3rd International Conference on Endocrinology November 02-04, 2015 Atlanta, Georgia, USA

Biography:

Dr. Yali Zhao received her M.D and Ph.D in China, undertook her post-doc training in neuroscience at Clinical Research Institute of Montreal in Canada. Her research is focused on neural circuits and synaptic plasticity in memory and reproduction. She currently serves as a research scientist in the Department of Physiology at the David Geffen School of Medicine at UCLA studying the development and plasticity of the gonadotropin-releasing-hormone neuronal system in zebrafish. She has published over 20 articles in peer-reviewed journals and also served as reviewer for numerous journals.

Abstract:

Understanding the biology of the gonadotropin-releasing hormone (GnRH) neuronal system is the key towards understanding the mechanism of central control of reproduction. In zebrafish, two forms of GnRH have been identified: GnRH2 and GnRH3. Here we have generated a transgenic zebrafish model system in which the GnRH3 promoter drove the expression of a bright variant of the green fluorescent protein (GnRH3:EMD).The unprecedented sensitivity allowed us to detect and image GnRH3 neurons dynamically during early embryogenesis in the transparent embryo. Using time-lapse confocal imaging to monitor the time course of the GnRH3:EMD expression in vivo, we described multiple populations of GnRH3:EMD neurons with details of emergence, development and interaction, including in the terminal nerve (TN) associated with the olfactory region, hypothalamus (HYPO), preoptic area (POA), and trigeminal ganglion (TG). Immunohistochemistry of synaptic vesicle protein 2 (SV2) suggests that the potential for synaptic transmission is occurring during early development of the GnRH3 neural network. Further, we successfully recorded electrical activity from TN-GnRH3 neurons in live embryos as early as 48 hours post fertilization. We found that neuron maturation was related to the pattern of the electrical activity. Kisspeptin is a neuropeptide essential for pubertal maturation and fertility. With the combination of electrophysiology and confocal imaging analysis, we further explored the effect of kisspeptin on the morphological and electrophysiological development of the GnRH3 neuronal system. Our findings suggest that kisspeptin regulates both the morphology and electrical activity of multiple populations of GnRH neurons within a complex neural network during zebrafish embryogenesis.

Biography:

Cédric Zimmer completed his PhD in 2010 at Strasbourg University in France. He is currently a research fellow at the School of Psychology and Neuroscience of the Univserity of St Andrews. He is mainly interested by the consequences of stress in animal models and particularly on the long-term effects of early life stress on brain, physiology and behaviour. He has published several papers in reputed journals. (Up to 100 words) Karen Spencer is currently a Lecturer within the School of Psychology and Neuroscience of the Univserity of St Andrews. Prior to this she held a BBSRC David Phillips Research Fellowship between 2007- 2014 at the Univresities of Glasgow and St Andrews. Karen is mainly interested in how early life experiences can shape long-term phenotypic traits, using an integrative approach which spans behaviour, physiology and neuroendocrinology. Karen currently leads the Mechanismsm of Behaviour research group (MoB url: https://mobgroup.wp.st-andrews.ac.uk/), which consisits of two postdoctoral fellows, five PhD students and a full time Technician.

Abstract:

Stress exposure during early-life is usually associated with detrimental effects on health and wellbeing. The hypothalamic-pituitary-adrenal (HPA) axis is one of the primary targets of this programming, which generally results in a hyperactive HPA axis and increased levels of anxious behaviours. Most research focused on these harmful effects. However, the environmental-matching hypothesis proposes that developmental stress programs physiology and behaviour in an adaptive way that can enhance fitness if early environments match those experienced later in life. We tested the potential beneficial effects that stress experienced during pre-natal development may have on adults at the neuroendocrine and behavioural level. We determined the effects of exposure to increased corticosterone during pre-natal development over two generations by quantifying: glucocorticoid (GR) and the mineralocorticoid (MR) receptor mRNA expression in the hippocampus, hypothalamus and pituitary gland; the acute CORT stress response and exploration in a stressful novel environment. We showed that pre-natal stress modified GR and MR expression in accordance with a more efficient negative-feedback within the HPA axis resulting in an attenuated stress response. In return these physiological responses mediated increased activity levels and exploration in a novel environment. This phenotype programmed by pre-natal stress was transmitted to offspring independently of their own developmental experience. Pre-natal stress could therefore program phenotypes in a way that may increase fitness when early and later environmental conditions match. This phenotype can also be transmitted to the next generation which may enhance offspring capacity to cope with stressful conditions.

Biography:

Andrew C. Shin received PhD in Neuroscience at Michigan State University in 2008. Thereafter, he worked as a postdoctoral fellow at Pennington Biomedical Research Center and at Icahn School of Medicine at Mount Sinai. He was promoted to a junior faculty at Mount Sinai in 2013. Dr. Shin is mainly interested in studying how brain controls acute nutrient metabolism as well as long-term energy homeostasis using genetic, molecular, surgical, and integrative physiological approaches. He has published more than 25 papers in peer-reviewed journals like Cell Metabolism, Endocrinology, Neuroscience, and International Journal of Obesity.

Abstract:

Circulating branched-chain amino acid (BCAA) levels are elevated in obese and diabetic individuals, and are the earliest and most predictive marker for risk of diabetes. Furthermore, supplementation of amino acids or BCAAs has been shown to induce insulin resistance in rodents and humans, implicating BCAAs in the pathogenesis of diabetes. Thus, identifying the regulatory mechanisms of BCAAs is critical for understanding their rise seen in obese and/or diabetes. We have shown that insulin dose-dependently lowers plasma BCAAs while glucose per se does not seem to be an important regulator of BCAA metabolism. Insulin induced the hepatic expression and activity of branched-chain α keto-acid dehydrogenase (BCKDH), the rate-limiting enzyme in BCAA degradation pathway. Selective induction of hypothalamic insulin signaling in rats as well as inducible and lifelong genetic modulation of brain insulin receptors in mice demonstrated that brain insulin signaling is a major regulator of BCAA metabolism by inducing hepatic BCKDH. Further, short-term overfeeding impaired the ability of brain insulin to lower circulating BCAA levels in rats. Chronic high-fat feeding in non-human primates and obesity and/or diabetes in humans were associated with reduced hepatic BCKDH protein expression. Lastly, C. elegans that lack insulin receptor homologue (Daf-2) in neurons showed increased BCAAs. These findings demonstrate that neuroendocrine pathways control BCAA homeostasis and these are evolutionarily conserved from worms to mammals. The findings also suggest that hypothalamic insulin resistance may account for impaired BCAA metabolism in obesity and diabetes, and that plasma BCAAs may be a marker for hypothalamic insulin action.

Biography:

Dr. Sasha Shafikhani has completed his PhD from University of California at Berkeley and postdoctoral studies from University of California at San Francisco. He has published more than 22 papers in reputed journals and has been serving as an editorial board member of several reputed journals. As a cellular microbiologist, Dr. Shafikhani focuses his research on immune dysregulation that renders diabetic wound vulnerable to infection and microbiome shift toward pathogenic bacteria. He also studies the virulence strategies that pathogenic bacteria use to drive a diabetic wound toward non-healing chronic state.

Abstract:

Diabetic foot ulcers are the leading cause of lower extremity amputations in the US and are responsible for more hospitalizations than any other complication of diabetes. The sheer number of diabetic ulcers that progress to amputation underscores the inadequacy of conventional therapies and the need for novel approaches. Bacterial infection and hyper-inflammation are two major comorbidities associated with impaired healing in diabetic chronic ulcers. However, the mechanism(s) underlying these effects remain poorly understood. Most studies have focused on old chronic diabetic wounds and found these ulcers to be infected and locked in a hyper-inflammatory mode. However, very little is known about the dynamics of inflammatory responses and infection control early after injury in diabetic wound. We have used a well-established wound model for type II diabetes, (db/db mouse and their normal littermates, C57BL/6), to study the early dynamics of bacterial infection control in diabetic and normal wound tissues. Our data demonstrate that diabetic skin harbors a significantly higher number of bacteria prior to injury and is severely defective in preventing bacterial colonization in a manner that is independent of its initial high bacterial loads. Surprisingly, we have found that unlike chronic diabetic ulcers which are known to be in a persistent inflammatory state, the acute phase of inflammation, which is needed to counter invading pathogens, is significantly delayed in diabetic wounds early after injury. This delay in inflammatory responses is partly due to reduced chemokine expression and partly due to impaired chemotactic response in diabetic leukocytes during the acute phase of healing early after injury. Our data indicate that reduced inflammatory responses early after injury in diabetic wounds is just as harmful as the persistent and hyper-inflammatory state that dominates diabetic wounds as they become chronic. Importantly, onetime treatment with a pro-inflammatory chemokine, CCL2, was able to jumpstart inflammatory response and significantly stimulated wound healing. Chemokine based therapy may offer an alternative approach to stimulate wound healing in diabetic ulcers.

Biography:

Mary Cataletto M.D. is Professor of Clinical Pediatrics at SUNY at Stony Brook and member of the clinical staff at the Prader Willi Center at Winthrop University Hospital in Mineola, New York. She serves as a member of the scientific advisory committee for the Prader-Willi Association USA and has presented at regional, national and international meetings on the topic of sleep and breathing in Prader-Willi syndrome. Dr. Cataletto is editor in chief of Pediatric Allergy, Immunology and Pulmonology, an international and peer reviewed publication of the Mary Anne Liebert Publishers , Inc.

Abstract:

Prader-Willi Syndrome Center at Winthrop University Hospital, Mineola, N.Y. Prader-Will syndrome is a complex, multisystem genetic disorder caused by lack of expression of genes located on the paternally inherited chromosome 15q11.2-q13 region. The phenotype is likely due to hypothalamic dysfunction which is responsible for hyperphagia, temperature instability and multiple endocrine abnormalities including growth hormone and thyroid stimulating hormone deficiencies. Hypersomnolence is an important feature of Prader Willi syndrome, reported in 70 to 100 % of adults with PWS and has been a major focus of clinical research over the past ten years. This presentation will update practitioners on clinical issues surrounding hypersomnolence, sleep disordered breathing and daytime function in individuals with Prader-Willi syndrome.

