4^th International Conference and Exhibition on Immunology September 28-30, 2015 Houston, Texas, USA

Biography:

Michelle completed both her Bachelor and Master Science degrees in Biology and she is finishing up her PhD in the Health Sciences program. Michelle currently holds the Technical Director position responsible for clinical diagnostics, clinical trials and R & D groups at the Amerimmune Immunology Laboratory. Previously, she has worked in the pre-clinical and clinical studies of different therapeutic areas at Hoffmann La-Roche, Inc. and Merck & Co. Inc. She utilizes her expertise in different technologies as the basis not only to study the biologics and mechanisms of immune cells in different diseases but to develop assays that support major clinical decisions and impact lives. With more understanding in how immune cells function or not function in immu-nodeficiencies patients, our lab strives to contribute in this field and achieve a new milestone in medicine.

Abstract:

Primary immune deficiencies (PIDs) affect approximately 1 in 1200 persons in the United States. Despite attempts to increase awareness and detection of PID, diagnosis is delayed over 10 years in 45% of the cases. In addition, the traditional diagnosis of immune disorders is taught as a step-wise approach and there are no clear guidelines on which step comes first or how far to progress the evaluation. We hypothesized that physicians lack understanding of immune disorders, the components of an immune deficiency evaluation and its interpretation as being the three main obstacles in identifying PIDs. We designed a diagnostic method called “curbside consultation” and offered it to physicians in Northern Virginia. We then calculated the prevalence of PID before and after our intervention by surveying 328 primary care providers (PCPs) and specialists asking the number of PID patients they have diagnosed. We provided them with the 10 warning signs of immunodeficiency and offered to perform the curbside consultation in patients they suspected of having an immunodeficiency. Patients’ clinical history and pertinent findings were reported to us and a blood sample to perform the immunological assays. Laboratory results were interpreted by an immunologist based on the supporting clinical data provided. A total of 9,265 patients were involved in the study over a two-year period. Prevalence of PID was 5.3:100,000 before the curbside consultation was implemented and increased to 33:100,000 afterwards (P<0.01). The most significant change in prevalence was observed in otolaryngology, pulmonary and pediatric gastroenterology patients. The addition of a qualitative assay and immune profiling, each by itself had a statistically significant impact on identifying additional cases of PID. Furthermore, the value each one of these immune tests differed between specialties. For example, T and NK cell abnormalities are more common in pediatric cardiology patients whereas B cell abnormalities are more predominant in pulmonary, primary care, and otolaryngology referrals. Hereby, we demonstrate the need for a complete assessment of the immune system, in a quantitative and qualitative manner. There is a statistically significant impact in improving accurate diagnosis of immune disorders. We believe that our approach saves healthcare costs by reducing patient referrals, decreasing exhaustive diagnostic evaluations and interventions and likely lessening morbidity by shortening delays in diagnosis.

Biography:

Ricardo Rosales has completely a PhD from Louis Pasteur University-France and Post-doctoral studies at the NIH (National Institutes of Health)-USA. He is a Full Professor at the México University. He is the President of Virolab S de RL de CV. He has published more than 30 papers in reputed journals.

Abstract:

Vaccinia virus was developed and tested as a safe smallpox vaccine. It was also found to be avirulent for normal or immunosuppressed individuals, and not to have negative side effects in all human tested up to now. The approach of expressing a foreign protein via vaccinia virus vectors has already been used to protect animals from other virus infections. Also, it is well known that Human papilloma viruses can induce warts, condylomas, and other intraepithelial cervical lesions that can progress to cancer. Cervical cancer is a serious problem in developing countries because early detection is difficult, and thus proper early treatment is many times missing. Based on this, we evaluate the potential of the MVA E2 recombinant MVA-Virus Vaccine in Phase I, II and III clinical trials to eliminate all types of papillomavirus lesions. 89.3% female patients showed complete elimination of lesions after treatment with MVA E2. In men, all lesions were completely eliminated. All MVA E2-treated patients developed antibodies against the MVA E2 vaccine and generated a specific cytotoxic response against papilloma–transformed cells. Papillomavirus DNA was not detected after treatment in 83% of total patients treated. MVA E2 did not generate any apparent side effects. These data suggest that therapeutic vaccination with MVA E2 vaccine is an excellent candidate to stimulate the immune system and generate regression in intraepithelial lesions when applied locally.

Biography:

Tatiana Barichello concluded her Master degree in 2002 and PhD in 2007 in Biological Sciences-Biochemistry in the Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil. She received the award Brazilian Academy of Sciences/L´Oreal/UNESCO for Women in Science in 2011. At the UT Health she is Assistant Professor at the Department of Psychiatric and Behavioral Sciences and at UNESC is Professor of Post-Graduate Program in Health Sciences University of Southern Santa Catarina, Brazil. She is author of 80 research papers (H-index=17, Thompson Reuters).

Abstract:

Bacterial meningitis is a life threatening infection associated with cognitive impairment in many survivors. The pathogen invades the central nervous system (CNS) by penetrating through the luminal side of the cerebral endothelium, which is an integral part of the blood-brain barrier (BBB). The replication of bacteria within the subarachnoid space occurs concomitantly with the release of their compounds that are highly immunogenic. These compounds known as pathogen-associated molecular patterns (PAMPs) are recognized by antigen-presenting cells through the binding of Toll-like receptors, triggering an inflammatory cascade. This in turn produces cytokines and chemokines, increases adhesion molecule expression and attracts leukocytes from the blood. This cascade leads to lipid peroxidation, mitochondrial damage and blood-brain barrier permeability. In spite of effective antibacterial treatments, approximately one third of survivors suffer from long-term sequelae, such as hearing loss, cerebral palsy, seizures, hydrocephaly or cognitive impairment. Our understanding of the pathophysiology of bacterial meningitis is mostly based on observations of human cases and studies in rodent experimental models. In experimental bacterial meningitis the levels of tumour necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and cytokine-induced neutrophil chemoattractant-1 (CINC-1) were detectable in the brain in the first 24 hours post-infection. These cytokines were increased simultaneously with a decrease of enzymatic defence, an increase of oxidative stress production, and the BBB disruption. The rodents also showed long-term cognitive impairment, depressive-like, and anxiety-like behaviours however, the imipramine treatment reversed depressive-like and anxiety-like behaviours, re-established hippocampal brain-derived neurotropic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) expression, and normalized adrenocorticotropic hormone(ACTH) levels in the blood. In an attempt to minimise the long-term cognitive impairment, rodents that were subjected to bacterial meningitis were exposed to different adjuvant treatments: N-acetylcysteine and deferoxamine, inhibition of matrix metalloproteinases, complex B vitamins, erythropoietin, and tryptophan pathway inhibition. These compounds presented neuro-protective properties and prevented long-term cognitive impairment in experimental bacterial meningitis.

Biography:

Xiubo Fan has completed her PhD from Dalian University of Technology in 2008 and worked as Research Scientist in Singapore General Hospital, Singapore since then. She has published 14 papers in international peer reviewed journals and has been serving as an Editorial Board Member of Autoimmune Diseases and Therapeutic Approaches.

