Context. In late Nov. 2013 the fifth eruption in five years of the M 31 recurrent nova M 31N 2008-12a was announced. Aims. In this Letter we address the optical lightcurve and progenitor system of M ...31N 2008-12a. Methods. Optical imaging data of the 2013 eruption from the Liverpool Telescope, La Palma; Danish 1.54 m Telescope, La Silla; and archival Hubble Space Telescope near-IR, optical, and near-UV data are astrometrically and photometrically analysed. Results. Photometry of the 2013 eruption, combined with three previous eruptions, enabled construction of a template lightcurve of a very fast nova (\hbox{$t_{2}\left(V\right)\simeq4$}t2V)(≃4 days). The archival data allowed recovery of the progenitor system in optical and near-UV data, indicating a red-giant secondary with bright accretion disk, or alternatively a system with a sub-giant secondary but dominated by a disk. Conclusions. The eruptions of M 31N 2008-12a, and a number of historic X-ray detections, indicate a unique system with a recurrence timescale of ~1 yr. This implies the presence of a very high-mass white dwarf and a high accretion rate. The recovered progenitor system is consistent with such an elevated rate of accretion. We encourage additional observations, especially towards the end of 2014.
A coupled channel analysis of the centrally produced
K
+
K
−and
π
+
π
−final states has been performed in
pp collisions at an incident beam momentum of 450 GeV/c. The pole positions and branching ...ratios to
ππ and
K
K
of the
f
0(980),
f
0(1370),
f
0(1500) and
f
0(1710) have been determined. A systematic study of the production properties of all the resonances observed in the
π
+
π
−and
K
+
K
−channels has been performed.
To examine the association of both individual and community socioeconomic status (SES) with inflammatory mediators relevant to cardiovascular pathophysiology, i.e., interleukin (IL)-6 and C-reactive ...protein (CRP), in a midlife community sample. Growing evidence suggests that socioeconomic attributes of both individuals and communities confer risk for cardiovascular morbidity and mortality.
Subjects were 851 men and women, 30 to 54 years of age (Caucasian = 77%, African-American = 23%). Individual SES was indexed by a composite of educational attainment and family income, and community SES was indexed by corresponding indicators derived from US Census data for participants' census tracts of residence. Plasma concentrations of IL-6 and CRP were determined from blood samples.
Regression analyses adjusting for age, sex, and race showed individual SES to be associated inversely with IL-6 (B = -0.126, p < .01), and community SES to be associated inversely with both IL-6 and CRP (B = -0.144, p < .01, B = -0.097, p < .01, respectively). The relationship of community SES with IL-6, but not CRP, persisted on multivariable adjustment for both lifestyle risk factors (smoking, alcohol consumption, sleep, exercise, body mass index) and individual SES (IL-6: B = -0.084, p < .05; CRP: B = -0.047, p > .10). After adjustment for lifestyle factors, however, individual SES was no longer associated with IL-6.
Independent of personal income or educational attainment, midlife adults living in less advantaged neighborhoods exhibit higher levels of circulating proinflammatory markers than residents of more affluent areas. This association may help explain the increased risk of atherosclerotic cardiovascular morbidity and mortality conferred by low community-level SES.
The reaction pp -> pf (eta eta) ps has been studied at 450 GeV/c. For the first time a partial wave analysis of the centrally produced eta eta system has been performed. Signals for the f0(1500), ...f0(1710) and f2(2150) are observed and the decay branching fractions of these states are determined.
Bilateral visual loss secondary to inherited optic neuropathies is an important cause of registrable blindness among children and young adults. The two prototypal disorders seen in clinical practice ...are Leber hereditary optic neuropathy (LHON) and autosomal dominant optic atrophy (DOA). About 90% of LHON cases are due to one of three mitochondrial DNA (mtDNA) point mutations: m.3460G>A, m.11778G>A, and m.14484T>C, which affect critical complex I subunits of the mitochondrial respiratory chain. The majority of patients with DOA harbour pathogenic mutations within OPA1, a nuclear gene that codes for a multifunctional inner mitochondrial membrane protein. Despite their contrasting genetic basis, LHON and DOA share overlapping pathological and clinical features that serve to highlight the striking tissue-specific vulnerability of the retinal ganglion cell (RGC) layer to disturbed mitochondrial function. In addition to severe visual loss secondary to progressive optic nerve degeneration, a subgroup of patients will also develop a more aggressive syndromic phenotype marked by significant neurological deficits. The management of LHON and DOA remains largely supportive, but major advances in our understanding of the mechanisms underpinning RGC loss in these two disorders are paving the way for novel forms of treatment aimed at halting or reversing visual deterioration at different stages of the disease process. In addition to neuroprotective strategies for rescuing RGCs from irreversible cell death, innovative in vitro fertilisation techniques are providing the tantalising prospect of preventing the germline transmission of pathogenic mtDNA mutations, eradicating in so doing the risk of disease in future generations.
The reactions
pp→
p
f
(
X
0)
p
s
, where
X
0 is observed decaying to
π
0
π
0
π
0
π
0 ,
π
+
π
−
π
+
π
− and
π
+
π
−
π
0
π
0 , have been studied at 450 GeV/
c. There is evidence for an
a
2(1320)
π ...decay mode of the
η
2(1645) and
η
2(1870) in the
π
+
π
−
π
0
π
0 and
π
+
π
−
π
+
π
− final states. The
f
2(1950) is consistent with being a single resonance with a dominant
f
2(1270)
ππ decay mode. The
f
0(1370) is found to decay dominantly to
ρρ while the
f
0(1500) is found to decay to
ρρ and
σσ.