Biography:

Irma Zamora-Ginez; MA and PhD in Biochemistry and Molecular Biology, she is originally from the city of Puebla, México; She is graduate of the Faculty of Medicine and Pharmacobyology Chemystry. She is currently coordinator of the Master of Medical and Research and she is member of Nacional System of Research. Her career has focused largely on the research of pathophysiology, genetics and risk factors of diseases affecting Mexican society, such as type 2 diabetes and cardiovascular disease.

Abstract:

Recently the association of genetic polymorphisms with different diseases has highlighted the importance in the presentation, evolution and prognosis of chronic degenerative diseases, making it a priority to assess the genetic diversity of specific populations. Mexico has a population of extraordinary genetic diversity, which results in populations with a different genetic background; this has not only historical, but also medical importance, because this diversity can affect characteristics of clinical interest and propensity to many diseases. Several studies have reported that type 2 diabetes is a chronic degenerative disease whose presentation is due to different risk factors, with a pathophysiology associated with low-intensity chronic inflammation; however this association depending on polymorphism of proinflammatory cytokines. In this context, our study group has studied the association of -598, -572 and -174 IL-6 polymorphism with the risk of developing diabetes, concluding that in subjects from central Mexico were not found all haplotypes and those associated with a lower risk for diabetes are at lower prevalence. On the other hand, the major complication of diabetes is cardiovascular disease due among others to the presence of oxidative stress, we have recently reported that GPx3 is increased in obese subjects and in subjects with metabolic syndrome, moreover the rs8177409 polymorphism is associated with increased cardiovascular risk measured by Triglyceride/HDL-C index. Currently our study group is conducting studies to determine if the presence of genetic polymorphism of IL6 and GPx3 influence the response of subjects to preventive advice on the risk of developing diabetes and cardiovascular disease.

Biography:

Marco Antônio Peliky Fontes has completed his PhD at the age of 32 years from Federal University of Minas (UFMG), Brazil and Post Doctoral studies from University of Sydney, Australia. He is Associate Professor in the Dept. of Physiology and Biophysics at the UFMG. He has published more than 50 papers in reputed Physiology and Neuroscience journals. Member of the American Physiological Society and INCT Nanobiofar / Brazil. The central area of his research is Cardiovascular Neuroscience with focus in circuits involved in the cardiovascular response to emotional stress and the central contribution of peptides for cardiovascular control.

Abstract:

Maintenance of homeostasis depends upon mechanisms controlling autonomic output. Sympathetic output depends on neuronal activity from different brain regions. Central requirement for changes in sympathetic output must be adjusted to the input signals from neural and humoral factors for an optimum cardiovascular performance. Consequently, abnormal inputs to one or more brain regions involved in the sympathetic control can lead to cardiovascular disease. Contributing factors may involve; abnormal feedforward and feedback mechanisms and altered humoral factors including angiotensinergic and leptinergic inputs. The dorsomedial hypothalamus is a key central region for the control of sympathetic outflow to the cardiovascular system. Recently, the descending sympathetic pathways from dorsomedial hypothalamus have been revealed. Reviewing the descending pathways from dorsomedial hypothalamus we discuss the interactions between mechanisms controlling the sympathetic output to the cardiovascular system and the possible implications in cardiovascular disease. Support: CNPq, FAPEMIG, CAPES.

Biography:

Matteo MARIANO has completed his PhD at the age of 25 years from BOLOGNA University School of Medicine; Specialist in Pediatrics and Pediatric Endocrinology to IRCSS GASLINI hospital Genoa University Specialist in Gastroenterology to L’Aquila University. Partner SIEDP (Italian Society of Pediatric Endocrinology and Diabetology)Partner SIGENP (Italian Society of Pediatric Gastroenterology Hepatology and Nutrition)

Abstract:

The craniopharyngioma and hypothalamic hamartoma are two tumors location in the brain (above)saddle and hypotalamus, with a histologically benign but uncertain behavior. Aim of the study: to value auxo-endocrinological changes to the diagnosis and after surgical and/or medical treatments. Matherial and method: mean of follow-up 7.0±5.2 years. Were studied 25 babies with craniopharyngioma and 1 baby with hypothalamic Hamartoma. For each subject, at diagnosis and during follow-up were detected at least once a year: Height (H),Weight (W) Pubertal development (In females: breast (B), Pubic Hair (PH), Menarche ; in the male: Genital (G), Pubic Hair (PH), Vol.Testicolare). H and W were evaluated by the standards of Tanner et al.; mass index (BMI) was evaluated with the standards of Rolland- Cacher etal. pubertal development was assessed by the standards of Marshalland Tanner. Endocrine features: baseline and / or after stimulation of GH, IGF-I, TSH, FT4, PRL, ACTH, cortisol, DEAS, insulin, E2, T, LH and FSH in pubertal Serum electrolytes, plasma osmolality and urinary. Conclusion: despite adequate replacement therapy, children with craniopharyngioma leave open several issues: High incidence of short stature 2DS (6 / 25 cases) High incidence of obesity (15/25 cases) Marked hyperphagia (binge eating) with difficulty in controlling appetite Increased behavioral disorders and psychosocial. The baby with hypothalamic hamartoma showed only hyperactivity during follow-up.

Biography:

Abraham Haim has his PhD in environmental physiology from the Hebrew University of Jerusalem and post-doc, the MRI University of Pretoria South Africa, Zoologist, Eco-physiologist and Chronobiologist. Since 1976 he is a faculty member at the University of Haifa and since 1996 a full professor. Was chair person of several departments, between the years 2002-2008, dean of natural- sciences faculty. Published over 170 papers in pre-reviewed journal and two years ago together with professor Portnov published a book entitled: Light Pollution as a New Risk Factor for Human breast and Prostate Cancers, by Springer. Supervised many M.Sc. and Ph.D. students.

Abstract:

Disappearance of dark nights is the most dramatic change that took place on our plant throughout the 20th century emerging from electrical illumination. The out-come is noted in great changes taking place in human lifestyle as activity extending to 24h/day, seven days a week. No doubt this has a positive effect on our economy and social activity but, what about the environment and our health? We have been studying the effects of Artificial Light at Night (ALAN) on the circadian system, production and secretion of pineal hormone melatonin (MLT), known as a "jack of all traits" among others as an antioxidant, anti-ageing and anti-oncogenic agent. MLT-suppression is wavelength depended where short wavelength illumination (SWI) is effective in MLT-suppression and among SWI natural light emitting diode (LED) has the greatest MLT-suppression. Epigenetically modifications as global DNA Methylation (GDM) are an expression to environmental changes. Results of studies carried out in our center revealed that exposure to ALAN caused GDM-reduction in cells from different organs this hypo-methylation was emerged presumably from MLT-suppression. However, addition of MLT in drinking water during the dark-period reversed the process and GDM level increased. These results support the idea that hormones, in our case MLT, are important mediators between the environment and epigenetically modifications.

Biography:

Beatriz is doing her PhD at the Hospital Irmandade Santa Casa de São Paulo, in Brazil, and will do part of her research at Joslin Center Diabetes. She is endocrinologist at Hospital Samaritano, researcher at Endoclinica, and have been presented a few paper at many congress, as well as having been awarded.

Abstract:

The hospital hyperglycemia is a frequent event initiated in patients with and without diabetes. The glycated hemoglobin (HbA1c), provides differentiation between hyperglycemia caused due glycemic variability secondary to other factors of hospitalization or diabetes mellitus without previous diagnosis. Thus, because of the deleterious effects triggered by hyperglycemia, justifies our interest in evaluating the HbA1c and its relationship to clinical outcome of patients admitted, either with or without diagnosis of DM. Objective: To use the HbA1c as a diagnostic and predictive tool outcome of patients with and without diagnosis of diabetes mellitus, performed during hospital stay and its relationship with the hospital complications. Method: Analysis of 100 patients with HbA1c hospital hyperglycemia hospitalized for other clinical disorders. According to the American Diabetes Association (ADA) as defined hyperglycemia hospital blood glucose levels above 140 mg / dl. Used HPLC method, employed by Fleury, with certificate from The National Glycohemoglobin Standardization Program. Was considered statistically significant at p <0.05. Results: There were 100 patients with mean age of 63.15 years, and 75% had previous diagnosis of DM, and 25% with hyperglycemia, but no previous diagnosis, 52% were diagnosed with DM. Patients without prior diagnosis of DM had HbA1c between 5.8% and 7.5%, with the median length of stay of nine days without complications. Patients with DM who developed complications had HbA1c between 7.3% and 12.4% and accounted for 20% of the study, with hospital stay of 34.5 days. DM patients without complications had HbA1c between 5.9% and 11.5% with length of stay of 11.12 days. Complications included pulmonary infections (50%), septic shock (15%), skin infection (15%), urinary tract infection (10%), kidney (10%). Discussion: Our study demonstrated that the HbA1c was increased in proportion to the increase in complications independent of hospital pathology associated with the patient. The deleterious effects of hyperglycemia and healing compromised immunity, increased oxidative stress, endothelial dysfunction, increase in pro-inflammatory and pro-thrombotic factors, enhanced mitogenesis, electrolyte changes, and potential exacerbation of myocardial and cerebral ischaemia, thus providing the increase of these complications. Conclusion: The analysis of HbA1c is presented as an important parameter to evaluate the length of stay and the risk of hospital complications independent of the patient's pathology.

Biography:

Dr. Laxmi S. Inamdar obtained her M.Sc. and Ph.D. degree in Zoology from Karnatak University, Dharwad. Currently, she is Professor and Chairperson of Zoology Department. Her areas of research interest include Endocrinology, Reproduction and Development principally focusing on the sex determination and differentiation. Her group is the first one to show a novel FMFM pattern of temperature dependent-sex determination in the developing embryos of a reptile, Calotes versicolor (Daud.). Currently, her research group is concentrating on: 1) Endocrine and Molecular mechanism of sex determination and differentiation, 2) Wnt signalling during early embryonic development in mouse Mus musculus, 3) Biochemical and Pharmacological Impact of Anabolic - Androgenic Steroids. She has been INSA visiting Scientist to Indian Institute of Science twice. She has published 21 papers in international journals of repute. She has received grants from UGC and DAE, India. She is life member for several scientific bodies. She is the recipient of Best Research Publication Award (2012-13).

