- Cairo University, Egypt
- Title:Stimulation of Bladder Acupoints by Cloprostenol for Treating Back Soreness in Athletic Horses.
- Time :
Twenty-five Thoroughbred jumper geldings suffered back soreness with poor performance, and 5 control horses were assessed by archived computer data, clinical examination, and laboratory analyses of complete blood picture, serum enzymes, and cortisol level, before and after cloprostenol-aquapuncture. The 25 diseased horses before therapy showed significant increases in aspartate aminotransferase and creatine phosphokinase with clinical pains scored mild in 15 horses, moderate in 9 horses, and severe in one horse, without changes in the hormonal and hematological data. After therapy, they responded by an increase of heart rate (57.8 ± 4.3 bpm), body temperature (38.5 ± 0.7 ºC), respiration rate (28.3 ± 2.1 bpm), and capillary refilling time (CRT) (1.0 ± 0.0). On the 2nd day, a significant decrease in the mean levels of aspartate aminotransferase and creatine phosphokinase (P ═ 0.001) was detected, while on the 4th day, they mimed the level of the 5 controls, and on the 6th day, they showed a significant decrease (P ═ 0.002). The serum cortisol level showed a significant increase on the 6th day of treatment (P ═ 0.013). The blood picture showed significant increases in red blood cells, mean corpuscular volume, platelets, white blood cells, hemoglobin, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, mean platelet volume, platelet distribution width, lymphocytes, plateletcrit, and large platelet concentration ratio (P < 0.05) and nonsignificant changes in hematocrit, granulocytes, and midocytes. The improved blood parameters, enzymes, hormones, and performance progress after cloprostenol-aquapuncture proved its effectiveness in treating back soreness in athletic horses. Biography:
Eldessouky Sheta has been a Professor at Department of Surgery, Anesthesiology and radiology since 2003. He was graduated from Cairo University in 1981, obtained his M.V.Sc., in 1986 and Ph.D., in 1990 from Cairo University.He has been trained on experimental liver transplantation 6-months in Heidelberg – Germany in 1988.He has attended veterinary conferences in Russia (Saint Petersburg, 2009), Italy (Arezzo, 2013).He is the constructor of International Horse Care Center in Kuwait since 2004.He has been trained on veterinary acupuncture in China (Beijing, 2010).He published several scientific works in equine acupuncture.Currently, he is the president of Egyptian Veterinary Acupuncture Society (EVAS).
- Charles Sturt University , Australia
- Title:Unique Gender- and Age-Specific Therapeutic Functions of Phyto-Pharmaceutical Preparations Derived from Peruvian Maca Phenotypes (Lepidium Peruvianum) and their Selective Applications in Regenerative Medicine.
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Peruvian Maca hypocotyls (Lepidium peruvianum synonym L. meyenii) grown as a blend of differently-coloured phenotypes in a mixed native Maca crops in high Peruvian Andes is cultivated at altitudes above 4,000m a.s.l.. It has been traditionally used by natives as an energizing and revitalising food additive with claimed “gender specific medicinal properties”. Several brands of dietary supplements based on processed Maca hypocotyls and designed specifically for men and/or women are now marketed around the world with wide ranging health claims – some of them being confirmed in clinical studies. Glucosinolates profiles and their individual ratios are used to identify products’ origin and plant phenotype responsible for expected specific physiological effects and biological potency of resultant individual Maca product.
In 1990s’ Maca was introduced to China, Yunnan Province, initially for research purpose, but with reported health benefits and potential advantages to local economy under local environmental and soil conditions, Peruvian Maca was propagated to the level of a commercial local crop, eventually in 2002 obtaining approval by Chinese Government for its cultivation in China (under the Latin name L. meyenii) and in 2012 Maca products were formally permitted to be marketed as a “food resource for health”. Recent research demonstrated that geographic location where Maca is cultivated (either in Peruvian Andean highlands or locations in Peru or China) has profound influence on percentage participation of individual phenotypes in Maca crop, their shape, weight and Glucosinolates profiles – all these differences most likely contributing to biochemical status of harvested Maca, hence, influencing bioactive potency of resultant Maca products.
In this presentation phenotypical target action of Maca preparations and their specific health effects on – or influencing medical conditions experienced by men and/or women of different age and physiological stages is presented. The phytopharmaceutical effects of standardised Maca preparations based on individual Maca phenotypes or their blends with characteristic Glucosinolates profiles based on Maca cultivated in High Peruvian Andes where Maca originates and is cultivated for centuries without changes until today according to traditional “single stage” cultivation system is compared with Glucosinolates characteristics of the products derived from cultivation in Shangri-La (Yunnan – China) according to a “two stage” commercial Chinese planting system.
Based on presented results, further research is recommended to help explaining dynamics of changes in Glucosinolates and other active Maca components induced by different cultivation practices and to what degree observed changes in phytochemistry could alter therapeutic functions expected from Maca used as functional dietary supplement originated and derived from traditional Peruvian and/or Chinese commercial cultivation system.
Dr Henry O MEISSNER – is a native of Poland, graduated from Cracow University where back in 1963 has obtained MSc degree in Environmental Sciences followed by PhD in Nutritional Biochemistry in 1968. Next 50 years which followed he settled initially in New Zealand and later in Sydney, Australia, where from 1978 he lived and worked at Universities and government research Organisations with frequent overseas senior academic appointments and various project assignments in the USA, South America, Europe and Asia.
His earlier research centred on correcting various metabolic symptoms induced by dietary imbalances, physiologically-induced stress, toxicity or environmental factors with their practical correction to restore metabolic equilibrium in treated groups of subjects exhibiting various dietary imbalances linked to specific health conditions.
The last 20 years Professor Meissner has devoted most of his time to research and clinical study on use of standardized Peruvian medicinal plant “Maca” and its prime phenotypes in alleviating gender-related health disorders and designing lines of standardised phyto-pharmaceutical products for a wide range of gender- and age-related health symptoms.
He has published over 300 peer-reviewed scientific papers, books and textbook chapters on wide spectrum of research topics, related to his professional interest. Now retired (semi-), still maintains his research base in Sydney continuing his collaborative research and development in biomedical and phytopharmaceutical areas with various institutions around the world.