Abstract:

In vitro, the effect of mesenchymal stromal cell (MSC) on immune suppression has been well studied. However, in vivo, questions regarding MSC optimal therapeutic strategy, homing, survival, and timing for immune suppression are still elusive. To address these questions for systemic lupus erythematosus (SLE), autoimmune lymphoproliferative syndrome (ALPS) and Sjogren’s syndrome, a MLR/MpJ-Faslpr/J (Faslpr) mice model was employed. Multipotency of bone marrow derived MSC (BM-MSC) was determined by phenotypic analysis and multipotential differentiation assay. Four- to six-month-old Faslpr mice showed onset of autoimmune disease with lymphoproliferation. Optimal infusion dose was determined by serial dilution. Homing and survival of MSC were monitored by fluorescent microscopy. Infusion frequency was deduced from immunomodulatory kinetics study. BM-MSC with passage number less than 10 could properly maintain multi-lineage differentiation capacity and stem cell phenotypes. Eight rounds administration of 10×106 cells/kg BM-MSC improved mouse survival from 62.5% to 92.9% and reversed lymphoproliferation to normal levels at day-21 post-transplantation (PT) (p=0.189). BM-MSC mainly and eventually homed to immune organs at four months PT. Immunomodulatory kinetics showed that the optimal immunosuppression period of BM-MSC occurred from day-7 to day-21 PT in immune organs, lung, and kidney; hence, optimal infusion frequency was deduced as 21 days. In conclusion, an appropriate therapeutic strategy in a pre-clinical autoimmune disease mouse model was established with a defined MSC source as well as optimal infusion dose, frequency, and administration number. It will help to standardize cell preparation, characterization and administration protocol, and minimize the outcome discrepancies between different centers worldwide.

Biography:

Ahmad G Hegazi worked as a Professor of Microbiology & Immunology, National Research Center National Research Center, Dept. Parasitology, 1997-2000, Chair of Faculty of Medicine, Zagazig University, 1981-1997, part-time Professor and Supervisor of Immunology Section, National Research Center, 1990- up till now. He is also Prof. of Microbiology & Immunology, African Federation of Apiculture Associations (AFAA), 2001- up till now, Standing Commission on Apitherapy (APIMONDIA), 1999 - up till now, Member of Standing Scientific Committee, National Research Center, 1998 –up till now. He was awarded the Excellent Medal of the First Class, 1995, received the Senior Scientist Prize of National Research Center, 1996, and won The Second Best Research Paper award from International Congress of Propolis, Argentina, 2000. He has published in Egyptian Journal of Immunology, 1995, was in the Editorial Board of The Egyptian Association of Immunologists, 1992 –1997, Secretary General, Referee in 37 international journals patents: 4 Patents Educational Activities. He has published 193 articles in national and international scientific journals, 6 books in English and 7 books in Arabic.

Abstract:

Bee venom acupuncture (BVA) from honeybee (Apis mellifera) was potentially used as complementary modality for treatment of many diseases. The aim of this study is to evaluate the efficacy of bee venom acupuncture as alternative medicine therapy for the long term treatment of rheumatoid arthritis (RA). This study is a randomized, controlled clinical trial with two parallel arms. The study intend to compare the effects of BVA by bee sting or bee venom collected by the electric shock device and p with pharmacotherapy only in patients with RA. Forty patients with Rheumatoid arthritis disease are allocated to group of patients with RA are treated with BVA (bee sting) therapy or bee venom collected by the electric shock device at apiacupoints twice a week with convention drug therapy. While other group of patient with Rheumatoid arthritis disease on convention drug therapy. Tender joint count, swollen joint count, morning stiffness, visal analog scal (VAS), health assessment Q, ESR, CRP, Tumor Necrosis Factor (TNF), Interleukin 1(IL1) Interleukin 6,(IL6), Nuclear Factor and Kappa B (NF-KB). All these parameters will be assessed before and after treatment. The results revealed that the bee venom apiacupuncture showed significant improvement in patients received bee venom group compare to patients received pharmacotherapy only. It is concluded that both modes of treatment for RA gave improvement regarding pain intensity, disability and quality of life being more evident in bee venom group supported with improved serum TNF, IL1. IL6 and NF-KB.

Biography:

Paulo R Z Antas has completed his PhD from Fiocruz and Post-doctoral studies from Vanderbilt University Medical Center. He is the Vice-Head of Clinical Immunology Laboratory, Oswaldo Cruz Institute-Fiocruz, a public health organization in Brazil. He has published more than 30 papers in reputed journals and has been serving as an Editorial Board Member of repute.

Abstract:

The inflammatory response plays an important role during the induction of several neonatal diseases. Previous studies have shown that during newborn infections, the natural imbalance between pro- and anti-inflammatory responses shifts towards the production of pro-inflammatory cytokines. In this study, we employed an array system to detect 9 pro- and anti-inflammatory cytokines and performed ELISA for 6 other cytokines. We then compared the immune response profiling in umbilical cord blood (UV) plasma samples with circulating levels in otherwise healthy donors (HD). Concentrations of ex vivo monokine levels, such as interleukins (IL)-18, IL-23 and IL-27, were profoundly reduced in the UV in relation to the HD group (p-values of 0.003, 0.009 and <0.0001, respectively). Conversely, UV-plasmatic TGF-1 levels displayed marked enhancement (p-value=0.005) in relation to HD. Several factors may be implicated in these neonatal alterations and additional characterization of a broader cytokine panel is warranted to reveal other possible candidates.

Biography:

Praveena T is currently pursuing her PhD under the supervision of Prof. Jamie Rossjohn, Department of Biochemistry and Molecular Biology, Monash University. She has been awarded Monash Graduate Scholarship (MGS) and Faculty of Medicine International Post-graduate Scholarship (MIPS) for undertaking her Doctoral studies in Australia. Her PhD work presented in the abstract has contributed to a paper that is currently under re-review in Nature Communications journal.

Abstract:

Natural killer T cells (NKT) are an innate-like population of T lymphocytes that recognize lipid antigens presented on the major histocompatibility complex (MHC)-like molecule CD1d. Upon activation, NKT cells release an array of Th1 and Th2 cytokines that confers ability to influence immune outcomes in a broad range of diseases, including cancer, tumor immunity, autoimmunity, allergy and infection.Thus their immunomodulatory potential enables them to be of important therapeutic targets. NKT cells are widely studied in mice and humans and possess two main subsets, type I and type II. Type I NKT cells typically express an invariant α-chain (Vα14-Jα18 in mice, Vα24-Jα18 in humans) paired with a broad spectrum of β-chains (Vβ8.2, Vβ7 and Vβ2 in mice and Vβ11 in humans) and recognize α-Galactosylceramide (α-Galcer) and termed as ‘semi-invariant’ (iNKT) cells. Type II NKT cells express a diverse TCR repertoire and do not recognize α-Galcer. We have identified a new subset of NKT cells in humans that do recognize α-Galcer presented by CD1d but express different TCRs from that of Inkt cells and termed as ‘Vα24- or non-canonical TCRs’. It is important to note, the prototypical NKT cell antigen, α-Galcer is undergoing phase I/II clinical trials. In our study, we have solved the crystal structure of a non-canonical NKT TCR-CD1d/α-Galcer complex and investigated the structural and molecular basis of glycolipid recognition. Thus, our results shed light in understanding the mechanism of lipid antigen recognition and would aid in designing new immunotherapeutic agents to modulate immune responses in various clinical settings.

Biography:

Hana Zelenková has been active in Dermatovenerology since 1973. Since 2000 she has been directing her own Private Clinic of Dermatovenereology. Orientation: Psoriasis vulgaris, atopic dermatitis, mycosis, aesthetic dermatology (anti aging medicine, keloid and scar). She has given more than 650 expert lectures in Slovak Republic as well as abroad, and has 420 scientific publications. She is the Founder and President of the Slovak Society for Aesthetic and Cosmetic Dermatology President of the traditional international DERMAPARTY congress.

