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We give a natural sufficient condition which ensures the finiteness of the number of integral points on a projective space omitting finitely many hyperplanes defined over a one-dimensional function field of positive characteristic. In this setting, when the number of hyperplanes is 2 n + 2 , where n is the dimension of the ambient projective space, we use this natural condition to explain and sharpen an earlier result of the second named author, which provides a concrete condition on the coefficients of the linear forms producing hyperplanes such that the above finiteness property is satisfied. [ABSTRACT FROM AUTHOR]

Abstract: Büchiʼs problem asks if there exists a positive integer M such that all satisfying the equations for all must also satisfy for some integer x. Hensleyʼs problem asks if there exists a positive integer M such that, for any integers ν and a, if is a square for , then . It is not difficult to see that a positive answer to Hensleyʼs problem implies a positive answer to Büchiʼs problem. One can ask a more general version of the Hensleyʼs problem by replacing the square by n-th power for any integer which is called the Hensleyʼs n-th power problem. In this paper we will solve Hensleyʼs n-th power problem for complex meromorphic functions and non-Archimedean meromorphic functions. [Copyright &y& Elsevier]

Abstract: We study the degeneration dimension of non-archimedean analytic maps into the complement of hypersurface divisors of smooth projective varieties. We also show that there exist no non-archimedean analytic maps into where , , are hypersurfaces of degree at least 2 in general position and intersecting transversally. Moreover, we prove that there exist no non-archimedean analytic maps into when , are generic plane curves with . [Copyright &y& Elsevier]

Abstract: We deduce an effective version of Schmidt''s subspace theorem over function fields of characteristic zero for arbitrary homogeneous polynomials in place of linear forms. We will then apply this result to study the S-integral points of a general Thue''s equation. [Copyright &y& Elsevier]

Abstract: Common variable immunodeficiency (CVID) is associated with autoimmunity, most commonly immune thrombocytopenic purpura (ITP) and autoimmune hemolytic anemia (AIHA). In a retrospective chart review of 326 CVID patients, 35 (11%) patients had a history of autoimmune hematologic disease. Fifteen patients had ITP, 9 had AIHA, and 11 had Evans syndrome (both ITP and AIHA). The age at diagnosis for CVID ranged from 5 to 66 years and for autoimmunity, from 2 to 66 years. There were 16 males and 19 females. Nineteen patients (54%) had the first episode of thrombocytopenia or hemolytic anemia prior to the diagnosis of immunodeficiency, 11 (32%) were diagnosed concurrently, and 5 (14%) developed one or both of these autoimmune diseases following the diagnosis of CVID. Eight patients were known to have granulomatous changes in one or more organs. Treatments for autoimmunity included corticosteroids, anti-Rh immunoglobulin, and intravenous immunoglobulin; 11 patients underwent splenectomy. While 5 patients had recurrences of autoimmune hemolytic disease while receiving maintenance intravenous immunoglobulin, most episodes occurred for subjects not yet on this therapy (P <0.0001). Most patients with frequent infections and hematologic autoimmunity should be evaluated for CVID. [Copyright &y& Elsevier]

We propose a function-field analog of Pisot's d -th root conjecture on linear recurrences, and prove it under some "non-triviality" assumption. Besides a recent result of Pasten-Wang on Büchi's d -th power problem, our main tool, which is also developed in this paper, is a function-field analog of a GCD estimate in a recent work of Levin and Levin-Wang. As an easy corollary of such a GCD estimate, we also obtain an asymptotic result. [ABSTRACT FROM AUTHOR]

Hypertension-induced tunica media thickening (TMT) is the most important fundamental for the subsequent complications like stroke and cardiovascular diseases. Pathogenically, TMT originates from both vascular smooth muscle cells (VSMCs) hypertrophy due to synthesizing more amount of intracellular contractile proteins and excess secretion of extracellular matrix. However, what key molecules are involved in the pathogenesis of TMT is unknown. We hypothesize that formin homology 2 domain-containing protein 1 (FHOD1), an amply expressed mediator for assembly of thin actin filament in VSMCs, is a key regulator for the pathogenesis of TMT. In this study, we found that FHOD1 expression and its phosphorylation/activation were both upregulated in the arteries of three kinds of hypertensive rats. Ang-II induced actin filament formation and hypertrophy through activation and upregulation of FHOD1 in VSMCs. Active FHOD1-mediated actin filament assembly and secretions of collagen-1α/collagen-3α played crucial roles in Ang-II-induced VSMCs hypertrophy in vitro and hypertensive TMT in vivo. Proteomics demonstrated that activated FL-FHOD1 or its C-terminal diaphanous-autoregulatory domain significantly upregulated RNF213 (ring finger protein 213), a 591-kDa cytosolic E3 ubiquitin ligase with its loss-of-functional mutations being a susceptibility gene for Moyamoya disease which has prominent tunica media thinning in both intracranial and systemic arteries. Mechanistically, activated FHOD1 upregulated its downstream effector RNF213 independently of its classical pathway of decreasing G-actin/F-actin ratio, transcription, and translation, but dependently on its C-terminus-mediated stabilization of RNF213 protein. FHOD1-RNF213 signaling dramatically promoted collagen-1α/collagen-3α syntheses in VSMCs. Our results discovered a novel signaling axis of FHOD1-RNF213-collagen-1α/collagen-3α and its key role in the pathogenesis of hypertensive TMT. [Display omitted] • FHOD1 was activated in hypertensive rats and angiotensin-II-stimulated VSMCs. • Inactivated FHOD1 alleviated angiotensin-II-induced hypertension and TMT. • Activated FHOD1 promoted the hypertrophy, migration and fibrosis of VSMCs. • Activated FHOD1 upregulated RNF213 through a novel mechanism. • This study deepens our understanding of the pathogenesis of hypertensive TMT. [ABSTRACT FROM AUTHOR]

