Journal of World Mitochondria Society最新文献_第5页

A molecular biosensor reveals regulation of mitochondrial protein import by the PINK1 kinase-driven Parkin ubiquitin ligase 一种分子生物传感器揭示了PINK1激酶驱动的Parkin泛素连接酶对线粒体蛋白进口的调节

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1964

Maxime Jacoupy, D. Guédin, F. Cogé, J. Corvol, A. Brice, C. Gautier, O. Corti

{"title":"A molecular biosensor reveals regulation of mitochondrial protein import by the PINK1 kinase-driven Parkin ubiquitin ligase","authors":"Maxime Jacoupy, D. Guédin, F. Cogé, J. Corvol, A. Brice, C. Gautier, O. Corti","doi":"10.18143/JWMS_V2I2_1964","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1964","url":null,"abstract":"The Parkinson’s disease (PD) related proteins PINK1 and Parkin act jointly as a mitochondrial quality control system, linking loss of mitochondrial import efficiency to the autophagy-dependent degradation of dysfunctional mitochondria. The aim of this study was to evaluate a possible involvement of the PINK1/Parkin system in the regulation of mitochondrial protein import. We engineered an inducible biosensor for monitoring the main presequence-mediated import pathway in living cells with a quantitative bioluminescence-based readout. Validation of this probe in HEK293T cells showed that it was appropriately targeted to mitochondria and sensitive to import impairment caused by pharmacological or genetic approaches. By using complementary tools to mimic or antagonize the activation of Parkin by PINK1 on mitochondria (siRNA-mediated downregulation of PINK1 or Parkin; overexpression of Parkin, PD-causing Parkin variants, phosphomimetic or non-phosphorylatable Parkin ; co-expression of ubiquitin, phosphomimetic, non-phosphorylatable or lysine-less ubiquitin), we show that the PINK1/Parkin system stimulates mitochondrial import in a kinase- and ubiquitin ligase-dependent manner. Use of the biosensor in primary skin fibroblasts from PD patients revealed lower levels of import compared to controls in a subset of PARK2 (Parkin) and PINK1 patients. Altogether, our results suggest that mitochondrial import defects may contribute to PD pathogenesis.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"63 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122565709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prevention of Mitochondrial Disease Caused by mtDNA Mutation through Mitochondrial Replacement Therapy (MRT) 线粒体替代疗法(MRT)预防mtDNA突变引起的线粒体疾病

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1971

Zitao Liu, Hui Liu, Zhuo Lu, S. Luo, Alejandro Chavez, Mingxue Yang, Z. Merhi, S. Silber, S. Munné, M. Konstantinidis, D. Wells, Taosheng Huang, John Zhang

{"title":"Prevention of Mitochondrial Disease Caused by mtDNA Mutation through Mitochondrial Replacement Therapy (MRT)","authors":"Zitao Liu, Hui Liu, Zhuo Lu, S. Luo, Alejandro Chavez, Mingxue Yang, Z. Merhi, S. Silber, S. Munné, M. Konstantinidis, D. Wells, Taosheng Huang, John Zhang","doi":"10.18143/JWMS_V2I2_1971","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1971","url":null,"abstract":"Objective: We investigated the role of MRT in preventing mitochondrial diseases caused by mtDNA mutation. Method: MRT was conducted by spindle nuclear transfer (SNT) between human oocytes. Mutant mtDNA load was analyzed. Results: of 18 oocytes collected from a female carrier (24.5% mtDNA 8993T>G) of Leigh Syndrome, 7 oocytes (haplogroup I) were attempted for MRT to enucleated donor oocytes (haplogroup L2c). Of the 4 blastocysts created from the 5 reconstituted oocytes, 1 euploid embryo was achieved, carrying 5.73% mtDNA 8993T>G mutation load comparing to 3.66% in an aneuploid embryo. The calculated mtDNA 8993T>G load was about 100% in both carrier’s oocytes, from which the above two embryos were created. A boy was delivered after euploid embryo transfer to the carrier. The mutant mtDNA load was differentiated expressed among the fetal and fetal appendage tissues, ranging from 0% to 9.23%. The child is still asymptomatic of Leigh Syndrome or other diseases at 5-month old now. Conclusions: Mitochondrial disease caused by mtDNA mutation may be prevented by MTR through SNT among different haplogroups. More cases and a long term follow-up are warranted to evaluate the safety of this technique.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131471871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of Parkin in innate immunity: crosstalk between mitochondrial dysfunction and NLRP3 inflammasome signaling Parkin在先天免疫中的作用:线粒体功能障碍和NLRP3炎性小体信号传导之间的串扰