Abstract:

Cyclosporine A is an immunosuppressant cyclic polypeptide isolated from the Tolypocladium inflatum fungus. Indications: organ transplantations (kidney, liver, heart, lungs, pancreas, skin), bone marrow transplantations, autoimmune disorders, and selected dermatoses such as psoriasis or AD. The indication window is opening wider and wider. In most indications the recommended administration form is oral. Transplanted patients require routine monitoring of CyA levels in blood. In non-transplantation indications the monitoring of CyA levels in blood is of limited importance, only. In dermatology, Cyclosporine A is administered in three groups of indications: Group I – dermatoses treated with maximum efficacy drugs, where CyA represents an extraordinarily effective first choice drug. Group II - dermatoses with the possibility to administer an alternative systemic drug based on the therapist’s choice, however, with CyA still being the best choice. Group III - other dermatoses (with individual therapy assessment due to presumed disease development and possible relapses). The window of indications is still widening (chronic urticaria, vitiligo). The commencement of CyA therapy in line I – III requires erudition and experience. In patients with severe dermatoses CyA therapy rapidly improves the local finding and radically improves the quality of patients’ life. Cyclosporine A must be only administered according to evidence based medicine!!!

Biography:

S Catherine Alexander is an Associate Professor in Research Centre and PG Department of Zoology, Jayaraj Annapackiam College for Women (Autonomous), Periyakulam, India. She has completed her PhD in Fish Immunology from Madural Kamaraj University, India and has 23 years of teaching and research experience in immunology. She is the Principal Investigator in major research project funded by University Grants Commission, Government of India. She has published research articles in reputed journals with high impact factor and guiding PhD scholars.

Abstract:

Immunotoxicity is simply defined as the study of the interaction of xenobiotics with the immune system, a definition which incorporates the ability of chemicals both to compromise immune function and to produce specific tissue damage or allergy. The immune responses to chronic exposures to specific immunotoxicological contaminants can be monitored and correlated to disease resistance and overall health. Even very low sub lethal doses of contaminants can have profound effects upon the structure and/or function of the immune system that could be almost as harmful as direct toxic doses, when a disease outbreak occurs. Fish and their immune system may also represent an important scientific tool in the monitoring of environmental quality, particularly immunotoxic environmental pollution. Only in the last few years environmental toxicologists have started to consider effects of aquatic pollution on the immune competence of fish. The impact of contaminants and other environmental factors on the immune system of fish and shellfish is an issue of ecological and economical concern, because it may result in clinical pathology and disease, by increasing the susceptibility of affected organisms to pathogens. Hence, the present study is aimed at investigating the direct effect of sub lethal concentrations of industrial effluents in the nearby areas (tannery industry, coffee industry and electroplating industry) on the specific immune response in terms of antibody level and nonspecific immune mechanisms in terms of serum lysozyme activity, anti protease activity and myeloperoxidase activity and disease resistance against live virulent fish pathogens in selected fin fish species. The results of this study re-emphasize the importance of integration of immunological assays into environmental monitoring with reference to industrial effluents. It also demonstrates the sensitivity of immune mechanisms in relation to environmental contamination, indicating their possible use as immunological indicators.

Biography:

Sadaf Hasan completed her PhD in November 2013 from Interdisciplinary Biotechnology Unit, Aligarh Muslim University, India. She was a recipient of Doctoral Fellowship award (UGC-MANF). She worked on oral biofilms and is currently working as a Research Associate studying antibiotic resistance. She has participated in several national and international conferences. She has published her work in 5 journals of international repute viz., PLoS One, BMC Microbiology and Future Medicine. She is a member of Biochemical Society, UK and has been serving as a reviewer for some international journals.

Abstract:

Antibiotics have revolutionized medicine in many respects and their discovery was a turning point in human history. Unfortunately, the use of these wonder drugs has been accompanied by the rapid appearance of resistance. The acquisition of Extended-spectrum-β lactamases (ESBLs) and Metallo-β lactamases (MBLs) by bacteria confer resistance against the majority of available antibiotics. The outbreak of such multi drug-resistant bacteria has posed a serious concern globally, by jeopardizing the optimism of therapeutic success against future infectious diseases. Monotherapy has been a choice to treat invasive infections since ages. Neverthe¬less, combination therapy has proved to be a promising substitute over monotherapy for infections that do not respond to standard treatments, such as infections occurring by MDR species. Infact, combination therapy is persistently recommended as empirical treatment for bacterial infections in intensive care units, where mono¬therapy fails to combat infections. Hence, we have conducted a study to explore the potential synergistic combinations of different antibiotics against extended-spectrum β-lactamase and metallo β-lactamase producers. The MICs were determined against 12 strains, harboring different resistant markers (blaNDM, blaCTX-M, blaTEM, blaSHV, blaOXA and armA), followed by in vitro synergy testing using microdilution, chequerboard and time-kill assays against different antibiotics. Results suggested that, of all the tested combinations, cefoxitin gave highest rate of synergy when paired with streptomycin and cefotaxime, thus forming effective synergistic combination against multidrug-resistant bacteria. Interestingly, the combination of cefotaxime/cefoxitin showed synergistic activity even against the atrocious NDM-1 producing strains. Therefore, this novel synergistic combination can be used against different resistant strains, including NDM-1 producers.

Biography:

Postdoctoral Research at Mayo Clinic, Rochester, USA (2014-2015), University of Illinois at Chicago, USA (2010-2014), Indian Institute of Toxicology Research, Lucknow, India (2009-2010). His research interests focus on the role of macrophages in the initiation, progression and resolution of inflammatory processes. The long term research interest is to elucidate the inflammatory signaling in macrophages during chronic and acute inflammation. Macrophage recruitment and plasticity are key components of several inflammatory diseases including asthma, fibrosis/cirrhosis, rheumatoid arthritis and atherosclerosis. Understanding the mechanisms that regulate macrophage phenotypic plasticity in tissues is critical for the identification and validation of markers and therapeutic targets in inflammatory diseases.
Awards 2010: Ramanujan Fellowship Award
2014: Ramalinga Swami Fellowship Award
2013: Mirus Research Award, Mirus Bio LLC, USA
2009: Research Bursary Award, UK
2008: FEBS Pre Doctoral Award , Greece
e Cheminfo Award, USA
2007: EMBL International Ph.D Fellow Award
2007: Research Travel Grant Award, USA

Abstract:

Nitric oxide synthases are a family of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. NO is an important cellular signaling molecule, having essential roles in many biological processes including the control of blood pressure, regulation of neuronal activity and immune responses. NOS3 (endothelial NOS or e NOS) and NOS2 (inducible NOS or I NOS) have been appreciated as mediators of inflammatory processes. However, considerably less is known about the role of NOS1 (neuronal NOS or n NOS) in inflammation. We have uncovered an important role for this enzyme in regulating TLR4 signaling. We demonstrate that in contrast to the enhanced susceptibility of NOS2-/- and NOS3-/- mice to LPS, NOS1-/- mice are, in fact, more resistant to LPS-induced lethality and tissue injury. We demonstrate that the loss of NOS1 attenuates TLR4-stimulated cytokine production and NF-κB activity in vivo and in vitro. Macrophages from NOS1-/- animals demonstrate an LPS-induced decrease in protein levels of the p65 subunit of NF-κB. This decrease in p65 protein correlates with an increase in protein levels of suppressor of cytokine signaling-1 (SOCS1) and increased physical association between SOCS1 and p65. On studying the mechanism of NOS1-regulation of inflammation we found that an early pulse of NOS1-derived NO was required to stabilize p65 in the nucleus of macrophages via the inhibitory S-nitrosation of suppressor of Cytokine Signaling-1 (SOCS1). NOS1-derived NO through nitrosation of Cys147 and Cys179 on SOCS1 permits p65-mediated pro-inflammatory gene transcription and is essential for the mechanism of inflammation. Taken together, our results demonstrate that NOS1 is a fundamental early regulator of gene transcription of the inflammatory response thereby heavily impacting the course, type and duration of the inflammatory process.

