Avoidance of filial cannibalism in the amphipod Gammarus pulex.

Adult animals that cannibalise juvenile conspecifics may gain energy but also risk filial cannibalism, that is, consumption of their own offspring. However, individuals vary in the magnitude of the costs and benefits of cannibalism depending on factors such as their current energy reserves or the probability that they have offspring in the vicinity. They may therefore also vary in the extent to which they participate in cannibalism. This study investigated whether the sex or brooding status of adult amphipods (Gammarus pulex) influenced whether they participated in cannibalism of juveniles. For females carrying embryos within their brood pouch, we also investigated two hypotheses to explain the presence or absence of cannibalistic behaviour by determining whether cannibalism was correlated with factors that might reflect energy demands (body length, brood size), or that might reflect a temporal change in cannibalistic behaviour (corresponding to stage of brood development). All reproductive classes of adults participated in some level of juvenile cannibalism, but females carrying offspring at an advanced stage of development (close to emergence from the brood pouch) consumed significantly fewer juveniles than other groups. Females thus appear to significantly reduce cannibalism of juveniles concurrent with the time when their own eggs are hatching within the brood pouch, prior to the release of their offspring. Because the experiment tested female responses to unfamiliar juveniles, this reflects a temporal change in behaviour rather than a response to phenotypic recognition cues, although additional direct recognition cannot be ruled out. Brooding females with large brood sizes or large body lengths, which might have disproportionately greater energetic demands, were not more likely to cannibalise juveniles. We also noted that juveniles that survived in trials where cannibalism occurred were significantly more likely to be found at the water surface, suggesting a possible adaptation to escape cannibalistic adults. Overall, our results provide evidence that amphipods use indirect temporal cues to avoid filial cannibalism.

Work-place social capital and smoking cessation: The Finnish Public Sector Study

AIMS:
To examine whether high social capital at work is associated with an increased likelihood of smoking cessation in baseline smokers.
DESIGN:
Prospective cohort study.
SETTING:
Finland.
PARTICIPANTS:
A total of 4853 employees who reported to be smokers in the baseline survey in 2000-2002 (response rate 68%) and responded to a follow-up survey on smoking status in 2004-2005 (response rate 77%).
MEASUREMENTS:
Work-place social capital was assessed using a validated and psychometrically tested eight-item measure. Control variables included sex, age, socio-economic position, marital status, place of work, heavy drinking, physical activity, body mass index and physician-diagnosed depression.
FINDINGS:
In multi-level logistic regression models adjusted for all the covariates, the odds for being a non-smoker at follow-up were 1.26 [95% confidence interval (CI)=1.03-1.55] times higher for baseline smokers who reported high individual-level social capital than for their counterparts with low social capital. In an analysis stratified by socio-economic position, a significant association between individual-level social capital and smoking cessation was observed in the high socio-economic group [odds ratio (OR) (95% CI)=1.63 (1.01-2.63)], but not in intermediate [(OR=1.10 (0.83-1.47)] or low socio-economic groups [(OR=1.28 (0.86-1.91)]. Work unit-level social capital was not associated with smoking cessation.
CONCLUSIONS:
If the observed associations are causal, these findings suggest that high perceived social capital at work may facilitate smoking cessation among smokers in higher-status jobs.

Ischemic A/D transition of mitochondrial complex I and its role in ROS generation

Mitochondrial complex I (NADH:ubiquinone oxidoreductase) is a key enzyme in cellular energy metabolism and provides approximately 40% of the proton-motive force that is utilized during mitochondrial ATP production. The dysregulation of complex I function – either genetically, pharmacologically, or metabolically induced – has severe pathophysiological consequences that often involve an imbalance in the production of reactive oxygen species (ROS). Slow transition of the active (A) enzyme to the deactive, dormant (D) form takes place during ischemia in metabolically active organs such as the heart and brain. The reactivation of complex I occurs upon reoxygenation of ischemic tissue, a process that is usually accompanied by an increase in cellular ROS production. Complex I in the D-form serves as a protective mechanism preventing the oxidative burst upon reperfusion. Conversely, however, the D-form is more vulnerable to oxidative/nitrosative damage. Understanding the so-called active/deactive (A/D) transition may contribute to the development of new therapeutic interventions for conditions like stroke, cardiac infarction, and other ischemia-associated pathologies. In this review, we summarize current knowledge on the mechanism of A/D transition of mitochondrial complex I considering recently available structural data and site-specific labeling experiments. In addition, this review discusses in detail the impact of the A/D transition on ROS production by complex I and the S-nitrosation of a critical cysteine residue of subunit ND3 as a strategy to prevent oxidative damage and tissue damage during ischemia–reperfusion injury.