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Search Results: 1 - 10 of 461866 matches for " Arshed A Quyyumi "
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Endothelium-Derived Hyperpolarizing Factor and Vascular Function
Muhiddin A. Ozkor,Arshed A. Quyyumi
Cardiology Research and Practice , 2011, DOI: 10.4061/2011/156146
Abstract: Endothelial function refers to a multitude of physiological processes that maintain healthy homeostasis of the vascular wall. Exposure of the endothelium to cardiac risk factors results in endothelial dysfunction and is associated with an alteration in the balance of vasoactive substances produced by endothelial cells. These include a reduction in nitric oxide (NO), an increase in generation of potential vasoconstrictor substances and a potential compensatory increase in other mediators of vasodilation. The latter has been surmised from data demonstrating persistent endothelium-dependent vasodilatation despite complete inhibition of NO and prostaglandins. This remaining non-NO, non-prostaglandin mediated endothelium-dependent vasodilator response has been attributed to endothelium-derived hyperpolarizing factor/s (EDHF). Endothelial hyperpolarization is likely due to several factors that appear to be site and species specific. Experimental studies suggest that the contribution of the EDHFs increase as the vessel size decreases, with a predominance of EDHF activity in the resistance vessels, and a compensatory up-regulation of hyperpolarization in states characterized by reduced NO availability. Since endothelial dysfunction is a precursor for atherosclerosis development and its magnitude is a reflection of future risk, then the mechanisms underlying endothelial dysfunction need to be fully understood, so that adequate therapeutic interventions can be designed. 1. Introduction Endothelial function refers to a multitude of physiological processes of the vascular endothelium that maintain healthy homeostasis of the vascular wall and may be used as a “barometer” of the injury/repair inflicted by multiple environmental and genetic factors [1–3]. Vascular endothelial dysfunction is associated with a reduction in nitric oxide (NO) bioavailability, an increase in generation of potential vasoconstrictor substances such as superoxide anions and endothelin–1, and a potential compensatory increase in other mediators of vasodilation. This remaining non-NO, nonprostaglandin-mediated endothelium-dependent vasodilation has been partly attributed to endothelium-derived hyperpolarizing factor/s (EDHF). Endothelial hyperpolarization is likely due to several factors that are site- and species-specific, ultimately causing vascular smooth muscle hyperpolarization and relaxation. Experimental studies suggest that the contribution of EDHFs increase as the vessel size decreases, with predominant EDHF activity in the resistance vessels and a compensatory upregulation of EDHFs in
Progenitor Cell Therapy to Treat Acute Myocardial Infarction: The Promise of High-Dose Autologous CD34+ Bone Marrow Mononuclear Cells
Joseph C. Poole,Arshed A. Quyyumi
Stem Cells International , 2013, DOI: 10.1155/2013/658480
Abstract: ST elevation myocardial infarction (STEMI) is associated with an increased risk for congestive heart failure and long-term mortality despite the widespread use of thrombolysis and catheter-based revascularization. The need for improved post-STEMI therapies has led to a surge of novel therapeutics, especially regenerative approaches using autologous mononuclear cells. Indeed, the past decade has been marked by a number of human trials studying the safety and efficacy of progenitor cell delivery in the post-STEMI setting. While a variety of cell types and delivery techniques have been utilized, directed therapy to the infarct-related artery has been the most widely used approach. From over 1300 subjects randomized in these studies, there is sufficient evidence to conclude that cell therapy after STEMI is uniformly safe, while the efficacy of this intervention for improving outcomes is less clear. Recent meta-analyses have highlighted the importance of both timing of cell delivery, as well as the type, quantity, and mobility of delivered cells as determinants of response. Here, we show the case in which higher doses of CD34+ cells, which are more potent in terms of their migratory capacity, offer the best hope for preserving cardiac function following STEMI. 