- University of Chicago, USA
- Title:Modeling the Origins of Small Cell Lung Cancer from Human Embryonic Stem Cells
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Small cell lung cancer (SCLC) remains a major challenge in public health because of its frequency, its lethality, and the paucity of convenient models for exploring its pathogenesis and potential therapeutic vulnerabilities. Despite recent research advances, fundamental features of SCLC, especially its initiation and progression, are not fully understood. One of the main obstacles is the development of a feasible and tractable system that allows molecular events to be evaluated for their functional changes towards the hallmarks of neoplasia during lung lineage differentiation.
To understand how and why certain constellations of genetic changes drive carcinogenesis in specialized human cell lineages, we are developing cell culture models based on directed differentiation of human embryonic stem cells (hESCs). In this report, we show for the first time that up to 10 percent of lung progenitor cells derived from hESCs can be induced to form pulmonary neuroendocrine cells (PNECs), the putative normal precursors to SCLCs, by inhibition of NOTCH signaling. In such cultures, reduction of the retinoblastoma (RB) protein, the product of a tumor suppression gene commonly mutated in SCLCs, significantly expanded the number of PNECs. But reduction of TP53 protein, the product of another tumor suppressor gene uniformly mutated in SCLCs, or expression of mutant KRAS or EGFR genes, each of which is commonly found in human lung adenocarcinomas, did not induce or expand PNECs, suggesting a lineage-specific sensitivity to loss of RB function. Subcutaneous injection of PNEC-containing cultures in which expression of both RB and TP53 was blocked produced tumors resembling early stage SCLC in immunodeficient mice. Single-cell RNA profiles of PNECs were heterogeneous; when RB levels are reduced, the profiles show similarities to RNA profiles from early stage SCLC. Taken together, these findings suggest that genetic manipulation of hESC-derived pulmonary cells will enable studies of the initiation, progression, and treatment of this recalcitrant cancer.
Huanhuan Joyce Chen received her Pharm.D. degree in Pharmaceutical Sciences at Zhejiang University in China, M.S. and Ph.D. degrees in Biomedical Engineering at Cornell University. She will be enrolled as an Assistant Professor in Pritzker school of molecular engineering and the Ben May department for cancer research at The University of Chicago in May 2020, and is currently a postdoctoral fellow with Dr. Harold Varmus at Weill Cornell Medicine.
She received a number of awards including NIH Pathway to Independence Award (K99/R00), Arnold O. Beckman Postdoctoral Fellowship, National Cancer Institute Physical Sciences in Oncology Young Investigator award and National Science Foundation Graduate Research Fellowship. She has published more than 19 papers in reputed journals, including Nature Biotechnology, Nature Medicine, Nature Communication, Cell Stem Cell, Journal of Experimental Medicine, Journal of Clinical Investigation, Lab on Chip and eLife. Her research is focused on stem cell technology and tissue engineering for modeling and studying cell biology and genetic diseases.
- University General Hospital of Patras, Greece
- Title:Virulence Factors of Gram Positive Bacteria Related to Ocular
- Time :
The ocular surface is constantly exposed to the dangers of the environment, including pathogenic bacteria. Bacterial infections of the human eye by gram positive bacteria can cause severe visual impairments. S. aureus is a major ocular pathogen as it possesses potent virulence factors in its armamentarium: fibronectin-binding protein A (FnbpA) and Fnbp B, fibrinogen binding proteins (ClfA and ClfB), iron regulated surface determinant A (IsdA), wall teichoic acid (WTA), b-defensins 2 and 3, cathelicidin, RNase 7, cytokines, chemokines, adhesion molecules, and granulopoiesis factors, alpha-toxin, phenol soluble modulins (PSM), and Panton-Valentine leukocidin (PVL), protein A (SpA), Exfoliative toxins (ETA and ETB) and toxic shock syndrome toxin (TSST), LukAB (LukGH) and PSMs, staphylocoagulase. S. pneumoniae in eye infections is most involved in keratitis, conjunctivitis, and endophthalmitis. The microorganism firstly colonizes the nasopharynx via the neuraminidases NanA, NanB, and NanC. Then, acts through hyaluronate lyase, pneumococcal capsule, autolysin, pneumolysin, zinc metalloproteinases. Streptococcus pyogenes is most involved in blepharitis and hospital acquired conjunctivitis. Its virulence factors include: cysteine proteinase, streptococcal pyrogenic erythrogenic toxin B, streptokinase, cell envelope protease, Streptococcus secreted esterase, streptolysin O and streptolysin S, M protein, endo-β-N-acetylglucosaminidase. E. faecalis is implicated in postoperative endophthalmitis cases. These strains produce a cytolysin with a large lytic subunit (CylLL) and a small lytic subunit (CylLS) and are related with poor visual outcome. Bacillus cereus can cause a rapidly destructive endophthalmitis via its peptidoglycan, flagella, hemolysins, lipases, enterotoxins, proteases, cereolysin AB, cereolysin O, and collagenase. Corynebacterium (non-diphtheriae) species: They possess pili with tissue tropism to colonize host tissues. After initial attachment additional minor pilins help anchoring, and provide proximity between the bacterial surface and the host cell plasma membrane. The arsenal of gram positive microorganisms that can cause ocular infections and the understanding of their mechanisms of action can elucidate further therapeutic targets and promote rapid treatment.
Panagiota Xaplanteri has graduated from Medical School, Patras University in 1999 and acquired the medical specialty of Biopathology (Laboratory Medicine) in 2007. She has completed her PhD in 2008 from Medical School, Patras University, Greece and her MSc in Health Care Management, Hellenic Open University in 2018. She has worked in the following positions: Senior Assistant, Department of Microbiology, University General Hospital of Patras, Greece, 2015-today, Part time Assistant Professor, School of Rehabilitation Sciences, University of Patras, Greece, 2019-today, Part time Lecturer/Assistant Professor, School of Sciences of Health and Care, Technological Educational Institute of Western Greece, Patras, 2007-2019. She has published more than 20 papers.
- University Hospital of Cologne, Germany
- Title:Exosomal ncRNAs, Novel Frontier of Tumor Detection by Liquid Biopsies
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Locally advanced adeno- and squamous cell carcinoma of the esophagous (EAC, ESCC) and oral squamous cell carcinoma (OSCC) result in worse prognosis upon late diagnosis. We aim to identify tumor indicating ncRNAs in serum exosomes of tumor patients for earlier non-invasive diagnosis to contribute to a better outcome.
