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| 1 | Role of alcohol in the regulation of iron metabolism显示文摘Patients with alcoholic liver disease frequently exhibit increased body iron stores, as reflected by elevated serum iron indices (transferrin saturation, ferritin) and hepatic iron concentration. Even mild to moderate alcohol consumption has been shown to increase the prevalence of iron overload. Moreover, increased hepatic iron content is associated with greater mortality from alcoholic cirrhosis, suggesting a pathogenic role for iron in alcoholic liver disease. Alcohol increases the severity of disease in patients with genetic hemochromatosis, an iron overload disorder common in the Caucasian population. Both iron and alcohol individually cause oxidative stress and lipid peroxidation, which culminates in liver injury. Despite these observations, the underlying mechanisms of iron accumulation and the source of the excess iron observed in alcoholic liver disease remain unclear. Over the last decade, several novel iron-regulatory proteins have been identified and these have greatly enhanced our understanding of iron metabolism. For example, hepcidin, a circulatory antimicrobial peptide synthesized by the hepatocytes of the liver is now known to play a central role in the regulation of iron homeostasis. This review attempts to describe the interaction of alcohol and iron-regulatory molecules. Understanding these molecular mechanisms is of considerable clinical importance because both alcoholic liver disease and genetic hemochromatosis are common diseases, in which alcohol and iron appear to act synergistically to cause liver injury. | Duygu Dee Harrison-Findik | 2007 | World Journal of Gastroenterology2007，13，37： | 10 |
| 2 | Is the iron regulatory hormone hepcidin a risk factor for alcoholic liver disease?显示文摘Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the progression of the disease. Over the years, many such factors have indeed been identified, including iron. Despite being crucial for various important biological processes, iron can also be harmful due to its ability to catalyze Fenton chemistry. Alcohol and iron have been shown to interact synergistically to cause liver injury. Iron-mediated cell signaling has been reported to be involved in the pathogenesis of experimental alcoholic liver disease. Hepcidin is an iron-regulatory hormone synthesized by the liver, which plays a pivotal role in iron homeostasis. Both acute and chronic alcohol exposure suppress hepcidin expression in the liver. The sera of patients with alcoholic liver disease, particularly those exhibiting higher serum iron indices, have also been reported to display reduced prohepcidin levels. Alcohol-mediated oxidative stress is involved in the inhibition of hepcidin promoter activity and transcription in the liver. This in turn leads to an increase in intestinal iron transport and liver iron storage. Hepcidin is expressed primarily in hepatocytes. It is noteworthy that both hepatocytes and Kupffer cells are involved in the progression of alcoholic liver disease. However, the activation of Kupffer cells and TNF-α signaling has been reported not to be involved in the down-regulation of hepcidin expression by alcohol in the liver. Alcohol acts within the parenchymal cells of the liver to suppress the synthesis of hepcidin. Due to its crucial role in the regulation of body iron stores, hepcidin may act as a secondary risk factor in the progression of alcoholic liver disease. The clarification of the mechanisms by which alcohol disrupts iron homeostasis will allow for further understanding of the pathogenesis of alcoholic liver disease. | Duygu Dee Harrison-Findik | 2009 | World Journal of Gastroenterology2009，15，10： | 9 |
