Biography:

Kevin Contrepois is an expert in metabolite profiling using LC-MS. He is the director of metabolomics and lipidomics in Pr. Michael Snyder laboratory at Stanford University, California, USA. By integrating multi-omics data sets, he is interested in the discovery of biomarkers and in understanding the pathogenesis of common diseases (i.e. diabetes, and cardiovascular disorders), with a special emphasis on host-gut microbiome interactions. He has published 9 peer-reviewed articles in top-tier journals (Nature Communications, Cell Systems, Cell Reports) that were cited 146 times. He received his Ph.D. from the University of Paris-Sud (France) in 2012.

Abstract:

Abstract (300 word limit)

Lack of physical activity (PA) has been identified as the fourth leading risk factor for global mortality (WHO, 2009) and a major contributor to disability from non-communicable diseases such as metabolic disorders (e.g., type 2 diabetes, T2D), cardiovascular, neurological diseases, and cancer. Conversely, PA has multiple physiological benefits (physically and mentally) and effectively prevents and treats non-communicable diseases. Despite undisputable evidence that regular PA has a profound beneficial impact, the molecular mechanisms by which PA promotes human health remains poorly understood and have not been characterized at a personalized level. In this context, we present an integrated Personal Omics Profiling (iPOP) for the comprehensive molecular profiling of blood-based analytes that we apply to track the molecular changes associated with exercise.

Multi-omic profiling (transcriptome, proteome, immunome, metabolome, and lipidome, etc.) revealed significant differences between prediabetics and healthy controls at rest, implicating pathways related to chronic inflammation and insulin regulation as well as novel connections to T2D. Participants went throught an acute bout of exercise (maximal cardiopulmonary exercise) that was followed by a dense sampling at 2 min, 15 min, 30 min, 1h, 2h, 4h, 6h and 24h post-exercise. The exercise perturbation was associated with a wealth of biomolecular changes spanning multiple omes that culminated at 15 min post-exercise including inflammation, glucose and energy metabolism. Interestingly, the omic response to exercise differed between prediabetics and healthy controls.

This study represents the most in-depth profiling of molecular changes associated with exercise and may offer new strategies for preventing and treating T2D.

Biography:

Kevin Contrepois is an expert in metabolite profiling using LC-MS. He is the director of metabolomics and lipidomics in Pr. Michael Snyder laboratory at Stanford University, California, USA. By integrating multi-omics data sets, he is interested in the discovery of biomarkers and in understanding the pathogenesis of common diseases (i.e. diabetes, and cardiovascular disorders), with a special emphasis on host-gut microbiome interactions. He has published 9 peer-reviewed articles in top-tier journals (Nature Communications, Cell Systems, Cell Reports) that were cited 146 times. He received his Ph.D. from the University of Paris-Sud (France) in 2012.

Abstract:

Lack of physical activity (PA) has been identified as the fourth leading risk factor for global mortality (WHO, 2009) and a major contributor to disability from non-communicable diseases such as metabolic disorders (e.g., type 2 diabetes, T2D), cardiovascular, neurological diseases, and cancer. Conversely, PA has multiple physiological benefits (physically and mentally) and effectively prevents and treats non-communicable diseases. Despite undisputable evidence that regular PA has a profound beneficial impact, the molecular mechanisms by which PA promotes human health remains poorly understood and have not been characterized at a personalized level. In this context, we present an integrated Personal Omics Profiling (iPOP) for the comprehensive molecular profiling of blood-based analytes that we apply to track the molecular changes associated with exercise.

Multi-omic profiling (transcriptome, proteome, immunome, metabolome, and lipidome, etc.) revealed significant differences between prediabetics and healthy controls at rest, implicating pathways related to chronic inflammation and insulin regulation as well as novel connections to T2D. Participants went throught an acute bout of exercise (maximal cardiopulmonary exercise) that was followed by a dense sampling at 2 min, 15 min, 30 min, 1h, 2h, 4h, 6h and 24h post-exercise. The exercise perturbation was associated with a wealth of biomolecular changes spanning multiple omes that culminated at 15 min post-exercise including inflammation, glucose and energy metabolism. Interestingly, the omic response to exercise differed between prediabetics and healthy controls.

This study represents the most in-depth profiling of molecular changes associated with exercise and may offer new strategies for preventing and treating T2D

Biography:

Anuri Shah is currently pursuing a fully funded Joint Ph.D. between The University of Hong Kong and King’s College London. Her doctoral thesis is aimed at understanding pathways involved in Parkinson’s disease and subsequently studying the protective effects of herbal medicine. Her expertise lies in cellular and animal models, coupled with molecular biology and metabolomics. She has a Masters in Pharmacology from the University of Southern California, where she also studied protein chemistry in the context of Parkinson’s disease.

 

Abstract:

Abstract

Parkinson’s disease (PD) is a debilitating neurodegenerative disorder, with no cure at present. An in-depth understanding of the pathology of PD will pave ways for effective treatment options. In recent years metabolomics has emerged as a powerful tool to identify biomarkers and mechanisms for a range of diseases. The aim of this study was to use systems metabolomics to identify changes in an in-vivo model of PD.

Male Sprague- Dawley rats were injected with the toxin 6-hydroxydopamine (6-OHDA) into the mid-brain, to induce Parkinsonism. Animals injected with saline were used as the control group. Two weeks after the injection, behaviour tests were carried out to assess motor dysfunction, followed by plasma and brain collection for untargeted metabolic profiling.