Differential gene and protein expression comparing tumor and normal tissues identified diagnostic, response predictive and prognostic tumor markers. Transfer to liquid biopsies now seems practicable by exosomes, components of the novel communication system of living cells. In addition to protein expressing genes, non-coding (nc-) RNAs like lnc-, circ-, and mi-RNA have been recognized as regulatory active key components with high impact for cancer development. Exosomal cargo provides an imense potential for creation of diagnostic marker signatures for earlier diagnosis. We profiled exosomal miRNAs, identified 80 exosomal miRNAs differentially concentrated between 12 OSCC tumor patients and 8 healthy blood donors. miRNome analysis was performed by TaqMan miRNA arrays. Six miRNA candidates have been selected for verification by 25 OSCC patients and 22 healthy blood donors. miR-409-3p has been identified as potential diagnostic candidate, p=0.001, fold change 0.203.
As an essiential step to detect tumor-indicative differences in exosomal cargo with better sensitivity 1. we need membrane proteins on the surface of the microvesicles, discriminating tumor cell secreted „oncosomes“ from exosomes originating from normal cells, 2. we aim to separate tumor cell derived „oncosomes“ from normal cells secreted exosomes, present in large abundance in serum of tumor patients.
By whole genome gene expression arrays we detected highly overexpressed membrane proteins as diagnostic signature which will be now examined in „oncosomal“ membranes for transfer to liquid biopsies.
Ute Warnecke-Eberz, molecular- and microbiologist, obtained PhD at the Freie University of Berlin, Germany in 1990. As head of lab for antiinfectiva research at Bayer Pharmaceutical Research in Wuppertal, Germany, she develoved screening assays to find antibacterials inhibiting protein-DNA interaction. 1999 establishing the lab for molecular oncology of the General-, Visceral- and Cancer Surgery at University Hospital of Cologne, she started research on diagnostic, response predictive and prognostic tumor markers for esophageal, gastric, oral and lung cancer. Since 2017 Prof. at University Hospital of Cologne focussing on real-time quantification of gene expression, and transfer of tumor marker results to liquid biopsy format. Actually evaluating the diagnostic use of serum exosomes and exosomal non-coding RNAs.
- University of Montreal, Canada
- Title:The Dual Regulatory Roles of miR-181a in Breast Cancer
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Breast cancer is the most common malignant tumor in females. It represents a complex heterogeneous group of tumors that display significant diversity with respect to histopathological features and therapeutic responses. Many researchers have focused on biomarkers, which will facilitate detection of breast cancer in its early stages, and microRNAs have shown immense potential for this purpose. microRNAs are a family of highly conserved noncoding single˗stranded RNA molecules of 21-25 nucleotides. microRNAs have been shown to have important roles in oncogenesis, invasion, and metastasis via epigenetic post-transcriptional gene regulation. Recent evidence indicates that the expression of miR-181a is altered in breast tumour tissues and in the serum of breast cancer patients. Some studies have demonstrated the involvement of miR-181a in the control of gene expression in breast cancer. The main thrust of this presentation is to explain the potency of miR-181a as a prognostic and/or diagnostic biomarker and to discuss the targeting therapeutics, as well as the associated challenges.
Pierre Hardy, MD, PhD is a clinical scientist, Professor of Pediatrics, Pharmacology and Physiology at the University of Montreal who has extensive experience in translational medicine regarding solid tumors, cancer biology, gene therapy and biotechnologies (application of nanomedicines in cancer therapy). He has published over 150 papers in peer-reviewed journals. Some of his recent publications include Journal of controlled release 298 (2019): 177-185; Experimental Cell Research 386 (2020): 111737.
- Carol Davila University of Medicine and Pharmacy,Romania
- Title:The Frequency of HLA Alleles in the Romanian Population
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Knowledge of human leukocyte antigen (HLA) allele frequencies is essential for bone marrow and kidney donor searches. The Romanian Caucasian population is heterogeneous and information on HLA polymorphism has not been well studied. We characterized the HLA genetic profile and allele frequencies of regional populations in Romania. HLA-A, B and DRB1 alleles were examined in 8252 individuals, belonging to the four main regions of Romania. The most common alleles found in the Romanian population are: HLA-A*01, A*02, A*03, A*11, A*24; HLA-B*18, B*35, B*44, B*51 and HLA-DRB1*01, DRB1*03, DRB1*07, DRB1*11, DRB1*13, DRB1*15, DRB1*16. More than half of the alleles are non-homogeneously spread in Romania.These results provide a starting point for future analyses of genetic heterogeneity in Romania.
I have started my medical activity as a PhD fellow at the University Hospital of Wales, Cardiff, UK, working on growth factors involved in the pathogenesis of pituitary tumours. My interest centres arround transplantation immunology, cancer immunology and virology. I have concentrated my efforts on three challenging topics: immunogenetics, new biomarkers, new genes involved in early cancer diagnosis, prognosis, immune system genetics in various diseases. At present I am Editor-in-chief at Immunogenetics: Open Access Journal and professor of immunology at Carol Davila Medical and Pharmacy University, Bucharest, Romania.
- University of Szeged ,Hungary
- Title:The Neonatal Isoform of Sarco/Endoplasmic Reticulum Calcium ATPase 1 has a Paradox between its Structure and Function
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The neonatal splice variant of the sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA1b) is expressed specifically in myotubes and developing skeletal muscle1. This pump has a functional difference from its adult isoform, SERCA1a. The SERCA1a is expressed in myofibres of fast twitch muscle and has more capacity to pump against high vesicular Ca2+ concentration than SERCA1b does2. The only structural variance – the octapeptide tail in SERCA1b instead of the C-terminal glycine of SERCA1a3 – does not seem to explain the functional difference because the C-terminal tail protrudes into the sarcoplasm, not the lumen of the sarcoplasmic reticulum where the concentration of Ca2+ is accumulated4. This paradox hints to a possible regulatory mechanism exerted by micro peptides recently found abundant in developing muscle5. A developmental effect of this possible regulation will be presented.
- Pharmaceutical University, Japan
- Title:Chronic Epipharyngitis: a Missing Background of Autonomic Nervous System Disorder and Autoimmune Disease
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It has been noticed since ancient times that colds may cause all kinds of diseases. However, its underlying mechanism has not been fully elucidated so far. Located at the back of the nasal cavities, the epipharynx is a unique tissue that is vulnerable to the effects of upper respiratory tract infections and air pollution. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. In addition, the epipharynx has abundant distribution of vagal nerve fibers. Chronic epipharyngitis is not a widely understood condition. However, because of its close link with the nervous system and immune systems, it may play an important role as a trigger for the development of autoimmune diseases and neuroendocrine disorders, including chronic fatigue syndrome and other somatic symptoms. Thus, the epipharynx-brain interaction and epipharyngitis related immunity are worth consideration in managing patients with autonomic nervous disorder and patients with autoimmune disease. Given that chronic epipharyngitis and its brain interactions are not fully understood, it is important to focus future research on this condition.
