Biography:

Haval Shirwan is Dr. Michael and Joan Hamilton Endowed Chair in Autoimmune Disease, Professor of Microbiology and Immunology, Director of Molecular Immunomodulation Program at the Institute for Cellular Therapeutics. He conducted his Graduate studies at the University of California in Santa Barbara, CA, and Postdoctoral studies at California Institute of Technology in Pasadena, CA. He joined the University of Louisville in 1998 after holding academic appointments at various academic institutions in the United States. His research focuses on the modulation of immune system for the treatment of immune-based diseases with particular focus on type 1 diabetes, transplantation, and development of prophylactic and therapeutic vaccines against cancer and infectious diseases.  He is an inventor on over a dozen of worldwide patents, founder and CEO/CSO of FasCure Therapeutics, LLC, widely published, organized and lectured at numerous national/international conferences, served on study sections for various federal and non-profit funding agencies, and is on the Editorial Board of a number of scientific journals. He is member of several national and international societies and recipient of various awards.

Abstract:

Type 1 diabetes (T1D) is a chronic autoimmune disease that impacts millions of people world-wide. Presently, there is no cure for T1D and treatment with exogenous insulin to manage diabetes is ineffective in controlling euglycemia in a substantial population of type 1 diabetics.  Transplantation of pancreatic islets as a source of beta cells producing insulin has proven effective in improving metabolic control in type 1 diabetic individuals. However, graft rejection is a major limitation of clinical islet transplantation that is controlled by chronic immunosuppression. Systemic use of immunosuppression is associated with various adverse effects that compromises the life quality of graft recipients.  We have been pursuing the development of targeted and localized immunomodulatory approaches as a safe and effective alternative to chronic immunosuppression. In particular, we developed biomaterials based on polyethylene glycol microparticles engineered with immunomodulatory ligands targeting islet destructive pathogenic T effector cells for physical elimination within the graft microenvironment. The application of this novel concept to the induction of tolerance to islet allografts as a cure for T1D will be discussed. 

Biography:

• Dr Paul J Davis is a graduate of Harvard Medical School and had his postgraduate medical training at Albert Einstein College of Medicine and the NIH. His academic positions have included Chair, Department of Medicine at Albany Medical College. He has served as President of American Thyroid Association, as a member of the Board of Directors of the American Board of Internal Medicine and he is Co-Head, Faculty of 1000 – Endocrinology. He serves on multiple Editorial Boards of His scientific interests include molecular mechanisms of actions of nonpeptide hormones, particularly, thyroid hormone. He and his colleagues described the cell surface receptor for thyroid hormone on integrin αvß3 that underlies the pro-angiogenic activity of the hormone and the proliferative action of the hormone on cancer cells. He has co-authored more than 200 original research articles and 30 textbook chapters and he has edited three medical textbooks.

Abstract:

Biography:

Diana Anderson (H index 54) holds the Established Chair in Biomedical Sciences at the University of Bradford. She obtained her first degree in the University of Wales and second degrees in the Faculty of Medicine, University of Manchester. She has 450+ peer-reviewed papers, 9 books, has successfully supervised 30 PhDs, is an Editorial Board Member of 10 international journals. She is Editor-in-Chief of a book series on Toxicology for the Royal Society of Chemistry. She gives key note addresses at various international meetings. She is a consultant for many international organisations, including WHO, EU, NATO, TWAS, UNIDO, OECD.

Abstract:

