11^th World Congress and Expo on Cell & Stem Cell Research March 25-26, 2019 Hong Kong, China

Biography:

Paul J Davis obtained the MD degree at Harvard Medical School and had his internal medicine clinical and endocrine research training, respectively, at Albert Einstein College of Medicine (NY) and the NIH. He has served in a number of senior administrative positions in academic institutions and in national societies. His research is focused on the molecular mechanisms of thyroid hormone actions. He has co-authored 275 research publications and 40 textbook chapters; he has co-edited four textbooks. He and colleague SA Mousa described the cell surface receptor for thyroid hormone on integrin αvβ3. They also co-founded NanoPharmaceuticals LLC (Rensselaer, NY).

Abstract:

Integrin α_Vβ₃ is a structural protein of the plasma membrane that is generously expressed by cancer cells and dividing endothelial cells; until recently, important functions of the integrin have been seen to relate to cell-cell and cell-extracellular matrix protein interactions. The extracellular domain of αvβ₃ is now appreciated to contain a small molecule receptor for thyroid hormone, primarily, L-thyroxine (T4). From this cell surface hormone receptor, the expression of a large panel of cancer-relevant genes is differentially regulated by thyroid hormone analogues. These genes include multiple cell division regulating cyclins and HRAS and KRAS genes linked to uncontrolled cell division; KRAS is also related to cancer stem cell (CSC) maintenance and to tumor recurrence. Transcription of these genes is downregulated by P-bi-TAT, consisting of a thyroid hormone analogue, tetraiodothyroacetic acid (tetrac), chemically coupled to polyethylene glycol (PEG). IDH2 is involved in tumor cell mitochondrial metabolism; P-bi-TAT decreases IDH2 transcription, thus promoting apoptosis by the intrinsic (mitochondrial) pathway. Expression of ERBB2 is important to tumor cell invasiveness and metastasis and is downregulated by P-bi-TAT. The ERBB family of proteins is also important to tumor cell chemoresistance. αvβ3 regulates via the thyroid hormone receptor the transcription of ABCB1, whose gene product—the P-glycoprotein of the plasma membrane—exports a number of chemotherapeutic agents from tumor cells as a component of chemoresistance. Expression of pro-angiogenic VEGFA, bFGF and PDGF genes is also decreased by P-bi-TAT action at αvβ₃, as is the EGFR gene whose transcription is important to angiogenesis and tumor cell proliferation. Matrix metalloproteinase (MMP) gene expression is critical to cell migration/metastasis and to angiogenesis; P-bi-TAT induces a signal at the integrin to reduce MMP production. The EGFR protein is a tyrosine kinase and thus P-bi-TAT, by downregulating expression of EGFR, functions as a tumor cell-relevant tyrosine kinase inhibitor (TKI). Another TKI gene affected by P-bi-TAT is KIT. This complex set of actions of P-bi-TAT on gene expression implies that T4 may act on tumor cell αvβ₃ to support, rather than inhibit, the expression of these genes whose products are linked to tumor cell survival. We have shown that T4 via αvβ3 does stimulate expression of VEGFA and bFGF, of MMPs, ABCB1 in tumor cells. Transduction of thyroid hormone and hormone analogue signals downstream of αvβ₃ is a function of MAPK/ERK1/2 and PI3K, the genes and enzyme activities of which are regulated by thyroid hormone. These observations indicate that the importance of αvβ₃ to cancer cell function and survival also includes the actions of thyroid hormone analogues on the integrin.

Biography:

Keating received her Bachelors of Science degree in Chemistry from the University of Wisconsin, Madison and her PhD in Chemistry from the University of California, Davis. She was a Postdoctoral Fellow at Emory University and at Pacific Northwest National laboratory. She has worked as an analytical and physical chemist at AT&T BellLaboratories, Wyeth, and the University of Illinois, specializing in NMR spectroscopy of proteins and small molecules. Dr. Keating transitioned to scientific editing in 2009 and currently is Science Editor/Medical Writer at the Pharmaceutical Research Institute at the Albany College of Pharmacy and  Health Sciences in Rensselaer, NY.

