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Mutations of PSEN1 have been reported in dilated cardiomyopathy pedigrees. Understanding the effects and mechanisms of PSEN1 in cardiomyocytes might have important implications for treatment of heart diseases. Here, we showed that PSEN1 was downregulated in ischemia‐induced failing hearts. Functionally, cardiovascular specific PSEN1 deletion led to spontaneous death of the mice due to cardiomyopathy. At the age of 11 months, the ratio of the heart weight/body weight was slightly lower in the Sm22a‐PSEN1‐KO mice compared with that of the WT mice. Echocardiography showed that the percentage of ejection fraction and fractional shortening was significantly reduced in the Sm22a‐PSEN1‐KO group compared with the percent of these measures in the WT group, indicating that PSEN1‐KO resulted in heart failure. The abnormally regulated genes resulted from PSEN1‐KO were detected to be enriched in muscle development and dilated cardiomyopathy. Among them, several genes encode Ca2+ ion channels, promoting us to investigate the effects of PSEN1 KO on regulation of Ca2+ in isolated adult cardiomyocytes. Consistently, in isolated adult cardiomyocytes, PSEN1‐KO increased the concentration of cytosolic Ca2+ and reduced Ca2+ concentration inside the sarcoplasmic reticulum (SR) lumen at the resting stage. Additionally, SR Ca2+ was decreased in the failing hearts of WT mice, but with the lowest levels observed in the failing hearts of PSEN1 knockout mice. These results indicate that the process of Ca2+ release from SR into cytoplasm was affected by PSEN1 KO. Therefore, the abnormalities in Ca2+ homeostasis resulted from downregulation of PSEN1 in failing hearts might contribute to aging‐related cardiomyopathy, which might had important implications for the treatment of aging‐related heart diseases. [ABSTRACT FROM AUTHOR]

Recently, PSEN1 has been reported to have mutations in dilated cardiomyopathy pedigrees. However, the function and mechanism of PSEN1 in cardiomyopathy remains unresolved. Here, we established four types of genetically modified mice to determine the function of PSEN1 in cardiac development and pathology. PSEN1 null mutation resulted in perinatal death, retardation of heart growth, ventricular dilatation, septum defects, and valvular thickening. PSEN1 knockout in adults led to decreased muscle fibers, widened sarcomere Z lines and reduced lengths of sarcomeres in cardiomyocytes. Cardiovascular loss of function of PSEN1 induced by Sm22a-Cre or Myh6-Cre/ER/tamoxifen also resulted in severe ultrastructural abnormalities, such as relaxed gap junctions between neighboring cardiomyocytes. Functionally, cardiovascular deletion of PSEN1 caused spontaneous mortality from birth to adulthood and led to diastolic heart dysfunction, including decreased volume of the left ventricle at the end-systolic and end-diastolic stages. Additionally, in a myocardial ischemia model, deletion of PSEN1 in the cardiovascular system first protected mice by inducing adaptive hypertrophy but ultimately resulted in severe heart failure. Furthermore, a collection of genes was abnormally expressed in the hearts of cardiac-specific PSEN1 knockout mice. They were enriched in cell proliferation, calcium regulation, and so on. Taken together, dynamic regulation and abnormal function of PSEN1 underlie the pathogenesis of cardiovascular diseases due to ultrastructural abnormality of cardiomyocytes. [ABSTRACT FROM AUTHOR]

The pentadentate amine-bis(phenolate) ligand 6,6'-(dipyridin-2-ylmethylazanediyl)bis(methylene)bis(2,4-dimethylphenol) (H2L) was prepared and characterized. This ligand readily coordinates with FeIII or CoIII ions, and the resulting complexes [FeIIILCl] (1) and [CoIIIL(H2O)]Cl (2) were characterized by elemental analysis. X-ray structural studies show that the ligand in complexes 1 and 2 acts as a pentadentate ligand, leaving one coordination side of the transition metal available for exogenous ligands such as chloride ion (1) or water (2) ligand, and the central metal atoms are hexacoordinate in a similar distorted octahedral arrangement. Electrochemical studies reveal that each of the complexes exhibits multiple redox processes in the potential window investigated. Complex 1 shows one reversible oxidative event at 0.32 V and one quasi-reversible reduction event at -1.03 V, while the complex 2 displays one reversible oxidative event at 0.18 V and one quasi-reversible reduction at -0.64 V. [ABSTRACT FROM AUTHOR]

