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| 1 | Iron and liver fibrosis: Mechanistic and clinical aspects显示文摘Liver fibrosis is characterised by excessive deposition of extracellular matrix that interrupts normal liver functionality. It is a pathological stage in several untreated chronic liver diseases such as the iron overload syndrome hereditary haemochromatosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and diabetes. Interestingly, regardless of the aetiology, iron-loading is frequently observed in chronic liver diseases. Excess iron can feed the Fenton reaction to generate unquenchable amounts of free radicals that cause grave cellular and tissue damage and thereby contribute to fibrosis. Moreover, excess iron can induce fibrosis-promoting signals in the parenchymal and non-parenchymal cells, which accelerate disease progression and exacerbate liver pathology. Fibrosis regression is achievable following treatment, but if untreated or unsuccessful, it can progress to the irreversible cirrhotic stage leading to organ failure and hepatocellular carcinoma, where resection or transplantation remain the only curative options. Therefore,understanding the role of iron in liver fibrosis is extremely essential as it can help in formulating iron-related diagnostic, prognostic and treatment strategies. These can be implemented in isolation or in combination with the current approaches to prepone detection, and halt or decelerate fibrosis progression before it reaches the irreparable stage. Thus, this review narrates the role of iron in liver fibrosis. It examines the underlying mechanisms by which excess iron can facilitate fibrotic responses. It describes the role of iron in various clinical pathologies and lastly,highlights the significance and potential of iron-related proteins in the diagnosis and therapeutics of liver fibrosis. | Kosha J Mehta Sebastien Je Farnaud Paul A Sharp | 2019 | World Journal of Gastroenterology2019，25，5： | 39 |
| 2 | Systematic review and meta-analysis on the association of tuberculosis in Crohn's disease patients treated with tumor necrosis factor-α inhibitors(Anti-TNFα)显示文摘AIM To perform a meta-analysis on the risk of developing Mycobacterium tuberculosis(TB) infection in Crohn's disease(CD) patients treated with tumor necrosis factoralpha(TNFα) inhibitors.METHODS A meta-analysis of randomized, double-blind, placebocontrolled trials of TNFα inhibitors for treatment of CD in adults was conducted. Arcsine transformation of TB incidence was performed to estimate risk difference. A novel epidemiologically-based correction(EBC) enabling inclusions of studies reporting no TB infection cases in placebo and treatment groups was developed to estimate relative odds.RESULTS Twenty-three clinical trial studies were identified, including 5669 patients. Six TB infection cases were reported across 5 studies, all from patients receiving TNFα inhibitors. Eighteen studies reported no TB infection cases in placebo and TNFα inhibitor treatment arms. TB infection risk was significantly increased among patients receiving TNFα inhibitors, with a risk difference of 0.028(95%CI: 0.0011-0.055). The odds ratio was 4.85(95%CI: 1.02-22.99) with EBC and 5.85(95%CI: 1.13-30.38) without EBC.CONCLUSION The risk of TB infection is higher among CD patients receiving TNFα inhibitors. Understanding the immunopathogenesis of CD is crucial, since using TNFα inhibitors in these patients could favor mycobacterial infections, particularly Mycobacterium avium subspecies paratuberculosis, which ultimately could worsen their clinical condition. | Brent L Cao Ahmad Qasem Robert C Sharp Latifa S Abdelli Saleh A Naser | 2018 | World Journal of Gastroenterology2018，24，25： | 4 |
| 3 | 急性儿茶酚胺暴露引起可逆的无心脏细胞再生的心肌细胞损伤显示文摘儿茶酚胺增加心脏收缩力,但暴露于高浓度儿茶酚胺或长时间暴露可引起心脏损伤。最近的一项研究表明,小鼠单次皮下注射异丙肾上腺素(isoproterenol,ISO;200 mg/kg)导致急性心肌细胞死亡(8%-10%),但在1个月之内心脏完整修复。心脏再生是通过内源性原癌基因蛋白质cKit+心脏干细胞介导新的心肌细胞形成。 | 刘莉 叶鹏 Wallner M Duran JM Mohsin S Troupes CD Vanhoutte D Borghetti G Vagnozzi RJ Gross P Yu D Trappanese DM Kubo H Toib A Sharp TE Harper SC Volkert MA Starosta T Feldsott EA Berretta RM Wang T Barbe MF Molkentin JD Houser SR | 2016 | 中华高血压杂志2016，24，8： | 4 |
| 4 | Role of PTPN2/22 polymorphisms in pathophysiology of Crohn's disease显示文摘AIM To establish the relationship of protein tyrosine phosphatase non-receptor type 2 and 22(PTPN2/22) polymorphisms and mycobacterial infections in Crohn's disease(CD). METHODS All 133 subjects' blood samples were genotyped for nine single nucleotide polymorphisms(SNPs) in PTPN2/22 using TaqMan^(?) genotyping, while the effect of the SNPs on PTPN2/22 and IFN-γ gene expression was determined using RT-PCR. Detection of Mycobacterium avium subspecies paratuberculosis(MAP) IS900 gene was done by nPCR after DNA extraction from the isolated leukocytes of each subjects' blood samples. T-cells isolated from the patient samples were tested for response to phytohematoagglutonin(PHA) mitogen or mycobacterial antigens by Brd U proliferation assays for T-cell activity. RESULTS Out of the nine