Abstract:

In vertebrates, the offspring sex is known to be influenced by a variety of sex-determining mechanisms (SDMs). In birds and mammals, sex is determined at fertilization of zygotes by sex chromosome composition, known as genotypic sex determination (GSD). In some species the gender is dependent on environmental cues, predominantly temperature, often called temperature-dependent sex determination (TSD) as reported in fish, amphibians and reptiles. In reptiles with TSD, temperature initiates a cascade of events, involving steroid hormones and culminating in sex determination. How does TSD differ from GSD? It is proposed that sex steroids are the main factor and there is evidence to support that endogenous E2 levels are influencing gene expression in the developing gonad and consequently, sex determination, by up-regulating SF-1 and aromatase expression in the female gonad while decreasing it in the male gonad. Nevertheless, the key role of aromatase and estrogen in the early steps of ovarian differentiation is still controversial in many reptilian species. The Indian garden lizard, Calotes versicolor that lacks heteromorphic sex chromosomes is an excellent model to study the molecular cascades of sex differentiation pathway which exhibits a unique pattern of TSD. The novel sex-determining pattern that we have reported for the first time in this lizard, neither compares to Pattern I [Ia (MF) and Ib (FM)] nor to Pattern II (FMF) and we refer to it as FMFM pattern of TSD. This pattern is likely to have an adaptive significance in maintaining the sex ratio in C. versicolor with increasing global warming. The gonadal expression of ER-α and aromatase enzyme (CYP 19A1) in embryos of this species revealed two protein bands with apparent molecular weight of ~55 kDa and ~45 kDa for ER-α and 58 kDa for aromatase in the total protein extracts of adrenal-kidney-gonadal (AKG) complex suggesting the occurrence of isoforms of ER-α. The increase in expression of ER-α variants and aromatase enzyme during later stages of development divulge responsiveness of AKG to estrogen suggesting the up regulation of estrogen. Further, the apparent surge in endogenous estradiol coincides with the first indication of gonadal sex differentiation at FPT and reveals that estrogen signalling is crucial for sexual differentiation of gonad in this lizard, thereby suggesting the synergistic action of incubation temperature as well as steroid hormones.

Biography:

Professor Aasem Saif has got his PhD from Cairo University. He completed his postgraduate training as a Clinical Fellow at the Royal Hallamshire Hospital, Sheffield University (UK), before obtaining his MRCP. He is a member of the European Society of Endocrinology (ESE), European Association for the Study of Diabetes (EASD) and American Diabetes Association (ADA). He currently works as a Professor of Internal Medicine and Endocrinology at Cairo University. He is also a Fellow of the Royal College of Physicians of Edinburgh (FRCPE). He has many international publications in addition to his contribution as an investigator in clinical trials.

Abstract:

Adiponectin is known to be associated with anti-atherosclerotic mechanisms. Carotid intima-media thickness (IMT) has been shown to correlate well with general atherosclerotic status. It also reflects the cardiovascular risk in type 2 diabetes. Plasma adiponectin levels were found to be lower in patients with atherosclerotic arterial disease. Decreased plasma adiponectin levels have also been reported in type 2 diabetes and were inversely related to insulin resistance. Some studies have also reported a negatively-significant correlation between adiponectin and carotid IMT, as a marker of atherosclerosis, in patients with type 2 diabetes and suggested that increased carotid IMT in those patients may, in part, be explained by lower plasma adiponectin. But these studies included obese and non-obese patients in the study group and it is not clear to what extent the relationship between plasma adiponectin and carotid IMT could be explained by other risk factors associated with obesity and metabolic syndrome. A group of 112 non-obese Egyptian patients with type 2 diabetes in addition to 40 age, sex and weight matched normal Egyptian subjects had assessment of their plasma adiponectin and carotid IMT. A non-significant inverse correlation was found between plasma adiponectin and carotid IMT in the study group. Multiple regression analysis revealed that plasma adiponectin was not a determinant of carotid IMT in those patients. These results point to the fact that the previously-reported inverse relation between plasma adiponectin and carotid IMT in type 2 diabetes could be explained, at least partially, by obesity.

Biography:

Robert A.A has published more than 50 research papers in the national and international peer reviewed journals. Currently, working as a Clinical Researcher at Endocrinology and Diabetes Department, Diabetes Treatment Center, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.

Abstract:

It is well established that diabetes mellitus is associated with high early mortality, morbidity, vascular complications, and loss of health-related quality of life. In Saudi Arabia, it is emerging as an epidemic of massive proportions, threatening to negate the benefits of modernization and economic revival. According to a recent World Health Organization report, Saudi Arabia has the second highest rate of diabetes in the Middle East region and is seventh highest in the world. The projected number of people living with diabetes in Saudi Arabia is about 7 million, and nearly 3 million people have pre-diabetes, leading to a public health problem. On the other hand, more worrying perhaps, is the rising trend of diabetes observed in Saudi Arabia over recent years, and diabetes has seen an almost 10-fold increase over the past three decades. In addition, Saudi Arabia faces a number of challenges in diabetes management, including rising prevalence, lifestyle transition, delayed diagnosis, lack of awareness, and high cost of treatment. According to earlier studies from Saudi Arabia, many young adults are diagnosed with the devastating disease; therefore, it is recommended that every Saudi aged 30 years or more should be screened for both type 2 diabetes and pre-diabetes to comprise the disease. It is clear that the burden diabetes mellitus will have on Saudi Arabia is likely to increase to tragic levels unless a comprehensive epidemic control program/multidisciplinary approach is rigorously executed. Such an approach would include promoting healthy diet, exercise, and active lifestyles as well as curbing obesity. Also, a national prevention program which will screen for diabetes and address the modifiable risk factors at the community level, focusing on high-risk groups, needs to be executed as early as possible.

Biography:

Riyaz Mohammed has completed his post graduation in Internal medicine from Prestigious Deccan College of Medical College and then did his masters in Endocrinology from Texilla American University and Dip in Endocrinology from University of South Wales ,UK . He is the director of Esani Diabetes and Mutlispeciality Research Centre in India. At the young age he was heading the department of medicine and endocrinology at Basvatarakam Indo American Hospital. He has published more than 30 papers in reputed journals and has more than20 oral presentations as speaker to his credit. He has been serving as an editorial board member of repute as Reviewer for Journal of Evidence based Medicine & Health care and Journal of Evolution of Medical and Dental Sciences.

Abstract:

The increased prevalence of type 2 diabetes mellitus is a major concern for the health providers. We have done an observation study in the diagnosed IGT patient who received α-glucosidase inhibitor (voglibose), which could prevent the development of type 2 diabetes in high-risk individuals.

Methods: This study was an observational study comprising of voglibose and placebo in individuals with impaired glucose tolerance.60 eligible patients were on the standard diet and taking regular exercise with impaired glucose tolerance were randomly assigned to oral voglibose 0.2 mg three times a day (n=60) or placebo (n=50) in this study. Treatment was continued until participants developed type 2 diabetes (primary endpoint) or normoglycaemia (secondary endpoint). In the final analysis, 60 registered individuals fulfilled the inclusion criteria: 36 were randomly assigned to receive voglibose and 24 placebos (two participants in the placebo group did not take their medication and were excluded). The mean duration of treatment was 48•4 weeks (SD 36•5)—i.e., 45•3 weeks (34•6) for voglibose and 51•6 weeks (37•5) for placebo.

Conclusion: Voglibose, in addition to lifestyle modification, can reduce the development of type 2 diabetes in high risk individuals with impaired glucose tolerance.

Biography:

Miguel Escalante has completed his PhD at the age of 25 years from Universidad de Guadalajara and specialized studies from Universidad Nacional Autonoma de Mexico School of Medicine. Head On the Departament of Endocrinology, in the Natonal West Medical Center of Mexican Institute of Social Security He is the director of Endo-Clinic, an organization for private practice and research protocols. He has published more than 28 Indexed Publications an 12 book chapters, 285 citations to their publications.

Abstract:

Diabetes Prevention Programs have been implemented in our country's health institutions, including by Mexican Institute of Social Security (IMSS); These programs are intended to reduce the incidence of new cases of Diabetes Mellitus, through the promotion of a healthy lifestyle , including maintaining a healthy weight, food intake caring and encouraging physical activity in the general population. On the Mexican Institute of Social Security, and other health institutions the prevalence and incidence of Diabetes Mellitus is monitored, as well as Diabetes complication

Biography:

Roberta Modica is specialist in Endocrinology and at present works at Federico II University in Naples.

Abstract:

Ectopic ACTH syndrome (EAS) is commonly caused by bronchial carcinoid tumors, whose detection can be challenging. Hypercortisolism requires rapidly effective medical therapy to avoid severe complications. We report a case of a 65-year-old woman with EAS due to an ACTH-secreting typical lung carcinoid, successfully and rapidly managed with cabergoline (CAB) and octreotide (OCT) before surgery. She presented with rapidly worsening Cushing’s syndrome and laboratory findings consistent with EAS. Initially the ACTH source was not localized, thereby acute tests with OCT (100 μg subcutaneous, 150 min) and CAB (1 mg oral, 6 h) were performed. Based on the significant reduction of ACTH and cortisol obtained with both tests, a combined medical treatment with OCT (0.05 mg/8 h) and CAB (0.5 mg three times/week) was started. Only 2 weeks after, biochemical data normalized together with cushingoid features. After the rapid fall of cortisol levels, severe urticaria occurred, thus OCT and CAB were withdrawn. Two weeks later urticaria improved but ACTH and cortisol levels increased again. Therefore CAB only was started again (0.5 mg/week), allowing restoration of normal cortisol levels. One month later, a contrast enhanced chest CT scan revealed a left lung nodule and a low-grade neuroendocrine tumor was removed (15 mm, pT1N0). Low doses of CAB and OCT showed a rapid onset of action with long-lasting effect both on clinical and biochemical parameters without any side effect and without recurrence. In summary, CAB and OCT, in mono- or combined therapy, are a safe and effective approach in EAS before surgery.