Spermatogonial stem cells (SSCs) are responsible for transmission of genetic information from males to their progeny. SSCs play pivotal roles in spermatogenesis and reproductive biology of gametes and treatment of infertility. Many chemicals have a negative impact on the SSCs, either directly, or indirectly through the somatic nursing cells. Eventually, these effects can inhibit fertility, and they may have negative consequences for the development of the offspring. Oxaliplatin is a platinum-organic drug with antineoplastic properties used for colorectal cancer and cytotoxicity due to platinum binding to DNA and the formation of intrastrand cross-links between neighbouring guanines. This study was to establish an oxidative stress model for antioxidant activity of some drugs investigated in SSCs in in vitro culture. The effects of oxaliplatin on SSCs were evaluated by standard cytotoxicity assays and the potential biochemical and molecular effects on the antioxidant system. Administration of oxaliplatin showed significant increases in DNA damage, p53 and bcl-2 gene expression levels concomitant with significant decreases in endogenous antioxidant enzymes SOD, CAT and GPx-mRNA gene expression. Glial cell line–derived neurotrophic factor (GDNF) is important for SSC self-renewal in vitro and in vivo, so we also assessed oxaliplatin on GDNF-mediated signalling in these cells and oxaliplatin significantly decreased GDNF-mRNA and associated protein. Oxaliplatin-induced DNA damage causes an increase in intracellular superoxide anions which are reduced by the exogenous antioxidant flavonoid, quercetin. This study highlights evidence that SCCs have antioxidant and antiapoptotic properties that could reverse oxaliplatin-induced testicular toxicity, in addition to their role in spermatogenesis.

Biography:

Jack A Coleman has earned his MD from the University of Cincinnati College Medicine in 1979, did his internship and General Surgery requirement at Cincinnati General Hospital and residency in Otolaryngology - Head and Neck Surgery at the University of Pittsburgh Eye and Ear Hospital as well as a fellowship at English Plastic and Cosmetic Surgery Center. He has been an Assistant Professor at Vanderbilt University and Clinical Assistant Professor at Eastern Virginia Medical School. Currently he is National Medical director for the Lung Institute. He has published over 23 articles in refereed journals, many book chapters and 5 books related to his various interests in medicine as well as national and international guest lecturer.

Abstract:

 

The Lung Health Institute has been treating chronic lung diseases with regenerative therapy for over four years and has treated over 5,000 patients. The diseases treated are in two broad categories: chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD). The common factor in these diseases that the treatment addresses is chronic inflammation. Up to this point these diseases have been treated with symptomatic control only with lung transplant being the only “curative” therapy. By utilizing autologous cells and Platelet Rich Plasma (PRP) the disease progress can be positively affected in the majority of patients treated. The cells and cytokines used will be reviewed as well as proposed mechanisms of action. Protocols utilized for the treatment will be reviewed along with changes that have been made over time. Two studies have been completed and will be summarized. The first is a review study of 568 patients with COPD treated in 2015. Self-reported quality of life measures using the Clinical COPD Questionnaire and pulmonary function tests were measure before treatment and 6 months after. 73% of patients had positively affected quality of life scores and no significant changes were noted in the PFT scores. The second study is a prospective study of 207 patients with COPD (167) or ILD (40). 124 patients completed the 6 month study period. Paired sample T-tests were used for data analysis. 90/124 reported CCQ score unchanged or improved (72.5%), increases of greater or equal to 0.4 (considered significant change for CCQ) was 61/124 (49.2%). We will also discuss need for further testing such as randomized control studies and review potential new therapies to improve treatments for these patients.

Biography:

J Koudy Williams is a DVM with over 35 years of experience in performing translational research using different animal models of human disease. He has published over 120 full length manuscripts and 20 chapters and reviews. His focus is on women’s health and recently on Regenerative Medicine approaches to restoration of the urinary sphincter for women with urinary incontinence.

Abstract:

Regenerative Medicine offers the promise of an unlimited amount of tissue and organ repair and replacement. Great progress has been made in preclinical studies and many applications are now in the clinical stage. Regenerative Medicine is beginning to explore the potential effects of efficacy in different patient populations. The risk urinary incontinence in women is age and obesity related, and is a chronic disease influenced by the sex hormone milieu. It is well known that aging and diabetes reduce the ability of tissue to regenerate. It also stands to reason that these changes may also influence the efficacy of Regenerative Medicine approaches to urinary incontinence. In fact, this may explain, in part, why cell therapies for urinary incontinence are so successful in preclinical studies (which historically use younger health animals with acute UI)? In contrast, the results of clinical studies in older women with varying body weights, sex hormone status and chronicity of disease. This presentation will first review select studies identifying the effects of age, gender and hormone status on the ability of cells to stimulate regeneration of tissues. The majority of this presentation will introduce a female nonhuman primate (NHP) model of induce intrinsic urinary sphincter deficiency (ISD) and then present results of several studies describing the effects of skeletal muscle precursor cell (skMPC) treatment in acute vs. chronic fibrotic ISD; older and younger NHPs and in NHPs with stress-induced dysmenorrhea. The presentation will close with the results of recent studies identifying the use of chemokines on sphincter regeneration in this animal model. 