Biography:

Mehmet Sen has completed his PhD from theUniversity of Houston, Department of Biology and Biochemistry with Glen Legge, M.D., Ph.D., and postdoctoral studies from Harvard Medical School, Department of Biological Chemistry and Molecular Pharmacology with Timothy Alan Springer, Ph.D.He is currently establishing his lab at the University of Houston. His research interests lie in the structural and functional basis of receptor/ligand interactions, which are relevant to human health and disease.

Abstract:

The 2 integrins, which are expressed only on leukocytes, must be activated rapidly to restrict integrin-dependent firm adhesion and emigration of leukocytes from the bloodstream only to sites where cues for inflammation or homing are locally displayed. All 2 integrin subunits contain I domains that bind ligand. Here, we describe two 2 integrin structures: a cocked, metastable state of the leukocyte integrin X2 ectodomain that primes it for rapid conformational change, and reveals how allostery is relayed to activate the I domain, and a closed state of the leukocyte integrin L2 headpiece. The X2 crystal structure reveals the X2 ectodomainin a bent conformation; however, its ligand-binding XI domain is in a high affinity, open conformation. Compared to the closed conformation, much of the I 7-helix unwinds, loses contact with the I domain, and reshapes to form an internal ligand that binds to a hydrophobic and metal ion-containing pocket at the interface with the X -propeller and 2I domains. An analogous pocket binds external ligand in integrins that lack I domains. In comparison of the the2 subunits of the cocked X2 and the closed L2 structures, I domain undergoes unexpected conformational change which reveals ratchet-like changes in positions of conserved hydrophobic residues located in the both N- and C-terminals of the 1-helix, despite absence of change in the neighboring I domain 7-helix, which pistons in integrin headpiece opening. Mutations of these residues demonstrate a key role for ratchet residues in stabilizing active and inactive 2 integrin states Comparisons to other integrins suggest that the cocked state is a specialization of the 2 integrin subunit. My two structures together with mutational analysis demonstrate the metastability of the cocked state, and suggest that it potentially catalyze rapid equilibrium between bent-closed, extended-closed, and extended-open states for rapid upregulation of leukocyte adhesiveness in 2 integrins.

Biography:

Rundk Ahmed Hwaiz is PhD student at Lund University. She was a Lecturer at Hawler Medical University at Erbil/ Kurdistan, Iraq. She has 10 published papers. She will defend her thesis in April 2015.

Abstract:

Accumulating evidence suggest that platelets play an important role in regulating neutrophil recruitment in septic lung injury. Herein, we hypothesized that platelet-derived CCL5 might facilitate sepsis-induced neutrophil accumulation in the lung. Abdominal sepsis was induced by cecal ligation and puncture (CLP) in C57/BL6 mice. CLP increased plasma levels of CCL5. Platelet depletion and treatment with the Rac1 inhibitor NSC23766 markedly reduced CCL5 in the plasma of septic mice. Moreover, Rac1 inhibition completely inhibited proteinase-activated receptor4-induced secretion of CCL5 in isolated platelets. Immunoneutralization of CCL5 decreased CLP-induced neutrophil infiltration, edema formation and tissue injury in the lung. However, inhibition of CCL5 function had no effect on CLP-induced expression of Mac-1 on neutrophils. Blocking CCL5 decreased plasma and lung levels of CXCL1 and CXCL2 in septic animals. CCL5 had no effect on neutrophil chemotaxis in vitro, suggesting an indirect effect of CCL5 on neutrophil recruitment. Intratracheal challenge with CCL5 increased accumulation of neutrophils and formation of CXCL2 in the lung. Administration of the CXCR2 antagonist SB225002 abolished CCL5-induced pulmonary recruitment of neutrophils. Isolated alveolar macrophages expressed significant levels of the CCL5 receptors CCR1 and CCR5. In addition, CCL5 triggered significant secretion of CXCL2 from isolated alveolar macrophages. Notably, intratracheal administration of clodronate not only depleted mice of alveolar macrophages but also abolished CCL5-induced formation of CXCL2 in the lung. Taken together, our findings suggest that Rac1 regulates platelet secretion of CCL5 and that CCL5 is a potent inducer of neutrophil recruitment in septic lung injury via formation of CXCL2 in alveolar macrophages.

Biography:

Mohammed Yousif Merza is a PhD student and permanent staff at Hawler Medical University, Kurdistan. He has graduated from Salahadin University, Hawler in 2003 and completed a Master’s degree at Glasgow University, UK in 2008. He has published 5 papers in reputed journals.

Abstract:

Leukocyte infiltration and acinar cell necrosis are hallmarks of severe acute pancreatitis (AP) but the signaling pathways regulating inflammation and organ injury in the pancreas remain elusive. In the present study, we investigated the role of CXCL4 in AP. Male C57BL/6 mice were treated with an anti CXCL4 antibody (20 µ/kg) prior to induction of pancreatitis by infusion of taurocholate into the pancreatic duct. Pretreatment with anti CXCL4 Ab reduced blood amylase levels, pancreatic neutrophil recruitment and hemorrhage and edema formation in taurocholate-evoked pancreatitis. Moreover, administration of anti CXCL4 Ab decreased the taurocholate-induced increase of myeloperoxidase activity in the pancreas and lung. Treatment with anti CXCL4 Ab markedly reduced levels of CXCL2 in the pancreas and IL-6 in the plasma in response to taurocholate challenge. Notably, inhibition of CXCL4 had no direct effect on secretagogue-induced activation of trypsinogen in pancreatic acinar cells in vitro. A significant role of CXCL4 was confirmed in an alternate model of AP induced by L-arginine challenge. Our findings show that CXCL4 regulates neutrophil accumulation and tissue damage via CXCL2 formation in AP. Thus, these results reveal new signaling mechanisms in pancreatitis and indicate that targeting CXCL4 might be an effective way to ameliorate severe AP.

Biography:

Abdel-Azeem M El-Mazary has completed his MBBCH and MD degree a from Minia University, Egypt. He did Post-doctoral workshops and training courses in Pediatrics in both Cairo and Mansoura Universities, Egypt. He is the Director of Neonatology Unit Clinic of Minia University Hospital. He is working as Associate Professor in Pediatrics, Pediatric Department, Minia University. He has published more than 16 papers in reputed journals and has been serving as an Editorial Board Member of (Science Research Journal) and as a Reviewer in (European Journal of Clinical Nutrition).