Osamu Hotta, Medical Doctor (Ph.D.-medicine), now is a Director of Hotta Osamu Clinic, Clinical professor of Tohoku Medical and Pharmaceutical University, Councilor of Japanese Society of Nephrology, and Chairman for Japanese Focal Inflammation related Disease Research Group (JFIR). Osamu Hotta is a nephrologist, got Medical Doctor’s degree (Ph.D) at Tohoku University in 1993.
- University of Silesia , Poland
- Title:Cd-Induced Autophagy Markers in Hemocytes and Gut Cells of the Moth Spodoptera Exigua of Increased Tolerance to Cadmium.
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Autophagy is a natural process which in physiological conditions is aimed at the elimination of destroyed or malfunctioning cell parts, organelles or molecules. Also, autophagy gets induced under stressing conditions in response to, for example, infection, starvation or oxidative stress. Cadmium as the metal regarded as highly toxic induces numerous harmful effects and reactions, including DNA damage, molecule function inhibition and oxidative stress, may also induce autophagy either directly, by interaction with molecules or indirectly through generation of free radicals. However, Cd also is known as a factor, the exposure to which may, after several generations, contribute to the selection of animal strains of increased tolerance to this element. In the Institute of Biology, Biotechnology and Environmental Protection, University of Silesia in Katowice, there is an unique strain of the moth S. exigua, selected to Cd for 170 generations (18 years). The strain exhibits cellular and organismal reactions that after the period of selection, resemble the ones noted for the control strain. Also, we have strains that are intermediate referring to both Cd concentration and time of exposure. Therefore, the aim of this study was to check whether the autophagy markers differs in insects of various Cd exposure history, including also additional acute intoxication. To reach the aim, two complementary methods: ELISA (LC3 protein level) and flow cytometry were used. Autophagy induction appeared to be significant only in the highest intensity of acute exposure.
Agnieszka Babczyńska, PhD, DSc In my research work I concentrate on relations between humans, animals and environment. As an enthusiastic ecophysiologist, in my work I apply widely understood biomarkers, from molecular markers to life history parameters, if they are able to throw a new light on the tolerance, adaptation, plasticity or selection processes of animals in response to external, especially anthropogenic factors. As animal models, I usually use invertebrates, with spiders and insects as my favorites. Equally eagerly I spend my scientific time in the laboratory and in the field. I am also an academic teacher and, I often organize and take part in popularization of researches among children and adults.
- University of Silesia , Poland
- Title:DNA Damage in Spodoptera Exigua after Multigenerational Cadmium Exposure - A Trade-off between Maintaining DNA Stability and Adaptation Requirements
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Human activity is a serious cause of huge changes in the environment and a constant reason for the emergence of new stress factors. Thus, to survive and reproduce, organisms must constantly implement a program of adaptation to continuously changing conditions. Presented here research are focused on tracking slow changes occurring in Spodoptera exigua (Lepidoptera: Noctuidae), that were caused by multigenerational exposure to sub- lethal cadmium doses. The insects received food containing cadmium at concentrations of 5, 11, 22 and 44 µg per g of dry mass of a food. The level of DNA stability was monitored by the Comet assay in subsequent generations, up to 36th generation. In the first three generations, the level of DNA damage was high, especially in the groups receiving higher doses of cadmium in the diet. In the fourth generation, a significant reduction in the level of DNA damage was observed, which could indicate that the desired stability of the genome was achieved. Surprisingly, however, in subsequent generations alternating increase and decrease of DNA stability was observed. The observed cycles of changing DNA stability were lasting longer in insects consuming food with a lower Cd content. Thus, a transient reduction in genome stability can be perceived as an opportunity to increase the number of variants which then undergo the selection. This phenomenon occurs faster if the severity of the stress factor is high, but low enough to allow the population to survive.
Professor, PhD, DSc Maria Augustyniak is working in the Institute of Biology, Biotechnology and Environmental Protection, University of Silesia in Katowice, Poland. Major scientific interests of professor Maria Augustyniak are: aging theory, stress theory and the theory of natural selection under anthropogenic pressure; ecotoxicology; assessment of DNA stability under the influence of various environmental stress factors, including nanoparticles. Results of her works are published in prestigious journals, including: Carbon, Journal of Hazardous Materials, Fish & Shellfish Immunology, Chemosphere, Environmental Research, Scientific Reports, Environmental Pollution and many others.
- Delta University for Science and Technology, Egypt
- Title:Modulation of Wound Processing by the Effect of Roselle Extract through TGF-β Signaling Pathway
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Wound healing consists of an organized cascade of biochemical and cellular events that involve tissue repairs and regeneration. Hibiscus sabdariffa (HS) content of polyphenols may participate by its antioxidant and anti-inflammatory properties necessary for wound healing. The purpose of this study is to assess the effect of HS loaded in ointment base applied topically to rats exposed to burning compared to standard Iruxol® ointment. Methodology: to assess wound healing potency, burn injury model was employed. Rats were divided into four groups, Group I: Normal topically applied with ointment base (Control). Group II: Burned rats were left without any treatment. Group III: Burned rats applied with topical Iruxol® ointment. Group IV: Burned rats topically applied with prepared HS extract ointment. The groups were treated with respective ointments three times through 24 hours. The wound tissues were collected to detect the oxidative stress and inflammatory effect in tissues as compared to control group. Histological analysis for tissue samples also were being endorsed the results by promoting collagen formation, re-epithelialization and angiogenesis. Results implicate that HS enhances the healing potential of the skin by stimulating the levels of biomarkers required for skin regeneration through its strong antioxidant in HS ointment applied group. In addition, HS suppressed the inflammatory effect induced by burning through its down regulation of TNF-α level. Moreover, it shows that HS topical treatment significantly reduces the hypertrophic scarring by its effect against TGF-β level. Altogether, these results suggest that HS is a valuable bioactive compound to use in wound healing and may be used with Iruxol® as synergistic product to accelerate wound processing.
Rania Khalil has her experiences in molecular biology in improving the health and protection from diseases. Her papers based on expression of genes which develop new pathways for improving healthcare. She has written these papers after several trials in research, teaching and publishing. The basis is founded on comparing gene expression before and after treatment either with a drug, complementary medicine and or food supplement. This approach has different ways of focusing that may be correlated to genetically or environmentally point of view.