Abstract:

Integrin α_Vβ₃ is a structural protein of the plasma membrane that is generously expressed by cancer cells and dividing endothelial cells; until recently, important functions of the integrin have been seen to relate to cell-cell and cell-extracellular matrix protein interactions. The extracellular domain of αvβ₃ is now appreciated to contain a small molecule receptor for thyroid hormone, primarily, L-thyroxine (T4). From this cell surface hormone receptor, the expression of a large panel of cancer-relevant genes is differentially regulated by thyroid hormone analogues. These genes include multiple cell division regulating cyclins and HRAS and KRAS genes linked to uncontrolled cell division; KRAS is also related to cancer stem cell (CSC) maintenance and to tumor recurrence. Transcription of these genes is downregulated by P-bi-TAT, consisting of a thyroid hormone analogue, tetraiodothyroacetic acid (tetrac), chemically coupled to polyethylene glycol (PEG). IDH2 is involved in tumor cell mitochondrial metabolism; P-bi-TAT decreases IDH2 transcription, thus promoting apoptosis by the intrinsic (mitochondrial) pathway. Expression of ERBB2 is important to tumor cell invasiveness and metastasis and is downregulated by P-bi-TAT. The ERBB family of proteins is also important to tumor cell chemoresistance. αvβ3 regulates via the thyroid hormone receptor the transcription of ABCB1, whose gene product—the P-glycoprotein of the plasma membrane—exports a number of chemotherapeutic agents from tumor cells as a component of chemoresistance. Expression of pro-angiogenic VEGFA, bFGF and PDGF genes is also decreased by P-bi-TAT action at αvβ₃, as is the EGFR gene whose transcription is important to angiogenesis and tumor cell proliferation. Matrix metalloproteinase (MMP) gene expression is critical to cell migration/metastasis and to angiogenesis; P-bi-TAT induces a signal at the integrin to reduce MMP production. The EGFR protein is a tyrosine kinase and thus P-bi-TAT, by downregulating expression of EGFR, functions as a tumor cell-relevant tyrosine kinase inhibitor (TKI). Another TKI gene affected by P-bi-TAT is KIT. This complex set of actions of P-bi-TAT on gene expression implies that T4 may act on tumor cell αvβ₃ to support, rather than inhibit, the expression of these genes whose products are linked to tumor cell survival. We have shown that T4 via αvβ3 does stimulate expression of VEGFA and bFGF, of MMPs, ABCB1 in tumor cells. Transduction of thyroid hormone and hormone analogue signals downstream of αvβ₃ is a function of MAPK/ERK1/2 and PI3K, the genes and enzyme activities of which are regulated by thyroid hormone. These observations indicate that the importance of αvβ₃ to cancer cell function and survival also includes the actions of thyroid hormone analogues on the integrin.

Biography:

Diana Anderson (H index 62) 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 500+ peer-reviewed papers, 10 books, has successfully supervised 32 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 plenary and key note addresses at various international meetings. She is a consultant for many international organizations, including WHO, EU, NATO, TWAS, UNIDO, OECD.

Abstract:

Germline stem cells are susceptible to anticancer drug induced-DNA damage and oxidative stress, and even low doses to the testicular cells may pose reproductive risks with possible treatment-related infertility. DNA damage in spermatogonial stem cells, caused by chemotherapy, could induce cell cycle arrest and germ cell apoptosis, with the potential to cause infertility in men. Spermatogonial stem cells are the only cell type capable of transmitting genetic information to future generations. Various compounds have a negative impact on the germline stem cells, either directly, or indirectly affecting them through their action on the spermatogonial cells. Eventually, these effects can inhibit fertility, and may have toxic consequences for the progress of the progeny. Oxaliplatin is a platinum-based anti-cancer drug with antineoplastic properties used mainly for colorectal cancer. It is cytotoxic due to platinum binding to DNA and the formation of intrastrand cross-links between neighbouring guanines. To examine the effects of oxaliplatin on spermatogonial cells separated using STAPUT unit-gravity velocity sedimentation. DNA damage was assessed in the Comet assay. The effects of oxaliplatin on mRNA and their proteins of P53, P21 and BLC2 were also studied using quantitative polymerase chain reaction (qPCR) and Western blot methods. Results indicated that oxaliplatin induced DNA damage and significantly increased levels of P53, P21 and decreased BLC2 mRNA and their proteins.

Understanding the mechanisms of action of oxaliplatin in spermatogonial stem cells is an important way to examine emerging new protection strategies for the reproductive system.