Abstract:

Background: Fever is one of the most frequently encountered pediatric problems, accounting for 25% of visits to pediatric emergency room. The vast majority of young children with fever have an infectious etiology, like cold, upper respiratory tract infections (ear infection, croup, bronchiolitis and pneumonia), gastroenteritis, UTI and other infections, but there are also other important causes of fever in children under five years as immunization reaction, collagen vascular disease, chronic inflammatory disease, metabolic disease, transfusion reaction, drug fever, or poisoning. The cause of fever in young children can be a diagnostic challenge because it is often difficult to identify the exact cause as in most cases the acute illness is due to self - limiting viral infection however; fever may also be the presenting feature of serious bacterial infections such as meningitis or severe pneumonia. Objective: This study aimed to compare between two different approaches; the standardized approach of IMCI (Integrated Management of Childhood Illness) versus the traditional approach in management of fever in children less than five years old. Methods: This is a prospective study carried out on 50 children less than five years old represented with fever attended the outpatient clinic of Minia University Hospital for children during the period from September 2012 to January 2014. These 50 children were divided into 2 main groups: Group 1: Included 25 children subjected to standardized (IMCI) approach of management which designed with limited diagnostic tools, limited medications and opportunities to practice complicated clinical procedures to reach a classification rather than diagnosis, and group II: Included 25 children subjected to traditional approach of management which designed to use serial investigations and procedures with many medications to reach to a specific cause or diagnosis. Results: Most of children in standardized approach (64%) were diagnosed at 1st day, while most of children in traditional approach were diagnosed at 4th (34%) or 5th day (20%), these differences were statistically significant, and 60% of children treated with the standard approach was improved compared to only 12% of children treated with traditional approach, 40% of treated with traditional approach had worse outcome compared to 16% of treated with the standard approach and these differences were statistically significant. Conclusions: This study showed that the standardized approach of IMCI designed to reach a classification and/or a diagnosis earlier with much better outcome than the traditional approach in majority of cases which is better for practical applications especially in developing countries.

Biography:

Yongxin zhang is currently doing his research work at Zyxell Inc., headquartered in Carrollton, Texas, USA. It is a cell science- and technology-based company.

Abstract:

Antigen-specific T immunocyte in vitro expansion provides effective cells in cancer therapy, but a successful expansion partially depends on the activity of the harvested cells. Ideally, the cells should be harvested at the point of maximum function. However, the activities of most, if not all, immunocytes decline when the cells are cultured in vitro. Therefore, the determination of the peak time point is critical for the efficient expansion of effective antigen-specific T immunocytes. Our previous studies demonstrated that hematopoietic stem cells reduce their engraftment potency during ex vivo expansion due to non-specific differentiation and has a optimal harvest time point for their highest engraftment potency during the expansion. Similar to hematopoietic stem cells, lymphocytes also cannot keep the activity at their highest level following in vitro culture. Antigen-specific cytotoxic T lymphocyte (asCTL) is a typical example, in which the total cytotoxicity increases for a certain period as cell number increases at the early expansion stage, but decreases at late stage because individual cell-based killing function always gradually declines and drops very fast at the late stage. In this study, CMV asCTLs and cancer cell-induced asCTLs were expanded in ZYX bioreactor, the correlation between cell number and their total antigen-specific cytotoxicity was established, and the peak time point of total antigen-specific cytotoxicity was determined. From this data, a computer program was used to predict the peak time point of total antigen-specific cytotoxicity by real-time monitoring the cell number changing in the CTL expansion. The results showed that our system could determine the optimal time point for the asCTL harvest without needing a series of CTL assays.

Biography:

Hadeel Faisal Gad has graduated from faculty of Veterinary Medicine, University of Khartoum in 2002 and earned her PhD degree in Immunology in 2013 from Institute of Endemic Diseases, studying the cellular immunology of Pulmonary Tuberculosis and Visceral Leishmaniasis co-infection. She investigates the role of gene mutations as a susceptibility to the two diseases co-infection. She worked as a part time Lecturer and Researcher at King Saud University.

Abstract:

Background: Leishmaniasis-tuberculosis co-infection has been reported many times mainly in the east region of Africa, but little is known about the immunological interactions of the co-infection. A case control study was carried out to analyze in-vitro cytokines responses in visceral leishmaniasis (VL) patients and pulmonary tuberculosis (TB) patients. Method: The cytokine profiles of 30 leishmaniasis patients, 30 tuberculosis patients and 10 healthy individuals were compared after stimulation with live Leishmania Promastigotes and BCG. Th-1 (IFN-γ and TNF-α), Th-2 (IL-10) and inflammatory cytokine IL-15 were measured in the supernatants of stimulated whole blood samples whole blood using ELISA. Results: The concentration of Th-1 cytokines (IFN-γ and TNF-α) were significantly higher in the supernatants of stimulated whole blood of VL patients compared with TB patients mainly when stimulated by L.donovani antigen. Th-2 cytokine IL-10 was significantly produced by whole blood of TB patients particularly stimulated with BCG. A significant concentration was detected in stimulated whole blood of VL and TB patients compared by healthy controls. Conclusion: The Th-1 cytokines expressions to the homologous antigen stimulation in visceral leishmaniasis patients were higher compared to the non-stimulated which suggests a strong adaptive response. Meanwhile, the Th-2 cytokine IL-10 expression to the homologous antigen stimulation in TB patients was higher than the non-stimulated which led to strong suppression the protective Th-1 cytokines expression. This finding suggests that a re-occurring TB infection may generate a weak protective immune response which could lead to a more persistent infection.

Biography:

Christian Pasquali has completed his Master and PhD between the Vienna IMP Institute and Compiegne University respectively. He was Director of Operational Research and Technology Transfer at xigen Pharmaceutical and is now Directing the unit of Preclinical Research at vifor Pharma, Geneva. He has published more than 35 papers in peer reviewed journals and has been serving as an chairs and speakers in various scientific congress.

Abstract:

Secondary bacterial infections following influenza infection are a pressing problem facing respiratory medicine. Although antibiotic treatment has been highly successful over recent decades, fatalities due to secondary bacterial infections remain one of the leading causes of death associated with influenza.We have assessed whether administration of a bacter-ial extract alone is sufficient to potentiate immune responses and protect against primary infection with influenza, and secondary infections with either Streptococcus pneumoniae or Klebsiella pneumoniae in mice.We show that oral administration with the bacterial extract, OM-85 (Broncho Vaxom), leads to a maturation of dendritic cells and B-cells characterized by increases in MHC II, CD86, and CD40, and a reduction in ICOSL. Improved immune responsiveness against influenza virus reduced the threshold of susceptibility to secondary bacterial infec-tions, and thus protected the mice.The protectionwas associated with enhanced polyclonal B-cell activation and release of antibodies thatwere effective at neutralizing the virus. Taken together, these data show that oral administration of bacterial extracts provides sufficient mucosal immune stimulation. Further to these findings and to potentiate the various mechanistic means by which OM-85 can modulate the host immune response, a general overview on other recent findings including other therapeutic indication such as asthma will be discussed.

Biography:

I am a post-doctoral researcher working in the laboratory of Dr. Richard Simpson at the University of Houston. I joined Dr. Simpson’s lab in 2009 and was funded his first two years as a teaching fellow and the last three years as a research assistant working on NASA grant NNX12AB48G. I am interested in cancer immunotherapy using NK-cells, especially how exercise and Cytomegalovirus (CMV) infection modulate NK-cell activity against hematologic malignancies. My goal is to understand the mechanisms underlying the effects of exercise and CMV infection on the phenotype, cytotoxicity, proliferative capacity, and persistence of NK-cells with an eye toward developing adjuvants for allogeneic adoptive transfer of NK-cells. My research thus far has been funded by a NASA grant awarded to Dr. Richard Simpson and he will continue to have access to these resources if awarded this fellowship. Through this collaboration with NASA, I have acquired expertise in cell culture techniques, cytotoxicity assays, and flow cytometry methods that have led to multiple publications in prestigious peer-reviewed journals.

