Biography:

Abstract:

Inhibitory S-nitrosylation of the deacetylase SIRT1 blocked EMT by Honokiol and inhibited gastriccancer peritoneal dissemination
The epithelial-to-mesenchymal transition (EMT) may play a key role in tumor peritoneal dissemination of epithelial tumors that involves loss of cell -- cell adhesion and increased cell mobility; however, the molecular mechanisms underlying PTM by S-nitrosylation modulates signal transduction are not fully elucidated. We previously reported that Honokiol preferentially evoked ER stress-calpain activity and degrades COX-2 via AhR cleavage. The expression of silent information regulator 1 (SIRT1) has been reported to predict poor
survival, associated with the clinical features and prognosis of patients with gastric cancer. Herein, we propose a novel mechanism through which the inhibitory S-nitrosylation of the deacetylase SIRT1 by Honokiol
regulates EMT in gastric cancer cells through interfere with the EMT reducing transcription factor Slug.Importantly, we found that Honokiol specifically reduced iNOS and induced eNOS enzymatic activity and protein expression. eNOS drive nitrosylation of Sirt1. Honokiol-induced S-nitrosylation of the deacetylase SIRT1 by direct methods analyzed by LC/MS/MS using ESI quadrupole time of flight (QTOF) mass
spectrometry and biotin-switch technique. In addition, over-expression of SIRT1 in gastric epithelial cells disrupts the epithelial morphology concomitant with decreased expression of the epithelial marker, E-cadherin,
and increased expression of mesenchymal markers. In contrast, exposure to Honokiol or silencing SIRT1 in metastatic gastric tumor cells restores cell -- cell adhesion and induces a shift toward an epithelial morphology
concomitant with increased expression of E-cadherin and decreased expression of mesenchymal markers. We also found that SIRT1 has a physiologically relevant role in endogenous EMT induced by kynurenine (KYN)
signaling in gastric cancer cells. We propose that the regulation of EMT by SIRT1 involves modulation of,and cooperation with, the EMT inducing transcription factor Slug. Specifically, we show that SIRT1 silencing
reduces expression of Slug and that SIRT1 is recruited to the E-cadherin proximal promoter by Slug to deacetylate histone H3 and to reduce binding of RNA polymerase II, ultimately suppressing E-cadherin
transcription. We thus identify a necessary role for Slug in SIRT1-mediated EMT. Finally, we show that Snitrosylation of the SIRT1 or reduction of SIRT1 decreases gastric cancer cell migration in vitro and metastasis
in vivo in immunodeficient mice, which is largely independent of any general effects of SIRT1 on cancer growth and survival. We therefore identify SIRT1 as a positive regulator of EMT and metastatic growth of
gastric cancer cells and our findings implicate S-nitrosylation of the SIRT1 by Honokiol as a potential therapeutic target to reverse EMT and to prevent gastric cancer progression.

Biography:

To be updated soon

Abstract:

Abstract

Preeclampsia is defined as hypertension associated with proteinuria arising de novo after the 20^th week of gestation in a previously normotensive woman and resolving completely by the 6^th postpartum week. It is a major cause of morbidity and mortality during pregnancy. In UK, preeclampsia affects 3-5% of pregnancies. Its aetiology remains incompletely understood, and is considered as a disease of theories. One of these theories refers to the effect of heavy metals, trace, and ultra trace elements in the corresponding patients. In the present study some trace and ultra trace elements were estimated to identity  their role in the pathogenesis of pre-eclampsia. This study was carried out in Babylon Teaching Hospital for Gynecology and Pediatrics, in Babylon Province, Hilla City. All samples were collected from November 2014 till February 2015. This is a case control study which included 120 women, sixty were patients diagnosed with preeclampsia in the third trimester and the other sixty were healthy pregnant women (controls) in the third trimester. Cases with age over 40, BMI > 30, previous history of  pre-eclampsia, family history of  pre-eclampsia, multiple pregnancy and hydrops fetalis, pre-existing hypertension or renal disease, pre-existing vascular disease,  antiphospholipid syndrome, and smoking were excluded. Serum levels of iron, zinc, magnesium were measured by using a colorimetric method,  while serum concentrations of copper, chromium, cobalt, manganese, molybdenum, and selenium were measured by using graphite furnace atomic absorption spectrophotometric technique.

The results were expressed as mean ± standard error of mean. T-test and the linear regression analysis were used for the determination of the level of significance. Statistical analysis were performed with Statistical Package for the Social Sciences (SPSS) version 21.0 software. A P value of < 0.05 was considered to be statistically significant.

