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<title>Thrombosis RSS : Gourt</title>
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<description></description>
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<dc:rights>Copyright 2007, Gourt.com</dc:rights>
<dc:date>2012-02-09T11:26+25:00
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<dc:publisher>rtruog@gourt.com</dc:publisher>
<dc:creator>rtruog@gourt.com</dc:creator>
<dc:subject>Thrombosis RSS : Gourt</dc:subject>
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<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/e13?rss=1">
<title>Vascular Incorporation of Endothelial Colony-Forming Cells Is Essential for Functional Recovery of Murine Ischemic Tissue Following Cell Therapy [Integrative Biology/Experimental Medicine]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/e13?rss=1</link>
<description><![CDATA[
Objective&mdash;
Cord blood&ndash;derived human endothelial colony-forming cells (ECFCs) bear a high proliferative capacity and potently enhance tissue neovascularization in vivo. Here, we investigated whether the leading mechanism for the functional improvement relates to their physical vascular incorporation or perivascular paracrine effects and whether the effects can be further enhanced by dual-cell&ndash;based therapy, including mesenchymal stem cells (MSCs).

Methods and Results&mdash;
ECFCs or MSCs were lentivirally transduced with thymidine kinase suicide gene driven by the endothelial-specific vascular endothelial growth factor 2 (kinase insert domain receptor) promoter and evaluated in a hindlimb ischemia model. ECFCs and MSCs enhanced neovascularization after ischemic events to a similar extent. Dual therapy using ECFCs and MSCs further enhanced neovascularization. Mechanistically, 3 weeks after induction of ischemia followed by cell therapy, ganciclovir-mediated elimination of kinase insert domain receptor+ cells completely reversed the therapeutic effect of ECFCs but not that of MSCs. Histological analysis revealed that ganciclovir effectively eliminated ECFCs incorporated into the vasculature.

Conclusion&mdash;
Endothelial-specific suicide gene technology demonstrates distinct mechanisms for ECFCs and MSCs, with complete abolishment of ECFC-mediated effects, whereas MSC-mediated effects remained unaffected. These data strengthen the notion that a dual-cell&ndash;based therapy represents a promising approach for vascular regeneration of ischemic tissue.

