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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.ashjournal.com/?rss=yes"><title>Journal of the American Society of Hypertension</title><description>Journal of the American Society of Hypertension RSS feed: Current Issue. The  Journal of the American Society of Hypertension (JASH)  publishes peer-reviewed articles on the topics of basic, applied 
and translational research on blood pressure, hypertension and related cardiovascular disorders and factors. Original research studies, 
reviews, hypotheses, editorial commentary and special reports spanning the spectrum of human and experimental animal and tissue research 
will be considered. All research studies must have been conducted following animal welfare guidelines.  Studies involving human subjects 
or tissues must have received approval of the appropriate institutional committee charged with oversight of human studies and informed 
consent must be obtained. 
 
This  Journal  is covered in MEDLINE, Chemical Abstracts Service, EMBASE, and Scopus.</description><link>http://www.ashjournal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 American Society of Hypertension. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:issn>1933-1711</prism:issn><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:publicationDate>July 2010</prism:publicationDate><prism:copyright> © 2010 American Society of Hypertension. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001221/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS193317111000121X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110000884/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001191/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001166/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001154/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001233/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001208/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001294/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ashjournal.com/article/PIIS1933171110001324/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001221/abstract?rss=yes"><title>From the Editor</title><link>http://www.ashjournal.com/article/PIIS1933171110001221/abstract?rss=yes</link><description>I hope that you found the 25th Anniversary ASH meeting as stimulating and informative as I did and as all of the attendees with whom I spoke acknowledged. Moreover, it was reassuring to see such a great turnout at the meeting in view of current economic issues.</description><dc:title>From the Editor</dc:title><dc:creator>Myron H. Weinberger</dc:creator><dc:identifier>10.1016/j.jash.2010.06.003</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>155</prism:startingPage><prism:endingPage>156</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS193317111000121X/abstract?rss=yes"><title>ASH Hypertension Community Outreach Program: taking action to address a “neglected disease”</title><link>http://www.ashjournal.com/article/PIIS193317111000121X/abstract?rss=yes</link><description>The Institute of Medicine (IOM) panel recently declared that high blood pressure (BP) is a “neglected disease” that costs the US health care system $73 billion per year. The IOM authors encouraged the Center for Disease Control and Prevention to promote policies to persuade Americans to exercise and consume a healthy diet to control their BP and to stimulate physicians to treat the condition more aggressively. It is time to shift the burden of hypertension prevention and treatment efforts from individuals to society, the report concluded, and to recognize that high BP has not been given appropriate attention, despite the simplicity of diagnosis, treatment, and prevention. Attacking hypertension from the aspect of public policy and systems is realistic and practical, particularly given the economic burden of suboptimal primary and secondary approaches. As noted by the IOM chair, Dr. David Fleming of the Public Health Department of Seattle and King County, Washington, individuals who live long enough are almost guaranteed to develop hypertension. Thus, uncontrolled high BP should be a universal concern.</description><dc:title>ASH Hypertension Community Outreach Program: taking action to address a “neglected disease”</dc:title><dc:creator>Keith C. Ferdinand</dc:creator><dc:identifier>10.1016/j.jash.2010.06.002</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>157</prism:startingPage><prism:endingPage>162</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110000884/abstract?rss=yes"><title>Antihypertensive drug development: current challenges and future opportunities</title><link>http://www.ashjournal.com/article/PIIS1933171110000884/abstract?rss=yes</link><description>Abstract: The growing rate of obesity and diabetes, and an aging population has led to increased demand for new antihypertensive compounds. This review highlights the challenges and opportunities associated with each phase of drug discovery and development of novel antihypertensive agents. Discovery and development starts with identification of a protein hypothesized to be linked to hypertension. Using the information gathered during this early stage, several potential candidates are often synthesized and moved on through preclinical evaluations, eventually leading to selection of one or more compounds for testing in humans. The compounds then enter preclinical safety studies in laboratory animal species and subsequently are tested in tiered clinical studies. As the compounds enter clinical testing, there is an exponential increase in the investment of resources to demonstrate that a new compound is a viable and worthy therapeutic agent for hypertension. The review provides some forecasting of issues that are likely to impact drug development of novel antihypertensives in the future.