Biography:

Dr Rajiv Kumar Jaiswal has completed his post graduation in Internal medicine from St. Petersburg State Medical Academy and then to Pursue Pain Management he had completed his Post Graduation Diploma in Anaesthesiology. He is working as a HOD Pain clinic in Esani Diabetes and Mutlispeciality Research Centre in India. He has published more than 10 papers in reputed journals.

Abstract:

Diabetes mellitus is not only characterized by hyperglycemia but it is a clinical syndrome associated with hyperglycemia, which may lead to chronic debilitating problem such as peripheral neuropathy (PN). This review was done to emphasise the importance of diagnosing PN in a clinical setting as PN is characterised by pain and discomfort in lower extremities, loss or absence of protective sensations in the lower limbs which can lead to balance problems, and these patients are at risk of foot ulcerations, and a reduced quality of life in adults with type 2 diabetes. Several methods are available for the evaluation of both subjective and objective measures of peripheral nerve functions. Vileikyte et al. designed a specific scale for neuropathic patients in especially Type 2 diabetes with an aim to measure the problems of foot and its impact of DPN on quality of life. Nabuurs- Franssen et al., in 2005 has described that patients with healed ulcers had a better quality of life than patients with persisting ulcers It is of utmost importance to understand that evaluating PN as a routine practice in a simple way may also play a vitally important role in preventing foot ulcers or fall-related morbidity and mortality in adults with type 2 diabetes. At present there is a need for a trial to address the current situation of DPN in India, where the quality of life of patients with DPN in/or response to a therapy remains to be evaluated.

Biography:

Amal zaghloul Moustafa is working as a professor in clinical pathology hematology, Umm Al-Qura University

Abstract:

Background and objective: Endothelial dysfunction in diabetes mellitus (DM) is an important factor in the pathogenesis of micro and macrovascular complications. We aimed to measure soluble endothelial protein C receptor (sEPCR) and high sensitivity C reactive protein (hsCRP) levels as markers of endothelial damage in both types of diabetes mellitus and to determine if they can be used as predictors of vascular complications. Methods: Fifty patients with DM, 20 with type 1 and 30 with type 2 as well as 30 healthy subjects were included. All were subjected to measurement of sEPCR and hsCRP by enzyme linked immunosorbent assay. Results: sEPCR and hsCRP were significantly increased when compared to the control group in both types of DM. sEPCR was a significant predictor of macrovascular complications and thrombosis in type 1 p = 0.02, and p = 0.015, respectively. hsCRP was a significant predictor of macrovascular complications in type 2 p = 0.04. Conclusion: Patients with type 1 and type 2 DM exhibit higher sEPCR and hsCRP levels compared to healthy controls which suggesting endothelial damage. sEPCR could be used as a predictor of macrovascular complications and thrombosis in type 1 DM, whereas, hsCRP might be used as a predictor of macrovascular complications in type 2 DM.

Biography:

Domenico Tavella was graduated in Cardiology at the Verona University in the 2000th. His fields of interest have always been Interventional Cardiology, Acute Coronary Care, Diabetic Coronary Artery Disease and Contrast Induced Nepropathy. Master II Level in Advanced Acute Cardiac Care Therapy at Florence University. Post-Doctoral in Amsterdam on functional evaluation of coronary stenosis, Transradial percutaneous procedures and percutaneous treatment of small coronary vessels. Member of ACCA and EAPCI, Editorial Board Member in Italian and International journals, he has published several papers in reputed journals and has participated as Spiker and Chairman to several Italian and International meeting.

Abstract:

It is well known that Diabetes Mellitus (DM) is the most powerful risk factor for Coronary Artery Disease (CAD). More than half the mortality and a vast amount of morbidity in people with DM is related to CAD. A quarter of myocardial revascularization procedures are performed in patients with DM. There are wide differences in the prevalence of CAD in patients with type 1 or 2 diabetes, being more represented in the second both in terms of incidence and severity of coronary involvement and worse intra/extra-hospital prognosis. 38yo-female, type1-diabetic in insulinic-therapy since the age of 8 years was admitted to our institution for a recurrent chest pain. Poor glycaemic control (fasting glucose 158 mg/dL; HbA1c 9.8%), extensive organ damage (already known peripheral vascular disease 5 years ago, severe hypertensive retinopathy 10 years ago treated by Laser-Therapy with current proliferative evolution, EPH-Gestosis), normal kidney function (Creatinin 1,07 mg/dL; GFR 56 ml/min/1.73m2) was evident. Treadmill Test was negative at 90%. CA-MSCT “unexpectedly” showed severe and extensive multifocal coronary disease on both very small LAD and RCA, confirmed by coronary angiography (CA) with successive PCI/DES on LAD and RCA, starting long ASA/Clopidogrel therapy. 3-months CA showed excellent result on LAD and tight intrastent re-stenosis on RCA with distal disease progression, treated by DEB intrastent and DES on distal. The therapy was shifted from ASA/Clopidrogrel to ASA/Prasugrel. While i’m writing, after 14 months since last procedure, the patient, asymptomatic and cardiac event-free, is admitted for temporal stroke and severe kidney failure bringing to dialysis.

Biography:

Ayman A. Al Hayek is working in the Department of Endocrinology and Diabetes, Diabetes Treatment Center, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.

Abstract:

Objectives: To explore the impact of insulin pump therapy on treatment satisfaction and glycemic control among patients with type 1 Diabetes Mellitus (T1DM). Methods: This was a 6 months, prospective study conducted among 47, T1DM patients aged 17-24 years who were attended the diabetes clinic during April 2014 to November 2014 at Insulin Pump Clinic, Diabetes Treatment Center, Prince Sultan Military Medical City, Riyadh, Saudi Arabia. The respondents were purposively and conveniently selected and educated about the correct use of the insulin pump device (Paradigm(®) Veo (™) system Medtronic Minimed, Northridge, CA) and they were interviewed using the Arabic version of the Diabetes Treatment Satisfaction Questionnaire (DTSQ) at baseline, 3 and 6 months. Demographics, duration of diabetes mellitus and HbA1c were also collected. Results: The mean age of the study cohort was 19.4±1.72 (mean±SD) years. Seventeen were males (36.2%) and 30 were females (63.8%). Compared to baseline significant positive differences were found in treatment satisfaction in both gender and patients those who have higher duration of diabetes mellitus at 6 months. Frequency of hyperglycemia and hypoglycemia decreased in female at 6 months and patient those who have shorter duration of diabetes mellitus. Compared to baseline significant positive differences were found in HbA1c among female and those who have shorter duration of diabetes mellitus. Both gender showed significant decreased in insulin necessity at 6 months and those with shorter duration of diabetes mellitus at 6 months. Conclusion: Although MDI is a feasible preference for insulin delivery, the use of insulin pumps also should be considered for patients with T1DM as it increased patients treatment satisfactions, decreased the frequency of hypoglycemia, hyperglycemia and dropped the HbA1c level.

Biography:

Caren HE is working in the The Chinese University of Hong Kong, China

Abstract:

Aims/Introduction: Type 2 diabetes is characterized by dysregulation of immunity, oxidative stress and reduced incretin effects. Experimental studies suggest that glucagon-like peptide (GLP-1) might have immuno-modulating effects. We hypothesize that GLP-1 receptor agonist, exendin-4, may reduce inflammatory response in type 2 diabetes. Materials and Methods: Using peripheral blood mononuclear cells (PBMC) sampled from 10 type 2 diabetes and 10 sex- and age-matched control subjects and supernatants from PBMC culture, the expression of phospho-mitogen activated protein kinase (MAPK) signaling pathways in CD4+ T helper lymphocytes and monocytes was analysed using flow cytometry. Cytokines/chemokines and superoxide anion before and after treatment with exendin-4 were measured by cytometric bead array and chemiluminesence assay, respectively. Results: Compared to control subjects, PBMC from type 2 diabetes patients showed activated MAPK (P38, JNK and ERK) signaling pathway, elevated superoxide anion, increased proinflammatory cytokines (TNF-α, IL-1β, IL-6), and chemokines (CCL5/RANTES and CXCL10/IP-10). These changes were attenuated by exendin-4, possibly through the suppression of p38 MAPK. Conclusions: These results suggest that exendin-4 might down-regulate proinflammatory responses and reduce oxidative stress by suppressing MAPK signaling pathways in type 2 diabetes.

Biography:

Prof. Fatchiyah F., PhD., has completed PhD program at the Graduate University for Advances Studies, School of Life Sciences, Department of Molecular Biomechanics, Okazaki, and Aichi, Japan, 2006. She is senior lecturer on molecular genetics at Biology Dept. Faculty of Sciences, Brawijaya University. Malang, Indonesia since 1989 till present; as director of Central Laboratory of Life Sciences, Brawijaya Universiy during 2007-2012; as director of Biosains Laboratory of Brawijaya Universiy, 2012-present, and as a head of SMONAGENES research group with research interest focus on: Nutrigenomics study of Natural Genetics Resources, Molecular Biomechanics of Gene Cascade of Metabolic and Degenerative Diseases and Genes Mapping.

Abstract:

Most of biological signaling pathway was orchestrated at the level of proteins and biological active compounds, that both molecules recognition have ability to interact and modulate molecular mechanisms underlying an organism’s physiological functions. Differentiation of structural and physicochemical properties of bioactive compounds is important factor to determine the biological function. Local Indonesian goat Ethawah breed milk is one of nutritionally enriched dairy breed milk to provide biological function modulation without health risks. Recently our study, we found the high amount of caprine alpha-S2 casein of goat Ethawah breed milk exclusively isolated from 36kDa, and identified the eight of bioactive peptides fragments of caprine alpha-S2 casein by MALDI-TOF analysis. This study focuses on elucidating the biological function of caprine milk alpha-S2 casein protein provides by in vivo, in vitro and in silico analyses. We found that alpha-S2 casein protein in high MG environment inhibits the decreasing of viability due to increasing the proliferation of MC3T3E1pre-osteoblast cell. In animal model, this protein able to down regulated cytokine pro-inflammation on some tissues target and controlled RAGE-AGE signaling pathway related with ROS and oxidative stress. These data also confirmed by in silico analysis, we detected each of bioactive peptide of caprine milk alpha-S2 casein protein has display a wide range of physiological functions as anti-inflammation, anti-oxidative, and immunomodulatory mechanism to regulate the cellular and molecular signaling mechanism to promote health life improvement.