Additional neurological features have recently been described in seven families transmitting pathogenic mutations in OPA1, the most common cause of autosomal dominant optic atrophy. However, the ...frequency of these syndromal ‘dominant optic atrophy plus’ variants and the extent of neurological involvement have not been established. In this large multi-centre study of 104 patients from 45 independent families, including 60 new cases, we show that extra-ocular neurological complications are common in OPA1 disease, and affect up to 20% of all mutational carriers. Bilateral sensorineural deafness beginning in late childhood and early adulthood was a prominent manifestation, followed by a combination of ataxia, myopathy, peripheral neuropathy and progressive external ophthalmoplegia from the third decade of life onwards. We also identified novel clinical presentations with spastic paraparesis mimicking hereditary spastic paraplegia, and a multiple sclerosis-like illness. In contrast to initial reports, multi-system neurological disease was associated with all mutational subtypes, although there was an increased risk with missense mutations odds ratio = 3.06, 95% confidence interval = 1.44–6.49; P = 0.0027, and mutations located within the guanosine triphosphate-ase region (odds ratio = 2.29, 95% confidence interval = 1.08–4.82; P = 0.0271). Histochemical and molecular characterization of skeletal muscle biopsies revealed the presence of cytochrome c oxidase-deficient fibres and multiple mitochondrial DNA deletions in the majority of patients harbouring OPA1 mutations, even in those with isolated optic nerve involvement. However, the cytochrome c oxidase-deficient load was over four times higher in the dominant optic atrophy + group compared to the pure optic neuropathy group, implicating a causal role for these secondary mitochondrial DNA defects in disease pathophysiology. Individuals with dominant optic atrophy plus phenotypes also had significantly worse visual outcomes, and careful surveillance is therefore mandatory to optimize the detection and management of neurological disability in a group of patients who already have significant visual impairment.
Objectives The aim of this study was to determine the impact of fat gain and its distribution on endothelial function in lean healthy humans. Background Endothelial dysfunction has been identified as ...an independent predictor of cardiovascular events. Whether fat gain impairs endothelial function is unknown. Methods A randomized controlled study was conducted to assess the effects of fat gain on endothelial function. Forty-three normal-weight healthy volunteers were recruited (mean age 29 years; 18 women). Subjects were assigned to gain weight (approximately 4 kg) (n = 35) or to maintain weight (n = 8). Endothelial function (brachial artery flow-mediated dilation FMD) was measured at baseline, after fat gain (8 weeks), and after weight loss (16 weeks) for fat gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition was measured by dual-energy X-ray absorptiometry and abdominal computed tomographic scans. Results After an average weight gain of 4.1 kg, fat gainers significantly increased their total, visceral, and subcutaneous fat. Blood pressure and overnight polysomnography did not change after fat gain or loss. FMD remained unchanged in weight maintainers. FMD decreased in fat gainers (9.1 ± 3% vs. 7.8 ± 3.2%, p = 0.003) but recovered to baseline when subjects shed the gained weight. There was a significant correlation between the decrease in FMD and the increase in visceral fat gain (rho = −0.42, p = 0.004), but not with subcutaneous fat gain (rho = −0.22, p = 0.15). Conclusions In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral rather than subcutaneous fat predicts endothelial dysfunction. (Fat Gain and Cardiovascular Disease Mechanisms; NCT00589498 )
Leber hereditary optic neuropathy (LHON) is currently estimated as the most frequent mitochondrial disease (1 in 27,000-45,000). Its molecular pathogenesis and natural history is now fairly well ...understood. LHON also is the first mitochondrial disease for which a treatment has been approved (idebenone-Raxone, Santhera Pharmaceuticals) by the European Medicine Agency, under exceptional circumstances because of the rarity and severity of the disease. However, what remains unclear includes the optimal target population, timing, dose, and frequency of administration of idebenone in LHON due to lack of accepted definitions, criteria, and general guidelines for the clinical management of LHON. To address these issues, a consensus conference with a panel of experts from Europe and North America was held in Milan, Italy, in 2016. The intent was to provide expert consensus statements for the clinical and therapeutic management of LHON based on the currently available evidence. We report the conclusions of this conference, providing the guidelines for clinical and therapeutic management of LHON.
The WA97 experiment has measured the transverse mass \(({m_{\mathrm T}})\) spectra for negative hadrons (\(\mathrm{h}^-\)) and strange particles produced at mid–rapidity in Pb–Pb collisions. The ...increased statistics of analysed data samples allowed us to perform a study of the spectra of \({\rm K_S^0}\), \(\mathrm{\Lambda}\), \(\mathrm{\Xi}\), \(\mathrm{\Omega}\) and \(\mathrm{h}^-\) as a function of the collision centrality. The data, which correspond to the most central 40% of the total inelastic cross section, have been divided into four centrality classes according to the estimated number of nucleons taking part in the collision. The \(m_{\mathrm T}\) spectra, analysed separately for each centrality bin, exhibit only weak (\(\leq\) 15%) centrality dependence. The deviation of the \(\mathrm{\Omega}\) inverse slope from the linear dependence on the particle mass is confirmed even for the most central Pb–Pb collisions.
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