Abstract:

We showed previously that acute exercise is associated with a preferential redeployment of highly-differentiated NK-cells and increased cytotoxicity against HLA-expressing tumor cell lines during exercise recovery. In this part II study, we retrospectively analyzed these findings in the context of latent cytomegalovirus (CMV) infection and performed additional experiments to explore potential mechanisms underpinning the marked reduction in NK-cell redeployment with exercise in CMV-seropositive individuals. We show here that latent CMV infection impairs NK-cell mobilization with exercise, only when the intensity of the exercise bout exceeds the individual blood lactate threshold (BLT). This impaired mobilization is associated with increased proportions of poorly exercise-responsive NK-cell subsets (NKG2C+/KIR-, NKG2C+/NKG2A-, and NKG2C+/CD57+) and decreased NK-cell β2-adrenergic receptor (AR) expression in those with CMV. As a result, NK-cell production of cyclic AMP (cAMP) in response to in vitro isoproterenol (synthetic β-agonist) stimulation was drastically lower in those with CMV (6.0 vs. 20.3 pmol/mL, p<0.001) and correlated highly with the proportion of NKG2C+/CD57+ NK-cells (R2 = 0.97). Moreover, NK-cell cytotoxic activity (NKCA) against the K562 (36.6% vs. 22.7%, p<0.05), U266 (23.6% vs. 15.9%, p<0.05), and 221.AEH (41.3% vs. 13.3%, p<0.001) cell lines was increased at baseline in those infected with CMV; however, latent CMV infection abated the post-exercise increase in NKCA as a result of decreased NK-cell mobilization. Additionally, NKCA per cell against the U266 (0.24 vs. 0.12, p<0.01), RPMI-8226 (0.17 vs. 0.11, p<0.05), and 221.AEH (0.18 vs. 0.11, p<0.05) cell lines was increased 1h post-exercise (relative to baseline) in CMV-seronegative subjects, but not in those infected with CMV. Collectively, these data indicate that CMV may compromise NK-cell mediated immunosurveillance after acute exercise due to an increased proportion of “CMV-specific” NK-cell subsets with impaired β-adrenergic receptor signaling pathways.

Biography:

Abstract:

Heavy metals like arsenic and lead are toxic to humans and animals. Arsenic is carcinogenic and plays its role through drinking water and by entering the food chain via the water bodies. There are numerous reports of the toxic effects of arsenic and with time, research on arsenic has only gained impetus. In this study we tried to address the immunotoxicological effects of arsenic contamination and subsequent effect of its oxidative stress-induced dysfunction of both the critical defences viz. the antioxidant mechanisms as well as innate immunity in the fish Channa punctatus Bloch. Fish were treated with sub-lethal doses of sodium arsenite solution (0.24 mg/L) for 4 days and when analysed for its effect on the intestinal macrophages, it was observed that it altered the bacterial phagocytosis and the intracellular killing activity which correlated with the decrease in the release of the antimicrobials viz, nitric oxide and myeloperoxidase and the inflammatory cytokines, thus rendering the fish prone to infections. Severe damages in terms of disarrangement and fragmentation of the mucosal epithelial lining of the intestine, as observed by transmission electron microscopy emphasizes on arsenic-induced oxidative stress. While the decrease in pro-inflammatory cytokines suggests the involvement of MAPK and NFκ pathways in the portrayal of immune dysfunction, loss of antioxidant homeostasis could be a result of direct inhibition of enzymes by arsenic. We therefore, conclude that arsenic affects the fish C. punctatus Bloch. by suppressing its immune system and antioxidant defences due to an increase of the oxidative stress, making it more susceptible to microbial attack.

Biography:

Haleh Talaie has completed her MD at the age of 28 years from Shahid Beheshti University of Medical Sciences and Research fellow, Division of Clinical Pharmacology & Toxicology, University of Toronto, Canada (2004). she is the director of Iranian Healing Oriented Integrative Medicine Institute.she has published more than 30 papers in reputed journals. Spring/Autumn 2014 : Accepted as postdoctoral integrative medicine fellowship in Arizona Center for Integrative Medicine University of Arizona ,USA(financial support not yet approved) March 2011- up to present: Integrative Medicine self education in Toxicological Research Center (TRC) and in Taleghani General Hospital,SBMU. April 2009 – Feb 2011: Integrative Medicine Courses in Clinical Excellence Center of SBMU. Oct. 2005- Nov 2005: Participation in Toxicology Rounds of Toronto, Canada poison center and Clinical pharmacology and toxicology of HSC of university of Toronto. Oct. 2003- May 2004: Research fellow, Division of Clinical Pharmacology & Toxicology by supervision of Dr Gideon Koren, M.D., A.B.M.T., F.R.C.P.C The Hospital for Sick Children, University of Toronto, Canada March 1997- 2003: Trainer & coordinator of Medical Education, Shahid Beheshti University (formerly Melli University) Medical Sciences & Health Services (SBUM), Tehran, Iran 1994 -1997: Board of Infectious Diseases specialty (SBUM) 1995-1997: Master in Public Health, Tehran University of Medical Sciences, Tehran, Iran 1987-1994: Training in Emergency ward & Outpatient clinic, Gillan Medical university,Iran 1978-1987: Shahid Beheshti University of Medical Sciences, (SBUM), Tehran, Iran

Abstract:

Background: Ventilator-associated pneumonia (VAP) is the main cause of acquired infections in ICUs. Every year, millions of people suffer from poisoning by various substances. Our aim was to determine the association between VAP incidence and different kinds of toxicity among Toxicological ICU (TICU) patients. Materials and Methods: Poisoned patients with diagnosis of VAP were enrolled to our retrospective study at TICU of Loghman Hakim Hospital. Data was collected through the medical records. The statistical analysis was performed with SPSS (version 16, Chicago, IL, USA). Results: Among 675 patients with MV > 48 h, 150 patients had the diagnosis of VAP. Mean age was 36.6 years. 74.7% were males. Intentional poisoning was 70.3%. The incidence of VAP was 22%. The higher incidence of VAP was recorded in anti depressants and opioid toxicities. The majority of bacterial isolates (81.3%) were multi drug resistance. MRSA accounted for 50.7% of VAP cases. Non survivors' hospital length of stay (mean = 18.7days) was significantly higher than survivors (12.8). The hospital length of stay in VAP patients was highest in the Acinetobacter spp (mean > 20 days). Mortality rate of VAP cases was 18.6%. Conclusion: No specific association was detected between incidence of VAP and different kinds of toxicity, while Anti Depressants and opioids had high VAP incidence, in a Quarter of this population. It is noticeable that pesticide had the lowest incidence for its short hospitalization. In our TICU, MRSA and Acinetobacter spp were the main agents leading to VAP and prolonged ICU stay, respectively.

Biography:

Abstract:

Hermansky-Pudlak Syndrome (HPS) comprises a group of inherited disorders caused by mutations that alter the function of lysosome-related organelles. Pulmonary fibrosis is the major cause of morbidity and mortality in BLOC-3 mutant HPS-1 and HPS-4 patients. Chitinase 3-like-1 (CHI3L1), a prototypic chitinase-like protein, plays a protective role by ameliorating cell death and stimulating fibroproliferative repair. Here we demonstrate that circulating CHI3L1 levels are higher in HPS patients with pulmonary fibrosis compared to those that remain fibrosis-free, and that these levels associate with disease severity. Using murine models we also demonstrate that a defect in CHI3L1 inhibition of epithelial apoptosis and exaggerated CHI3L1-driven fibroproliferation play important roles in HPS fibrosis. Lastly we demonstrate that these divergent responses are mediated by differences in the trafficking and effector functions of two CHI3L1 receptors. Specifically, the enhanced sensitivity to apoptosis is due to the BLOC-3 dependent, and thus abnormal, trafficking of IL-13Ra2. In contrast, the fibrosis is due to interactions of CHI3L1 and CRTH2, which traffics normally in BLOC-3 HPS.

