| pubmed-article:11684638 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11684638 | lifeskim:mentions | umls-concept:C0078058 | lld:lifeskim |
| pubmed-article:11684638 | lifeskim:mentions | umls-concept:C0020542 | lld:lifeskim |
| pubmed-article:11684638 | lifeskim:mentions | umls-concept:C1171892 | lld:lifeskim |
| pubmed-article:11684638 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:11684638 | lifeskim:mentions | umls-concept:C1517499 | lld:lifeskim |
| pubmed-article:11684638 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:11684638 | pubmed:dateCreated | 2001-10-30 | lld:pubmed |
| pubmed-article:11684638 | pubmed:abstractText | Pulmonary arterial hypertension is characterized by increased pulmonary vascular resistance secondary to a decrease in the caliber and number of pulmonary vascular channels. We hypothesized that the targeted overexpression of an angiogenic factor within the lung would potentially minimize the development and progression of pulmonary arterial hypertension by preventing the loss of existing vessels or by inducing the development of new blood vessels within the lung. | lld:pubmed |
| pubmed-article:11684638 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11684638 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11684638 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:11684638 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11684638 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11684638 | pubmed:issn | 1524-4539 | lld:pubmed |
| pubmed-article:11684638 | pubmed:author | pubmed-author:StewartD JDJ | lld:pubmed |
| pubmed-article:11684638 | pubmed:author | pubmed-author:SandhuRR | lld:pubmed |
| pubmed-article:11684638 | pubmed:author | pubmed-author:ZhaiSS | lld:pubmed |
| pubmed-article:11684638 | pubmed:author | pubmed-author:CampbellA IAI | lld:pubmed |
| pubmed-article:11684638 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11684638 | pubmed:day | 30 | lld:pubmed |
| pubmed-article:11684638 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:11684638 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11684638 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11684638 | pubmed:pagination | 2242-8 | lld:pubmed |
| pubmed-article:11684638 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:11684638 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11684638 | pubmed:articleTitle | Cell-based gene transfer of vascular endothelial growth factor attenuates monocrotaline-induced pulmonary hypertension. | lld:pubmed |
| pubmed-article:11684638 | pubmed:affiliation | Division of Cardiac Surgery, University of Toronto, Terrence Donnelly Heart Centre, St Michael's Hospital, Toronto, Ontario, Canada. | lld:pubmed |
| pubmed-article:11684638 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11684638 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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