We have scheduled our Programs dividing them into Day 1, Day 2, Day 3 in order to make it convenient for you to attend in absolute comfort.
Time : 09:00 - 09:45
Giovana Aparecida Gonçalves is Professor of the Padre Albino University Center - UNIFIPA. Assistant Professor of Master's and PhD Degrees by the Department of Gynecology of Federal University of São Paulo - UNIFESP. PhD in Sciences by InCor.HC-FMUSP (2008) and postdoctoral fellow by the Department of Gynecology-UNIFESP (2009-2014) and by the Laboratory of Angiogenesis and Vascular Metabolism - Vesalius Research Center / KULeuven-Leuven / Belgium under the supervision of Prof. Peter Carmeliet (2014-2015). Develops projects in the area of Gene Therapy and Cell Therapy as a focus in angiogenesis.
p27kip1 is a cyclin-dependent kinase (CDK) inhibitor whose specific late G1 destruction allows progression of the cell across the G1/S boundary. There is a direct relationship between low level of p27 and rapid proliferation occurring in several benign states and in many malignances. In the glandular cells of the normal endometrium, the level of p27kip1 is exceedingly low during the proliferative phase, whereas it is markedly increased during the secretory phase. The expression of p27kip1 in endometriosis is very low but has been found to increase following treatment with progesterone. However, estrogen exposure is considered as a major risk factor in developing endometrial cancer. Endometriosis endometrial cells cultures have also lower levels of p27kip1 compared to heath endometrial cells cultures and restore the cell cycle balance when transduced with an adenoviral vector carring the p27kip1 coding gene (Adp27EGFP). More uniform and rigorous studies are required to confirm these and additional markers utility in a diagnostic and possible treatment panel. As a major clinical priority is to determine which lesions can be treated medically and which require surgical intervention, focusing future studies on markers that distinguish response to hormone therapy or are involved in hormone regulation, will be important future considerations. The goal of this highlight review is to provide a broad overview of the advancements in studies about endometriosis mainly correlating the cytokine p27kip1 expression with the diagnostic and disease treatment
Time : 09:45 - 10:30
Anna Cornelia Beyer is Senior Lecturer at the University of Hull. She has published 7 monographs and about 30 articles on war and terrorism, their causes and how to prevent them. Recently, she has published a self-help book for schizophrenia, entitled Health and Safety for Spirit Seers, Telepaths and Visionaries – Self-help for Schizophrenia
Schizophrenia is a debilitating illness that includes the main symptom of voice hearing and delusions, which can become as painful as strong physical pain and very frightening. Many patients with this illness live on disability income, unemployment and suicide are high, life expectancy is 15 years reduced. From a patients perspective, and from the perspective as a scientist, this paper will describe a holistic treatment approach that might work better than reliance on medication alone. It will describe the use of vitamin therapy, a healthy lifestyle, and spirituality. It will also point out the role of caffeine and nicotine abuse for contributing to the symptoms of schizophrenia.
Time : 10:45 - 11:30
Kathleen Hefferon received her PhD in Molecular Virology at the University of Toronto. She worked as a post-doc at the Boyce Thompson Institute for Plant Research and later as the Director of the Human Metabolic Research Unit in the Division of Nutritional Science at Cornell University. Most recently, Kathleen has written two books on agricultural biotechnology and is currently teaching Virology at the University of Toronto.Research Interest :Virology, biotechnology, vaccines, nutrition, global health
For over two decades now, plants have been explored for their potential to act as production platforms for biopharmaceuticals, such as vaccines and monoclonal antibodies. Without a doubt, the development of plant viruses as expression vectors for pharmaceutical production have played an integral role in the emergence of plants as inexpensive and facile systems for the generation of therapeutic proteins. More recently, plant viruses have been designed as non-toxic nanoparticles which can target a variety of cancers and thus empower the immune system to slow or even reverse tumor progression. The following presentation describes the employment of plant virus expression vectors for the treatment of some of the most challenging diseases known today. The presentation concludes with a projection of the multiple avenues by which virus nanoparticles could impact developing countries.
