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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 | High omega arachidonic acid/docosahexaenoic acid ratio induces mitochondrial dysfunction and altered lipid metabolism in human hepatoma cells显示文摘BACKGROUND Non-alcoholic fatty liver disease(NAFLD) is a common cause of liver disease worldwide and is a growing epidemic. A high ratio of omega-6 fatty acids to omega-3 fatty acids in the diet has been implicated in the development of NAFLD. However, the inflicted cellular pathology remains unknown. A high ratio may promote lipogenic pathways and contribute to reactive oxygen species(ROS)-mediated damage, perhaps leading to mitochondrial dysfunction.Therefore, these parameters were investigated to understand their contribution to NAFLD development.AIM To examine the effect of increasing ratios of omega-6:3 fatty acids on mitochondrial function and lipid metabolism mediators.METHODS Hep G2-derived VL-17 A cells were treated with normal(1:1, 4:1) and high(15:1,25:1) ratios of omega-6: omega-3 fatty acids [arachidonic acid(AA):docosahexaenoic acid(DHA)] at various time points. Mitochondrial activity and function were examined via MTT assay and Seahorse XF24 analyzer, respectively.Triglyceride accumulation was determined by using Enzy Chrom? and levels of ROS were measured by fluorescence intensity. Protein expression of the mediators of lipogenic, lipolytic and endocannabinoid pathways was assessed by Western blotting.RESULTS High AA:DHA ratio decreased mitochondrial activity(P < 0.01;up to 80%) and promoted intracellular triglyceride accumulation(P < 0.05;40%-70%).Mechanistically, it altered the mediators of lipid metabolism;increased the expression of stearoyl-Co A desaturase(P < 0.05;22%-35%), decreased the expression of peroxisome proliferator-activated receptor-alpha(P < 0.05;30%-40%) and increased the expression of cannabinoid receptor 1(P < 0.05;31%).Furthermore, the high ratio increased ROS production(P < 0.01;74%-115%) and reduced mitochondrial respiratory functions such as basal and maximal respiration, ATP production, spare respiratory capacity and proton leak(P < 0.01;35%-68%).CONCLUSION High AA:DHA ratio induced triglyceride accumulation, increased oxidative stress and disrupted mitochondrial functions. Stimulation of lipogenic and steroidal transcription factors may partly mediate these effects and contribute to NAFLD development. | Reem Ghazali Kosha J Mehta SW Annie Bligh Ihab Tewfik Dahn Clemens Vinood B Patel | 2020 | World Journal of Hepatology2020，12，3： | 2 |
| 3 | Predictors of bone mineral loss in patients with ovaria cancer treated with anticancer agents显示文摘 | Douehi T Kosha S Kan R | 1997 | Obstet Gynecol1997，90，1： | 1 |
| 4 | Application of chromogenic media for rapid detection water and food-borne pathogens显示文摘 | TAVAKOLI H R BAYAT M KOSHA M | | 0，，06： | 1 |
| 5 | Direct comparison of the BD ProbeTec ET system with in-house LightCycler PCR assays for detection of Chlamydia trachomatis and Neisseria gonorrhoeae from clinical specimens显示文摘 | Koenig M G Kosha SL Doty BL | 2004 | J Clin Microbiol2004，42，12： | 1 |
| 6 | Predictors of bone mineral loss in patients with ovarian cancer treated with anticancer agents显示文摘 | Duchi T Kosha S Kan R | 1997 | Obstet Gynecol1997，90，： | 1 |
| 7 | Predictors of bone mineral loss in patients with ovarian cancer treated with anticancer agents显示文摘 | Duchi T Kosha S Kan R | 1997 | Obstet Gynecol1997，90，1： | 1 |
| 8 | Adverse events and bone health during anastrozole therapy in postmenopausal Japanese breast cancer patients显示文摘 | Yasuaki Sagara Shoichiro Kosha Shinichi Baba Fumiko Dokiya Shugo Tamada Yoshiaki Sagara Yoshito Matsuyama Yasuyo Ohi Mitsutake Ando Yoshiaki Rai Yoshiatsu Sagara Tsutomu Douchi | 2010 | Breast Cancer2010，，3： | 1 |
| 9 | Detection of influenza virus from throat and pharyngeal swabs with anested duplex light cycler RT-PCR显示文摘 | Koenig M Kosha S Hickman M | 2003 | Diag Microbiol Inf Dis2003，46，： | 1 |
| 10 | Direct comparison of the BD ProbeTec ET system with in-house LightCycler PCR assays for detection of Chlamydia trachomatis and Neisseria gonorrhoeae from clinical specimens 显示文摘 | Koenig MG Kosha SL Doty BL | 2004 | J Clin Microbiol2004，42，12： | 1 |
| 11 | Predictors of bone mineral loss in patients with ovarian cancer treated with anticancer agents显示文摘 | Douchi T Kosha S Kan R | 1997 | Obstetrics and Gynecology1997，90，3： | 1 |
| 12 | 显示文摘 | Iwamoto I Douchi T Kosha S | 2000 | Acta Obstet Gynecol Scand2000，79，12： | 1 |
| 13 | 6-8, 2002; TRIZHPJapan, Sept, 2002 显示文摘 | Toru Nakagawa Hideaki Kosha and Yuji Mihara: 'Reorganizing TRIZ Solution Generation Methods intoSimple Five in USIT' ETRIA World Conference 'TRIZ Future 2002' held at Strasbourg France on Nov | 2002 | Nov2002，，： | 1 |
| 14 | Direct comparison of the BD ProbeTec ET system with in-house light cycler PCR assays for detection of Chlamydia trachomatis and Neisseria gonorrhoeae from clinical specimens显示文摘 | Koenig M G Kosha S L Doty B L | 2004 | J Clin Microbiol2004，12，： | 1 |
| 15 | Direct comparison of the BD ProbeTec ET system with in-house LightCyeler PCR assays for detection of Chlamydia trachomatis and Neisseria gonorrhoeae from clinical specimens显示文摘 | Koenig M G Kosha S L Doty B L etal | 2004 | J Clin Microbiol2004，42，12： | 1 |
| 16 | Relationships be-tween serum leptin level and regional bone mineral density,bone metabolic markers in healthy women显示文摘 | Iwamoto I Douchi T Kosha S | 2000 | Acta ObstetGynecol Scand2000，79，： | 1 |
| 17 | Predictors of bone mineral loss in patients with ovarian canner treated with anticancer agents显示文摘 | KOSHA S KAN R | 1997 | Obstet Gynecol1997，90，1： | 1 |
| 18 | A mathematical model of the adaptive control of human arm motions 显示文摘 | Robert M Sanner Makiko Kosha | 1999 | Biological Cybernetics1999，80，： | 1 |
| 19 | Relationships between serum leptin level and regional bone mineral density,bone metabolic markers in healthy women显示文摘 | Iwamoto I Douchi T Kosha S | 2000 | Acta Obstet Gynecol Scand2000，79，： | 1 |
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