</description><dc:title>Antihypertensive drug development: current challenges and future opportunities</dc:title><dc:creator>Peter U. Feig, Sophie Roy, Robert J. Cody</dc:creator><dc:identifier>10.1016/j.jash.2010.04.003</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-06-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-06-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Review Article</prism:section><prism:startingPage>163</prism:startingPage><prism:endingPage>173</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001191/abstract?rss=yes"><title>The insular cortex and cardiovascular system: a new insight into the brain-heart axis</title><link>http://www.ashjournal.com/article/PIIS1933171110001191/abstract?rss=yes</link><description>Abstract: The classical literature on neurocardiology has focused mainly on the subcortical regions of the central autonomic nervous system. However, recent studies have supported the notion that the cardiovascular system is regulated by cortical modulation. Modern neuroimaging data, including positron emission tomography and functional magnetic resonance imaging, have revealed that a network consisting of the insular cortex, anterior cingulate gyrus, and amygdala plays a crucial role in the regulation of central autonomic nervous system. Because the insular cortex is located in the region of the middle cerebral arteries, its structure tends to be exposed to a higher risk of cerebrovascular disease. The insular cortex damage has been associated with arrhythmia, diurnal blood pressure variation disruption (eg, a non-dipper or riser pattern), myocardial injury, and sleep disordered breathing, as well as higher plasma levels of brain natriuretic peptide, catecholamine, and glucose. This review article focuses on the role of the insular cortex as a mediator for the cardiovascular system and summarizes current knowledge on the relationships between cerebrovascular disease and cardiovascular system dysregulation. Finally, a hypothesis of the neural network involved in cortical cardiovascular modulation, including modulation of the insular cortex, is provided.</description><dc:title>The insular cortex and cardiovascular system: a new insight into the brain-heart axis</dc:title><dc:creator>Michiaki Nagai, Satoshi Hoshide, Kazuomi Kario</dc:creator><dc:identifier>10.1016/j.jash.2010.05.001</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Research Article</prism:section><prism:startingPage>174</prism:startingPage><prism:endingPage>182</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001166/abstract?rss=yes"><title>A non-blood pressure-measuring student of hypertension looks at blood pressure variability</title><link>http://www.ashjournal.com/article/PIIS1933171110001166/abstract?rss=yes</link><description>We take blood pressure measurement for granted. Similar to body-temperature determination, the measurement of blood pressure has become a clinical banality. Clinicians engaged in treating hypertensive patients and researchers into hypertensive mechanisms or hypertension-induced target-organ damage often hardly give blood pressure measurement itself another thought. Or perhaps I should speak for myself (which I do). Recently, Webb et al published a systematic review and meta-analysis on antihypertensive drug classes, individual variation in blood pressure, and stroke risk that gave me food for thought. They claimed that, on the basis of their analysis, drug-class effects on interindividual variation in blood pressure could account for differences in the effects of antihypertensive drugs on risk of stroke, independent of effects on mean systolic blood pressure. According to the authors, interindividual variation in systolic blood pressure was reduced by calcium-channel blockers and non–loop diuretic drugs, but increased by angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, and beta-blocking drugs.</description><dc:title>A non-blood pressure-measuring student of hypertension looks at blood pressure variability</dc:title><dc:creator>Friedrich C. Luft</dc:creator><dc:identifier>10.1016/j.jash.2010.04.006</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-06-11</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-06-11</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>183</prism:startingPage><prism:endingPage>186</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001154/abstract?rss=yes"><title>Enhanced blood pressure variability in a high cardiovascular risk group of African Americans: FIT4Life Study</title><link>http://www.ashjournal.com/article/PIIS1933171110001154/abstract?rss=yes</link><description>Abstract: High blood pressure (BP) levels in African Americans elicit vascular inflammation resulting in vascular remodeling. BP variability (BPV) correlates with target organ damage. We aimed to investigate the relationship between inflammatory markers and BPV in African Americans. Thirty-six African Americans underwent 24-hour ambulatory BP monitoring (ABPM). BPV was calculated using the average real variability index. Fasting blood samples were assayed for high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), and white blood cell (WBC) count. Significant associations between hs-CRP and 24-hour systolic variability (r = 0.50; P = .012) and awake systolic variability (r = 0.45; P = .02) were identified after adjusting for age, body mass index, and 24-hour mean BP. ABPM variables were compared between the hs-CRP tertile groups. In post-hoc analysis, there was a significant difference in 24-hour and awake periods for both systolic and diastolic variability among the groups. TNF-α and WBC count showed no associations with ABPM variables. hs-CRP was associated with systolic variability, and higher levels of hs-CRP were related with greater BPV. Higher inflammatory status influences wider fluctuations in systolic BP, which in turn could facilitate early progression to target organ damage independent of absolute BP levels in African Americans.