Time : 11:30 - 12:00
Fan has completed his PhD from Michigan State University and Post-doctoral studies from The Scripps Research Institute and University of California Berkeley. He is currently an Associate Professor in the Department of Biochemistry and Director of Macromolecular X-ray Crystallography Core Facility at University of Califorani Riverside. He has published many papers in peer-reviewed journals including Cell, Molecular Cell, PNAS, Nucleic Acid Research, etc. Research projects in his laboratory focus on structure and function studies on proteins or enzymes important to fundamental biological processes including DNA repair and recombination, amino acid metablism, and bacteria-host interactions.
XPB helicase is essential for unwinding DNA at the damage site in nucleotide excision repair and melting the promoter during transcription. Inherited xpb mutations are associated with disease xeroderma pigmentosum (xp), Cockaye Syndrome (CS), and trichothiodystrophy (TTD). Here we explored two most important questions about XPB: 1) How does XPB open double-stranded (ds) DNA at promoters for transcription and at DNA lesions for DNA repair? 2) Why and how different xpb mutations are associated with different disease phenotypes?
Using a combination of X-ray crystallography and biophysical methods, we observed that ATP-binding induces domain rotation in XPB, allowing XPB to open dsDNA as a molecular wrench. Our results clearly distinguish XPB from a conventional helicase, which unwinds dsDNA by translocating along one strand DNA driven by ATP hydrolysis and breaking the base-pairing along the way. The molecular wrench model strongly support the important roles of XPB in both transcrition initiation and DNA repair. In addition, we investigated the distinguished biochemical properties of three disease-causing mutations including one frame shift mutation XP11BE (for XP/CS) and two point-mutions F99S (for XP/CS) and T119P (for TTD). Our results provide the molecular basis to explain why different mutations cause different clinical manifestations.
Keywords: XPB, helicase, DNA repair, transcription, TFIIH.
Time : 12:00 - 12:30
Huanxiang Zhang has completed his Ph.D from Beijing Normal University, China and postdoctoral studies from Geneva University School of Medicine, Switzerland. He is now working in the Department of Cell Biology, Medical College of Soochow University, China. His research focuses on the control of the directed migration and differentiation of stem cells, including neuralstem cells, mesenchymal stem cells and embryonic stem cells, and tissue engineering, especially the interaction between stem cells and the silk fibroin scaffolds with a variety of physical and chemical properties. Recently, his group demonstrated the close relationship between the chemotactic migration of stem cells and their differentiation states, the transdifferentiation of astrocytes to neural stem/progenitor cells or neurons, and further systematically studied the underlying mechanisms, thereby shedding light on optimization of the therapeutic potential of stem cells to be employed for tissue regeneration after injury
Injury to central nervous system triggers the pronounced reactivity of astrocytes, leading to the glial scar formation and rendering the lesion unfavorable to nerve regeneration. Recent studies have shown that astrocytes, the most plentiful cells in the central nervous system, hold great promise, especially upon transdifferentiation into neurons or neural stem/progenitor cells (NSCs) that can be used to replace the lost cells or ameliorate the lesion conditions, for nerve repair after injury. Our intriguing results indicate that overexpression of NEDD9 (neural precursor cell expressed, developmentally downregulated 9) can transdifferentiate astrocytes into NSCs or neurons. In this talk, I’ll summerize our data regarding the effects of NEDD9 overexpression on the conversion of astrocytes into neurons and/or NSCs in relation to the specificity of the produced neurons and the expression of the neurogenic transcription factors, and further the signaling molecules that participate in the transdifferentiation of astrocytes into neurons by NEDD9. Moreover, I’ll introduce the results about the contribution of the reactive astrocytes that have migrated to the lesion sites, and overexpression of NEDD9 to the structural and functional recovery of the injured spinal cord. These results will surely shed light on the new therapeutic strategy for nerve repair by using astrocytes as a powerful and plentiful cell source.
