3^rd International Conference on Predictive, Preventive and Personalized Medicine & Molecular Diagnostics September 01-03, 2015 Valencia, Spain

Biography:

Vincent S. Gallicchio has 42 years experience in academic medicine and research covering experimental hematology, immunology, and developmental therapeutics for human diseases such as AIDS and cancer. He has earned national and international respect and recognition for his efforts. In a first time study reporting on academic scholarly productivity in the Journal of Clinical Laboratory Science, Gallicchio was rated the number one academic biomedical laboratory science researcher in the United States. In addition to his passion for research, Gallicchio is equally passionate to teach, mentor and advise students. He has mentored many doctoral and post-doctoral students, dozens of master’s level students and hundreds of undergraduate students both foreign and domestic, many of whom are now esteemed researchers themselves at institutions such as: Oxford University, Eastern Kentucky University, University of Cincinnati, University of Florida, University of Kentucky, University of Limpopo (South Africa), Jewish and Mercy Hospitals in Cincinnati and major pharmaceutical companies such as Procter & Gamble and Johnson & Johnson. As a board certified medical laboratory scientist by the American Society of Clinical Pathology (ASCP), Gallicchio also serves as the Clinical Laboratory Director of the Lab Tree Clinical Biochemical Research Laboratory in Greenville, SC. He also serves as a consultant to Minerals Resources International, Inc on matters related to the health benefits of trace elements; and is a consulting Vice-President of Technology Development for Conversion Laboratories, LLC, and West Columbia, SC. He has served on the faculty and academic staff at the Yale University School of Medicine, the University of Kentucky Medical Center, the University of Central Lancashire (England) and the University of Wolver hampton (England). He has served as President of Alpha Eta Honor Society, the International Society for Lithium Research, International Federation of Biomedical Laboratory Science and currently serves as Vice President of the Educational and Research Centers in Trace Elements program operated under the auspice of UNESCO.

Abstract:

Lithium (Li) salts have been widely used in psychiatry as mood stabilizing agents for 60 years. Li found in variable amounts in foods, especially grains, vegetables, and in some areas, the drinking water provides a significant source of the element. Therefore, dietary intake in humans depends on location, type of foods consumed, and fluid intake. Traces of Li have been detected in human organs and tissues, leading speculation that the element was responsible for specific functions in the human body. It was not until the 20th century that studies performed in the 1970’s and 1990’s, primarily in rats and goats, maintained on Li-deficient diets demonstrated higher mortality, altered reproductive and behavioral abnormalities. Such deficiencies have not been detected in humans; however, studies performed on populations living in areas with low Li levels in water sup- plies have been associated with higher rates of suicides, homicides, and the arrests rate for drug abuse and other crimes. Li appears to play a significant role in early fetal development as evidenced by high Li levels during the early gestational period. Biochemically, the mechanism of Li action involves multi- factor and interconnected pathways with enzymes, hormones, vitamins, and growth and transforming factors. This body of evidence now appears sufficient to label Li as an essential element with the recommended RDA for a 70 kg adult of 1000 mg/day. Of extreme importance for the future is the growing body of evidence indicating Li can be used effectively for the treatment of acute brain injuries, e.g., ischemia and chronic neurodegenerative dis- eases such as Alzheimer’s disease, Parkinson’s disease, Tauopathies, and Huntington’s disease. This conclusion is based upon evidence showing Li as important in neurogenesis as well as protecting neurons from neurotoxicity. Li influences stem cells, both neuronal and marrow derived, thus additional therapeutic implications for this element in clinical medicine to treat disorders associated with the faulty production of blood and nerve cells or as a tool to enhance blood stem cell mobilization for transplantation.

Biography:

Mohamed Abdulla Primary care center, Olofström, Sweden 6th International Conference on Fermented Foods, Health and Social Well-being Anand Agricultural college, Anand, India December 6-7, 2013

Abstract:

MAIN TOPICS TO DISCUSS Diet and aging Diet, gut flora and health Diet and chronic diseases Diet, gut flora and social well-being

Biography:

Vincent S. Gallicchio has 42 years experience in academic medicine and research covering experimental hematology, immunology, and developmental therapeutics for human diseases such as AIDS and cancer. He has earned national and international respect and recognition for his efforts. In a first time study reporting on academic scholarly productivity in the Journal of Clinical Laboratory Science, Gallicchio was rated the number one academic biomedical laboratory science researcher in the United States. In addition to his passion for research, Gallicchio is equally passionate to teach, mentor and advise students. He has mentored many doctoral and post-doctoral students, dozens of master’s level students and hundreds of undergraduate students both foreign and domestic, many of whom are now esteemed researchers themselves at institutions such as: Oxford University, Eastern Kentucky University, University of Cincinnati, University of Florida, University of Kentucky, University of Limpopo (South Africa), Jewish and Mercy Hospitals in Cincinnati and major pharmaceutical companies such as Procter & Gamble and Johnson & Johnson. As a board certified medical laboratory scientist by the American Society of Clinical Pathology (ASCP), Gallicchio also serves as the Clinical Laboratory Director of the Lab Tree Clinical Biochemical Research Laboratory in Greenville, SC. He also serves as a consultant to Minerals Resources International, Inc on matters related to the health benefits of trace elements; and is a consulting Vice-President of Technology Development for Conversion Laboratories, LLC, and West Columbia, SC. He has served on the faculty and academic staff at the Yale University School of Medicine, the University of Kentucky Medical Center, the University of Central Lancashire (England) and the University of Wolver hampton (England). He has served as President of Alpha Eta Honor Society, the International Society for Lithium Research, International Federation of Biomedical Laboratory Science and currently serves as Vice President of the Educational and Research Centers in Trace Elements program operated under the auspice of UNESCO.

Abstract:

Trace elements possess important therapeutic properties. First, binding to specific macromolecules (enzymes, nucleic acids, etc.) they influence important chemical and biological processes; second, they interact amongst themselves synergistically to amplify their individual reactions. Metals have been used therapeutically for hundreds of years. Use of metals in the treatment of human diseases began with discoveries with gold used initially in patients with tuberculosis followed by rheumatoid arthritis. Gold identified an immunological pathogenesis in the etiology of rheumatoid arthritis, thus metals may be efficacious in other human conditions that are immunological in etiology. The antineoplastic potential of metals was further disseminated by the development of less toxic compounds such as platinum. Third, metals in human cancers have increased their therapeutic effectiveness and increased the diversity of cancers responding to these treatments. Fourth, lithium use in clinical medicine revolutionized treating psychiatric mood disorders. Central to the biological action of lithium is its ability to influence brain and central nervous system chemistry, thereby providing spectacular results in the treatment of affective and other psychiatric mood disorders, in particular, suicide prevention. Discoveries defining alternative non-­‐psychiatric clinical use of lithium continue to intrigue clinical medicine based upon a key discovery demonstrating lithium can effectively influence stem cells. Halotherapy is using salt compounds as initial and maintenance therapy of human respiratory aliments. Used by the Greeks and Romans, halotherapy has existed for thousand of years. It is associated with the therapeutic effectiveness attributed to spas. Today halotherapy has gained resurgence with its use as personalized medicine in the treatment of human diseases.

Biography:

Ananda S. Prasad was born in Buxar, a small town in the state of Bihar, India. After graduation from high school, he joined Patna Science College, Patna University where he was top student in chemistry and received B.Sc degree with honors in mathematics. Prasad entered the Patna Medial College in Bihar, graduating there in 1951 with high distinction in physiology. In 1952 Prasad went to St. Paul’s Hospital, Dallas, Texas, for residency training in pathology, accompanied by his wife, who sought further training in obstetrics and gynecology. Contrary to the route taken by his classmates, Ananda Prasad decided not to seek Membership in the Royal College of Physicians (MRCP), England, and looked for additional training in the USA. He was accepted by Dr. C.J. Watson, a well known outstanding Professor of Medicine, for training in internal medicine at the University of Minnesota Medical School. He was trained at Minnesota to be a clinical scientist with research interests in calcium and magnesium metabolism. Thus began a lifelong interest in the metabolism of various elements, including zinc. Prasad then went to Iran at the invitation of Hobart A. Reimann, who had preceded Dr. Watson as Chief of Medicine in Minnesota, and was Chief of Medicine at the Nemazee Hospital of Pahlevi University in Shiraz, Iran. He was a personal friend of the Shah of Iran. Prasad left Iran in January 1961 and joined the department of Biochemistry and Medicine of Vanderbilt University under Dr. William J. Darby. Although Dr. Darby wanted Prasad to study porphyrin metabolism in Pellagra in Egypt, Prasad shared with Darby his speculation that zinc deficiency in the Middle East was prevalent and was responsible for widespread growth retardation. Darby approved plans to investigate zinc metabolism in growth-retarded subjects and Prasad was able to join the U.S. Naval Medical Research unit No.3 (NAMRU-3), in Egypt. Studies in Egypt showed that the growth retardation and gonadal hypofunction in these subjects were related to zinc deficiency. The anaemia was due to iron deficiency and responded to oral iron treatment. Ananda S. Prasad, M.D., Ph.D., has been at the WSU School of Medicine since 1963, when he took a position as director of the Division of Hematology. Dr. Prasad was appointed a Distinguished Professor of Medicine, Division of Hematology- Oncology, in 2000. Ananda Prasad has published over 300 papers and fifteen books. He was founding editor of two journals,American Journal of Hematology and Journal of Trace Elements in Experimental Medicine. Prasad has received much recognition for his contributions. These include AMA Goldberger Award, American College of Physicians Award for outstanding work in science as related to Medicine, Medal of Honor from Mayor of Lyon, France, First Raulin Award for pioneering research in zinc from International Society for Trace Elements Research in Humans (ISTERH), Robert H. Herman Award from American Society of Clinical Nutrition, Mastership from the American College of Physicians, inducted in the Heritage Hall of Fame, International Institute Foundation, Detroit, Michigan and Asian Academy Hall of Distinction Award, Washington, DC. Most importantly Prasad received the 2010 Prince Mahidol Award from Bangkok.

Abstract:

In the Middle East nearly 50 years ago we established the essentiality of zinc for human and documented for the first time occurrence of zinc deficiency in the villages of Iran and Egypt. During the past five decades we have witnessed tremendous advances in both clinical and basic science areas of zinc metabolism. Currently WHO estimates that nearly 2 billion subjects in the developing countries are zinc deficient and widespread growth retardation, immune dysfunction and cognitive impairment are related to zinc deficiency. Therapeutic use of zinc for treatment of acute diarrhea in infants and children in developing countries has saved millions of lives. Zinc is very effective in reducing the incidences of blindness in patients with age related macular degeneration (AMD). Zinc is an approved therapy for patients with Wilson’s disease. Zinc administration is effective in decreasing the incidences of infection in the elderly, patients with sickle cell disease and head and neck cancer patients. Zinc is a molecular signal for immune and neuronal cells. In our experimental model of human zinc deficiency we reported that measurement of zinc and ecto 5’ nucleotidase in lymphocytes, are sensitive indicators of zinc deficiency. Serum active thymulin and generation of Th1 cytokines, IL-2 and IFN-γ and their mRNAs are most sensitive indicators of acute zinc deficiency. We have now established a new method of zinc assay in nails and plasma by LIBS (laser induced background spectroscopy) technique which is simple, exportable and cost effective and is an excellent indictor of chronic human zinc deficiency.

Biography:

After medical studies at Aristotelian University in Greece, Constantin Polychronakos specialized in pediatric endocrinology in Canada and had post-doctoral research training at McGill University in Montreal, where he is now full professor in the Department of Paediatrics with cross-appointment in Human Genetics. He is credited with the discovery of the effect of the INS locus in the thymus in type 1 diabetes, with two of the first GWAS for type 1 and type 2 diabetes and one of the first uses of exon capture combined with NGS to elucidate the cause of a rare monogenic form of diabetes.

Abstract:

Background: Type 1 diabetes (T1D) is due to the autoimmune destruction of the pancreatic -cells. Autoantigen specificity is determined by the T-cell receptors (TCRs) of autoreactive lymphocytes but their characteristics are poorly understood. Next-generation sequencing now offers methodological possibilities for exploring the vast diversity of the somatically rearranged TCRs for possibilities of personalized diagnosis and intervention. Objective: To define the TCRs reactive to whole proinsulin, the most important T1D autoantigen. Methods: We examined T-cells from the peripheral blood of nine children with T1D and two normal controls, by proliferated in vitro after 12 days of activation with proinsulin and isolated by CFSE dye-dilution flow-sorting. TCRs were amplified from whole RNA by 5’RACE and amplicons sequenced on the Illumina miSeq with a 250x2 protocol. Beta-chain reads were analysed by a paired-end modification of the standard algorithm. Results: Response to proinsulin was highly polyclonal in the T1D patients but much fewer clones were seen in the two controls, where 29% and 80% of all proliferating clones had the same TCR (p=0.018, rank test). Interestingly, 562 out of the 5,446 clones that showed at least 20-fold expansion were “public”, i.e. exactly the same in different subjects. These clones tended to have a higher ratio of expansion (mean 123 vs. 103, p=0.04 Conclusion: TCR clonality of proinsulin specificities appears to distinguish cases from controls and, if confirmed, may be an important predictor of diabetes, and immune-progress biomarker. Definition of the main TCR clones in early pre-diabetes may provide opportunities for antigen-specific immunosuppression.

Biography:

María A. Pajares completed her PhD from the Universidad Complutense de Madrid (Spain) in 1986, and her postdoctoral studies from the Harvard Medical School (Boston, USA) in 1989. She is a Senior Research Scientist from the CSIC since 2006, where her own group works in the structure/function relationships that govern methionine metabolism in health and disease. She has authored more than 60 original papers in reputed international journals, she serves as referee for a large number of journals and several grant agencies and is now also serving as an Editorial Board member for the World Journal of Biological Chemistry.

Abstract:

The methionine cycle produces S-adenosylmethionine (AdoMet) the main methyl donor for cellular transmethylations, including several epigenetic modifications. Alterations in this pathway and specifically in the AdoMet synthesis by methionine adenosyltransferases (MATs) have been reported in a large variety of diseases, although most studies have been performed in liver. The enzymes involved, excluding methyltransferases, are oligomers that were classically consider cytoplasmic. Thus, the AdoMet synthesized in the cytoplasm was expected to be transported to other compartments as required, a hypothesis further sustained by identification of an AdoMet mitochondrial transporter. However, in the last decade several reports have shown that this is not the case for the cell nucleus, where most of these enzymes have been identified in very low quantities. Work of my laboratory has recently provided evidences showing nuclear accumulation of several proteins of the methionine cycle in two models of acute liver injury. Moreover, we demonstrated that the nucleocytoplasmic distribution is governed by the ratio between glutathione species (GSH/GSSG). In fact, the oxidative stress induced by D-galactosamine or acetaminophen produces opposite effects on MAT I/III isoenzymes according to the subcellular compartment examined. This opposite regulation leads to decreased AdoMet production in the cytoplasm, whereas the nuclear levels of active MAT I increase, as well as certain epigenetic methylations. Prevention by N-acetylcysteine administration did not avoid all the drug-induced changes. Hence, we propose that alterations in the subcellular localization pattern of several enzymes of this cycle show a potential as biomarkers of liver disease.