Biography:

Abstract:

Introduction: A better understanding of the impacts of malaria control interventions on Anopheles mosquito vector and Plasmodium falciparum parasite populations, acquired immunity, and burden of the disease, is needed to guide malaria elimination strategies. Therefore the impacts of implemented strategies need to be monitored overtime to anticipate the consequences of changing malaria epidemiology. To gain insights on the impact of malaria control interventions on anti-malarial antibodies responses, we closely investigated the dynamics of IgG antibodies responses to P. falciparum antigens in relation to decrease malaria transmission resulting from successful control interventions in a West African setting. Methods: A total of 1235 sera obtained in 2000 (n=218), 2002 (n=186), 2008 (n=269), 2010 (n=288) and 2012 (n=274) from inhabitants of Dielmo (Senegal) aged 3.4 to 90.9 years old were tested by ELISA to investigate the prevalence and magnitude of antibody responses to crude schizont extracts obtained from a locally adapted P. falciparum strain (Pf0703). The threshold for positivity was defined as an OD ratio >2. Statistical analyses were performed using R software and threshold of significance was set at 0.05 Results: The prevalence of anti-sch0703 antibodies progressively decreased from 97.25% in 2000 to 57.3% in 2012. When categorized between various age groups, the seroprevalence increased significantly (P<0.5) with age from 47.19% in children <7 years old to 89.45% in >=15 years old. The seroprevalence within age groups through the different periods significantly dropped after the implementation of insecticides nets in 2008. Similarly, the magnitude of IgG antibody responses in positive responders decreased progressively from 2000 to 2012 despite limited variation in the different age groups. Mean levels of IgG antibodies fluctuated from 2002 to 2012 indicating a moderate to no relationship between the magnitude of IgG antibodies responses and malaria interventions. Discussion and conclusion: While the data suggest that all implemented control strategies (rapid diagnostic test, ACT treatment and LLINs use) contributed to the decrease of immune responses to P. falciparum antigens, the role of LLINS was the most pronounced as revealed by the significant decline in seroprevalence and magnitude of antibodies responses observed after 2008. Implementation of LLINS was reported associated with a substantial reduction of Anopheles mosquitos and a decreased of the entomological inoculation rates to its lowest value in 2012 when parasite carriage almost disappeared in Dielmo villagers. The rapid decrease of protective immunity allows new infections to be rapidly detected and treated, but also favors the re-establishment of human-vector contacts contributed in boosting immune responses to P. falciparum malaria antigens.

Biography:

Hana Zelenková has been active in Dermatovenerology since 1973. Since 2000 she has been directing her own Private Clinic of Dermatovenereology. Orientation: Psoriasis vulgaris, atopic dermatitis, mycosis, aesthetic dermatology (anti aging medicine, keloid and scar). She has given more than 650 expert lectures in Slovak Republic as well as abroad, and has 420 scientific publications. She is the Founder and President of the Slovak Society for Aesthetic and Cosmetic Dermatology President of the traditional international DERMAPARTY congress.

Abstract:

Cyclosporine A is an immunosuppressant cyclic polypeptide isolated from the Tolypocladium inflatum fungus. Indications: organ transplantations (kidney, liver, heart, lungs, pancreas, skin), bone marrow transplantations, autoimmune disorders, and selected dermatoses such as psoriasis or AD. The indication window is opening wider and wider. In most indications the recommended administration form is oral. Transplanted patients require routine monitoring of CyA levels in blood. In non-transplantation indications the monitoring of CyA levels in blood is of limited importance, only. In dermatology, Cyclosporine A is administered in three groups of indications: Group I – dermatoses treated with maximum efficacy drugs, where CyA represents an extraordinarily effective first choice drug. Group II - dermatoses with the possibility to administer an alternative systemic drug based on the therapist’s choice, however, with CyA still being the best choice. Group III - other dermatoses (with individual therapy assessment due to presumed disease development and possible relapses). The window of indications is still widening (chronic urticaria, vitiligo). The commencement of CyA therapy in line I – III requires erudition and experience. In patients with severe dermatoses CyA therapy rapidly improves the local finding and radically improves the quality of patients’ life. Cyclosporine A must be only administered according to evidence based medicine!!!

Biography:

Arnie Berk is a virologist and cell biologist in the Molecular Biology Institute and Department of Microbiology, Immunology and Molecular Genetics at UCLA. As a postdoctoral fellow, his analysis of adenovirus mRNA synthesis led to the initial discovery of RNA processing of spliced mRNAs from pre-mRNA precursors containing introns, and his analysis of early SV40 mRNA lead to the initial discovery of alternatively spliced mRNA isoforms encoding distinct, but related proteins. At UCLA his research has focused on the mechanisms of transcriptional activation and control of the cell cycle by the adenovirus E1A and E1B proteins. Work from his laboratory demonstrated that the tumor suppressor activity of p53 depends on its activity as a transcriptional activator. His laboratory discovered that activation of transcription by the adenovirus large E1A protein results from its interaction with the human mediator of transcription complex, and that this promotes assembly of pre-initiation complexes on promoter DNA and stimulation of elongation by promoter proximal paused RNA polymerase II. The small E1A protein was shown to regulate host cell transcription and cell cycle progression through modifications of chromatin structure. He is a Fellow of the American Academy of Arts and Sciences and holds the UCLA Presidential Chair in Molecular Cell Biology.

Abstract:

To analyze control of host cell gene expression by adenovirus small E1A protein, we performed experiments with structure-based e1a mutants completely defective for binding to either p300/CBP or RB-family proteins. RNA-seq and ChIP-seq for e1a, RB1, RBL1 (p107), RBL2 (p130), p300, pol2, H3K9ac, H3K18ac, H3K27ac and H3K4me1 revealed that p300/CBP acetylation of RB1 K873/K874 (1) in a trimeric p300/CBP-e1a-RB complex (2) inhibits RB phosphorylation by cyclin/CDKs, thereby locking RB1 in a repressing conformation (1,3) that interacts with repressive chromatin modifying enzymes (3). e1a then delivers these repressing p300/CBP-e1a-RB complexes to host cell genes that have unusually high p300 association within the gene body and are highly enriched for cytokine signaling pathway genes, repressing their transcription. The p300/CBP-e1a-RB complex condenses chromatin as assayed by confocal microscopy of an amplified lacO array (4). e1a-induced chromatin condensation requires simultaneous binding of e1a to an RB and p300/CBP, e1a-binding to the chromatin remodeler p400 (5), HDAC activity, p300 KAT activity, the p300 bromo-ring-PHD domain (6), and acetylation of RB1 K873/K874 (2) and e1a K239 (7). Our data suggests a model for how the p300/CBP-e1a-RB complex spreads over repressed genes. 1. Chan HM doi:10.1038/ 35083062 2. Wang HG PMID 8416379 3. Dick FA, Rubin SM doi:10.1038/nrm3567 4. Verschure PJ doi: 10.1128 /MCB.25.11.4552-4564 5. Fuchs M doi:10.1016/S0092-8674(01) 00450-0 6. Delvecchio M doi:10.1038/nsmb.2642 7. Zhang Q doi: 10.1073/pnas.011283598

Biography:

Rongtuan Lin is an Associate Professor in the Department of Medicine, McGill University and a Senior Investigator at the Lady Davis Institute for Medical Research. Dr. Lin received his Ph.D. degree from Concordia University and he completed Post-doctoral training at the Lady Davis Institute for Medical Research. He have published more than 120peer-reviewedpapers,which have been cited for more than 10,000 times. He made important contributions in the fields ofinnate antiviral immunity.