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1962

F. Mouton-Liger, Julia E. Sepulveda, P. Michel, A. Brice, J. Corvol, O. Corti

{"title":"Role of Parkin in innate immunity: crosstalk between mitochondrial dysfunction and NLRP3 inflammasome signaling","authors":"F. Mouton-Liger, Julia E. Sepulveda, P. Michel, A. Brice, J. Corvol, O. Corti","doi":"10.18143/JWMS_V2I2_1962","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1962","url":null,"abstract":"Mitochondrial dysfunction and chronic neuroinflammation are central mechanisms in the pathogenesis of Parkinson’s disease (PD). Studies provided evidence that microglial overactivation of the NLRP3-inflammasome, a signaling complex that senses reactions to tissue damage, contributes to neurodegeneration in PD. The PD-linked gene PARK2/Parkin plays a central role in the regulation of mitochondrial quality control. Recent links have been established between mitochondria, Parkin and innate immunity responses. The objective of this project was to determine to what extent and by which mechanisms Parkin deficiency and mitochondrial dysfunction affect microglial response to pro-inflammatory stimuli and inflammasome activation. Cells from WT and Park2-knockout mice were obtained using an innovative in house protocol for the isolation of highly enriched microglia and then exposed to specific inducers of the NLRP3-inflammasome (nigericin…). Microglial activation was evaluated by measuring morphological changes and cytokines production. Our results show that Parkin deficiency exacerbates the increase in NLRP3 levels and IL-1β release triggered by nigericin in microglial cells, accompanied by corresponding morphological changes. This hyperactivaton profile was reversed by the selective inhibitor of NLRP3-inflammasome complex formation, MCC950. This work will foster integrated consideration of the deleterious crosstalk between these two key pathological mechanisms underlying PD in animal models and patients.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"35 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116039006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Merm1: a novel regulator of mitochondrial transcription and function Merm1:一种新的线粒体转录和功能调节因子

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1965

M. Baxter, P. Guiomar, M. Minczuk, P. Chinnery, A. Loudon, D. Ray

{"title":"Merm1: a novel regulator of mitochondrial transcription and function","authors":"M. Baxter, P. Guiomar, M. Minczuk, P. Chinnery, A. Loudon, D. Ray","doi":"10.18143/JWMS_V2I2_1965","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1965","url":null,"abstract":"Metastasis-related methyltransferase 1 (Merm1) is a highly conserved protein which mediates N7-methylation of G1639 on ribosomal 18S RNA (1). Here, we identify a novel role for Merm1 in modulating mitochondrial transcription and thereby function. Merm1 function was investigated by siRNA mediated knockdown followed by RNAseq analysis, revealing reduced abundance of all mitochondrially encoded transcripts. This observation was corroborated by qPCR analysis, and there was no change in mitochondrial genome copy number. The changes in mitochondrial transcript abundance induced by Merm1 knockdown were found to be functionally important, reducing basal mitochondrial respiration, spare respiratory capacity and ATP production, as measured by Seahorse™ XF analyser. Immunofluorescence imaging combined with subcellular fractionation studies in A549 cells did not co-localise Merm1 within mitochondria. We therefore propose that Merm1 is eliciting these effects from outside the mitochondria, through its role as a ribosomal modulator. Importantly, in a panel of ~400 exomes from patients with unexplained mitochondrial defects, three heterozygous exonic missense mutations were identified in the Merm1 gene. Delineating the mechanism by which Merm1 regulates mitochondrial function may inform new therapies with clinical impact.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"20 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125966201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical ischemia reperfusion injury directly associates with postreperfusion metabolic failure 临床缺血再灌注损伤与灌注后代谢衰竭直接相关

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1938

L. Wijermars, S. Schaapherder, S. Kostidis, J. Lindeman

{"title":"Clinical ischemia reperfusion injury directly associates with postreperfusion metabolic failure","authors":"L. Wijermars, S. Schaapherder, S. Kostidis, J. Lindeman","doi":"10.18143/JWMS_V2I2_1938","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1938","url":null,"abstract":"Delayed graft function (DGF) is the manifestation of ischemia reperfusion injury (I/R) in the context kidney transplantation. Elucidation of DGF may provide critical clues for mechanisms underlying clinical I/R. In earlier studies we excluded ROS formation, complement, thrombocyte and neutrophil activation as drivers of clinical I/R, whereas the eminent inflammatory response following reperfusion appears protective. Using a comprehensive approach that includes sequential assessment of postreperfusion arteriovenous concentration (AV) differences over the human graft, along with metabolomic analyses on graft biopsies it is concluded that I/R injury is preceded by a profound postreperfusion metabolic deficit. Grafts with later DGF failed to recover aerobic respiration and showed persistent ATP catabolism as indicated by a persistently low post reperfusion tissue glucose/lactate ratio (mean (s.e.m.)): 0.2 (0.06) vs. 0.9 (0.16) in + and – I/R (P<0.002) and low phosphocreatinine, and continued post-reperfusion lactate and hypoxanthine release (net AV difference for lactate and hypoxanthine at t=30 minutes: 1.7 (0.67) mmol/l (P<0.00004) and 12.17 (4.63) µmol/l P<0.003 respectively). Respirometry showed the archetypical mitochondrial stabilizing peptide SS-31 preserved mitochondrial function in human kidney biopsies following simulated I/R (P<0.016). In conclusion, clinical I/R directly associates with a severe post-reperfusion metabolic deficit due to mitochondrial damage.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"34 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134200755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Drainage of fatty acids from blood in a liver-specific manner -associated with increased hepatic mitochondrial fatty acid oxidation, lowering triacylglycerol levels in liver and plasma. 以肝脏特异性方式从血液中排出脂肪酸-与肝脏线粒体脂肪酸氧化增加有关，降低肝脏和血浆中的甘油三酯水平。