Biography:

Milos JENICEK, MD, Canadian citizen, is currently holding a position as Professor (Part-Time) at the Department of Clinical Epidemiology and Biostatistics, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada. He is also Professor Emeritus at the University of Montreal and he held also until recently an adjunct position of Professor at McGill University Faculty of Medicine, Montréal, Québec, Canada. In 2009, he was elected Fellow of The Royal Society of Medicine, London, UK. Born October 9, 1935 in Prague, Milos Jenicek received his undergraduate medical education at Charles University, Prague (MD, 1959), a graduate degree in 1965 (PhD) and later a postgraduate clinical training at McGill University Teaching Hospitals. He is a licentiate of the Medical Council of Canada (LMCC), a Fellow of the Royal College of Physicians and Surgeons of Canada (FRCPC, Preventive Medicine and Public Health), a specialist of the Province of Québec (CSPQ, santé communautaire/community health). He holds a regular permit to practice medicine in Ontario and Québec. He contributes to the evolution of epidemiology as a general method of objective reasoning and decision making in medicine. To further enhance his teaching and research, he has committed himself to short sabbaticals during which he visited Harvard and Johns Hopkins, Yale, North Carolina at Chapel Hill and Uniformed Services at Bethesda Universities. He also lectured and visited numerous institutions in Hong Kong, Singapore, Japan, South Korea, Portugal, Brazil, France and Switzerland. He has been a visiting professor to various universities and governments. Earlier in his career, three years of University teaching and field practice of preventive medicine and public health in North Africa (1965-1968) has given him valuable insight and understanding of the realities in this part of the world. During his term as Acting Chairman of the Department of Social and Preventive Medicine, University of Montreal (1988-1989), he founded the graduate program in Clinical Epidemiology at the University of Montreal, his core course being also part of the graduate program at McGill University. Until 1991, he was member of the Board of Examiners of the Medical Council of Canada (Committee on Preventive Medicine). In 2000, he was invited as External Examiner by the Kuwait University. Also, Milos Jenicek is a consultant to various national and international public and private bodies, Editorial Consultant for the Journal of Clinical Epidemiology and the Case Reports & Clinical Practice Review and Honorary Editorial Board Member of Evidence-Based Preventive Medicine. In addition to numerous scientific papers, Milos Jenicek has published fifteen textbooks: "Introduction to Epidemiology" (in French, 1975). "Epidemiology. Principles, techniques, applications" (in French with R. Cléroux, 1982, and in Spanish, 1987), "Clinical Epidemiology, Clinimetrics" (in French with R. Cléroux, 1985), and "Meta-Analysis in Medicine. Evaluation and Synthesis of Clinical and Epidemiological Information" (in French, 1987), by the James Lind Library recognized first textbook of meta-analysis in medicine. The "Epidemiology. The Logic of Modern Medicine" (EPIMED International,1995) was also published in Spanish (1996) and Japanese (1998). His sixth book, "Medical Casuistics. Proper Reporting of Clinical Cases" (in French, 1997) is again produced jointly by Canadian (EDISEM) and French (Maloine) publishers. The ”Clinical Case Reporting in Evidence-Based Medicine” (Butterworth Heinemann,1999) appears again as an expanded second edition in English (Arnold/Oxford University Press, 2001), Italian (2001), Korean (2002) and Japanese (2002). His “Foundations of Evidence-Based Medicine” was published in 2003 by Parthenon Publishing/CRC Press. The tenth, Evidence-Based Practice. Logic and Critical Thinking in Medicine” (with D Hitchcock) was released by the American Medical Association (AMA Press, 2005) as well as his “A Physician’s Self-Paced Guide to Critical Thinking” (AMA Press, 2006) and Fallacy-Free Reasoning in Medicine. Improving Communication and Decision Making in Research and Practice (AMA Press, 2009). His Medical Error and Harm. Understanding, Prevention, and Control was published by CRC Press/Taylor & Francis (2011). Followed A Primer on Clinical Experience in Medicine. Reasoning, Decision Making, and Communication in Health Sciences (CRC Press/Taylor & Francis, 2013) and Writing, Reading, and Understanding in Modern Health Sciences. Medical Articles and other Forms of Communication (CRC Press/Taylor & Francis, 2014). Current interests: Development of methodology and applications of logic, critical thinking, decision making and communication in health sciences, enhancement of evidence-based medicine and evidence-based public health, health policies and program evaluation, decision oriented (bedside) clinical research.

Abstract:

Modern health sciences and practice require both a solid grounding in the scientific method and attention to individuals who must benefit, and rightly so, from the best possible understanding and decision making about individuals and groups of individuals in clinical and community settings. Until now, evidence-based medicine has contributed mainly to the former, especially with regards to dealing with cause-effect relationships between noxious and beneficial factors affecting health as seen through sets of cases. Defining improved clinical expertise, patient values and patient circumstances must be approached with equally structured methodological rigor and practice, reproducible and evaluable in various prevailing settings of care. The current and rapidly developing interest in the attention given to individual patient characteristics, patient environment and type of care is created, developed and increasingly practiced by more than one entity: Patient-centered care, patient-centered medicine, personalized medicine, patient-centered health care. These fields all focus on individuals and very often with few or unique cases, but are they identical? A clinical-epidemiological and biostatistical approach to patient health problem solving is not enough. It must be expanded through qualitative research, case studies, clinical case reporting, broader ways of critical thinking and argumentation as well as through patient care ethics from a modern philosophy perspective in increasingly operational manners, forms, and techniques. Are these patient-focused entities equally well or better defined in their identity, objectives, practices and evaluation as pertains to their content, structure, and impact? Patient-centered care and medicine are complementary to evidence-based medicine. They are the trigger of care as well as the endpoint of evidence-based practice and its end-decision step in individual care. Their equal importance must be emphasized, understood and further justified. And then, what next?

Biography:

After qualifying in Medicine from the King George’s Medical College (now a University), Lucknow, India, I completed postgraduate training in Paediatrics with an MD. Since 1980 I have pursued a career in Medical Genetics in the UK. In 1990 I became a Diplomate of the American Board of Medical Genetics and later on elected a Fellow of the American College of Medical Genetics (FACMG). I serve as a Fellow of the main Royal Colleges- FRCP-London, FRCP-Ireland and FRCPCH- Paediatrics & Child Health. Visiting Professor to the Genomic Policy Research Unit, Faculty of Life Sciences and Education, the University of South Wales, UK. He is also the Adjunct Professor to the Public Health Epidemiology Unit at the Chinese Capital Medical University, Beijing, China and Visiting Professor to the Chettinad Health University, Chennai, India. Prior to my current appointment as Consultant in Clinical Genetics at the University Hospital of Wales, Cardiff, I have had several other NHS appointments in Sheffield, Oxford, Exeter and Nottingham. My current role includes clinical, teaching and research commitments along with professional duties including senior R&D roles in NHS Wales. As the lead Clinical Geneticist for the Multi-Disciplinary Inherited Cardiovascular Conditions service, I have devoted my professional time and skills in setting up a benchmark service supported by an active teaching and research programme. My current clinical and research interests are focused on sudden cardiac death, molecular studies in chronic heart failure and inherited arteriopathies (Marfan syndrome). The biennial Cardiff International Cardiovascular Genetic Symposium, that I organised and lead, is hugely popular and attracts the cardiology and genetic communities engaging in learning, sharing research and developing good clinical practice through active networking. In addition, I have actively contributed in major nation wide efforts for raising awareness and profile for clinical cardiovascular genetics and took a lead role in setting up the dedicated professional group (Association for Inherited Cardiac Conditions- AICC) that I continue to serve on the Council and as the Treasurer.

Abstract:

Cancer is a genetic disease at the cellular level leading to successive organ/ system structural and functional dysfunction. This fundamental concept has led to the ‘gene-molecule’ family basis of carcinogenesis leading to development of the ‘targeted molecular therapy’ and ‘stratified medicine’ approaches in clinical oncology. Designing and developing the new therapeutic approaches in clinical oncology require understanding of the complex molecular pathways involved in common cancers. This is often facilitated by the outcome of molecular genetic analyses in rare Mendelian cancer family syndromes. Investigations in dominantly inherited cancer predisposing disorders, for example tuberous sclerosis (TSC) and neurofibromatosis type 1 (NF1), have led to the identification of activated mTOR molecules as one of the major steps in carcinogenesis. Clinical trials using the potential mTOR inhibitors, for example Rapamycin & Sirolimus, have shown promising results in substantially limiting development and progression of TSC tumors (pulmonary lymphangiomas and renal cell cancers). The scope of mTOR inhibitors is extended to NF1 and other cancer predisposing syndromes sharing the mTOR molecular pathway. Several protein kinase inhibitors targeting epidermal growth factor receptors (EGFRs) are now licensed for treating various cancers. NICE recommends transtuzumab (Herceptin) with or without paclitaxel or docetaxel in HER2 positive early breast cancer and with cisplatin for metastatic gastric cancer. K-RAS mutation testing is recommended in sporadic and inherited colorectal cancer (CRC). Mutations in K-RAS are shown to have negative predictive power in CRC patients treated with Cetuximab and panitumumab, EGFR binding monoclonal antibodies, in combination with irinotecan for improved response rates. If the K-RAS mutation was present, the patient should not be offered cetuximab, avoiding additional toxicity and expense of cetuximab, Thus CRC patients with wild K-RAS gene might benefit from cetuximab or panitumumab. The non–small cell lung cancer (NSCLC) is the most common type of lung cancer with specific cellular characteristics and genetic constitution. Up to 7 percent of NSCLC have an abnormal version of the anaplastic lymphoma kinase (ALK) gene, most common among non-smokers and contribute to the growth of cancer cells. The most common drug for treating lung cancer, crizotinib (Xalkori) targets the protein produced by the abnormal ALK gene. Studies provide evidence for ALK-positive NSCLC show significant tumor shrinkage. FDA has now approved ALK gene test as a requirement for prescribing Xalkori in NSCLC. Patients with malignant melanoma, another common cancer among Caucasians, are likely to benefit from targeted approach using the mutation testing in the BRAF and c-kit-activating genes. The multiple kinase inhibitor, Sorafenib does not work in BRAF-mutated melanoma compared to good response of the second-generation PLX4720. Drugs that target BRAF may also be important in treating other tumours in which BRAF mutations are common including thyroid cancer (45%), ovarian cancer (10 %) and colorectal cancers (13 %). The practice of molecular stratification and targeted specific cancer pharmacotherapy has generated wide interest and rapid acceptance. This approach supports the concept of personalized therapy and is the basis of Stratified Medicine, a major revolution of clinical medicine in the genome era.

Biography:

Founder and Chief Executive Officer Global Genomics Group, LLC Richmond, VA June 1, 2012-Present Executive Vice President Chief Clinical Strategy Officer Health Diagnostic Laboratory, Inc. Richmond, VA August 1, 2012-Present Visiting Professor of Radiology and Cardiology Department of Radiology and Cardiology Stony Brook University Medical Center State University of New York Stony Brook, NY March 26, 2012-Present

Abstract:

Complex biological networks of atherosclerosis are largely unknown. Objective: The main objective of the Genetic Loci and the Burden of Atherosclerotic Lesions study is to assemble comprehensive biological networks of atherosclerosis using advanced cardiovascular imaging for phenotyping, a panomic approach to identify underlying genomic, proteomic, metabolomic, and lipidomic underpinnings, analyzed by systems biologyedriven bioinformatics. Methods: By design, this is a hypothesis-free unbiased discovery study collecting a large number of biologically related factors to examine biological associations between genomic, proteomic, metabolomic, lipidomic, and phenotypic factors of atherosclerosis. The Genetic Loci and the Burden of Atherosclerotic Lesions study (NCT01738828) is a prospective, multicenter, international observational study of atherosclerotic coronary artery disease. Approximately 7500 patients are enrolled and undergo nonecontrast-enhanced coronary calcium scanning by CT for the detection and quantification of coronary artery calcium, as well as coronary artery CT angiography for the detection and quantification of plaque, stenosis, and overall coronary artery disease burden. In addition, patients undergo whole genome sequencing, DNA methylation, whole bloodebased transcriptome sequencing, unbiased proteomics based on mass spectrometry, as well as metabolomics and lipidomics on a mass spectrometry platform. The study is analyzed in 3 subsequent phases, and each phase consists of a discovery cohort and an independent validation cohort. For the primary analysis, the primary phenotype will be the presence of any atherosclerotic plaque, as detected by cardiac CT. Additional phenotypic analyses will include per patient maximal luminal stenosis defined as 50% and 70% diameter stenosis. Single-omic and multi-omic associations will be examined for each phenotype; putative biomarkers will be assessed for association, calibration, discrimination, and reclassification.

Biography:

Dr Gayane Badalian-Very (MD, PhD) is a leading physician of the world and a Top Doctor. Dr. Badalian-Very has obtained her Medical degree from Semmelweis University and attended Harvard Medical School for a fellowship. During her fellowship trainingDr. Badalian-Very and her collaborators at Dana Farber Cancer Institute and Harvard Medical School had a breakthrough when they demonstrated that Langerhans cell histiocytosis -an orphan childhood disease which had an unknown etiology for the past two centuries since the disease was defined by Langerhans- is a neoplasia. Currently the primary research focuses of Dr. Badalian-Very are secondary hepatic tumors, where lack of effective treatment gets manifested in 6-12 months of overall survival of affected individuals. Dr. Badalian-Very is a prominent speaker in international meetings and conferences and she serves as board member in several scientific societies. Dr. Badalian-Very has received several awards and recognitions from International societies such as Histiocytosis Association, Leading Physician of the World, National Association of Distinguished Professionals, Executive of the Year and Who’s Who in America. Gaia Medical Diagnostics and Intervention (GMDI) was Founded by Dr. Badalian-Very where she serves as Chief Executive Officer. GMDI focuses on personalized medicine andcompanion diagnostics to promote the medicine of future.

Abstract:

Personalized medicine attempts to identify tailored treatment based on the susceptibility profile of each individual. Although this approach has generated much excitement, few personalized-medicine therapies have achieved high levels of clinical adoption. To personalized medicine, one needs robust diagnostics and a clear understanding of disease pathomechanism. We have observed four main obstacles to the advancement of personalized medicine: scientific challenges (a poor understanding of molecular mechanisms or a lack of molecular markers associated with some diseases, for instance), economic challenges (poorly aligned incentives and high cost of new medications), lack of outcome based data (a comprehensive study of cost effectiveness/health benefit of personalized medicine) and operational issues. Although economic challenges remain, the scientific shortcomings and operational issues now seem to be the biggest hurdle. Diagnostics/companion diagnostics is the key to personalized medicine, yet it is hard to identify which tests truly save costs and select effective responders. On the other hand experimental testing leads to fears that although individual tests may not be very expensive, the overall eventual costs could be unjustifiably high. A third concern is the difficulty of enforcing standard protocols to ensure that physicians follow through with appropriate patient care based on test results. Fourth, test information could be misused—particularly in the early stages of investigation and development—which could harm patients and payers. Finally, there is no longitudinal accounting, which would enable payers to capture long-term cost savings from near-term testing. Even if operational issues get resolved within a particular stakeholder group,overcoming the scientific burden and correcting the incentive structure and modifying the relationships between stakeholders could be more complex.