Biography:

Aibing Wang obtained BS and MS from Hunan Agricultural University (HUNAU) in 1998 and 2001, respectively; PhD majored in Biochemistry and Molecular Biology from Peking Union Medical College (PUMC) in 2005. He was a Visting and Research Fellow in National Heart, Lung and Blood Institute (NHLBI) of National Institutes of Health (NIH) during 2005-2011. He worked as a Biologist and Senior Biologist in NIH during 2011-2016; He joined in CVpath Insitute Inc as a Senior Scientist in 2016; Currently, he is a Professor of Molecular biology and virology in the School of Veterinary Medicine of Hunan Agricultural Univesity since 2016. He has obtained 3 awards from NIH and 3 grants from the Chinese government, applied for 3 patents and published 45 peer-reviewed publications. His current research interests mainly include: investigating the gene functions or molecular mechanisms associated with virus infection and other diseases; exploring the development of virus detection and vaccine using cutting-edge technologies such as CRISPR/Cas9.

Abstract:

Targeted integration of exogenous genes into so-called safe harbors/friend sites, offers the advantages of expressing normal levels of target genes and preventing potentially adverse effects on endogenous genes. However, the ideal genomic loci for this purpose remain limited. Additionally, due to the inherent and unresolved issues with the current genome editing tools, traditional embryonic stem (ES) cell-based targeted transgenesis technology is still preferred in practical applications. Here, we report that a high and repeatable homologous recombination (HR) frequency (>95%) is achieved when an approximate 6kb DNA sequence flanking the MYH9 gene exon 2 site is used to create the homology arms for the knockout/knock-in of diverse nonmuscle myosin II (NM II) isoforms in mouse ES cells. The easily obtained ES clones greatly facilitated the generation of multiple NM II genetic replacement mouse models, as characterized previously. Further investigation demonstrated that though the targeted integration site for exogenous genes is shifted to MYH9 intron 2 (about 500bp downstream exon 2), the high HR efficiency and the endogenous MYH9 gene integrity are not only preserved, but the expected expression of the inserted gene(s) is observed in a pre-designed set of experiments conducted in mouse ES cells. Importantly, we confirmed that the expression and normal function of the endogenous MYH9 gene is not affected by the insertion of the exogenous gene in these cases. Therefore, these findings suggest that like the commonly used ROSA26 site, the MYH9 gene locus may be considered a new safe harbor for high-efficiency targeted transgenesis and for biomedical applications.

Biography:

Lin received his PhD degree at SUNY Buffalo in 1991. Dr. Lin has served at the VA Hospital and Ordway Research Institute in Albany, NY as a senior scientist. Later, he worked at the Pharmaceutical research Institute (PRI) at the Albany College of Pharmacy and Health Sciences, Albany, NY. Dr. Lin joined Taipei Medical University as full professor in 2012. For the past three years, his research has focused on mechanisms involved in thyroidhormone-induced pathogenesis in colorectal cancer and other types of cancers.

Abstract:

The checkpoint programmed cell death protein 1 (PD-1)/ programmed death-ligand 1(PD-L1) plays an important role in cancer proliferation. Thyroid hormone, L-thyroxine (T4), induces the expression of PD-L1 and promotes cell proliferation in cancer cells. Resveratrol inducesanti-proliferation in various types of cancer cells via binding to integrin αvβ3 to increase nuclear inducible cyclooxygenase (COX)-2 accumulation, complex with p53, and induce p53-dependent anti-proliferation. We investigated the mechanism by which L-thyroxine impairs resveratrolinduced anti-proliferation in human cancer cells. L-thyroxine increased expression and cytoplasmic accumulation of PD-L1. The increased PD-L1 retained  resveratrol-induced COX- 2 in cytoplasm and prevented COX-2 nuclear accumulation. Byinhibiting activated PI-3K-STAT3 signal transduction axis by thyroid hormone, anodiamino-tetrac (NDAT) was able to inhibit thyroid hormone-induced PD-L1 and relieved the inhibitory effect of L-thyroxine on resveratrolinduced nuclear accumulation of COX-2. DAT is a thyroid hormone derivative. The NDAT-inhibited consequences were re-establishingCOX-2/p53-dependent gene expression and anti-proliferation. These findings provide new insights into the antagonizing effect of NDAT on L-thyroxineinduced interference withresveratrol-induced anticancer properties.