</description><dc:title>Enhanced blood pressure variability in a high cardiovascular risk group of African Americans: FIT4Life Study</dc:title><dc:creator>Praveen Veerabhadrappa, Keith M. Diaz, Deborah L. Feairheller, Kathleen M. Sturgeon, Sheara Williamson, Deborah L. Crabbe, Abul Kashem, Debra Ahrensfield, Michael D. Brown</dc:creator><dc:identifier>10.1016/j.jash.2010.04.005</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-05-31</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-05-31</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>187</prism:startingPage><prism:endingPage>195</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001233/abstract?rss=yes"><title>Urinary albumin excretion among nondipper hypertensive patients is closely related with the pattern of nondipping</title><link>http://www.ashjournal.com/article/PIIS1933171110001233/abstract?rss=yes</link><description>Abstract: The relationship between 24-hour urinary albumin excretion (UAE) rate and the pattern of nondipping (isolated systolic nondipping, isolated diastolic nondipping, and both systolic and diastolic nondipping) is not known. Medical history, physical examination, laboratory analysis, and office and ambulatory blood pressure measurements were performed. Twenty-four hour urine specimens were collected to determine creatinine clearance and UAE. In total, 158 essential hypertensive patients (104 dippers, 54 nondippers) were included. Fourteen patients were isolated systolic nondippers, 7 patients were isolated diastolic nondippers, and 33 patients were both systolic and diastolic nondippers. Among nondipper patients, 17 had microalbuminuria and, among dipper patients, 9 had microalbuminuria (P &lt; .0001). The median UAE of dippers was lower when compared with nondippers (5.25 mg/day vs.23 mg/day, P &lt; .0001). The median UAE of isolated systolic nondippers, isolated diastolic nondippers, and both systolic and diastolic nondippers were 8.45 mg/day, 7.7 mg/day, and 25.5 mg/day, respectively (P = .001). Subgroup comparison of patients revealed that UAE was higher in patients with both systolic and diastolic nondippers when compared with dippers (P &lt; .0001), isolated systolic nondippers (P = .001), and isolated diastolic nondippers (P =  .017). Not only nondipping itself, but nondipping profile may be related with UAE in essential hypertensive patients.</description><dc:title>Urinary albumin excretion among nondipper hypertensive patients is closely related with the pattern of nondipping</dc:title><dc:creator>Baris Afsar, Rengin Elsurer</dc:creator><dc:identifier>10.1016/j.jash.2010.06.004</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>196</prism:startingPage><prism:endingPage>202</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001208/abstract?rss=yes"><title>Flow-mediated dilatation has an additive value to stress ECG for the diagnosis of angiographically significant coronary atherosclerosis</title><link>http://www.ashjournal.com/article/PIIS1933171110001208/abstract?rss=yes</link><description>Abstract: The objective of this study is to determine if flow-mediated endothelial-dependent vasodilatation (FMD) performed after stress electrocardiogram (ECG) test has an additive value for the diagnosis of significant coronary artery disease (CAD). We studied 322 patients who underwent stress ECG test, coronary arteriography (CAG), and FMD evaluation. The pretest probability (preTP) for the presence of significant CAD (≥50% stenosis) was 73%. The probability for the disease after positive or negative ECG test (postTP) was 75% and 62%, respectively. A positive FMD response after a positive stress test resulted in 86% postTP with prevalence of advanced CAD in this subgroup −70.4%. A negative FMD response after a positive treadmill test decreased the postTP to 50% (prevalence of significant CAD 25.5%) and could change clinical behavior – additional tests before proceeding to CAG. After negative stress test the postTP increased to 78% when FMD was positive (prevalence of the disease 50%), necessitating the performance of CAG. It decreased to 36% after a negative FMD (prevalence of the disease 11.5%), directing to conservative behavior. In a group with a high pretest probability for the presence of advanced coronary atherosclerosis, FMD has an additive value to stress ECG for the diagnosis of significant CAD and could guide clinical behavior.</description><dc:title>Flow-mediated dilatation has an additive value to stress ECG for the diagnosis of angiographically significant coronary atherosclerosis</dc:title><dc:creator>Iana Simova, Tsvetana Katova, Stefan Denchev, Nikolay Dimitrov</dc:creator><dc:identifier>10.1016/j.jash.2010.06.001</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Research Articles</prism:section><prism:startingPage>203</prism:startingPage><prism:endingPage>208</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001294/abstract?rss=yes"><title>Editorial Board</title><link>http://www.ashjournal.com/article/PIIS1933171110001294/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1933-1711(10)00129-4</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A2</prism:endingPage></item><item rdf:about="http://www.ashjournal.com/article/PIIS1933171110001324/abstract?rss=yes"><title>Table of Contents</title><link>http://www.ashjournal.com/article/PIIS1933171110001324/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1933-1711(10)00132-4</dc:identifier><dc:source>Journal of the American Society of Hypertension 4, 4 (2010)</dc:source><dc:date>2010-07-01</dc:date><prism:publicationName>Journal of the American Society of Hypertension</prism:publicationName><prism:publicationDate>2010-07-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S1933-1711(10)X0005-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A5</prism:startingPage><prism:endingPage>A5</prism:endingPage></item></rdf:RDF>