Biography:

Vladimír Štrbák has worked at Institute of Experimental Endocrinology, Slovak Academy of Sciences. He was Organizer and Chairman of the five International Symposia on Hormones in Milk, resident of the International Symposium on Cell Volume and function 1997. He was Organizer and Chairman Symposium Cell Volume, physiological and pathophysiological aspects, 5th International Congress of Pathophysiology, June 28-July 1, 2006, Beijing, China, published in Chinese Journal of Pathophysiology, June 2006, Volume 22, No 13, Supplement p. 167. Organizer and Chairman of the session Cell Volume Regulation and Cell Functions The Physiology of Anion Transport and Cell Volume Regulation (August 3-6, 2009, Okazaki, Japan) Symposium following the IUPS Congress (Kyoto). His most important activities in last three years: 6th Global Diabetes Summit and Medicare Expo, November 02-04, 2015, Dubai, UAE, Organizing Committee Member, Keynote Speaker, 13th Global Diabetes Conference and Medicare Expo, August 8-10, 2016, Birmingham, UK: Organizing Committee Member Keynote Speaker and 16th Global Diabetes Conference and Medicare Expo, March 22-23, 2017 Rome, Italy Organizing Committee Member, Keynote Speaker, Chair of the Session.

 

Abstract:

Thyrotropin releasing hormone (TRH; pGlu-His-ProNH2) is colocalized in pancreatic β cells in secretory granules with insulin. TRH secretion from pancreatic islets is stimulated by glucose and inhibited by insulin. Disruption of the TRH gene in knockout mice results in hyperglycemia accompanied by impaired insulin secretory response to glucose. To understand role of TRH we blocked the last step of biosynthesis of α−amidated peptides, including TRH by Disulfiram (DS) treatment of adult male rats subcutaneously with 200 mg/kg for five days. TRH in physiological concentration (1 nM) does not affect basal insulin secretion from intact islets. In contrast, basal insulin secretion from islets of DS-treated rats is four times higher compared to controls and could not be stimulated by high-glucose. The addition of 1 nM TRH into medium decreased immediately basal insulin secretion in DS (TRH lacking) islets to control level and normalized also their response to glucose. Absence of the secretory response to glucose in islets from TRH depleted rats is connected with their increase of insulin content. Glucose stimulation together with 1 nM TRH normalized also insulin content in DS islets. Apparently, high insulin content in islets from TRH depleted animals is a result of block of regulatory secretion pathway which is corrected by the addition of TRH. In conclusion, presence of TRH in β cells ensures appropriate low basal (constitutive) insulin secretion and high response to stimulation. Release of TRH induced by glucose has autocrine effect resulting in directing insulin secretion to regulatory pathway. 

 

Biography:

Francesco Lippi was graduated in Medicine, Surgery at the University of Pisa, Albo Pisa 1879/79, and specialization in Endocrinology at the University of Pisa July 1982 and specialization in Nuclear Medicine at the University of Florence July 1987. He has taught at the Institute of Clinical Methodology and the Institute of Endocrinology of the University of Pisa. From 1990 as a Professor of Endocrinology at the University Hospital of Pisa, he conducted the study (pahe se III) on effects of recombinant human TSH (rhTSH) adjuvant therapy in compassionate use program for patients with differentiated thyroid carcinoma.

 

 

Abstract:

Thyroid cancer is represented in most cases by differentiated thyroid carcinoma (DTC) (papillary or follicular), although the histological prevalence is papillary (90%). DTC is not particularly frequent, affecting only one in 25,000 people in Europe but increasing in the world, and has a higher incidence in women than in men (ratio 3-5:1). The DTC is asymptomatic, since in the great majority of cases the thyroid function appears normal. Secondary lymphadenopathy may rarely occur as a first event. Therefore the prevention, in particular the palpation and the ultrasound of the neck, becomes particularly important. A first cause is the area of origin (iodine deficiency). Another ascertained cause is the previous irradiation on the neck in pediatric age for benign pathologies. Other causes are the familiarity and genetic predisposition. It’s often the same patient who becomes aware of a swelling in the neck region. However, many of the nodules are so small in size that they are not discovered by the patient or the doctor, but require an adequate instrumentation (ultrasound). As soon as a thyroid nodule is discovered, it is advisable to carry out a specialist examination, blood test to measure serum FT3, FT4, TSH, anti-thyroglobulin antibodies and anti-thyroperoxidase (AbTg and AbTPO), and calcitonin (Ct). Following this phase, the neck ultrasound study follows. Often the ultrasound finding can already be suggestive of a suspicious nodule due to the presence of "spray" microcalcifications or to an incomplete halo sign or an increase in intra-nodular vascularity. The examination that still allows the diagnosis is the fine needle aspiration biopsy with cytological examination and international classification. In case of DTC, surgical therapy (total thyroidectomy) was generally followed by radioiodine therapy (RIT) which allows the elimination of residual thyroid tissues (ablation) and reduces the recurrences. Recently the new anatomopathological staging has reduced the RIT. Therefore, both papillary microcarcinoma and multifocal carcinoma, and papillary carcinoma with focal infiltration of the peri-thyroid soft tissues, are not treated with RIT if there are not different variants to the classical one. However, there are still authors who continue to treat patients (except microcarcinoma) still with RIT. This therapy can be performed both in conditions of hypothyroidism, or more recently without therapy withdrawal, but in euthyroid status after stimulation with recombinant human TSH. Moreover, the high serum TSH it’s the condition necessary for the thyroid cells stimulation, both for the production of thyroglobulin (Tg), and for the ability to concentrate radioiodine. The percentages of ablation and therefore of remission of the disease vary between 90 and 98% depending on the series published. RIT is followed by total body post-therapy scintigraphy that allows the visualization of radioactive iodine concentration in the body. About 10-15% of patients need an additional dose of radioiodine to complete the ablation of thyroid residues, while, in a small percentage of patients, for local or distant metastases or for detectable serum Tg levels

Biography:

Eduardo J Simoes is a Chair, Wesbury and HMI Alumni Distinguished Professor of the Department of Health Management and Informatics-University of Missouri School of Medicine. His Medical degree is from Faculdade de Medicina, Universidade de Pernambuco-Brazil (1981), Diploma and Master of Science degree from the University Of London School Of Hygiene Tropical Medicine (1987) and Master of Public Health degree from Emory University School of Public Health (1991). He is a Fellow of the American College of Epidemiology. He has published more than 135 papers and served as an Editorial Board Member of reputable journals

Abstract:

About more than 500 million adults worldwide now have diabetes mellitus, 90% of whom have type-2 diabetes (T2D). Successful glycemic control key to prevent and reduce complications of T2D and reduce death related to the disease. However, maintaining optimal glycemic control through ongoing monitoring and treatment can be costly and challenging. The development of innovative self-care strategies to improve diabetes management is necessary. Advances in health information technologies (HITs) aim to increase the support of effective and affordable health-care delivery and patient education. There is evidence that HIT approaches using mobile, computer, e-mail, and internet enhance chronic disease management. This research provides an overview of the HITs in use for T2D management. We synthesize the latest findings on HITs’ effect in reducing HbA1c and managing complications from cardiovascular diseases. We discuss the current research limitations and implications for future research. Finally, we present barriers to applications of HITs in T2D management and suggested steps to move forward

Biography:

 

Wei-Chiang Shen is a Professor in Pharmaceutical Sciences at the University Of Southern California School Of Pharmacy. His research interests focus on the development of novel systems for improving peptide and protein drug delivery. He has published more than 150 papers in different areas of biomedical sciences. He is a Co-Author of the textbook “Immunology” for Pharmacy Students and a Co-editor of the book “Antibody-Drug Conjugates – the 21st Century Magic Bullets for Cancer”. He was elected to Fellow of the American Association of Pharmaceutical Scientists in 1992 and Fellow of the American Association for the Advancement of Sciences in 2000

Abstract:

We have recently prepared a recombinant proinsulin-transferrin fusion protein (ProINS-Tf). ProINS-Tf is an inactive form of insulin analog, but can be selectively absorbed, activated, and retained in the liver. We have demonstrated in type 1 diabetes mouse models that ProINS-Tf is a highly liver-targeted and long-lasting insulin prodrug. Due to the binding to both insulin and transferrin receptor, the liver-activated ProINS-Tf exhibited a significantly higher affinity to insulin receptor when compared with the native insulin. The bivalent binding of activated ProINS-Tf induces a longer and stronger activation of insulin receptor as demonstrated in the enhanced and prolonged Akt phosphorylation with hepatoma cells. Furthermore, ProINS-Tf can overcome insulin resistance in palmitate-treated HepG2 cells, as well as in severe hyperglycemic NOD mice. Therefore, ProINS-Tf can potentially be developed into a safe and effective insulin prodrug for the control of basal glycaemia in diabetes and for the treatment/prevention of insulin resistance- associated diseases

Biography:

Ravi Muppirala is a Biophysicist who has held academic appointments at TIFR, Carnegie-Mellon, Syracuse University and University of Michigan. His expertise and interests span bio-molecular structure-dynamics, origins of primitive cells and type-2 diabetes

Abstract:

It is argued - why the preferred method to maintain euglycemia in type-2 should be prioritizing the endogenous insulin secretion, while suggesting possible approaches to research further in that direction. It is known, that most types of peripherally administered insulin (PAI) have drawbacks; viz. being non-native, lacking c-peptide, not mimicking physiological insulin secretion oscillations (ISO) that reduce insulin receptor saturation, contributing to weight gain (often as visceral fat). Also, PAI is far less effective in countering gluconeogenesis, a contributor to hyperglycemia, as it doesn’t mimic pancreatic release of insulin into the hepatic entrance of the portal vein as triggered by feeding. Merely maintaining tight-glycemic control may not necessarily reduce endothelial dysfunction. Hence, it may be more beneficial to steer away from PAI as well as exogenous insulin. Although, recent research demonstrates the merits of portally administered insulin, access to the portal vein is not practical. Clearly, stem cells are the right approach and deserve high priority. While DPP4-I/GLP-1, even with concomitant Glitazones, is good therapeutic approaches, they remain insufficient to achieve tight glycemic control. They, also, fail to mimic the ISO and feeding correlated hepatic portal secretion. Meanwhile it may be beneficial to revisit insulin secretagogues (IS) and modify traditional therapy, while improving approaches to endogenous secretion and concomitantly minimizing side effects. Dosage of sulfonylureas should be reduced to maintain a very basal secretion. This should be co-administered with a short acting IS (e.g. meglitinides) prior to feeding. This approach can be titrated to mimic native secretion. Effort should be made to find new molecules that enhance secretion efficiency while minimizing side effects. While β-cell ion channels have been exploited, more effort is needed to exploit the glycolysis/glucokinase aspect

Biography:

Walid Al-Qerem has received his PhD in Clinical Pharmacy Sunderland University in 2013. He has been working as an Assistant Professor at the Faculty of Pharmacy of Al-Zaytoonah University of Jordan since 2014. His research interests include Quality of Life especially for diabetics and respiratory medicine, which involves the standardization of spirometry

Abstract:

Diabetes quality of life (DQOL) instrument has been broadly used to evaluate quality of life among diabetics. This study aims to develop a revised validated Arabic version of DQOL questionnaire in diabetic patients in Jordan. Patients were enrolled in this cross-sectional study from 1^st, January through April/2019 at several public health clinics in Jordan. The original DQOL questionnaire was translated to Arabic and then back-translated by a different translator, then the two versions were compared. Prior to circulating the final version of the questionnaire cognitive validity test were applied to ensure that all the questions were clear. Then a questionnaire that included demographical and other health related questions in addition to the final Arabic version of the DQOL was circulated to the participants. The data of the questionnaire were analyzed using exploratory factor analysis and confirmatory factor analysis after excluding duplicated questions and questions that included more than 15% missing data, also Cronbach alpha was conducted to confirm internal consistency. This study developed a validated Arabic version of DQOL that can measure quality of life of diabetics in the Arabic speaking world. 