Biography:

Lucero Alvarado has done her B.S from The University of Texas at San Antonio 2014, she is currently pursuing her M.S. from the University of Texas at San Antonio (2017). Her research  interests is developing cell –based products for use in combat casualty care and healthcare settings. She has three years experience in manurfacturing cell-derived extra-cellular matrices in a GMP setting at the San Antonio based biotechnology company, StemBioSys, Inc. Published in Stem Cell Research and Therapy and presented at RegenMed SA conference in San Antonio, TX

Abstract:

Acute Respiratory Distress Syndrome (ARDS) is a form of acute lung injury that causes morbidity and mortality in ill patients. Current therapies for ARDS include lung protective ventilation and fluid clearance, but do not treat the underlying cause. Mesenchymal stem cells (MSCs) have been proposed as a promising form of therapy to treat ARDS. Currently, it is unknown which MSC type is best-suited to treat ARDS. The goals of these study were therefore three-fold: 1. Create a model of ARDS in vitro; 2.Identify which MSC source, bone marrow (BM) or adipose (AD)-MSC, is more suitable to treat ARDS; and 3. Evaluate the ability of MSCs to mitigate the ARDS-like injury.

To accomplish this, we utlized injurious signals typically manifested in ARDS, such as low oxygen concentration (i.e., hypoxia) and lipopolysaccharide (LPS). LPS is a bacterial endotoxin that induces ARDS in vivo and mimics infection in vitro. We then subjected a co-culture system of lung epithelial and endothelial cells to these signals to induce the injury. Finally, we added MSCs to this sustem to evaluate their ability to mitigate the injury.

After subjecting the co-culture system to hypoxia and LPS, we observed an increase in apoptosis as evidenced by increase in mitochondrial membrane potential and Annexin V analysis. In comparing MSC types, both BM-MSCs and AD-MSCs suppressed T-cell proliferation in a mixed lymphocyte reaction assay; however, AD-MSCs were more potent following a LPS challenge. Additionally, both cell types diminished the secretion of the pro-inflammatory cytokines IFN-γ, IL-13, IL-1α, and IL-1β; yet, unlike BM-MSCs, AD-MSCs showed a significant increase in the anti-inflammatory IL-1RA after LPS exposure. Following the addition of AD-MSCS, there was a significant decrease in protein pearmeability in the co-culture system.

Taken together, in the co-culture system, we successfully established a injurios environment rmimicking an ARDS-like condition. Compared to BM-MSCs, AD-MSCs appear to be a more suitable candidate for ARDS due to their superior anti-inflammatory function.  Therefore, Addition of AD-MSCs to an in vitro co-culture system of ARDS mitigated the injury as evidenced by reduction in membrane permeability.

Biography:

Abstract:

Background: In the last few decades, thousands of patients have benefited from platelet-rich plasma (PRP) therapies, emerging as a safe alternative in many different medical fields. The use of Platelet-Rich Plasma (PRP) in medicine has become increasingly more widespread during the last decade. Eczema (atopic dermatitis) is a complex disorder caused by the interplay between multiple genetic and environmental factors. Particularly in patients with severe disease, the effect is not just an itchy rash but also the secondary effects on the psychological well-being of the patient and their carers, particularly disturbed sleep. The aim of the study was to treat the patient by using the platelet-rich plasma.

Materials and Methods: 15cc blood sample was collected from the patient. The baseline parameters included complete blood count (CBC), erythrocyte sedimentation rate(ESR), fasting blood sugar/ransom blood sugar(FBS/RBS), urea, creatinine and uric acid, We also checked for the inflammation by performing C-Reactive Protein(CRP) and immunoglobulin IgE for the allergy. The rest of the blood sample was used for the PRP.The platelet-rich plasma (PRP) was collected with the help of spiral needle in sterilized falcon tube which was then place in Adilight 2 for the activation of PRP for 15minutes.

Result: In baseline reports, it was noted that eosinophil was elevated, with ESR. The sugar level, urea, creatinine and Uric acid were at the normal range. The CRP was high and igE was abnormal. She underwent three consecutive platelet-rich plasma therapy with a gap of 15 days in between. We assessed the patients by taking the photograph and repeating the parameters which were elevated before the second and third treatment. After the first therapy, the images showed improvement. However, after the second therapy, the patient reported marked control on the itchy and disappearance of rash. She was quite satisfied with the treatment because of the treatment she was taking increasing the rashes.