Biography:

Growing up in Tokyo, Munich, and Michigan, Dr Shinichiro Koga is now an attending physician in systems disorder section of Internal Medicine, an affiliate teaching hospital of The University of Tokyo, Japan. On his way from medical school student to board certifications in both Medicine and Pediatrics, he diagnosed several severe cases with single gene mutation: a mother whose frequent miscarriage has come from coagulation factor XIII deficiency 1); an asphyxia neonate whose mother was thereafter diagnosed as having myotonic dystrophy; then this time he reported genetic diagnosis, clinical relationship, and individual preventive eduction for a case with RHUC type 1. Thus Dr Koga has contributed to public health promotion with concentation to personalized medicine in gene mutation, clinical diagnosis, and molecular prevention. Graduate with MD, Yamagata University 2001; PhD, stem cell biology, Tohoku University 2007. MPH, Tokyo University 2014. Grant: Informatics, Mochida Foundation for Medical/Pharmaceutical Research 2009; Grant B, Japan-North America Medical Exchange Foundation 2009.

Abstract:

BACKGROUND: Hypouricemia has reported to a risk factor to develop cardiovascular event in men and women 1). In adults with renal hypouricemia (RHUC), excercise-induced acute kidney injury (EIAKI) is major commorbidity, but its prediction and prevention is not yet satisfied. Japanese RHUC frequently has mutation in exons 1 and 4 in urate transporter 1 (URAT1). In Japanese type 1 RHUC, W258X in exon 4 is the most frequent mutation that extincts urate transportation 2)3). CLINICAL PRESETATION: A healthy 33-year-old male consulted to primary care physician with chief complaint of epigastric dullness and anorexia 3 days after 1.2 miles anaerobic road race. He was immediately transferred to our institute because serum creatinin 3.6 mg/dL and blood urea nitrogen 33.7 mg/dL implied him acute kidney injury. As past medical history, he has received no further evaluation for hypertension from preschool age and serum hypouricemia in annual health check. No abnormality was shown in urine dipstick so far. No relevant medical history on his family. Abdominal US show no difference, atrophy, hydronephrosis, nor lithiasis. Contrast CAT imaging was not performed in acute phase. Hypouricemia was detected on admission, so EIAKI on RHUC was raised as clinical diagnosis. After admission, hydration 1,500-2,500mL/day was continued for 5 days and symptoms had dissappeared soon, but serum uric acid had linearly decreased from 2.4 mg/dL (FEUA 57.1%; day 1) to 1.0 mg/dL (54.8 %; day 10). Serum creatinine decreased gradually from 3.69 to 1.52 mg/dL so he discharged in day 10 of hospitalization after preventive education. MOLECULAR DIAGNOSIS: Peripheral blood on day 9 was subjected to URAT1/SLC22A12 exons 1 and 4 DNA sequence, as described elsewhere 4). No mutation was detected in exon 1. W258X homologous mutation was detected in exon 4 on URAT1 DNA; This is the causative gene mutation of RHUC type 1. Extracellular release and degradation pathways of this blunted protein has not reported. History and clinical course of patient was agree with genetic diagnosis described above. DISCUSSION: Having URAT1 DNA mutation, excercise, particularly anaerobic, generally need to have enough prerequisite water to prevent dehydration. Anaerobic exercise should avoid in having cold, or having antipyretics. Frequency of EIAKI recurrence is not well known in experienced patients with EIAKI. It has not yet shown whether antioxydatives (vitamin C, E) is effective for EIAKI prevention. REFERENCES: 1) Odden MC, et al. Am J Kidney Dis 2014;64:550-7. 2) Enomoto A, et al.Nature 2002;417:447-52. 3) Kamatani Y, et al. Nat Genet 2010;42:210-5. 4) Matsuo H, et al. Am J Hum Genet 2008;83:744-51.

Biography:

Dr. Giulio Maria Pasinetti is a Professor of Psychiatry, Professor of Neuroscience and Professor of Geriatrics and Adult Development, in the Department of Psychiatry at Mount Sinai School of Medicine, New York. Dr. Pasinetti graduated from Milan University School of Medicine in 1982, and he received his Ph.D. from the University of Milan in 1988. He joined the Mount Sinai School of Medicine's faculty in 1996 and has consistently maintained an outstanding record of excellence and exceptional productivity. Dr. Pasinetti is a recipient of several academic awards including the prestigious Zenith and Temple awards from the Alzheimer's Association. Most recently, Dr. Pasinetti was awarded ''The Faculty Council Award'' for academic excellence at Mount Sinai School of Medicine and "The Charles Dana Alliance for Brain Research Award" from Dana Foundation, recognizing productivity and the worldwide leadership in his field of expertise, which further emphasizes his standing as an academic role model. Dr. Pasinetti was also recently awarded with an NIH funded research grant supporting a ''Center of Excellence for Research in Complementary and Alternative Medicine in Alzheimer's disease,'' of which he is the Principal Investigator and Director. Dr. Pasinetti also serves as the Director of the Basic and Biomedical Research and Training Program, GRECC James J. Peters Veterans Affairs Medical Center at the Bronx VA.

Abstract:

The convergence of several unique features of Alzheimer’s disease (AD) [e.g., heterogeneity, complex polygenic etiology, and prolonged asymptomatic pre-clinical phase of neurodegeneration] indicates the need for very large cohorts of well-characterized populations from diverse genetic/cultural backgrounds as potential volunteers for both: 1) longitudinal epidemiological studies to discover and/or validate putative risk factors, and 2) clinical studies for prospective validation of potential preventive interventions. In addition, many epidemiological studies indicate that people with diabetes are at higher risk of eventually developing AD or other dementias. A massive longitudinal database involving at-risk populations is an essential infrastructure needed in order to address the future needs of a major prevention initiative. Along with ‘Big-Data’, the field of therapy development will require novel computational capabilities to not only sort out the complex interactions between type 2 diabetes(T2D) and cognitive deterioration in AD, but also to discover-validate technologies for the early and accurate detection of the disease.We used data from public genome-wide association studies (GWAS) to explore the associationsingle-nucleotide polymorphisms (SNPs) between T2D and AD. Next, we explored the function of the T2D-AD shared GWAS SNPs by integrating pathway data withgene ontology data, expressional quantitative trait loci (eQTL), and co-expression networks.We found a significant overlap (p=4.9E-19) between association SNPs from large scale GWAS of T2D and AD.927 SNPs were associated with both ADand T2D with p≤0.01, and we found that these SNPs influence 190 genes in brain tissue and 416 genes in T2D-relevant peripheral tissues (liver and adipose). Interestingly, we found that certain mitochondria pathways and innate immune response pathways are particularly enriched in the AD and T2D GWAS. Collectively, by leveraging GWAS, eQTLs, gene co-expression networks, etc., we found that T2D and AD share common genetic risk factors, which may partially explain the epidemiological observation of the disease incidence correlation. A massive longitudinal database on health aging and pre-dementia or at-risk populations, such as T2D subjects, is essential to address the future needs of a major prevention initiative in AD.

Biography:

Head the molecular Neuro-Oncology Laboratory in the Departments of Neurology and Oncology at the Hadassah-Hebrew University Medical Center. Completed her PhD at 1999. The main research interests of her Lab are in the field of molecular characteristics of brain tumors and personalized medicine for patients with brain tumors and neurodegenerative diseases. The results of her studies have been published in 28 scientific papers. Several of her findings have been patented and were shown to have clinical applications in terms of potential implementation in the development of new therapeutic approaches.

Abstract:

Identification of tumor-specific circulating miRNAs may offer biomarkers to evaluate prognosis and response to therapy in patients with the incurable tumor Glioblastoma (GBM). The salvage therapy for recurrent GBM who have failed the standard-of-care of radiation and temozolomide chemotherapy, is bevacizumab, a recombinant human monoclonal anti-VEGF antibody. We previously demonstrated that among others, four of the hypoxia-mediated-miRNAs (miR-210, miR-21, miR-10b and miR-196b), are up-regulated in gliomas as compared to normal brain. We hypothesized that the expression of these miRNAs will be altered in response to hypoxia following treatment with anti-angiogenic drug and might serve as circulating biomarkers to the drug efficiency. Thus we aimed to develop a strategy for a rapid, sensitive and noninvasive technique for monitoring anti-angiogenic therapy dynamics by analysis of circulating tumor-specific microRNAs. For that purpose the expression these miRNAs were evaluated by real-time-RT-PCR from circulating RNA that was collected longitudinally from 15 patients with GBM treated with bevacizumab. Radiographic evaluation was based on measurable changes in tumor dimensions using MRI by fluid-attenuated inversion recovery (FLAIR) and contrast enhanced T1-weighted images. The quantification of miR-10b and miR-21 were significantly negatively correlated to MRI measurements, especially to sum product contrast diameter (R=0.51/p=0.002; R=0.568/p<0.0001 respectively). There was even higher correlation between the quantification of both miRNA and the contrast measurements than the correlation of each of them separately ((R=-0.648/ p<0.0001). This non-invasive procedure may lead to the routine use of circulating micro-RNA as a strategy for a rapid, sensitive and noninvasive technique for monitoring anti-angiogenic therapy dynamics.

Biography:

1980 Ph.D Biochemistry Postgraduate Inst of Medical Education and Research, Chandigarh, India 1981 - 83 Postdoc Research Inst of Scripps Clinic, La Jolla, CA 1983 - 87 Res. Assoc Dept of Biochemistry, USC School of Medicine Los Angeles, CA 1987 - 88 Asst Prof Div. GI, Dept of Pediatrics, Children's Hosp Univ. of Cincinnati, Cincinnati, OH 1988 - 96 Assoc. Res. Sci Div GI, Dept of Pediatrics, Yale Univ. Sch Med. New Haven, CT 1996 -2010 Assoc. Prof. Dept of Pediatrics, Mount Sinai Sch. Med. New York, NY 2011 - to date Sen. Res Sci Div. of GI, Dept of Medicine, Yale Univ. Sch. Med New Haven, CT Over the last decades, my research has focused on the mechanisms of regulation of bile acid transporters in liver during development and in pathological situations such as the human liver disease cholestasis. My main focus over the last decade has been on the role of Nuclear Receptors (with specific reference to FXR) on the regulation of Bile salt export pump (BSEP) a canalicular transporter for bile acids in the hepatocytes. I have recently also explored the role of microRNAs (mIRs) in regulating bile salt transporters in liver in physiology and pathophysiology. Since the beginning of this year, I am conducting research into molecular mechanisms of regulation of Inositol 3-phosphate receptors (IP3Rs) that act as Ca-channels in the endoplasmic reticulum (ER) with specific focus on the promoters of the Type 2 and 3 isoforms and their regulation by microRNAs.

Abstract:

The type III isoform of the inositol 1,4,5-trisphosphate receptor (InsP3R3) is apically localized and triggers Ca2+ waves and secretion in a number of polarized epithelia. However, nothing is known about epigenetic regulation of this InsP3R isoform. We investigated miRNA regulation of InsP3R3 in primary bile duct epithelia (cholangiocytes) and in the H69 cholangiocyte cell line, because the role of InsP3R3 in cholangiocyte Ca2+ signaling and secretion is well established and because loss of InsP3R3 from cholangiocytes is responsible for the impairment in bile secretion that occurs in a number of liver diseases. Analysis of the 3’-UTR of human InsP3R3 mRNA revealed two highly conserved binding sites for miR-506. Transfection of miR-506 mimics into cell lines expressing InsP3R3-3’UTR-luciferase led to decreased reporter activity, while co-transfection with miR-506 inhibitors led to enhanced activity. Reporter activity was abrogated in isolated mutant proximal or distal miR-506 constructs in miR-506 transfected HEK293 cells. InsP3R3 protein levels were decreased by miR-506 mimics and increased by inhibitors, and InsP3R3 expression was markedly decreased in H69 cells stably transfected with miR506 relative to control cells. miR506-H69 cells exhibited a fibrotic signature. In situ hybridization revealed elevated miR506 expression in vivo in human diseased cholangiocytes. Histamine-induced, InsP3-mediated Ca2+ signals were decreased by 50% in stable-miR-506 cells compared to controls. Finally, InsP3R3-mediated fluid secretion was significantly decreased in isolated bile duct units (IBDU) transfected with miR-506, relative to control IBDU. Together, these data identify miR-506 as a regulator of InsP3R3 expression and of InsP3R3-mediated Ca2+ signaling and secretion.

Biography:

Vincent S. Gallicchio has 42 years experience in academic medicine and research covering experimental hematology, immunology, and developmental therapeutics for human diseases such as AIDS and cancer. He has earned national and international respect and recognition for his efforts. In a first time study reporting on academic scholarly productivity in the Journal of Clinical Laboratory Science, Gallicchio was rated the number one academic biomedical laboratory science researcher in the United States. In addition to his passion for research, Gallicchio is equally passionate to teach, mentor and advise students. He has mentored many doctoral and post-doctoral students, dozens of master’s level students and hundreds of undergraduate students both foreign and domestic, many of whom are now esteemed researchers themselves at institutions such as: Oxford University, Eastern Kentucky University, University of Cincinnati, University of Florida, University of Kentucky, University of Limpopo (South Africa), Jewish and Mercy Hospitals in Cincinnati and major pharmaceutical companies such as Procter & Gamble and Johnson & Johnson. As a board certified medical laboratory scientist by the American Society of Clinical Pathology (ASCP), Gallicchio also serves as the Clinical Laboratory Director of the Lab Tree Clinical Biochemical Research Laboratory in Greenville, SC. He also serves as a consultant to Minerals Resources International, Inc on matters related to the health benefits of trace elements; and is a consulting Vice-President of Technology Development for Conversion Laboratories, LLC, and West Columbia, SC. He has served on the faculty and academic staff at the Yale University School of Medicine, the University of Kentucky Medical Center, the University of Central Lancashire (England) and the University of Wolver hampton (England). He has served as President of Alpha Eta Honor Society, the International Society for Lithium Research, International Federation of Biomedical Laboratory Science and currently serves as Vice President of the Educational and Research Centers in Trace Elements program operated under the auspice of UNESCO.

Abstract:

Lithium (Li) salts have been widely used in psychiatry as mood stabilizing agents for 60 years. Li found in variable amounts in foods, especially grains, vegetables, and in some areas, the drinking water provides a significant source of the element. Therefore, dietary intake in humans depends on location, type of foods consumed, and fluid intake. Traces of Li have been detected in human organs and tissues, leading speculation that the element was responsible for specific functions in the human body. It was not until the 20th century that studies performed in the 1970’s and 1990’s, primarily in rats and goats, maintained on Li-deficient diets demonstrated higher mortality, altered reproductive and behavioral abnormalities. Such deficiencies have not been detected in humans; however, studies performed on populations living in areas with low Li levels in water sup- plies have been associated with higher rates of suicides, homicides, and the arrests rate for drug abuse and other crimes. Li appears to play a significant role in early fetal development as evidenced by high Li levels during the early gestational period. Biochemically, the mechanism of Li action involves multi- factor and interconnected pathways with enzymes, hormones, vitamins, and growth and transforming factors. This body of evidence now appears sufficient to label Li as an essential element with the recommended RDA for a 70 kg adult of 1000 mg/day. Of extreme importance for the future is the growing body of evidence indicating Li can be used effectively for the treatment of acute brain injuries, e.g., ischemia and chronic neurodegenerative dis- eases such as Alzheimer’s disease, Parkinson’s disease, Tauopathies, and Huntington’s disease. This conclusion is based upon evidence showing Li as important in neurogenesis as well as protecting neurons from neurotoxicity. Li influences stem cells, both neuronal and marrow derived, thus additional therapeutic implications for this element in clinical medicine to treat disorders associated with the faulty production of blood and nerve cells or as a tool to enhance blood stem cell mobilization for transplantation.