Biography:

Sergio Wehinger Wehinger has completed his PhD in Biomedical Sciences from University of Chile in 2013 and actually is an Associate Professor and Director of Magister in Biomedical Sciences of University of Talca in Chile. He had published papers in the field of Metabolism and Diabetes and he is currently investigating the molecular mechanisms involved in the cellular failure of the beta pancreatic islets, which is induced by elevated free fatty acids and oxidative stress levels, to elucidate how to prevent these processes

Abstract:

Background: Deleterious effects of high levels of free fatty acids lead to a phenomenon known as “lipotoxicity”, associated with insulin resistance and beta pancreatic cell damage, key events in development of type 2 diabetes mellitus. Lipotoxicity has been associated with cellular oxidative stress and beta-cell apoptosis. Caveolin-1 is a membrane protein that has been associated with many cellular functions as cell signalling regulation and apoptosis, and it is normally present in beta pancreatic cells. We previously reported that the expression of the membrane protein Caveolin-1 promotes free fatty acids-induced apoptosis in vitro in a mouse beta cell line; remains to be elucidated if this phenomenon is relevant in vivo.

Methods: We used C57BL6J mice lacking expression of Caveolin-1 (CAV-1 K.O. mice). We evaluated free fatty acids and triglycerides levels in blood in fasting conditions, oral glucose tolerance test (OTTG), carbonylated proteins in serum and C-peptide in wild type (WT) and Caveolin-1 K.O. and wild type mice exposed to a high fat diet for three months. Also, the presence of apoptosis was evaluated by TUNEL staining in beta pancreatic islets.

Results: The results indicated that we found that CAV-1 K.O. mice fed with high fat diet showed higher levels of triglycerides, cholesterol, free fatty acids and carbonylated proteins, although also a better response OGTT and C-peptide levels. Islets from K.O. mice showed lower levels of apoptosis.

Conclusion: Although K.O. mice showed a lipotoxic profile, our results suggest that their pancreatic islets were more resistant to the high fat diet deleterious effects over beta cells

Biography:

Kseniia Sokolova entered PhD student’s courses at Ural Federal University in 2016. She is a Junior Researcher at the Chair of Medicine Biochemistry and Biophysics of Ural State University and at the Laboratory of Biochemistry and Biophysics of Institute of Immunology and Physiology Ural Branch Russian Academy of Science. She is interested in Diabetes and Regeneration. Since 2016 she has published 14 papers and conference abstracts.

 

Abstract:

Introduction: Diabetes mellitus type 2 (DM2) is always accompanied by inflammation and destruction of β-cells. Cytokines, secreted by macrophages, are the main mediators of inflammatory and regenerative processes. In previous studies we demonstrated partial recovery of functional activity of β-cells at the injections of sodium phthalhydrazide, which changes macrophage phenotype M1→M2 and reduce inflammation.

Objective: The main objective of this study is the peculiarities of islet β-cells regeneration at DM2 and at modulation activity of macrophages.

Materials & Methods: Twenty (20) Wistar adult rats were divided into four groups: one –control; two and three – 30 and 60 days of streptozotocin/nicotinamide-induced diabetes correspondingly; four – 30 days of diabetes + injections of sodium phthalhydrazide. White blood parameters were evaluated on a hemoanalyzer. Cytokines were measured in blood and pancreas using ELISA method. Insulin+, KI67+cells were detected by immunohistochemistry. Detection of DNA fragmentation in apoptotic cells was made by TUNEL method kits.

Results: The results indicated that at the experimental diabetes quantity of white blood cells (WBC), lymphocytes and pro-inflammatory cytokines TNFα and Ifnγ in blood significantly increases. Concentration of anti-inflammatory TGFβ decreases both in blood and in pancreas. Sodium phthalhydrazide reduces quantity of WBC and lymphocytes and concentration of Ifnγ in blood and level of TNFα in pancreas. At 30th day of diabetes quantity of apoptotic β-cells increases and Ki67+β-cells are appeared. At sodium phthalhydrazide, quantity of Ki67+ β-cells increases significantly, while the quantity of apoptotic cells decreases. General and local inflammation at diabetes leads to the destructive-degenerative processes in pancreas, while modulation activity of macrophages, which reduces inflammation, intensifies islet regeneration.

 

Biography:

Angelo Michele Carella (MD) has completed his graduation in Medicine, after graduating he has obtained specialization in Internal Medicine, university Master in Healthcare Management and postgraduate courses on Diabetes and Obesity. He is a Medical Doctor at the Internal Medicine in the Department of "T. Masselli - Mascia" Hospital in San Severo (Italy). He was a past teacher in Health Professions degree course of Foggia University.And served as an Editorial Board Member/Reviewer of several scientific journals, author of about 50 scientific publications (Google Scholar h-index 5). He is a Member of D&CVD EASD Study Group, Investigator in clinical studies (DAVID, ESPORT, ATA-AF, DIAMOND) published in international journals, and Speaker at numerous scientific congresses and meetings. Rregistered in Google Scholar and Research Gate.

