Day 1 :
Keynote Forum
Hailong An
Hebei University of Technology, China
Keynote: Identification of the calcium-dependent gating and targeted-drug discovery of CaCCs
Time : 09:00
Biography:
Abstract:
Keynote Forum
Vaughn Smider
Scripps Research Institute, USA
Keynote: Cow antibodies: Unusual biology and new opportunities.
Time : 12:20-13:00
Biography:
Dr. Vaughn Smider received his M.D. and Ph.D. degrees from Stanford University School of Medicine. He is currently on the faculty of the Scripps Research Institute in the Cell and Molecular Biology Department, and is also the Chief Scientific Officer of Sevion Therapeutics. Dr. Smider’s research focuses on both basic biology and applied technology in the antibody field, including antibody genetics, structure, engineering and development.
Abstract:
Typical mouse or human antibodies have CDR H3 loop lengths of 10-15 amino acids, which often form a flat binding surface for contact with antigen. In contrast, cows can form CDR H3 regions of over 70 amino acids, which form novel ‘stalk’ and ‘knob’ domains that protrude far from the antibody surface. These antibodies utilize an unusual diversity generating system that alters cysteine positions and disulfide bonding patterns in the knob. The functional importance of this antibody system is illustrated by recent experiments showing that cows, unlike other species, can make a broad and potent neutralizing antibody response to spike antigens of HIV.
Keynote Forum
Iftikhar Ahmed
University of Southampton, Southampton, UK
Keynote: Volatile organic metabolites as novel, non-invasive diagnostic biomarkers in inflammatory Bowel Disease
Time : 11:40-12:20
Biography:
Abstract:
Keynote Forum
Orkid Coskuner-Weber
Turkısh-German University, Turkey
Keynote: Mitochondrial Dysfunction, Oxidative Stress and Genetic Factors in Alzheimer´s Disease
Biography:
Orkid Coskuner-Weber is an expert in Alzheimer´s and Parkinso´s disease mechanism studies and monoclonal antibody design. She recived her Ph.D. degree from the Universitaet zu Koeln in Germany. She was a postdoc at Johns Hopkins and Stanford Universities. She was an assistant professor at George Mason University and at the University of Texas at San Antonio. She recently took a position in Istanbul for opening the Alzheimer´s and Parkinson´s disease research center. She has been associated with the National Institute of Standards and Technology since 2005. She develops and uses quantum chemical, statistical mechanical, bioinformatics, artificial intelligence and experimental tools in her research activities.
Abstract:
Alzheimer`s disease affects 10 million Americans and 44 million people worldwide. There are various biochemical mechanisms and processes that play a role in Alzheimer´s disease. These mechanisms are debated in the literature and there is currently no efficient drug that halts the progress of the disease. Efficient and effective drug design studies require detailed understanding of associated biochemical and biophysical mechanisms at the atomic level with dynamics. We investigate all biochemical processes and mechanisms associated with Alzheimer´s disease using quantum chemistry, statistical mechanics, bioinformatics, artificial intelligence and experiments. Using the information that we gain from biochemical investigations, we design monoclonal antibodies in collaboration with pharmaceutical companies. In this talk, we will present some of our studies about the roles of genetics, mitochondrial dysfunction and oxidative stress mechanisms in Alzheimer´s disease. Our theoretical and experimental results show that ATP reduces the fibrillization of disordered amyloid-β, transition metal ion coordination with amyloid-β increases the fibrillization progress and genetic factors significantly impact the fibrillization and aggregation properties of amyloid-β alloforms. Furthermore, we will provide insights into monoclonal antibody design for the treatment of Alzheimer´s disease.
Keynote Forum
Jun-ichi KADOKAWA
Kagoshima University, Japan
Keynote: Enzymatic preparation of nanostructured supramolecular assemblies from biological macromolecules
Time : 09:55-10:35
Biography:
Jun-ichi Kadokawa received his Ph.D. in 1992. He then joined Yamagata University as a Research Associate. From 1996 to 1997, he worked as a visiting scientist at the Max-Planck-Institute for Polymer Research in Germany. In 1999, he became an Associate Professor at Yamagata University and moved to Tohoku University in 2002. He was appointed as a Professor of Kagoshima University in 2004. His research interests focus on polysaccharide materials. He received the Award for Encouragement of Research in Polymer Science (1997) and the Cellulose Society of Japan Award (2009). He has published more than 200 papers in academic journals.