Biography:

Amosy E. M’Koma, M.D., M.S., Ph.D.

Abstract:

Mass spectrometry (MS) and imaging mass spectrometry (IMS) [1] are non-invasive technologies that can measure individual molecules in complex endoscopic and surgical clinical specimens [2,3]. These analyses provide quantitative and qualitative data about cellular systems, and can differentiate diseased from normal tissue, and can identify and differentiate diseases within the same organ [2-4]. These characteristics offer significant diagnostic and prognostic potential for clinical medicine and could supplement known clinicopathologic variables for delineating IC into UC or CC at a patient’s first clinical visit. Established techniques like MS and IMS, which are affordable, non-invasive, easier, accurate and faster at screening for potential delineation of IBD, ought to be considered for personalized medicine in clinical applications in IBD laboratories. Predicting the phenotypic outcomes of “indeterminate colitis” (IC), given its unpredictable clinical presentation and disease course, is challenging [5,6]. Inadequate differentiated diagnoses of the two predominantly colonic inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohn’s colitis (CC), may lead to the inconclusive IC diagnosis even when a state-of-the-art classification system of combined clinical, endoscopic, radiologic and histologic tools [5,6] are used. Unless there is a unique and yet unclassified class of colitis, the field needs to develop supplemental molecular biomarker tools for precise and rapid distinction between UC and CC for patients that will otherwise be diagnosed with IC. Previous studies using mucosal biopsy [7,8] have been successful as prognostic indicators for IBD whether the colitis is in a quiescent or active state, but have not been able to distinguish UC from CC [7,8]. Patients with IC are significantly younger at diagnosis (M±SEM, 9.53±4.8 years) [9-12] with onset of symptoms before the age of 18 years [13-17]. IC shows an equal gender distribution [12,18,19]. In contrast, UC is predominant among males and the mean age at onset is 36-39 years [18-22]. These figures have not changed over the past 3 decades despite the introduction of newer diagnostic modalities [5,6,9,14,15,17,23]. Even after long-term surveillance, a substantial number of patients with IC still have an unchanged diagnosis [9,23,24], with significant patient suffering in the interim [9,23,24]. The continued presence of an IC diagnosis over a long period of time supports part of our hypothesis that IBD may represent a spectrum of diseases rather than just two entities, Crohn’s disease (CD) and UC [25]. The need for IC classification into either UC or CC is important for proper care in patients suffering from IBD, with obvious therapeutic and prognostic implications [26]. Early and accurate diagnosis and sub-classification of UC and CC is therefore the cornerstone for personalized and evidence-based interventional care [27-29]. These two pathologies have differing therapeutic strategies and prognoses. Most patients with UC, or IC likely to develop UC [26], will require pouch surgery for resolution [30-34]. Pouch surgery is well-established [26] and restores gut continuity, defecation, deferral, and discrimination, but is only successful if the UC and/or IC likely to develop UC diagnosis is correct [35,36]. However, IC and UC are mistakenly diagnosed in patients with CC [5,37]. Current data show that 15% of IBD patients who undergo pouch surgery for presumed definitive UC (or IC likely to develop UC) subsequently are diagnosed with de novo Crohn’s disease (CD) in the ileal pouch [38,39]. Identifying patients with CC and positive outcomes after pouch surgery is a painstaking clinical experience [4,38,39]. Ileal pouch anal anastomosis (IPAA) is acceptable standard care for UC patients, and restorative proctocolectomy (RPC) should be contraindicated for CC patients [4,40,41]. Pouch complications are significantly higher in patients with CC (+/- 64%) and IC (+/- 43%) vs. patients having UC (+/- 22%) (p< 0.05) [27,42,43]. This diagnostic dilemma holds potential morbidity from unnecessary and/or inappropriate surgery, and underscores the need for a research strategy focused on developing molecular biometrics to improve diagnosis of colitides at initial endoscopic biopsy [1-3,44,45. De novo CD in the ileal pouch is the diagnosis most feared by IBD patients and doctors due to its intractable nature and associated complications which often necessitate excision of the pouch with a permanent end-ileostomy [46-50]. The proteomic patterns can shed new light for the differential diagnosis in IBD, better reflecting diverse disease phenotype to avoid complications, misdiagnoses and unwanted surgeries.

Biography:

After finishing med school, Wendy Onstenk started working at the Laboratory of Translational Cancer Genomics and Proteomics, workgroup circulating tumor cells, at the Erasmus MC Cancer Institute. This workgroup has a long standing track record in the identification of prognostic gene signatures on the one hand and detection of rare cell populations in the circulation on the other hand. The combined expertise has resulted in several important publications in the field of CTC enumeration and characterization. Also, different multicenter clinical trials in metastatic breast, prostate, colon cancer, and bladder cancer and mesothelioma are still running.

Abstract:

A Circulating tumor cells (CTCs) count is a strong established prognostic factor in both primary and metastatic breast cancer (MBC). Moreover, characterization of CTCs is expected to become an invaluable tool to predict treatment response and personalize cancer treatments. Shed from different tumor lesions into the circulation, CTCs may provide a comprehensive view of metastatic tumor cell characteristics at a certain time-point, including inter- and intratumoral heterogeneity. Obtained through a simple venipuncture, CTCs could this way serve as a “liquid biopsy”. However, isolation and subsequent characterization of CTCs is technically extremely challenging, mainly due to the small number of cells amidst a large majority of leukocytes. A wide range of assays has been developed, but only the CellSearch System® (Veridex, Raritan, NJ, USA) has obtained FDA approval for CTC enumeration so far. For characterization purposes, no assay has been validated at all. Still, different studies already investigate the predictive value of the expression of ER and HER2 on CTCs. We developed a robust method to measure the expression of up to 96 genes in CTCs, including HER2 and ER, and have this way set up gene expression profiles to discriminate patients with <5 CTCs in a good and intermediate prognosis group. Also, we have developed a profile to predict resistance to aromatase inhibitors. Lastly, we have shown that CTCs differ from the primary tumor in approximately half of the MBC patients, suggesting evolution in tumor characteristics and the value of CTCs as liquid biopsy.

Biography:

Technological advancements in the molecular characterization of cancers have enabled researchers to identify an increasing number of key molecular drivers of cancer progression. These discoveries have led to multiple novel anticancer therapeutics, and clinical benefit in selected patient populations. Despite this, the identification of clinically relevant predictive biomarkers of response continues to lag behind. In this presentation, strategies for the molecular characterization of cancers and the importance of biomarkers for the development of novel antitumor therapeutics are discussed. We also review critical successes and failures in oncology, as well as the lessons learnt, which may aid in the acceleration of anticancer drug development and biomarker discovery are reviewed.

Abstract:

Dr Timothy Yap is a NIHR BRC Clinician Scientist and Consultant in Medical Oncology at the Royal Marsden Hospital and The Institute of Cancer Research in London, UK. He is based in in the Drug Development and Lung Cancer Units, and Cancer Biomarkers Laboratory Group. His research includes the first-in-human development of molecularly targeted agents and their acceleration through clinical studies using novel predictive and pharmacodynamic biomarkers. Dr Yap is Principal Investigator for clinical trials evaluating novel strategies for targeting the DNA damage response in lung and other cancers, such as PARP inhibitors, as well as the blockade of signaling pathways, with a focus on PI3K/AKT inhibitors. He is Lead Investigator for the AZD5363 AKT inhibitor arm of the National Lung Matrix Trial. His laboratory interests include the development of tumours, plasma DNA and circulating tumour cells as predictive biomarkers in clinical trials. He has published widely in peer-reviewed journals, including the New England Journal of Medicine, Journal of Clinical Oncology and Nature Reviews Cancer.

Biography:

Noha Amer has completed his PhD at the age of 32 years from Faculty of pharmacy (Girls) Al-Azhar University, Cairo, Egypt. She is Assistant Lecturer of biochemistry-Faculty of pharmacy (Girls) Al-Azhar University. She has published 1 paper in a national journal (Egyptian Journal of Biomedical Sciences).

Abstract:

Background: Taq IB polymorphic site of the CETP gene has been studied for a possible relation to the development of cardiovascular diseases in some ethnic groups. So far there are no data concerning the CETP Taq IB polymorphism in Egyptians. Our study aimed to investigate the frequency of different CETP Taq IB polymorphism genotypes in Egyptian acute coronary syndrome (ACS) patients and healthy controls and investigate whether this polymorphism predisposes to ACS. Methods: The Current study was conducted on 70 hospitalized patients with ACS and 30 control subjects which are age and sex matched to the patients. The patients were subdivided into two groups: MI group: 40 patients with myocardial infarction and UA group: 30 patients with unstable angina. CETP Taq IB genotyping was determined using TaqMan real time PCR. Results: The CETP genotype frequencies were: 42.86%, 44.28% and 12.86% in all patients, 30%, 60% and 10% in MI patients, 60%, 23.33% and 16.67% in UA group, 30%, 53.33% and 16.67% in controls for GG, GA and AA genotypes respectively. The frequency of GA genotype was significantly lower in UA patients than that in the control group (P<0.05). Conclusions: The frequency of CETP Taq IB genotypes and alleles in Egyptian ACS patients and healthy controls was similar to that in other ethnic groups with GA genotype was the most common genotype and G allele was the major allele. Taq IB GA genotype carriers may have lower risk of UA.

Biography:

O.O. BogomoletsNationalMedicalUniversity, Department of Pediatrics â„–4 Kyiv, Ukraine, Tolstogostreet 10, 01004

Abstract:

Hypoxia-related disorders play an important role in irreversible tissue damage via activation of certain secondary processes. The objective of the current project was to study the levels of cellular hypoxia, apoptosis controlling factors in relation to the value of kidney function impairment and to evaluate possible protective effects of the treatment with antioxidant agent tocopherol in pediatric patients with nephrotic syndrome. An examination ofrenalbiopsies of 53 patients (agedfrom 10 to 15years) withnephrotic syndromewasdone. Conventional clinical investigations, immunogistichemistry, immunoblotting have been applied in this study. We show that nephrotic patients reveal a high level of cellular hypoxia marker HIF-1α and its dependence on the level of kidney function impairment and proteinuria. The progression of the sclerosis as a sign of irreversible kidney damage was accompanied by gradual increase in expression of proapoptotic factor Bax. Administration of the antioxidant tocopherol in addition to the conventional scheme (immunosuppressive agents, ACE inhibitors)resulted in an improvement of hypoxia level, proapoptotic factor Bax expression, clinical symptoms. Thus, hypoxia-induces disorders in nephrotic children presented by disturbances in apoptosis controlling system can be attenuated by the antioxidants application in addition to the conventional treatment.

Biography:

Jack Kushner MD, MGA, FACS, FICS, FAANS, HDG (Oxford)

Abstract:

The prospect of treating gliomas effectively with the aid and information from genomics has so far been an illusion, but hope remains. This article will review advances in the therapy for gliomas including surgery, radiation treatment, medical therapy, immunotherapy, and gene therapy with the replacement of defective genes. There will be a brief discussion about vascular enabled nanosecond pulse or VEIN pulse and 3-D printing.

Biography:

Professor and Associate Dean for Faculty Affairs, College of Pharmacy,, University of South Florida Health,12901 Bruce B Downs Blvd, MDC 030, Tampa, FL 33612, Tel: 813-974-1026

Abstract:

Modern nutritional sciences are following new trends in analyzing the needs of human being based on their genetic backgrounds leading to new areas of nutrigenetics and nutrigenomics. The information gathered for the nutrients especially after the genomic studies is widely used for catering the nutritional needs of a particular group, providing measures for prevention of the diseases as well as better health to the end users. Nutrigenetics provides the individual genetic disposition, manifesting as single nucleotide polymorphism, and epigenetic phenomena. While Nutrigenomics provides information on diet which influencesthe gene transcription, protein expression and metabolism. Life style changes can be leading to better nutrition training, can be utilized for disease prevention and also helpful in providing global health to the masses. Knowledge which has been acquired during last decades in the area of nutrigenetics and nutrigenomics can really be used to provide a healthy lifestyle modification. Some of the information available provides lot of insight into application of nutritional principles in disease manipulation especially in the areas of digestive system, allergy, diabetes, obesity and other disease conditions. Nutritional intervention for better health is a new trend gaining momentum in western world. The presentation will discuss various aspects of Omics driven trends in nutrition, disease prevention and better health.

Biography:

David Cheng completed a PhD in Biomedical Physics from UCLA and a dual residency in Internal Medicine and Nuclear Medicine at Montefiore Medical Center, the hospital for the Albert Einstein College of Medicine in Bronx, NY. He has served as the Chief of Nuclear Medicine for more than 10 years at Yale-New Haven Hospital. He has joined Sidra Medical and Research Center in July 2014 as the Chief of Nuclear Medicine and Molecular Imaging to develop his own research.

Abstract:

With continued advancement in personalized therapies in medicine, there is a need for improvements in diagnostic imaging. This talk will give a brief update in equipment (such as PET/MRI) and in biomarkers currently under investigation and being used in clinical practice

Biography:

Izhak Haviv has completed his Ph.D at the age of 32 years from Weizmann Institute of Science and postdoctoral studies from University of California, Berkeley (c/o Tjian lab, head, HHMI). He is the director of cancer research center of excellence in the Faculty of medicine in the Galilee of Bar Ilan University, an academic clinical and translational research organization. He has an affiliate position in the University of Melbourne for 11 years, and at Peter MacCallum Cancer Centre, Australia for 16 years. He has published more than 59 papers in reputed journals.

Abstract:

Recent successes of targeted drugs on end stage cancer patients highlight the value of mutation-based biomarkers for drug response. However, the impact of these drugs is often temporary, and the patients progress to acquired resistance. A common mechanism of drug evasion involves feedback mechanisms that increase expression or phosphorylation-driven activation of an alternative oncogenic pathway. The objective of this work was to set up a streamlined methodology (kinome profiling, shRNA negative RNAi screens, evolution tracking, etc.) for rational drug combination designs. It includes pre-clinical assessment of the novel drugsfocused oncancer cases, refractory to biomarker predicted targeting, and seeking combination therapies that would block the spontaneous drug evasion. We explored the efficacy of the combination approach on a panel of cancer patient derived xenografts in mice, using tumor size, or metabolic imaging as an end point. Each cancer case was subject to target somatic mutation screening, which resulted in a targeted drug recommendation, and then, mouse groups were treated either with sequeincing-based therapy, or with combination of these therapies with blockers of the suspected evasion mechanisms. As a blocker of the evasion mechanism and epithelial to mesenchymal transition, we characterized the utility of a molecule that leads to the destruction of IRS1/2 of the IGF1R pathway. Usetargeted drugs, such as Erlotinib, Zelboraf, Afinitorand Gleevec, all increase the attenuation of the cancer growth temporarily, followed by acquired resistance, while inclusion of the IRS1/2 destruction lead to sustained efficacy, and even lead to regression of the recurrent tumor mass.

