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Robert M. Hackman,John A. Polagruto,Heidrun B. Gross,Faranak Kamangar,Ken-Ichi Kosuna,Buxiang Sun,Hajime Fujii,Carl L. Keen 한국식품영양과학회 2007 Journal of medicinal food Vol.10 No.4
Epidemiological studies suggest that a high dietary intake of flavanols, a subclass of flavonoids, is associatedwith reduced risk of vascular disease. Clinical studies have also shown that the consumption of certain flavanol-rich foods(e.g., cocoa, tea, red wine), as well as intake of the individual flavanol (-)-epicatechin, can result in improvement in a num-ber of parameters associated with vascular disease, including improved endothelial function, reduced platelet reactivity, andreduced oxidative stress. The present study assessed the effects of a flavanol-rich supplement on platelet reactivity and plasmaoxidant defense in a group of smokers, a population at an elevated risk for vascular disease. Male smokers were randomlyassigned to a placebo (n . 10) or a flavanol-rich grapeseed extract (FRGSE; n . 13) group, and after an overnight fast, bloodsamples were collected before and at 1, 2, and 6 hours following consumption of the placebo or supplement. The FRGSE sup-plement, but not the placebo, significantly decreased ADP-stimulated platelet reactivity at 1, 2, and 6 hours following intake(P. .05) compared to baseline levels. Similarly, the supplement, but not the placebo, decreased epinephrine-stimulated plateletreactivity 2 hours following consumption. Plasma antioxidant capacity (total radical trapping antioxidant potential), lipid ox-idation (plasma thiobarbituric acid-reactive substances), and serum uric acid concentrations were not affected in either group.Thus smokers may obtain some health benefits from the consumption of certain flavanol-rich foods, beverages, and supple-ments.
Teo, Ruijie D.,Hwang, Jae Youn,Termini, John,Gross, Zeev,Gray, Harry B. American Chemical Society 2017 Chemical reviews Vol.117 No.4
<P>Corroles are exceptionally promising platforms for the development of agents for simultaneous cancer-targeting imaging and therapy. Depending on the element chelated by the corrole, these theranostic agents may be tuned primarily for diagnostic or therapeutic function. Versatile synthetic methodologies allow for the preparation of amphipolar derivatives, which form stable noncovalent conjugates with targeting biomolecules. These conjugates can be engineered for imaging and targeting as well as therapeutic function within one theranostic. assembly. In this review, we begin with a brief outline of corrole chemistry that has been uniquely useful in designing corrole-based anticancer agents. Then we turn attention to the early literature regarding corrole anticancer activity, which commenced one year after the first scalable synthesis was reported (1999-2000). In 2001, a major advance was made with the introduction of negatively charged corroles, as these molecules, being amphipolar, form stable conjugates with many proteins. More recently, both cellular uptake and intracellular trafficking of metallocorroles have been documented in experimental investigations employing advanced optical spectroscopic as well as magnetic resonance imaging techniques. Key results from work on both cellular and animal models are reviewed, with emphasis on those that have shed new light on the mechanisms associated with anticancer activity. In closing, we predict a very bright future for corrole anticancer research, as it is experiencing exponential growth, taking full advantage of recently developed imaging and therapeutic modalities.</P>
Chung-Il Wi,W. Ray Kim,John B. Gross, Jr,Linda M. Stadheim,John J. Poterucha 거트앤리버 소화기연관학회협의회 2016 Gut and Liver Vol.10 No.4
Background/Aims: Despite the potent suppression of the hepatitis B virus with modern antiviral agents, only a minority of HBeAg-positive patients achieve hepatitis B e antigen seroconversion. We aimed to explore the potential efficacy of combination therapy consisting of pegylated interferon (p-IFN) and an oral antiviral agent in patients with HBeAgpositive chronic hepatitis B. Methods: The treatment protocol consisted of p-IFN-a-2a at 180 μg/wk for 48 weeks, with either entecavir or tenofovir added 8 weeks after the initiation of p-IFN and continued for at least 6 months after HBe seroconversion was achieved. Results: To date, 10 patients have been treated under the protocol (eight adults, mean age 36±8 years; two adolescents, aged 12 and 16 years). All eight adult patients experienced loss of HBeAg at a mean of 72.3±66.9 weeks, including six patients who also developed anti-HBe and one patient who had HBs seroconversion. Although both adolescents remain on therapy, one adolescent had HBs seroconversion without HBe seroconversion. A total of nine of our 10 patients experienced a favorable serological transition. Conclusions: The combination of p-IFN and a modern oral antiviral agent may be more effective than monotherapy with either class of agent in the treatment of HBeAg-positive chronic hepatitis B patients.
CBFβ Stabilizes HIV Vif to Counteract APOBEC3 at the Expense of RUNX1 Targen Gene Expression
( Dong Young Kim ),( Eunju Kwon ),( Paul D Hartley ),( David C Crosby ),( Sumanjit Mann ),( Nevan J Krogan ),( John D Gross ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
The HIV-1 accessory protein Vif hijacks a cellular Cullin-RING ubiquitin ligase, CRL5, to promote degradation of the APOBEC3 (A3) family of restriction factors. Recently, the cellular transcription cofactor CBFβ was shown to form a complex with CRL5-Vif and to be essential for A3 degradation and viral infectivity. We now demonstrate that CBFβ is required for assembling a well-ordered CRL5-Vif complex by inhibiting Vifoligomerization and by activating CRL5-Vif via direct interaction. The CRL5-Vif-CBFβ holoenzyme forms a well-defined heterohexamer, indicating that Vif simultaneously hijacks CRL5 and CBFβ. Heterodimers of CBFβ and RUNX transcription factors contribute toward the regulation of genes, including those with immune system functions. We show that binding of Vif to CBFβ is mutually exclusive with RUNX heterodimerization and impacts the expression of genes whose regulatory domains are associated with RUNX1. Our results provide a mechanism by which a pathogen with limited coding capacity uses one factor to hijack multiple host pathways.