Biography:

Esmaiel Jabbari has completed his PhD at Purdue University and Post-doctoral studies at Monsanto, Rice University, and Mayo Clinic. He is the Director of Tissue Engineering and Drug Delivery Laboratory and Full Professor of Chemical and Biomedical Engineering at University of South Carolina. He received the Berton Rahn Award from AO Foundation in 2012 and the Stephen Milam Award from Oral and Maxillofacial Surgery Foundation in 2008. He was elected to the College of Fellows of AIMBE in 2013. He has published >250 peer-reviewed articles and presented >260 conference lectures. He serves as Academic Editor of PLOS ONE.

Abstract:

Osteogenesis and vascularization during development are coupled by spatiotemporal regulation of paracrine signaling in which the invading vascular endothelial progenitor cells secrete osteogenic morphogens to stimulate cell differentiation and bone formation. Conversely, the committed mesenchymal stem cells (MSCs) in the vicinity of the vascular endothelial cells release vasculogenic morphogens to further stimulate vasculogensis for the metabolically highly active osteoblasts. The objective of this work was to investigate the effect of micro-patterning of mesenchymal stem cells (MSCs) and endothelial colony forming cells (ECFCs) within a 3D hydrogel matrix combined with localized delivery of osteogenic and vasculogenic morphogens BMP-2 and VEGF on synergistic expression of paracrine signaling factors and coupling of osteogenesis and vasculogenesis. Human MSCs and sustained release BMP-2 nanogels were encapsulated in a slow-resorbing polyethylene glycol-based hydrogel matrix containing micro-channels. Next, a combination of human MSCs, human ECFCs, and on-time release VEGF nanogels were delivered to the micro-channels of the matrix in a fast-resorbing galatin-based hydrogel. This approach resulted in spatial patterning of MSCs and ECFCs and spatiotemporal delivery of BMP-2 and VEGF morphogens. The effect of cell and morphogen patterning on vascularized osteogenesis and paracrine signaling was assessed by biochemical, mRNA, protein analysis, and immunofluorescent staining. The localization of MSCs to the matrix and MSCs+ECFCs to the microchannels combined with temporal release of BMP-2 in the matrix and VEGF in the channels sharply increased the expression of paracrine signaling factors basic fibroblast growth factor (bFGF, vasculogenic and osteogenic), platelet-derived growth factor (PDGF, vasculogenic), and transforming growth factor-beta (TGF-β, osteogenic) by the encapsulated human MSCs and ECFCs. These results suggest that osteogenesis and vascularization are coupled by localized secretion of paracrine signaling factors by the differentiating MSCs and ECFCs.

Biography:

Bruce K. Young is a graduate of Princeton University and New York University School of Medicine. He is internationally known as a leader and innovator in Obstetrics and Gynecology.  His  122 peer-reviewed publications report various fetal heart rate patterns and their relationship with fetal acid base metabolism and adverse neonatal outcome, referred to in the major obstetrics textbooks, estriol conjugates in amniotic fluid as a marker of fetal kidney function, fetoscopic surgery, risk assessment for high risk pregnancies, incompetent cervix, recurrent miscarriage, the fetal immune system, maternal-fetal immunologic cross-talk, and currently, human amniotic fluid derived stem cells. He has edited 2 books on Maternal-Fetal Medicine and written 2 books for the general reader.  He is a member of the Helen Kimmel Srem Cell Research Center, emeritus Director of the New York University-Langone Medical Center Division of Maternal-Fetal Medicine and presently directs the Pregnancy Loss Prevention Center there.