Biography:

Dr. Zhan received his undergraduate and graduate training in the fields of preventive medicine and epidemiology and statistics at the West China University of Medical Sciences in China during 1989 to 1999. He received his post-doctoral training in oncology and cancer proteomics for two years at the Cancer Research Institute of Human Medical University in China. In 2001, he went to the University of Tennessee Health Science Center (UTHSC) in USA, where he was a post-doctoral researcher and focused on mass spectrometry and cancer proteomics. Then, he was appointed as an Assistant Professor of Neurology, UTHSC in 2005. He moved to the Cleveland Clinic in USA as a Project Scientist/Staff in 2006 where he focused on the studies of eye disease proteomics and biomarkers. He returned to UTHSC as an Assistant Professor of Neurology in the end of 2007, engaging in proteomics and biomarker studies of lung diseases and brain tumors, and initiating the studies of predictive, preventive, and personalized medicine (PPPM) in cancer. In 2010, he was promoted to Associate Professor of Neurology, UTHSC. Currently, he is a Professor at Xiangya Hospital of Central South University in China, the European EPMA National Representative in China, Associate Editors of BMC Genomics and of BMC Medical Genomics. He has published 75 peer-reviewed research articles including about 50 articles in the field of disease proteomics and transcriptomics, 7 book chapters, and 2 US patents. His current main research interest focuses on the studies of cancer proteomics and biomarkers, and the use of modern omics techniques and systems biology for PPPM in cancer.

Abstract:

Tumor heterogeneity and individual difference are actually derived from individualized variations. No two completely same individuals exist in the world. Variations are involved in each aspect of healthcare. Cancer contains highly heterogeneous cell types that are the distinguishing pathophysiological basis and causes the proteomic variation. In combination with multiple endogenous and exogenous factors, that proteome variation is the basis for personalized patient treatment. Differences in the proteins (the proteome) can distinguish among those heterogeneity structures. The components of a proteome dynamically change as a cancer progresses. Changes in protein expression, protein modifications, and protein molecular network, individually or in combination, might be biomarkers to predict the disease, monitor the tumor progression, and develop an accurate molecular classification for personalized patient treatment. The modalities of proteomic variation might also be useful in the interventional prevention and personalized treatment of patients to halt the occurrence and progression of a tumor.

Biography:

Department of Biomedical Sciences for Health, University of Milan, Segrate, Milan, Italy

Abstract:

Inflammatory bowel diseases (IBD) are chronic and relapsing inflammatory conditions of the gastrointestinal tract and comprise Crohn’s disease (CD) and ulcerative colitis (UC). Both CD and UC are characterized by a great extent of heterogeneity, in terms of phenotypic presentation and response to different therapies; in fact, whereas some patients present limited bowel involvement and a very mild course of disease, others develop very extensive, aggressive disease, displaying extraintestinal manifestations as well. On the same line, the efficacy of different therapeutic strategies is extremely variable from patient to patient. As such, a subset of IBD may require the use of biological drugs targeting TNF, which is a key mediator in IBD inflammatory response; however, up to 10-20% of patients do not respond to anti-TNF agents. Thus, studies to define subgroups of patients with UC and CD who may benefit from TNF-blockade are needed. To this purpose, a study based on serum and lipid profiling of patients affected by UC and CD has been performed utilizing Maldi mass spectrometry profiling to identify specific markers of therapeutic response. The study was conducted on UC and CD patients of both genders andpatients were followed up to the fourth infusionin order to evaluate response to anti-TNF antibody treatment. Results indicated a difference in serum profiling between men and women after treatment. The analysis of UC responders and non-responders to anti-TNF treatment revealed the presence of 43 peaks, so called best separators between cohorts. Concerning CD, Maldi profiles indicated significant statistical difference in 48 peaks. Comparing UC and CD, the presence of peaks (29 for men, 15 for women) characteristics of the disease was determined. The identification of peaks is in progress and will determine target molecules contributing to clarify the physiopathological mechanisms associated to anti-TNF response. Nevertheless, the serological profile provided by this study will contribute to select the right candidates to anti-TNF treatment.

Biography:

Alice Zemljic-Harpf, MD VA San Diego Healthcare System 3350 La Jolla Village Drive Department of Anesthesiology Cardiac/Neuro Protection Laboratories Mail Code: 151, Room 5005 San Diego, CA 92161

Abstract:

With more than 25 years of clinical trial data cholesterol-lowering statin drugs are used as the first-line treatment for prevention and treatment of cardiovascular disease. Currently statins are among the most widely prescribed drugs. The occurrence of statin adverse events (AEs) was underestimated in clinical trials. In November 2013 the American Heart Association and the American College of Cardiology published new guidelines that are expected to expand statin use. Gene variations have been identified that modify statin response and increase susceptibility to statin AEs (e.g. SLCO1B1, CoQ2, variants in liver transport genes, variants in drug metabolism). Over the last decade Dr. Golomb’s group investigated statin AE’s, both those reported in patients that were enrolled in the UCSD Statin Effects Study (patient-targeted AE surveillance); and in the UCSD Statin Study (>1000 person randomized double-blind placebo controlled trial). For the former, >5000 patient surveys were submitted, including patient contact information and willingness to be contacted, and these data sets are available for further analysis, with the majority of participants expressing willingness to subjects that reported AEs as well as unaffected controls that previously participated in the UCSD Statin Study. The goal would be to develop predictive models, including questionnaires and pharmacogenomic screening before initiation of statin therapy as well as follow up questionnaires, by which statin therapy/drug choice may be tailored based on the patient’s genetic profile. The hope would be to move toward safer prescribing, to reduce the adverse effect toll from this widely used drug class.

Biography:

Mohammadreza Hajjari has completed his Ph.D in Molecular genetics at the age of 29 years in Tarbiat Modares university of Tehran, Iran. He had an internship fellowship in Seoul National University, South Korea in 2013. He got the best researcher award from the Tarbiat Modares University, 2014. He is now the assistant Professor of Molecular Genetics in Shahid Chamran University of Ahvaz. He has published more than 13 papers in reputed journals and serving as an editorial board member of different journals. He is now the Guest associate editor of the Frontiers in genetics, RNA and is managing a research topic on the role of non-coding RNAs in multifactorial diseases. His field of interest is “lncRNAs in cancers”.

Abstract:

Long non-coding RNAs are usually more than 200 nucleotides in length and do not encode any protein. They are mostly transcribed from the regions that previously known to be as “Junk DNA”. The discovery of numerous lncRNAs in human has dramatically altered our understanding of cell biology. Different studies indicate that these RNAs are involved in different biological processes such as gene regulation, epigenetic mechanisms, protein trafficking and stability, etc. Recently, different roles including tumor suppressor and oncogenic functions have been attributed to these RNAs. The dysregulation of different lncRNAs in some cancers has been observed in different studies. Various databases are also designed to report the comparison of the expression of these RNAs between normal and tumor tissues. Based on the different studies, some lncRNAs such as HOTAIR are considered as oncolncRNAs, and some of them such as MEG3 are considered as TSlncRNAs (Tumor suppressor). Finding novel biomarkers and therapeutic targets for cancers has been always important. Some proteins have been considered as biomarkers for some cancers. However, the discovery of novel biomarkers with high sensitivity/specificity are still challenging. Due to the stability of lncRNAs in various biological samples such as urine and serum, the lncRNAs have attracted different researchers trying to find novel biomarkers/therapeutic targets for cancer. This would be more interesting when we know that one of the lncRNAs named PCA3 has been approved as a prostate cancer biomarker by FDA. So, it seems that lncRNAs are rapidly becoming essential pieces in cancer puzzles.

Biography:

Abstract:

Introduction:The role of pharmacokinetics (PK), pharmacogenetics (PG) and clinical and therapeutic drug monitoring (TDM), are essential for improving the efficacy and safety of medicines. In the last years, in Mexico the individualization of medicine and therapeutics has become a priority for chronic and oncologic patients, and it demanded the establishment of pilot programs for MPPU. Objective:To show the experiences, mission and vision of MPPU as a resource to improve the individualization of treatment in chronic or/and critical patients. Methods: We have twonewintra-hospital UMPPin the states ofDurangoandBajaCalifornia underagreementacademia, government andprivate institutions.The service offerspharmacogenetictests (FG) such asqPCR, RFLP's, gene expressionand identificationof nucleotidevariationsbyautomated sequencing, that identifygenetic polymorphismsencodingdrugmetabolizing enzymessuch asCYP450, TPMT, MTHFR, FPGS, XO; drug transportersandreceptors(SLC19A1, ABCB1, ABCC5, OCT), etc. In addition we give aserviceclinicalPKandtherapeutic drug monitoring(TDM) fordose adjustmentfor cancerandchronic patients. Results:Based onthePGprofile, monitoring of drug concentrationsand /orthe population pharmacokineticstudy (PopPK), trainedpersonnelin analysisand interpretation are able toevaluate the therapeuticschemeestablished, design a new personalized treatment regimenin orderto reduce therisk of adverseeventsand maintaining optimal drug concentrationswithin the therapeutic range. Conclusion: Expertise gained in the first Clinical Pharmacokinetics Laboratory of the National Institute of Pediatrics and the implementation of a program for Optimizing Drug Therapy in Pediatrics, it led to creating the Laboratory of Pharmacogenomics and Molecular Biomedicine at the National Polytechnic Institute, CIIDIR-Unit Durango , Mexico to study FG in indigenous, mestizos and Caucasian populations of northern and northwestern Mexico, which has improved the differential diagnosis and personalized treatment in critical and/or chronic patients

Biography:

Alireza Haghighi, MD, DPhil is a clinician scientist. He graduated from University of Oxford and is currently based at theDepartment of Genetics of Harvard Medical School and Brigham and Women’s Hospital. Dr.Haghighi's research focuses onclinical and genetic investigation of inherited diseases, using state of the art technologies such as high throughput genotypingand next generation sequencing. He is also working on translating basic research discoveries into better diagnostics and improved management strategies.

Abstract:

Personalized Medicine can be described as making correct diagnosis and providing the right patient with the right drug at the right dose at the right time. Rapidly evolving advances in genetic technologies, including next-generation sequencing (NGS), has opened up a revolutionary era in genetics of human diseasesand is transforming medicine into precise, personalized health-care. NGS or "High throughput sequencing" includes different technologies of massively parallel sequencing and microarray analysis that determine the precise order of nucleotides within a DNA molecule in a few hours. Whole exome sequencing technologies have helped us discover the genetic bases of many monogenic diseases and identify novel pathways involved in the pathogenesis and progression of complex disease. Using targeted sequencing, we are now able to rapidly test a large set of candidate genes (for a disease) in a single test, which is a faster and much more efficient substitute for the conventional gene-by-gene approaches. The continuing decrease in costs and run times is expanding NGS into routine clinical practice. Yet the major challenges are not in the technology itself, but in the big amount of data generated by these methods that identify millions of variants among of which one or two may be the cause of a disease; a shift from the identification to the interpretation phase.NGS tools will very soon be adopted by physicians who are consulted to assist in providing a diagnosis for patients with complex clinical manifestations, particularly in cases where genetic contributions are suspected but have proven difficult to identify.Physicians are in a unique position to benefit from these advancements in genetics and further promote this approach.NGS can assist them to tailor the treatment of patients to alterations in their genome. These technologies also enable clinicians to re-classify diseases based on genome sequence and subsequently, take a targeted therapeutic approach to optimise treatment outcome.There are, however, challenges that need to be overcome, which include the identification of clinically relevant causative genomic variations across the whole genome and the ability to rapidly and easily analyze and interpret the vast quantity of dataproduced by genomic techniques.

Biography:

Abstract:

The organic cation transporter 1, OCT 1 (also called SLC22A1-Solute Carrier Family 22 member 1), appears to play a role in the efficacy and disposition of variety of organic cation including drugs. Genetic polymorphisms in the drug transporter have been increasingly recognized as a possible source of variation in drug disposition and response. Genetic variants in OCT1 have been identified largely in European, Asian (Japanese, Chinese and Korean) populations. Interestingly, eight genetic variations were found in the human SLC22A1 gene, which encodes OCT 1, from 50 type 2 diabetes mellitus individuals (T2DM), in West Bengal population. The purpose of this study was to investigate genetic variants of OCT1 in West Bengal populations. We detected the three previously reported non-synonymous variations, 480 G>C (L160F); 1022 C>T (P341L); 1222 A>G (M408V) and one synonymous variations 156 T>C (S52S) at a minor allele frequencies (MAF) of 0.63, 0.20, 0.43 and 0.27 respectively. We also found four previously reported intronic variations: IVS1-43(T>G), IVS2 -99(C>T), IVS5 -61(G>A), IVS9 +43(C>T) with minor allele frequencies of 0.20, 0.17, 0.18, and 0.37 respectively.In conclusions, we identified eight genetic variants including four exonic ones in SLC22A1 in 50 type 2 diabetes mellitus patients of West Bengal. This is the first report of SLC22A1 variations among Indian, especially West Bengal’s type 2 diabetes mellitus patients. The present results would be useful for haplotype analysis and pharmacogenetic studies on OCT1.

Biography:

Jang-Ung Park achieved his Ph.D from University of Illinois at Urbana-Champaign (UIUC) in 2009. After that, he went on to work as Postdoctoral Fellow at Harvard University. He is now an Associate Professor in the School of Materials Science and Engineering at UNIST (Ulsan National Institute of Science and Technology). His current research is focused on wearable electronics

Abstract:

Flexible and transparent conductive materials have been vigorously investigated as the next-generation electrodes to cover the disadvantages of conventional indium tin oxide (ITO) such as poor mechanical robustness on fl exible substrates. A variety of materials such as carbon nanotubes (CNTs), graphene, metal nanowires and conducting polymers have been appliedto fl exible electrodes in transparent electronics. Especially, graphene-silver nanowires (AgNWs) hybrid structures have been considerably researched due to their high transparency and conductivity.Also, graphene and AgNWs hybrid fi lmscouldprevent the oxidation of AgNWs and complement relatively high sheet resistance of graphene. In this talk, we present the fabricationof fl exible and transparent electronic devices, including fi eld eff ect transistor (FET) sensors, using graphene-AgNW hybrid fi lms as electrodes. These transistors show relatively high mobility (~3000 cm2V-1s-1) because of the low graphene-AgNW contact resistance (~0.3 kΩ·μm). In addition, the devices could be directly integratedon very thin andfl exible substrates as well as human skin, exhibiting their versatility and bio-compatibility. Furthermore, we demonstrate the real-time wireless nanosensors for monitoring the materials operating at radio frequency (~-30 dB at the center frequency of 4.4 GHz) without power consumption. Th is device can be used as ultrasensitive mannan-binding lectin (MBL, Concanavalin A) sensors. Fabrication of fl exible, transparent transistors using the hybrid electrodes demonstrates the substantial promise of future electronics

Biography:

A.LLerena has completed his Ph.D in 1988, and postdoctoral studies from Karolinska Institute in Stockholm, Sweden. He is the director of a University Hospital Clinical Research Center, member of the Spanish Network for Clinical Research SCREN. He has published more than 154 papers (indexed) in reputed journals and serving as an editorial board member of reputated Journals, is Editor in Chief of Drug Metabolism and Personalized Therapeutics (De Gruyter), Current Pharmacogenomics and Personalized Medicine (Bentham) and Associate Editor of the Pharmacogenomics Journal (Nature).

