Solar light driven transition metal codoped ZnO (Ag, Ni- codoped ZnO) photocatalyst for environmental remediation

 Visible light efficient Ag, Ni-codoped ZnO photocatalyst has been synthesised in the nano form by co-precipitation and sonochemical method using ZnSO4ꞏ7H2O as a precursor. The structural, morphological and elemental observations of synthesised photocatalyst have been characterized using X-ray diffraction (XRD), FTIR, UV-DRS, SEM with EDX and HRTEM analysis. Incorporation of metal ions into ZnO lattice caused a red shift in the absorption band thus extending its absorption towards visible region through inhibition of electron hole recombination reaction and through the property of surface plasmon resonance (SPR). However the addition of silver and nickel ions has modified the electronic and optical properties of the photocatalyst thus improving the photocatalytic performance of the sample. The photocatalytic performance of Ag, Ni-codoped ZnO nanoparticles have been tested for degradation of Direct Red 81 dye (DR-81), as pollutant in aqueous solution. Under the optimum conditions (20 ppm dye and 10 mg/L photocatalyst), complete mineralization of dye solution under study was achieved within 40min of time duration. The Ag, Ni-codoped ZnO photocatalyst is thermally stable and efficient for five successive consecutive runs thus retaining its efficiency towards degradation. The overall results thus obtained have suggested that a suitable method for the detoxification of environmental pollutants emerging from industries.

8-Meth­oxy-3-(4-methyl­benzyl­idene)-6-(prop-1-en­yl)chroman-4-one

In the title compound, C21H20O3, the tolyl ring makes a dihedral angle of 31.11 (6)° with the benzene ring of the chromanone unit. The pyrone ring adopts a half-chair conformation. The mol­ecular structure is stabilized by a weak intra­molecular C—H⋯O inter­action and the crystal packing is stabilized by weak inter­molecular C—H⋯O inter­actions and a C—H⋯π inter­action

A comparison of rat models that best mimic immune-driven preeclampsia in humans

Preeclampsia (PE), a hypertensive pregnancy disorder, can originate from varied etiology. Placenta malperfusion has long been considered the primary cause of PE. However, we and others have showed that this disorder can also result from heightened inflammation at the maternal-fetal interface. To advance our understanding of this understudied PE subtype, it is important to establish validated rodent models to study the pathophysiology and test therapies. We evaluated three previously described approaches to induce inflammation-mediated PE-like features in pregnant rats: 1) Tumor necrosis factor-α (TNF-α) infusion via osmotic pump from gestational day (GD) 14-19 at 50ng/day/animal; 2) Polyinosinic:polycytidylic acid (Poly I:C) intraperitoneal (IP) injections from GD 10-18 (alternate days) at 10mg/kg/day/animal; and, 3) Lipopolysaccharide (LPS) IP injections from GD 13-18 at 20ug-70ug/kg/day per animal. Maternal blood pressure was measured by tail-cuff. Upon sacrifice, fetal and placenta weights were recorded. Placenta histomorphology was assessed using H&E sections. Placenta inflammation was determined by quantifying TNF-α levels and inflammatory gene expression. Placenta metabolic and mitochondrial health were determined by measuring mitochondrial respiration rates and placenta NAD+/NADH content. Of the three rodent models tested, we found that Poly I:C and LPS decreased both fetal weight and survival; and correlated with a reduction in region specific placenta growth. As the least effective model characterized, TNF-α treatment resulted in a subtle decrease in fetal/placenta weight and placenta mitochondrial respiration. Only the LPS model was able to induce maternal hypertension and exhibited pronounced placenta metabolic and mitochondrial dysfunction, common features of PE. Thus, the rat LPS model was most effective for recapitulating features observed in cases of human inflammatory PE. Future mechanistic and/or therapeutic intervention studies focuses on this distinct PE patient population may benefit from the employment of this rodent model of PE

GCN5 maintains muscle integrity by acetylating YY1 to promote dystrophin expression

Protein lysine acetylation is a post-translational modification that regulates protein structure and function. It is targeted to proteins by lysine acetyltransferases (KATs) or removed by lysine deacetylases. This work identifies a role for the KAT enzyme general control of amino acid synthesis protein 5 (GCN5; KAT2A) in regulating muscle integrity by inhibiting DNA binding of the transcription factor/repressor Yin Yang 1 (YY1). Here we report that a muscle-specific mouse knockout of GCN5 (Gcn5(skm)(−/−)) reduces the expression of key structural muscle proteins, including dystrophin, resulting in myopathy. GCN5 was found to acetylate YY1 at two residues (K392 and K393), disrupting the interaction between the YY1 zinc finger region and DNA. These findings were supported by human data, including an observed negative correlation between YY1 gene expression and muscle fiber diameter. Collectively, GCN5 positively regulates muscle integrity through maintenance of structural protein expression via acetylation-dependent inhibition of YY1. This work implicates the role of protein acetylation in the regulation of muscle health and for consideration in the design of novel therapeutic strategies to support healthy muscle during myopathy or aging

Angiotensin-(1-7): A Target for Stem Cell Mobilopathy and Vascular Repair in Diabetes

Bone marrow stem/progenitor cells (BMPCs) accelerate vascular repair by re-endothelialization and revascularization of ischemic areas. Diabetes causes impairment of BMPC mobilization, a.k.a. stem cell mobilopathy, and reparative functions, which have now been considered as a major contributing factor for the development of macro and microvascular complications and end-organ damage. Therefore, autologous cell therapies for the treatment of diabetic vascular complications are currently not possible. In this study, I tested the effects of Angiotensin (Ang)-(1-7), a heptapeptide member of the protective arm of renin-angiotensin system, on mobilization of BMPCs and their ischemic vascular repair functions that are impaired in diabetes. Streptozotocin-induced diabetic or db/db mice were used. Circulating and bone marrow Lineage- Sca1+ c-Kit+ (LSK) cells were decreased in diabetes, which was normalized by Ang-(1-7). Ang-(1-7) specifically increases Rho-kinase (ROCK) activity in diabetic bone marrow (BM) LSK cells, and fasudil, a ROCK inhibitor, prevented the beneficial effects of Ang-(1-7). BM Slit3 levels were increased by Ang-(1-7), which might have activated ROCK in LSK cells and sensitized for stromal-derived factor-1 (SDF)-induced migration. In relation to ischemia, diabetes prevented LSK cell mobilization and blood flow recovery, which were reversed by Ang-(1-7). Ang-(1-7), in combination with G-CSF or plerixafor reversed the stem cell mobilopathy in diabetes. These beneficial effects of Ang-(1-7) were blunted in Mas receptor knockout (MasR-KO) mice. These results suggest that MasR is a promising target for the treatment of diabetic bone marrow mobilopathy and vascular disease. Overall, this study provided strong preclinical evidence, supporting Ang-(1-7) as a promising molecule for the treatment of diabetic stem cell mobilopathy and vascular disease.American Heart Association (13SDG16960025)COBRE Pilot Project Grant (Intramural)Center for Protease Research (P30 GM103332 – 01)