1. Introduction Despite early thrombolysis and revascularization, ST elevation myocardial infarction (STEMI) carries significant morbidity and mortality [1, 2]. Following acute STEMI, failure of prompt revascularization leads to myocardial necrosis that can cause ventricular chamber dilation through adverse remodeling, often leaving patients with permanent left ventricular (LV) systolic dysfunction and progressive congestive heart failure [3, 4]. Optimal medical therapy and cardiac rehabilitation in the postinfarct period helps minimize adverse remodeling; however, 12-month mortality for patients with STEMI and LV dysfunction still exceeds 10% [5]. In a landmark preclinical study, Orlic et al. demonstrated that direct injection into the infarcted myocardium of a highly defined bone marrow derived-cell (Lin? c-kitpos) population with hematopoietic and endothelial progenitor potential improved morbidity and mortality in a murine MI model. Within 3–5 hours of an induced anterior MI, mice received either Lin? c-kitpos cells, Lin+ cells, or no injection. In animals receiving Lin? c-kitpos cells, more than two-thirds of the infarcted myocardium was repopulated with regenerated myocytes; there was clear neovascularization, and cardiac function improved. The need for improved postinfarct therapies, together
The Arterial Pulse: Vascular Biology, Vascular Function Testing, and Therapies
A. Maziar Zafari,Arshed A. Quyyumi,Julian P. J. Halcox,Sanjay Rajagopalan
Cardiology Research and Practice , 2011, DOI: 10.4061/2011/151428
Abstract:
The Arterial Pulse: Vascular Biology, Vascular Function Testing, and Therapies
A. Maziar Zafari,Arshed A. Quyyumi,Julian P. J. Halcox,Sanjay Rajagopalan
Cardiology Research and Practice , 2011, DOI: 10.4061/2011/151428
Abstract:
MicroRNA Expression Profile in CAD Patients and the Impact of ACEI/ARB
Martina Weber,Meredith B. Baker,Riyaz S. Patel,Arshed A. Quyyumi,Gang Bao,Charles D. Searles
Cardiology Research and Practice , 2011, DOI: 10.4061/2011/532915
Abstract: Coronary artery disease (CAD) is the largest killer of males and females in the United States. There is a need to develop innovative diagnostic markers for this disease. MicroRNAs (miRNAs) are a class of noncoding RNAs that posttranscriptionally regulate the expression of genes involved in important cellular processes, and we hypothesized that the miRNA expression profile would be altered in whole blood samples of patients with CAD. We performed a microarray analysis on RNA from the blood of 5 male subjects with CAD and 5 healthy subjects (mean age 53 years). Subsequently, we performed qRT-PCR analysis of miRNA expression in whole blood of another 10 patients with CAD and 15 healthy subjects. We identified 11 miRNAs that were significantly downregulated in CAD subjects (<.05). Furthermore, we found an association between ACEI/ARB use and downregulation of several miRNAs that was independent of the presence of significant CAD. In conclusion, we have identified a distinct miRNA signature in whole blood that discriminates CAD patients from healthy subjects. Importantly, medication use may significantly alter miRNA expression. These findings may have significant implications for identifying and managing individuals that either have CAD or are at risk of developing the disease.
Elevated Circulating Angiogenic Progenitors and White Blood Cells Are Associated with Hypoxia-Inducible Angiogenic Growth Factors in Children with Sickle Cell Disease
Solomon F. Ofori-Acquah,Iris D. Buchanan,Ifeyinwa Osunkwo,Jerry Manlove-Simmons,Feyisayo Lawal,Alexander Quarshie,Arshed A. Quyyumi,Gary H. Gibbons,Beatrice E. Gee
Anemia , 2012, DOI: 10.1155/2012/156598
Abstract: We studied the number and function of angiogenic progenitor cells and growth factors in children aged 5–18 years without acute illness, 43 with Hemoglobin SS and 68 with normal hemoglobin. Hemoglobin SS subjects had at least twice as many mononuclear cell colonies and more circulating progenitor cell than Control subjects. Plasma concentrations of erythropoietin, angiopoietin-2, and stromal-derived growth factor (SDF)-1α were significantly higher in children with Hemoglobin SS compared to Control subjects. In a multivariate analysis model, SDF-1α concentration was found to be associated with both CPC number and total white blood cell count in the Hemoglobin SS group, suggesting that SDF-1α produced by ischemic tissues plays a role in mobilizing these cells in children with Hemoglobin SS. Despite having a higher number of angiogenic progenitor cells, children with Hemoglobin SS had slower migration of cultured mononuclear cells.