Abstract:

The Iberian American Network of Pharmacogenetics and Pharmacogenomics (RIBEF) was created with the aim of promoting collaborative pharmacogenetic research in Iberoamerica. Latinoamericans are diverse according to their genetic composition resulting from the inter-ethnic crosses between Amerindians, Europeans and Africans. The genetic polymorphism of the most studied CYPs are among the major determinants of the interindividual and interethnic variability of pharmacokinetics and drug response. \\\"Poor metabolizers\\\" (PM), and \\\"extensive metabolizers\\\" (EM) including a group of Ultra-rapid Metabolizers (UMs) have been described for CYP2D6 and CYP2C19, and “slow metabolizers” (SMs) have been described for CYP2C9, Therefore the CEIBA-RIBEF Network Consortium (European Ibero-American for Population Pharmacogenetics) aimed to evaluate the most relevant CYPs genetic polymorphism (CYP2D6, CYP2C9, CYP2C19) in Hispanics from Ibero-America. An standardized protocol for genetic analyse has been developed. To date the CYP2D6-2C9-2C19 genetic polymorphism have been studied in 6013 healthy volunteers from North (n=756), Central (n=250) and South Mexico (n=545), Cuba (n=713), Nicaragua (n=133), Costa-Rica (n=458), Colombia (n=294), Ecuador (n=401), Brazil (n=98), Peru (n=286), Argentina (n=426), Chile (n=285), Uruguay (n=32), Portugal (n=458) and Spain (n=878). The frequency of CYP2D6 PMs and UMs in Spain is 7-10% and 4.9%, respectively (Llerena et al., 2009). Differences have been found across Hispanics: the frequency of CYP2D6 PMs ranged from 0% (some groups from Mexico and Peru) to 10% (Amerindians from Costa Rica) and for UMs from 0% (some groups from Mexico and Peru) to 20% (some Amerindian groups from Mexico). For CYP2C19, the frequency of PMs varied from 0 (some groups from Brazil, Costa Rica, Mexico and Nicaragua) to 3.46% (Admixed from Cuba), and for UMs from 0 (some groups from Costa Rica, Mexico and Peru) to 39.29% (Admixed from Brazil). The frequency of CYP2C9 SMs ranged from 0-0.85%. Present data shows a large variability on CYPs polymorphism across Hispanics. The pharmacogenetics of CYP2D6, CYP2C19 and CYP2C9 may be a useful tool to predict unexpected side-effects, interactions, or therapeutic failures of many relevant drugs and may explain the interethnic differences observed the response to several drugs. Financial Support: Government of Extremadura-AEXCID (13/A001) MESTIFAR to the RIBEF Network IberoAmerican Society of Pharmacogenetics SIFF (www.ribef.com).

Biography:

Cecilia Gelfi is a Associate Professor of Clinical Biochemistry and Molecular Biology at the Faculty of Medicine, University of Milan. The scientifi c activity of Cecilia Gelfi has been focused on: the development of methodologies for the separation and identification of biomolecules. She contributed to the development of electrophoretic techniques transforming them into a physico-chemical tool for probing the structure and conformation of macromolecules; the investigation of the functional and morphological changes occurring in muscle in a number of physiological and pathological states. Recently, the interest have been focused on development of 1) clinical methods for monitoring drugs; 2) protocols for serological profi les for the clinical diagnosis of pancreatic and prostate cancer and infl ammatry bowel disease; 3) MALDI imaging methodologies for monitoring nano particles; 4) HPTLC-MALDI methodologies for recognition and quantitation of gangliosides and globosides in tissue extracts. Cecilia Gelfi published 213 scientifi c articles on international peer-reviewed journals (Scopus h-index 2015: 37)

Abstract:

Infl ammatory bowel diseases (IBD) are chronic and relapsing infl ammatory conditions of the gastrointestinal tract and comprise Crohn’s disease (CD) and ulcerative colitis (UC). Both CD and UC are characterized by a great extent of heterogeneity, in terms of phenotypic presentation and response to diff erent therapies; in fact, whereas some patients present limited bowel involvement and a very mild course of disease, others develop very extensive, aggressive disease, displaying extra intestinal manifestations as well. On the same line, the effi cacy of diff erent therapeutic strategies is extremely variable from patient to patient. As such, a subset of IBD may require the use of biological drugs targeting TNF, which is a key mediator in IBD inflammatory response; however, up to 10- 20% of patients do not respond to anti-TNF agents. Th us, studies to defi ne subgroups of patients with UC and CD who may benefi t from TNF-blockade are needed. To this purpose, a study based on serum and lipid profi ling of patients aff ected by UC and CD has been performed utilizing MALDI mass spectrometry profi ling to identify specifi c markers of therapeutic response. Th e study was conducted on UC and CD patients of both genders andpatients were followed up to the fourth infusionin order to evaluate response to anti-TNF antibody treatment. Results indicated a diff erence in serum profiling between men and women aft er treatment. Th e analysis of UC responders and non-responders to anti-TNF treatment revealed the presence of 43 peaks, so called best separators between cohorts. Concerning CD, MALDI profi les indicated signifi cant statistical diff erence in 48 peaks. Comparing UC and CD, the presence of peaks (29 for men, 15 for women) characteristics of the disease was determined. Th e identifi cation of peaks is in progress and will determine target molecules contributing to clarify the physio pathological mechanisms associated to anti-TNF response. Nevertheless, the serological profi le provided by this study will contribute to select the right candidates to anti-TNF treatment

Biography:

Iris Lavon is the Head of the Molecular Neuro-Oncology Laboratory in the Departments of Neurology and Oncology at the Hadassah-Hebrew University Medical Center. She completed her PhD in 1999. The main research interests of her lab are in the fi eld of molecular characteristics of brain tumors and personalized medicine for patients with brain tumors and neurodegenerative diseases. The results of her studies have been published in 28 scientifi c papers. Several of her fi ndings have been patented and were shown to have clinical applications in terms of potential implementation in the development of new therapeutic approaches

Abstract:

Identifi cation of tumor-specifi c circulating miRNAs may off er biomarkers to evaluate prognosis and response to therapy in patients with the incurable tumor Glioblastoma (GBM). Th e salvage therapy for recurrent GBM who have failed the standard-of-care of radiation and temozolomide chemotherapy, is bevacizumab, a recombinant human monoclonal anti-VEGF antibody. We previously demonstrated that among others, four of the hypoxia-mediated-miRNAs (miR-210, miR-21, miR-10b and miR-196b), are upregulated in gliomas as compared to normal brain. We hypothesized that the expression of these miRNAs will be altered in response to hypoxia following treatment with anti-angiogenic drug and might serve as circulating biomarkers to the drug effi ciency. Th us we aimed to develop a strategy for a rapid, sensitive and noninvasive technique for monitoring anti-angiogenic therapy dynamics by analysis of circulating tumor-specifi c microRNAs. For that purpose the expression these miRNAs were evaluated by real-time-RTPCR from circulating RNA that was collected longitudinally from 15 patients with GBM treated with bevacizumab. Radiographic evaluation was based on measurable changes in tumor dimensions using MRI by fl uid-attenuated inversion recovery (FLAIR) and contrast enhanced T1-weighted images. Th e quantifi cation of miR-10b and miR-21 were signifi cantly negatively correlated to MRI measurements, especially to sum product contrast diameter (R=0.51/p=0.002; R=0.568/p<0.0001 respectively). Th ere was even higher correlation between the quantifi cation of both miRNA and the contrast measurements than the correlation of each of them separately ((R=-0.648/ p<0.0001). Th is non-invasive procedure may lead to the routine use of circulating micro-RNA as a strategy for a rapid, sensitive and noninvasive technique for monitoring anti-angiogenic therapy dynamics

Biography:

Sangeeta Shukla is Vice Chancellor of Jiwaji University. She has wide experience of research in the fi eld of Reproductive Biology, Biochemical Pharmacology and Environmental Toxicology. She has been awarded fellowship from Welcome Trust, Indo-French Government Fellowship UK and many others. She has published 105 papers in SCI journals good citation indices. She has also edited book and contributed chapters in books. In recognition of her efforts, she held international positions as Vice President for Asian Continent of International Centers for Trace Element Study for UNESCO, France including Council Member of ISTERH. She has completed ten major research projects and supervised 18 PhD thesis and many dissertations of MPhil and MSc students

Abstract:

Liver disease including hepatitis, cirrhosis and liver cancer is the leading cause of death. Approximately 25,000 Americans die per year from chronic liver disease and more than 300,000 people are hospitalized per year due to cirrhosis. Th e harmful use of alcohol results in 2.5 million deaths worldwide per year. Excessive alcohol consumption is a major cause of preventable premature death, accounting for 1.4% of all deaths registered in England and Wales in 2012. Th us to create new herbal-based therapeutic approaches that are targeting the liver has been explored. Th is aims to develop effective drugs that can stimulate hepatic function or helps to regenerate hepatic cells. Artmisia absinthium, Rosa damascena, Butea monosperma, Nigella sativa, Rewand chini, Polygonum bistorta and polyherbal formulations were investigated against toxicants (CCl4, acetaminophen, alcohol, galactosamine, anti-tubercular drugs like isoniazid, rifampicin etc.) Research has also shown that herbals enhance the detoxifi cation rate of toxicants by reducing the oxidative stress/associated with drug metabolizing system, protected DNA from oxidative damage and reversed the level of hepatic markers. Choleretic activity, hexobarbitone-induced sleep time and plasma bromosulphalein retention also improved liver functions aft er herbal therapy. Th e histopathological observations revealed that cellular and ultra-structural pathological changes were reversed by mitigating of toxicant metabolic eff ects indicating improve hepatic morphology and physiological functions. Th e data suggests that herbals have an efficient protective mechanism against hepato toxicants. Statistical analysis of these herbal agents showed signifi cant hepato-protective index. Th us, it can be concluded that these herbal agents may be considered as a good hepatoprotective agent by medical practitioners for liver ailments

Biography:

Vincent S Gallicchio is Professor of Biological Sciences, Public Health and Microbiology at Clemson University. He is the Vice President of the Trace Element Research Centers operating under UNESCO and the immediate Past-President of the International Federation of Biomedical Laboratory Science. He has authored more than 200 peer-reviewed scientifi c articles, book chapters and textbooks. He is the Inventor on eleven US and one international patent focused on drug delivery. He has received more than $22 million in research funding. In 2003 he was presented to her majesty Queen Elizabeth of England for his efforts promoting higher education opportunities for British students

Abstract:

Trace elements possess important therapeutic properties. First, binding to specifi c macromolecules (enzymes, nucleic acids, etc.) they infl uence important chemical and biological processes; second, they interact amongst themselves synergistically to amplify their individual reactions. Metals have been used therapeutically for hundreds of years. Use of metals in the treatment of human diseases began with discoveries with gold used initially in patients with tuberculosis followed by rheumatoid arthritis. Gold identifi ed an immunological pathogenesis in the etiology of rheumatoid arthritis, thus metals may be effi cacious in other human conditions that are immunological in etiology. Th e antineoplastic potential of metals was further disseminated by the development of less toxic compounds such as platinum. Th ird, metals in human cancers have increased their therapeutic eff ectiveness and increased the diversity of cancers responding to these treatments. Fourth, lithium use in clinical medicine revolutionized treating psychiatric mood disorders. Central to the biological action of lithium is its ability to infl uence brain and central nervous system chemistry, thereby providing spectacular results in the treatment of aff ective and other psychiatric mood disorders, in particular, suicide prevention. Discoveries defi ning alternative non‐psychiatric clinical use of lithium continue to intrigue clinical medicine based upon a key discovery demonstrating lithium can eff ectively infl uence stem cells. Halo-therapy is using salt compounds as initial and maintenance therapy of human respiratory ailments. Used by the Greeks and Romans, halo-therapy has existed for thousands of years. It is associated with the therapeutic eff ectiveness attributed to spas. Today, halo-therapy has gained resurgence with its use as personalized medicine in the treatment of human diseases

Biography:

Kenney-Herbert Emma completed her PhD from Cambridge University, UK. She graduated in Entry Medicine at Imperial College London and qualifi ed in 2014. She is now working as a Junior Doctor at The Chelsea and Westminster Hospital, London. She plans to forge a career as an Oncologist and continue to play an active role in research

Abstract:

The prognosis for patients with glioblastoma (GB) remains poor. Recent research has focused on the hypothesis that the growth and regeneration of GB is sustained by a sub-population of self-renewing stem-like cells. Th is has led to the prediction that molecular markers for cancer stem cells in GB may provide a treatment target. One candidate marker is CD15; we wanted to determine if CD15 represented a credible stem cell marker in GB. We investigated CD15 as a potential marker for treatment in patient GB samples, primary GB cell lines (GBC) and in tumour forming assays in mouse models. We found that the prevalence of CD15+ cells was varied in 10 patient GB tumours and CD15+ cells were less proliferative than their CD15- counterparts. In vitro, CD15 did not confer a proliferative advantage. Furthermore, GBCs sorted for CD15+ and CD15- were not signifi cantly diff erent cytogenetically or in terms of gene expression profile. Sorted single CD15+ and CD15- cells were equally capable of reconstituting a heterogeneous population containing both CD15+ and CD15- cells over time; and both CD15+ and CD15- cells were able to generate tumours in vivo. Our data confi rms that CD15 does not identify a sub-population of cancer stem cells. Instead, detailed single cell analysis suggests that CD15+ cells are a component of the variegated clonal architecture typical of GB. However, we believe there is a role for our experimental models to assist in the fi nding of further GB therapeutic targets

Biography:

Mohamed Abdulla has completed his Md-PhD from the University of Lund, Sweden and currently working as professor of medicine for the Swedish medical board. He has published over 300 original publications and several chapters in textbooks. He is currently active in the fi eld of diet and aging

Abstract:

The relationship between the body and diet is a very intimate one compared to all other relations. During the 1960s and 1970s, dietary manipulations, especially caloric restrictions were found to retard aging. Research during the last couple of decades has shown that the number of independent molecules-processors contribute to human aging. Th is includes Metformin, Ratamycin, Resveratroan, Free radicals, hormones and gene modifi cations. Ratamycin and related compounds such as Everolimus and Temsirolimus are found to interfere with the activity of a protein called Mammalian Tor (mTor). All these compounds and processors are known to extend the lifespan of a number of experimental animals and postpone age-related disorders such as cardio vascular diseases and cancer. Metformin is a very commonly used drug against diabetes and recent studies in England have shown that it can prolong the lifespan of humans without having diabetes. Free radicals theory of aging has become less specifi c in animals as well as in humans during the last decade. Th ere are a number of genes that are known to interfere with human aging. Manipulation of some of these genes has found to increase human lifespan in some selected areas of the world. Telommeres are the time keepers of a self-life; each time a cell divides the length of the Telommeres is shortened and fi nally it disappears altogether. Many researchers are active at present in order to fi nd ways of keeping Telommeres intact. In young blood cells there is a protein (GD lever) that is abunded one is young and giving the blood from younger mice to older ones to increase the lifespan of the older mice. Th is paper will describe some of the details of the molecule processors involved in the aging process. It will also discuss the importance of microbiome that infl uences health and disease

Biography:

Ananda S Prasad has been at Wayne State University since 1963 when he took a position as Director of the Division of Hematology, a post he held until 1984 when he became the Director of the Division of Research. He has also been a Professor of Medicine at Wayne from 1968 until the present. He was appointed as Distinguished Professor of Medicine, Division of Hematology-Oncology in 2000. He is author of twelve books and over three hundred scientifi c articles. He has received many awards, which include Medal of Honor from the Mayor of Lyon, France, Honorary Doctorate from Claude Bernard University, France, election as corresponding member of The European Academy of Sciences, Arts and Humanities, and American College of Physicians’ (ACP) highest award for outstanding work in science as related to Medicine. In 2010, he received the prestigious Mahidol Award from Royal Highness King of Thailand for his discovery of zinc as an essential element for human health. In 2011, he received a Congressional Commendation for his lifelong studies involving zinc as an element essential for human survival. In May of 2012, he received The Lawrence M. Weiner Award, honoring outstanding contributions of non-alumni to the School of Medicine through the exceptional performance of his research at Wayne State University. Most recently, The American College of Nutrition will honor him as a distinguished Professor of Internal Medicine, with its 2014 Alexander and Mildred Seelig Magnesium Award.

