Six new loci associated with body mass index highlight a neuronal influence on body weight regulation

Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.

Further clarifying the competition–performance relation: reply to D. W. Johnson et al. (2012)

In their commentary, D. W. Johnson, Johnson, and Roseth (2012) provided some laudatory statements about our article, but they also expressed a number of concerns. The concerns focus on the following issues: types and definitions of competition, our choice of control group, the nature of performance-approach and performance-avoidance goals, the comprehensiveness of the opposing processes model, and performance-approach goals and constructive competition. We respond to each of these issues in turn and conclude with a statement regarding working to build an integrative model of the competition–performance relation (and beyond).

Heme oxygenase-1 regulates cell proliferation via carbon monoxide-mediated inhibition of T-type Ca2+ channels

Induction of the antioxidant enzyme heme oxygenase-1 (HO-1) affords cellular protection and suppresses proliferation of vascular smooth muscle cells (VSMCs) associated with a variety of pathological cardiovascular conditions including myocardial infarction and vascular injury. However, the underlying mechanisms are not fully understood. Over-expression of Cav3.2 T-type Ca2+ channels in HEK293 cells raised basal [Ca2+]i and increased proliferation as compared with non-transfected cells. Proliferation and [Ca2+]i levels were reduced to levels seen in non-transfected cells either by induction of HO-1 or exposure of cells to the HO-1 product, carbon monoxide (CO) (applied as the CO releasing molecule, CORM-3). In the aortic VSMC line A7r5, proliferation was also inhibited by induction of HO-1 or by exposure of cells to CO, and patch-clamp recordings indicated that CO inhibited T-type (as well as L-type) Ca2+ currents in these cells. Finally, in human saphenous vein smooth muscle cells, proliferation was reduced by T-type channel inhibition or by HO-1 induction or CO exposure. The effects of T-type channel blockade and HO-1 induction were non-additive. Collectively, these data indicate that HO-1 regulates proliferation via CO-mediated inhibition of T-type Ca2+ channels. This signalling pathway provides a novel means by which proliferation of VSMCs (and other cells) may be regulated therapeutically.

And the night was kind. 'Ruskin's Ponds' book works by John Woodman

A journal article published in the Blue Notebook: Journal for artists' books. Vol 8 No 2, April 2014 exploring the work of video and book artist John Woodman and his relationship with John Ruskin's life and landscapes.

Handbook of institutional investment and fiduciary duty

Foreword by Al Gore, former Vice President of the United States Endorsements by Keith Ambachsheer, James Gifford, John Kay, Bob Monks, Knut Rostad and Anne Stausboll

John Wikins

My essay is an analysis of the paintings of John Wilkins that contextualizes his mode of abstract painting within the semiological turn of post eighties painting.