Biography:
PURUSHARTH KUMAR SHARMA is the student of BDS 1st year at RAJASTHAN DENTAL COLLEGE affiliated to RAJASTHAN UNIVERSITY OF HEALTH SCIENCE .
Abstract:
This is a condition which affect our heart they are of may type such as heart attack heart failure CAD aorta disease and many more there are many other ways through which we can prevent this so my research work is on that how we can manage these fatal disease at there early stages so we can prevent the death of patient . or some ways to manage this disease and I think these ways are very helpful to people and some technique which person can do at there level it they get heart attack and some medicine which has less side effect and more response .
Keynote Forum
Mohammed Elmujtba
Ph.D
Keynote: Echocardiography Effectiveness In Improving Diagnostic Rheumatic Heart Disease Guidelines
Biography:
Acute Rheumatic fever (RF) is an inflammatory disease caused by autoimmune responses to bacterial infection, commonly by group A β hemolytic Streptococci(GAS). Many organs are usually involved, including the heart, joints, skin and the brain. Rheumatic Heart disease (RHD) damages one or more heart valves with recurrent episodes of the ARF (1, 2). RHD and RF are diseases of poverty, overcrowding, low access and inadequate provision of health services(3). One to 5 per 1000 children in school age of poor countries have RHD, with an increased percentages in Sub Saharan Africa(4). RHD remains one of the major causes of mortality and morbidity in poor countries and imposes a high responsibility on health care systems with narrowing budgets.
Abstract:
Acute Rhumatic fever (ARF) is an inflammatory disease caused by autoimmune responses to bacterial infection, commonly group A β hemolytic Streptococci (GAS). Many organs can be involved including the heart, joint, skin and the brain. Rhumatic heart disease damages one or more heart valves through recurrent episodes of ARF. RHD and RF are diseases of poverty interpreted in low access to and inadequately provided health services. One to 5 cases per 1000 population suffered from rheumatic heart disease particularly children at school age in poor countries as Sudan
Keynote Forum
Arianna Pahlavan
Professor
Keynote: Solving Heterogeneities in Defibrillation for a Vascular Remodel of the Heart
Biography:
Working with Professor Glimm at Stony Brook University, Arianna Pahlavan was able to elucidate anatomical cardiac geometries for the first-ever efficacious vascular remodel of the human heart—a step necessary for the implication of painless defibrillation therapy in hospitals. She spent much of her time debugging tens of thousands of lines of code, in which Arianna’s solutions were often met with more debugging challenges. She savored the challenging and almost addictive cycle. These accomplishments helped Arianna to further define her career ambitions, and both came directly as rewards for her hard work and academic enthusiasm.
Abstract:
Acute cardiac arrhythmias are the main cause of death in industrialized countries; despite clinical importance, the mechanisms behind the onset and dynamics of cardiac arrhythmias are still poorly understood. The purpose of this work is twofold: (1) determine how smaller blood vessel radii affect the moving wave-front velocity, virtual electrode (VE) formation, and transmembrane potential induced by a shock (2) to elucidate a minimum radius correlative to shock strengths of interest. The model described here resolved tissue dynamics with a second-order solution to Poisson’s equation uniformly to boundaries. Through examining the role of small blood vessels, a minimum radius was identified at which a current will propagate, a range of 100-400µm. The velocity of the moving wave-front remained constant and no VEs form in the blood vessel region for all blood vessels below the size of the minimum radius. An alteration of fiber orientation, perpendicular to parallel, caused a twofold reduction in minimum radius. Blood vessels of radii 400µm do not affect the propagation of a 6V, 3V, 1.5V, .75V, and .33V induced shock strengths. Thus, 400µm blood vessels can be excluded in the first ever vascular mathematical model of the human heart at a feasible cost. An accurate anatomical model is needed to computationally verify the results of low energy antifibrillation pacing (LEAP) for the implication of painless defibrillation therapy in hospitals. The implementation of low energy automated defibrillators will save the US $1.1 trillion annually and universalize the CPR protocol for the minimization of anoxic encephalopathy. Future investigations may involve nanoparticles monitoring the cardiac ion channel currents and activating a painless electric shock where re-entry begins to occur, a potential solution to sudden cardiac arrhythmia death.
Keynote Forum
Duraid Al-Midfai
Ph.D
Keynote: Significant genetic association of a functional TFPI variant with circulating fibrinogen levels and coronary artery disease
Biography:
Dr. Duraid Al-Midfai considering the cardiovascular major for various reasons. Since I he was a child, he has been fascinated by the world around himself. When he traveled to China and Middle East, the conservation efforts of these two countries interested him and he knew that he wanted to do something related to the CAD disease in Genetics filed. He is currently a member of Fuwai Central China Cardiovascular Hospital As a post doctoral research in the cardio surgery department-in patient building as well as his work also collaborated with Henan Hospital in the Research Center building, which is a Big and famous hospital in central of china for cardiovascular disease treatment. A long-term goal of him, his goals is to one day manage and discover a novel genes associated with various diseases in human genome. Moreover, he is also curious to learn more about any medical field that is somehow related to genetics research.
Abstract:
The tissue factor pathway inhibitor (TFPI) gene encodes a protease inhibitor with a major role in regulation of blood coagulation. In this project, we performed a large population-based study with 2,313 study subjects for which blood coagulation data are available, including the Fg level, the PT level, the APTT level and the TT level. We selected a functional variant in the promoter of TFPI, rs10931292, which was found to reduce the transcription of TFPI and genotype it in the 2,313 study subjects using the TaqMan assay. We carried out the linear regression analysis under three different genetic models, including an additive model, an autosomal dominant model or an autosomal recessive model, for the genotyping data. Our analysis identified significant association of TFPI variant rs10931292 with increased plasma Fg levels (P=0.017 under a recessive model), but not with PT, APTT or TT (P>0.05). To the best of our knowledge, this is the first time to show that a TFPI variant is significantly associated with plasma Fg levels. These data identify a novel genetic variant for Fg levels and contributes importantly to the elucidation of the genetic basis and biological pathways for plasma Fg levels. An increased plasma Fg level is a well-established risk factor for cardiovascular disease. Therefore, we determined whether TFPI SNP rs10931292 was also associated with risk of CAD. Using a large case control association study population with 4,479 CAD patients and 3,628 controls, we identified significant association between TFPI SNP rs10931292 and CAD under a recessive genetic model (OR = 1.23, P = 0.005). Individuals with the GG/CC genotype had a significantly increased risk of CAD (OR = 1.23, P = 0.005). These data identify a new genetic variant that increases risk of CAD and contributes importantly to the elucidation of the genetic basis and biological pathways for the pathogenesis of CAD.