Conference Schedule

Day1: May 10, 2018

Keynote Forum

Biography

Thomas Boldicke has received his PhD in 1982 at the Max Planck Institute of Molecular Genetics, Berlin. He started his carrier as Postdoc at the German Research Centre for Biotechnology (GBF, Brunswick) in the Department of Genetics and Cell Biology by John Collins. Now he is a Senior Scientist at the Helmholtz Centre for Infection Research and Project Leader for intrabodies. In 2011, he qualified as a Professor in Molecular Biology and Cell Biology at the Technical University of Braunschweig. He is an expert in generating mouse and human hybridomas and in selecting and modifying recombinant antibodies. In the last decade he focused on the construction and characterization of intracellular antibodies. He has published 35 manuscripts.


Abstract

Intrabodies can be used to target and knock down virtually every protein inside the cell. The knockdown of intracellular cancer antigens by intrabodies is promising. Cancer antigens passing the endoplasmatic reticulum (ER) are inactivated by ER intrabodies retained inside the ER and expressed in the single-chain variable fragment (scFv) format. Cytosolic and nuclear cancer targets are inhibited by neutralizing single domain antibodies which comprises only the variable domain of the heavy chain derived from camels or sharks. This talk will give an overview of in vivo targeting of cancer antigens by intrabodies in mouse tumor models and will demonstrate an example of ER intrabodies inhibiting the polysialyltransferases in rhabdyomasarcoma cells in a xenograft tumor mouse model.

 

Biography

Pascal Rihet has a long lasting experience of research in the field of genetics and genomics of infectious diseases. He has mapped malaria and sepsis predisposing genes by using genetic linkage or association approaches. Furthermore, he has identified many variants associated with the disease; most of those genetic variants are located within noncoding regions. He has provided evidence that several variants have a cis-regulatory effect, suggesting that the regulation of gene expression is critical for the pathogenesis. In this way, he has investigated gene expression profiles in patients or in mouse models, and identified a number of genes whose expression is up- or down-regulated before or at the onset of the disease. He was the Deputy Director of the TAGC laboratory. Currently he is the Director of TAGC laboratory. The research scope of the laboratory is Genetics, Genomics and Bioinformatics. He is a Professor of Genomics and Immunology at AMU


Abstract

The contribution of host genetic factors to resistance or susceptibility to Plasmodium falciparum malaria has been widely studied. Nevertheless, a few genome scans have been performed, and few of them led to the discovery of loci significant at the genome level and to the identification of functional variants potentially causal. Here we describe loci genetically linked to malaria phenotype at the genome level and genetic variants located within those loci and associated with malaria phenotype in two independent populations. Furthermore, we provide evidence of a cis-regulatory effect of the genetic variants, suggesting that those variants are causal. We mainly focus on genes and genetic variants located within chromosome 6p21, which has been linked to mild malaria. These include TNF and NCR3, which encode a major actor of inflammation and a receptor of natural killer cells involved the cytotoxicity function, respectively. Also, the results are in line with those supporting the role of TNF in malaria on the one hand and allow us to propose a new biological model to explain the association of a cis-regulatory variant of NCR3 with mild malaria, on the other hand. Also, the genetic variation that alters the activation of natural killer cells may influence human malaria resistance

Tracks

  • Classical Immunology | Tissue Engineering and Regeneration | Immunoinformatics | Immunological Disorders | Autoimmune Diseases | Infectious Disease Drivers | Emerging and Re-emerging Infectious Diseases | Remedy for Immunity and Infection
Location: Spessart

Hadaf Dhafir Al Yaseen

University of Baghdad, Iraq

Chair

Yawei Liu

University of Copenhagen, Denmark

Co Chair

Biography

Manijeh holds a BSc. in microbiology and PhD in immunology and has about 17 years of research experience in infectious diseases and vaccines. Her research path started as research assistant at Pasteur Institute of Iran, where she was involved in recombinant vaccine studies against Leishmania major, and assisted the group leader to establish and run the “Molecular Immunology and Vaccine lab”. She fulfilled her PhD studies at Stockholm University on the general topic of “Human genetic factors involved in immunity to malaria”, while contributing to allergy studies as well. As Postdoctoral researcher and Assistant Professor her research focus turned towards genetic diversity of malaria parasite in relation to transmission intensity and prospective studies of malaria in travelers. Years of engagement with tropical diseases provided her with experience of filed study as well as broad collaborative network. Beside academic education, she schooled for ICH-GCP, Pharmacovigilance-Drug Safety, GMP, and coaching-leadership


Abstract

The rapid clearance of malaria parasite DNA from circulation has widely been accepted as a fact without being systemically investigated. In this longitudinal study, we examined the duration of PCR positivity as well as the presence of gametocytes in adult travelers treated for Plasmodium falciparum malaria in a malaria-free setting, using microscopy, species-specific qPCR, merozoite surface protein 2 (msp2)-genotyping PCR, and gametocyte-specific qPCR. Venous blood was collected at the time of admission and prospectively up to one year. Patients were treated with a full regimen of six doses of artemether-lumefantrine (AL). In 31 successfully treated individuals, asexual parasites were seen by microscopy until two days after treatment, whereas parasite DNA was detected by msp2- and species-specific PCR up to days 31 and 42, respectively. Statistical modelling predicted 26% (± 0•05 SE) species-specific PCR positivity until day 40 and estimated 48 days for all samples to become PCR negative. Gametocytes were detected by microscopy and PCR latest two days after treatment. CT values correlated well with microscopy-defined parasite densities before but not after treatment started. Duration of PCR positivity was correlated neither with the initial (asexual) parasite densities nor with the initial presence of gametocytes.

 

These results reveal that PCR positivity can persist several weeks after treatment without evidence of viable sexual or asexual parasites, and that the removal of dead parasites and their debris is not as rapid as it is believed, indicating that PCR may overestimate post-treatment parasite prevalence in epidemiological studies, and underestimate drug efficiency in clinical management and trials. This report underlines an important diagnostic matter essentially in infectious diseases and particularly in malaria, and points out the need for detection tool as sensitive as PCR and as accurate as microscopy

 

Biography

Hans Kollberg is Professor emeritus, Pediatrics, Children´s University Hospital, Uppsala. He has a Specialization in Pediatrics from Swedish Medical Board in 1966. He holds a Medical Doctors Degree (MD) in Pediatrics from Uppsala University, Sweden 1961. He started his career as Staff Physician, Good Samaritan Hospital, Phoenix, Arizona during 1959-1966. He extended his service as a Director of the CF Center, University Hospital, Uppsala in 1968-1982 and Umea in 1985-1999. He was Professor at the University of Kuwait during 1982-1985. He has been a recipient of many awards and grants. He is the Founder of the Swedish Cystic Fibrosis Association. His research experience includes various programs, contributions and participation in different countries for diverse fields of study. His research interests as a Research Scholar reflect in his wide range of publications in various national and international journals


Abstract

There is an increasing prevalence of antibiotic resistant bacteria. This makes traditional antibiotics less effective. More than 25000 people in Europe die each year from infections of resistant bacteria. This emphasizes the need to find alternatives to antibiotics. The drug should fight infections, it should not give resistant bacteria or viruses, it should be easy to scale up and it should be cheap. Such a drug exists. Avian antibodies from immunized hens act as strong weapons against a series of common infections. Hence these can be used either as a complement or an alternative to antibiotics. It is high time for health authorities, pharmaceutical companies, physicians, and researchers etc., to be involved in the fight against infectious diseases by joining this strong pull for avian antibodies-IgY. Clinical studies are carried out including use of IgY will diminish the development of antibiotic resistant microbes.

 

Biography

Huang Wei Ling has graduated in Medicine in Brazil, specializing in infectious and parasitic diseases, a General Practitioner and Parenteral and Enteral Medical Nutrition Therapist. She was in charge of the Hospital Infection Control Service of the City of Franca's General Hospital, she was responsible for the control of all prescribed antimicrobial medication, and received an award for the best paper presented at the Brazilian Hospital infection Control Congress in 1998. She was coordinator of both the Infection Control and the Nutritional Support Committee in Sao Joaquim Hospital in Franca, and also worked at the infectious Sexually Transmitted Disease Reference Center. She is the owner of the Medical Acupuncture and Pain Management Clinic, and since 1997 she has been presenting her work worldwide concerning the treatment of various diseases using techniques based on several medical traditions around the world


Abstract

Background: Furunculosis is a deep infection of the hair follicle leading to abscess formation with accumulation of pus and necrotic tissue. Furuncles appear as red, swollen, and tender nodules on hair-bearing parts of the body, and the most common infectious agent is Staphylococcus aureus, but other bacteria may also be causative. The management of recurrent furunculosis is problematic and may be disappointing. Simple incision and drainage may be sufficient in solitary lesions, but systemic antibiotic therapy may be required. S. aureus has the ability of developing resistance to different antibiotics. Traditional Chinese Medicine (TCM) believes furunculosis is mostly caused by invasion of dampness and heat. The treatment in TCM is intended to dissipate heat and detoxify the body
 
Purpose: The purpose of this study is to demonstrate that recurrent furunculosis can be treated without the use of antibiotics
 
Methods: Through the report of two clinical cases, both men, suffering from recurrent furunculosis, presented little improvement with the use of antibiotic therapy. Through earlier medicine theories, such as TCM, methods for energy balance of yin, yang, qi and blood were used, allied with apex ear bloodletting to withdrawal of internal heat, as well as dietary counseling. 
 