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1955

Carine Lindquist, B. Bjørndal, C. Rossmann, Deusdedit Tusubira, A. Svardal, G. Røsland, K. Tronstad, S. Hallström, R. Berge

{"title":"Drainage of fatty acids from blood in a liver-specific manner -associated with increased hepatic mitochondrial fatty acid oxidation, lowering triacylglycerol levels in liver and plasma.","authors":"Carine Lindquist, B. Bjørndal, C. Rossmann, Deusdedit Tusubira, A. Svardal, G. Røsland, K. Tronstad, S. Hallström, R. Berge","doi":"10.18143/JWMS_V2I2_1955","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1955","url":null,"abstract":"Hepatic mitochondrial function, apolipoproteinC-III and lipoprotein lipase are potential targets for triacylglycerol lowering drugs. We wanted to investigate whether a new drug could influence these parameters. After dietary treatment of male Wistar rats with 100mg/kg body weight of the compound 2-(tetradec-12-yn-1-ylthio)acetic acid (triple-TTA) for three weeks, the hepatic mitochondrial fatty acid oxidation increased 5-fold. Gene expression analysis in liver showed significant downregulation of ApoC-III, and upregulation of Lpl and Vldlr,. Hepatic and plasma triacylglycerol were reduced, accompanied by induction of liver-specific mitochondrial biomarkers such as mitochondrial DNA, cytochrome c and mitochondrial transcription factor A. Interestingly, triple-TTA lowered the plasma acetylcarnitine level whereas the concentration of betahydroxybutyrate was increased. The hepatic energy charge was lowered in triple-TTA treated rats, as reflected by increased AMP/ATP ratio, whereas energy charge remained unchanged in muscle and heart. Triple-TTA administration induced gene expression of uncoupling proteins 2 and 3 in liver. Altogether, triple-TTA may induce (re)uptake of VLDL to the liver, facilitating drainage of lipids from the blood to liver for beta oxidation and production of ketone bodies as extrahepatic fuel. The possibility that UCP2/3 mediate a moderate degree of mitochondrial uncoupling and thereby protect against ROS production should be considered.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"438 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121460075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Profiling of Environmental Chemicals for Mitochondrial Dysfunction 环境化学物质对线粒体功能障碍的影响

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1939

M. Xia

引用次数: 0

Mitochondrial electron transport chain complex III activity is essential for neural differentiation of mouse P19 cell line 线粒体电子传递链复合体III活性对小鼠P19细胞系的神经分化至关重要

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1961

N. Pashkovskaia, Uta Gey, G. Rödel

{"title":"Mitochondrial electron transport chain complex III activity is essential for neural differentiation of mouse P19 cell line","authors":"N. Pashkovskaia, Uta Gey, G. Rödel","doi":"10.18143/JWMS_V2I2_1961","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1961","url":null,"abstract":"Besides energy production as their main function mitochondria contribute to diverse regulatory pathways1. For instance, it has been reported that the activity of the mitochondrial electron transport chain (mETC) complexes I and III are essential for cell cycle, apoptosis and stem cell differentiation2–4. In our work, we show that mETC complex III activity is essential for neurogenic differentiation of P19 stem cells. P19 is an embryonic carcinoma mouse cell line that provides a powerful model for neurogenesis5. The efficiency of differentiation was estimated by the appearance of cells with neuron-like morphology and the detection of the neuron-specific marker protein beta-III-tubulin. The role of mETC role in P19 cell differentiation was analysed by including the mETC complex III inhibitors Antimycin A (250 nM) and Myxothiazol (10 nM), respectively, in the differentiation medium. Both Antimycin A and Myxothiazol prevented neurogenic differentiation of P19 cells. Interestingly, the inhibitors did not change the ATP/ADP ratio and hence did not affect energy production, but induced the release of reactive oxygen species (ROS) as estimated by MitoSox staining.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131124808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