| 3 | TLR4 signaling and the inhibition of liver hepcidin expression by alcohol显示文摘AIM:To understand the role of toll-like receptor 4(TLR4)signaling in the regulation of iron-regulatory hormone,hepcidin by chronic alcohol consumption.METHODS:For chronic alcohol intake studies,TLR4mutant mice on C3H/HeJ background and wildtype counterpart on C3H/HeOuJ background were pair-fed with regular(control)and ethanol-containing Lieber De Carli liquids diets.Gene expression was determined by real-time quantitative PCR.Protein-protein interactions and protein expression were determined by co-immunoprecipitation and western blotting.The occupancy of hepcidin gene promoter was determined by chromatin immunoprecipitation assays.RESULTS:Chronic alcohol intake suppressed hepcidin mRNA expression in the livers of wildtype,but not TLR4 mutant,mice.The phosphorylation and nuclear translocation of nuclear factor(NF)-κB p65 subunit protein was observed in alcohol-fed wildtype,but not in alcohol-fed TLR4 mutant,mice.Similarly,alcohol induced the binding of NF-κB p50 subunit protein to hepcidin gene promoter in wildtype,but not in TLR4mutant,mice.In contrast,the phosphorylation of Stat3in the liver was stronger in alcohol-treated TLR4 mutant mice compared to alcohol-treated wildtype mice.The occupancy of hepcidin gene promoter by Stat3was observed in alcohol-fed mutant,but not in wildtype,mice.An interaction between NF-κB p65 subunit protein and small heterodimer partner protein(SHP)was observed in the livers of both wildtype and TLR4mutant mice fed with the control diet,as shown by coimmunoprecipitation studies.Alcohol intake elevated cytosolic SHP expression but attenuated its interaction with NF-κB in the liver,which was more prominent in the livers of wildtype compared to TLR4 mutant mice.CONCLUSION:Activation of TLR4 signaling and NF-кB are involved in the suppression of hepcidin gene transcription by alcohol in the presence of inflammation in the liver. | Emily Zmijewski Sizhao Lu Duygu Dee Harrison-Findik | 2014 | World Journal of Gastroenterology2014，20，34： | 6 |
| 4 | 开窗畸形之基底动脉并发颅内多发性动脉瘤显示文摘 | 李文彬 李明华 H Grady Daniel Dee H Wu L.Tytle Rifat Karatas Yasemin Karatas William TC Yuh | 2003 | 实用放射学杂志2003，19，9： | 4 |
| 5 | Spatial assessment of forest cover and land-use changes in the Hindu-Kush mountain ranges of northern Pakistan显示文摘Anthropogenic activities and natural processes are continuously altering the mountainous environment through deforestation, forest degradation and other land-use changes. It is highly important to assess, monitor and forecast forest cover and other land-use changes for the protection and conservation of mountainous environment. The present study deals with the assessment of forest cover and other land-use changes in the mountain ranges of Dir Kohistan in northern Pakistan, using high resolution multi-temporal SPOT-5 satellite images. The SPOT-5 satellite images of years 2004, 2007, 2010 and 2013 were acquired and classified into land-cover units. In addition, forest cover and land-use change detection map was developed using the classified maps of 2004 and 2013. The classified maps were verified through random field samples and Google Earth imagery(Quick birds and SPOT-5). The results showed that during the period 2004 to 2013 the area of forest land decreased by 6.4%, however, area of range land and agriculture land have increased by 22.1% and 2.9%, respectively. Similarly, barren land increased by 1.1%, whereas, area of snow cover/glacier is significantly decreased by 21.3%. The findings from the study will be useful for forestry and landscape planning and can be utilized by the local, provincial and national forest departments; and REDD+ policy makers in Pakistan. | Sami ULLAH Muhammad FAROOQ Muhammad SHAFIQUE Muhammad Afra SIYAB Fazli KAREEM Matthias DEES | 2016 | Journal of Mountain Science2016，13，7： | 4 |
| 6 | Autophagy and cancer显示文摘Autophagy is a homeostatic and evolutionarily conserved mechanism of self-digestion by which the cells degrade and recycle long-lived proteins and excess or damaged organelles.Autophagy is activated in response to both physiological and pathological stimuli including growth factor depletion,energy deficiency or the upregulation of Bcl-2 protein expression.A novel role of autophagy in various cancers has been proposed.Interestingly,evidence that supports both a positive and negative role of autophagy in the pathogenesis of cancer has been reported.As a tumor suppression mechanism,autophagy maintains genome stability,induces senescence and possibly autophagic cell death.On the other hand,autophagy participates in tumor growth and maintenance by supplying metabolic substrate,limiting oxidative stress,and maintaining cancer stem cell population.It has been proposed that the differential roles of autophagy in cancer are disease type and stage specific.In addition,substrate selectivity might be involved in carrying out the specific effect of autophagy in cancer,and represents one of the potential directions for future studies. | Si-Zhao Lu Duygu Dee Harrison-Findik | 2013 | World Journal of Biological Chemistry2013，4，3： | 3 |