 

Abstract:

microRNAs (miRNAs), short noncoding RNA sequences, regulate several biological processes as cell differentiation, proliferation and development, cell-to-cell communication, cell metabolism and apoptosis. miRNAs seem also regulate insulin signaling, immune-mediated inflammation, adipokine expression, adipogenesis, lipid metabolism, and food intake. miRNAs may have a role in molecular mechanisms linked to cellular pathways of some diseases, as viral infections, cancer, diabetes, obesity and cardiovascular disease. Dysregulation of several miRNAs involves different aspects of diabetic disease: glycemic control, residual beta cell function, insulin secretion and sensitivity, micro- and macro-vascular complications as endothelial dysfunction, renal disease and retinopathy. The recent discovery of circulating miRNAs (c-miRNAs) easily detectable and measurable in plasma and other body fluids, led to the hypothesis of their potential role as disease indicators. Altered levels of several c-miRNAs were found to be linked to type 1 and type 2 diabetes, both at onset and in advanced disease. A lot of c-miRNAs are consistently dysregulated in diabetic patients and miR-126 was confirmed to be the most linked to pathways and development of type 1 and type 2 diabetes and their complications. Altered expression of other c-miRNAs correlates to obesity and its complications. Different levels of some c-miRNAs were found significantly associated with weight gain, but most of the data concern comorbidities and complications of obesity as insulin resistance, pre-diabetes, diabetes, dyslipidemia, adipogenesis dysregulation and inflammatory processes. Moreover, several evidences were obtained in obese children, in newborns and in maternal pre-gestational and gestational obesity. In particular the expression of some c-miRNAs differs in infants born to obese women compared with those born to lean women and these biomarkers might be useful in predicting future risk of obesity in children. At last, down-regulation of different c-miRNAs was observed in overweight/obese subjects after low or high glycemic index diet and after low-fat diet; c-miRNAs might also be potential novel biomarkers for the benefits of bariatric surgery and the effects of mild exercise. In conclusion, there are scientific evidences suggesting a potential role of c-miRNAs detection as diagnostic, prognostic and therapeutic biomarkers in obese and diabetic patients. Major limits: number, duration and sample size of clinical studies are small; source of c-miRNAs, extraction procedures, quantities of blood samples and methods of analysis were promiscuous and not well standardized; high costs required for c-miRNAs detection. The uncertainty observed in literature highlights the need for reproducible and well standardized methods as well as low-cost and wide availability assays to detect c-miRNAs with high sensitivity/specificity. Large, long-term and randomized controlled clinical studies are need to determine whether c-miRNAs can play a role as biomarkers for obesity and diabetes in daily clinical practice.

 

Biography:

Mukhlynina E A has completed her PhD from Ural Federal University. She is the Researcher of Institute of Immunology and Physiology, Laboratory of Morphology and Biochemistry. She has published more than seven papers in reputed journals. The field of her scientific interest belongs to connective tissue physiology and regeneration.

 

Abstract:

