pubmed-article:1302304 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1302304 | lifeskim:mentions | umls-concept:C0029418 | lld:lifeskim |
pubmed-article:1302304 | lifeskim:mentions | umls-concept:C0225369 | lld:lifeskim |
pubmed-article:1302304 | lifeskim:mentions | umls-concept:C0221284 | lld:lifeskim |
pubmed-article:1302304 | lifeskim:mentions | umls-concept:C0023175 | lld:lifeskim |
pubmed-article:1302304 | lifeskim:mentions | umls-concept:C0600688 | lld:lifeskim |
pubmed-article:1302304 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:1302304 | pubmed:dateCreated | 1993-6-7 | lld:pubmed |
pubmed-article:1302304 | pubmed:abstractText | The skeleton is a major repository for divalent cations, including toxic heavy metals such as lead. Unfortunately the effects of such agents on bone (and cartilage) have been minimally investigated in the past. With the current level of understanding of the mechanisms of bone formation and cartilage development it is now appropriate to begin to research the effects of lead on cellular processes. The following discussion describes some of the points of regulation in bone and cartilage formation where interference in metabolic processes could compromise the development of normal tissues as well as affect the homeostatic mechanisms of the skeleton. | lld:pubmed |
pubmed-article:1302304 | pubmed:language | eng | lld:pubmed |
pubmed-article:1302304 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1302304 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1302304 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1302304 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1302304 | pubmed:issn | 0161-813X | lld:pubmed |
pubmed-article:1302304 | pubmed:author | pubmed-author:PuzasJ EJE | lld:pubmed |
pubmed-article:1302304 | pubmed:author | pubmed-author:SickelM JMJ | lld:pubmed |
pubmed-article:1302304 | pubmed:author | pubmed-author:FelterM EME | lld:pubmed |
pubmed-article:1302304 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1302304 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:1302304 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1302304 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1302304 | pubmed:pagination | 783-8 | lld:pubmed |
pubmed-article:1302304 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:1302304 | pubmed:meshHeading | pubmed-meshheading:1302304-... | lld:pubmed |
pubmed-article:1302304 | pubmed:meshHeading | pubmed-meshheading:1302304-... | lld:pubmed |
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pubmed-article:1302304 | pubmed:meshHeading | pubmed-meshheading:1302304-... | lld:pubmed |
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pubmed-article:1302304 | pubmed:meshHeading | pubmed-meshheading:1302304-... | lld:pubmed |
pubmed-article:1302304 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1302304 | pubmed:articleTitle | Osteoblasts and chondrocytes are important target cells for the toxic effects of lead. | lld:pubmed |
pubmed-article:1302304 | pubmed:affiliation | Department of Orthopaedics, University of Rochester School of Medicine, New York 14642. | lld:pubmed |
pubmed-article:1302304 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1302304 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:1302304 | pubmed:publicationType | Review | lld:pubmed |
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http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1302304 | lld:pubmed |