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| 1 | Aging:A mitochondrial DNA perspective,critical analysis and an update显示文摘The mitochondrial theory of aging, a mainstream theory of aging which once included accumulation of mitochondrial DNA(mt DNA) damage by reactive oxygen species(ROS) as its cornerstone, has been increasingly losing ground and is undergoing extensive revision due to its inability to explain a growing body of emerging data. Concurrently, the notion of the central role for mtDNA in the aging process is being met with increased skepticism. Our progress in understanding the processes of mtDNA maintenance, repair, damage, and degradation in response to damage has largely refuted the view of mt DNA as being particularly susceptible to ROS-mediated mutagenesis due to its lack of 'protective' histones and reduced complement of available DNA repair pathways. Recent research on mitochondrial ROS production has led to the appreciation that mitochondria, even in vitro, produce much less ROS than previously thought, automatically leading to a decreased expectation of physiologically achievable levels of mtDNA damage. New evidence suggests that both experimentally induced oxidative stress and radiation therapy result in very low levels of mtDNA mutagenesis. Recent advances provide evidence against the existence of the 'vicious' cycle of mtDNA damage and ROS production. Meta-studies reveal no longevity benefit of increased antioxidant defenses. Simultaneously, exciting new observations from both comparative biology and experimental systems indicate that increased ROS production and oxidative damage to cellular macromolecules, including mtDNA, can be associated with extended longevity. A novel paradigm suggests that increased ROS production in aging may be the result of adaptive signaling rather than a detrimental byproduct of normal respiration that drives aging. Here, we review issues pertaining to the role of mtDNA in aging. | Inna N Shokolenko Glenn L Wilson Mikhail F Alexeyev | 2014 | World Journal of Experimental Medicine2014，4，4： | 6 |
| 2 | Gut Microbiota in Health and Disease显示文摘 | Inna Sekirov Shannon L RUSSELL L | 2010 | Physiol Rev2010，90，： | 1 |
| 3 | Gut Microbiota in Health and Disease显示文摘 | Inna S Shannon L Russell L | | 0，，03： | 1 |
| 4 | Cyclometalated ruthenium (II) complexes as efficient redox mediators in peroxidase catalysis显示文摘 | Inna S Alpeeva V S Soukharev L | 2003 | J Biol Inorg Chem2003，8，： | 1 |
| 5 | Caspase : pharmacological manipu- lation of cell death显示文摘 | Inna N L Alexander G Peter H K | 2005 | J Clin Invest2005，115，10： | 1 |
| 6 | The role of massspectrometry in vaccine development显示文摘 | Greory A P Inna G O Kenneth L J | 2001 | Vaccine2001，19，： | 1 |
| 7 | Dual effects of tetracaine on spontaneous calcium release in rat ventricular myocytes显示文摘 | Sandor G Valeriy L Inna G | | 0，，： | 1 |
| 8 | The role of massspectrometry in vaccine development显示文摘 | Greory A P Inna G O Kenneth L J | 2001 | Vaccine2001，19，： | 1 |
| 9 | Ertapenem Resistance among Extended-Speetrum-Lactamase-Produeing Klebsiella pneumoniae Isolates显示文摘 | Azita L Inna C Raul C | 2009 | J Clin Microbiol2009，47，4： | 1 |
| 10 | The role of mass spectrometry in vaccine development 显示文摘 | Greory A P Inna G O Kenneth L J | 2001 | Vaccine2001，19，1719： | 1 |
| 11 | The Role of Mass Spectrometry in Vaccine Development 显示文摘 | Greory A P Inna G O Kenneth L J | 2001 | Vaccine2001，19，： | 1 |
| 12 | Interactive effects of metal pollution and tem-perature on metabolism in aquatic ectotherms:implications of globalclimate change显示文摘 | Inna M S Gisela L | 2008 | Clim Res2008，37，： | 1 |
| 13 | Hepatitis C virus cures after direct acting antiviral-related drug-induced liver injury: Case report显示文摘The United States Food and Drug Administration recently warned that the direct acting antiviral(DAA) combination hepatitis C virus(HCV) treatment of Paritaprevir, Ombitasvir, Dasabuvir, Ritonavir, and Ribavirin(PODr + R) can cause severe liver injury in patients with advanced liver disease. Drug induced liver injury was observed in a small number of patients with decompensated cirrhosis treated with other DAAs, but has not been reported in patients with compensated cirrhosis. We report a case of a 74-year-old woman with chronic HCV and Child-Pugh class A cirrhosis(compensated cirrhosis) treated with PODr + R. The patient presented on day 14 of PODr + R therapy with jaundice and new-onset ascites. Her total bilirubin level increased to 23 mg/dL and international normalized ratio rose to 1.65, while aminotransferase levels remained relatively stable. Hepatitis C treatment was discontinued on day 24 and she gradually recovered. Follow-up testing showed that she achieved a sustained virologic response. In conclusion, hepatic decompensation developed within two weeks of starting treatment withPODr + R in a patient with Child-Pugh class A cirrhosis and was characterized by jaundice and ascites with stable aminotransferase levels. Careful monitoring is warranted in patients with HCV-related cirrhosis treated with PODr + R. | Yaakov Hasin Shimon Shteingart Harel Dahari Inna Gafanovich Sharon Floru Marius Braun Amir Shlomai Anthony Verstandig Ilana Dery Susan L Uprichard Scott J Cotler Yoav Lurie | 2016 | World Journal of Hepatology2016，8，20： | 1 |
| 14 | The role of massspectrom- etry in vaccine development 显示文摘 | Greory A P Inna G O Kenneth L J | 2001 | Vaccine2001，19，： | 1 |
| 15 | Overexpression of plastidic protoporphyrinogenⅨoxidase leads to resistance to the diphenyl-ether herbicide acifluorfen显示文摘 | Inna L Bernhard G | 2000 | Plant Physiology2000，122，1： | 1 |
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