Biography:

Gregory Lee received his Ph. D from the California Institute of Technology and completed his postdoctoral studies at the University of California, San Diego. He became a full Professor at the University of British Columbia in 1989, and retired in 2012 with the title of Professor Emeritus. He is the co-founder of Vancouver Biotech Ltd. He has published more than 200 papers, including 30 papers in cancer research. He has been serving as an editorial board member of the Journal of Carcinogenesis and Mutagenesis, and the Journal of Cancer Science and Therapy since 2012.

Abstract:

GHR106 monoclonal antibody (Mab) was generated against the extracellular domain (N1-29) of the GnRH receptor and belongs to a new class of bioequivalent long-acting GnRH analogs. Through various biological and immunological studies, it was revealed that Mabs in both murine (mGHR106) and humanized (hGHR106) forms have comparable specificity and affinity to intact GnRH receptor on cancer cells and to N1-29 synthetic peptides from humans and monkeys. By terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, both Mabs were shown to act in a similar manner to the decapeptide GnRH antagonist, Antide, in inducing apoptosis of cultured cancer cells from various tissue origins. Furthermore, both mGHR106 and hGHR106 were shown to induce complement-dependent cytotoxicity (CDC) reaction to cancer cells, an immune property which is not shared by decapeptide GnRH analogs. Through semi-quantitative polymerase chain reaction both GHR106 and its humanized forms were revealed to be bioequivalent to Antide in terms of their respective effects on the expression of genes related to cell proliferation and apoptosis. In addition. GHR106 Mabs demonstrate a longer circulating half-life than GnRH peptide analogs (days. vs hours). Therefore, based on the results of these studies, it can be concluded that both mGHR106 and hGHR106 are bioequivalent to the GnRH decapeptide antagonist, Antide, and can serve as a long-acting alternative to current GnRH decapeptide antagonists for applications in cancer immunotherapy and for fertility regulations.

Biography:

Aydin Sav has completed his pathology residency in Istanbul University in 1984. In 1988, he was a visiting professor in Mayo Clinic, Rochester, MN (Dr. BW Scheithauer); AFIP, Washington D.C. (Dr. J Parisi); University of Vienna, Obersteiner Institute for Neuropathology (Dr. H Budka); Saint Michael’s Hospital, University of Toronto (Dr. K Kovacs). He worked in Marmara University (1989-2008) and Acıbadem University as tenure (2008-2014). He directed Marmara University Institute of Neurological Sciences and neuropathology laboratory (1994-2008). He has published more than 250 papers in reputed journals. He has been serving as an editorial board member of two national and 4 international journals.

Abstract:

Pituitary adenomas can be classified according to pathologic, radiological, or clinical behavior as typical or atypical, invasive or noninvasive, and aggressive or nonaggressive adenomas. World Health Organization classification categorizes pituitary adenomas as typical and atypical. Pathologic features of atypical adenoma are defined as a Ki-67 labeling index greater than 3%, and/or extensive p53 immunoreactivity. Invasive adenomas show pathologic or radiological signs of invasion to the cavernous or sphenoid sinuses, bone, or nasal mucosa. According to clinical behavior, a pituitary adenoma can be either aggressive or nonaggressive, and the use of biomarkers in differentiating aggressive adenomas has a limited place in determining the prognosis. Pituitary carcinomas are rare, show cerebrospinal and/or systemic metastasis; show a higher index of Ki-67 and p53 protein than aggressive adenomas, and they usually are resistant to radiotherapy.

Biography:

In 1982 Prof. Alessandro Antonelli has completed his degree in Medicine, cum laude; in 1985 Post-graduate Specialization in Endocrinology, in 1987 in Occupational Health and in 1992 in Oncology from University of Pisa, Italy. In 1995 he was Visiting Professor, Allegheny-Singer Research Institute of the Medical College of Pennsylvania and Hahneman University in Pittsburgh (USA). He is Associate Prof., Department of Clinical and Experimental Medicine, Pisa, Italy. He has published more than 240 articles on international journals (Impact Factor > 800; HI 44) and has been serving as an editorial board member and reviewer for several international journals.

Abstract:

The prevalence of autoimmune thyroid diseases (AITD) is estimated to be about 5%. AITD are generally of low severity, but can affect significantly the quality of life, and they are a cause of considerable medical costs. The AITD comprise two main clinical presentations, Graves' disease and Hashimoto's thyroiditis, whose clinical features are thyrotoxicosis and hypothyroidism, respectively. AITD is characterized by lymphocytic infiltration of the thyroid parenchyma; recruited T helper 1 lymphocytes are responsible of IFN-γ and TNF-α secretion, which stimulates CXCL10 (the main IFN-γ-inducible chemokines) production from the thyroid cells, generating an amplification feedback loop, that induces the autoimmune process. Epidemiological data show an interaction among environmental triggers and genetic susceptibility as the key factor leading to the initiation of AITD. An association of AITD and papillary thyroid cancer has been suggested. Moreover, AITD have been shown to be associated with other autoimune disorders (type 1 diabetes, Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, cryoglobulinemia, etc). These above mentioned data suggest that AITD patients need to be monitored for the appearence of thyroid dysfunctions, thyroid nodules, or other autoimmune disorders.

Biography:

Eloisa Loss has completed her PhD in physiology at the age of 27 years from Ferderal University of Rio Grande do Sul, Porto Alegre, Brasil. She is specialized in electrophysiology of endocrine tissues. Nowadays, she is head of Department of Physiology in this University. She has published more than 18 papers in reputed journals.

Abstract:

Sertoli cells (SCs) are essential for sustaining spermatogenesis in adulthood. The total number of SCs determines the daily gamete production, since SCs can support only a limited number of developing germ cells. Considering that human SCs proliferation only occurs during the immature period, proper development and proliferation of the SCs during the proliferative phase are crucial to male reproductive health in adulthood. Coordinated mainly by follicle-stimulating hormone (FSH) and androgens, the proliferation process is regulated by an assortment of hormonal and paracrine/autocrine factors, which regulate the rate and extent of proliferation. Insulin and IGF-1 signaling are intimately involved in such processes and seem to be the most important signals in regulating the final number of SCs during the pre-pubertal period. Actually, several studies show that metabolic diseases such as Diabetes mellitus are related to male infertility, especially altering insulin, LH, FSH and IGF-I plasma levels. Since insulin/IGF-I has an important role in the regulation of SC proliferation, this deregulation is a possible mechanism by which insulin lack may be involved in the development of infertility. The electrophysiological recording of immature rat SCs from whole seminiferous tubules has enabled several observations, which introduce new concepts regarding the mechanisms of action of hormones especially FSH and androgens. Both, insulin and IGF-I cause depolarization on the membrane potential and increase calcium uptake in immature SCs acting on the IGF-I receptor through the PI3K/Akt pathway. Knowing the mechanisms by which insulin and IGF regulate SC function can provide new insights regarding diabetes-related infertility.

Biography:

Dr. Mei-Chyn Chao had graduated from Kaohsiung Medical University and is an associate professor of Kaohsiung Medical University. She was a chief director of Pediatric Department and a director, Division of Pediatric Genetics, Endocrine and Metabolism of Kaohsiung Medical University Hospital. Now, She is a director, Division of Pediatirc Genetics, Changhua Christian Children’s Hospital Taiwan.

Abstract:

TSHR mutations result in a wide spectrum of clinical manifestations ranging from mild to severe congenital hypothyroidism (CHT) and thyroid hypoplasia. To date, several loss of function mutations in the TSHR gene have been reported in patients with CHT. In this study, we found that the frequency of heterozygous and homozygous p.R450H (c.1349G/A and A/A) TSHR mutations was approximately 7.0% in the Taiwanese CHT patients study. The thyrotropin-releasing hormone (TRH) test is useful for differentiating central and primary hypothyroidism. We reviewed a 228 cases with eutopic thyroid glands and neonatal hyperthyrotropinemia under levothyroxine replacement for 3 years. Analyzed the clinical use of the TRH test in the re-evaluation of CHT. At the age of 3 years, 31.6% of the patients still had hypothyroidism. There was no significant difference between basal TSH level and TRH test in the diagnosis of hypothyroidism (p = 0.23). The negative predictive value of the basal TSH level was 100%, however, the positive predictive value was only 43.6%. When the TSH level was near the upper limit of the normal range (4.5–8.5 mIU/L), the TRH test result had a better correlation with hypothyroidism than the basal TSH level (p = 0.03). The threshold of the TRH test set at 60 mIU/L had the greatest area under the curve, with a negative predictive value of 95.2% and a positive predictive value of 80.2%.

Biography:

Yolanda de Rijke has completed her PhD in biochemistry and has been registred as laboratory specialist since 2000. She is the deputy head of the department of Clinical Chemistry, Erasmus MC. She published over 100 peer-reviewed papers and her special interests are endocrinology and pediatrics. She is an active member of the Netherlands Society for Clinical Chemistry and Laboratory Medicine.

Abstract:

Chromogranin A (CgA) is used as an aid in the diagnosis and follow-up of neuroendocrine tumors. We evaluated the ThermoFisher Brahms CgA Kryptor assay against the CisBio assay. Recently, we evaluated also the new generation CgA assay (CgA II). Methods: Analytical validation of the CgA II assay was performed and included precision, linearity and recovery studies as well as a comparison study with the current CgA assay and a stability study. For the stability study, individual serum samples were aliquoted and stored at different storage temperatures (room temperature, 4⁰C and -20⁰C) until assayed. Results: The CgA II assay showed a good correlation with the current CgA assay. Although the current assay was not stable at 4°C, the CgA II assay is stable at 4°C for at least 48 hr and therewith comparable to the stability we used to with the CisBio assay. Conclusion: Our study showed that the CisBio assay can conveniently be replaced by the Kryptor assay which is a robust assay with good performance. The CgA II assay uses antibodies directed against different epitopes and the results have demonstrated that this epitope is stable over time and at different temperatures, including 4°C.

