) ligands, a thiazolidinedione, rosiglitazone (RG) and the prostaglandin D2 metabolite 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) on the proliferation of human cultured airway smooth muscle (HASM) was examined.

2. The increases in HASM cell number in response to basic fibroblast growth factor (bFGF, 300 pm) or thrombin (0.3 U ml−1) were significantly inhibited by either RG (1–10 μm) or 15d-PGJ2 (1–10 μm). The effects of RG, but not 15d-PGJ2, were reversed by the selective PPARγ antagonist GW9662 (1 μm).

3. Neither RG nor 15d-PGJ2 (10 μm) decreased cell viability, or induced apoptosis, suggesting that the regulation of cell number was due to inhibition of proliferation, rather than increased cell death.

4. Flow-cytometric analysis of HASM cell cycle distribution 24 h after bFGF addition showed that RG prevented the progression of cells from G1 to S phase. In contrast, 15d-PGJ2 caused an increase in the proportion of cells in S phase, and a decrease in G2/M, compared to bFGF alone.

5. Neither RG nor 15d-PGJ2 inhibited ERK phosphorylation measured 6 h post mitogen addition. The bFGF-mediated increase in cyclin D1 protein levels after 8 h was reduced in the presence of 15d-PGJ2, but not RG.

6. Although both RG and 15d-PGJ2 can inhibit proliferation of HASM irrespective of the mitogen used, only the antiproliferative effects of RG appear to be PPARγ-dependent. The different antimitogenic mechanisms of 15d-PGJ2 and synthetic ligands for PPARγ may be exploited to optimise the potential for these compounds to inhibit airway remodelling in asthma.

Auranofin increases apoptosis and ischaemia-reperfusion injury in the rat isolated heart

1. Auranofin, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and glutathione peroxidase. These enzymes play an important role in protecting cardiac tissue from oxidative stress generated during ischaemia–reperfusion.

2. Auranofin (100 mg/kg) was administered to rats and their hearts were subjected to an in vitro model of ischaemia–reperfusion. The activity of thioredoxin reductase and glutathione peroxidase was determined in liver and heart tissues in an attempt to correlate enzymatic activity with heart recovery after ischaemia–reperfusion.

3. There was significantly less thioredoxin reductase activity in rat liver extracts, whereas the level of glutathione activity remained unchanged, demonstrating that the dose of auranofin used was able to selectively inhibit one of these enzyme systems. Rats administered auranofin displayed significantly impaired recovery from ischaemic insult. The end diastolic pressure was increased, whereas the rate pressure product was significantly decreased.

4. The level of postischaemic apoptosis was also assessed by examining caspase-3 activity in tissue homogenates. Auranofin significantly increased the degree of postischaemic apoptosis, leading to poor postischaemic recovery.

Effects of predator control on behaviour of an apex predator and indirect consequences for mesopredator suppression

1. Apex predators can benefit ecosystems through top–down control of mesopredators and herbivores. However, apex predators are often subject to lethal control aimed at minimizing attacks on livestock. Lethal control can affect both the abundance and behaviour of apex predators. These changes could in turn influence the abundance and behaviour of mesopredators.

2. We used remote camera surveys at nine pairs of large Australian rangeland properties, comparing properties that controlled dingoes Canis lupus dingo with properties that did not, to test the effects of predator control on dingo activity and to evaluate the responses of a mesopredator, the feral cat Felis catus.

3. Indices of dingo abundance were generally reduced on properties that practiced dingo control, in comparison with paired properties that did not, although the effect size of control was variable. Dingoes in uncontrolled populations were crepuscular, similar to major prey. In populations subject to control, dingoes became less active around dusk, and activity was concentrated in the period shortly before dawn.

4. Shifts in feral cat abundance indices between properties with and without dingo control were inversely related to corresponding shifts in indices of dingo abundance. There was also a negative relationship between predator visitation rates at individual camera stations, suggesting cats avoided areas where dingoes were locally common. Reduced activity by dingoes at dusk was associated with higher activity of cats at dusk.

5. Our results suggest that effective dingo control not only leads to higher abundance of feral cats, but allows them to optimize hunting behaviour when dingoes are less active. This double effect could amplify the impacts of dingo control on prey species selected by cats. In areas managed for conservation, stable dingo populations may thus contribute to management objectives by restricting feral cat access to prey populations.

6. Synthesis and applications. Predator control not only reduces indices of apex predator abundance but can also modify their behaviour. Hence, indicators other than abundance, such as behavioural patterns, should be considered when estimating a predator's capacity to effectively interact with lower trophic guilds. Changes to apex predator behaviour may relax limitations on the behaviour of mesopredators, providing enhanced access to resources and prey.