Findings: Both cases obtained a significant improvement with dietary counseling according to TCM and auricular acupuncture sessions associated with apex ear bloodletting to clear out the internal heat.
 
Conclusion: By reporting these two clinical cases, we can conclude that recurrent furunculosis can be treated without the use of antibiotics. For this goal, we must resort to earlier medicine theories like TCM to treat the root of the problem, not only the symptom.

 

Biography

Desheng Hu has received his PhD degree in Immunology at the Leibniz Institute for Ageing Research, Jena University, Germany in 2012. After that he did his Postdoc training in the Institute for Immunology of Helmholtz Zentrum Munich and in the Institute for Immunology of Ludwig Maximilian University of Munich. In 2017, he went back to China and established his own research group in Wuhan Union Hospital, Wuhan, China. His research focuses on Vascular Immunology. So far, he has published several papers in high impact factor journals, such as Nature Immunology, Immunity and Circulation Research.

 


Abstract

Tertiary lymphoid organs (TLOs) emerge during non-resolving peripheral inflammation, but their impact on disease progression remains unknown. We have found in aged Apoe-/- mice that artery TLOs (ATLOs) controlled highly territorialized aorta T cell responses. ATLOs promoted T cell recruitment, primed CD4+ T cells, generated CD4+ , CD8+ , T regulatory (Treg) effector and central memory cells, converted naive CD4+ T cells into induced Treg cells, and presented antigen by an unusual set of dendritic cells and B cells. Meanwhile, vascular smooth muscle cell lymphotoxin b receptors (VSMC-LTbRs) protected against atherosclerosis by maintaining structure, cellularity, and size of ATLOs though VSMC-LTbRs did not affect secondary lymphoid organs. Atherosclerosis was markedly exacerbated in Apoe-/- Ltbr-/- and to a similar extent in aged Apoe-/-Ltbrfl/fl, Tagln-cre mice. These data support the conclusion that the immune system employs ATLOs to organize aorta T cell homeostasis during aging and that VSMC-LTbRs participate in atherosclerosis protection via ATLOs.

Biography

Rochelle is a registered medical practitioner, completed her studies in 2010 at the University of Pretoria. She finished her Diploma in Emergency Medicine in 2017 along with her certificate in Travel Medicine in 2016. She accomplished her dispensing license and have been updated with ATLS, ACLS and PALS in South Africa. She works for one of the busiest, private hospital, Emergency departments in South Africa seeing a multitude of trauma and medical emergencies. She is interested in Family and Travel Medicine practice affiliated with the ED with a special interest in Aesthetic Medicine. She is currently serving on the executive board for the Society of Travel Medicine in South Africa working closely with the NICD with all infectious disease monitoring in SA and submitting interesting case studies to Federation of Infectious Diseases in SA (FIDSSA) on behalf of SASTM


Abstract

Listeriosis is the new and deadly disease emerging after years of being the quiet one sitting in the corner while HIV and Malaria caused havoc and massive outbreaks and mortality rates sky rocketing. Our population is well informed and up to date on most of the diseases and as soon as listeria was mentioned in the same sentence as processed foods, we created mass hysteria in all the emergency departments with worried patients, ill-informed patients and really sick patients, with very little knowledge about listeria. I want to discuss the pathogenicity as a re-emerging disease we have not heard from in a long time with very little information regarding pandemic and epidemics. Being in the midst of the hysteria, I think giving an inside view and up close, first-hand experience on what happened as soon as the outbreak was confirmed leading up to the massive explosion of patients literally running to ED after the source was confirmed as one of our leading manufacturers and producers of processed meat. We have had around 180 deaths in SA due to Listeria especially in the age groups of the very young, elderly, pregnant and immunosuppressed patients. The biggest factor leading to the outbreak initially was that we were not looking for it as we were so focused on Malaria as leading cause of fever and confusion etc. at the time of the outbreak and NICD confirmed that Malaria deaths doubled in 2017 vs. 2016. Listeriosis was monitored and regarded as a minor infection, but, while everyone was focused on travel history, Listeria was silently killing dozens. I would like to include the basic information as to what, where and how as the simple things were missed while we were looking for complicated illnesses

 

Biography

J Di Cristofaro has her experience in Human Genetics applied to Personal Medicine. She graduated PhD in Oncology from the Aix Marseille University, Immunological Therapies in Paris Descartes University and Forensics in Bordeaux University. After completing her PhD at INSERM, she has joined the French Blood Center to set up a genetic analysis platform dedicated to Immunogenetics, Immunohematology and Anthropogenetics. She has worked on molecular carcinogenesis and set up markers to help carcinomas classification and worked in anthropogenetics on Y chromosome phylogeny. Her current researches focus is HLA Ib molecules in immunization and inflammatory responses. Her aim is to validate inflammatory and/or alloimmunization prognostic markers in blood transfusions, pregnancies, transplantation or inflammatory diseases. Her team works on genetic polymorphisms, transcriptional expression variation both at qualitative level and quantitative level, protein expression and function.


Abstract

Today topic is human leukocyte antigen (HLA) non-classical class Ib genes, HLA-G, -E and -F, involved in immune tolerance. HLA-G immune-inhibitory role acting directly on immune cells is extensively documented. HLA-G inhibits natural killer (NK) cytotoxicity. This molecule is also able to negatively influence antigen presentation of dendritic cells (DC), B and T lymphocytes activation and proliferation. HLA-G gene is characterized by few coding alleles and polymorphic regulatory regions, organized in a restricted number of haplotypes (UTR). Both HLA-G genetic polymorphism and expression are correlated to clinical outcome in different pathologies, particularly in inflammatory disease and organ transplantation. HLA-G phylogeny reflects HLA-G haplotype specific association with different clinical conditions. HLA-G sequences associated with immune impairments in pathological conditions are grouped in same phylogenetic clades. Furthermore, this molecule displays several isoforms, soluble or membrane bound, generated by alternative splicing. Besides its expression in immune cells, HLA-G is expressed by the epithelium and is implicated in cell proliferation and differentiation. However, little is known about the qualitative and quantitative HLA-G expression in epithelial cells. HLA-E gene is the least polymorphic of the HLA class Ib genes. While its transcripts have been detected in several tissues, membrane expression appears to be limited in physiological condition to endothelial cells, T and B lymphocytes, macrophages and trophoblast cells. HLA-E peptide-binding groove, composed by α1 and α2 domains, loads highly conserved peptides mainly derived from classical HLA class I leader peptide sequences. HLA-E binds preferentially HLA-G signal peptide. HLA-E inhibit NK cytotoxicity trough the CD94/NKG2A inhibitory receptor. HLA-F appears to be expressed mostly in intracellular compartment; its surface expression is detected on activated B, T, and NK cells in vitro and on extravillous-trophoblast that had invaded the maternal decidua in vivo. HLA-F, expressed as an open conformer molecule, binds the inhibitory receptor KIR3DS1.

Biography

Hepatitis C virus (HCV) is a serious infectious disease that can cause lifelong infection. Infection with chronic hepatitis C virus (HCV) can lead to autoimmune hepatitis (AIH) in a minority of patients. Viral infection induces, both (in vivo and in vitro) tumor necrosis factor (TNF-alpha) production in hepatocytes, and these findings suggest that TNF-alpha may have an important role in human liver diseases induced by viruses, together with the prolactin hormone, which is an endocrinal hormone that acts like a cytokine involved in immune response. Our study showed that chronic hepatitis C virus infection associated with a statistical significant increase in the antismooth muscle antibody, while no statistical significant increase in antinuclear antibody were shown in this study.  The study elucidated a statistically non-significant increase in mean value of prolactin hormone in chronic hepatitis C patients but a significant increase in tumor necrosis factor-alpha. No significant correlations were found between prolactin hormone and tumor necrosis factor-alpha. The study concluded that chronic hepatitis C associated with an immunological abnormality mainly represented with antismooth muscle antibody. Tumor necrosis factor-alpha increased in chronic hepatitis C virus infection with no significant correlations with prolactin hormone


Abstract

Prof. Dr. Hadaf El-Yassin was faculty in University of Baghdad in the Department of Biochemistry, College of Medicine at University of Baghdad. She finished her Post Doctorate in Clinical Biochemistry at Al-Nahrain University. She is currently the head of the Department of Clinical Biochemistry, University of Baghdad, Iraq. She actively participated in 43 local conferences in Iraq and 26 abroad, making a total of 69 conferences attendance and paper presentation. She also published 85 articles

Biography

Yawei Liu has a medical doctor background and has been doing medical research for more than 10 years. Since her Ph.D., she mainly focused on the role of neurons in the regulation of auto-reactive T cells and central nervous system (CNS) inflammation. We reported a novel function for neurons as being highly immune-competent cells, based on their crucial role in the regulation of T-cell responses and CNS inflammation in models of multiple sclerosis