Abstract: Prior studies showed that Toll-like receptor (TLR) signaling pathway genes were upregulated in the liver of rats fed ethanol, but not in rats fed ethanol plus S-adenosylmethionine (SAMe). These results were obtained using a PCR microplate array analysis for TLRs and associated proteins such as proinflammatory cytokines and chemokine mRNA levels. A large number of genes were upregulated by the ethanol diet, but not the ethanol plus SAMe diet. In the present study, using the same experimental rat livers, DNA methylation analysis was done by using an Epitect Methyl DNA Restriction Kit (Qiagen, 335451) (24 genes). The results of all the genes combined show a highly significant increase in methylation in the ethanol-fed group of rats, but not in the dextrose-fed, SAMe-fed or ethanol plus SAMe-fed groups of rats. There was also an increase in DNA methylation in rats with high blood alcohol levels compared to a rat with a low blood alcohol level. The individual genes that were upregulated as indicated by the increased mRNA measured by qPCR correlated positively with the increased methylation of the DNA of the corresponding genes as follows: Cd14, Hspa1a, Irf1, Irak1, Irak2, Map3k7, Myd88, Pparα, Ripk2, Tollip and Traf6. [Copyright &y& Elsevier]

Abstract: We have previously demonstrated that quercetin, a bioflavonoid, blocks hepatitis C virus (HCV) proliferation by inhibiting NS5A-driven internal ribosomal entry site (IRES)-mediated translation of the viral genome. Here, we investigate the mechanisms of antiviral activity of quercetin and six additional bioflavonoids. We demonstrate that catechin, naringenin, and quercetin possess significant antiviral activity, with no associated cytotoxicity. Infectious virion secretion was not significantly altered by these bioflavonoids. Catechin and naringenin demonstrated stronger inhibition of infectious virion assembly compared to quercetin. Quercetin markedly blocked viral translation whereas catechin and naringenin demonstrated mild activity. Similarly quercetin completely blocked NS5A-augmented IRES-mediated translation in an IRES reporter assay, whereas catechin and naringenin had only a mild effect. Moreover, quercetin differentially inhibited HSP70 induction compared to catechin and naringenin. Thus, the antiviral activity of these bioflavonoids is mediated through different mechanisms. Therefore combination of these bioflavonoids may act synergistically against HCV. [Copyright &y& Elsevier]

Cell specific and cytokine targeted therapeutics have underperformed in systemic lupus erythematosus (SLE). Mesenchymal stem cells (MSCs) have emerged as a novel therapy to address the dysregulation in autoimmune diseases but also have limitations. Human gingiva derived MSCs (GMSCs) are superior in regulating immune responses. Here, we demonstrate that the adoptive transfer of GMSCs homes to and maintains in the kidney and has a robust therapeutic effect in a spontaneous lupus nephritis model. Specifically, GMSCs limits the development of autoantibodies as well as proteinuria, decreases the frequency of plasma cells and lupus nephritis histopathological scores by directly suppressing B cells activation, proliferation and differentiation. The blockage of CD39−CD73 pathway dramatically abrogates the suppressive capacities of GMSCs in vitro and in vivo and highlights the significance of this signaling pathway in SLE. Collectively, manipulation of GMSCs provides a promising strategy for the treatment of patients with SLE and other autoimmune diseases. • GMSCs suppress B cell activation, proliferation and plasma cell differentiation in vitro and in vivo by clearing the extracellular ATP via CD39-CD73 pathway. • GMSCs can home and maintain to the kidney and display a robust therapeutic effect on a spontaneous lupus nephritis model by directly targeting B cells. • Administration of GMSCs or the targeting of the CD39-CD73 signaling axis may have a promising therapeutic role in patients with SLE and other autoimmune diseases. [ABSTRACT FROM AUTHOR]