Biography:

Joy Varghese MCH. FINR .is Sr. consultant Neurosurgeon &Head of the department ,Dept.of Neurointervention. Global health city Chennai. He completed MCH in neurosurgery from Mumbai University, India and Fellowship in Interventional neuroradiology [FINR] from Zurich University ,Switzerland. Endovascular and micro vascular neurosurgery always fascinated him and has been working in this field for last ten years .He is the Neuro interventional surgeon incharge of Global Hospital India stroke programme. He has published several papers in reputed journals.

Abstract:

The concept of ‘Neurovascular unit’[NVU]introduced in 2001 ,by stroke progress review group under the National Institutes of Neurological Disorders and Stroke, emphasize that brain function and dysfunction arises from integrated interaction between a network of neurons ,glia and cerebral endothelium i.e. a functioning NVU .This phenomenon is partly mediated by the ability of cerebral endothelium ,astrocytes , pericytes and oligodentrocytes to secrete a rich repertoire of trophic factors .More data are available now regarding endothelial –neuron /endothelial –astrocyte /endothelial –oligodentrocyte trophic coupling. Brain derived neurotrophic factors, Fibroblast growth factor-2, Transforming growth factor – beta ,adrenomedullin, vascular endothelial growth factor , matrix metalloproteinases etc. play multiple ,specific roles in neurovascular unit to accomplish its functions of homeostasis and damage repair. Neurovascular unit participates in the establishment and function of the Blood brain barrier[BBB] .Astrocytes contribute support to the BBB via the release of factors including Glial cell line-derived neurotrophic factor ,angiopoetin -1 and angiotensin -11. Through releasing trophic factors cerebral endothelial cells guide developing axons and protect neurons against stress . It also provide a niche for supporting neural stem /progenitor cells [NSPCs]. NSPCs are shown to have direct coupling with cerebral endothelial cells .In neurovascular unit cell-cell signaling between cerebral endothelial cells and neuronal precursor cells help mediate and sustain pockets of ongoing neurogenesis and angiogenesis in adult brain . Under the remodeling phase after brain injury these close relationships are maintained and both neurogenesis and angiogenesis occur in the neurovascular niche to promote repairing the brain .Thus rather performing as a passive conduit for blood stream ,cerebrovascular system with its actively interacting cellular network and trophic mediators plays more active role in maintaining CNS homeostasis .As more and more acute ischemic stroke patients are undergoing endovascular recanalisation after the successful MR CLEAN[2014] & ESCAPE[2015] trials ,more clinical and radiological evidences are surfacing supporting the existence of this integrated endocrine CNS homeostasis .This presentation will discuss some of them .

Biography:

Sutrisno, MD, is an Obstetrics and Gynecologist , senior lecturer and Consultant in Gynecology laparoscopy, female reproductive endocrinology and infertility of Brawijaya University Faculty of Medicine, Malang, East Java , Indonesia. He also to be senior lecturer in Midwifery master programme in Brawijaya University. The current position is head of the Obstetrics and gynecology section of Saiful Anwar General Hospital, Malang, Indonesia. The main topics of research is Endometriosis and Immunocontraceptions and published the papers in International and Indonesia Journal of medicine.

Abstract:

Objective: To investigate the effect of genistein on proinflammatory cytokines, NF-kB activation, and estrogen receptor- β expression in a mice model of endometriosis. Methods: Forty female mice (Mus musculus) were divided into eight groups (n=5 each), including the control (untreated) group, endometriosis group, and the endometriosis groups were given various doses of genistein (at doses of 50; 100; 200; 300; 400; 500 mg/day). Analysis of TNF-α, IL-1 β, IL-6, and IL-8 level were done by ELISA technically. Analysis of estrogen receptor-β and NF-kB were done by immunohistochemistry. Results: The level of TNF-α, IL-1β, IL-6, and IL-8 were significantly higher in the EM group compared to the untreated control group (P<0.05). All doses genistein significantly prevented EM-induced increase in TNF-α level (P<0.05), but only at dose of 300 mg/day reach the level in the control group (P>0.05). These increased levels of IL-1β, IL-6, adn IL-8 in the EM group were significantly reduced by all doses of genistein. There were significantly (P<0.05) increased estrogen receptor-β expression and NF-kB activation in EM group compared to untreated group. Only first and fourth dose significantly (P<0.05) decreased the estrogen receptor-β expression compared to the EM group, to reach a level in the control group (P>0.05). All doses genistein significantly prevented EM-induced increase in NF-kB activation (P<0.05). Conclusion: In conclusion, genistein prohibits the increase in proinflammatory cytokines, NF-kB, and estrogen receptor-β expression in a mice model of endometriosis.

Biography:

Leonardo Romano Torres MD : Assistant General and Endocrine Surgeon.University General Hospital of Puebla “Eduardo Vasquez” (México). Post Graduate Studies in Endocrine surgery (Masters degree) at the Catholic University of Rome- Agostino Gemelli in Rome Italy at the age of 35 years, continuing The Same at The Hospital Universitario del Mar in Barcelona Spain (fellowship degree).

Abstract:

Evaluation of cervical lymph nodes for staging and surgical planning in thyroid cancer is necessary to determine the extend of surgery. CND (central neck dissection) in differentianted thyroid cancer remains controvertial due to low potential benefits and increase complications such as dysphonia, hypoparathyroidism (temporal/permanent).There is a large proportion of patients with subclinical disease during thyroidectomy (50 %). the presence of metastatic positive lymph in the central compartment during the procedure increases the risk of local recurrence (N1 31% - N0 8%). There is debate whether if its necessary the PND (prophylactic neck dissection) during thyroidectomy in PTC (papillary thyroid cancer), because do not change survival rate ,but increases local recurrence. The study of Antonio Sitges ( Nodal Yield, morbidity, and recurrence after CND for papillary thyroid carcinoma) proved prevalence nodal metastasis rate of 60% in those patients with no local recurrences after thyroidectomy of PTC. Tissel study meticulous CND improves the prognosis PTC even without the use of I 131. To date there is no study has demonstrated significantly reduced recurrence or mortality rates with PND. the controvercy remains whether perform or not PND in PTC.

Biography:

Jun Ming Wang has completed his PhD at the University of Antwerp, Belgium, and postdoctoral studies from University of Ottawa, Canada. He was a Research Assistant Professor in the University od Southern California. He is now an Associate Professor in University of Mississippi Mecical Center, directing a Neurodegenrerative Diseases Research Laboratory. He has published more than 63 papers in reputed journals and has been serving as an editorial board member of Frontiers of Aging Neuroscience.

Abstract:

Dementia and depression disproportionately affect women in both prevalence and severity. Particularly related to deficiency of ovarian hormones which impairs the homeostasis of the brain microenvironment, reduces neurogenesis, and leads to neurodegeneration. Accumulated data suggest that estradiol-17β (E2), the primary ovarian hormone, promotes hippocampal neural progenitor cell (NPC) proliferation in vitro, in vivo, and after brain injury. Our earlier work indicated that activation of estrogen receptor (ER) β by the ERβ-specific ligand, diarylpropionitrile, led to an increase in phosphorylated extracellular signal-regulated kinase in human neural progenitor cells and increased these cell proliferation. Our resent work suggested that ovariectomy (OVX) increased alternative splicing of ER β and the ERβ splice variants might mediate the differential effects of estrogen therapy (ET) in early and late post-menopause. To further understand the mechanism, we used a customized RT2 Profiler PCR Array to examine expressions of RNA splicing factors in brain of female rats treated with E2, ERβ or ERα specific agonists, or vehicle 6-day (early) or 180-day (late) after OVX. Early ET reversed OVX-increased (SFRS7 and SFRS16) or -decreased (ZRSR2 and CTNNB1) mRNA levels of splicing factors and ERβ splicing changes in brains and leukocytes, and improved mood/cognitive performances. While only DPN (an ERβ specific agonist), but not E2 (an ERα and ERβ agonist) nor PPT (an ERα specific agonist), achieved similar results in late treatment. These data suggests ERβ plays an important role in ET and ET efficiency may be indicated the expression of ERβ splice variant in circulation.

Biography:

Narayana Kilarkaje has completed his PhD from Manipal University, India, in the year 2001. At present, he is employed as an Associate Professor of Human Anatomy at the Kuwait University. He has taught human anatomy to medical students since 1995 and actively involved in administrative affairs. Currently, he is the Director of Animal Resources Center at the Kuwait University. He has conducted several research projects on genetic toxicology, hepatology and molecular reproductive biology and published around 60 research papers in high impact journals. Currently, his research interest focusses on DNA damage and its repair mechanisms in germ cells and hepatocytes.

Abstract:

Hyperglycemia up-regulates oxidative stress, which forms a basis for the onset of both macro- and micro-vascular diseases. In addition, hyperglycemia in males also induces hypogonadism, alterations in hypothalamo-hypophyseal-testicular hormonal axis, erectile dysfunction and infertility in both humans and animals. One of the serious effects of hyperglycemia in males is the induction of DNA damage in germ cells and spermatozoa. Hyperglycemia causes DNA single- and double-strand breaks. TUNEL and DNA fragmentation assays have reproducibly shown that hyperglycemia induces DNA double-strand breaks in immature germ cells, Sertoli cells and mature spermatozoa. Moreover, ELISA and immunohistochemistry/ immunofluorescence studies have shown significant increases in stage-dependent expression of 8-oxo-dG, a marker for base oxidation in the testes and also in spermatozoa. Although DNA repair mechanisms repair the damaged DNA, which seems to be associated with several molecular mechanistic pathways, including poly(ADP-ribose) polymerase, MAPKs and p53-p21 signaling, not all damaged DNA is recovered in germ cells. The cells with huge amount unrepaired DNA damage undergo apoptosis. Interestingly, supplementation of some antioxidants, for example, Resveratrol (trans-trihydroxystilbene) appears to be promising to alleviate the DNA damage in germ cells, at least in diabetic animals, but such attempts in humans have not been undertaken. Taken together, published scientific data from our laboratory and from that of other researchers indicate that diabetes-induced DNA damage in germ cells have widespread implications as regards to fertility and quality of offspring. Thus, there is a need to develop a counteracting strategy to alleviate the induced DNA damage.