Abstract

Neurons reprogram encephalitogenic T cells (T(enc)) to become regulatory T(reg) cells FoxP3+Tregs or FoxA1+Tregs. We reported previously that neuronal ability to generate FoxA1+Tregs was central to preventing neuroinflammation in experimental autoimmune encephalomyelitis (EAE). Mice lacking the cytokine interferon (IFN)b were defective in generating FoxA1+Tregs in the brain. Neuron-induced FoxA1+Tregs were capable of preventing chronic and demyelinating EAE in mice lacking IFNb. Here we show that lack of neuronal IFNb-signaling was associated with lack of neuronal expression of program death-ligand1 (PDL1), which also prevented their ability to reprogram Tenc cells to FoxA1+Tregs. Transfer of IFNb competent encephalitogenic T cells to mice lacking IFNb or its receptor; IFNAR in the brain (NesCre:Ifnarfl/fl) led to the absence of FoxA1+Tregs generation and aggravated neuroinflammation. We identified that IFNb activated neuronal PI3K/Akt signaling. Phosphorylated Akt consequently bound to transcription factor FoxA1, which upon translocation to the nucleus induced neuronal PDL1 expression. Conversely, inhibition of PI3K/Akt, or FoxA1 and PDL1 knock-down blocked neuronal ability to generate FoxA1+Tregs. Our study identified crucial molecular player’s central for neuronal ability to reprogram pathogenic T-cells and to generate FoxA1+Tregs, which could be a therapeutic target to prevent neuroinflammation

Biography

Sameh Elmorsy Hassan has an experience in Neurosurgery for nine years in educational hospitals, currently pursuing his MD of Neurosurgery in Cairo University. He has completed his MSc in Neurosurgery. He is a Member of ESA, SPINE, Member of ESNS a lot of conferences about Neurosurgery and Spine Administrator of Egyptian and World Neurosurgeons Community on telegram

 


Abstract

Discitis accounts for nearly 2.2 of 100,000 populations and its presence is an indicator for immunocompromisation, as its risk factors includes diabetes mellitus, IV drug abuse and hemodialysis. As disc nutrition is through diffusion from end plates. So once you diagnose discitis you have to search for immunocompromized agent asking for lab is mandatory to manage medically is the best choice, unless there is refractory pain or neurological deficits, following up of patient by erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) first sign of improvement is decrease of CRP it occurs in two weeks. In acute stage of inflammation surgical intervention is not recommended but in chronic stage you can manage it surgically. Discitis is a serious problem which may cause death and it's a vicious circle as risk factors are immunocompromization and results are more compromising most probably septicaemia or viraemia is the cause of death. Most appropriate antibiotics should be selected for 3-6 months; intradiscal injection of antibiotics may decrease postoperative discitis as proved by meta-analysis. How discitis happen, risk factors, medical treatment, surgical, what to choose when you choose

Biography

Sopita Wongin is a posdoctoral fellow in Biological Engineering Program, Faculty of Engineering, King Mongkut's University of Technology Thonburi. Sopita got a scholarship from the Royal Golden Julilee PhD Program and completed her PhD at King Mongkut's University of Technology Thonburi, Thailand in 2017. During her PhD, she worked as a special research student for a year in Laboratory of BioProcess Systems Engineering (BPSE), Department of Biotechnology, Graduate School of Engineering, Osaka University, Japan. Her research interests lie in the area of cell sheet technology, tissue engineering and advanced cell technology. Her recent publications include Chondrogenesis and Hypertrophy in Response to Aggregate Behaviors of Human Mesenchymal Stem Cells on a Dendrimer-Immobilized Surface (2017), Effect of Cell Sheet Manipulation Techniques on The Expression of Collagen Type II by Altering Stress Fiber Formation (2018) and Maintenance of the human chondrocyte phenotype on a dendrimer-immobilized surface for chondrocyte sheet engineering (2018).

 


Abstract

Human chondrocyte sheets have attracted attention as tissue-engineered cartilage for the treatment of articular cartilage defects. However, the process of transferring the human chondrocyte sheets to cartilage defects is complicated because the cell sheets are thin and fragile. This study investigated whether human chondrocyte sheets could adhere to human cancellous bone and express cartilage-specific markers. Human chondrocyte sheets were constructed using osteoarthritic chondrocytes and temperature-responsive culture plates. Monolayer and triple-layered chondrocyte sheets were placed on the top of cancellous bones and cultured in basal medium. The expressions of cartilage surface (lubricin) and hypertrophic chondrocyte (collagen type X) markers in the tissue structure were observed by immunofluorescence staining. After one month, all the chondrocyte sheets were firmly attached, with growth inside the cancellous bones, as shown by fluorescence staining of the nuclei and stress fibers. The cells also adhered and proliferated to reach confluence on the tissue culture surface outside the cancellous bone, indicating cell growth and viability. Moreover, the expressions of lubricin and collagen type X were found in chondrocyte cultures. Our results indicated that the human chondrocyte sheets showed potential to adhere to cancellous bone with expression of cartilage surface markers; although hypertrophic markers were found in the cultures as we used osteoarthritic chondrocytes. Attachment of human chondrocyte sheets to cancellous bone could enhance the thickness and support the structure of engineered cartilage tissue transferred to the defective areas. This would be beneficial for researchers to develop a protocol for the treatment of articular cartilage defects.

 

Biography

Kajal Chaudhry is a PhD student in the Graduate School of Biomedical Engineering at University of New South Wales. She completed her MTech in Biochemical Engineering at Harcourt Butler Technical University, India. Her research interests include Genetic Engineering, Live Cell Imaging and Immunology


Abstract

Adoptive therapy with chimeric antigen receptor (CAR)-modified T cells has induced long-term remission in patients with CD19+ leukaemia but limited success in solid tumors. The cellular mechanisms driving the immune responses mediated by CART-cells still remain obscure. The aim of this study is to directly observe immune synapse formation, tumor cell killing and kinetics of CART cell activation by live cell imaging to explore its potential against different types of cancer. Second-generation CAR specific for CD19 antigen-expressing CD28 co-stimulatory domain were co-cultured with CD19+ leukaemia Nalm6 and visualized in real time using time-lapse microscopy. The infiltration and cytotoxicity of solid tumors by both natural killer (NK) and T cells was studied against SK-N-As neuroblastoma cell line spheroids to determine their synergy. Live cell imaging of CART cell antitumor response showed that CART cells not only induced direct cytolysis of tumor cells but arrest cell division and migration. CART cells have also demonstrated the indirect killing where they induce leukemic cell apoptosis without stable conjugation. Thus non-cytolytic mechanisms may play an important role in determining the anti-leukemic activity of CART cells. Live cell imaging has shown that both T and NK cells are capable of infiltrating neuroblastoma spheroids. However, NK cells reduced the size of spheroids more than T cells. Unlike T cells, NK cells were also able to completely dissociate day 3 immature neuroblastoma spheroids. Future studies will examine whether NK cells can enhance the potency of GD2 ligand specific T cells targeting solid tumors by dissociating the tumor capsule.

 

Biography

Yosra Bouraoui is experienced in immunology, inflammatory and prostate cancer. Yosra worked on prostate tissue by immunohistochemistry to analyze several signaling pathways in response to inflammatory cytokines such as IL-6, IL-1 and TNF alpha. She is expertized in prostate cell culture to study AKT signaling and NF kappa B mediated by IL1. At this moment she is working on petri net model (In silico model) my experiment results on pro inflammatory cytokines and its network in prostate pathologies. Yosra is currently working on the relation between inflammatory cytokine and immune metabolic in prostate tissue


Abstract

Introduction: The major signaling transduction of the pro-inflammatory cytokine IL-6 is through the transcription factor STAT3. However, PI3-K/AKT signaling pathway can also activated by IL-6 under prostate pathological conditions.

Objectives: The aim of this study is to evaluate the tissues levels of STAT3/IL-6/ AKT axis signaling in prostate tissues from patients with benign prostatic hyperplasia (BPH) and prostate cancer (PC).

Material & Methods: Immunohistochemical analyses for IL-6, Gp130, phospho-STAT3 (Tyr705) and phospho-AKT (Ser473) were carried out in 25 samples of BPH, 16 samples of PC.

Results: Immunoreactivity to IL-6 was consistently observed in stroma compartment of BPH and cytoplasmic epithelial cell in PC samples. Phospho-AKT was mainly expressed in membrane and the cytoplasm in PC compared to BPH. Immunoreactivity for phospho-STAT3 (Tyr705) was found in the stroma and the nucleus of epithelial and tumoral cells. No significant association was determined (r=0.153, P=0.518) when IL-6 and phospho-AKT (S473) were analyzed within BPH patients; whereas a positive correlation emerged between phospho-STAT3 (Tyr705) in the stroma and phospho-AKT (S473). In PC patients, significant relationship was documented between IL-6 and phospho-AKT (Ser473) (r=0.725, P=0.02). In addition, the correlation between phospho-AKT (Ser473) and phospho-STAT3 (Tyr705) as well as detected in the nucleus and the stroma were significant.