Abstract:

The innate immune response to virus infection plays a critical role in limiting virus multiplication and pathogenesis. Central to the innate antiviral response is the rapid induction of type I interferon (IFN) expression; IFN gene expression is tightly regulated by the recognition of extra- and intra-cellular signals, generated during primary infection.The viral genome or viral replicative intermediates containing 5’triphosphate (5’ppp) RNA binds to RIG-I and ultimately leads to the production of pro-inflammatory cytokines and anti-viral factors, as well as type I interferons (IFNs) that amplifies the antiviral immune response.Given that viral RNA-RIG-I interaction is the initial trigger of the innate and adaptive immune response, an attractive strategy for the development of an efficient and broad spectrumantiviral therapy to inhibit virus infection involves the use of RIG-I agonist that mimic viral RNA to activate the host defense. Our previous study demonstrated that treatment of various cell lines and primary cells with 5’pppRNA in vitro led to protection against infection and replication of a broad range of RNA and DNA viruses. In vivo, intravenous administration of 5’pppRNA protected mice from a challenge with H1N1 and H5N1 Influenza virus. Our recent study shown that5’pppRNA has the ability to counteract Ebola virus infectivity in vitro. We identified STING among a plethora of differentially expressed genes induced by the RIG-I agonist 5’ppp RNA. STING has been identified as an RIG-I signaling cofactor and a critical adaptor protein required for cytosolic DNA and cyclic dinucleotides (CDNs) triggered immune responses.We further detailthe mechanism of STING regulation.Furthermore, our results also unveiled an essential contribution of STING in the establishment of the 5’pppRNA induced antiviral responses during HSV1 infection.Taken together, these observations demonstrate that the STING is induced via RIG-I signaling and up-regulated STING is essential for 5’ppp RNA mediated HSV restriction.

Biography:

Kimihiko Okazaki graduated from Kyoto University, Faculty of Medicine in 1959. He was then engaged in medical chemical research till 1981 and started working as an internist as of July 16, 1981. His main achievements are discoveries of (1) A novel coenzyme in Baker’s yeast, (2) Initiator of rat liver regeneration, and (3) A radical cure method of immune diseases.

Abstract:

It has long been taken for granted that all of antibody molecules rigidly combine with their receptors. On the other hand, it is well established that an equilibrium state exists among antibody molecules in the vicinity of their receptors. These two concepts obviously disagree with each other. Namely, either one of these two concepts ought to be wrong. However, the concept of existence of equilibrium can't be wrong since it has been established more recently than the other one, which used to be believed presumptively. Apparently, contemporary immunologists should be aware of the contradiction. Unfortunately, they don't seem to be so. It seems to me that authoritative immunologists, at least, are aware of it because they must not be stupid enough not to be aware of the contradiction. I'm afraid that they are just too egocentric to admit the irrelevancy. For them, it is more important to keep their research problems unfinished than to heal autoimmune diseases. In my opinion, purpose of medical research is to save sick people applying the best treatment for their diseases. Applying the relevant concept, the pathogenic antibodies can easily be replaced from the responsible cells, i.e., cytolytic T lymphocytes, by accumulating non- pathogenic antibodies in the body of the patient. The latter can be accomplished by repeating intradermal injections with non-specific antigens. I do have numerous cases of successful healing of autoimmune and allergic diseases. I have no case of failure. In conclusion, it is about time for authoritative contemporary immunologists to admit my idea.

Biography:

Abstract:

This work has been presented in several national and international ENT meetings and has been awarded "Prof. Dr. Juan Carlos Arauz " First Prize for "A new technique for treating recurrent respiratory papillomatosis using chromoendoscopy associated with Endoscopic Laryngotracheal Surgery (ELS)" research paper. It was granted by the Argentine Society of Otolaryngology and Children Phonoaudiology at the IX Argentinian Congress of Pediatric Otolaryngology and Children Phonoaudiology during the III IAPO Regional Meeting, Córdoba, May 24, 2007

Introduction
Chromoendoscopy is an endoscopic technique which uses acontrast stain to paint the aerodigestive tractmucosal liningfollowed by an optical assessment to highlightingany epithelial abnormalities. Detailed and high-definition magnified views achieved with the aid of rigid endoscopes can often allow for identification of the tissue type or pathology based upon the pattern uncovered.According to the literature we reviewed, we may have been the first ones to use indigo carminein the field of otolaryngology.Tiny lesionsthat usually go overlooked with conventional microlaryngoscopy become visible upon the instillation of indigo carmine and further decreasing the chances of an early lesion postoperativerecurrence. Chromoendoscopy, in recurrent respiratory papillomatosis (RRP), helpsidentify unsuspected intraoperative lesions byclearly enhancing the view of their boundaries and surface type. It is also suitable to assess the presence of residual lesions, if any, after theirsurgical removal.

Objectives:
To demonstrate the usefulness of chromoendoscopy in RRP in laryngotracheal surgery. Material and Methods: We used indigo carmine associated with endoscopic laryngeal surgery. Before staining, the mucosa may need to be treated with a mucolytic agent to get rid of excess mucus to boost staining. Rigid suspension laryngoscopes of different proximal and distal diameters were used with chromoendoscopy. Patients underwent chromoendoscopy associated with endoscopic laryngeal surgery under general anesthesia in the O.R.

Results:
In this second phase of our research work, this diagnostic technique was applied toeighteen patients with recurrent laryngeal papillomatosis and two patients with suspected carcinoma of the larynx. We were able to optimize the intraoperative diagnosis and reduce the likelihood of the relapse risk in all patients.

Conclusion:
Chromoendoscopy associated with endoscopic laryngeal surgery is an excellent low-cost intraoperative diagnostic method for the treatment of invasive diseases of the larynx such as laryngeal papillomatosis

Keywords:
larynx, papillomatosis, chromoendoscopy, respiratory, surgery, diagnosis, intraoperative, rigid endoscope, RRP.

Biography:

Rajiv Mahendru possessed Post-Graduate Degree in Obstetrics and Gynaecology from Himachal Pradesh University at the age of 29 years and became one of the youngest Professors. Presently, Head of the Department in the only second women medical college of India. He has 41 Publications in reputed journals and is the recipient of a prestigious Award for excellence in Medical field. Appointed as the Chief-editor of the Special issue of an international journal of repute and has numerous presentations to his credit at international arena as an invited Guest Speaker. He is the member of editorial board of international journals, Academic Board of many universities, member of recruitment for medical teachers, and assessor for establishing Medical colleges. He has chaired numerous sessions in the National and International conferences

Abstract:

Thyroid autoimmunity is the most common autoimmune disorder in women of reproductive age, with a prevalence varying between 5 and 15%. Many studies show a significant association between the presence of thyroid autoantibodies, infertility and recurrent pregnancy loss. The aim of study was to find out an association between anti-TPO-Ab, TSH and infertility among female patients attending the Gynaenecologycal OPD for the management of infertility. A cross-Sectional study was conducted for the period of six months from Jan. 2011 to June 2011 in the Department of Obstetrics and Gynaecology in collaboration with the Department of Biochemistry in a rural medical Institute of India. Fifty infertile females of reproductive age group with both primary and secondary infertility were selected for the study and fifty age-matched non pregnant healthy females who had no problem of infertility were taken as controls. Serum anti-TPO Ab, TSH levels were evaluated by Enzyme linked Immunosorbant assay method. The results obtained from the study showed statistical significance between anti-TPO Ab levels, TSH levels, age and infertility in both the groups. The parameters observed may be considered as a valuable aid in investigation and diagnosis of autoimmune thyroid disease in patients with unexplained infertility.