Abstract:
Biological macromolecules, such as polysaccharide and protein (peptide) exhibit specific in vivo functions in living systems, which are appeared by their controlled primary and higher-order assembled structures. Many kinds of conjugates, which are assembled from such biological macromolecules, are present as vital materials in nature. Therefore, artificial assemblies from biological macromolecules can be expected as new bio-based functional materials, which have a potential for practical applications in biomedical and tissue engineering fields. Polysaccharides are known to form nanostructured higher-order assemblies by non-covalent linkages such as hydrogen bonds. Accordingly, the construction of hierarchically assembled structures, so-called supramolecules, from polysaccharides has attracted much attention to obtain new polysaccharide-based functional materials. For example, amylose, which is a linear polysaccharide linked through a(1g4)-glycosidic linkages and well-known as a component of starch, forms regularly controlled assemblies, that is, inclusion complex and double helix, depending on whether guest compounds are present or not. Amylose with well-defined structure is synthesized by phosphorylase-catalyzed enzymatic polymerization using a-d-glucose 1-phosphate (G-1-P) and a(1g4)-oligoglucan (maltooligosaccharide) as monomer and primer, respectively. As the polymerization is initiated from the non-reducing end of the maltooligosaccharide primer, the enzymatic polymerization can be conducted using primers covalently linked to other polymeric materials (immobilized primers) at the reducing end, giving rise to amylose-grafted bio-based polymeric materials.1,2 By means of the property of spontaneously double helix formation from the enzymatically synthesized amylose, the phosphorylase-catalyzed enzymatic polymerization using the immobilized primers produces supramolecular assemblies comprising the double helix cross-linking points.3,4 For example, the phosphorylase-catalyzed enzymatic polymerization using the immobilized primers on chitin nanofibers was investigated to produce amylose-grafted chitin nanofiber assemblies.5 Owing to supramolecular network structure by the double helix cross-linking points, the product formed hydrogels, which were further converted into porous materials with controlled nano- and microstructures by lyophilization.
Location: Los Angeles
Session Introduction
Bill Shelander
CEO, Anven Biosciences, Inc., USA
Title: Identification of pathogenic antigen:antibody complexes of Alzheimer’s disease using “proxy antigensâ€
Biography:
Bill Shelander is a co-founder and CEO of Anven Bioscience. Previously he held an appointment at Lawrence Berkeley National Lab as a commercialization expert, building on a career focused on science and technology ventures. He has directed international funds with major investors from Japan, Taiwan, and the United States and continues to serve as an advisor for high tech enterprises. He earned a BS in Systems Engineering at Georgia Tech, an MSE in Chemical Engineering from West Virginia College of Graduate Studies, and an MBA from Stanford University. He also teaches innovation and entrepreneurship at Haas School of Business at UC Berkeley and at the Civil and Environmental Engineering Department of Stanford University.
Abstract:
Alzheimer’s disease (AD) is a progressive, neurodegenerative disease and believed by many to be associated with extracellular amyloid plaques and intracellular neurofibrillary tangles1, 2. Researchers have also long suspected that as neurodegeneration occurs in the brain, the immune response propagates disease-related antibodies in the blood, which will lastingly present in the serum of AD patients. However, despite enormous efforts through decades of research, no definitive early blood-based biomarker for AD has yet been validated3. A new approach involving “proxy antigens” provides profound new insights into the pathogenesis of Alzheimer’s disease. By isolating the pathogenic antigen:antibody complexes directly involved in the causation and progression of Alzheimer’s, a direct biomarker of the neurodegenerative disease can measure and monitor the subject’s immune response at the earliest stages of the disease.
Proxy antigens are biosimilar, but otherwise non-native, molecules that bind to antibodies in the hypervariable region with exquisite sensitivity and specificity4-7. Using this unprecedented capability, a systematic, step-by-step procedure first isolated the complexes unique to subjects exhibiting Alzheimer’s pathology (figure 1). Thereafter, the Alzheimer’s-specific proxy antigens provide a clear diagnostic tool to detect whether the Alzheimer’s complexes are present or absent in blood samples. One high value application of AD-specific proxy antigens can profile and stratify clinical trial populations, i.e. differentiate and predict which subjects would respond to a drug and which would not. For example, retrospective analysis of archived blood samples from a past clinical trial can be used to unambiguously reassess subgroups of subjects and offer an enriched population for a guided prospective clinical trial. Additionally, and perhaps most importantly, the identified Alzheimer’s complexes provide definitive targets for future therapeutic development.
Hailong An
Hebei University of Technology, Tianjin, China
Title: Identification of the calcium-dependent gating and targeted-drug discovery of CaCCs
Biography:
Professor Hailong An received his Ph.D. degree in Biophysics in Hebei University of Technology in 2005. After that, he was appointed to the faculty in Institute of Biophysics, Hebei University of Technology. From 2006 to 2008, he worked in Hebei Medical University under supervision by Prof. Hailin Zhang as a postdoc. Awarded by China Scholarship Council, he spent 20 months in Prof. Diomedes E. Logothetis’ Lab as a visiting scholar.