 

 

 

Abstract:

Amniotic fluid cells from second trimester amniocentesis(hAFSC) have been found to be a source of multipotent stem cells which might overcome the limitations of expansion, histocompatibility, tumorigenesis and ethical issues associated with the use of human embryonic cells. Previous work by others demonstrated pluripotency and growth patterns in c-Kit selected cells. We sought to perform a more comprehensive investigation of their  pluripotency  and the culture characteristics and distribution of stem cell markers in c-Kit selected cells compared to c-Kit negative cells.  Using MACS & FACS we found less than 5% of HAFSC were c-Kit positive. However when cultured,  between 15-90% of the c-Kit negative cells expressed CD90, SSEA4 or TRA-1-60, in varying amounts . There was persistence of stem cell markers including expression of SSEA4, TRA-1-60, CD90 in vitro through multiple passages and subpopulations in a high percentage of cells. There was increased Oct4, Nanog and Sox2 mRNA expression in cells derived from 15-17 gestation week amniotic fluid samples versus longer gestational ages. Double and triple labeled cell populations were identified by MACS .  5.5% of c-Kit negative cells were triple positive for SSEA4, TRA-1-60 and CD90 expression. This may be a more efficient method than c-kit selection of hAFSC  because  stem cell markers expression was equal to or exceeded by the c-kit negative cells in our results. Differentiation of amniotic fluid cells was successfully induced for neural, bone and cartilage lineages using specific induction media as demonstrated by morphologic staining and fluorescent histochemistry. The occurrence of triple-labeled cell populations poses the intriguing possibility of cells with a closer resemblance to embryonic stem cells.  Our results confirm  that hAFSC  maintain pluripotency markers in culture over enough passages to provide sufficient numbers of cells for clinical use.  Current studies with serum-free media  offer  therapeutic promise.

 

Biography:

Mari Dezawa is graduated from Chiba University School of Medicine in 1989, and got PhD degree in 1995 at the same institution. She moved to Yokohama City University as Assistant Professor of Dept Anatomy in 2000 where she started to work with mesenchymal stem cells (MSCs). After moving to Kyoto University Graduate School of Medicine as Associate Professor in 2003, she discovered methods to induce neurons and skeletal muscle cells from human MSCs. In 2008, she became Professor and Chair of Department of Stem Cell Biology and Histology, Tohoku University Graduate School of Medicine, where she discovered muse cells (PNAS, 2010, PNAS, 2011, Nat Protocol, 2013, JASN, 2017). 

Abstract:

Multilineage-differentiating stress enduring (muse) cells are naturally existing unique endogenous stem cells that are non-tumorigenic and are pluripotent-like. They express pluripotent markers, can generate cells representative of all three germ layers from a single cell and are able to self-renew. Since they express specific receptor for damage signal, they can preferentially home into damaged site after topical injection or intravenous injection with lower entrapment in the lung and spleen. After integration, they replenish lost cells by spontaneous differentiation into tissue-compatible cells, leading to robust tissue and functional regeneration. The unique reparative functions of Muse cells were demonstrated in animal models of liver cirrhosis, partial hepatectomy, stroke, skin ulcer of diabetes mellitus and chronic kidney disease. They do not have to be “induced,” or genetically manipulated, to be pluripotent or be purposive cells before transplantation as required with some other cell varieties. They can be collected as cells positive for SSEA-3, a surface marker for pluripotent stem cells, from readily accessible sources such as the bone marrow (~0.03% of the total mononucleated cell population), and from cultured fibroblasts (several %), as well as from the dermis and adipose tissue. Recently, Muse cells are shown to circulate in peripheral blood in healthy donors, and the number increases in stroke patients in an acute phase, suggesting that endogenous Muse cells are mobilized into peripheral blood to repair tissues while their number is not sufficient to recover, and that supply of exogenous Muse cells is expected to deliver statistically meaningful functional recovery. Overall, Muse cells are a feasible source for cell-based approaches，and may safely provide clinically relevant regenerative effects compatible with the ‘body’s natural repair systems’ by simple cost-effective strategy-collection of Muse cells from sources, large scale expansion and intravenous injection.