Conclusion: This suggests that IL-6/AKT axis could be one of mechanism to activate STAT3 by facilitating inflammatory cell migration and chronic inflammation in BPH and promote cancer progression by promoting cell growth in PC

Day2: May 11, 2018

Keynote Forum

Biography

Huang Wei Ling has graduated in Medicine in Brazil, specializing in infectious and parasitic diseases, a General Practitioner and Parenteral and Enteral Medical Nutrition Therapist. Once in charge of the Hospital Infection Control Service of the City of Franca's General Hospital, she was responsible for the control of all prescribed antimicrobial medication, and received an award for the best paper presented at the Brazilian Hospital infection Control Congress in 1998. She was coordinator of both the Infection Control and the Nutritional Support Committee in Sao Joaquim Hospital in Franca, and also worked at the infectious Sexually Transmitted Disease Reference Center. She is the owner of the Medical Acupuncture and Pain Management Clinic, and since 1997 she has been presenting her work worldwide concerning the treatment of various diseases using techniques based on several medical traditions around the world.


Abstract

Statement of the Problem: Very few publications provide sound scientific data used to determine which components are essential for infection prevention and control (IPC) programs in terms of effectiveness in reducing the risk of infection. In recent years, a range of regional best practice or policy principles have been developed that address what could be considered as core components of IPC programs. However there remains a major gap in relation to the availability of international best practice principles for core components of IPC programs.

Purpose: The purpose of this study was to show why patients still catch hospital infections despite IPC programs. A better understanding of a variety of theories is needed that could explain the physiopathology of diverse diseases described in the medical past history, which are usually disregarded clinically today. A broader view seems to show the necessity of seeing the patient as a whole; not only focusing on the disease in the prevention of these hospital infections.  

Methodology: A review of these theories such as those presented by Hippocrates (Natural forces within us are the true healers of disease), as well as others from oriental medicine, which explain that diseases originate from three factors: external (exposure to cold, heat, humidity, wind and dryness), internal (emotional) and dietary.       

Findings: Having a broader view of the patient as a whole (Yin, Yang, Qi, blood energy and heat retention), we can understand better the formation of hospital infection which is a systemic energy reaction of our body undergoing normal hospital treatment.

Conclusion: To understand better why a patient is still catching hospital infections, despite these IPC programs, we need to broaden our view observing all emotional, environmental and dietary factors, as well as studying the patient’s energy situation at the moment of admittance identifying the risk of hospital infection

Biography

Thomas Grundström has completed his Doctorate at Umeå University in 1981 and his Medical degree in 1982. He was a Postdoc during 1982-1984 in the laboratory of Professor Pierre Chambon, Institut de Chimie Biologique, Strasbourg, France, where he characterized the first discovered enhancer of transcription. He is a Professor at the Department of Molecular Biology at Umeå University since 1994. He has been studying Ca2+ sensor proteins and eukaryotic transcription and discovered the first direct Ca2+/calmodulin inhibition of a transcription factor. He has characterized the Ca2+ regulation of many transcription factors and other regulatory proteins with a main focus on the immune system. He is presently studying regulation of production of antibodies. He studies how somatic hypermutation (SH) and class switch recombination (CSR) are targeted and the regulation of the protein complex that performs SH and CSR.

 


Abstract

B-lymphocytes can modify their immunoglobulin (Ig) genes to generate antibodies with a new isotype and enhanced affinity. Activation-induced cytidine deaminase (AID) is the key mutagenic enzyme that initiates these processes. How somatic hypermutation (SH) and class switch recombination (CSR) are targeted and regulated to understand how we achieve good antibodies. The trans-acting factors mediating specific targeting of AID and thereby SH and CSR have remained elusive. How AID is recruited was still a big mystery. We show that mutant E2A transcription factor with defect inhibition by the Ca2+ sensor protein calmodulin results in reduced B cell receptor (BCR), IL4- plus CD40 ligand-stimulated CSR to IgE. AID is shown to be together with the transcription factors E2A, PAX5 and IRF4 in a complex on key sequences of the Igh locus in activated mouse splenic B cells. Calmodulin shows proximity with them after BCR stimulation. Direct protein-protein interactions are shown to enable formation of the complex. BCR signaling reduces binding of the proteins to some of the target sites on the Igh locus, and calmodulin resistance of E2A blocks this reduction. Thus, E2A, AID, PAX5 and IRF4 are components of a CSR and SH complex that calmodulin binding redistributes on the Igh locus. We present also that initiation of antibody diversification leads to formation of a mutasome, a complex between many proteins that enable repair at high error rate of the uracils made by AID on Ig genes but not on most other genes. We show also that BCR activation, which signals end of successful SH, reduces interactions between some proteins in the complex and increases other interactions in the complex with varying kinetics. Furthermore, we show increased localization of SH and CSR coupled proteins on switch regions of the Igh locus upon SH/CSR and that BCR signaling differentially change the localization.

 

Biography

Sasha Berdichevski is a Post-doctoral Research Associate in Engineering Department at University of Cambridge, UK. She has obtained a Blavatnik Fellowship by the Blavatnik Family Foundation, British Council and University of Cambridge, and currently she holds a Marie Curie Fellowship. She has been awarded as outstanding Researcher in Engineering and Science Award and Prize for Excellence in Nano-science and Nanotechnology during her PhD in the Technion, Israel. She has published her research in leading journal papers, and co-authored publications in three books. Her research interests include “Biomaterials, tissue engineering, scaffold-tissue/cell interactions, and scaffolds’ 3D geometry function relationship”.

 


Abstract

One of the main goals in producing engineered tissues at clinically relevant dimensions is creating perusable vascular networks, since cell viability and function cannot be sustained through diffusion alone. Therefore a great deal of research in the field of regenerative medicine has been devoted to establish in-vitro pre-vascularization approaches. In this context, we propose to create capillary-like networks using human umbilical cord endothelial cells, cultured with human osteoblasts, as these cells were demonstrated to have both direct and indirect pro-vasculogenic effects, within freeze-dried collagen scaffolds with tailored pore architecture. We guided scaffold pore architecture by manipulation of the freeze-drying conditions; producing porous scaffolds with randomly oriented (isotropic) or uniaxially aligned (anisotropic) pore architectures. We characterized the scaffolds’ structural, permeability and mechanical properties and showed that pore architecture affected the invasion, morphology and self-organization of the endothelial cells, in both mono- and co-cultures. Results showed that cell proliferation and metabolic activity were affected by pore architecture as well. Pore anisotropy promoted more uniform cell infiltration deeper within the scaffold, and improved cell organization into multi-cellular vessel-like networks. Co-culture conditions further improved the network quality. We suggest that deeper cell infiltration, along with more efficient medium perfusion within the anisotropic scaffolds account for these findings. However, the exact mechanism and conditions for optimal 3D vascular network formation as function of pore architecture have yet to be established.

 

 

Biography

Roman Bauer is an MRC Research Fellow at Institute of Neuroscience-Newcastle University, with joint affiliation with the School of Computing. His research involves computational models to better understand how neural tissue evolves during development. He received his Bachelor's and Master's Degree in Computational Science and Engineering from ETH Zurich, Switzerland. Afterwards, he did his Doctoral studies at Institute for Neuroinformatics (INI)-ETH and University Zurich, working on simulations of cortical development. After Postdoctoral work at Newcastle University from 2013 to 2016, he took up a prestigious MRC fellowship. His research interests include “Neural development, neural degeneration, neural disorders, gene regulatory networks and cryopreservation”.

 


Abstract

Biological tissue often exhibits extraordinary complexity. For example, neural tissue comprises large numbers of neurons with cell-type specific axonal and dendritic arborisation, highly structured synaptic connectivity, and fine-tuned electrical activity. A better understanding of how such tissue complexity develops is often essential for tissue engineering purposes. To this end, author will present some of his computational models of neural tissue development, demonstrating how complex structure and function can be generated based solely on simple genetic rules. These multi-scale models comprise intracellular as well as extracellular dynamics in a detailed, physical 3D environment. In particular, author will elaborate on computational models of cortical and retinal structure and function, ranging across different spatial scales. By modelling the biological self-organization of such tissue, predictions are made and so novel hypotheses are generated, which can be experimentally validated. Moreover, these models can inform and guide tissue engineering protocols. Finally, author will discuss modern computational approaches, including the BioDynamo software, which is a collaborative project with project partner CERN Openlab. Overall, author will emphasize the importance of computer models as a tool to advance tissue engineering approaches.

 

Tracks

  • Clinical Immunology | Tissue Engineering and Regeneration | Immunological Variability | Immunity and Host defence | Immune Adverse Effects | Microbiology and Clinical Infections | Versatile Immunology | Study of Evolution
  • Poster Presentations
  • E-poster presentation
Location: Spessart

Hans Kollberg

Uppsala Universitet, Sweden

Chair

Manijeh Vafa Homann

Karolinska Institute, Sweden

Co Chair

Biography

Dr. Aarti Sharma born 1983 did Bachelor of Ayurvedic medicine and surgery (BAMS) from one of the premier Ayurvedic College, Govt. Ayurvedic College, Patiala (India) in 2007. Since then she has been practicing Ayurveda for the treatment of lifestyle disorders, stress, gynecological issues, hepatic disorders, arthritis and other chronic ailments in her own clinic named Govindrakshak Ayurvedic and Acupuncture Centre, Ludhiana. During these years, she also completed Masters in nutrition and dietetics, Post graduate diploma in Acupuncture and moxibustion, and in yoga and naturopathy along with a short term course in panchkarma. Suggesting a patient about diet, yoga, naturopathy, panchkarma along with Ayurvedic medicines and healthy lifestyle has always helped her patients for better recovery in a short span. She has been presenting her findings at various national and International conferences.

