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Articles by H Xie
Total Records ( 7 ) for H Xie
  S. R Costford , S Bajpeyi , M Pasarica , D. C Albarado , S. C Thomas , H Xie , T. S Church , S. A Jubrias , K. E Conley and S. R. Smith
 

In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD+). NAD+ is an obligate cosubstrate for mammalian sirtuin-1 (SIRT1), a deacetylase that activates peroxisome proliferator-activated receptor- coactivator-1 (PGC-1), which in turn can activate mitochondrial biogenesis. Given that mitochondrial biogenesis is activated by exercise, we hypothesized that exercise would increase NAMPT expression, as a potential mechanism leading to increased mitochondrial content in muscle. A cross-sectional analysis of human subjects showed that athletes had about a twofold higher skeletal muscle NAMPT protein expression compared with sedentary obese, nonobese, and type 2 diabetic subjects (P < 0.05). NAMPT protein correlated with mitochondrial content as estimated by complex III protein content (R2 = 0.28, P < 0.01), MRS-measured maximal ATP synthesis (R2 = 0.37, P = 0.002), and Vo2max (R2 = 0.63, P < 0.0001). In an exercise intervention study, NAMPT protein increased by 127% in sedentary nonobese subjects after 3 wk of exercise training (P < 0.01). Treatment of primary human myotubes with forskolin, a cAMP signaling pathway activator, resulted in an ~2.5-fold increase in NAMPT protein expression, whereas treatment with ionomycin had no effect. Activation of AMPK via AICAR resulted in an ~3.4-fold increase in NAMPT mRNA (P < 0.05) as well as modest increases in NAMPT protein (P < 0.05) and mitochondrial content (P < 0.05). These results demonstrate that exercise increases skeletal muscle NAMPT expression and that NAMPT correlates with mitochondrial content. Further studies are necessary to elucidate the pathways regulating NAMPT as well as its downstream effects.

  W Sun , H Xie , J Ji , X Zhou , D Goltzman and D. Miao
 

We used mice with targeted deletion of 25-hydroxyvitamin D 1-hydroxylase [1(OH)ase–/–] to investigate the effects of calcium and phosphorus on defects in the reproductive system of 1,25-dihydroxyvitamin D [1,25(OH)2D]-deficient female mice. The 1(OH)ase–/– mice and their wild-type littermates were fed either a normal diet or a rescue diet (high calcium, phosphate, and lactose) starting from weaning until 3 mo of age. We then determined serum calcium and phosphorus levels, assessed gonadotropin and gonadal hormone production, and evaluated folliculogenesis, corpus luteum formation, ovarian angiogenesis, uterus development, and fertility. Results showed that hypocalcemic and hypophosphatemic female 1(OH)ase–/– mice developed infertility accompanied by decreased estrogen and progestogen levels, elevated follicle-stimulating hormone and luteinizing hormone levels, defects in follicular development and corpus luteum formation, uterine hypoplasia, and decreased ovarian expression of angiogenic factors including vascular endothelial growth factor (VEGF), angiopoietin-1 and -2, and Tie-2. When serum calcium and phosphorus were normalized by the rescue diet, the defective reproductive phenotype in the female 1(OH)ase–/– mice, including the dysfunction in the hypothalamic-pituitary-ovarian axis, and ovarian angiogenesis were reversed. These results indicate that the infertility seen in 1,25(OH)2D-deficient mice is not a direct effect of active vitamin D deficiency on the reproductive system but is an indirect effect mediated by extracellular calcium and phosphorus.

  J Huang , S Ma , H Xie and C. H. Zhang
 

In multiple regression problems when covariates can be naturally grouped, it is important to carry out feature selection at the group and within-group individual variable levels simultaneously. The existing methods, including the lasso and group lasso, are designed for either variable selection or group selection, but not for both. We propose a group bridge approach that is capable of simultaneous selection at both the group and within-group individual variable levels. The proposed approach is a penalized regularization method that uses a specially designed group bridge penalty. It has the oracle group selection property, in that it can correctly select important groups with probability converging to one. In contrast, the group lasso and group least angle regression methods in general do not possess such an oracle property in group selection. Simulation studies indicate that the group bridge has superior performance in group and individual variable selection relative to several existing methods.

  T. H Shaikh , X Gai , J. C Perin , J. T Glessner , H Xie , K Murphy , R O'Hara , T Casalunovo , L. K Conlin , M D'Arcy , E. C Frackelton , E. A Geiger , C Haldeman Englert , M Imielinski , C. E Kim , L Medne , K Annaiah , J. P Bradfield , E Dabaghyan , A Eckert , C. C Onyiah , S Ostapenko , F. G Otieno , E Santa , J. L Shaner , R Skraban , R. M Smith , J Elia , E Goldmuntz , N. B Spinner , E. H Zackai , R. M Chiavacci , R Grundmeier , E. F Rappaport , S. F.A Grant , P. S White and H. Hakonarson
 

We present a database of copy number variations (CNVs) detected in 2026 disease-free individuals, using high-density, SNP-based oligonucleotide microarrays. This large cohort, comprised mainly of Caucasians (65.2%) and African-Americans (34.2%), was analyzed for CNVs in a single study using a uniform array platform and computational process. We have catalogued and characterized 54,462 individual CNVs, 77.8% of which were identified in multiple unrelated individuals. These nonunique CNVs mapped to 3272 distinct regions of genomic variation spanning 5.9% of the genome; 51.5% of these were previously unreported, and >85% are rare. Our annotation and analysis confirmed and extended previously reported correlations between CNVs and several genomic features such as repetitive DNA elements, segmental duplications, and genes. We demonstrate the utility of this data set in distinguishing CNVs with pathologic significance from normal variants. Together, this analysis and annotation provides a useful resource to assist with the assessment of CNVs in the contexts of human variation, disease susceptibility, and clinical molecular diagnostics.

