A Hot Gap Around Jupiter's Orbit in the Solar Nebula

The Sun was an order of magnitude more luminous during the first few hundred thousand years of its existence, due in part to the gravitational energy released by material accreting from the Solar nebula. If Jupiter was already near its present mass, the planet's tides opened an optically-thin gap in the nebula. We show using Monte Carlo radiative transfer calculations that sunlight absorbed by the nebula and re-radiated into the gap raised temperatures well above the sublimation threshold for water ice, with potentially drastic consequences for the icy bodies in Jupiter's feeding zone. Bodies up to a meter in size were vaporized within a single orbit if the planet was near its present location during this early epoch. Dust particles lost their ice mantles, and planetesimals were partially to fully devolatilized, depending on their size. Scenarios in which Jupiter formed promptly, such as those involving a gravitational instability of the massive early nebula, must cope with the high temperatures. Enriching Jupiter in the noble gases through delivery trapped in clathrate hydrates will be more difficult, but might be achieved by either forming the planet much further from the star, or capturing planetesimals at later epochs. The hot gap resulting from an early origin for Jupiter also would affect the surface compositions of any primordial Trojan asteroids.Comment: 25 pages, 10 figures. ApJ in press. Discussion of Jupiter's volatile enrichment revised in sec. 4.

Electron Spin Resonance in S=1/2 antiferromagnetic chains

A systematic field-theory approach to Electron Spin Resonance (ESR) in the $S=1/2$ quantum antiferromagnetic chain at low temperature $T$ (compared to the exchange coupling $J$) is developed. In particular, effects of a transverse staggered field $h$ and an exchange anisotropy (including a dipolar interaction) $\delta$ on the ESR lineshape are discussed. In the lowest order of perturbation theory, the linewidth is given as $\propto Jh^2/T^2$ and $\propto (\delta/J)^2 T$, respectively. In the case of a transverse staggered field, the perturbative expansion diverges at lower temperature; non-perturbative effects at very low temperature are discussed using exact results on the sine-Gordon field theory. We also compare our field-theory results with the predictions of Kubo-Tomita theory for the high-temperature regime, and discuss the crossover between the two regimes. It is argued that a naive application of the standard Kubo-Tomita theory to the Dzyaloshinskii-Moriya interaction gives an incorrect result. A rigorous and exact identity on the polarization dependence is derived for certain class of anisotropy, and compared with the field-theory results.Comment: 53 pages in REVTEX, 7 figures in EPS included; revised version with missing references and correction

JNK modulates FOXO3a for the expression of the mitochondrial death and mitophagy marker BNIP3 in pathological hypertrophy and in heart failure

Bcl-2 E1B 19-KDa interacting protein 3 (BNIP3) is a mitochondrial death and mitophagy marker, which is involved in inducing cardiac remodeling post myocardial infarction. In this study, we show that BNIP3 expression increases in stressed cardiomyocytes in vitro and in response to pressure overload in vivo, and that its transcription is directly related to JNK activity. BNIP3 expression gradually increased in the first weeks after pressure overload and peaked at the heart failure stage. Ultrastructurally, the mitochondrial area was inversely proportional to BNIP3 expression. Both JNK and AKT activities increased with pressure overload; however, JNK signaling dominated over AKT signaling for the activation of the transcription factor FOXO3a and for the transcription of its effector, BNIP3. 3-methyladenine attenuated JNK signaling and significantly decreased BNIP3 expression and reversed cardiac remodeling in heart failure. Ultrastructurally, the mitochondrial area was significantly increased in the 3-methyladenine group compared with placebo. Moreover, adenoviral gene delivery of dominant negative JNK in a rat model of pressure overload hypertrophy abolished the increase in BNIP3 expression in response to pressure overload. These results suggest that JNK signaling is a critical modulator of the transcription factor FOXO3a driving the expression of its effector, BNIP3, in heart failure and that JNK, through BNIP3, induces mitochondrial apoptosis and mitophagy

ADP Ribosylation Factors 1 and 4 and Group VIA Phospholipase A2 Regulate Morphology and Intraorganellar Traffic in the Endoplasmic Reticulum–Golgi Intermediate Compartment

In search of morphological determinants for the endoplasmic reticulum-Golgi intermediate compartment (ERGIC), we found that a concerted action of Arf1, Arf4, and PLA2G6-A controls the architecture of the ERGIC by regulating tubular carriers. This is predicted to impact the rate of transport and destination of cargos in the ERGIC

Augmented Cardiac Hypertrophy in Response to Pressure Overload in Mice Lacking ELTD1

BACKGROUND: Epidermal growth factor (EGF), latrophilin and seven transmembrane domain-containing protein 1 (ELTD1) is developmentally upregulated in the heart. Little is known about the relationship between ELTD1 and cardiac diseases. Therefore, we aimed to clarify the role of ELTD1 in pressure overload-induced cardiac hypertrophy. METHODS AND RESULTS: C57BL/6J wild-type (WT) mice and ELTD1-knockout (KO) mice were subjected to left ventricular pressure overload by descending aortic banding (AB). KO mice exhibited more unfavorable cardiac remodeling than WT mice 28 days post AB; this remodeling was characterized by aggravated cardiomyocyte hypertrophy, thickening of the ventricular walls, dilated chambers, increased fibrosis, and blunted systolic and diastolic cardiac function. Analysis of signaling pathways revealed enhanced extracellular signal-regulated kinase (ERK) and the c-Jun amino-terminal kinase (JNK) phosphorylation in response to ELTD1 deletion. CONCLUSIONS: ELTD1 deficiency exacerbates cardiac hypertrophy and cardiac function induced by AB-induced pressure overload by promoting both cardiomyocyte hypertrophy and cardiac fibrosis. These effects are suggested to originate from the activation of the ERK and JNK pathways, suggesting that ELTD1 is a potential target for therapies that prevent the development of cardiac disease