 


Abstract

An autoimmune disease condition arises due to abnormal immune system response. Psoriasis is one of very common auto immune disease. Case presented here is of thirty two year old male patient who have been suffering from psoriasis since last ten years. He had red itchy patches on both limbs and scalp with white silvery scales on its top. Ayurvedic treatment was started for his psoriasis, in which he was given purification therapy procedure known as Vamana followed by Takradhara for 21 days. Along-with, this he was given Mahatiktaka ghrit 20 ml with Mahamanjishtadi Kashaya 40 ml twice a day during Takradhara procedure. During Takradhara he was also given Virechana, another purification (Shodhana therapy) with Avipathi Churna. In continuation of this treatment he was given Talapodichhil (panchkarma procedure) treatment for another fourteen days along with Rasayana (rejuvenate) therapy with the herb Plumbago zeylanica. After these panchkarma procedures patient was given mahamanjishtadi kashayam 40ml and kaishore guggulu two tablets twice day for six months. With above treatment patient showed relief in all clinical parameters, particularly his itching and silvery scales disappeared. After 6 months, it was found that Ayurvedic treatment showed improvement in both Psoriasis Area and Severity Index (PASI) score along with Dermatological Life Quality Index (DLQI). The above case study shows that Ayurveda is a ray of hope for such chronic autoimmune disease like psoriasis and further extensive studies should be carried out for such treatment modalities which may prove very beneficial for people suffering from psoriasis.

 

Biography

Thomas Boldicke has received his PhD in 1982 at the Max-Planck-Institut of Molecular Genetics, Berlin. He started his carrier as Postdoc at the German Research Centre for Biotechnology (GBF, Brunswick) in the Department of Genetics and Cell Biology by John Collins. Now he is a Senior Scientist at the Helmholtz Centre for Infection Research (HZI, former GBF) and Project Leader of intrabodies. In 2011, he qualified as a Professor in Molecular Biology and Cell Biology at the Technical University of Braunschweig. He is an expert in generating mouse and human hybridomas and in selecting and modifying recombinant antibodies. In the last decade he focused on the construction and characterization of intracellular antibodies. He has published 35 manuscripts.

 


Abstract

IFN-α activates the transcription of various IFN-stimulated genes (ISGs) in virus infected cells. Proteins encoded by ISGs block viral transport into the host cell and inhibit viral gene transcription and translation. Due to the existence of 13 different high homologous isoforms of mouse IFN-α, an IFN-α knockout mouse has not yet been established by conventional knockout strategies and CRISPR/Cas. We used an IFN-α knockdown strategy based on ER-intrabodies to inhibit IFN-α secretion in macrophages and dendritic cells, the main producers of IFN-α  after virus infection. To realize this strategy an ER intrabody was constructed from an anti-mouse IFN-α rat hybridoma recognizing five mice IFN-α isoforms. We follow the hypothesis that an intrabody recognizing five high homologous isoforms of the proteins will be able to knockdown all isoforms. The secretion of IFN-α was significantly inhibited by the intrabody in stable intrabody expressing RAW 264.7 macrophages and D1 dendritic cells as demonstrated by ELISA, Mx2-dependent luciferase assay and immunofluorescence. This antibody has the potential to knockdown IFN-α in transgenic intrabody mice. These animals might be very valuable in the future to study in detail the role of IFN-α during active and chronic viral infections and in autoimmune diseases.

 

Biography

Katja Bettina Ferenz has completed her PhD in Pharmaceutical Chemistry from Westfaelische-Wilhelms-University Muenster in Germany. From 2011 to 2018, she led her own research group development of artificial oxygen carriers at University Hospital Essen, Institute of Physiological Chemistry, Germany. Since February 2018, she continues her research on artificial blood and organ regeneration as Assistant Professor at University Hospital Essen, Institute of Physiology. Since 2017, she is a member of the editorial boards for the Journal of Nanochemistry and Nanotechnology and Journal of Nanoscience and Nanomedicine. Her research interests are artificial oxygen carriers, regeneration of tissue/organs, micro- and nanoparticles, nanomedicine, perfluorocarbons, drug delivery and biomaterials.

 


Abstract

At present, despite long lasting efforts, a harmless, effective artificial oxygen carrier is missing for clinical use both in Europe and USA. To bypass this bottleneck albumin-derived perfluorocarbon-based nanocapsules (nanocapsules) were designed as a novel artificial oxygen carrier. Nanocapsules do not contain any chemical emulsifier and can be synthesized in different size ranges (Ø 100-1500 nm). Physical assessment of size, oxygen transport capacity and repeated loading and unloading of respiratory gases was already performed and in vitro functionality was successfully proven using a flow-controlled Langendorff heart. Functionality in vivo was shown using a normovolemic hemodilution model. Up to 95% of the blood (final hematocrit of ~5%) was exchanged stepwise against plasma-like medium with nanocapsules (treatment) or without nanocapsules (control) in order to dilute below the critical hematocrit of a rat (~10%). Rats were monitored throughout the experiment (e.g. heart rate, mean arterial pressure (MAP), body core temperature and blood gas analysis). Furthermore rat kidneys were assessed for expression of erythropoietin using RNA scope technique to track effects of oxygen shortage on cellular level. Compared to control group all animals of the treatment group survived longer, showed a significant higher MAP and presented a continuous physiological temperature. Importantly, within the observation period erythropoietin mRNA was detected only in control animals. In conclusion nanocapsules provide enough oxygen to supply an organism when erythrocytes are not sufficiently present anymore, whereas plasma-like medium fails in the absence of any oxygen carrier. These positive results are confirmed on cellular level with the oxygen-dependent presence of erythropoietin.

Biography

Huang Wei Ling has graduated in Medicine in Brazil, specializing in infectious and parasitic disease, a General Practitioner and Parenteral and Enteral Medical Nutrition Therapist. She was in charge of the Hospital Infection Control Service of the City of Franca's General Hospital, she was responsible for the control of all prescribed antimicrobial medication, and received an award for the best paper presented at the Brazilian Hospital infection Control Congress in 1998. She was coordinator of both the Infection Control and the Nutritional Support Committee in Sao Joaquim Hospital in Franca, and also worked at the infectious Sexually Transmitted Disease Reference Center. She is the owner of the Medical Acupuncture and Pain Management Clinic, and since 1997 she has been presenting her work worldwide concerning the treatment of various diseases using techniques based on several medical traditions around the world.


Abstract

Introduction: Autoimmune hepatitis (AIH) occurs when the liver is attacked by rogue immune cells that mistake it for foreign tissue or pathogen, causing inflammation, being the goal of the treatment to slow or stop the immune system attack on the liver. Treatment with prednisone is generally used initially and a second medication, azathioprine may be recommended as well. Prednisone, especially when taken long term, can cause a wide range of serious side effects, including diabetes, thinning bones (osteoporosis), broken bones (osteonecrosis), high blood pressure, cataracts, glaucoma and weight gain. Most people need to continue taking the prednisone for at least eighteen to twenty four months, and many remain on it for life. Although the patient may experience remission a few years after starting treatment, the disease often returns if the drug is discontinued. In traditional Chinese medicine (TCM) Yin deficiency plays a central role in autoimmune disease.

Purpose: The purpose of this study is to demonstrate that autoimmune hepatitis can be treated without the use of corticosteroids.

Methods: An autoimmune hepatitis treatment literature review has been done through earlier medicinal theories such as traditional Chinese medicine.

Results: The general principle in TCM is to eliminate pathogenic heat from the blood, remove blood stasis, nourish liver and kidney yin. The treatment is based neither on Chinese herbal treatment and acupuncture nor ever including corticosteroids and immunosuppressive drugs.

Conclusion: The conclusion of this study is that autoimmune hepatitis can be treated without the use of corticosteroids and immunosuppressive drugs according to the teachings of traditional Chinese medicine, reducing the side effects caused by these drugs.

Biography

Özlem Vural studied Biotechnology at Technical University of Berlin. After working as a student assistant on in-vitro chondrogenesis in the Group of Prof. Dr. Roland Lauster, she started her PhD studies focusing on the generation of a human 3D thyroid model for substance testing. Her research interests include “Human organ models, tissue engineering and thyroid”.

 


Abstract

The thyroid gland plays a crucial role during embryonic development and organogenesis. It further controls the metabolism of various adult organs. Mechanisms that drive thyroid morphogenesis have not been fully elucidated. The inter-follicular extra cellular matrix supports the interaction of the functional units, the thyroid follicles, where thyroid hormone (T3 & T4) biosynthesis takes place. The development of 3D structures in vivo requires cell-cell interactions and crosstalk. Thus, we are aiming an imitation of cellular crosstalk in order to acquire functional organoids by culturing primary human thyrocytes in a 3D environment in vitro. Isolated human primary thyrocytes are expanded in monolayer culture and cells are seeded in ultra-low attachment plates to allow aggregation and cellular interaction. Within two weeks of in vitro culture, primary human thyrospheres restore their transcriptional status similar to the native thyroid. Based on the multi-organ-chip technology, developed by tissue GmbH, the interaction between selected organs can be mimicked. Due to the major impact of thyroid hormone on the metabolism, we want to investigate the interaction and influence between thyroid and organs such as liver or cardiac tissue by emulating the endocrine impact. Furthermore, based on our thyroid model, possible endocrine disruptors can be identified using our in vitro test system.