SNPs examined, subjects with either heterozygous(TC)/minor(CC) alleles in PTPN2:rs478582 occurred in 83% of CD subjects compared to 61% healthy controls(P-values < 0.05; OR = 3.03). Subjects with either heterozygous(GA)/minor(AA) alleles in PTPN22:rs2476601 occurred in 16% of CD compared to 6% healthy controls(OR = 2.7). Gene expression in PTPN2/22 in CD subjects was significantly decreased by 2 folds compared to healthy controls(P-values < 0.05). IFN-γ expression levels were found to be significantly increased by approxiately 2 folds in subjects when either heterozygous or minor alleles in PTPN2:rs478582 and/or PTPN22:rs2476601 were found(P-values < 0.05). MAP DNA was detected in 61% of CD compared to only 8% of healthy controls(P-values < 0.05, OR = 17.52), where subjects with either heterozygous or minor alleles in PTPN2:rs478582 and/or PTPN22:rs2476601 had more MAPbacteremia presence than subjects without SNPs did. T h e average T-cell proliferation in CD treated with PHA or mycobacteria antigens was, respectively, 1.3 folds and 1.5 folds higher than healthy controls without any significant SNP. CONCLUSION The data suggests that SNPs in PTPN2/22 affect the negative regulation of the immune response in CD patients, thus leading to an increase in inflammation/apoptosis and susceptibility of mycobacteria. | Robert C Sharp Shazia A Beg Saleh A Naser | 2018 | World Journal of Gastroenterology2018，24，6： | 2 |
| 5 | Complete genomes of two clinical Staphylococcus aureus strains:evidence for the rapid evolution of virulence and drug resistance显示文摘 | Holden MT Feil EJ Lindsay JA Peacock SJ Day NP Enright MC Foster TJ Moore CE Hurst L Atkin R Barron A Bason N Bentley SD Chillingworth C Chillingworth T Churcher C Clark L Corton C Cronin A Doggett J Dowd L Feltwell T Hance Z Harris B Hauser H Holroyd S Jagels K James KD Lennard N Line A Mayes R Moule S Mungall K Ormond D Quail MA Rabbinowitsch E Rutherford K Sanders M Sharp S Simmonds M Stevens K Whitehead S Barrell BG Spratt BG Parkhill J | 2004 | Proc Natl Acad Sci USA2004，101，26： | 1 |
| 6 | Production of hydrogen from chemical hydrides via hydrolysis with steam 显示文摘 | AIELLO R SHARP J H MATTHEWS M A | 1999 | International Journal of Hydrogen Energy1999，24，12： | 1 |
| 7 | BAG-1 prevents stress-induced long-term growth inhibition in breast cancer cells via a chaperone-dependent pathway显示文摘 | Townsend PA Cutress RI Sharp A | 2003 | Cancer Res2003，63，14： | 1 |
| 8 | The production of elastic waves by explosion pressures: Ⅰ, Theory and empirical observations显示文摘 | Sharpe J A | 1942 | Geophysics1942，7，： | 1 |
| 9 | Activities of several noveloxazolidinones against Mycobacterium tuberculosis in a murine model显示文摘 | Cynamon M H Klemens S P Sharpe C A | 1999 | Atimicrob AgentsChemother1999，43，： | 1 |
| 10 | Comparisons between FLUENT and ADMS for atmospheric dispersion modeling显示文摘 | RIDDLE A CARRUTHERS D SHARPE A | 2004 | Atmospheric Environment2004，38，7： | 1 |
| 11 | Case study:a state space condition monitoring model for furnace erosion prediction and replacement显示文摘 | Christer A H Wang W Sharp J M | 1997 | European Journal of Operational Research1997，101，1： | 1 |
| 12 | The influence of the MAPK pathway on T cell lineage commitment显示文摘 | SHARP L L SCHWARZ D A BOTT C M | 1997 | Immunity1997，7，5： | 1 |
| 13 | Feasibility of a novel deformable image registration technique to facilitate elassifieation, targeting, and monitoring of tumor and normal tissue 显示文摘 | Brock K K Dawson L A Sharpe M B | 2006 | Int J Radiat Oneol Biol Phys2006，64，4： | 1 |
| 14 | Urachal carcinoma-a clinico-pathologic analysis of 24 cases with outcome correlation显示文摘 | Copalan A Sharp DS Fine SW | 2009 | Am J Surg Pathol2009，33，5： | 1 |
| 15 | Expression and Regulation of Lhx6 and Lhx7, a Novel Subfami?ly of LIM Homeodomain Encoding Genes, Suggests a Role in Mammalian Head Development显示文摘 | GRIGORIOU M TUCKER A S SHARPE P T | 1998 | Development1998，125，11： | 1 |
| 16 | Pitfalls in the prenatal di- agnosis of peroxisomal beta-oxidation defects by chorionic villus sampling 显示文摘 | Carey WF Poulos A Sharp P | 1994 | Prenat Diagn1994，14，9： | 1 |
| 17 | FGFR1 amplification drives endocrine therapy resistance and is a therapeutic target in breast cancer 显示文摘 | Turner N Pearson A Sharpe R | 2010 | Cancer Res2010，70，5： | 1 |
| 18 | A state space condition monitoring model for furnace erosion prediction and replacement显示文摘 | Christer A H Wang W Sharp J M | 1997 | European Journal of Operational Research1997，101，1： | 1 |
| 19 | Mucosal reactive oxygen species decrease virulence by disrupting Campylobacter jejuni phosphotyrosine signaling显示文摘 | CORCIONIVOSCHI N ALVAREZ L A SHARP T H | 2012 | Cell Host Microbe2012，12，1： | 1 |
| 20 | Association between circulating 25-hydroxyvitamin D and incident type 2 diabetes: a mendelian randomisation study显示文摘 | Zheng Ye Stephen J Sharp Stephen Burgess Robert A Scott Fumiaki Imamura Claudia Langenberg Nicholas J Wareham Nita G Forouhi | 2015 | The Lancet Diabetes & Endocrinology2015，，1： | 1 |
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