]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/161?rss=1">
<title>Targeting Angiogenesis as Treatment for Obesity [Editorial]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/161?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/163?rss=1">
<title>Humanizing the Problem of Transplant Vasculopathy [Editorials]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/163?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/165?rss=1">
<title>Endothelial-to-Mesenchymal Transition and MicroRNA-21: The Game Is On Again [Editorials]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/165?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/167?rss=1">
<title>Intraplaque Hemorrhage: An Imaging Marker for Atherosclerotic Plaque Destabilization? [Editorials]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/167?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/169?rss=1">
<title>Life After GWAS: Functional Genomics in Vascular Biology [ATVB in Focus: Life After GWAS: Functional Genomics in Vascular Biology]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/169?rss=1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/170?rss=1">
<title>Strategies Beyond Genome-Wide Association Studies for Atherosclerosis [ATVB in Focus: Life After GWAS: Functional Genomics in Vascular Biology]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/170?rss=1</link>
<description><![CDATA[
Atherosclerotic diseases, including coronary artery disease (CAD) and myocardial infarction (MI), are the leading causes of death in the world. The genetic basis of CAD and MI, which are caused by multiple interacting endogenous and exogenous factors, has gained considerable interest in the last years as genome-wide association studies (GWASs) have identified many new susceptibility loci for CAD and MI, and the underlying genes provide new insights into the genetic architecture of these diseases. Here we summarize the recent findings from GWASs of atherosclerosis and discuss their functional and biological implications. We also discuss the different post-GWAS strategies that are currently used for refining the location of causal variants, understanding their role, and shedding light on molecular mechanisms explaining their association to CAD. We finally discuss potential clinical translations of GWAS findings for individual risk prediction, advanced clinical strategies, and personalized treatments.
]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/182?rss=1">
<title>The Use of High-Throughput Technologies to Investigate Vascular Inflammation and Atherosclerosis [ATVB in Focus: Life After GWAS: Functional Genomics in Vascular Biology]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/182?rss=1</link>
<description><![CDATA[
The greatest challenge of scientific research is to understand the causes and consequences of disease. In recent years, great efforts have been devoted to unraveling the basic mechanisms of atherosclerosis (the underlying pathology of cardiovascular disease), which remains a major cause of morbidity and mortality worldwide. Because of the complex and multifactorial pathophysiology of cardiovascular disease, different research techniques have increasingly been combined to unravel genetic aspects, molecular pathways, and cellular functions involved in atherogenesis, vascular inflammation, and dyslipidemia to gain a multifaceted picture addressing this complexity. Thanks to the rapid evolution of high-throughput technologies, we are now able to generate large-scale data on the DNA, RNA, and protein levels. With the help of sophisticated computational tools, these data sets are integrated to enhance information extraction and are being increasingly used in a systems biology approach to model biological processes as interconnected and regulated networks. This review exemplifies the use of high-throughput technologies&mdash;such as genomics, transcriptomics, proteomics, and epigenomics&mdash;and systems biology to explore pathomechanisms of vascular inflammation and atherosclerosis.
]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/196?rss=1">
<title>Recent Studies of the Human Chromosome 9p21 Locus, Which Is Associated With Atherosclerosis in Human Populations [ATVB in Focus Life After GWAS: Functional Genomics in Vascular Biology]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/196?rss=1</link>
<description><![CDATA[
The chromosome 9p21 (Chr9p21) locus was discovered in 2007 by independent genome-wide association studies for coronary artery disease. Since then, the locus has been replicated numerous times and can be considered the most robust genetic marker of coronary artery disease today. Subsequent work has shown associations of Chr9p21 with a number of additional cardiovascular disease traits, such as carotid artery plaque, stroke, aneurysms, peripheral artery disease, heart failure, and cardiovascular mortality, suggesting a more general role in vascular pathology. Importantly, Chr9p21 lacks associations with common cardiovascular risk factors, such as lipids and hypertension, indicating that the locus exerts its effect through a completely novel mechanism. One of the challenges is that the core haplotype block at Chr9p21 resides in a region of the genome devoid of protein-coding genes. Recent progress has been made by functional studies focusing on differential expression of antisense noncoding RNA in the INK4 locus (ANRIL), which is transcribed from the Chr9p21 locus, as well as neighboring protein-coding genes at the INK4/ARF locus. The emerging concept suggests that ANRIL might constitute a regulator of epigenetic modification and thus modulate cardiovascular risk. Here, we review the current clinical, mechanistic, and diagnostic implications of the Chr9p21 locus in cardiovascular disease.
]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/207?rss=1">
<title>Beyond Genome-Wide Association Studies: The Usefulness of Mouse Genetics in Understanding the Complex Etiology of Atherosclerosis [ATVB in Focus: Life After GWAS: Functional Genomics in Vascular Biology]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/207?rss=1</link>
<description><![CDATA[
The development of population-based genome-wide association studies has led to the rapid identification of large numbers of genetic variants associated with coronary artery disease (CAD) and related traits. Together with large-scale gene-centric studies, at least 35 loci associated with CAD per se have been identified with replication. The majority of these associations are with common single-nucleotide polymorphisms exhibiting modest effects on relative risk. The modest nature of the effects, coupled with ethical/practical constraints associated with human sampling, makes it difficult to answer important questions beyond gene/locus localization and allele frequency via human genetic studies. Questions related to gene function, disease-causing mechanism(s), and effective interventions will likely require studies in model organisms. The use of the mouse model for further detailed studies of CAD-associated loci identified by genome-wide association studies is highlighted herein.
]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/216?rss=1">
<title>Use of Functional Genomics to Identify Candidate Genes Underlying Human Genetic Association Studies of Vascular Diseases [ATVB in Focus Life After GWAS: Functional Genomics in Vascular Biology]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/216?rss=1</link>
<description><![CDATA[
Recent genome-wide association studies have identified hundreds of genetic loci as being associated with vascular diseases or traits and their risk factors. Many of the loci uncovered represent novel discoveries with no obvious candidate genes and molecular mechanisms, testifying to the complexity of vascular diseases. To understand the functional consequences of genetic variations and help pinpoint the underlying genes and mechanisms of common complex diseases, functional genomics that integrate genetic variations and intermediate molecular traits such as gene expression has been extensively studied in the past few years. This review summarizes the key concepts of functional genomics, the current state of the field, and its application in vascular diseases.
]]></description>
</item>

<item rdf:about="http://atvb.ahajournals.org/cgi/content/short/32/2/223?rss=1">
<title>S100A8 and S100A9 in Cardiovascular Biology and Disease [Brief Review]</title>
<link>http://atvb.ahajournals.org/cgi/content/short/32/2/223?rss=1</link>
<description><![CDATA[
There is recent and widespread interest in the damage-associated molecular pattern molecules S100A8 and S100A9 in cardiovascular science. These proteins have a number of interesting features and functions. For example, S100A8 and S100A9 (S100A8/A9) have both intracellular and extracellular actions, they are abundantly expressed in inflammatory and autoimmune states, primarily by myeloid cells but also by other vascular cells, and they modulate inflammatory processes, in part through Toll-like receptor 4 and the receptor for advanced glycation end products. S100A8/A9 also have anti