- Zhejiang University School of Medicine, China
- Title:Role of CD97 in Insulinoma Extracellular Vesicles Induced Differentiation of Mesenchymal Stem Cells into Islet β-like Cells
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Obtaining sufficient donor islet β-like cells is the key to islet transplantation for type 1 diabetes mellitus. Bone marrow mesenchymal stem cells (BMMSCs) are expected to be ideal sources to obtaining islet β-like cells, however the low differentiation rate is an urgent bottleneck that need to be solved. Our group demonstrate that extracellular vesicles (Evs) derived from insulinoma can differentiate BMMSCs into islet β-like cells, and exosomes (Exos), a core component of Evs, had higher differentiation rate than Evs. In addition, we show that CD97 overexpressed Exos had higher differentiation rate than that of CD97 knockdown Exos. Furthermore, we clarify that CD97 promotes differentiation of mesenchymal stem cells into islet β-like cells through MAPK/Smad/Ngn3 pathway. Taken together, we demonstrate that insulinoma Evs, especially the Exos, were able to differentiate BMMSCs into islet β-like cells, and that CD97 plays a crucial role in the differentiation process.
Chao Li (M.D. Ph.D.) is currently fellow of Department of Surgery,Second Affiliated Hospital of Zhejiang University, School of Medicine. In 2011, Dr. Li finished his bachelor training of clinical medicine at Tongji Medical College, Huazhong University of Science and Technology. From 2011 to 2016, Dr. Li received his M.D./Ph.D. education in Zhejiang University, School of Medicine, and undertook a half year visiting scholar training in the Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada. Dr. Li’s research focuses on diabetes mellitus and malignant tumors of digestive system, specialized in the treatment of diabetes mellitus using extracellular vesicles derived from mesenchymal stem cells, as well as the metastatic mechanism of pancreatic cancer.
- Louisiana State University, USA
- Title:Aluminum-Stimulated Production of Lipopolysaccharide (LPS) from the Human Gastrointestinal (GI)-Tract Microbiome-Resident Bacteroides Fragilis
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Gram-negative obligate anaerobic bacteria of the human GI-tract-microbiome and their immunogenic secretory products have significant potential to serve as a dynamic, life-long source of extremely potent pro-inflammatory enterotoxigenic compounds highly toxic to the central nervous system (CNS). These microbes and their secreted products: (i) are capable of generating a broad-spectrum of highly neurotoxic, pro-inflammatory and potentially pathogenic molecules; and (ii) these include a highly immunogenic class of amphipathic surface glycolipids known as lipopolysaccharide (LPS). Bacteroides fragilis (B. fragilis), a commensal, Gram negative, non-motile, non-spore forming obligatory anaerobic bacillus, and one of the most abundant bacteria found in the human GI tract, produces a particularly pro-inflammatory and neurotoxic LPS (Bf-LPS). Bf-LPS: (i) is secreted from the B. fragilis outer membrane into the external-medium; (ii) can damage biophysiological barriers via cleavage of zonula adherens cell-cell adhesion proteins, thereby disrupting both the GI-tract barrier and the blood-brain barrier (BBB); (iii) is able to transit GI-tract barriers into the systemic circulation and cross the BBB into the human CNS; and (iv) accumulates within CNS neurons in neurodegenerative disorders such as Alzheimer’s disease (AD). This presentation will provide evidence that the incubation of B. fragilis with aluminum sulfate [Al2(SO4)3] is a potent inducer of Bf-LPS. The results suggest for the first time that the pro-inflammatory properties of aluminum may not only be propagated by aluminum itself, but by a stimulation in the production of microbiome-derived Bf-LPS and other pro-inflammatory pathogenic microbial products normally secreted from human GI-tract-resident microorganisms.
- Can Tho University of Medicine and Pharmacy, Vietnam
- Title:Molecular and Cellular Mechanisms Underlying the Interaction between the Host and Crohn Disease-Associated Adherent-Invasive Escherichia Coli: A Focus on the Role of Autophagy and Exosomes
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Our group has been working on the implication of adherent-invasive Escherichia coli (AIEC) in the etiology of Crohn’s disease (CD). We have showed that AIEC abnormally colonize the intestinal mucosa of CD patients, adhere to and invade intestinal epithelial cells (IECs), survive and replicate within macrophages, promote pro-inflammatory cytokine production, and colonize the gut and induce intestinal inflammation in genetically susceptible mouse models. We also showed that upon AIEC infection, autophagy is activated in host cells to restrain AIEC replication and to inhibit AIEC-induced inflammation. We showed recently in vitro and in vivo that activation of the metabolic stress response pathway EIF2AK4-EIF2A-ATF4 upon AIEC infection serves as a host defense mechanism to induce a functional autophagy, independently of mTOR, to control AIEC intracellular replication and to inhibit AIEC-induced inflammation1. Given that most of the current strategies based on modulating autophagy by targeting mTOR can have undesirable effects, targeting the EIF2AK4-EIF2A-ATF4 pathway could be a promising strategy to inhibit specifically AIEC colonization and inflammation. While host cells induce a functional autophagy as a defense mechanism to control AIEC replication, AIEC can subvert autophagy by up-regulating the levels of miR-30c and miR-130a in IECs, thus inhibiting levels of two key autophagy-related proteins ATG5 and ATG16L1. AIEC also inhibit autophagy by impairing host SUMOylation, a eukaryotic-reversible post-translational modification, in which SUMO, an ubiquitin-like polypeptide, is covalently linked to target proteins. Thus, we demonstrated the AIEC-induced impaired autophagy via the modulation of host miRNAs or host SUMOylation consequently leads to increased AIEC intracellular replication and AIEC-induced inflammation. We also showed a role for autophagy in the control of gut microbiota composition and host susceptibility to AIEC infection using genetically manipulated mouse models with a defect in autophagy. This was accompanied with increased AIEC colonization in the gut and enhanced intestinal inflammation. Of interest, upon AIEC infection, IECs and macrophages secrete an increased amount of exosomes, which are extracellular vesicles of 30 to 100 nm playing a role in cell-to-cell communication. Furthermore, the exosomes secreted by AIEC-infected cells can increase pro-inflammatory cytokine production and AIEC replication in exosome-receiving cells. Of interest, exosomes secreted by AIEC-infected IECs inhibit autophagy in exosome-receiving IECs. Mechanistically, this is mediated miR-30c and miR-130a, which are transferred via exosomes from donner cells to recipient cells, in which they directly target and inhibit expression of ATG5 and ATG16L1, respectively (unpublished data). This consequently leads to impaired autophagy response and increased intracellular replication of AIEC in cells that receive exosomes from AIEC-infected cells. These data show that exosomes are an important player in cell-to-cell communication during AIEC infection, which can carry and transfer specific miRNAs, leading to autophagy inhibition and favoring AIEC colonization. Altogether, our researches help to understand better the mechanism underlying the interaction between the host and AIEC strains. In the future, this work could contribute to the development of a personalized therapeutic strategy based on autophagy modulation for patients with abnormal AIEC colonization.