Biography

Dr. Dehghani is a professor of Veterinary Surgery, Dr. Haghani is a graduate student at the department of Surgery, Dr. Namazi is an assistant professor of Pathology, school of Veterinary Medicine, Shiraz University. And Dr. Ghaderi is a professor at the Cancer research centre of the Shiraz University of Medical Science, Shiraz, Iran. His research interest includes Stem Cell and Tissue regeneration.

 


Abstract

Liver cirrhosis is a chronic disease which normal liver tissue is replaced by fibrosis and scar leading to liver malfunction. The purpose of this study was to induce cirrhosis in rat as an animal model and treat cirrhosis by Mesenchymal stem cells derived from adipose tissue. 45 adult rats were used in this study. Group 1(30 rats) were treated by the mixture of CCL4 and olive oil for 16 weeks till cirrhosis signs appeared. Group 2 (15 rats) were not treated. Following the confirmation of cirrhosis, under anaesthesia, the linea alba was incised, the Stem cells were injected into the Portal vein.  5 weeks later, the rats were euthanized. Samples of liver tissue were collected for histopathological investigation. They were stained by H&E and Masson trichrome and studied by light microscope. Grossly the Cirrhosis liver appeared, Nodular, Pale and yellowish, with adhesion. Microscopic signs were: Diffused fibrosis, fatty changes, diffused necrosis, heterogeneous hepatic parenchyma. The clinical results of treated rats included: Increased movements, appetite, improved behaviour and decreased abdomen size. The histopathologic results of liver cirrhotic rats treated by stem cells indicated: although different stages of liver fibrosis was observed, however the structural parenchymal lesions were not found and this indicates that liver cells were renewing and regenerating and forming new colonies. In conclusion Liver cirrhosis was induced by IP injection of CCL4. The stem cells were developed from adipose tissue and cirrhotic livers were regenerated by injection of stem cells derived from adipose tissue in the portal vein.

 

Biography

Post implant insertion disease is not uncommon according to recent systematic reviews. Frequency has been classified in relation to affected biologic entity, number of implants and number of individuals involved: peri–implant mucositis affected 63.4% of identified participants compared to 30.7% of implants inserted; peri-implantitis was detected in 18.8% of participants and 9.6% of implants. Different treatment protocols are described in the literature. Critical appraisal of the evidence based upon long term outcome predictability could not sufficiently support and/or favorize particular treatment protocols. The consensus report of the sixth European workshop on periodontology (2008) concluded that there was no evidence that so-called regenerative procedures had additional beneficial effects on treatment outcome when used for peri-implantitis lesions. The consensus report of the tenth European workshop on periodontology (2014) related skin wound healing to oral soft tissue healing both in teeth and implants. The aim of the presentation is to introduce regenerative and maintenance protocols borrowed from wound healing and addressing both implant affected entities: soft tissues and supporting bone. The suggested protocols follow established requests related to the biology of wound healing and modification of the implant surface, application of self-induced regenerative, anti-bacterial and anti-bio adhesion coating.

 


Abstract

Liviu Steier served as Clinical and Course Director of the MSc in Endodontics at University of Warwick. He is Specialist in Prosthodontics and Dental Materials and Specialist in Endodontics. He served as Visiting Professor at University of Florence and Tufts Dental School. He published numerous papers and book chapters. He serves as a Reviewer and editorial board for different scientific journals worldwide. His research interest includes Dental Bio-Material Science.                                                      

 

Location: Foyer

Biography

Hans Kollberg is Professor emeritus, Pediatrics, Children´s University Hospital, Uppsala. He has a Specialization in Pediatrics from Swedish Medical Board 1966. He holds a Medical Doctors Degree (MD) in Pediatrics from Uppsala University, Sweden 1961. He started his career as Staff physician (1959-1966), Resident Good Samaritan Hospital, Phoenix, Arizona (1966-1967). He extended his service as a Director of the CF Center, University Hospital, Uppsala and Umea in 1968-1982 and 1985-1999. He was professor at the University of Kuwait 1982-1985. He has been a recipient of many awards and grants. He is the Founder of the Swedish Cystic Fibrosis Association, 1969. His research experience includes various programs, contributions and participation in different countries for diverse fields of study. His research interests as a Research Scholar reflect in his wide range of publications in various national and international journals.

 


Abstract

Objectives: Clinical studies have been running in Sweden and in Europe for 22 years with CF-patients on Anti-pseudomonas IgY (Anti-PA IgY) to prevent infections with Pseudomonas aeruginosa (PA) to find out efficacy and adverse events. The promising results gave Anti-PA IgY an Orphan Drug Designation in 2016.

Studies: Phase II study was conducted during 1995 -2002: Two groups with intermittently PA-infected patients: one group got Anti-PA IgY, the other group was without IgY. Microbiologists did not know from which group the analyses came from. A prolonged study in Sweden continued 2002-2011. Pregnancy: Two CF women, whereof one twice, were on Anti-PA IgY during pregnancies. Transplanted: One boy transplanted 12 years ago due to infections w. PA and Atyp.Mycobact. Phase III study 2002 -2017: A multicenter study from nine European countries.

Results: Phase II: Group with Anti-PA IgY: 2.35 positive PA cultures/100 months; Untreated group: 7 positive PA/100 months. The duration from first to second colonization with PA was significantly prolonged for the treated versus the control group (Kaplan-Meier p=0.015). The time from first PA infection until chronic infection occurred was prolonged in the Anti-PA IgY treated group. The time until PA was transformed to the severe mucoid form was prolonged. Lung function and BMI were well preserved. Prolonged group: similar effects as those in the first study. Three pregnancies have been carried out well and gave birth to three healthy babies. Transplanted pat.: No new pseudomonas or atypical mycobacterium after transplantation. The few infections in the treated group minimized the need for antibiotics. Phase III: The study was finished in June 2017. Totally 144 countable patients had been included. The results will be ready in spring 2018. All patients have gargled more than 250.000 times and no adverse events have been reported.

Discussion: Anti-PA IgY has shown good results both in efficiency and absence of adverse events. It reduces the use of antibiotics and thus also the risk of resistant bacteria. Gargling is convenient to use. Treatment is cost effective. Cost for Anti-PA IgY is much less than the costs for antibiotics. The costs for days of illness and for hospitalization will be much lower.

Conclusion: Hopefully the now running double-blind, randomized phase III study will give results as expected and Anti-PA IgY might be registered and physicians will be able to give anti-PA IgY to all eligible CF patients.

 

Biography

Rochelle is a registered medical practitioner, completed her studies in 2010 at the University of Pretoria. She finished her Diploma in Emergency Medicine in 2017 along with her certificate in Travel Medicine in 2016. She accomplished her dispensing license and has been updated with ATLS, ACLS and PALS in South Africa. She works for one of the busiest, private hospital, Emergency departments in South Africa seeing a multitude of trauma and medical emergencies. She is interested in Family and Travel Medicine practice affiliated with the ED with a special interest in Aesthetic Medicine. She is currently serving on the executive board for the Society of Travel Medicine in South Africa working closely with the NICD with all infectious disease monitoring in SA and submitting interesting case studies to Federation of Infectious Diseases in SA (FIDSSA) on behalf of SASTM.

 


Abstract

Today topic is Malaria, one of the deadliest infections in Sub-Saharan Africa causing more deaths per day than any other outbreak in recent years.  Malaria accounts for one of the highest Mortality and Morbidity rates in the world amongst Children esp. in poverty stricken countries with poor socio-economic status with malnutrition and immunosuppression.  It also has a very high morbidity rate amongst travelers not taking prophylaxis due to myths regarding the medication, uneducated regarding the signs and symptoms and to seek early treatment. 

Due to the above, resistance to medication and options for prophylaxis are limited with poor outcome if not detected early with a very low parasite count and no co-morbidities.  Patients are diagnosed with Malaria and are admitted to an ICU setting due to the high infection count and other complications, also increasing the length of stay in hospital, hospital acquired infection rate increasing, complications due to prolonged admission and illness including Thrombi and cardiac complications, malnutrition and Hepato-renal complications.  This in itself has a major burden on the economy due to the high cost of ICU management and care.

