Understanding the multiwavelength observation of Geminga's TeV halo: the role of anisotropic diffusion of particles

In this letter we propose that the X-ray and the TeV observations in the vicinity of Geminga can be understood in the framework of anisotropic diffusion of injected electrons/positrons. This interpretation only requires the turbulence in the vicinity of Geminga to be sub-Alfv\'enic with the local mean magnetic field direction approximately aligned with our line of sight towards Geminga, without invoking extreme conditions for the environment, such as an extremely small diffusion coefficient and a weak magnetic field of strength $<1\mu$G as suggested in previous literature.Comment: 7 pages, 4 figures, including Supplemental Material, PRL accepte

On the Unusually Large Spatial Extent of the TeV nebula HESS J1825-137: Implication from the Energy-Dependent Morphology

Deep observation of the High Energy Stereoscopic System (HESS) on the most extended pulsar wind nebula HESS J1825-137 reveals an enhanced energy-dependent morphology, providing useful information on the particle transport mechanism in the nebula. We find that the energy-dependent morphology is consistent with a diffusion-dominated transport of electrons/positrons. It provides an alternative possible interpretation for the unusually large spatial extent (i.e., $\gtrsim 100$pc) of the nebula, which could then be attributed to the diffusion of escaping electrons/positrons from a compact plerion. The influence of various model parameters on the energy-dependent extent of the nebula is studied in the diffusion-dominated scenario. We also show that the energy-dependent morphology of the nebula may also be used to study the spin-down history of the pulsar.Comment: 11 pages, 10 figures, section 4 has been significantly rewritten; accepted by MNRA

On the minimum jet power of TEV BL Lac objects in the p-γ\gamma model

We study the requirement on the jet power in the conventional p-$\gamma$ models (photopion production and Bethe-Heitler pair production) for TeV BL Lac objects. We select a sample of TeV BL Lac objects whose SEDs are difficult to be explained by the one-zone leptonic model. Based on the relation between the p-$\gamma$ interaction efficiency and the opacity of $\gamma\gamma$ absorption, we find that the detection of TeV emission poses upper limits on the p-$\gamma$ interaction efficiencies in these sources and hence minimum jet powers can be derived accordingly. We find that the obtained minimum jet powers exceed the Eddington luminosity of the supermassive black holes. Implications for the accretion mode of the supermassive black hole in these BL Lac objects and the origin of their TeV emissions are discussed.Comment: 11 pages, 4 figures, 2 tables, accepted for publication in Ap

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction.

Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling. Transiently or stably overexpression of mitochondria Omi/HtrA2 in H9C2 cells enhance apoptosis as evidenced by elevated caspase-3, -9 activity and TUNEL staining, which was completely blocked by Ucf-101, a specific Omi/HtrA2 inhibitor. Mechanistic studies revealed mitochondrial Omi/HtrA2 overexpression degraded the mitochondrial anti-apoptotic protein HAX-1, an effect attenuated by Ucf-101. Additionally, transfected cells overexpressing mitochondrial Omi/HtrA2 were more sensitive to hypoxia and reoxygenation (H/R) induced apoptosis. Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor, blocked translocation of Omi/HtrA2 from mitochondrial to cytoplasm, and protected transfected cells incompletely against H/R-induced caspase-3 activation. We report in vitro and in vivo overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction. Thus, strategies to directly inhibit Omi/HtrA2 or its cytosolic translocation from mitochondria may protect against heart injury

Adiponectin improves coronary no-reflow injury by protecting the endothelium in rats with type 2 diabetes mellitus.

To determine the effect of adiponectin (APN) on the coronary no-reflow (NR) injury in rats with Type 2 diabetes mellitus (T2DM), 80 male Sprague-Dawley rats were fed with a high-sugar-high-fat diet to build a T2DM model. Rats received vehicle or APN in the last week and then were subjected to myocardial ischemia reperfusion (MI/R) injury. Endothelium-dependent vasorelaxation of the thoracic aorta was significantly decreased and serum levels of endothelin-1 (ET-1), intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were noticably increased in T2DM rats compared with rats without T2DM. Serum APN was positively correlated with the endothelium-dependent vasorelaxation, but negatively correlated with the serum level of ET-1. Treatment with APN improved T2DM-induced endothelium-dependent vasorelaxation, recovered cardiac function, and decreased both NR size and the levels of ET-1, ICAM-1 and VCAM-1. Hypoadiponectinemia was associated with the aggravation of coronary NR in T2DM rats. APN could alleviate coronary NR injury in T2DM rats by protecting the endothelium and improving microcirculation