METABOLIC RE-PROGRAMMING IN CANCER CELLS: LIPOGENESIS, OXIDATIVE STRESS, AND THE MITOCHONDRIAL CONNECT 癌细胞中的代谢重编程:脂肪生成、氧化应激和线粒体连接

Journal of World Mitochondria Society Pub Date : 2016-09-19 DOI: 10.18143/JWMS_V2I2_1933

R. DeepaP, Krishnakumar Subramanian

{"title":"METABOLIC RE-PROGRAMMING IN CANCER CELLS: LIPOGENESIS, OXIDATIVE STRESS, AND THE MITOCHONDRIAL CONNECT","authors":"R. DeepaP, Krishnakumar Subramanian","doi":"10.18143/JWMS_V2I2_1933","DOIUrl":"https://doi.org/10.18143/JWMS_V2I2_1933","url":null,"abstract":"Mitochondrial metabolic re-modeling in cancer cells re-routes the glycolytic intermediates to biosynthetic reactions (instead of the physiological oxidative-phosphorylation fate).1 One such effect is the neoplastic activation of lipid biosynthesis. Lipogenic activation in cancer cells endows them with exceptional growth advantage through high membrane lipids turnover and lipid-rafts, mitochondrial redox-energy homeostasis, oncogenic signaling activation, pro-apoptotic pathway suppression, drug resistance and cancer cell stemness.2 This presentation will demonstrate the association of abnormal lipogenesis (catalysed by fatty acid synthase, FASN) with altered redox-energy balance and cancer cell proliferation. Using the ocular cancer model of retinoblastoma, experimental and clinical correlations between abnormal fatty acid metabolism, lipid peroxidation, aberrant cell cycle and apoptotic regulation, cell invasion and metastasis, will be discussed. While lipogenesis is largely linked with the cytosolic FASN I, there exists its lesser studied, structurally-distinct mitochondrial counterpart, FASN II (or mtFASN).3 What are the functional roles of mtFASN in human cancer cells? Is there a regulatory connect between cytoplasmic and mitochondrial FASN? Insights from global gene profiling and biochemical analyses using FASN enzyme inhibitors4 and FASN gene-silencing,5 will be presented.","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131348185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cytobiochemical biomarkers of the state of mitochondria in humans. II. Small but clear differences between elderly people with bronchial asthma and these with no clinical symptoms or middle-aged examinees 人类线粒体状态的细胞生化生物标志物。2老年支气管哮喘患者与无临床症状者或中年受试者之间存在微小但明显的差异

Journal of World Mitochondria Society Pub Date : 2016-09-16 DOI: 10.18143/JWMS_v2i2_1930

M. Zakharchenko, N. Kosyakova, N. V. Khunderyakova, E. G. Litvinova, N. I. Fedotcheva, Polina Sсhwartsburd, M. N. Kondrashova

{"title":"Cytobiochemical biomarkers of the state of mitochondria in humans. II. Small but clear differences between elderly people with bronchial asthma and these with no clinical symptoms or middle-aged examinees","authors":"M. Zakharchenko, N. Kosyakova, N. V. Khunderyakova, E. G. Litvinova, N. I. Fedotcheva, Polina Sсhwartsburd, M. N. Kondrashova","doi":"10.18143/JWMS_v2i2_1930","DOIUrl":"https://doi.org/10.18143/JWMS_v2i2_1930","url":null,"abstract":"Quantitative indicators of mitochondria functions and dysfunctions were estimated by the activity of dehydrogenases (DH): succinate DH (SDH), lactate DH (LDH), LDH/SDH as glycolysis-respiration ratio or Warburg effect (WEF) measure proposed by our group. The measurements were carried out by our advanced cyto-BIO-chemical method in mitochondria within lymphocytes in a smear of blood [1, 2]. In this study we have added α-ketoglutarate (KGL) DH (KDH) measurement by blue staining of nitroblue tetrazolium and estimation of KGL influence on red staining of nucleus (KNU) by neutral red (NR). Part I of the work showed that given the great differences between the states of examinees DH activity served as sensitive biomarker [3]. WEF reveals these changes with even greater amplitude. We have shown that DH do not distinctly reveal smaller differences between elderly people with chronic bronchial asthma and control group of the same age or with healthy middle-aged examinees. However, WEF detects the smaller distinctions clearly (Fig1). Strict distribution of examinees by this indicator completely corresponds to the physician’s opinion on the clinical data. But even WEF cannot reveal very mild differences between elderly and middle-aged people within the range of norm. However, KDH and KNU detect this differences (Fig2).","PeriodicalId":266249,"journal":{"name":"Journal of World Mitochondria Society","volume":"73 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127324695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0