Abstract:

In the Middle East, nearly 50 years ago, we established the essentiality of zinc for human and documented for the fi rst time occurrence of zinc defi ciency in the villages of Iran and Egypt. During the past fi ve decades we have witnessed tremendous advances in both clinical and basic science areas of zinc metabolism. Currently WHO estimates that nearly 2 billion subjects in the developing countries are zinc defi cient and widespread growth retardation, immune dysfunction and cognitive impairment are related to zinc defi ciency.Th erapeutic use of zinc for treatment of acute diarrhea in infants and children in developing countries has saved millions of lives. Zinc is very eff ective in reducing the incidences of blindness in patients with age related macular degeneration (AMD). Zinc is an approved therapy for patients with Wilson’s disease. Zinc administration is eff ective in decreasing the incidences of infection in the elderly, patients with sickle cell disease and head and neck cancer patients. Zinc is a molecular signal for immune and neuronal cells. In our experimental model of human zinc defi ciency we reported that measurement of zinc and ecto 5’ nucleotidase in lymphocytes, are sensitive indicators of zinc defi ciency. Serum active thymulin and generation of Th 1 cytokines, IL-2 and IFN-γ and their mRNAs are most sensitive indicators of acute zinc defi ciency. We have now established a new method of zinc assay in nails and plasma by LIBS (laser induced background spectroscopy) technique which is simple, exportable and cost eff ective and is an excellent indictor of chronic human zinc deficiency.

Biography:

Constantin Polychronakos specialized in Pediatric Endocrinology in Canada after medical studies at Aristotelian University in Greece, and fi nished his Post-doctoral research training at McGill University in Montreal, where he is now Full Professor in the Department of Paediatrics with cross-appointment in Human Genetics. He is credited with the discovery of the effect of the INS locus in the thymus in type 1 diabetes, with two of the fi rst GWAS for type 1 and type 2 diabetes and one of the fi rst uses of exon capture combined with NGS to elucidate the cause of a rare monogenic form of diabetes

Abstract:

Background: Type 1 diabetes (T1D) is due to the autoimmune destruction of the pancreatic -cells. Autoantigen specifi city is determined by the T-cell receptors (TCRs) of autoreactive lymphocytes but their characteristics are poorly understood. Nextgeneration sequencing now off ers methodological possibilities for exploring the vast diversity of the somatically rearranged TCRs for possibilities of personalized diagnosis and intervention. Objective: To defi ne the TCRs reactive to whole proinsulin, the most important T1D autoantigen. Methods: We examined T-cells from the peripheral blood of nine children with T1D and two normal controls, by proliferated in vitro aft er 12 days of activation with proinsulin and isolated by CFSE dye-dilution fl ow-sorting. TCRs were amplifi ed from whole RNA by 5’RACE and amplicons sequenced on the Illumina miSeq with a 250 x 2 protocol. Beta-chain reads were analysed by a paired-end modifi cation of the standard algorithm. Results: Response to proinsulin was highly polyclonal in the T1D patients but much fewer clones were seen in the two controls, where 29% and 80% of all proliferating clones had the same TCR (p=0.018, rank test). Interestingly, 562 out of the 5,446 clones that showed at least 20-fold expansion were “public”, i.e. exactly the same in diff erent subjects. Th ese clones tended to have a higher ratio of expansion (mean 123 vs. 103, p=0.04. Conclusion: TCR clonality of proinsulin specifi cities appears to distinguish cases from controls and, if confi rmed, may be an important predictor of diabetes, and immune-progress biomarker. Defi nition of the main TCR clones in early pre-diabetes may provide opportunities for antigen-specifi c immunosuppression

Biography:

María Ángeles Pajares completed her PhD from the Universidad Complutense de Madrid (Spain) in 1986, and her Post-doctoral studies from the Harvard Medical School (Boston, USA) in 1989. She is a Senior Research Scientist from the CSIC since 2006, where her own group works in the structure/function relationships that govern methionine metabolism in health and disease. She has authored more than 60 original papers in reputed international journals. She serves as referee for a large number of journals and several grant agencies and is now also serving as an Editorial Board Member for the World Journal of Biological Chemistry

Abstract:

The methionine cycle produces S-adenosylmethionine (AdoMet) the main methyl donor for cellular transmethylations, including several epigenetic modifi cations. Alterations in this pathway and specifi cally in the AdoMet synthesis by methionine adenosyltransferases (MATs) have been reported in a large variety of diseases, although most studies have been performed in liver. Th e enzymes involved, excluding methyltransferases, are oligomers that were classically consider cytoplasmic. Th us, the AdoMet synthesized in the cytoplasm was expected to be transported to other compartments as required, a hypothesis further sustained by identifi cation of an AdoMet mitochondrial transporter. However, in the last decade several reports have shown that this is not the case for the cell nucleus, where most of these enzymes have been identifi ed in very low quantities. Work of my laboratory has recently provided evidences showing nuclear accumulation of several proteins of the methionine cycle in two models of acute liver injury. Moreover, we demonstrated that the nucleocytoplasmic distribution is governed by the ratio between glutathione species (GSH/GSSG). In fact, the oxidative stress induced by D-galactosamine or acetaminophen produces opposite eff ects on MAT I/III isoenzymes according to the subcellular compartment examined. Th is opposite regulation leads to decreased AdoMet production in the cytoplasm, whereas the nuclear levels of active MAT I increase, as well as certain epigenetic methylations. Prevention by N-acetylcysteine administration did not avoid all the drug-induced changes. Hence, we propose that alterations in the subcellular localization pattern of several enzymes of this cycle show a potential as biomarkers of liver disease

Biography:

David Cheng completed a PhD in Biomedical Physics from UCLA and a dual residency in Internal Medicine and Nuclear Medicine at Montefi ore Medical Center, the hospital for the Albert Einstein College of Medicine in Bronx, NY. He has served as the Chief of Nuclear Medicine for more than 10 years at Yale-New Haven Hospital. He has joined Sidra Medical and Research Center in July 2014 as the Chief of Nuclear Medicine and Molecular Imaging to develop his own research

Abstract:

With continued advancement in personalized therapies in medicine, there is a need for improvements in diagnostic imaging. Th is talk will give a brief update in equipment (such as PET/MRI) and in biomarkers currently under investigation and being used in clinical practice. It is an exciting time to integrate and translate scientifi c knowledge into clinical practice Understand basic principles in order to diff erentiate promising eff orts from confusing fl awed data New technology and radiotracers need time for validation

Biography:

Sadhana Shrivastava completed her PhD from Jiwaji University and Post-doctoral studies from the same University. She has published more than 40 papers in reputed journals and books. She has been awarded many national fellowships. She has presented papers in international conferences

Abstract:

Kaempferol is a natural fl avonol, a type of fl avonoid that has been isolated from broccoli, grapefruit, cabbage, tomato, grapes and apples. Acryl amide (AA) is an industrial chemical with neurotoxic, carcinogenic eff ects in humans and has been known as an occupational hazard for decades. However, in recent years, AA has been found to form in fried and baked starchy foods like potato chips, French fries etc during cooking. Th e aim of the present study was to evaluate the therapeutic effi cacy of Kaempferol against AA induced toxicity in rats. AA was administered at the dose of 19.13 mg/Kg for 28 days to albino rats followed by therapy with 20 mg/ Kg dose of Kaempferol. Th e various toxicity symptoms were observed which include signifi cant reduction of body weight, hair loss, hind-limb splaying, dragging of back legs and irritation on skin. Th ere was signifi cant elevation in the level of AST, ALT and ALPase with reduction in levels of hemoglobin and blood ALAD and ALAS in brain aft er AA exposure. Activities of acetyl cholisterase, GST, GR and GPx were also declined in AA treated groups as compared to control group. Aft er AA intoxication, activities of drug metabolizing enzymes (AH, AND, CYT P-450) were depleted with increase in G-6-PDH, microsomal lipid peroxidation and also induced DNA damage. Histo-pathological observations also supported biochemical studies. Kaempferol has a therapeutic potential for the protection of AA induced toxicity to prevent harmful eff ects

Biography:

Jean Gabert is a Biochemist and Molecular Biologist, who has spent 10 years in the Cancer Centre in Marseilles (France) as Assistant Professor in Haematology after getting his PhD in Immunology. From 1999 to till date, he has been working as a Professor of Biochemistry and Molecular Biology, Head of the department at the University Hospital in Marseilles. His work has always been in the transfer research and availability for patients of new biological tests allowing improving health care. He has been the coordinator of a very successful European network under the Europe against Cancer program (SANCO Commission). He is currently the Head of the molecular platform for cancer in the PACA West region. He has 5 patents and greater than 75 peer review international publications in reputed journals. He recently obtained honour of Executive Master in Health from Science Po Paris (2011).

Abstract:

A new mutated cancer gene (CALR) has been discovered in December 2013 aff ecting mainly primary myelo-proliferative syndromes (MPS). Th e patients with mutated CALR have a lower risk of thrombosis and longer overall survival than patients with mutated jak2 gene and the clinicians continue to face challenges during diagnosis of un-mutated MPS. CALR mutations are present in 70 to 80% of un-mutated Jak2 MPS. Th e mutations are located on exon 9 of the gene with a loss of KDEL sequence (signal sequence for endoplasmic reticulum) and loss of calcium biding sites with a new basic (instead of acidic) C terminal region. We will present our data: although the fi rst papers were based on new generation sequencing, we wanted to set up a prospective screening based on High Resolution Melting (HRM) followed by Sanger sequencing using the same pair of primers to speed up the process. We tested 180 samples including for suspicion of Essential Th rombocytemia (ET) and primary myelo-fi brosis. We found 21 CALR mutations including one deletion which has not been reported so far. Until 12 years ago the diagnosis of MPS patients was only on elimination; Jak2 and MPL mutations, we can today, with CALR mutations in addition, fi nd one mutated gene for 90% of the MPS patients which improves the medical care of such patients. Th e personalized therapeutic approach is under process

Biography:

Vincent S Gallicchio is Professor of Biological Sciences, Public Health and Microbiology at Clemson University. He is the Vice President of the Trace Element Research Centers operating under UNESCO and the immediate Past-President of the International Federation of Biomedical Laboratory Science. He has authored more than 200 peer-reviewed scientifi c articles, book chapters and textbooks. He is the Inventor on eleven US and one international patent focused on drug delivery. He has received more than $22 million in research funding. In 2003 he was presented to her majesty Queen Elizabeth of England for his efforts promoting higher education opportunities for British students

Abstract:

Lithium (Li) salts have been widely used in psychiatry as mood stabilizing agents for 60 years. Li found in variable amounts in foods, especially grains, vegetables, and in some areas, the drinking water provides a signifi cant source of the element. Th erefore, dietary intake in humans depends on location, type of foods consumed, and fl uid intake. Traces of Li have been detected in human organs and tissues, leading speculation that the element was responsible for specifi c functions in the human body. It was not until the 20th century that studies performed in the 1970’s and 1990’s, primarily in rats and goats, maintained on Li-defi cient diets demonstrated higher mortality, altered reproductive and behavioral abnormalities. Such defi ciencies have not been detected in humans; however, studies performed on populations living in areas with low Li levels in water supplies have been associated with higher rates of suicides, homicides, and the arrests rate for drug abuse and other crimes. Li appears to play a signifi cant role in early fetal development as evidenced by high Li levels during the early gestational period. Biochemically, the mechanism of Li action involves multi- factor and interconnected pathways with enzymes, hormones, vitamins, and growth and transforming factors. Th is body of evidence now appears suffi cient to label Li as an essential element with the recommended RDA for a 70 kg adult of 1000 mg/day. Of extreme importance for the future is the growing body of evidence indicating Li can be used eff ectively for the treatment of acute brain injuries, e.g., ischemia and chronic neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Tauopathies, and Huntington’s disease. Th is conclusion is based upon evidence showing Li as important in neurogenesis as well as protecting neurons from neurotoxicity. Li infl uences stem cells, both neuronal and marrow derived, thus, the additional therapeutic implications for this element in clinical medicine to treat disorders associated with the faulty production of blood and nerve cells or as a tool to enhance blood stem cell mobilization for transplantation

Biography:

Manuel Perez Alonso has a degree in Biology and PhD in Molecular Genetics. He is currently working as a Professor in Genetics at the University of Valencia. He participated in fi ve international genome sequencing consortia (as Principal Investigator) and in a number of basic research projects. He is Promoter and Founding partner in six biomedical companies: Valentia Bio-Pharma, The Institute of Genomic Medicine, Gen A Gen, Genera Biotech, Medi-Gene Press, all of them located at the University of Valencia Science Park. His research is now focused on the development of genomic tools for genetic testing. He also contributes to biopharmaceutical research through the study of the pathways leading to rare genetic disease. He is President of the Valencia Bio-Region (BIOVAL) and President of the Spanish Association of Entrepreneurs in Science

Abstract:

Detecting gene mutations related to rare disease pathogenesis is a major need in patient healthcare. More than 3,000 rare diseases are known to be caused by mutations in the corresponding genes. Th is kind knowledge can be used for medical genetics and medical genomics, i.e., thousands of diff erent gene tests may be developed internally in reference laboratories. Despite the obvious medical interest of this kind of genetic tests, there are only a few global labs off ering more than 1,000 diff erent gene tests in their portfolios. In this talk the professional pathway leading to the creation of the Institute of Genomic Medicine as well as the fast evolution of this reference laboratory will be described. Aft er fi nding this genetics reference laboratory, in 2009, the Institute has developed into one of the main Reference Laboratories for the Genetic Testing of Rare Genetic Diseases, providing more than 6,000 gene tests per year. Only six years aft er establishment, the portfolio of available molecular tests from the Institute includes more than 1,300 genes corresponding to more than 1,200 rare genetic diseases. Th is list grows every week on demand, i.e., we accept requests from clinics or hospitals in Europe, America or Asia for new tests to be developed in our labs. Now the company includes a service for exome sequencing by Next Generation Sequencing. Th e key points for our development that can be summarized in (1) the creation of interdisciplinary teams between biologists, bio-informaticians and IT experts; (2) international collaboration; (3) active collaboration with the academia, small biotech companies worldwide and business people; (4) a strong commitment of the founders of the company on the idea that research has to benefi t the Society; and (5) strong commitment within our team with business ethics will be described

Biography:

Lars Von Olleschik-Elbheim completed his PhD in Medical Microbiology from Westfälische Wilhelms-Universität, Germany. In the past 17 years he has been working for both pharmaceutical and diagnostics companies in various positions. Dealing with the diagnostics and treatment of environmental, diet and behaviour related diseases, his interest became focussed on the effects of personalized nutrition within the frameset of personalized medicine. Within this context he is currently focussing on the effects of Vitamin D and adaptogens, when it comes to stress and age related diseases and anti–ageing in general. The proper use of companion diagnostics for consultation and monitoring is one of his additional topics of interest in regard to personalized nutrition and anti-ageing

Abstract:

In the mid-20th century the Soviet scientists Nicolai Lazarevand Israel I. Brekhman came up with the term adaptogen. Th e term refers to a group of secondary metabolites, based on plant extracts that can help the body adapt to stress, regardless of the source: heat, cold, exertion, trauma, sleep deprivation, toxic exposure, radiation, infection, or psychological duress. By defi nition, an adaptogen causes no side eff ects, treats a wide variety of illnesses, and helps return an organism back toward balance (homeostasis) no matter in what manner it has moved out of balance. Intensive research has been made on this topic in Russia and Asia, fi rst of all in the area of sports and military. Th ere is strong evidence that there is a positive correlation between frequent adaptogen extracts uptake, enhanced physical endurance and enhanced mental capacity. Th e talk will give an overview on the most imporant adaptogenic plants, the secondary plant metabolites involved and the current use of adaptogenic extracts on various health conditions. It shall also discuss the adaptogenic eff ects on bioliogical ageing. In order to estimate how much an individual will benefi t from the use of adaptogens, the measurement of cortisol levels has become like a biomarker. Recently an easy to use home test has been developed in Canada. It estimates how much an individual might benefi t from the use of adaptogens. Th is test is also dedicated to monitor long term eff ects of adaptogen intake on the individual stress level and thus may soon become part of the diagnostics toolbox for personalized medicine

Biography:

Anatoly V Skalny has completed his PhD at the age of 28 years from All-Union Centre for Narcology, Moscow, USSR. He is a vice-president of Trace Element Institute for UNESCO, the chairman of Russian Society of Trace Elements in Medicine, a member of advisory board of Federation of European Societies on Trace Elements and Minerals (FESTEM). He has published more than 200 journal articles, abstracts and book chapters in English. Prof. Skalny is a member of editorial board of Journal of Trace Elements in Medicine and Biology, the leading journal in the fi eld of trace elements science.