We have studied 2-aminopropylmorpholino-5-phenyl-6H-1, 3, 4-thiadisine dihydrobromide (L-14) and 2-morpholino-5-phenyl-6H-1, 3, 4-thiadiazine hydrobromide (L-17), which combine antioxidant and antiglycative properties. The absence of myelotoxic effect is required for antidiabetic agents. So the aim of this research is to reveal hematological changes in diabetes rats treated with L-14 and L-17. Forty (40) male Wistar rats were used in accordance with the ethical principles of the Directive 2010/63/EU, divided into four groups: control, alloxan diabetes (AD), alloxan diabetes plus L-14, alloxan diabetes plus L-17. Rats were given alloxan injections (100 mg/kg/day, i.p., three days) to induce type-1 diabetes. L-14 and L-17 was injected intramuscularly (40 mg/kg/day, simultaneously with alloxan, 12 injections for four weeks). Hematological analysis of peripheral blood was performed by hemoanalyser Celly70 (Biocode Hycel). Alloxan diabetes after 30 days leads to significantly increase of mean corpuscular hemoglobin concentration (MCHC), erythrocyte anisocytosis (RDW), neutrophilic leukopenia, low platelet count and mean platelet volume (MPV). L-14 reduces MCH, MCHC and WBC, but not the RDW-changes. L-14 also causes significant increase in platelet count in comparison to control rats and MPV-recovery. L-17-treatment leads to increase in hemoglobin, MCH, MPV and platelet distribution width. But MCHC and RDW return to the physiological norm. Neutrophilic leukopenia persists at the level of AD-group. We have not found any myelotoxic effects of L-14 and L-17. Some hematological changes of AD-rats were recovered by investigated compounds, so, L-14 and L-17 are promising for the metabolic correction in diabetic conditions. The study was supported by the Russian Science Foundation grant 16-15-0039-П

Biography:

Will Jervis has graduated in Medicine and Surgery from Newcastle University in 2017. He has recently completed his Foundation Training in East Yorkshire at Hull Royal Infirmary in 2019. During his foundation training he has worked in Diabetes and Endocrinology and developed a keen interest in Thyroid Disorders and Osteoporosis. Over the past year he has created and organized a regional teaching programme for medical students in association with Hull York Medical School and has a publication in BMJ case reports.

 

 

Abstract:

Denosumab is a monoclonal antibody that is approved in the United States and Europe for the treatment of osteoporosis. Denosumab is typically given every six months and there is no current requirement for monitoring or dose adjustment in renal impairment. We present a case of a patient with chronic kidney disease stage four who presented with a generalized tonic clonic seizure and prolonged QT secondary to severe hypocalcaemia (1.43 mmol/L) 13 days after receiving a single dose of denosumab as treatment for osteoporosis. The patient was therefore commenced on an intravenous calcium infusion, which restored her calcium to near normal range and she had no further seizure activity. This report highlights the severe hypocalcaemia that can develop from a single dose of denosumab. We recommend that further monitoring of eGFR/serum calcium/vitamin D is required prior and post dosing of denosumab to help immediately recognize and treat life-threatening hypocalcaemia following denosumab administration.

 

Biography:

Kamila Szymanska is a third year PhD student in the Department of Biochemistry and Molecular Biology at Medical University of Lublin. Her project under the supervision of Prof. Adolfo Rivero-Müller is aimed to create a molecular characterization of gonadotropins and gonadotropin receptors. She has published 12 papers, in which she is either an author or co-author, she took part in more than 15 conferences and received many scholarships for her scientific achievements. Furthermore, she is a Principal Investigator of pre-doctoral grant PRELUDIUM funded by National Science Centre in Poland

Abstract:

Three novel compound heterozygous mutations in LHCGR gene were identified in male patient with disorder of sex development (DSD). Two of these mutations, p.L16Q missense mutation and a deletion p.K12_L15del were of paternal origin, whereas the third of the mutations was a duplication p.L10_Q17dup of maternal origin. In order to understand the effect of these mutations on the phenotype observed in the patient, a number of molecular studies were carried out. First, we separated the missense mutation from p.K12_L15del and p.L10_Q17dup mutations, so we could study them separately. Analyses include the measurement of the membrane expression of the receptors, gene and protein expression, measurement of cAMP production and investigation of its cellular localization and transport. The results of the study revealed that the surface expression of mutants was decreased as compared to the WT LHCGR. Confocal microscopy showed intracellular expression of p.L10_Q17dup and p.L16Q mutations, whereas the intracellular expression of p.K12_L15del was negligible. The cAMP production was significantly lower in the case of p.L10_Q17dup mutant as compared to the WT LHCGR stimulation. The cAMP production of p.L16Q was 2.4 times lower, whereas p.K12_L15del did not show any response upon stimulation. Furthermore, both mRNA and protein expression of all three mutant receptors was decreased. We present here three novel mutations that lead to complete inactivation of LHCGR. Duplication mutant is most likely being degraded within the endoplasmic reticulum, p.K12_L15del results in mRNA degradation, whereas the expression of p.L16Q receptor is associated with decreased membrane expression of the receptor