Day 2 :
ReMed Natural Medicine Clinic, Australia
Time : 09:05-09:30
Keonie Moore completed her studies at the renowned School for Complementary and Natural Medicine, Southern Cross University, Australia. As the Director of ReMed Natural Medicine Clinic, a multi-modality clinic that exemplifies scientific implementation in the Australian Health sector, she tours nationally to involve additional integrative clinics and practitioners in the assimilation of research findings and evidence into clinical practice. Most recently, she has presented on Metabolic Syndrome to the Integrative Medicine Education and Research Group, Alfred Hospital and published ‘Metabolic Syndrome: A case for collaborative care’ in the reputable journal, Advances in Integrative Medicine.
Metabolic syndrome is a known and well-documented forerunner to both Type 2 Diabetes Mellitus (T2DM) and cardiovascular disease. However, it is rarely viewed as a window of opportunity; a period of time where the long-term consequences are potentially reversible. Early detection with dietary and lifestyle interventions have been shown to reduce the incidence of progression to T2DM by almost 60%. Even though early detection can potentially alter the disease progression, there is still a significant lag between onset and diagnosis of T2DM. Whilst healthcare professionals have easy and clinically relevant point of care screening available, they are rarely conducted consistently in a clinical setting. As healthcare professionals and researchers, we need to ask ourselves ‘what is the cost?’ to the healthcare system, to the workforce and most of all to the health of the individual. Case studies will be used as a guide to highlight the use of implementation science; to promote the integration of research findings and evidence into healthcare policy and practice. There will be a strong practice-based focus on point of care screening, early detection and diet/lifestyle interventions to halt or slow the progression of metabolic syndrome and to address major flaws with current practices that impede effective implementation of new approaches to improving health outcomes.
Mayo Clinic, USA
Time : 09:30-09:55
Thomas J Sebo has been a Mayo Clinic Rochester Surgical Pathologist and Cytopathologist for 21 years completing a PhD in molecular biology prior to medical school, then coming to Mayo Clinic in 1987 for post-graduate training, first, in Internal Medicine then in Anatomic/Clinical Pathology, joining the Anatomic Pathology\\\\\\\\r\\\\\\\\nstaff January 1, 1993. He is Professor of Pathology (Mayo Medical School) with 185 publications in urologic, endocrine, and molecular pathology, and cytopathology, He has been Section Head of Frozen Section Laboratory, Urologic Pathology, and (currently) Endocrine Pathology. He began Mayo’s Molecular Cytology and, Imaging Laboratory combining digital image analysis and FISH.
The clinical utility of thyroid fine needle aspiration (TFNA) interpretation as a necessary step in the management of patients\\\\\\\\r\\\\\\\\nwith thyroid nodules has been an unquestioned success. However, the impact of TFNA has recently come under greater\\\\\\\\r\\\\\\\\nscrutiny. This is due to 3 main drivers: (1) the utilization of ultrasonography has led to an increase in detection of thyroid\\\\\\\\r\\\\\\\\nnodules, in turn, leading to an increase in the number of TFNA performed; (2) the introduction of the Bethesda classification\\\\\\\\r\\\\\\\\nscheme of TFNA has set the stage for “equivocation creep,” in which pathologists are increasingly reluctant to classify TFNA\\\\\\\\r\\\\\\\\nas unequivocally benign or malignant; and (3) the introduction of molecular testing into clinical practice has coincided with\\\\\\\\r\\\\\\\\nequivocal TFNA results leading clinicians to demand expensive molecular tests in hopes of more accurately defining a nodule’s\\\\\\\\r\\\\\\\\nbiology. This lecture focuses on these drivers and defines the criteria necessary for accurate and cost-effective interpretation\\\\\\\\r\\\\\\\\nof TFNA. This is an important topic because in the past decade, the number of thyroid malignancies per year has increased\\\\\\\\r\\\\\\\\nfrom roughly 21,000 (2002) to almost 60,000 (2012) while the death rate has been halved from 6.3% to 3.2%. In the coming\\\\\\\\r\\\\\\\\nera of cost-containment, it is essential that we apply common sense and critical data analysis to the interpretation of TFNA. If\\\\\\\\r\\\\\\\\nanything, the importance of traditional TFNA evaluation is as great today as it was when first introduced – to the extent that\\\\\\\\r\\\\\\\\nthe main purpose of TFNA now is to “reduce the risk of surgery.”
Biomarker Core Laboratory, USA
Ngoc-Anh Le completed his PhD in 1979 from University of California San Diego and his post-doctoral training with the SCOR-Atherosclerosis at Columbia\r\nUniversity, NYC. He has served as laboratory director for several multicenter trials, including the Strong Heart Study, CARDIA, SAMMPRIS, and BIOSIS. He is\r\ncurrently the director of the Biomarker Core Laboratory, Atlanta Research and Education Foundation, Atlanta VAMC. He has published more than 90 papers in\r\npeer reviewed journals.
T2DM is associated with increased risk for cardiovascular disease. Oxidatively modified LDL (oxLDL) is the primary\r\ncontributor. oxLDL have been measured in plasma but association with disease risk has been mixed. Plasma oxLDL are\r\naffected by pro- and anti-oxidant metabolites as well as circulating autoantibodies against oxLDL. Oxidative susceptibility of\r\nLDL to Cu++ induced oxidation as measured by lag time (min) is a functional assay for oxLDL. We hypothesize that with meal\r\nconsumption, oxidative susceptibility of LDL is increased and reduction of postprandial lipemia may reduce this susceptibility.\r\nPatients with metS participated in a randomized, double-blind, placebo-controlled study with cross-over with fenofibric acid\r\n(FA). After each treatment period, fasting (f) and postprandial (pp) plasma after a standardized mixed meal were collected for\r\nlipoprotein isolation. Both fasting (f) and postprandial (pp) LDL undergoes spontaneous oxidation (no Cu++) with comparable\r\nlag times (169 and 172). With FA, ppLDL is more protected, i.e. longer lag time (212 vs 151). In the presence of Cu++, lag\r\ntimes of fLDL are reduced for both periods (37 and 44). Compared to fLDL, reductions in ppLDL lag times were statistically\r\nsignificant only during placebo (37 vs 30) and not during FA (44 vs 38). Co-incubation with autologous HDL failed to protect\r\nLDL from oxidative modification. In summary, (1) ppLDL is more susceptible to oxidative modification, (2) treatment with FA\r\nreduced postprandial lipemia and oxidative susceptibility of ppLDL, and (3) HDL from metS appears to be dysfunctional and\r\nthis was not normalized by FA therapy.