362 research outputs found

    7,11,15,28-Tetra­methyl-1,21,23,25-tetra­kis(2-phenyl­ethyl)resorcin[4]arene ethyl acetate clathrate

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    The title compound, C68H64O8·C4H8O2, is a new resorcin­[4]arene cavitand synthetic precursor, obtained by alkyl­ation of a previously reported resorcin[4]arene. The additional alkyl bridges significantly rigidify the structure and enforce a ‘bowl’ shape on the mol­ecular cavity. In the crystal structure, the mol­ecule lies on a crystallographic mirror plane, and a single ethyl acetate mol­ecule (also lying on the mirror plane) is present within the compound cavity, illustrating the host capabilities of the mol­ecule

    7,11,15,28-Tetra­kis[(2-formyl­phen­oxy)methyl]-1,21,23,25-tetra­methyl­resorcin[4]arene cavitand ethyl acetate clathrate at 173 K

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    The title compound, C68H56O16, was synthesized as a novel synthetic inter­mediate towards deeper and more elaborate resorcin[4]arene cavitands. The structure is the first reported example of a resorcin[4]arene cavitand bearing aromatic aldehyde functional groups at the extra-annular rim of the mol­ecule. The 2-formyl­phen­oxy residues are found to assume two different orientations above the mol­ecular cavity. One half of the resorcin[4]arene cavitand mol­ecule appears in the asymmetric unit; the complete resorcin[4]arene cavitand structure was generated across a mirror plane. In addition, a highly disordered ethyl acetate solvent mol­ecule is present within the mol­ecular cavity

    β2-microglobulin modified with advanced glycation end products modulates collagen synthesis by human fibroblasts

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    β2-microglobulin modified with advanced glycation end products modulates collagen synthesis by human fibroblasts. β2-microglobulin amyloidosis (Aβ2m) is a serious complication for patients undergoing long-term dialysis. β2-microglobulin modified with advanced glycation end products (β2m-AGE) is a major component of the amyloid in Aβ2m. It is not completely understood whether β2m-AGE plays an active role in the pathogenesis of Aβ2m, or if its presence is a secondary event of the disease. β2-microglobulin amyloid is mainly located in tendon and osteo-articular structures that are rich in collagen, and local fibroblasts constitute the principal cell population in the synthesis and metabolism of collagen. Recent identification of AGE binding proteins on human fibroblasts lead to the hypothesis that the fibroblast may be a target for the biological action of β2m-AGE. The present study demonstrated that two human fibroblast cell lines exhibited a decrease in procollagen type I mRNA and type I collagen synthesis after exposure to β2m-AGE for 72 hours. Similar results were observed using AGE-modified albumin. Antibody against the RAGE, the receptor for AGE, attenuated this decrease in synthesis, indicating that the response was partially mediated by RAGE. In addition, antibody against epidermal growth factor (EGF) attenuated the decrease in type I procollagen mRNA and type I collagen induced by β2m-AGE, suggesting that EGF acts as an intermediate factor. These findings support the hypothesis that β2m-AGE actively participates in connective tissue and bone remodeling via a pathway involving fibroblast RAGE, and at least one interposed mediator, the growth factor EGF

    The Iowa Homemaker vol.39A, no.5

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    People Without a Country, Carol Shellenbarger, page 4 Foster Parent Plan Aids Needy Children, Marcena Christian, page 5 The Music Goes Round and Round, Tom Emmerson, page 6 The History of Hose, Diane Houser, page 8 Milady’s Heels, Martha Glenn, page 9 Knit Your Own Squaw Valley Sweater, Suzanne Guernsey, page 10 Mincemeat – a Rich History, Sue Ellen Lieder, page 12 Christmas in Our Newest States, Beth Beecher, page 14 Christmas Shopping Section, Kay Thompson Maas, page 16 Futuristic Music Sphere, Mary Stoner, page 1

    BNip3 regulates mitochondrial function and lipid metabolism in the liver

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    BNip3 localizes to the outer mitochondrial membrane, where it functions in mitophagy and mitochondrial dynamics. While the BNip3 protein is constitutively expressed in adult liver from fed mice, we have shown that its expression is superinduced by fasting of mice, consistent with a role in responses to nutrient deprivation. Loss of BNip3 resulted in increased lipid synthesis in the liver that was associated with elevated ATP levels, reduced AMP-regulated kinase (AMPK) activity, and increased expression of lipogenic enzymes. Conversely, there was reduced β-oxidation of fatty acids in BNip3 null liver and also defective glucose output under fasting conditions. These metabolic defects in BNip3 null liver were linked to increased mitochondrial mass and increased hepatocellular respiration in the presence of glucose. However, despite elevated mitochondrial mass, an increased proportion of mitochondria exhibited loss of mitochondrial membrane potential, abnormal structure, and reduced oxygen consumption. Elevated reactive oxygen species, inflammation, and features of steatohepatitis were also observed in the livers of BNip3 null mice. These results identify a role for BNip3 in limiting mitochondrial mass and maintaining mitochondrial integrity in the liver that has consequences for lipid metabolism and disease

    In vivo antiviral efficacy of prenylation inhibitors against hepatitis delta virus

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    Hepatitis delta virus (HDV) can dramatically worsen liver disease in patients coinfected with hepatitis B virus (HBV). No effective medical therapy exists for HDV. The HDV envelope requires HBV surface antigen proteins provided by HBV. Once inside a cell, however, HDV can replicate its genome in the absence of any HBV gene products. In vitro, HDV virion assembly is critically dependent on prenyl lipid modification, or prenylation, of its nucleocapsid-like protein large delta antigen. To overcome limitations of current animal models and to test the hypothesis that pharmacologic prenylation inhibition can prevent the production of HDV virions in vivo, we established a convenient mouse-based model of HDV infection capable of yielding viremia. Such mice were then treated with the prenylation inhibitors FTI-277 and FTI-2153. Both agents were highly effective at clearing HDV viremia. As expected, HDV inhibition exhibited duration-of-treatment dependence. These results provide the first preclinical data supporting the in vivo efficacy of prenylation inhibition as a novel antiviral therapy with potential application to HDV and a wide variety of other viruses

    Coronary flow velocity reserve after percutaneous interventions is predictive of periprocedural outcome

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    BACKGROUND: Because heterogeneous results have been reported, we assessed coronary flow velocity changes in individuals who underwent percutaneous transluminal coronary angioplasty (PTCA) and examined their impact on clinical outcome. METHODS AND RESULTS: As part of the Doppler Endpoints Balloon Angioplasty Trial Europe (DEBATE) II study, 379 patients underwent Doppler flow-guided angioplasty. All patients were evaluated according to their coronary flow velocity reserve (CFVR) results (> or =2.5 or < 2.5) at the end of the procedure. A CFVR < 2.5 after angioplasty was associated with an elevated baseline blood flow velocity in both the target artery and reference artery. CFVR before PTCA and CFVR in the reference artery were independent predictors of an optimal CFVR after balloon angioplasty (CFVR before PTCA: odds ratio [OR], 2.26; 95% confidence interval [CI], 1.57 to 3.24; CFVR in reference artery: OR, 1.90; 95% CI, 1.21 to 2.98; both P<0.001) and stent implantation (before PTCA: OR, 2.54; 95% CI, 1.47 to 4.36; reference artery: OR, 1.97; 95% CI, 1.07 to 3.87; both P<0.05). A low CFVR at the end of the procedure was an independent p
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