Biography:

Philippe Touraine, M.D, Ph .D., is the Head of the Department of Endocrinology and Reproductive Medicine at the GH Pitié Salpêtrière, Paris, France and a full professor at ParisVI, Université Pierre et Marie Curie, Paris. Dr Touraine directs the Clinical Fellowship in Endocrinology and Metabolism at the GH Pitié Salpêtrière Hospital. He is the current organizer of the Program of Endocrinology and metabolism in Paris VI University. Major research interests include the pathogenesis and treatment of pituitary tumors, the role of prolactin in human breast diseases, the pathogenesis and the genetics of Premature Ovarian Failure, and finally the treatment of growth hormone deficiency in adults. Society memberships include The Endocrine Society, The French Endocrine Society and the French Internal Medicine Society. He’s currently member of the Editorial Board of the JCE&M. Finally he received consultant and lecture fees from Pfizer and lecture fees from Ipsen.

Abstract:

Premature ovarian failure (POF) occurs in almost 1% of women under the age of 40. This encompasses a heterogeneous spectrum of conditions with phenotypic variability among patients. However, in most cases, the etiology remains unknown and POF is mostly irreversible. In such context, we had the opportunity to set up a network to better understand the current diagnosis management but also to discuss, on a case-by-case basis, the genetic studies and the opportunity for proposing hormonal regimens, to potentially increase their fertility prognosis. We performed a mixed retrospective and prospective study between 1997 and 2014. Five hundred and fifty-seven patients were included. Seventy-six percent of the patients presented normal puberty and secondary amenorrhea, and 28% were under the age of 20 at the time of diagnosis. Forty-five percent of women had detectable estradiol levels and 38% had detectable inhibin B levels. Fifty-six (15.7%) patients presented highly variable hormonal and clinical profiles, leading to the definition of a subgroup of patients with fluctuating POF. The presence of follicles was suggested at ultrasonography in 50% of patients, and in 29% at histology. The negative predictive value of ultrasonography for detection of follicles was 77%. According to us, AMH measure appeared to be a better marker for detecting a remaining ovarian reserve. Finally, a bone mineral density study revealed different patterns: 43% presented a normal BMD, whereas 44% had osteopenia and 13% osteoporosis. Karyotype and Xfra screening were systematically performed, at least in the most recent patients included for the last criteria, whereas genetic studies concerning genes involved in follicular maturation were performed, depending on the presence of follicles, and observed either on ultrasonography or ovarian biopsy. Various genetic mutations have been identified. Overall, the etiology of POF could be suspected or identified in 27 patients (7.5%). POF remained idiopathic in all other cases. Finally, a current prospective follow up of these patients is under evaluation in order to define the natural history of POF in these women, as well as of a subgroup of patients likely to be concerned by therapeutics in order to increase their fertility. Preliminary data suggest that patients who became spontaneously pregnant did so within the first year after POF diagnosis. Finally, different therapeutic strategies will be discussed.

Biography:

I have M.Sc and PhD in Anatomical Sciences from the University of Shiraz and the University of Tehran, Iran. My PhD thesis was entitled, “Effects of supraphysiological doses of nandrolone decanoate on the apoptosis of spermatogenic cells”. I published papers in peer-review journal which cited many times by the others. At the end of my PhD studies I had the chance to visit the University of Newcastle, Australia. I worked on a project supervised by Prof. Robert John Aitken in his laboratory on the topic, "Insulin signal transduction cascades in human spermatozoa". Working at the University of Newcastle extended my knowledge to new techniques like immunocytochemistry, computer assisted sperm analysis, flowcytometry, and western blot analysis. After comming to my own country I have started my job as an assistant prodessor of anatomy in Zanjan University of medical sciences from 2010 to 2014. Now I am working at department of translational medicine, clinical research center, molecular genetics reproductive medicine research group as a Visiting researcher in Lund University, Sweden.

Abstract:

Male dysfunction is common in patients with temporal lobe epilepsy (TLE). We evaluated whether melatonin, as a supplement, can play a positive role in reducing the epileptogenesis imposing abnormalities of spermatozoa and testes in epileptic rats. Status epilepticus was induced based on the TLE lithium-pilocarpine model. Two patterns of melatonin were administered to the epileptic animals along the mean durations of latent (14 days) and chronic (60 days) phases. Sperm parameters, different antioxidant enzyme levels, germ cell apoptosis, body and relative sex organ weights were evaluated in all groups 60 days following SE induction. Chronic TLE caused a significant reduction in sperm parameters. In the testis, the reduced level of antioxidant enzymes was accompanied by a significant increase in malondialdehyde concentration. The presence of oxidant condition in the testes of epileptic animals caused expanded apoptosis in the germ cell layer. Moreover, the amount of weight gain in epileptic animals was more prominent. Melatonin administration was able to improve sperm motility by increasing the total antioxidant level. There was also a significant reduction in the spermatogenic cell line apoptosis and the extra weight gain of melatonin-treated animals. Melatonin supplementation might be considered as an acceptable cotreatment in epileptic patients.

Biography:

Philip D. Houck, M.D. MSc. is a cardiologist associate professor of medicine Texas A&M University currently working at Baylor Scott & White Healthcare. He started his academic career in Engineering Science at Penn State University, received an MSc in Biomedical Engineering and MD from Northwestern University. He retired from the Air Force serving at the Aerospace Medical Research Laboratory, School of Aerospace Medicine, and Wilford Hall Medical Center. Research interests include weather and myocardial infarction, increasing circulating stem cells with EECP, electrical remodeling of the heart, peripartum immune disease, lymphatics role in decompensated heart failure, and fundamental laws of biology.

Abstract:

Fundamental Laws are not accepted in biological sciences. At present there are no accepted laws of biology. The laws below represent empirical facts. 1. Biology must be consistent with the fundamental laws of physics and chemistry. 2. Life, as opposed to non-living, exhibits negative entropy; developing order out of chaos. (The energy to support negative entropy is yet to be defined.) 3. The cell is the fundamental unit of biology 4. The cell must be in homeostasis with the environment. (This property allows for Evolution. The environment changes life.) 5. There must be a distinction between self and the environment. ( Immunity and inflammation are the defenses against invaders from the environment and responsible for repair of damaged and senile cells) 6. Electromagnetic information transfer is necessary for development and regeneration. (Life, regeneration of tissue will not exist in a non-electromagnetic environment, denervation. Lacking the additional information of the Y chromosome, Law 2 states that women have less entropy than men explaining greater female longevity. The most significant differences between men and women are reflected in law 5. Women, during pregnancy, are able to carry a fetus with foreign antigens. In order to accomplish this feat the immune system must adapt under the influence of sex hormones. The answer to the questions: Why is there a young female advantage? Why is it lost?; is the cyclic response of the immune system to sex hormones. Females lose this advantage after menopause when their immune system becomes similar to a male.

Biography:

Long Cheng has completed his PhD at the age of 28 years from Beijing Institute of Biotechnology. He has published more than 20 papers in reputed journals.

Abstract:

The transcription factor estrogen receptor β (ERβ) plays roles in the central nervous, endocrine, cardiovascular, and immune systems. ERβ can be SUMOylated. However, the underlying mechanism remains unclear. Here, we show that RSRC1/SRrp53 interacts with ERβ and SUMOylation of RSRC1 is required for regulation of PIAS1-mediated ERβ SUMOylation. RSRC1 promotes ERβ SUMOylation through enhanced interaction between ERβ and PIAS1. RSRC1 represses ERβ transcriptional activity through regulation of ERβ SUMOylation. By establishing RSRC1 as a novel cofactor for SUMOylation, our data provide insight into regulation of ERβ SUMOylation and indicate that SUMOylation of one protein can regulate another protein SUMOylation.

Biography:

Abstract:

The development of breast cancer is frequently associated with enhanced expression of tumor-promoting estrogen receptor α (ERα) protein and reduced expression of tumor-suppressive ERβ protein. Here we show that a microRNA-PES1 axis can regulate the balance between ERα and ERβ in breast cancer. PES1 controlled many estrogen-responsive genes by increasing the transcriptional activity of ERα while decreasing transcriptional activity of ERβ. Consistent with this modulation of ERα and ERβ transcriptional activity, PES1 promoted the stability of the ERα protein and inhibited that of ERβ through the ubiquitin-proteasome pathway, mediated by the carboxyl terminus of Hsc70-interacting protein (CHIP). A microRNA (miR-A) downregulated PES1 expression by targeting its 3’-untranslated region. Contrary to PES1, miR-A decreased the transcriptional activity and expression of ERα but increased those of ERβ. miR-A inhibited PES1-induced breast cancer growth. Further analysis of clinical samples showed that expression of miR-A, which is downregulated in breast cancer, inversely correlated with PES1, which is upregulated in breast cancer. Our data indicate that PES1 contributes to breast tumor growth through modulating the balance between ERα and ERβ. miR-A mimics may be a better drug than commonly used endocrine drugs that repress both ERα and ERβ activities.

Biography:

Dr. Awatif AlBahar is Medical Director, Senior Consultant, Obstetrics/Gynaecology, Reproductive Endocrinology at the Dubai Gynaecology & Fertility Centre, DUBAI HEALTH AUTHORITY. After completing her graduation, she specialized in Obstetrics & Gynaecology from the German Board, Koln and has a membership in Endocrine and Infertility from Academic University in Bonn. Dr. Awatif had been selected in 2002 in Dubai Excellency Programme. Her name is mentioned in the U.A.E Book of Special Personalities of All Fields (i.e. Medicine, Politics, Art etc.). Been awarded by his highness Amro Mosa in 2004 as to be the leader in medicine and social services in Middle East. She was awarded as hero of health care in 2012 by his highness ruler of Ajman, She has held multiple posts in various capacities in the OBS/GYN and is currently the director of the IVF Board of the Ministry of Health of UAE. Dr. Awatif is the Chairperson of the Emirates Obs/Gyne & Fertility Forum (EOFF) and a regular speaker on U.A.E activities in mother and child health via media – television, radio, ladies association, universities etc. She has had many publications on polycystic ovaries and infertility.