Abstract:

Chemical elements are the structural basis of all living organisms. At the same time, chemical elements and their organic and inorganic compounds exist in the human organism not as inert and independent units. Th erefore, a term “bioelement” was proposed earlier. Bioelement is not a single chemical element (atom) inside a large molecule, but a temporarily formed biocomplex where the element is bound to an organic molecule with a specifi c biological function. In particular, certain chemical element is a physicochemical unit whereas bioelement is a precursor of biological unit. Consequently, clinical medicine aims at analysis of bioelements rather than chemical elements alone. Taking into account the fact that bioelementology is an integrative science that includes the knowledge on bioorganic chemistry, bioinorganic chemistry, biochemistry and biophysics, molecular biology, medicine and other parts of life sciences, analysis of bioelemental status of the human organism may provide more essential information on the condition of the human organism than chemical analysis of metals and other compounds in human biosamples alone. Finally, this results in the formation of a complex metabolic profi le of the organism. Th e availability and the use of such information may help the physician to successfully correct the disturbed metabolic pathways in the human organism and fi nally increase the effi ciency of treatment. Th erefore, it can be proposed that bioelementology is not just a tool in a large arsenal of the physician but a basis for personalized medicine

Biography:

Abstract:

Biography:

Guilherme Martins Santos completed his Bachelor in Veterinary Medicine in 1997, at the University of Uberlandia, Brazil. In 1998, he started his masters studies in the University of Brasilia, and then went on to do a PhD in Molecular Pharmacology at the University of Brasilia and INSERM-Paris, France. In 2006 he went to the UK to start a post-doc at the MRC-Laboratory of Molecular biology in Cambridge, followed by a post-doc at the University of Leicester, focused on the structural studies of nuclear receptor and chromatin. He is currently a Professor of Pharmacology of the Pharmacy School at the Universidade de Brasilia. He has published several articles in important journals such as Nature, Cell and Trends in Pharmacological Science. In April 2015, he founded Nucleosantos Therapeutics, a start-up that is working on the discovery and development of exogenous Nucleosome-Binding Molecules

Abstract:

Chromatin is the major regulator of gene expression and genome maintenance. Proteins that bind the nucleosome, the repetitive unit of chromatin, and the Histone H4 tail are critical to establish chromatin architecture and phenotypic outcomes. Intriguingly, nucleosome-binding proteins (NBPs) and H4 tail peptide compete for the same binding site at an acidic region on the nucleosome surface. Although the essential facts about the nucleosome were already revealed 17 years ago, new insights into its atomic structure and molecular mechanisms are still emerging. In this talk, I will feature the nucleosome surface as a drug target to control chromatindynamics and, consequently, gene expression and genome maintenance. I will cover the key aspects of chromatin architecture upon binding of protein and exogenous molecules (exogenous Nucleosome Binding Molecules - eNBMs) to the nucleosome. Moreover, I will discuss the impact and development of eNBMs, presenting some of our results in silico, in vitro and in cell-based assays

Biography:

Lars Von Olleschik-Elbheim has completed his PhD in medical microbiology at the age of 33 years from Westfälische Wilhelms-Universität, Münster, Germany. In the past 17 years he has been working for both pharmaceutical and diagnostics companies in various positions. Dealing with the diagnostics and treatment of environmental, diet and behaviour related diseases, his interest became focussed on the effects of personalized nutrition within the frameset of personalized medicine. Within this context he is currently focussing on the effects of Vitamin D and adaptogens, when it comes to stress and age related diseases and anti-ageing in general. The proper use of companion diagnostics for consultation and monitoring is one of his additional topics of interest in regard to personalilized nutrition and anti ageing.

Abstract:

Clinoptilolite is an outstanding microporuous material with a superlarge surface of volcanic rock origin with special selective binding capacities towards heavy metals, small positive charged molecules, and even viruses. Its very interesting, thqt encages mainly the “bad boys” and thus supports their inactivation and depletion from the human body. Used since thousands of years by men and even being part of instincive activities in some animals it was more or less fogotten until the Tschernobyl catastrophy led to intense research activities in order to protect the health of the people as good as possible. Clinoptilolite showed to be the best material to prevent the environment from further intoxication and it is even capable of depleting substances like radioactive Cesium out of the human body. Nowadays there is a rising amount of publications with case reports and clinical studies showing that the “typical diseases of the elderly”, like e.g. diabetes, cancer, ostephorousis, some forms of brain damage can be slowed down or stopped in their progression, sometimes eff ectively treated by the use of clinopotilolite. By blocking toxic compounds from interfering with internal regulatory processes and the capability to deplete them from the human body it shows anti-aging eff ects e.g. on skin, liver, heart, brain, bones, wound healing, hair, and overall endurance. Combined with the right diagnostics clinoptilolite is more and more prooving as a very good part of the medical toolbox

Biography:

Reda Mohamed El badawy has completed her MD at Banha University ,Faculty Medicine. She is worked at King Saud University and King Khaled University Saudi Arabia. She has published more than 25 papers in reputed journals

Abstract:

The relation between Non –Alcoholic liver disease(NAFLD) and cardiovascular diseases (CVD)has not been elucidated with non diabetic obese normal healthy subjects. Th e aim: Was to evaluate the use of simple biomarkers as predictors for NAFLD and consequanly CVD. Seventy seven Subjects divided into two groups: Group( 1) included 37 patients known to have diabetes mellitus type 2 , Group( 2) included 40 healthy subjects who have no medical illness. Results: Th ere was a statistical signifi cant diff erence for all laboratory parameters between the 2 groups except for total bilirubin, direct bilirubin and ALT/AST ratio. In DM group fatty liver was diagnosed in 22/37(54%) by abdominal ultrasound. Th e median values of TG, insulin, leptin, insulin resistant, ALT ,GGT,AST and ALT/AST ratio in diabetic patients were statistically signifi cant higher in those with fatty liver compared with those without fatty liver (P values <0.05). In group 2 fatty liver was diagnosed by abdominal ultrasound in 12/40( 30%). Th e median values of FBS,TG, cholesterol, insulin, leptin, insulin resistant, ALT ,GGT,AST and ALT/AST ratio in the healthy subjects were statistically signifi cant higher in those with fatty liver compared with those without fatty liver (P values <0.05).Th e sensitivity and specifi city of GGT, ALT/AST ratio was as follow 100.%, 59% and 73%, 55% at a cut off value of 45 IU/l and 1.9 respectively. Conclusion: Elevated liver enzymes, although in normal ranges, play a role in early diagnosis of fatty liver disease which has a predict for the presence of cardiovascular diseases especially carotid intimal thickning

Biography:

Guo-Hui Fu has completed her MD from Jiamusi Medical College, China and then completed PhD from Harbin Medical University, China and Post-doctoral studies from Kyushu University School of Medicine, Japan. She is the Dean and Professor of Pathology Center, Shanghai Jiao Tong University School of Medicine. She has published more than 81 papers in reputed journals and has been serving as an Editorial Board Member of repute

Abstract:

Epidermal Growth Factor receptor 2 (HER2) is expressed in 6%-23% gastric cancer tissues. Administration of Trastuzumab, a fully humanized monoclonal antibody targeted to the HER2, is associated with survival rate in HER2-positive gastric cancer (GC) patients. Gastrin is a major gastrointestinal hormone proven to have an inhibitory eff ect on GC in vitro and in vivo. Here, we report the synergistic inhibitory eff ects of Trastuzumab and Gastrin on HER2-negative GC cells through the Gastrin/Cholecystokinin B receptor (CCKBR) pathway. Trastuzumab upregulated CCKBR protein levels but could not initiate its signal transduction, whereas Gastrin increased the levels and activation of CCKBR. Molecular experiments indicated that Trastuzumab and Gastrin co-treatment synergistically enhanced the stability of CCKBR. Moreover, their combined treatment synergistically arrested GC cells at G0/G1 phase, down-regulated levels of GC-related proteins, including anion exchanger (AE) 1, Cyclin D1, β-catenin and Cytoplasmic p16, and promoted nuclear translocation of p16. In addition, combination treatment upregulated AE2 levels, which are reduced in GC tissues. Th e in vivo synergistic anti-GC eff ect of combined treatment was confi rmed in xenograft experiments. Th e results demonstrated the synergistic eff ect of Gastrin and Trastuzumab in the suppression of GC

Biography:

Maysa Kamal Salama has completed her PhD from Cairo University School of Medicine. She was the head of Medical Biochemistry and Molecular Biology Department. She has published more than 30 papers in reputed journals and serving as an Editorial Board Member of repute

Abstract:

To investigate the association of the functional monocyte chemotactic protein-1 (MCP-1) promoter polymorphism (A-2518G) with spontaneous bacterial peritonitis (SBP). Fift y patients with post-hepatitis C liver cirrhosis and ascites were categorized into two groups; group I included 25 patients with SBP and group II included 25 patients free from SBP. In addition, a group of 20 healthy volunteers were included. We assessed the MCP-1 gene polymorphism and gene expression as well as interleukin (IL)-10 levels in both blood and ascitic fl uid. A signifi cant MCP-1 gene polymorphism was detected in groups I and II (P=0.001 and 0.02 respectively). Group I was associated with a signifi cantly higher frequency of AG genotype [control 8 (40%) vs SBP 19 (76.0%), P < 0.001], and group II was associated with a signifi cantly higher frequency of GG genotype when compared to healthy volunteers [control 1 (5%) vs cirrhotic 16 (64%), P < 0.001]. Accordingly, the frequency of G allele was signifi cantly higher in both groups (I and II) [control 10 (25%) vs SBP 27 (54%), P < 0.001 and vs cirrhotic 37 (74.0%), P < 0.001, respectively]. Th e total blood and ascetic fl uid levels of IL-10 and MCP-1 gene expression were signifi cantly higher in group I than in group II. Group I showed signifi cant reductions in the levels of MCP-1 gene expression and IL-10 in the whole blood and ascetic fl uid aft er therapy. MCP-1 GG genotype and G allele may predispose HCV infected patients to a more progressive disease course, while AG genotype may increase the susceptibility to SBP. Patients carrying these genotypes should be under supervision to prevent or restrict further complications.

Biography:

Cardiac metabolism is essential in myocardial contraction. Here, we analyzed the eff ect of metabolic substrates (fatty acids, pyruvate and lactate in normal Tyrode’s solution, termed NF) on myocyte contractility in rat left ventricular myocytes. Our results showed that NF signifi cantly increased myocyte contraction and intracellular Ca2+ transients. L-type Ca2+ current or Na+- Ca2+ exchanger activity was not increased and myofi lament Ca2+ sensitivity was reduced by NF, suggesting key role of myofi lament on cardiac Ca2+ homeostasis and contraction with NF. Furthermore, NF diminished insulin-dependent tyrosine phosphorylations of insulin receptor or receptor substrate and eNOS-Ser1177. Beta-adrenergic stimulation with isoprenaline signifi cantly increased spontaneous myocyte contraction during diastole in NF. Collectively, NF impairs insulin signaling and reduces bioavailability of eNOS-derived NO, which desensitizes myofi lament Ca2+ sensitivity, increases Ca2+ level and contraction. In addition, it predisposes beta-adrenergic arrhythmogenesis in cardiac myocytes. Th e results reveal that it resembles an in vitro model of cardiac metabolic syndrome

Abstract:

Yin Hua Zhang has completed her PhD in 1999 from Seoul National University, College of Medicine and Post-doctoral studies from Oxford University, Cardiovascular Medicine. She directs Cardiovascular Laboratory studying Physiology and Pathology of the heart. She has published more than 40 papers in high ranking journals and is holding a number of national grants

Biography:

Abstract:

Drugs and specifi c supplements used for personalized medicine can be used to manage neurological disorders based on an individual’s personal genomic profi le. Th e development of an improved evidence-base for personalized and patient-decision making about the choice to use a dietary supplement can be a wise decision that provides health benefi ts. Addresses the wide variation in biological response to fi xed-dose supplementation, allow the researchers to advance personalized clinical care by estimating the specifi c supplement dosage needed to achieve the targeted blood concentration. Th e goal is to develop patient-specifi c therapeutic strategies aimed at improving patient health when it comes to getting the right drug and the right supplement to the right patient for optimal results. During the last 40 year, patients with Spielmeyer-Sjögren disease were treated with antioxidant supplementation. Th e patients were supplemented with a combination of vitamin E, vitamin C, methionine and butylated hydroxytoluene (BHT). As the disease began to progress, the treatment was changed to a combination of sodium selenite and vitamin E in some patients. Th e same combination was also given to children (vitamins B2 and B6 were also added for several years.) who had not received previous antioxidant supplementation. Th e latter combination (called the Westermarck formula) appeared to be helpful to some patients. Statistical correlations between various neurological items and relevant laboratory data were sought. In the older patients a signifi cant correlation was found between neurological dysfunction and ceruloplasmin, and also between epilepsy and ceruloplasmin, while a negative correlation was noticed between neurological dysfunction and glutathione peroxidase. In the younger patients, a negative correlation was observed between superoxide dismutase and epilepsy. Serum apolipoprotein B levels were below the normal range in the 6 patients investigated. So far the Westermarck formula seems to have been the best treatment devised yet in Spielmeyer-Sjögren disease, but further studies are needed for a better understanding of the pathogenesis of neuronal ceroid-lipofuscinoses disorders. For treating various health problems, it makes sense to take into account diet, genetic makeup, pathogens, pollutants and environment exposure, and to then judiciously use supplements to counter any nutrient defi ciencies. Making dietary changes alone frequently helps correct some of the most common. A good diet is a foundation but, for optimum health, we need to look aft er all aspects of being.