Keywords: Astrocytes,NEDD9, neural stem/progenitor cells, cell differentiation
Title: Targeting the CD200 Checkpoint Blockade with a Peptide Inhibitor Ligand as a Novel Approch for Glioblastoma Immunotheapy Targeting the CD200 Checkpoint Blockade with a Peptide Inhibitor Ligand as a Novel Approch for Glioblastoma Immunotheapy
Time : 12:30 - 13:00
Olin is an Associate professor in the Department of Pediatrics, Division of Hematology/Oncology at the University of Minnesota. Dr. Olin graduated from the University of Minnesota, Duluth, in 1995 with a BS in biochemistry and a BA in chemistry completing his PhD in Veterinary Medicine (Infectious Disease) in 2005. Dr. Olin has dedicated his efforts to developing immunotherapy for brain tumors developing a novel peptide checkpoint inhibitor, demonstrating promising results with minimal toxicity. He recently founded a company “OX2 Therapeutics” and holds the position of Chief Scientific Officer to raise money to run a Phase I trial in2019.
The discovery of immune checkpoints has dramatically advanced immunotherapy; however, current FDA-approved checkpoint inhibitors have only modest effects on patients with glioblastoma multiforme (GBM), thus requiring alternative approaches to be pursued. Our research has focused on the CD200 immune checkpoint, which suppresses the immune system through binding of the inhibitory CD200 protein to the inhibitory receptor (CD200R1) expressed on immune cells, In addition, the CD200 checkpoint includes activation receptors (CD200AR), which we are targeting with a peptide inhibitor ligand surmounting the inhibitory effects of the CD200 protein, activating antigen-presenting cells, enhances dendritic cell maturation, cytokine production, and antigen specific T-cell activation significantly extending survival in two murine glioma models. In an ongoing pilot study, spontaneous high-grade glioma dogs receive a canine specific CD200 peptide in combination with the autologous tumor lysate vaccine increased median overall survival to 9 months, compared to 6.3 with lysate alone resulting in an overall 36 month survival of 21%. However, unlike any other treatment, we have a 45% event free (progression-free), dogs that died of non-tumor related deaths. Six dogs remain on trial. 100% of the dogs receiving tumor lysate-only died of tumor recurrence within 6 months. Serum chemistry profiles and physical examinations showed that the peptide did not induce any systemic toxicity. To determine why our peptide inhibitor responded so well, we looked at the molecular pathway of the CD200ARs. We discovered the molecular connection between CD200, PD-1 and CTLA4. We demonstrated that our peptide inhibitor downregulates the inhibitory PD-1 and PD-L1 and inhibits the upregulation of CTLA4. For translation, we developed human CD200 paptides to develop an immunotherapy approach for CNS tumors, we will conduct a Phase I trial utilizing the peptide inhibitor concomitantly with an allogeneic GBM6-AD cell line as a tumor vaccine and the adjuvant imiquimod
Keywords: Immunotherapy, Glioblastoma Multiforme, Peptide inhibitor.
Time : 14:00 - 14:30
May Alqurashi, a postdoctoral fellow, was born and raised in the coastal city of Jeddah, Saudi Arabia. The passion for scientific research commenced in 2013 with her PhD degree in proteomics from KAUST. Postdoctoral experience includes working at KAUST and Cambridge Centre for Proteomics, University of Cambridge, UK with Professor Kathryn Lilley. Research interests include abiotic stresses and their effect on the plant proteome, second messengers and their role in signal transduction and the utilisation of computational and bioinformatic approaches toward improving the proteomic field. She authored multiple publications, a book chapter and is an active researcher.
Environmental factors such as abiotic stresses can cause constraints on the growth, development and productivity of plants. To alleviate the impact of stress, plants initiate a complex and intertwined network of responses including hormones and signalling molecules among others. In planta, the hormone abscisic acid (ABA) has been shown to induce reactive oxygen species (ROS) production through the action of plasma membrane-associated NADPH oxidases. Although quantitative proteomics studies have been performed to identify ABA- or hydrogen peroxide (H2O2)-dependent proteins, little is known about the ABA- and H2O2-dependent proteome changes. By using 50 µM of either H2O2 or ABA on the Arabidopsis microsomal proteome and utilizing tandem mass spectrometry we idintified H2O2- and ABA-dependent proteins that are differentially expressed as well as common significant peoreins shared by both. Main observations showed accumulation of proteins involved in the TCA cycle, RNA biology and enrichment of ‘response to stress’ and ‘transport’ gene ontology categories suggesting that H2O2 and ABA directly and/or indirectly are involved in a complex and partly overlapping cellular responses.