| 7 | Adenoma detection with cap-assisted colonoscopy versus regular colonoscopy: a randomised controlled trial显示文摘 | Thomas R de Wijkerslooth Esther M Stoop Patrick M Bossuyt Elisabeth M H Mathus-Vliegen Jan Dees Kristien M A J Tytgat Monique E van Leerdam Paul Fockens Ernst J Kuipers Evelien Dekker | 2012 | Gut2012，，10： | 3 |
| 8 | Lack of hepcidin expression attenuates steatosis and causesfibrosis in the liver显示文摘AIM: To investigate the role of key iron-regulatory protein, hepcidin in non-alcoholic fatty liver disease(NAFLD). METHODS: Hepcidin(Hamp1) knockout and floxed control mice were administered a high fat and high sucrose(HFS) or a regular control diet for 3 or 7 mo. Steatosis, triglycerides, fibrosis, protein and gene expression in mice livers were determined by histological and biochemical techniques, western blotting and realtime polymerase chain reaction. RESULTS: Knockout mice exhibited hepatic iron accumulation. Despite similar weight gains, HFS feeding induced hepatomegaly in floxed, but not knockout, mice. The livers of floxed mice exhibited higher levels of steatosis, triglycerides and c-Jun N-terminal kinase(JNK) phosphorylation than knockout mice. In contrast, a significant increase in fibrosis was observed in knockout mice livers within 3 mo of HFS administration. The hepatic gene expression levels of sterol regulatoryelement-binding protein-1c and fat-specific protein-27, but not peroxisome proliferator-activated receptoralpha or microsomal triglyceride transfer protein, were attenuated in HFS-fed knockout mice. Knockout mice fed with regular diet displayed increased carnitine palmitoyltransferase-1a and phosphoenolpyruvate carboxykinase-1 but decreased glucose-6-phosphatase expression in the liver. In summary, attenuated steatosis correlated with decreased expression of lipogenic and lipid storage genes, and JNK phosphorylation. Deletion of Hamp1 alleles per se modulated hepatic expression of beta-oxidation and gluconeogenic genes. CONCLUSION: Lack of hepcidin expression inhibits hepatic lipid accumulation and induces early development of fibrosis following high fat intake. Hepcidin and iron may play a role in the regulation of metabolic pathways in the liver, which has implications for NAFLD pathogenesis. | Sizhao Lu Robert G Bennett Kusum K Kharbanda Duygu Dee Harrison-Findik | 2016 | World Journal of Hepatology2016，8，4： | 3 |
| 9 | 制定科学合理的生物安全措施显示文摘在当今的生猪产业,生物安全措施是保护和维持猪群健康和有效利用率的重要科学基础程序。 | Scott Dee Andrea Pitkin Satoshi Otake 贾海燕(翻译) | 2009 | 猪业科学2009，26，12： | 3 |
| 10 | Rho A signaling and blood pressure: The consequence of failing to “Tone it Down”显示文摘Uncontrolled high blood pressure is a major risk factor for heart attack, stroke, and kidney failure and contributes to an estimated 25% of deaths worldwide. Despite numerous treatment options, estimates project that reasonable blood pressure(BP) control is achieved in only about half of hypertensive patients. Improvements in the detection and management of hypertension will undoubtedly be accomplished through a better understanding of the complex etiology of this disease and a more comprehensive inventory of the genes and genetic variants that influence BP regulation. Recent studies(primarily in pre-clinical models) indicate that the small GTPase Rho A and its downstream target, Rho kinase, play an important role in regulating BP homeostasis. Herein, we summarize the underlying mechanisms and highlight signaling pathways and regulators that impart tight spatial-temporal control of Rho A activity. We also discuss known allelic variations in the Rho A pathway and consider how these polymorphisms may affect genetic risk for hypertension and its clinical manifestations. Finally, we summarize the current(albeit limited) clinical data on the efficacy of targeting the Rho A pathway in hypertensive patients. | Xue Bai Rachel Dee Kevin D Mangum Christopher P Mack Joan M Taylor | 2016 | World Journal of Hypertension2016，6，1： | 3 |
| 11 | Hydrothermal carbonization of livestock mortality for the reduction of pathogens and microbially-derived DNA显示文摘 | Thomas F. Ducey Jessica C. Collins Kyoung S. Ro Bryan L. Woodbury D. Dee Griffin | 2017 | Frontiers of Environmental Science & Engineering2017，11，3： | 3 |