Serum total iron level was significantly higher in patients with pre-eclampsia compared to control group (186.498 µg/dl versus 94.392 ,            P value < 0.05). While no significant difference was found in molybdenum level between them (2.304 µg/dl versus 2.670, P value ˃ 0.05).  Finally,  serum total concentrations of the other elements were significantly lower in patients with pre-eclampsia compared to control group as illustrated below:

• Copper (143.153 µg/dl versus 209.657 µg/dl, P value < 0.05)
• Chromium (0.382 µg/dl versus 0.678 µg/dl, P value < 0.05)
• Cobalt (0.143 µg/dl versus 0.330 µg/dl, P value < 0.05)
• Magnesium (2.115 mg/dl versus 2.456 mg/dl, P value < 0.05)
• Manganese (7.617 µg/dl versus 10.847 µg/dl, P value < 0.05)
• Selenium (2.546 µg/dl versus 4.306 µg/dl, P value < 0.05)
• Zinc (57.283 µg/dl versus 87.535 µg/dl, P value < 0.05).

In conclusion, alteration in the levels of serum trace and ultra trace elements could contribute to the pathogenesis of pre-eclampsia.

Biography:

Ya-Ju Hsieh has her expertise in mass spectrometry of metabolomics and proteomics analysis. Her study is major in using quantitative metabolomics profiling approaches to investigate urine samples of cardio surgery patients with or without cardioplegia treatment. The platform was developed by Prof. Liang Li from University of Alberta, Canada, which is based on modified metabolites with dansyl group which can efficiently improve the ionization efficiency of metabolites for 1~3 orders. Using this method, we detected
more than 14,000 metabolites from 100 samples which provides systemic analysis of metabolomicsalteration. This method was focused on metabolites with amine and phenol  functional groups, and the platform to label alcohol, aldehyde and acid are still working on.

Abstract:

The discovery of Bretschneider’s histidine-tryptophan-ketoglutarate (HTK) cardioplegia solution had been one of major advancement in cardiac surgery to offer myocardial protection. However, metabolic alteration of these additive in the whole body has not been systematically investigated. Using non-targeted mass spectrometry-based method, the deep urinary metabolome may provide a systemic view of metabolic shifts in patients receiving HTK. Prospective urine samples were collected from 100 patients underwent cardiac surgery and the metabolomic changes were profiled by a high-performance chemical isotope labeling liquid chromatography (LC-MS) method. Over 14642 metabolites were quantified using differential 13C-/12C-dansyl labeling LC-MS, which targeting the amine/phenol submetabolome from the urine specimens. We identified 285 significantly differential metabolites (fold change more than 5) and assembled several potential metabolic pathway map derived from dysregulated metabolite hits. Our data indicated an up-expressed histidine metabolism with subsequent increased glutamine/glutamate metabolism, altered purine and pyrimidine metabolism, and up-expressed vitamin B6 metabolism in patients receiving HTK. Such information provides solid evidence outlining the shift in metabolic pathways and establishes a basis for further study regarding the key mechanisms of HTK solution in organ protection or potential harm.

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:

Dr. Joseph Fomusi Ndisang is an Associate Professor in the University of Saskatchewan College of Medicine, Department of Physiology. He received postdoctoral training in Physiology at the University of Saskatchewan College of Medicine from 2000-2005. He obtained a PhD in Pharmacology & Toxicology from the University of Florence, Italy, 2000. He obtained a Doctor of Pharmacy degree from University of Florence, Italy in 1995. He has received several distinguished awards and distinctions including: (i) Fellow of the Canadian Cardiovascular Society (FCCS) in 2016,  (ii) Fellow of the American Heart Association (FAHA) in 2011; (iii) Fellow of the International College of Angiology (FICA) in 2007; (iv) Young Investigator Award by International College of Angiology (2007); (v) Young Investigator Award by the American Society of Pharmacology & Experimental Therapeutics-Division for Drug Discovery, Development & Regulatory Affairs (2005); (vi) Young Investigator Award by the Society of Experimental Biology and Medicine (2005); (vii) Caroline tum Suden/Frances A Hellebrandt Professional Opportunity Award for Meritorious Research by the American Physiological Society (2005); and (viii) Recognition Award for Meritorious Research by a Young Investigator by the American Physiological Society (2004).

Top 5% of cited authors in journals of Biology and Biochemistry in 2011, by Thomson-Reuters.

Currently, Dr. Ndisang is an Editor for Frontiers in Bioscience (impact factor 3.8) and Executive Guest Editor for Current Medicinal Chemistry (impact factor 3.7) He has published more than 64-full length manuscripts in peer-reviewed journals and more than 80 abstracts. Dr. Ndisang has served as external PhD examiner for several universities in Canada, has given more than 30-invited talks, and has also served as peer-reviewer for several reputed journals and granting agencies in United States, United Kingdom, Canada, New Zealand and Poland.

Research Interest: His research is mainly focused on investigating the role of the heme oxygenase system in hypertension, diabetes (types-1 and -2), and obesity.