With a PhD degree in 2006 at University of Aix-Marseille III, France and a postdoc training at Department of Medicine, Emory University, USA (2006-2011), H. Nguyen has obtained a tenured position as an assistant professor at the M2iSH (Microbe, intestine, inflammation and Susceptibility of the Host), UMR1071 Inserm, University of Clermont Auvergne since 2012. H. Nguyen has been deeply working on the molecular and cellular mechanisms involved in the etiology of intestinal diseases such as inflammatory bowel diseases (IBD) and colorectal cancer (CRC). Her current researches focus on the infectious etiology of these diseases, and in particular on the interaction between the host and the pathogens involved in these diseases.
- National Research Centre ,Egypt
- Title:Molecular Cytogenetic Analysis of Patients with Disorders of Sex Development Associated With Congenital Anomalies: A Single Centre Egyptian Experience
- Time :
Disorders of sex development (DSD) represent a diverse group of clinical conditions, which have a very wide phenotypic spectrum associated with a complicated molecular background. Such conditions are considered among the most common birth defects and are frequently associated with congenital abnormalities.
Herein we present 66 patients with DSD associated with somatic anomalies, who were selected from clinical genetics dept., NRC. The patients underwent detailed clinical and genital assessment, Quigley scoring of external genitalia, pubertal staging, hormonal profiling, and imaging analysis. Chromosomal analysis of the peripheral blood lymphocytes was performed using GTG banding technique for all patients. FISH analysis was performed whenever indicated. MLPA was carried out for selected patients and chromosomal microarray (CMA) were conducted for 15 patients.
12 patients had numerical sex chromosomal abnormalities of them 3 had a translocation of a sex chromosome to an autosome; 13 patients had autosomal abnormalities; 25 patients had 46,XY karyotype, of them 8 were clinically diagnosed as having recognizable syndromes; 19 patients had 46,XX karyotype, one of them was clinically diagnosed as having Rubinstein Taybi syndrome. CMA detected significant copy number abnormalities in 7 patients, which were correlated to the phenotype.
The study emphasizes the crucial need to improve the clinical utility of genetic analysis in patients with DSD. CMAs can dramatically assist diagnosis in patients with multiple anomalies, not specific to a well-delineated genetic syndrome, and help more understanding of the molecular basis of DSD.
Improving the diagnostic yield for such complicated disorders will be reflected on the patients and their families, regarding possible therapeutic interventions, recurrence risk and carrier detection.
Dr. Mona Kamal Mekkawy, associate professor of Human genetics, Human Cytogenetics department , National Research Centre (NRC), Cairo, Egypt. Graduated in the Faculty of Medicine, Ain Shams University. Had M.Sc. degree in Pediatrics, Ain Shams University and PhD in Human Genetics, Alexandria University. Major research interests are: human cytogenetics and molecular cytogenetics and its recent diagnostic applications in human genetics, especially experienced in the field of disorders of sex development (DSD).
Supervised many MSc. and PhD thesis for student from National Research Centre and Cairo university in the field of chromosomal disorders in DSD patients, gonadal tissue culture, FISH analysis and microdeletion detection by MLPA techniques and copy number variation detection by chromosomal microarray. In addition to micronucleus assays for DNA damage detection.
Experienced practical teaching in many training courses held in the human cytogenetics dept. Also participated as a speaker in many courses and lectures carried out in the department and in the division of human genetics and genome research and in many activities and courses held in NRC and in other Egyptian universities.
- Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Poland
- Title:New Insights into MS Pathomechanisms: On the Track to Control Inflammation and Neurodegeneration
- Time :
Multiple sclerosis (MS) is a chronic disorder characterized by multifocal inflammatory infiltrates (T cells, B cells, macrophages) within the central nervous system (CNS) and concomitant degradation of myelin, oligodendrocytes and axons, along with reactive microgliosis. Disease background is thought to include two overlapping processes: polyphasic myelin destruction (inflammatory demyelination) and progressive axonopathy (neurodegeneration) with little capacity for repair. The pathology is generally believed to reflect autoimmune attack upon myelin auto-antigens but the mechanisms resulting in the escalation of the autoimmune response and leading to the damage of white and gray matter in the CNS have not been so far fully clarified.
Lipid antigens are substantial myelin components and they also may constitute potential candidates for autoimmune attack in MS. We have recently explored the seem to be role of bioactive lipids, particularly ceramide, in the pathomechanism of autoimmune demyelination in MS. Specifically, we examined TNF- and IFN- effect, the two Th1 pro-inflammatory cytokines known to be accumulated in MS brain, upon a human oligodendroglioma (HOG) cell line. Our results suggested an exosome-mediated new mechanism of synergistic cytotoxicity of TNF- and IFN-. Ceramide-laden exosomes, when released from stressed or cytokine-targeted oligodendrocytes in vivo, may “broadcast” the cell death signal and promote the immune response that occurs under demyelinating conditions in the CNS. For this reason exosomes offer new molecular insights into MS pathology and perhaps could be used in the future as bioactive markers for the disease activity. On the other hand, it is well known that ceramide play a central role in sphingolipids metabolism which intricate scenario with numerous potential therapeutic targets, e.g. “engineered” exosomes can be used as an efficient vehicles for delivery of therapeutic agents across the blood-brain barrier.