Elevated Circulating Angiogenic Progenitors and White Blood Cells Are Associated with Hypoxia-Inducible Angiogenic Growth Factors in Children with Sickle Cell Disease
Solomon F. Ofori-Acquah,Iris D. Buchanan,Ifeyinwa Osunkwo,Jerry Manlove-Simmons,Feyisayo Lawal,Alexander Quarshie,Arshed A. Quyyumi,Gary H. Gibbons,Beatrice E. Gee
Anemia , 2012, DOI: 10.1155/2012/156598
Abstract: We studied the number and function of angiogenic progenitor cells and growth factors in children aged 5–18 years without acute illness, 43 with Hemoglobin SS and 68 with normal hemoglobin. Hemoglobin SS subjects had at least twice as many mononuclear cell colonies and more circulating progenitor cell than Control subjects. Plasma concentrations of erythropoietin, angiopoietin-2, and stromal-derived growth factor (SDF)-1α were significantly higher in children with Hemoglobin SS compared to Control subjects. In a multivariate analysis model, SDF-1α concentration was found to be associated with both CPC number and total white blood cell count in the Hemoglobin SS group, suggesting that SDF-1α produced by ischemic tissues plays a role in mobilizing these cells in children with Hemoglobin SS. Despite having a higher number of angiogenic progenitor cells, children with Hemoglobin SS had slower migration of cultured mononuclear cells. 1. Introduction Sickle cell anemia (Hemoglobin SS) is characterized by hemoglobin polymerization and the formation of inflexible sickled erythrocytes. Accumulation of sickled erythrocytes in the microcirculation causes acute vaso-occlusive events that lead to pain and acute organ injury. Chronic arterial vasculopathy, with intimal proliferation and arterial stenosis, can lead to complications such as stroke and pulmonary hypertension. The etiology of arterial stenosis in sickle cell anemia is poorly understood. We hypothesize that intimal proliferation in sickle cell anemia is due to abnormal reparative responses to ongoing vessel injury. Hemolytic anemia, vaso-occlusion, and abnormal flow dynamics in sickle cell anemia may contribute to vessel injury. Chronic intravascular hemolysis releases free heme, which binds avidly to nitric oxide (NO), causing NO depletion, and subsequent vaso-constriction and inflammation [1]. Erythrocyte-derived reactive iron and oxygen species are also directly injurious to endothelium [2]. Repetitive episodes of acute vaso-occlusion cause tissue ischemia and reperfusion, which also lead to inflammation and increased oxidative stress [3]. Evidence of ongoing inflammation and vascular injury is present in people with sickle cell anemia even when asymptomatic, with elevated levels of high sensitivity C-reactive protein (hsCRP) [4] and circulating endothelial cells [5]. Reendothelization after vascular injury is a critically important process to restoring and maintaining vascular homeostasis. Endothelial progenitor cells (EPCs) are recruited from the bone marrow and home to sites of vascular injury.
Assessment of Myocardial Contractile Function Using Global and Segmental Circumferential Strain following Intracoronary Stem Cell Infusion after Myocardial Infarction: MRI Feature Tracking Feasibility Study
Sabha Bhatti,Hussein Al-Khalidi,Kan Hor,Abdul Hakeem,Michael Taylor,Arshed A. Quyyumi,John Oshinski,Andrew L. Pecora,Dean Kereiakes,Eugene Chung,Gianni Pedrizzetti,Tomasz Miszalski-Jamka,Wojciech Mazur
ISRN Radiology , 2013, DOI: 10.5402/2013/371028
Abstract: Background. Magnetic resonance imaging (MRI) strain analysis is a sensitive method to assess myocardial function. Our objective was to define the feasibility of MRI circumferential strain ( ) analysis in assessing subtle changes in myocardial function following stem cell therapy. Methods and Results. Patients in the Amorcyte Phase I trial were randomly assigned to treatment with either autologous bone-marrow-derived stem cells infused into the infarct-related artery 5 to 11 days following primary PCI or control. MRI studies were obtained at baseline, 3, and 6 months. was measured in the short axis views at the base, mid and apical slices of the left ventricle (LV) for each patient (13 treatments and 10 controls). Mid-anterior LV improved between baseline ? and 3 months ? , . There were no significant changes in at 3 months and 6 months compared to baseline for other segments. There was excellent intraobserver and interobserver agreement for basal and mid circumferential strain. Conclusion. MRI segmental strain analysis is feasible in assessment of regional myocardial function following cell therapy with excellent intra- and inter-observer variability's. Using this method, a modest interval change in segmental was detected in treatment group. 