  A. N Freedman , L. B Sansbury , W. D Figg , A. L Potosky , S. R Weiss Smith , M. J Khoury , S. A Nelson , R. M Weinshilboum , M. J Ratain , H. L McLeod , R. S Epstein , G. S Ginsburg , R. L Schilsky , G Liu , D. A Flockhart , C. M Ulrich , R. L Davis , L. J Lesko , I Zineh , G Randhawa , C. B Ambrosone , M. V Relling , N Rothman , H Xie , M. R Spitz , R Ballard Barbash , J. H Doroshow and L. M. Minasian
 

Recent advances in genomic research have demonstrated a substantial role for genomic factors in predicting response to cancer therapies. Researchers in the fields of cancer pharmacogenomics and pharmacoepidemiology seek to understand why individuals respond differently to drug therapy, in terms of both adverse effects and treatment efficacy. To identify research priorities as well as the resources and infrastructure needed to advance these fields, the National Cancer Institute (NCI) sponsored a workshop titled "Cancer Pharmacogenomics: Setting a Research Agenda to Accelerate Translation" on July 21, 2009, in Bethesda, MD. In this commentary, we summarize and discuss five science-based recommendations and four infrastructure-based recommendations that were identified as a result of discussions held during this workshop. Key recommendations include 1) supporting the routine collection of germline and tumor biospecimens in NCI-sponsored clinical trials and in some observational and population-based studies; 2) incorporating pharmacogenomic markers into clinical trials; 3) addressing the ethical, legal, social, and biospecimen- and data-sharing implications of pharmacogenomic and pharmacoepidemiologic research; and 4) establishing partnerships across NCI, with other federal agencies, and with industry. Together, these recommendations will facilitate the discovery and validation of clinical, sociodemographic, lifestyle, and genomic markers related to cancer treatment response and adverse events, and they will improve both the speed and efficiency by which new pharmacogenomic and pharmacoepidemiologic information is translated into clinical practice.

  T Tang , H Xie , Y Wang , B Lu and J. Liang
 

Rice grain filling is a process of conversion of sucrose into starch catalysed by a series of enzymes. Sucrose synthase (SUS) is considered as a key enzyme regulating this process. This study investigated the possible roles of sucrose and abscisic acid (ABA) in mediating the activity and expression of SUS protein of grains during grain filling in rice (Oryza sativa). Field-grown rice plants and detached cultured panicles were used as experimental materials. Several treatments, including spikelet thinning, leaf cutting, and applications of different concentrations of exogenous sucrose and ABA, were imposed during grain filling. A higher SUS activity was found in superior grains than in inferior grains in the earlier stage of grain filling, which was significantly and closely related to a higher grain filling rate and starch accumulation. An increase in sucrose concentration in grains as a result of different treatments increased both SUS activity and SUS protein expression in grains. An increase in ABA concentration gave similar results. Furthermore, effects of interactions between sucrose and ABA on the activity and expression of SUS protein in grains were also found. It was suggested that sucrose- and ABA-mediated rice grain filling is largely due to an increase in SUS activity and SUS protein expression.

  J. C Strum , J. H Johnson , J Ward , H Xie , J Feild , A Hester , A Alford and K. M. Waters
 

Human adipose tissue secretes a number of proinflammatory mediators that may contribute to the pathophysiology of obesity-related disorders. Understanding the regulatory pathways that control their production is paramount to developing effective therapeutics to treat these diseases. Using primary human adipose-derived stem cells as a source of preadipocytes and in vitro differentiated adipocytes, we found IL-8 and monocyte chemoattractant protein-1 (MCP-1) are constitutively secreted by both cell types and induced in response to serum deprivation. MicroRNA profiling revealed the rapid induction of microRNA 132 (miR-132) in these cells when switched to serum-free medium. Furthermore, miR-132 overexpression was sufficient to induce nuclear factor-B translocation, acetylation of p65, and production of IL-8 and MCP-1. Inhibitors of miR-132 decreased acetylated p65 and partially inhibited the production of IL-8 and MCP-1 induced by serum deprivation. MiR-132 was shown to inhibit silent information regulator 1 (SirT1) expression through a miR-132 binding site in the 3'-untranslated region of SirT1. Thus, in response to nutritional availability, induction of miR-132 decreases SirT1-mediated deacetylation of p65 leading to activation of nuclear factor-B and transcription of IL-8 and MCP-1 in primary human preadipocytes and in vitro differentiated adipocytes.

 
 
 
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