A layer-by-layer deposition strategy was employed for the immobilization of tungstophosphoric acid (HPW) onto a pentaethylenehexamine (PEHA)-grafted ZrSBA-15 framework to a give HPW/PEHA/ZrSBA-15 composite. The resulting composite was characterized by XRD, SEM, TEM, FTIR, thermogravimetric analysis, N2 sorption, and X-ray photoelectron spectroscopy, and these methods showed that the composite was stable in polar environments. These properties were attributed to the method of preparation, which ensured that a dense and stable array of HPW was encapsulated within the pores of PEHA-modified ZrSBA-15. In the H2O2-mediated oxidation of benzyl alcohol, the 25 % HPW/PEHA/ZrSBA-15 catalyst exhibited high selectivity (>99 %) for benzaldehyde. Moreover, the oxidation reaction was performed under solvent-free conditions, and the catalyst was recycled several times with negligible loss in selectivity and conversion. This HPW-based catalyst was also efficient at selectively oxidizing other benzylic and alkyl alcohols to the corresponding aldehydes. [ABSTRACT FROM AUTHOR]

Two photocatalytic hydrogen evolution systems were constructed by assembling [FeFe]-hydrogenase mimics, either carboxyl group-containing ( C1) or not ( C2), on to the surface of ZnS using triethanolamine as electron donor in DMF-H2O (9/1, v/v) solution. Upon irradiation for 30 h, the turnover numbers of hydrogen evolution were 3400 and 4950 for the hybrid system C1/ZnS and C2/ZnS, respectively. The photocatalytic activity of the C2/ZnS system was five times higher than the activity of the pristine ZnS, suggesting that the [FeFe]-hydrogenase mimics are crucial toward improving the activity of ZnS. On the basis of the spectroscopic studies and analyses, the photogenerated electron transfer from ZnS to the mimics is probably responsible for the activity enhancement of ZnS. The time dependence of hydrogen generation shows that the mimic C2 is more active than C1. The different hydrogen evolution activity can be attributed to the different adsorption modes of the two [FeFe]-hydrogenase mimics on the surface of ZnS. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

A magnetically retrievable and stable composite, Fe3O4@SiO2-NH2/HPW@CS/HPW, in which H3PW12O40 (abbreviated as HPW hereafter) was successfully anchored onto the surface of a cross-linked chitosan coating on magnetic Fe3O4 cores, has been prepared by means of chemical bonding between the amino and HPW components. The resultant composites were characterized by different physicochemical techniques, such as TEM, SEM, FTIR, and vibrating sample magnetometry (VSM). An improved synthesis of methyl oleate from oleic acid and methanol was observed with the as-prepared material as catalyst with easy recovery by simply using an external magnet. A yield of 93.2 % of methyl oleate was achieved under the optimal reaction conditions, that is, a 20:1 molar ratio of methanol to oleic acid and 0.4 g catalyst at 60 °C for 4 h. It was demonstrated that improved catalytic performance and facilitated separation were simultaneously achieved in the esterification reactions as a result of the core@shell structures in which stabilized HPW and magnetic cores are integrated into one body. [ABSTRACT FROM AUTHOR]

Cardiac hypertrophy, which is characterized by the enlargement of cell size, reactivation of fetal genes, remains one of the most important triggers to heart failure. Increasing evidence shows that microRNA (miRNA) is extensively involved in the pathogenesis of cardiac hypertrophy. But the effects of miRNAs on cardiomyocyte hypertrophy have not been completely solved yet. Here, we showed that a collection of miRNAs was aberrantly expressed in hypertrophic cardiomyocytes induced by phenylephrine (PE) or angiotensin II (Ang II). Among them, miR-22 was the most strikingly up-regulated miRNA. To investigate the role of miR-22 in hypertrophy, both over-expression and knock-down assays were performed on cardiomyocytes. The results showed that up-regulation of miR-22 significantly increased the cell size and markedly influenced the expression of hypertrophic markers, including induction of nppa and reduction of myh6. In contrast, reduction of miR-22 level attenuated either PE- or Ang II-induced hypertrophic reaction. Furthermore, several genes, including PTEN, were identified as potential targets of miR-22 by bioinformatic algorithms. Using luciferase analysis, miR-22 could significantly suppress the luciferase activity of reporter fused with 3′ untranslated region of PTEN mRNA. Furthermore, up-regulation of miR-22 could suppress the protein level of PTEN and reduction of miR-22 level markedly increased the protein level of PTEN in cardiomyocytes by Western blot analysis, suggesting that the contribution of miR-22 to cardiomyocyte hypertrophy may be partially through targeting PTEN. Taken together, miRNAs were dynamically regulated in cardiomyocyte hypertrophy and attenuation of miR-22 in rat cardiomyocytes efficiently protected from hypertrophic effects through derepressing PTEN. J. Cell. Physiol. 227: 1391-1398, 2012. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]