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

Cryopreservation of cell/hydrogel constructs based on a new cell-assembling technique

Organ manufacturing products hold the promise to be used widely in the future for complex organ failings. The cryopreservation of the product is a very important step in the commercialization activities. In this article, a new cell cryopreservation technique, whereby, cryoprotectants were directly incorporated into the cell/hydrogel constructs, prototyped according to the predesigned structure and then subjected to a special freezing/thawing process. The rheological and hydration properties of the cryopreservation systems indicated that the hydratabilities of the gelatin/alginate hydrogels were greatly increased while the eutectic temperatures were greatly decreased by the addition of glycerol. Dextran-40 was found to be effective to improve the cell survival when incorporated with glycerol. The optimal volume concentration of the cryopretectans was 2.5% (v/v) glycerol and 5% (g/mL) dextran-40 in the gelatin/alginate hydrogel. Under these conditions, the cell viability in the construct was 96.3 ± 3.4%. Microscopic, thiazolyl blue (MTT) and hematoxylin and eosin (HE) staining results all indicated that the cells began to proliferate after thawing. The cells in the gelatin/alginate hydrogel with both glycerol and dextran-40 had greater proliferations than with only glycerol or dextran-40. This approach holds promise for a variety of applications in cell assembly for high-throughput drug screening and complex organ manufacturing areas

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

Satellite-like CdS nanoparticles anchoring onto porous NiO nanoplates for enhanced visible-light photocatalytic properties.

Novel CdS/NiO nanocomposites assembled by satellite-like CdS nanoparticles anchoring onto porous NiO nanoplates have been fabricated by a step synthesis process, which involves a chemical bathing method followed by a heat treatment, and a microwave-assisted aqueous chemical reaction. The structure and photocatalytic properties of products were characterized by various techniques. More significantly, benefiting from the synergistic effect of CdS/NiO heterojunction, the as-prepared CdS/NiO architectures exhibited superior photocatalytic activity for decolorization of Congo red. The degradation rate on CdS/NiO nanocomposites achieves about 3.5 times higher than that of pure CdS nanocrystals under visible light irradiation for 30 min, suggesting a promising application in water purification.This work was supported by the Key Projects of Support Program for Outstanding Young Talents of Anhui Province (gxyqZD2016151), the Natural Science Foundation of Anhui Province (1808085MB40), the Program of Study Abroad for Excellent Young Scholar of Anhui Province (gxfxZD2016221), the Natural Science Foundation of Anhui Province Educational Committee (KJ2014ZD08, KJ2015A145), and the Special Foundation for Scientists of Hefei University (15CR06)

Crystallization and preliminary crystallographic analysis of the ADP-ribosyltransferase HopU1. Corrigendum

A correction to the article by Lin et al. [(2010). Acta Cryst. F66, 932–934]

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