The Formation of the Double Pulsar PSR J0737-3039A/B

Recent timing observations of the double pulsar J0737-3039A/B have shown that its transverse velocity is extremely low, only 10 km/s, and nearly in the Plane of the Galaxy. With this new information, we rigorously re-examine the history and formation of this system, determining estimates of the pre-supernova companion mass, supernova kick and misalignment angle between the pre- and post-supernova orbital planes. We find that the progenitor to the recently formed `B' pulsar was probably less than 2 MSun, lending credence to suggestions that this object may not have formed in a normal supernova involving the collapse of an iron core. At the same time, the supernova kick was likely non-zero. A comparison to the history of the double-neutron-star binary B1534+12 suggests a range of possible parameters for the progenitors of these systems, which should be taken into account in future binary population syntheses and in predictions of the rate and spatial distribution of short gamma-ray burst events.Comment: To appear in MNRAS Letters. Title typo fix only; no change to pape

Discordance of physiological and biochemical response to smoking and to psychological stress

Both smoking and psychological stress produce marked effects upon cardiovascular function, and several studies have demonstrated that in combination they produce additive or potentiating effects. More recently, it has been reported that individuals strongly reactive to psychological stress are also strongly reactive to nicotine. In an attempt to replicate and extend those findings, we examined reactivity to smoking and competitive mental arithmetic across several physiological and biochemical variables. Despite stable responding across mental arithmetic trials, we were unable to demonstrate significant correlations between reactivity to smoking and to a psychological stressor. We further observed that anxiety level, when low, was a poor predictor of desire to smoke and of withdrawal, whereas higher anxiety levels were more tightly linked to these measures. These findings have implications for the iDentification of individuals at risk of cardiovascular disease as well as for the design of smoking treatment and relapse prevention programs.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72030/1/j.1360-0443.1990.tb01607.x.pd

Effects of exercise induced muscle damage on cardiovascular responses to isometric muscle contractions and post-exercise circulatory occlusion

Purpose: The aim of the present study was to investigate whether exercise-induced muscle damage (EIMD) influences cardiovascular responses to isometric exercise and post-exercise circulatory occlusion (PECO). We hypothesized that EIMD would increase muscle afferent sensitivity and, accordingly, increase blood pressure responses to exercise and PECO. Methods: Eleven male and nine female participants performed unilateral isometric knee extension at 30% of maximal voluntary contraction (MVC) for 3-min. A thigh cuff was rapidly inflated to 250 mmHg for two min PECO, followed by 3 min recovery. Heart rate and blood pressure were monitored beat-by-beat, with stroke volume and cardiac output estimated from the Modelflow algorithm. Measurements were taken before and 48 h after completing eccentric knee-extension contractions to induce muscle damage (EIMD). Results: EIMD caused 21% decrease in MVC (baseline: 634.6 ± 229.3 N, 48 h: 504.0 ± 160 N), and a 17-fold increase in perceived soreness using a visual-analogue scale (0–100 mm; VASSQ) (both p < 0.001). CV responses to exercise and PECO were not different between pre and post EIMD. However, mean arterial pressure (MAP) was higher during the recovery phase after EIMD (p < 0.05). Significant associations were found between increases in MAP during exercise and VASSQ, Rate of Perceived Exertion (RPE) and Pain after EIMD only (all p < 0.05). Conclusion: The MAP correlations with muscle soreness, RPE and Pain during contractions of damaged muscles suggests that higher afferent activity was associated with higher MAP responses to exercise

Effect of prenatal DHA supplementation on the infant epigenome: results from a randomized controlled trial

BACKGROUND: Evidence is accumulating that nutritional exposures in utero can influence health outcomes in later life. Animal studies and human epidemiological studies have implicated epigenetic modifications as playing a key role in this process, but there are limited data from large well-controlled human intervention trials. This study utilized a large double-blind randomized placebo-controlled trial to test whether a defined nutritional exposure in utero, in this case docosahexaenoic acid (DHA), could alter the infant epigenome. Pregnant mothers consumed DHA-rich fish oil (800 mg DHA/day) or placebo supplements from 20 weeks' gestation to delivery. Blood spots were collected from the children at birth (n = 991) and blood leukocytes at 5 years (n = 667). Global DNA methylation was measured in all samples, and Illumina HumanMethylation450K BeadChip arrays were used for genome-wide methylation profiling in a subset of 369 children at birth and 65 children at 5 years. RESULTS: There were no differences in global DNA methylation levels between the DHA and control group either at birth or at 5 years, but we identified 21 differentially methylated regions (DMRs) at birth, showing small DNA methylation differences (<5%) between the treatment groups, some of which seemed to persist until 5 years. The number of DMRs at birth was greater in males (127 DMRs) and in females (72 DMRs) separately, indicating a gender-specific effect. CONCLUSION: Maternal DHA supplementation during the second half of pregnancy had small effects on DNA methylation of infants. While the potential functional significance of these changes remains to be determined, these findings further support the role of epigenetic modifications in developmental programming in humans and point the way for future studies. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry (ANZCTR), ACTRN12605000569606 and ACTRN12611001127998.Susan J. van Dijk, Jing Zhou, Timothy J. Peters, Michael Buckley, Brodie Sutcliffe, Yalchin Oytam, Robert A. Gibson, Andrew McPhee, Lisa N. Yelland, Maria Makrides, Peter L. Molloy and Beverly S. Muhlhausle