Conclusion: This study suggests the use of platelet-rich plasma has a beneficial effect on skin diseases and can thus be attributed to various platelet-derived growth factors causing improvement in the function on skin and promotion to decrease the rashes and itching. It is safe, cheap and non-allergic and it appears to be a useful adjuvant in the management of eczema.

Biography:

Moses Kayongo holds a Masters and a Doctorate in Public Health (DrPH) has expertise in Preventive Health Care. He is currently working as Assistant Professor at University of Lay Adventists of Kigali (UNILAK) and Adventist University of Central Africa (AUCA) as an adjunct Lecturer teaching public health courses and research methodology. He has a research interest in self-care management of Noncommunicable diseases however after his Doctoral studies’ completion, his second child was diagnosed at 5years with sickle cell disease and suffered several strokes. Given his educational background, he developed a research interest in Sickle Cell self-care management and has since developed and supported several awareness programs for parents of children with sickle cell disease.

Abstract:

Statement of the Problem: Haplo Identical Stem Cell Transplant (SCT) procedure  in some countries is still considered experimental and performed only as part of research studies because of the complications during and after the transplant such as high risk for infections, Graft-versus-host disease (GVHD), Graft failure, Nutrition problem, Low blood counts, dermatological challenges, Social and emotional concerns and others. The number of Haplo Identical SCT procedures nonetheless, continues to rise as parents in many African countries seek treatment for the increasing diagnosis of sickle cell disease among children. Parents as caregivers are destined to face a greater number of challenges yet there has not been any documented shared experience of this specific procedure. The purpose of this study report is to describe the 2year caregiving experience and challenges by a family living in Rwanda, since their nine-year-old daughter’s Post Haplo-identical SCT, done on (December 28^th, 2016) at Christian Medical College Hospital, Vellore, India to further the understanding and knowledge of the caregiving aspects of this procedure.

Methodology/Finding: Using a case report approach, six key points emerge from a caregiving perspective of parents’ experiences and challenges namely: nutritional adjustments, continuous home monitoring and evaluation of the child’s general wellbeing, compliance to routine consultation / medications, father’s direct involvement and social interaction difficulties besides the mother’s role.

Conclusion: Despite this procedure being delicate and complex during and after transplant, our experience as caregivers has shown that Pre/Post-Haploidentical SCT orientation and existing experienced doctors in the different specialties’ related to the complications have so far greatly contributed to our post-transplant adaptation to care to give.

Biography:

Thomas J Lewis is a Medical Scientist. He holds a PhD in Chemistry from MIT and certification from the Harvard School of Public Health. He is an entrepreneur and healthcare professional with expertise in toxic substances, drug development, biotechnology, health technology and medical protocol development. For the past decades, he has worked closely with senior researchers and clinicians at Harvard Medical School and has developed a program for chronic disease root cause prevention, screening, diagnosis and treatment. Alzheimer’s disease and the most serious eye diseases, macular degeneration and glaucoma have been a particular focus. He has opened the first-of-its-kind Alzheimer’s prevention, screening, early detection and treatment centre in the Orlando, Florida area in 2014. He works closely with Dr. Clement Trempe, 41years at Harvard Medical School who is one of few doctors in the world who treats chronic eye diseases as systemic inflammatory conditions – and reverses these conditions with great success. It was through this work that Dr Trempe developed his protocol for diagnosing, treating and reversing Alzheimer's disease that is now an integral part of the Health Revival offering.

Abstract:

Critical to broad acceptance of newer technologies is an understanding of the causes behind both success and failure of treatments. As humans age, their immune system undergoes immunosenescence. The progressive deterioration of the immune system is one contributing factor to the characteristic decline in stem cell activity that also accompanies aging, at least with regard to certain types of stem cells. Underlying low-grade chronic disease and accompanying immune activation and inflammation also drive senescence processes and concomitantly impacts stem cell efficacy. It’s well established that inflammatory sites and an inflammatory milieu are hostile towards the survival of transplanted cells. Practitioners who apply stem cell therapy have a significant opportunity to take a leading role in understanding and reversing accelerated aging. Stem cell therapy, to be most impactful, should be delivered along with anti-inflammatory strategies. Key to this approach is understanding the immune system/inflammatory status of each patient. Presented here is a novel Harvard Medical School and MIT developed a systems approach to accurately and precisely measure immune and chronic inflammatory status. The Chronic Disease Assessment™ and Chronic Disease Temperature™ provide a subjective and objective measure of immune status and include a path to reducing inflammation. The eye plays an important role in this program. Cataract, for example, is a sign of systemic inflammation, stem cells disease, high cardiovascular risk, and early mortality. The lens of the eye uniquely acts like a single large stem cell. The connection between life risks, biomarkers and eye pathologies will be discussed in the context of a holistic approach to successful stem cell therapy.