Professor Hailong An focuses on understanding the structure-function relationship of ion channels, the relationship between ion channels and major diseases and drug screening targeting at ion channels. More than 50 papers have been published in academic journals such as Scientific Reports, Journal of Biological Chemistry, British Journal of Pharmacology etc., and more than 40 papers were included in the SCI (total impact factor: 126.52), the paper was cited more than 200 times.
Abstract:
Calcium-activated chloride channels (CaCCs) play vital roles in a variety of physiological processes. Transmembrane protein 16A (TMEM16A) has been confirmed as the molecular counterpart of CaCCs which greatly pushes the molecular insights of CaCCs forward. However, the detailed mechanism of Ca2+ binding and activating the channel is still obscure. To identify the calcium binding site, the authors presented a computational approach which combined the fragment homology modeling with molecular dynamics simulation. Our data show that the first intracellular loop serves as a Ca2+ binding site including D439, E444 and E447. The experimental results indicate that a novel residue, E447, plays key role in Ca2+ binding. Compared with WT TMEM16A, E447Y produces a 30-fold increase in EC50 of Ca2+ activation and leads to a 100-fold increase in Ca2+ concentrations that is needed to fully activate the channel.
It is well established that TMEM16A is a drug target in many diseases, including cystic fibrosis, hypertension, asthma, and various tumors. Therefore, identifying potent and specific modulators of the TMEM16A channel is crucial. Here, the authors identified two modulators from the traditional Chinese medicine, an activator, Ginsenoside Rb1 (GRb1) which can increase the amplitude and frequency of contractions in an isolated guinea pig ileum assay in vivo and serve as a lead compound for the development of novel drugs for the treatment of diseases caused by TMEM16A dysfunction, an inhibitor, matrine which can dramatically inhibit the growth of lung adenocarcinoma tumors in xenografted mice, and may function as an anti-lung adenocarcinoma drug targeting at TMEM16 channels.
Chibuzo Carole Nweze
Nasarawa State University, Nigeria
Title: Hypoglycemic, Hepatoprotective and Hypolipidemic Effect of Pleurotusostreatus in Alloxan-Induced Hyperglycemic Rats
Biography:
Chibuzo Carole Nweze has her expertise in nutritional and Food Biochemistry. She has passion for indigenous functional foods and significant of the foods phytochemicals especially, their antioxidants related properties in scavenging free redicals in the cells. Her interest to look at these foods may improve the health of the middle class in the country, as most of them cannot afford to purchase most nutritionally important antioxidants that are costly for the low-income earners. Chibuzo is a senior lecturer in Nasarawa State University Keffi, Nigeria where she has been in academics for ten years. She has a PhD in Biochemistry from University of Jos, Nigeria, MSc from University of Lagos, Nigeria and Bachelor degree from Federal University of Technology Owerri, Nigeria.
Abstract:
Statement of problem: Diabetes mellitus is a metabolic disorder characterized with hyperglycemia and often associated with many complications in several organs most especially in liver and kidney. The purpose of this study is to evaluate effect of Pleurotusostreatus (Oyster mushroom) in Diabete mellitus and its complications. Methodology and theoretical orientation: Experimental diabetes were induced following an overnight fast, by a single intraperitoneal (i.p.) injection of Alloxan monohydrate at dose 150 mg/kg b.wt. to rats in group II to V. Control animals (group I ) were injected with 0.5ml of normal saline. Hyperglycemia was confirmed three days after injection by measuring the blood glucose level. The Diabetic rats were then fed with broiler feeds supplemented with dried Oyster mushroom powder at doses of 10 and 20g daily for a period of four weeks whereas the control animals were given only broiler feeds. Findings: The results show that intraperitoneal (i.p.) injection of Alloxan significantly (p<0.05) elevated blood glucose level accompanied by significantly (p<0.05) increase in serum Aspartate aminotransferase AST, Alanine aminotransferase ALT, Alkaline phosphatase ALP, hyperlidemia, sodium Na+, bicarbonate ion HCO3 , potassium K+ and with a concomitant significant (p<0.05) decrease in serum total protein , high density lipoprotein and chloride. Conclusion: Supplementation of dried oyster mushroom powder at doses of 10 and 20gdaily for a period of four weeks resulted in a reversal of the above pathological conditions associated with diabetes. Recommendation: Therefore, the study indicated that oyster mushroom besides its hypoglycemic and hypolipidemic effects could also protect the liver and kidney against impairment due to hyperglycemia.