Abstract:

ABSTRACT

In diabetic subjects, dysfunctional insulin signaling and impaired glucose metabolism are associated with alterations and function of the heart and kidneys. We recently reported that upregulating heme-oxygenase (HO) potentiates insulin signaling and improve glucose metabolism in different animal models of type-1 and type-2 diabetes. Particularly, HO-inducers suppressed inflammatory/oxidative mediators such as cytokines (TNF-α, IL-6, IL-1β), chemokines (MCP-1, MIP-1α), macrophage-M1 infiltration, NF-κB, AP-1, AP-2, cJNk and 8-isoprostane but potentiated insulin-signaling proteins (IRS-1, GLUT4, PI3K, PKB) and reduced insulin/glucose intolerance. These were associated with reduced cardiac lesions (hypertrophy, collagen deposition in cardiomyocytes and left ventricular longitudinal muscle-fiber thickness) and renal lesions (glomerulosclerosis, tubular necrosis, tubular vacuolization, interstitial macrophage infiltration and pro-fibrotic/extracellular-matrix proteins like collagen and fibronectin that deplete nephrin, a protein which forms the scaffolding of the podocyte slit-diaphragm for filtration). Correspondingly, improved cardiac hemodynamics and reduced proteinuria was observed suggesting improved cardiac and renal functions.

 These data suggest that HO may be explored in the search for novel and effective remedies against cardio-renal complications

Biography:

Dr. Ali Alanazi has an extensive background in Biomedical engineering in Saudi Arabia and Japan, as a researcher, trainer, and organizer of biomedical engineering programs implementation.

In addition, skilled in management, development, implementation of new programs; train and supervise biomedical engineers in planning, maintenance, and inventory systems for newly installed equipment and instrumentation

Abstract:

Medical Application of Diamond like Carbon (DLC) Coating

Artificial heart forms a specific intervention that can be used for treating various heart diseases. Silicon oil is used as a pillar for the artificial heart. However, certain problems may arise with the silicon oil ions as they diffuse with the blood through ion penetration. There are seven various forms of Diamond like Carbon (DLC). All forms have a high value of sp3 hybridized carbon atoms. DLC can be found in more than one types primarily because the diamond is produced in two different crystalline poly-types. DLC coatings exhibit great combination chemical, mechanical, and electrical properties. As compared to the conventional hard coatings, they can be produced at very low temperatures without compromising its hardness. The study examined use of micro-hardness tester, the AFM, and the DLC films deposited because of R.F. plasma discharge. It is apparent that the roughness and hardness of films depend upon the bias voltage provided to the substrates and upon the pressure exerted on the deposition chamber. Artificial hearts contain power adapter, blood type diaphragm, two oval pumps, and multiple electronic modules. The power adapter plays an important role in delivering hydraulic silicone oil into the blood as it is pumped through a pair of oil channels. The rotating pulse of silicone oil makes circulation more flexible. Use of planar electrodes form the most popular method of operation while the RF plasma are used. It, therefore, is not easy to uniformly deposit the DLC film upon the surfaces of insulator material especially when a three-dimensional shape is used. DLC films are used for coating ellipsoidal diaphragm (polyurethane elastomer) and yet forms an influential biomaterial for functioning of the artificial hearts. Such coatings are done to prevent penetration of the hydraulic silicone oil to blood through the diaphragm.

Biography:

Prof. Hari Misra is currently Head, Molecular Biology Division, Bhabha Atomic Research Centre, Mumbai, India. For last 27 years, Dr Misra has been working on molecular and cellular responses of bacteria to both oxidative stress and DNA damage effects of gamma radiation. He has identified a novel antioxidant / radioprotector, which is found to be a ubiquitous response regulator from one of the most radioresistant bacterium, Deinococcus radiodurans. Catching tail of this molecule, his group discovered a new type of DNA damage response mechanism that seems to be an alternative to the missing classical LexA/RecA type SOS response in this bacterium. Dr. Misra’s current research interests are “Bacterial Genome Biology, Molecular and Cellular responses to oxidative stress and DNA damage, Molecular Genetics and structure-function of proteins, Metabolic engineering and antioxidant / radioprotector / redox biology. Dr Misra has published ~70 research papers in national and international journals of very high repute, with an aggregate IF ~198 and SCI >1000 (Scopus) and >1400 (Goggle scholar). For these contributions, Dr Misra is bestowed with a number of national /international recognitions / awards like “Indian Science Congress- Platinum Jubilee Lecture Award, Homi Bhabha Science and Technology Award, Sarma Memorial Award, DAE Science and Technology Excellence Award, INS Young Scientist Award”. He is elected member of “Guha Research Conference”. Dr Misra is a fellow of National Academy of Sciences, India (FNASc) and Maharashtra Academy of Sciences (FMASc) and Fulbright-Nehru Senior Fellow. Dr Misra has been visiting Scientist/Professor to Harvard Medical School Boston, UTSW-MC Dallas, LSU, Baton Rogue, Zhijiang University China and Korean Atomic Energy Research Institute, Republic of South Korea. He is a Member of BoS and Ph.D. thesis examiner to a number of highly reputed institutions in India. Dr Misra is a member of the American Society of Biochemistry and Molecular Biology (ASBMB), American Society of Microbiologists (ASM), Society of Biological Chemists of India, Association of Microbiologists of India, Environmental Mutagenic Society of India., Indian Society of Cell Biology and Indian Nuclear Society, and has been office bearers of academic societies in India.

Abstract:

To be updated soon

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.