Biography:

Kimberley Tam graduated from The University of Adelaide 2010, PhD in Medicine (Obstetrics and Gynaecology). He had completed  his postdoctoral career with Cancer Science Institute of Singapore till 2014 developing Patient-derived xenografts for drug testing. He had served in the Department of Obstetrics and Gynaecology at National University of Singapore investigating the effects of Human Wharton’s Jelly Stem Cells and wound healing till 2016 and is currently based at Singapore-MIT Alliance of Research and Technology establishing pre-clinical evaluations and critical quality attributes (cQAs) for stem cell manufacturing and precision medicine. Kimberley Tam’s Research and Interests include – Developing various animal models for pre-clinical evaluation, bringing bench to bedside therapies and also developing in-vitro diagnostic platform for stem cell cQAs.

Abstract:

Abstract

Introduction: MSCs are easily procured from bone marrow (BM) aspirates and may be suitable for adapting successfully to the environment of the intervertebral disc (IVD) to stimulate regeneration. Through novel technology for identifying and biophysically sorting MSC subpopulations, we demonstrate that implantation of MSC derived osteoprogenitors leads to the greatest efficacy in restoring IVD matrix and function in murine models.

Methods: We studied various biophysical traits of MSCs and created microfluidic sorters that isolate an osteoprogenitor subpopulation for clinical use. IVD cells were obtained from 5 patients for analysis (L3/4, L4/5, L5/S1). We correlated pain scores with gene expression of IVD cell-produced proteins to identify biomarkers relevant to DDD. We also evaluated pre-clinically the efficacy of different MSC subpopulations in reversing degeneration in IVD cells both in vitro and in vivo.

Results: MSC osteoprogenitors are defined biophysically from other subpopulations as cells with >20μm diameter, >375Pa stiffness and <1.2% nuclear fluctuation; functionally, MSC osteoprogenitors differentiate most readily into osteo/chondro-lineages and also secrete more Aggrecan, Fgf1, Ang-1, etc, making them potentially optimal for stimulating regeneration of both IVD cells and matrix. qPCR studies of patient IVD cells show a>5 fold Aggrecan decrease with a corresponding 3 point pain increase (scale of 0-10). Stimulation of patient IVD cells with osteoprogenitors in vitro greatly restored production of Aggrecan (~2.5 fold improvements compared to other MSC subpopulations). Protein expression of ANG-1 was also significantly higher when IVD cells were treated with MSC osteoprogenitors in vitro. In murine models, the administration of osteoprogenitors most potently restored the decrease in original disc height after injury using MRI and histopathological scoring system.

Conclusion: We demonstrate a facile and clinically relevant strategy for deriving an MSC osteoprogenitor subpopulation for cell-therapy in DDD, which may potentially be more efficacious in reversing the underlying degeneration in the IVD.

Biography:

Yogesh Kumar Verma, MNABS, is working as Scientist ‘D’ in INMAS, DRDO, Delhi, India. He has completed his MSc (Year 2000) and PhD (Year 2008) in Biomedical Science from Delhi University, India. He also has another MSc degree in Bioinformatics from Punjab Technical University, India. In 2008, he received Young Scientist award from DST under SERC scheme for carrying out research work as Principal Investigator. In year 2009, he joined INMAS, DRDO, Delhi, as Scienitst ‘C’. He has 23 publications and 04 patents (filed) to his credit. He is presently working in the area of stem cell research, microencapsulation, tissue engineering and omics data mining and analysis for decreasing various types of injuries.

