pubmed-article:15569094 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15569094 | lifeskim:mentions | umls-concept:C0001811 | lld:lifeskim |
pubmed-article:15569094 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:15569094 | lifeskim:mentions | umls-concept:C0948051 | lld:lifeskim |
pubmed-article:15569094 | lifeskim:mentions | umls-concept:C1442080 | lld:lifeskim |
pubmed-article:15569094 | lifeskim:mentions | umls-concept:C1522855 | lld:lifeskim |
pubmed-article:15569094 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
pubmed-article:15569094 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:15569094 | pubmed:dateCreated | 2004-11-30 | lld:pubmed |
pubmed-article:15569094 | pubmed:abstractText | The rapid growing population of elderly illustrates the importance of understanding the mechanisms responsible for ageing and the detrimental effects on health associated with increasing age. One of the primary mechanisms may be because of the accumulation of mtDNA damage and oxidative damage with age. Previous studies have examined this correlation in post-mitotic tissues such as skeletal muscle, heart and brain with decreased mitochondrial function, such as enzymatic activities of the electron transport chain and ATP production. However, regional differences in the subcellular location of mitochondria exist and most studies have failed to differentiate the effects of these two autonomous fractions, the subsarcolemmal and intermyofibrillar populations. Hence, while future research attempts to explain the mechanisms responsible for ageing in the mitochondrion, it should also take into account the independent pathways of these two distinctly different populations. | lld:pubmed |
pubmed-article:15569094 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15569094 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15569094 | pubmed:language | eng | lld:pubmed |
pubmed-article:15569094 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15569094 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15569094 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15569094 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15569094 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15569094 | pubmed:month | Dec | lld:pubmed |
pubmed-article:15569094 | pubmed:issn | 0001-6772 | lld:pubmed |
pubmed-article:15569094 | pubmed:author | pubmed-author:FordL MLM | lld:pubmed |
pubmed-article:15569094 | pubmed:author | pubmed-author:LeeuwenburghC... | lld:pubmed |
pubmed-article:15569094 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15569094 | pubmed:volume | 182 | lld:pubmed |
pubmed-article:15569094 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15569094 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15569094 | pubmed:pagination | 333-41 | lld:pubmed |
pubmed-article:15569094 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:15569094 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15569094 | pubmed:articleTitle | Ageing and subcellular distribution of mitochondria: role of mitochondrial DNA deletions and energy production. | lld:pubmed |
pubmed-article:15569094 | pubmed:affiliation | Biochemistry of Aging Laboratory, University of Florida, Gainesville, FL 32611, USA. | lld:pubmed |
pubmed-article:15569094 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15569094 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:15569094 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:15569094 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15569094 | lld:pubmed |