Keywords: ABA; Abiotic Stress; Mass Spectrometry; QuantitativeProteomics.
Time : 14:30 - 15:00
Brossard Clément started PhD in 2019 in Radiobiology of Medical Exposure Laboratory (LRMed) of the Institute of Radioprotection and Nuclear Safety. I hold a Master 2 degree in tissues, cells and genes biotherapies obtained in 2018 at the University of Paris Saclay. My doctorate is in line with my M2 internship, which aims to create a pre-clinical model of chronic radiocystitis and to provide an innovative therapeutic method using mesenchymal stem cells.
Introduction: Chronic radiocystitis (CRC) is a consecutive pathology of pelvic irradiation characterized by chronic inflammation sometimes progressing to fibrosis with symptoms such as pain and bleeding. There is no effective treatment and we propose to test mesenchymal stem cells (MSCs) as a new therapeutic method. Our previous studies on radiation rectitis have shown that MSCs can reverse chronic inflammation and fibrosis after irradiation.
Material and methods: Preclinical modelling of CRC in rats was implemented by localized irradiation guided by scanner imaging of the bladder from 20 to 40 Gray with a follow-up of 3 to 6 months post-irradiation. Gene and protein expression analyses as well as histological and functional parameters are carried out.
Results and Statistical Analysis: The analysis of urinary parameters revealed transient hematuria but no decrease in urinary volume over the 6 months. Transcriptomic analysis indicates a profile of chronic inflammation (IL1β, CCL2, IL6) and hypoxia (HIF1α) at 6 months. Histological observations reveal a disorganization of urothelium at 6 months, with a decrease in its thickness and vascular lesions, which is consistent with gene expression results.
Conclusion: These initial results attest to the relevance of the study by showing an initiation of CRC at 6 months with chronic inflammation, signs of hypoxia, hematuria and urothélium disorganization. The analysis of kinetics over later times will make it possible to characterize the evolution towards fibrosis and to have an established CRC. In a second step we will set up the treatment of this pathology by cell therapy.
Keywords: Chronic radiocystitis, preclinical modelling, pelvic irradiation, mesenchymal stem cells, MSC,
Time : 15:00 - 15:30
Wanessa Medina completed her doctorate at the age of 32 at the University of São Paulo and did postdoctoral studies at the Faculdade de Ciências Farmacêuticas de Ribeirão Preto. She is Director of Scientific Research at the University Center Padre Albino (UNIFIPA), an important university services organization in the interior of Brazil. Professor at UNIFIPA (Medicine, Biomedicine and Nursing courses). Coordinator of the Specialization Course in Aesthetic Health at UNIT, unit of Maceió (2012 to 2014). She is a member of the American Association of Pharmaceutical Scientists (AAPS), Advisory Director in Toxicology of INB (National Institute of Biomedicine), Advisory Director in Aesthetic Biomedicine of INB and Member of ABCFarm (Brazilian Association of Pharmaceutical Sciences) and Supervisor of the Student Chapter UNIFIPA since 2014. She has published more than 17 articles in renowned magazines and has acted as a member of the renowned editorial board.
We have designed a microemulsion (ME) containing Ketoprofen (KET) for anti-inflammatory effect evaluated using the rat paw edema model. The ME was prepared by adding propylene glycol (PG) loaded with 1% KET/water (3:1, w/w), to a mixture of sorbitan monooleate and polysorbate 80 (47.0%) at 3:1 (w/w) and canola oil (38.0%). The physicochemical characterization of KET-loaded ME involved particle size and zeta potential determination, entrapment efficiency, calorimetric analysis, and in vitro drug release. The in vivo anti-inflammatory study employed male Wistar rats. Measurement of the foot volume was performed using a caliper immediately before and 2, 4, and 6 h after injection of Aerosil. KET-loaded ME showed particle size around 20 nm, with zeta potential at -16 mV and entrapment efficiency at 70%. Moreover, KET was converted to the amorphous state when loaded in the formulation and it was shown that the drug was slowly released from the ME. Finally, the in vivo biological activity was similar to that of the commercial gel, but ME better controlled edema at 4 h. These results demonstrated that the ME formulation is an alternative strategy for improving KET skin permeation for anti-inflammatory effect. Furthermore, our findings are promising considering that the developed ME was loaded with only 1% KET, and the formulation was able to keep a similar release profile and in vivo effect compared to the commercial gel with 2.5% KET. Therefore, the KET-loaded developed herein ME is likely to have a decreased side effect compared with that of the commercial gel, but both presented the same efficacy.