Developmental origins of obesity-related hypertension

1. In the past 30 years the prevalence of obesity and overweight have doubled. It is now estimated that globally over 500 million adults are obese and a further billion adults are overweight. Obesity is a cardiovascular risk factor and some studies suggest that up to 70% of cases of essential hypertension may be attributable, in part, to obesity. Increasingly, evidence supports a view that obesity-related hypertension may be driven by altered hypothalamic signalling, which results in inappropriately high appetite and sympathetic nerve activity to the kidney.

2. In addition to the adult risk factors for obesity and hypertension, the environment encountered in early life may ‘programme’ the development of obesity, hypertension and cardiovascular disease. In particular, maternal obesity or high dietary fat intake in pregnancy may induce changes in fetal growth trajectories and predispose individuals to develop obesity and related sequelae.

3. The mechanisms underlying the programming of obesity-related hypertension are becoming better understood. However, several issues require clarification, particularly with regard to the role of the placenta in transferring fatty acid to the fetal compartment, the impact of placental inflammation and cytokine production in obesity.

4. By understanding which factors are most associated with the development of obesity and hypertension in the offspring, we can focus therapeutic and behavioural interventions to most efficiently reduce the intergenerational propagation of the obesity cycle.

Total and domain-specific sitting time among employees in desk-based work settings in Australia

Objective: To describe the total and domain-specific daily sitting time among a sample of Australian office-based employees. Methods: In April 2010, paper-based surveys were provided to desk-based employees (n=801) in Victoria, Australia. Total daily and domain-specific (work, leisure-time and transport-related) sitting time (minutes/day) were assessed by validated questionnaires. Differences in sitting time were examined across socio-demographic (age, sex, occupational status) and lifestyle characteristics (physical activity levels, body mass index [BMI]) using multiple linear regression analyses. Results: The median (95% confidence interval [CI]) of total daily sitting time was 540 (531-557) minutes/day. Insufficiently active adults (median=578 minutes/day, [95%CI: 564-602]), younger adults aged 18-29 years (median=561 minutes/day, [95%CI: 540-577]) reported the highest total daily sitting times. Occupational sitting time accounted for almost 60% of total daily sitting time. In multivariate analyses, total daily sitting time was negatively associated with age (unstandardised regression coefficient [B]=-1.58, p<0.001) and overall physical activity (minutes/week) (B=-0.03, p<0.001) and positively associated with BMI (B=1.53, p=0.038). Conclusions: Desk-based employees reported that more than half of their total daily sitting time was accrued in the work setting. Implications: Given the high contribution of occupational sitting to total daily sitting time among desk-based employees, interventions should focus on the work setting.

Depressive symptomatology, weight status and obesogenic risk among Australian adolescents: a prospective cohort study

OBJECTIVES: Adolescence is a period of increased risk for mental health problems and development of associated lifestyle risk behaviours. This study examined cross-sectional and longitudinal associations between obesogenic risk factors, weight status, and depressive symptomatology in a cohort of Australian adolescents.

DESIGN: Prospective cohort study.

SETTING: The study used repeated measures data from the Australian Capital Territory (ACT) It's Your Move project, an Australian community-based obesity prevention intervention. Intervention effect was non-significant therefore intervention and comparison groups were combined in this study.

PARTICIPANTS: Total sample was 634 secondary school students (female n=338, male n=296) with mean age 13 years (SD=0.6) at baseline (2012) and 15 years (SD=0.6) at follow-up (2014) recruited from 6 government secondary schools in the ACT.

PRIMARY AND SECONDARY OUTCOMES MEASURES: Primary outcome was depressive symptomatology measured by Short Mood and Feelings Questionnaire. Secondary outcomes were weight status, physical activity, screen time and diet related measures.

RESULTS: Increased physical activity was associated to lower depressive symptomatology among males (OR=0.35, p<0.05). Sweet drink (OR=1.15, p<0.05) and takeaway consumption (OR=1.84, p<0.05) were associated with higher levels of depressive symptomatology among females at follow-up. Males who were classified as overweight or obese at baseline, and remained so over the study period, were at increased risk of depressive symptomatology at follow-up (b=1.63, 95% CI 0.33 to 2.92). Inactivity among males over the 2-year study period was predictive of higher depressive symptomatology scores at follow-up (b=2.55, 95% CI 0.78 to 4.32). For females, those who increased their consumption of takeaway foods during the study period were at increased risk for developing depressive symptomatology (b=1.82, 95% CI -0.05 to 3.71).

CONCLUSIONS: There are multiple, probably complex, relationships between diet, physical activity and outcomes of obesity and mental health as well as between the outcomes themselves. Healthier diets and increased physical activity should be foundations for healthier body weight and mental health.