A complex and heterogeneous picture of MS immunopathology may suggest the presence of various immunoregulatory abnormalities in this disease. These may result from disturbed functional interactions of many cellular components of the immune system, especially regulatory T cells. Natural killer T (NKT) cells may perform major regulatory functions in immunity, however their function in MS is not yet fully understood. In our studies, we identified glycosphingolipid (GSL)-reactive CD1-restricted lymphocytes especially those of the NKT and NKR+ phenotype and with T cell regulatory functions. GSL-driven anergy of circulating lymphocytes in MS suggests that the altered immune response in MS is via robust invariant NKT (iNKT) activation with potent cellular and cytokine activities. Diverse GSLs including the endogenous myelin acetylated-galactosylceramides (FMCs) can drive activation critical to controlling CNS inflammation and fostering myelin repair. Rendering iNKT-cells hyporesponsiveness to an endogenous GSL is a novel insight into diseases manifesting aberrant iNKT-cell activation. Furthermore, the state of anergy following stimulation with the auto-antigen FMC-7 may have significant clinical implications, according to the theory of antigen-specific therapy of autoimmune diseases.
An equally important factor in the pathology of MS, apart from (sub)acute demyelination, is progressive axonal and neuronal damage, resulting in accumulating neurological deficit and disability. Earlier reports indicate that calpain has been implicated in MS autoimmune mechanism, including demyelination, axonal damage, loss of neurons and oligodendrocytes and modulation of proteins involved in apoptotic pathways. We hypothesized that this Ca2+ dependent cysteine protease plays a key regulatory role in immune activation of MS pathology and its deactivation (inhibition) causes remission with control of autoimmune inflammation and neurodegeneration. Our studies yielded new findings regarding the mechanism of progressive MS that have implications for potential treatment. Based on two primary culture models rat and human we identified calpain as a key neuron injury signal driving the toxic component of reactive microgliosis. Specifically, we determined that calpain, released upon neuron damage, activates microglia to produce reactive oxygen species and nitric oxide that are selectively toxic to neurons. Our findings indicate that damaged neurons themselves are culpable in propagating further neurotoxicity with pro-inflammatory signals to microglia. These studies provide much needed insight into the nature of progressive phase of MS, with emerging putative preventive and therapeutic options. These novel findings (e.g., targeting calpain inhibition) may provide valuable insight into the mechanisms by which Th1 cells elicit neurodegeneration and appear promising in the treatment of progressive types of MS but also other neurodegenerative disorders.
2019 Habilitation: Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland
2003 Ph.D.: Institute of Immunology & Experimental Therapy Polish Academy of Sciences, Wroclaw, Poland
1997 Master of Science & Engineer: Wroclaw University of Technology, Department of Chemistry, Wroclaw, Poland
since 1997 Ludwik Hirszfled Institute of Immunology & Experimental Therapy,
Polish Academy of Sciences, Wroclaw, Poland
2012 and 2014-2016 – Medical University of South Carolina, Charleston, SC, USA
2010-2011 – Heinrich Heine University, Düsseldorf, Germany
2004-2010 – Georgia Regents University, Augusta, GA, USA
Honors and Awards:
2016 Certificate of the Polish-American Fulbright Commission received at the Ministry of Science and Higher Education in recognition of merits to promote Polish science and culture and to strengthen friendships between the peoples of the Republic of Poland and the United States of America through participation in the program of Fulbright Senior Award 2015-2016.
2015 Fulbright Senior Award nomination by the Polish-U.S. Fulbright Commission approved by J. William Fulbright Foreign Scholarship Board, Washington, DC, USA.
2014 Fellowship award approved by the Kosciuszko Foundation, New York, NY, USA.
2011 Du Pré Grant award approved by the Multiple Sclerosis International Federation, London, United Kingdom.
2007 Wroclaw Medical University Rector’s award for scientific publication, conducted in collaboration between Medical University and IIET, published in 2006 in the journal of the highest IF value (Galactosylation of IgG from rheumatoid arthritis [RA] patients-changes during therapy; Glycoconj. J. 23, 463-471, 2006).
2003 Award for Ph.D. dissertation, Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
since 2016 Member of the Fulbright Scholar Alumni Program administered by the Council for International Exchange of Scholars, a division of the Institute of International Education, Washington, DC, USA
since 2015 Member of the Kosciuszko Foundation Research Alumni Program, Warsaw, Poland
since 2012 Member of the Multiple Sclerosis International Federation Research Alumni Program, London, United Kingdom
since 2008 Member, The International Society of Neuroimmunology
M. Podbielska, J. O’Keeffe, E. L. Hogan Autoimmunity in multiple sclerosis: role of sphingolipids, invariant NKT cells and other immune elements in control of inflammation and neurodegeneration J. Neurol. Sci. 385, 198-214, 2018.
N. M. Trager, J. T. Butler, J. Harmon, J. Mount, M. Podbielska, A. Haque, N.L. Banik and C.C. Beeson. A Novel Aza-MBP Altered Peptide Ligand for the Treatment of Experimental Autoimmune Encephalomyelitis. Mol. Neurobiol. 55(1), 267-275, 2018.
M. Podbielska, Z.M. Szulc, E. Kurowska, E.L. Hogan, J. Bielawski, A. Bielawska, N.R. Bhat. Cytokine-induced release of ceramide-enriched exosomes as a mediator of cell death signaling in an oligodendroglial cell line. J. Lipid Res. 57(11), 2028-2039, 2016.
M. Podbielska, A. Das, A. W. Smith, A. Chauhan, S. K. Ray, J. Inoue, M. Azuma, K. Nozaki, E.L. Hogan and N.L. Banik. Neuron-Microglia Interaction Induced Bi- directional Cytotoxicity Associated with Calpain Activation. J. Neurochem. 139(3), 440-455, 2016.
J. O’Keeffe, M. Podbielska, E.L. Hogan. Invariant natural killer cells and their ligands: focus on multiple sclerosis. Immunology 145, 468-475, 2015.
M. Podbielska, N.L. Banik, E. Kurowska, E.L. Hogan. Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination. Brain Sci. 3, 1282-1324, 2013.
E.L. Hogan, M. Podbielska, J. O’Keeffe. Implications of lymphocyte anergy to glycolipids in multiple sclerosis (MS): iNKT cells may mediate the MS infectious trigger. J. Clin. Cell. Immunol. 4, 144, 2013.
C. Gately, M. Podbielska, T. Counihan, M. Hennessy, T. Leahy, A.P. Moran, E. L. Hogan, J. O’Keeffe. Invariant natural killer T-cell anergy of circulating lymphocytes to myelin polyacetylated-β-galactosyl-ceramides in multiple sclerosis. J. Neuroimmunol. 259 (1-2), 1-7, 2013.
M. Podbielska, H. Krotkiewski and E.L. Hogan. Signaling and regulatory functions of bioactive sphingolipids as therapeutic targets in multiple sclerosis. Neurochem. Res. 37, 1154-1169, 2012.