Keywords : Aerosil-induced rat paw edema model, Ketoprofen, anti-inflammatory effect, microemulsion
Time : 15:30 - 16:00
Itoh is a Professor at the Akita University Graduate School of Engineering Science. He received a bachelor’s degree in sociology from Ibaraki University and a docor’s degree in Science from Akita University in Akita, Japan. His research interests include, science, Biochemistry and Molecular Biology
The AhR, so called the dioxin receptor, is a member of the nuclear receptor superfamily. The ligand-free AhR forms a cytosolic protein complex with the molecular chaperone HSP90, co-chaperone p23, and XAP2 in the cytoplasm. Following ligand binding like 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), the AhR translocates into the nucleus. Although it has been reported that HSP90 regulates the translocation of the AhR to the nucleus, the precise activation mechanisms of the AhR have not yet been fully understood. AhR consists of the N-terminal bHLH domain containing NLS and NES, the middle PAS domain and the C-terminal transactivation domain. The PAS domain is familiar as a ligand and HSP90 binding domain. In this study, we focused on the bHLH domain that was thought to be a HSP90 binding domain. We investigated the binding properties of bHLH to HSP90. We analyzed the direct interaction of bHLH with HSP90, p23 and XAP2 using purified proteins. We found that not only the PAS domain but also the bHLH domain bound to HSP90. The bHLH domain forms complex with HSP90, p23 and XAP2. We also determined the bHLH binding domain was HSP90 N-domain. The bHLH domain makes a complex with HSP90, p23 and XAP2 via the HSP90 N-domain. Although the NLS is closed in the absence of a ligand, the structure of AhR will be changed in the presence of a ligand, which leads to NLS open, result in the nuclear translocation of AhR.
Keywords: Ahr, HSP90, Molecular Chaperone
Time : 16:15 - 16:45
Chagas is a professor in the medical course at Padre Albino University Center, Catanduva, São Paulo, Brazil (UNIFIPA). He was a surgical fellowship at the European Institute of Oncology, Milan, Italy. Currently he is a postdoc researcher atGinecology Department – UNIFESP (Federal University of São Paulo) He is interested in breast reconstruction and surgical treatment of breast cancer.
Invasive breast cancer is a more common gynecological malignancy among women and the late diagnosis for women who end up performing a radical mastectomy. The two techniques of breast reconstruction, and those that practice the treatment of tissues, are common. A common complication is arterial ischemia and / or venous congestion that occurs in the flap. One of the strategies to obtain better vascularization is the use of hyperbaric therapy. Materials and methods: 30 rats were divided into 3 groups: 10 rats in the control group (5 rats with arterial ischemia and 5 rats with venous congestion), 10 rats with arterial ischemia and 10 rats with venous congestion. Each rat was anesthetized with 30 mg / kg injected phenobarbital and underwent surgery to make cutaneous tissue, following a technique described by Matsumoto (2017). Rats undergoing hyperbaric therapy performed a 90-?minute session, once a day for 7 days. The evaluation of the vitality of the flap occurred on day 7. Results: We evaluated the VEGF expression and a neoangiogenesis in the 3 groups. The flaps with ischemia were recorded in a smaller area oftissue necrosis by a clinical analysis and expressed more VEGF and the greater number of neoformed capillaries.Conclusion: it was possible to demonstrate that hyperbaric therapy has a greater effect on neoangiogenesis and VEGF expression in the flap with arterial ischemia.Key words: VEGF, neoangiogenesis, flap ischemia, flap congestion, breast reconstruction
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