Palmitic acid (p = 1.76 x 10^-2, q = 3.72 x 10^-2, FC = 1.81) and stearic acid (p = 2.56 x 10^-2, q = 3.84 x 10^-2, FC = 2.15) were significantly upregulated in the plasma of the PD group, while mono-palmitin (p = 2.4 x 10^-2, q = 4.8 x 10^-2, FC = -11.7), mono-stearin (p = 3.1 x 10^-2, q = 3.72 x 10^-2, FC = -15.1)  and myo-inositol (p = 3.81 x 10^-2, q = 3.81 x 10^-2, FC = -3.32)  showed a significant imbalance in their mid-brains. Receiver operating characteristic (ROC) curves showed that all these metabolites had an area under the curve (AUC) of > 0.8, which indicates good prediction ability. Furthermore, the plasma metabolites were significantly correlated with the behaviour test scores.

These results show that plasma saturated free fatty acids and their mono-glycerides in the brain were associated with 6-OHDA induced toxicity. All these metabolites showed a good prediction ability. The plasma fatty acids also had a strong correlation with motor dysfunction, an integral symptoms of PD, suggestive of their potential as biomarkers.

Biography:

Prof. Dr. Anil Batta is presently Associate professor and senior consultant in Baba Farid University of Health Sciences/ Govt. Medical College, Amritsar, Punjab, India. He did his M.B.B.S. and M.D. in Medical Biochemistry from Govt. Medical College, Patiala in 1984 and 1991, respectively. His research interest is mainly in clinical application especially cancer and drug de-addiction. He has supervised more than 20 M.D., M.Sc. and Doctorate researches and published more than 70 international research papers. He is the chief editor of America’s Journal of Biochemistry. He is also working as advisor to the editorial board of International Journal of Biological and Medical Research. Recently, he has been deputed advisor to Pakistan Medical Journal of Biochemistry. He has been attached as technical advisor to various national and international conferences in Biochemistry. He has been attached as hi-tech endocrinal, genetics and automated labs of GGS Medical College, Faridkot. He has chaired various sessions in the Biochemistry meets.

Abstract:

Biochemical approach to diagnose myocardial infarction

Diagnostic criteria for AMI have classically been based on the triad of history, ECG and measurement of cardiac enzymes. The choice of 'cardiac enzymes' has been dictated by the evolution of laboratory techniques, commencing with measurement of aspartate transaminase and progressing to measurement of creatine kinase (CK) and its MB isoenzyme (CK-MB). Measurement of CK-MB has been shown by both clinical studies and rigorous statistical analysis to represent the best test for the diagnosis of AMI. Development of immunoassays for the cardiac troponins, i.e. cardiac troponin T (cTnT) and cardiac troponin (cTnI), has enhanced diagnostic specificity. These measurements are completely specific for cardiac damage, allow quantization of the extent of infarction and are diagnostically superior to CK-MB measurement. The majority require risk stratification into high- and low-risk groups. It is here that cardiac troponins have a major role. The measurement of cTnT has been shown in a large number of studies to enable risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification which can be completed by 24 h from admission, as well as allowing a safe discharge policy from the ED. Measurements of cardiac troponins can also be used to predict prognosis in patients with other diagnostic categories. Patients with cardiac failure can be risk stratified according to cTnT status. cTnT status on admission allows subdivision into high- and low-risk groups in patients presenting with ST segment elevation. Certainly, cTnT measurement can be incorporated into a clinical decision-making strategy to assign patients to investigation and management pathways. There is evidence that cTnT may be useful to guide therapeutic options. Improvements in diagnostic accuracy can reduce inappropriate long-term drug therapy. Finally, use of point-of-care testing (POCT) means that biochemical testing can be précised. It is important to establish as soon as possible whether patients who present with chest pain are having an acute myocardial infarction (AMI). Ideally, sensitive and specific serum myocardial markers could provide the basis for early detection as well as determine the status of reperfusion following thrombolytic therapy. In the ED study, CK-MB, myoglobin, and cTnI were equally sensitive (100%) for the detection of AMI in patients who presented 7.4-14 h after onset of chest pain. However, cTnI was the most specific serum marker (specificity 91.9% compared to CK-MB 85.6 %,).. Within the reperfused group, the relative increase of cTnT was greater than CK-MB. These findings show the clinical utility of cardiac-specific troponins as markers for the early detection of AMI and monitoring of reperfusion following thrombolytic therapy. The cardiac troponins, in particular, have become the cardiac markers of choice for patients with ACS. Indeed, cardiac troponin is central to the definition of acute myocardial infarction (MI) in the consensus guidelines. These changes were instituted following the introduction of increasingly sensitive and precise troponin assays.Note that cardiac markers are not necessary for the diagnosis of patients who present with ischemic chest pain and diagnostic ECGs with ST-segment elevation. These patients may be candidates for thrombolytic therapy or primary angioplasty. Treatment should not be delayed to wait for cardiac marker results, especially since the sensitivity is low in the first 6 hours after symptom onset. The objective of this study was to compare the levels of troponins and enzymes levels in myocardial infarction and skeletal muscle injury. This study was carried out in GGS Medical College & Hospital, Faridkot, Punjab and India. Fifty subjects selected were cases suffering from myocardial infarction. Fifty patients were selected as control. These were the persons who were healthy & accompanying the patients. Creatine kinase, aspartate amino-transferase, lactate dehydrogenase and Troponin T were determined by kit methods. Troponin I level rises significantly (p<0.01) in patients suffering from myocardial infarction. Creatine kinase (CK), CKMB, aspartate aminotransferase and lactate dehydrogenase levels rises significantly (p<0.01) in disease group compared with controls. Troponin T is an early indicator of myocardial infarction and is superior to CKMB in diagnosis of myocardial injury. There is no increase in troponin T levels in skeletal muscle injury.