 

Biography

Yawei Liu has a medical doctor background and has been doing medical research for more than 10 years. Since her Ph.D., she mainly focused on the role of neurons in the regulation of auto-reactive T cells and central nervous system (CNS) inflammation. We reported a novel function for neurons as being highly immune-competent cells, based on their crucial role in the regulation of T-cell responses and CNS inflammation in models of multiple sclerosis

 


Abstract

Neurons reprogram encephalitogenic T cells (T(enc)) to become regulatory T(reg) cells FoxP3+Tregs or FoxA1+Tregs. We reported previously that neuronal ability to generate FoxA1+Tregs was central to preventing neuroinflammation in experimental autoimmune encephalomyelitis (EAE). Mice lacking the cytokine interferon (IFN)b were defective in generating FoxA1+Tregs in the brain. Neuron-induced FoxA1+Tregs were capable of preventing chronic and demyelinating EAE in mice lacking IFNb. Here we show that lack of neuronal IFNb-signaling was associated with lack of neuronal expression of program death-ligand1 (PDL1), which also prevented their ability to reprogram Tenc cells to FoxA1+Tregs. Transfer of IFNb competent encephalitogenic T cells to mice lacking IFNb or its receptor; IFNAR in the brain (NesCre:Ifnarfl/fl) led to the absence of FoxA1+Tregs generation and aggravated neuroinflammation. We identified that IFNb activated neuronal PI3K/Akt signaling. Phosphorylated Akt consequently bound to transcription factor FoxA1, which upon translocation to the nucleus induced neuronal PDL1 expression. Conversely, inhibition of PI3K/Akt, or FoxA1 and PDL1 knock-down blocked neuronal ability to generate FoxA1+Tregs. Our study identified crucial molecular player’s central for neuronal ability to reprogram pathogenic T-cells and to generate FoxA1+Tregs, which could be a therapeutic target to prevent neuroinflammation.

 

Biography

Prof. Dr. Hadaf Dhafir El Yassin was faculty in University of Baghdad in the Department of Biochemistry, College of Medicine at University of Baghdad. She finished her Post Doctorate in Clinical Biochemistry at Al-Nahrain University. She is currently the head of the Department of Clinical Biochemistry, University of Baghdad, Iraq. She actively participated in 43 local conferences in Iraq and 26 abroad, making a total of 69 conferences attendance and paper presentation. She also published 85 articles.

 


Abstract

Background:

Hepatitis C virus (HCV) is a serious infectious disease that can cause lifelong infection. Infection with chronic hepatitis C virus (HCV) can lead to autoimmune hepatitis (AIH) in a minority of patients. A genetic predisposition to autoimmune hepatitis from medication may lead to appearance of serum autoimmune antibodies especially anti smooth muscle antibodies (ASMA). Viral infection induces tumor necrosis factor (TNF-alpha) production in hepatocytes. These findings suggest that both parameters may have an important role in the patho-physiology and drug resistance of human liver diseases induced by viruses.  

Aim:

The aim of the presents study was to evaluate the role of the immunoendocrine system in the pathogenesis of the disease, by measuring serum TNF and antismoothmuscle antibodies (ASMA).

Subject and methods:

Sixty- one chronic hepatitis C patients were consequently selected from the Medical city, Gastrointestinal Hospital in Baghdad, Iraq, during the period from July 2014 to September 2014, their median age was 34.8 year, 29 of them were males and 32 were females. All patients were diagnosed having positive for HCV RNA by means of polymerase chain reaction. The study also included twenty apparently healthy adult ages and sex matched considered as controls, which were negatively screened with hepatitis C virus. Peripheral blood sample of 2 ml was aspirated using disposal syringes. Samples were collected between (9.00a.m-12.00p.m.). The blood was allowed to clot in plain tube for 30-45 minutes at room temperature. Sera were obtained by centrifugation of the collected blood and then stored in plain tubes at -20°C. ELISA method was used to measure serum TNF, while ASMA was measured by indirect immunofluoresent assay.

Results:

The results of this study showed an increase in mean value of serum TNF in chronic hepatitis C patients accompanied with a 65% increase in ASMS. Significant correlations were found between both parameters studied.

Conclusions:

Chronic hepatitis C is associated with an immunological abnormality. Results obtained might shed a light on the type of therapy and drug of choice when managing the disease.

 

Biography

Yosra Bouraoui is experienced in immunology, inflammatory and prostate cancer. Yosra worked on prostate tissue by immunohistochemistry to analyze several signaling pathways in response to inflammatory cytokines such as IL-6, IL-1 and TNF alpha. She is expertized in prostate cell culture to study AKT signaling and NF kappa B mediated by IL1. At this moment she is working on petri net model (In silico model) my experiment results on pro inflammatory cytokines and its network in prostate pathologies. Yosra is currently working on the relation between inflammatory cytokine and immune metabolic in prostate tissue.

 


Abstract

Introduction: The major signaling transduction of the pro-inflammatory cytokine IL-6 is through the transcription factor STAT3. However, PI3-K/AKT signaling pathway can also activated by IL-6 under prostate pathological conditions.

Objectives: The aim of this study is to evaluate the tissues levels of STAT3/IL-6/ AKT axis signaling in prostate tissues from patients with benign prostatic hyperplasia (BPH) and prostate cancer (PC).

Material & Methods: Immunohistochemical analyses for IL-6, Gp130, phospho-STAT3 (Tyr705) and phospho-AKT (Ser473) were carried out in 25 samples of BPH, 16 samples of PC.

Results: Immunoreactivity to IL-6 was consistently observed in stroma compartment of BPH and cytoplasmic epithelial cell in PC samples. Phospho-AKT was mainly expressed in membrane and the cytoplasm in PC compared to BPH. Immunoreactivity for phospho-STAT3 (Tyr705) was found in the stroma and the nucleus of epithelial and tumoral cells. No significant association was determined (r=0.153, P=0.518) when IL-6 and phospho-AKT (S473) were analyzed within BPH patients; whereas a positive correlation emerged between phospho-STAT3 (Tyr705) in the stroma and phospho-AKT (S473). In PC patients, significant relationship was documented between IL-6 and phospho-AKT (Ser473) (r=0.725, P=0.02). In addition, the correlation between phospho-AKT (Ser473) and phospho-STAT3 (Tyr705) as well as detected in the nucleus and the stroma were significant.

Conclusion: This suggests that IL-6/AKT axis could be one of mechanism to activate STAT3 by facilitating inflammatory cell migration and chronic inflammation in BPH and promote cancer progression by promoting cell growth in PC.

 

Biography

Alexandra Scheer completed her Master’s degree in Medical Biology in 2015. Since October 2015, she has been working on her Doctoral thesis at Institute of Physiological Chemistry-University Hospital Essen, Germany, in the working group of Dr Katja B Ferenz. Within the scope of this work, she is involved in the development and characterization of artificial oxygen carriers. Since February 2018, she followed Katja B Ferenz in the Institute of Physiology at University Hospital Essen, Germany, to continue her work. Her research interests include “Artificial oxygen carriers, biomaterials, nanoparticles and perfluorocarbons”.

 


Abstract

Currently, perfluorodecalin (PFD) and perfluorooctyl bromide (PFOB) are the majorly used perfluorocarbons in the field of artificial oxygen carriers. So far, in our investigations only PFD has been employed as core material of albumin-derived artificial oxygen carriers (A-AOCs). This led to the question of whether PFOB would display an equally safe alternative in A-AOCs. To investigate toxicity, we studied A-AOCs with a PFOB-core in a top load model (TL) and compared the data with results from our previous studies with a PFD-core. TL (+1/6 of blood volume) experiments with 16 healthy Wistar rats were performed with and without (control) A-AOCs (17 vol. %), respectively. After the infusion period (30 min) rats were further observed up to 180 min. During TL systemic parameters, plasma enzyme activities and acid base status were continuously monitored. To confirm hemolysis obtained in the in vivo model, supporting in vitro studies were performed additionally: whole blood was incubated varying temperature, A-AOCs-concentration and mechanical stress. Blood pressure showed a transient drop during infusion of A-AOCs but was unaffected in the control group. Compared to control animals the PFOB-group displayed increased plasma enzyme activities. All effects after application of only 17 vol. % A-AOCs with PFOB-core were considerably more pronounced compared to 32 vol. % A-AOCs with PFD-core. Furthermore, hemolysis caused by A-AOCs with PFOB-core was significantly more distinct compared to A-AOCs with PFD-core. In conclusion, PFOB should be avoided as core material for A-AOCs because of distinct side-effects already occurring at low dosage.

 

 

Biography

Yu-zhen Tan is a Professor in Department of Anatomy, Histology and Embryology at Shanghai Medical School of Fudan University. She completed her MD at Nanjing Medical University, China and; PhD at Shinshu University School of Medicine, Japan. In 1999, she became a Professor of Shanghai Medical School of Fudan University. She firstly designed and synthesized the self-assembling peptide modified with RGDSP, and investigated effects of the peptide carrying stem cells on repairing the infracted myocardium. She was also first to investigate effects of the PCL/gelatin nanofibrous patch on repairing the infracted myocardium after transplantation on the epicardium. Her research interests include “Stem cell differentiation and cardiovascular regenerative medicine”


Abstract

Recent studies suggest that the epicardium plays an important role in cardiomyogenesis during development, while it becomes quiescent in adult heart. Thymosin beta 4 (Tβ4) has an effect on activating the epicardium. However, effectiveness of Tβ4 administration is unsatisfactory. Therefore, this study prepared cardiac patch and investigated efficiency of activating the epicardium by Tβ4 released sustainedly from the cardiac patch. Mesenchymal stem cells (MSCs) isolated from bone marrow of rats and mice were transfected with Tβ4. Tβ4 release from the cells was determined with an acquity ultra-performance liquid chromatography system. For preparing of cardiac patch, the cells transfected with Tβ4 and Flag were seeded on PLACL/collagen membrane formulated by electrospinning. The survival and proliferation of the cells on the nanofibers were examined after treatment with hypoxia. In MI models of rats and Wt1CreERT2/+, R26mTmG mice, the patches were implanted on the epicardium of the infarcted region. In rat models, differentiation of the epicardium-derived cells (EPDCs) and the engrafted MSCs towards cardiomyocytes and vascular cells was examined by Wt1 immunostaining and Flag labeling. In transgenic mouse models, the activated EPDCs expressed GFP. At four week after implantation of the patches, cardiac function was improved significantly, scar area in the infarcted region was reduced obviously. EPDCs increased in subepicardium and myocardium, and some Wt1+ cells and GFP+ cells expressed CD31, α-SMA or cTnT. Moreover, c-kit+ cells were observed in subepicardium and myocardium, and a few of them expressed CD31, α-SMA or cTnT. Flag labeling showed that some engrafted MSCs migrated into subepicardium and myocardium. These results suggest that Tβ4 released from the transfected MSCs in PLACL/collagen nanofibrous patches may effectively attenuate left ventricular remodeling and improve cardiac function by activating the epicardial cells and recruiting endogenous stem cells. Our finding provides a novel strategy for myocardial regeneration by enhancing the endogenous regenerative mechanisms.