Abstract:

Effective homing of stem cells is a pre-requisite for successful hematopoietic stem cell transplantation (HCT) when there is a dearth of available hematopoietic stem cells (HSC). However, the transplanted cells face premature differentiation and death while en route to bone marrow. This causes decreased engraftment of transplanted HSC. In order to enhance the homing of stem cells to bone marrow as undifferentiated cells, in this study the mouse bone marrow cells were masked with fibronectin modified alginate (A-F). This biocompatible coat prevented the antibody from binding to its cognate receptor, i.e. CD49e, which is present on the cell surface. In addition, coating effectively abolished RBC’s clumping by reactive antibodies in haemagglutination assay. Bioluminescence imaging showed significant improvement in the efficiency of coated cells to home in bone marrow. This also provided protection to irradiated BALB/c mice (75% on sublethal irradiation). To further enhance the transplantation efficiency, we designed and evaluated Bax antagonist peptide (BAP-GR23) for decreasing the death of HSC and other tissues, which become morbid on preparatory or undesired radiation exposure. We found that administration of novel BAP and LiCl combination followed by A-F coated bone marrow cells transplantation and ascorbic acid supplementation Ad libitum was effective in preventing the imminent death of lethally irradiated BALB/c mice (100% survival). Radiation-induced aplasia was corrected after 10days of treatment. Histologically no toxicity of the treatment was observed. This combination also improved survivability and clonogenicity of cells with a concomitant decrease in DNA degradation in the comet assay. Microarray data analysis showed a specific role of LiCl in upregulation of cell survival genes’ expression along with downregulation of bile producing genes (CYP7A1 and FOXA2) having a role in radiation-induced gastrointestinal syndrome. These results suggest the development of a new multi-therapy paradigm to enhance the clinical efficacy of HCT.

Biography:

Pawan Kumar Raghav completed his MSc in Bioinformatics (2008) from Punjabi university Patiala, India; PG Diploma in Chemoinformatics (2009) from Jamia Hamdard; MPhil in Bioinformatics (2010) from The Global Open University, Nagaland; and PhD at the Institute of Nuclear Medicine and Allied Sciences (INMAS), DRDO, Delhi for Life Sciences in Bharathiar University, Coimbatore. During his PhD he had designed molecules and evaluated their applications through response modification that regulates stem cells proliferation, differentiation, and apoptosis. His main research interests are in the drug designing of anti-Cancer Stem Cells (CSCs). He is currently DST, SERB, Post-Doctoral Fellow in Computational Biology at the IIIT-D, Delhi, India under Prof. GPS Raghava. His current research activities are in the fields of machine learning, deep learning, and molecular biology, as well as in the development of new scoring function parameterizations for use in docking, simulations and complex network analysis. He has 08 publications and 03 abstracts to his credit.

Abstract:

Stem cells are being used to study aging, embryonic development and diseases including cancer, diabetes and neurodegenerative diseases. Stem cells possess two essential properties, self-renewal and differentiation. Stemness is defined as the potential of a cell to self-renewal and differentiation. Characterizing the genes involved in the regulation of these properties is fundamental to understand the concept of stemness, the underlying mechanisms which can be further used for therapy. Extensive data is available from various stem cell studies. However, yet, the prediction model of the stemness of genes is still not available. Therefore, molecular profiling assays experimental data of pluripotent stem cells have been collected. The analysis of the gene expression data revealed stem cells specific novel stemness genes. Afterward, we used machine learning to predict the stemness of the genes and established a reference for the pluripotent state. We have thus developed a machine learning model based on the random forest, support vector machine and artificial neural network methods of markers gene expression, which has been identified to regulate stemness. The training data was validated using stratified 5-fold cross-validations (CV) and corresponds to an 80:20 test and training set ratio. Finally, this developed classification model categorized the genes into pluripotent and non-pluripotent using the machine learning methods based on accuracy, sensitivity and specificity. The present work assessed the accurate performance of the method used to evaluate stemness that classifies pluripotent genes. Using automated classifiers based on the random forest machine-learning algorithm we are able to identify the hotspot pluripotent genes responsible for its stemness.

Biography:

Azzah Momenh from Saudi Arabia-Dammam  she is currently pursuing her masters education in The Catholic University of America. Bachelors and Diploma in University of Damman, Saudi Arabia.Her research and Laboratory experience include:She worked as a research assistant under the direct of John S.Choy at The Catholicuniversity of America. She was a member of John Hanover, Ph.D’s. research team in the same university.She served as an intern in the laboratory of John A. Hanover, Ph.D., Laboratory of Cell and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and worked with Agata Steenackers, Ph.D., in the project entitled “Protein Stabilization and Purification by Targeted domain swapping.”  