| 12 | 服务贸易壁垒的测量与建模——兼谈澳大利亚经验显示文摘 | Philippa Dee 蔡玉贞 王洋 | 2005 | 经济资料译丛2005，，4： | 3 |
| 13 | H^+,N^+和Ar^+离子束辐射诱导碳纳米结构的变化(英文)显示文摘在室温和高温下,以不同辐射剂量的H+、N+和Ar+离子辐照多壁碳纳米管和无定形碳纳米线。利用透射电镜和拉曼光谱研究多壁碳纳米管和无定形碳纳米线的结构变化及损伤。以70keV N+离子束辐射多壁碳纳米管在室温下可形成无定形碳纳米线。1000K下70keV的H+离子束照射导致无定形碳纳米线向金刚石结构转变。离子辐照多壁碳纳米管的有序程度足够高,70keV的N+和Ar+离子能够引起碳从多壁碳纳米管的剥落。离子辐射能够为缺陷的转化提供必需的动力学驱动力。 | A Ishaq Shahid Iqbal Naveed Ali A A Khurram A U Akrajas C F Dee Shahzad Naseem H M Rafique Yan Long | 2013 | 新型炭材料2013，28，2： | 2 |
| 14 | Effect of alcohol exposure on hepatic superoxide generation and hepcidin expression显示文摘AIM: To understand the role of mitochondrial-produced superoxide(O 2 ?) in the regulation of iron-regulatory hormone, hepcidin by alcohol in the liver. METHODS: For alcohol experiments, manganese superoxide dismutase knockout mice heterozygous for Sod2 gene expression(Sod2 +/) and age-matched littermate control mice(LMC), expressing Sod2 gene on both alleles, were exposed to either 10%(w/v) ethanol in the drinking water or plain water(control) for 7 d. Total cellular O 2 ? levels in hepatocytes isolated from the livers of mice were measured by electron paramagnetic resonance spectroscopy. The mitochondrial-targeted, O 2 ?-sensitive fluorogenic probe, MitoSOX Red and flow cytometry were utilized to measure O 2 ? in mitochondria. Gene and protein expression were determined by Taqman Real-time quantitative PCR and Western blotting, respectively. RESULTS: Sod2 +/- mice expressed 40% less MnSOD protein(SOD2) in hepatocytes compared to LMC mice. The deletion of Sod2 allele did not alter the basal expression level of hepcidin in the liver. 10% ethanol exposure for 1 wk inhibited hepatic hepcidin mRNA expression three-fold both in Sod2 +/ and LMC mice. O 2 ? levels in hepatocytes of untreated Sod2 +/ mice were three-fold higher than in untreated LMC mice, as observed by electron paramagnetic resonance spectroscopy. O 2 ? levels in mitochondria of Sod2 +/ mice were four-fold higher than in mitochondria of untreated LMC mice, as measured by MitoSOX Red fluorescence and flow cytometry. Alcohol induced a two-fold higher increase in O 2 ? levels in hepatocytes of LMC mice than in Sod2 +/ mice compared to respective untreated counterparts. In contrast, 1 wk alcohol exposure did not alter mitochondrial O 2 ? levels in both Sod2 +/- and control mice. CONCLUSION: Mitochondrial O2 ? is not involved in the inhibition of liver hepcidin transcription and thereby regulation of iron metabolism by alcohol. These findings also suggest that short-term alcohol consumption significantly elevates O 2 ? levels in hepatocytes, which appears not to originate from mitochondria. | Duygu Dee Harrison-Findik Sizhao Lu Emily M Zmijewski Jocelyn Jones Matthew C Zimmerman | 2013 | World Journal of Biological Chemistry2013，4，4： | 2 |
| 15 | Mesenchymal stromal cells may enhance metastasis of neuroblastoma via SDF-1/CXCR4 and SDF-1/CXCR7 signaling显示文摘 | Ming Ma Jie Yu Ye Ruixia Deng Cathleen Michelle Dee Godfrey Chi-Fung Chan | 2011 | Cancer Letters2011，，1： | 2 |
| 16 | 犊牛支原体感染的防控对策显示文摘支原体是一种微小的生物体,能够引起奶牛发生乳腺炎、子宫内膜炎、肺炎和跛行等,从而给牧场造成破坏性的经济损失,这些损失主要表现在产奶量下降、牛只淘汰率升高、治疗费用增加等方面。犊牛感染支原体常常会出现耳炎、关节炎及呼吸系统疾病等临床症状,并且影响其生长发育。本文对犊牛感染支原体的症状、诊断及治疗作以综述,以供参考。 | John Currin Dee Whittier Nancy Currin 张晓峰 王赞江 梁建光 | 2012 | 中国奶牛2012，，1： | 2 |
| 17 | The new paradigm of hepatitis C therapy: integration of oral therapies into best practices显示文摘 | N. H. Afdhal S. Zeuzem R. T. Schooley D. L. Thomas J. W. Ward A. H. Litwin H. Razavi L. Castera T. Poynard A. Muir S. H. Mehta L. Dee C. Graham D. R. Church A. H. Talal M. S. Sulkowski I. M. Jacobson | 2013 | J Viral Hepat2013，，11： | 2 |
| 18 | An improvement in hearing sensitivity following hearing-aid fitting in a child with an apparent sensorineural hearing impairment显示文摘 | Dees DD | 1996 | J Laryn Otol1996，110，： | 1 |
| 19 | American Joint Committee on Cancer tumor-node-metastasis stage after neoadjuvant chemotherapy and breast cancer outcome 显示文摘 | Carey LA Metzger R Dees EC | 2005 | J Natl Cancer Inst2005，97，15： | 1 |
| 20 | The proteasome as a target for cancer therapy显示文摘 | Vorhees PM Dees EC O Neil B | 2003 | Clin Cancer Res2003，9，： | 1 |
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