 

Biography

Hai-jie Wang is a Professor of Department of Anatomy, Histology and Embryology at Shanghai Medical School of Fudan University. He studied Clinical Medicine at Weifang Medical College, China. He completed his MD from Medical School of Shandong University, China in 1987 and PhD from Shinshu University School of Medicine, Japan in 1996. He studied Molecular Medicine at School of Medicine, Yale University from 2005 to 2006 as Visiting Professor. In 1999, he became a Professor of Shanghai Medical School of Fudan University. His research interests include “Differentiation and transplantation of endothelial progenitor cells”.

 


Abstract

Lymphatic vessels play a crucial role in draining excess fluid and transport macromolecular substances from extracellular spaces. Disfunction of lymphatic vessels may cause lymph edema and chronic inflammation, leading to fibrosis of the local tissue. This study investigated efficiency of transplantation of lymphatic endothelial progenitor cell (LEPCs) and sustained release of VEGF-C from self-assembling peptide (SAP) on promoting lymphangiogenesis after myocardial infarction (MI). CD34+VEGFR-3+ EPCs were isolated from rat bone marrow. Sustained release of VEGF-C from SAP nanofibers (SAPNs) was detected with ELISA. Compatibility of SAPNs with the cells was accessed with transmission electron microscopy and EB/AO staining. After rat MI models were established with ligation of the anterior descending branch of the left coronary artery, SAP carrying the cells and VEGF-C was injected at the border of the infarcted region. At four week after transplantation, the survival and differentiation of the cells labeled with GFP were examined, and repair of the infarcted myocardium was evaluated. Under induction with VEGF-C, CD34+VEGFR-3+ EPCs could differentiate into lymphatic endothelial cells. The cells spread well along SAPNs. SAPNs protected the cells from apoptosis in the condition of hypoxia, and released VEGF-C sustainedly. After transplantation, cardiac function was improved significantly. The number of the survived cells increased, and some cells differentiated into lymphatic endothelial cells. Density of lymphatic vessels increased, and cardiac edema was reduced. Moreover, angiogenesis and myocardial regeneration were enhanced. These results suggest that SAPNs load LEPCs and release VEGF-C effectively. VEGF-C released from SAPNs induces differentiation of LEPCs towards lymphatic endothelial cells. Loading stem cells and releasing growth factor with SAPNs is a promised strategy for MI therapy.

 

Biography

Dr. Tadjalli is a professor of Histology and Zarinfard is a graduate student at the department of Histology  School of Veterinary Medicine, Shiraz University, Shiraz and Dr. Razavi  is a professor of Histology Isfahan University of Medical Science, Isfahan, Iran. Her research interest includes Histology, stem cell, regeneration.

 


Abstract

The Schwann-like cells can be considered as promising in stem cell therapies, at least in experimental models. Human adipose-derived stem cells (ADSCs) are induced into Schwann-like cells (SC-like cells) and are cultured on either a plastic surface or laminin-coated plates. The findings here reveal that laminin is a critical component in extracellular matrix (ECM) of SC-like cells at in vitro. The survival rate of SC-like cells on a laminin matrix are measured through MTT assay and it is found that this rate is significantly higher than that of the cells grown on a plastic surface (P < 0.05). Schwann cell markers and the myelinogenic ability of SC-like cells at the presence versus absence of laminin are assessed through immunocytochemistry. The analysis of GFAP/S100β and S100β/MBP markers indicate that laminin can increase the differentiated rate and myelinogenic potential of SC-like cells. The expression levels of SCs markers, myelin basic proteins (MBP), and neurotrophic factors in two conditions are analyzed by real-time reverse transcription polymerase chain reaction(RT-PCR).The findings here demonstrated that gene expression of SCs markers, MBP, and  brain-derived neurotrophic factors (BDNF) increase significantly on laminin compared to plastic surface (P < 0.01). In contrast, the nerve growth factor(NGF) expression is down regulated significantly on laminin-coated plates (P < 0.05). The obtained data suggest that production of neurotrophic factors in SC-like cell in presence of laminin can induce appropriate microenvironment for nerve repair in neurodegenerative diseases.

 

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Biography

Aditi Singh has over seventeen years of experience in research and academics. After completing her Doctorate in the year 2000 from King Georges’ Medical College, she started teaching at undergraduate and post graduate level. During PhD thesis, she tried to understand the pathogenesis of Japanese encephalitis virus in disease confirmed patients; where in pro inflammatory cytokines were studied and evaluated. Her area of research interest is Microbiology, Immunology and Enzymology. Till now, she has authored more than thirty research papers in national and international journals and two book chapters. She has presented more than twenty papers in national and international conferences. Currently, she is working as Associate Professor in Amity University, a leading private University of India.

 


Abstract

Japanese encephalitis (JE) is one of the chief causes of acute encephalitis syndrome (AES) in North India with more than 15% confirmed cases. The disease is caused by Japanese encephalitis virus (JEV), a neurovirulent RNA flavivirus transmitted by Culex mosquitoes. The virus in natural cycle circulates between pig and mosquitoes or bird and mosquitoes, with pigs being the most important biological amplifiers. Though humans are accidental dead end hosts, JE has generated considerable public anxiety because it mainly remains a disease of children. The disease ranges from non-specific febrile illness to a severe meningoencephalomyelitis illness. The transmission of disease can occur throughout the year in endemic zone, with disease at a peak during monsoon season. Since there is no specific treatment available and vaccination is the best measure to get protection from the disease; it is important to understand the molecular mechanisms in host. The virus has been shown to induce neutrophil infiltration in neural and extra neural tissues. A neutrophil chemotactic protein derived from macrophages had been isolated from JEV induced animal models. It had variety of pathologic effects on host, including vascular permeability and breach in blood brain barrier. The presence of inflammatory chemokine IL-8 was also significantly detected in JE confirmed patients during acute phase of illness. The study had revealed a correlation between IL-8 levels and severity of illness as all severely ill and fatal cases showed higher levels of IL-8 in acute cerebrospinal fluid (CSF) and serum. In cases who recovered completely, the level of IL-8 declined markedly by convalescent phase. The study indicates important interaction between pro inflammatory cytokine, macrophages and neutrophils during JE infection.

 

Biography

Arnav Gupta is passionate about exploring causal relationships of drugs commonly used to treat neurodegenerative disorder.  Arnav is interested in pursuing a career in neuroscience. His passion in studying the brain and memory has inspired him to do research about Alzheimer’s disease. This common disorder presents so many unanswered questions, and Arnav is motivated to do further research in the future to answer some of these questions.

 


Abstract

Alzheimer’s disease is a very common type of dementia that destroys memory and other important mental functions. It is a neurodegenerative disorder which affects over 5 million people in the United States alone. In fact, it is the 6th leading cause of death in the United States, and on average, an American is diagnosed with Alzheimer’s disease every 66 seconds. This can be a familial or sporadic disease which is primarily caused by the destruction of neurons which starts from the hippocampus and spreads throughout the brain (cerebellum is spared). The apoptosis of the countless neurons seems to be caused by a multitude of factors including amyloid-beta plaques, Tau tangles, and neuronal loss. For the sake of this investigation, there will be a primary focus on the amyloid-beta plaques because the accumulation or buildup of neurotoxic plaques on the neurons seems to be a key factor in Alzheimer’s disease. Enzymes called γ-secretase and β-secretase cleave a protein called an amyloid precursor protein (APP) to form these amyloid-beta peptides which can accumulate and form neurotoxic plaques. Previous studies have found that DAPT, a dipeptide analogue, is effective in inhibiting γ secretase thus decreasing amyloid-beta concentration in the brain. This study confirms the efficacy of DAPT in inhibiting γ-secretase, but also investigates the alternative inhibitory effects of other drugs like Activase® rt-PA (alteplase), a tissue plasminogen activator typically used for treatment of stroke, and clonazepam (E64), a pill used to treat panic disorder and anxiety. Although the goal was to see the effects on Aβ40 (40 amino acid amyloid-beta chain) and Aβ42 (42 amino acid amyloid-beta chain) production, only the effects of Aβ40 production were examined due to possible contamination in the Aβ42 tests.