M. Podbielska, S.B. Levery and E.L. Hogan. The structural and functional role of myelin fast-migrating cerebrosides: pathological importance in multiple sclerosis. Clin. Lipidol. 6(2), 159-179, 2011.
M. Podbielska, S. Dasgupta, S.B. Levery, W.W. Tourtellotte, H. Annuk, A.P. Moran, E.L. Hogan. Novel myelin penta- and hexa-acetyl-galactosyl-ceramides: structural characterization and immunoreactivity in cerebrospinal fluid. J. Lipid Res. 51(6), 1394-1406, 2010.
M. Podbielska and E.L. Hogan. Molecular and immunogenic features of myelin lipids: incitants or modulators of multiple sclerosis? Mult. Scler. 15(9), 1011-1029, 2009.
- Center for Integrative Medical Sciences ,Japan
- Title:Role of mRNA Decay in Tissue Development and Homeostasis
- Time :
mRNA decay is required for many biological events, and dysregulation of the mechanism leads to disorders, including cancer, neurodegenerative diseases and diabetes. A shortening of poly(A) tails (deadenylation) triggers mRNA degradation, that is mainly mediated by the CCR4-NOT complex.
Liver development involves dramatic gene expression change mediated by transcriptional and post-transcriptional control. We generated mice lacking a Cnot3 gene, encoding an essential subunit of the CCR4-NOT complex, in liver from a neonatal stage (Cnot3-LKO mice). Hepatocyte death and inflammation were observed in the livers of Cnot3-LKO mice. Gene expression analysis showed increased expression of immune response-related, cell cycle-regulating, and immature liver genes in the livers of Cnot3-LKO mice. In contrast, genes, which are relevant to liver functions, such as oxidation-reduction and lipid metabolism, decreased, indicating impaired liver functional maturation. Highly expressed mRNAs possessed elongated poly(A) tails and were stabilized in the livers of Cnot3-LKO mice. Similar results were obtained when we suppressed the CCR4-NOT complex in adult mouse liver. These data suggest that the CCR4-NOT complex-mediated mRNA decay plays a critical role in liver maturation and function, providing novel insights into tissue development and homeostasis.
Dr. Toru Suzuki is a Senior Researcher at RIKEN, Center for Integrative Medical Sciences from 2016. Main research interests are roles of posttranscriptional mechanisms in biological processes.
He received Ph.D. from University of Tokyo in 2001. He became Research Associate at Division of Oncology, Department of Cancer Biology, Institute of Medical Sciences, University of Tokyo and did research to 2012. He moved to Okinawa Institute of Science and Technology Graduate University as a Staff Scientist at Cell Signal Unit in 2012 and worked until 2016.
- Title:Recent Developments in Cell-SELEX Technology for Aptamer Selection
- Time :
SELEX technique is employed to select aptamers against wide range of targets. The in vitro method of aptamer selection using live cells as the target is referred as CELL-SELEX. The use of aptamers as therapeutic and diagnostic agents is rapidly evolving, selection techniques such as Cell-SELEX could be beneficial in identifying aptamers when the target is in its native conformation and without prior information of the cognate target, thereby bringing the aptamer development one step closer to the clinic. The presentation provides a comprehensive description on the development of aptamers through various cell-SELEX methods. In addition, it pinpoints the advantages and limitations of the cell-SELEX process and its variants. The given information can be valuable for the design and development of futuristic oligonucleotide based diagnostics and therapeutics work.
Dr Harleen Kaur has been in the pharmaceutical industry for almost 8 years and most recently led the analytics and drug product tech transfer projects for two biologics products while working at AstraZeneca, USA. Prior to this, she worked in R&D division of Fujitsu Asia Pte Ltd in Singapore where she worked on aptamer development and played an integral role in identifying and purifying aptamers against different protein targets in collaboration with National University of Singapore, Agency of Science Technology and Research Singapore, and Japanese diagnostic enterprise Sysmex. In her current role, Dr Kaur is leading a team of analytical scientists at Aurobindo Biologics and her responsibilities include the method development, method qualification and method transfer for different biosimilar products. Dr Kaur completed her PhD in chemical and biomolecular engineering department at National University of Singapore.
- Utsunomiya University, Japan
- Title:Melanocyte Activation Mechanisms and Rational Therapeutic Treatments of Solar Lentigos
- Time :
To characterize the pathobiology of solar lentigos (SLs), analyses by semiquantitative RT-PCR, Western blotting, and immunohistochemistry revealed the upregulated expression of endothelin (EDN)-1/endothelin B receptors (EDNBRs), stem cell factor (SCF)/c-KIT, and tumor necrosis factor (TNF)α in the lesional epidermis, which contrasted with the downregulated expression of interleukin (IL) 1α. These findings strongly support the hypothesis that previous repeated UVB exposure triggers keratinocytes to continuously produce TNFα. TNFα then stimulates the secretion of EDNs and the production of SCF in an autocrine fashion, leading to the continuous melanogenic activation of neighboring melanocytes, which causes SLs. A clinical study of 36 patients with SLs for six months treated with an M. Chamomilla extract with a potent ability to abrogate the EDN1-induced increase in DNA synthesis and melanization of human melanocytes in culture revealed a significant improvement in pigment scores and color differences expressed as L values. Another clinical study using a tyrosinase inhibitor L-ascorbate-2-phosphate 3 Na (ASP) demonstrated that L values of test lotion (6% APS)-treated skin significantly increased in SLs and in non-lesional skin with a significantly higher ΔL value in SLs when compared with non-lesional skin. The sum of these findings strongly suggests that combined topical treatment with EDN signaling blockers and tyrosinase inhibitors is a desirable therapeutic choice for SLs.
Dr. Genji Imokawa (Ph.D.-medicine) now is Professor of Utsunomiya University, Center for Bioscience Research and Education as well as Visiting Professor of Chubu University, Research Institute of Biological Functions and of Ohio University, Edison Biotechnology Institute. Board of Directors in Japanese Society for Ceramide Research and Japanese Medical Society for Skin Aging and Council member for Japanese Medical Society for Anti-Aging. Research Activities: More than 175 original English papers including EMBO Journal, J Clinical Invest, J Cell Sci, Cancer Res, Am J Pathol, FASEB J, J Biol Chem, J Pathol and J Lipid Res; Research Field: Photo-aging/ Fibroblasts, Atopic Dermatitis/Sphingolipid Metabolism, Melanogenesis/Melanocyte Biology, Keratinization/Keratinocyte Biology.