Abstract:

O-GlcNAcylation is a dynamic post-translational modification (PTM) of thousands of nuclear, cytoplasmic and mitochondrial proteins. This PTM targets serine or threonine residues of proteins, resulting in crosstalk with phosphorylation. The protein phosphorylation is controlled by many different kinases and phosphatases, whereas only two enzymes regulate O-GlcNAcylation. The addition of N-Acetylglucosamine onto target proteins is controlled by O-GlcNActransferase(OGT), while removal of this molecule is catalyzed by O-GlcNAcase(OGA). OGT uses UDP-GlcNAc(uridine diphosphate-N-acetylglucosamine) as a donor, which is the product of the hexosamine biosynthetic pathway. Since, nutrient derivative molecules, including glucose, glutamine, acetyl CoA and uridine diphosphate are all used to synthesize UDP-GlcNAc, O-GlcNAc cycling is susceptible to cellular nutrient levels. Therefore, O-GlcNAc is suggested to connect the nutrient status to cellular machineries. Moreover, O-GlcNAc cycling is involved in many fundamental functions, including transcription, translation, cell signaling, and protein trafficking. Deregulation of O-GlcNAcylation dynamics is involved in the etiology of diverse pathologies, such as type 2-diabetes, Alzheimer and cancers.

Biography:

Bibitayo B Olayiwola is a two time alumni of Florida Agricultural and Mechanical University (FAMU.) She received her Bachelor’s degree in Accounting from the School of Business and Industry (2010). She also obtained her Masters in Healthcare Administration from School of Allied Health Sciences (2016), where she developed an interest for healthcare related matters. She graduated with honors from both programs. Bibitayo decided to pursue her doctoral degree in Pharmaceutical Science with a specialization in Health Outcome Research and Pharmacoeconomics. She is currently a third year PhD candidate at FAMU’s College of Pharmacy and Pharmaceutical Sciences. Bibitayo is a well-rounded student, she is a member of the honor society, Omicron Delta Kappa and Sickle cell – Lupus – Autoimmune Disease (SLAD), an organization established by her sister on the campus of FAMU to bring awareness to autoimmune diseases that are prevalent among people of color. Her topic of interest for her current doctoral program is Sickle Cell Disease (SCD) and the application of value-based pricing to pharmaceutical interventions. Her diverse experience includes HIV/AIDs testing and counseling, reconciliation, research, presentation and teaching. She has presented abstract at National Institute of Health among other conferences. She hopes to make a difference in Sub-Saharan African countries to improve the prevalence and knowledge of SCD.

Abstract:

Sickle cell disease (SCD) is the most common hereditary blood disease that affects roughly 100,000 births in the United States. Globally, there are 300,000 SCD births, annually. According to the National Institute of Health, SCD affects 1 in 365 African Americans, while 1 in 13 has the trait. SCD also affect people of Hispanic descent, Asian, Middle Eastern and southern Europe. In 2006, WHO declared SCD as a public health priority. In SCD patients, red blood cells (RBCs) become coarse and sticky making it difficult for blood and oxygen circulation. RBCs stick to the vessel walls and cause a blockage which results in vaso-occlusive crises. The aim of this review was to assess the knowledge of healthcare providers (HCPs) that SCD patients encounter during a painful episode. This review identified and screened published literature based on prior inclusion and exclusion criteria. Searches from PubMed and Ovid identified 45 articles in total. Of the 45 published materials, six of them met the inclusion criteria. In conducting this review, it was noted that HCPs lack knowledge of treating SCD patients. Seventy-eight percent of primary care physicians (PCPs) do not display confidence in treating SCD patients while experiencing vaso-occlusive crises. Patients do not like visiting PCPs to seek advice on managing painful episodes. Emergency department (ED) physicians tend to be more comfortable with SCD patients than any other HCPs. Subsequently, patients often receive conflicting information and are perceived as drug seekers, which affect the quality of care and health outcomes. Since SCD is more prevalent among people of color, race tends to play a major role in the treatment process. In addition to the lack of knowledge and race, perceptions of HCPs also affect the wait time experienced by SCD patients while visiting the ED for crises. To minimize wait time, the United States Department of Health and Human Services has categorized SCD as a priority health condition. This review shed light on the need for HCPs to have access to abreast educational conferences on SCD. The improvement in knowledge and comfort level will aid in treatment rendered to patients.