1. Introduction Circumferential strain ( ) analysis is an established method to assess myocardial function. has been demonstrated to detect changes in myocardial contractility across a variety of cardiac conditions including hypertensive [1] or hypertrophic cardiomyopathy [2] and Duchenne muscular dystrophy [3] before changes in left ventricular ejection fraction (LVEF) are observed. Cell therapy offers a promising approach for regeneration of damaged vascular and cardiac tissue after acute myocardial infarction (MI) [4–8]. The Amorcyte trial evaluated effect of autologous bone marrow derived CD34+ cell therapy on LVEF and myocardial perfusion [9]. Significant improvement in myocardial perfusion and a trend towards improvement in LV ejection fraction were reported. Because the changes seen in systolic function are modest and by design regional, the more sensitive myocardial strain techniques offer an attractive option for analyzing these results. Accordingly, we evaluated the feasibility of MRI-derived segmental analysis in patients treated with cell therapy following primary intervention for ST-segment elevation myocardial infarction (STEMI), using the feature tracking (FT) technique. The FT technique was previously validated for assessment against harmonic phase imaging (HARP) [10] and subsequently utilized for
Investigation of 95 variants identified in a genome-wide study for association with mortality after acute coronary syndrome
Thomas M Morgan, John A House, Sharon Cresci, Philip Jones, Hooman Allayee, Stanley L Hazen, Yesha Patel, Riyaz S Patel, Danny J Eapen, Salina P Waddy, Arshed A Quyyumi, Marcus E Kleber, Winfried M?rz, Bernhard R Winkelmann, Bernhard O Boehm, Harlan M Krumholz, John A Spertus
BMC Medical Genetics , 2011, DOI: 10.1186/1471-2350-12-127
Abstract: We examined 95 polymorphisms in 69 distinct gene regions identified in a GWAS for premature myocardial infarction for their association with post-ACS mortality among 811 whites recruited from university-affiliated hospitals in Kansas City, Missouri. We then sought replication of a positive genetic association in a large, racially diverse cohort of myocardial infarction patients (N = 2284) using Kaplan-Meier survival analyses and Cox regression to adjust for relevant covariates. Finally, we investigated the apparent association further in 6086 additional coronary artery disease patients.After Cox adjustment for other ACS risk factors, of 95 SNPs tested in 811 whites only the association with the rs6922269 in MTHFD1L was statistically significant, with a 2.6-fold mortality hazard (P = 0.007). The recessive A/A genotype was of borderline significance in an age- and race-adjusted analysis of the entire combined cohort (N = 3095; P = 0.052), but this finding was not confirmed in independent cohorts (N = 6086).We found no support for the hypothesis that the GWAS-identified variants in this study substantially alter the probability of post-ACS survival. Large-scale, collaborative, genome-wide studies may be required in order to detect genetic variants that are robustly associated with survival in patients with coronary artery disease.Genome-wide association studies (GWAS) have identified robust genetic associations in a variety of common diseases [1], including myocardial infarction (MI) [2-6]. The GWAS approach, with its emphasis on large sample sizes and inclusion of hundreds of thousands of genetic markers, has produced a degree of reproducibility that was generally lacking in earlier candidate gene studies of MI [7]. However, nine GWAS-identified genetic susceptibility markers, all meeting criteria for genome-wide statistical significance, collectively account for only 3% of the estimated heritability of early-onset myocardial infarction (MI), raising questions about t
Entanlement-Assisted Classical Capacity of Quantum Channels with Correlated Noise
Nigum Arshed,A. H. Toor
Physics , 2006, DOI: 10.1103/PhysRevA.73.014304
Abstract: We calculate the entanglement-assisted classical capacity of symmetric and asymmetric Pauli channels where two consecutive uses of the channels are correlated. It is evident from our study that in the presence of memory, a higher amount of classical information is transmitted over quantum channels if there exists prior entanglement as compared to product and entangled state coding.
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