Abstract:

The vitamin D receptor (VDR) and vitamin D metabolizing enzymes are found in reproductive tissues of women and men. Vitamin D plays a role in fertility on multiple levels, it has impact on in vitro fertilization (IVF) outcomes, endometriosis, polycystic ovary syndrome (PCOS), as well as it can boost levels of progesterone and estrogen, which decide the regulation of menstrual cycles and can increase the likelihood of successful conception The most critical role of vitamin D in pregnancy may be within the uterus, at the uterine lining. Improved fertility rate among women with sufficient levels of the hormone could be due to the vitamin D boosting production of good-quality eggs in the ovaries and improving the chances of embryos implanting successfully in the uterus. Vitamin D supplementation has its overall health benefits, which include bone health, pregnancy health, cancer and chronic disease risk reduction. Researchers recently found that low vitamin D levels may reduce pregnancy chances in women undergoing in-vitro fertilization. Many studies have implicated oxidative stress in the pathogenesis of infertility causing diseases of the female reproductive tract. Many studies have shown antioxidant supplementation to improve insulin sensitivity and restore redox balance in patients with PCOS. We will review through the lecture the recent literature showing the advantage of antioxidants & vitamins in male and female fertility.

Biography:

Amal Alhefdhi has completed her MBBS from King Saud University, MS at University of Wisconsin-Madison, and EdD at Edgewood College. She has the Arab and Saudi board in general surgery. She completed her fellowship in breast and endocrine surgery at university Wisconsin-Madison, USA. She is a breast and endocrine surgeon at King Faisal hospital & research center, Riyadh, KSA. He has published more than 20 papers in reputed journals.

Abstract:

Surgery is the only curative treatment for PHPT. Minimally invasive parathyroidectomy is now commonly performed, the successful removal of hypersecreting parathyroid glands is indicated by a decrease in intraoperative parathyroid hormone (IoPTH) levels by >50% within 15 min. However, the use of IoPTH testing in patients with mild PHPT whose PTH levels are within the normal range and that of a subsequent final set of IoPTH levels after all four glands are visualized remain questionable. The aim of this work was to optimize the surgical treatment of PHPT, focusing on the role of IoPTH testing in mild disease, the role of IoPTH after four-parathyroid gland exploration, and persistent and recurrent disease after surgery. A retrospective analysis was performed on the data from a prospectively collected database of more than 1,000 patients who received parathyroidectomy for PHPT at a single institution from 2001 to 2013 by two experienced endocrine surgeons. IoPTH testing plays an important role in the operative management in 14% of patients with mild hyperparathyroidism. Importantly, a 50% decline in IoPTH levels within 15 min of parathyroidectomy is 96.5% reliable in predicting a cure in patients with PTH levels within the normal range. Moreover, when experienced surgeons visualize all four parathyroid glands, drawing a subsequent final set of IoPTH levels serves a limited role and rarely changes the operative course. Recurrent and persistent PHPT occur more frequently in patients with double adenoma (DA), which suggests that DA in some cases may represent asymmetric or asynchronous hyperplasia.

Biography:

Ana Paula Jacobus has completed her PhD in Biological Sciences (Physiology) at Federal University of Rio Grande do Sul/Brazil (2009) and postdoctoral studies in Endocrine Physiology/Reproduction and Molecular Genetics at Magee Womens’ Research Institute-University of Pittsburgh (USA) (2011-2013). She published several papers on the subject of Sertoli cell hormonal regulation and development in international journals. Has been serving as reviewer for the reproduction and hormonal signaling papers. At the present, she is Research Associate in Dr. Gross’ lab at ESALQ-USP (Brazil) where her research is about sex and meiosis experimental evolution and genomics.

Abstract:

Spermatogenesis and male fertility are dependent upon a complex interplay of hormonal inputs. In the testis, Sertoli cells are required to support germ cell development and survival after puberty. Because Sertoli cells can support only a finite population of germ cells, the extent of Sertoli cell proliferation and its number defines the upper limit of sperm output and fertility. Follicle Stimulating Hormone (FSH) is a known regulator of Sertoli cell proliferation that ends with the establishment of the blood testis barrier. After that, FSH assumes a role on Sertoli cells differentiation. For this reason, it is expect that FSH-receptor downstream signaling differ during the two development stages (pre and post pubertal). FSH stimulates some mechanisms only on the pre pubertal stage such as Ca2+ uptake, MAPK/Erk phosphorylation and PI3k/Akt activation. On the other hand, cAMP can acts either way on proliferation and differentiation by different pathways mediating FSH signal. This fine tune on the timing regulation by the same molecules, show us the diversity and complexity of this hormonal signaling. We want to discuss the importance of pathways for the Sertoli cell development, demonstrate the expression of key molecules that change related to the pre and post-pubertal phases and have a broad view at the FSH role on proliferation and differentiation of Sertoli cells. Altogether, these data may contribute for the understanding of the signaling dynamics, especially for the development of the favorable seminiferous milieu for sperm production and for identifying better control points providing strategies for male contraception.

Biography:

Dr. Sudipta Maitra has completed his PhD at the age of 30 years from Visva-Bharati University, Santiniketan, India and postdoctoral studies from CSIR Indian Institute of Chemical Biology (CSIR-IICB), Kolkata, India. Presently he is serving as Associate Professor of Zoology at Visva-Bharati University, a premier institute of advanced learning and research. His research interest includes inter alia molecular mechanism involved in the endocrine regulation of ovarian function. He has published more than 25 papers in peer-reviewed international journals and six students have completed their PhD degree under his supervision.

Abstract:

In addition to pituitary gonadotropins and gonadal steroids, insulin and insulin-like growth factors (IGFs) are considered as important regulator of ovarian function. The present study aims at detection of cognate insulin receptors (IRs) and seeks to explore physiological significance of insulin action in the zebrafish ovary. Transcripts for insra and insrb were detected in liver, intact ovarian follicles and denuded oocytes through reverse transcriptase (RT)-PCR. Anti-IRβ immunoreactivity was detected in the ovary through fluorescence microscopy and immunoblot analysis using IRβ specific antibody could detect a single 95 kDa band in the membrane preparation from intact follicles and denuded oocytes harvested from adult zebrafish. In addition to its positive influence on follicular steroidogenesis, stimulation with recombinant human (rh)-insulin could trigger meiotic G2-M1 transition in a manner sensitive to translational activation in zebrafish defolliculated oocytes. Priming with insulin promotes resumption of meiotic maturation in PI3K/Akt-dependent manner and oocyte specific phosphodiesterase 3 (PDE3) has been implicated as a possible downstream target. Forced elevation of intra-oocyte cAMP attenuates rh-insulin action on germinal vesicle breakdown (GVBD), MAPK3/1 (ERK1/2) phosphorylation and p34cdc2 kinase activation. Conversely, PKA inhibition by H89/PKI-(6-22)-amide could successfully overcome negative regulation by cAMP and induces GVBD and MAPK activation. Interestingly, elevated phosphorylation of Akt and ERK1/2 concomitant with higher GVBD percentage was noticed in zebrafish oocytes in vivo prior to ovulation. Further, ovarian follicles harvested from streptozotocin (Stz)-injected (i.p.) gravid zebrafish showed poor oocyte quality and compromised ovarian function including steroidogenesis and maturational potential, indicating functional relevance of insulin action on female reproduction.

Biography:

Prof. Dilip Mukherjee is serving as a faculty in the Department of Zoology, Kalyani University, India since 1981-till date. His is doing research on vertebrate molecular endocrinology and published more than 63 papers in peer-reviewed International Journals and four book chapters. 16 research students have been awarded Ph. D degree under his direct supervision on hormonal regulation of fish ovarian steroidogenesis and oocyte maturation, gonadotropin regulation of uterine function in mammals and hormonal regulation of calcium ion metabolism. He is the member of Editorial Board and reviewer of many International and National Journals. He is the Fellow and Member of many Scientific Societies in India. At present 8 Ph. D students and one post-doctoral student are working in his laboratory.

Abstract:

Presence and activation of aromatase enzyme and its physiological relevance in mammalian uterus including human have been previously reported. Local estrogen production in human endometrium also was suggested to be important in development of cancer. However, the presence or absence of aromatase cytochrome P450arom (P45arom) transcript and aromatase enzyme in the endometrium of normal human and other mammals is controversial. To address this issue, we used RT-PCR and real time PCR techniques to evaluate the presence or absence of P450arom transcript and its physiological significance in endometrial tissues of non-pregnant mice under various culture conditions. Endometrium at metestrus stage of estrous cycle contained P450arom mRNA, essentially identical to that found in mouse ovary and LH caused significant increase in its expression levels. Endometrium also contained aromatase activity as evident from increased conversion of labeled testosterone to 17β-estradiol (E2) and de novo E2 synthesis. Non-steroidal inhibitor fadrozole significantly attenuated both aromatase activity and E2 synthesis. Most interesting finding was the inhibition of P450arom gene expression in vitro by fadrozole. LH-induced endometrial E2 synthesis was mediated through activation of steroidogenic factor-1 protein. Matrix metalloproteinases (MMPs) are expressed in the mice endometrium. We examined the steroidal regulation of MMP9 within mouse endometrium. Female mice were ovariectomized and treated with LH and E2 alone or E2 plus progesterone (P4) and MMP9 gene expression were studied. Results revealed that LH and E2 alone or E2 plus P4 increase MMP9 gene expression. All these findings are indicative of the presence of functional P450arom mRNA and its stimulation by LH leading to E2 synthesis in non-pregnant mouse endometrium. Results also suggest that E2 synthesis by the induction of LH in mouse endometrium regulates MMP9 expression and activity in vivo via a complex mechanism. This estrogen regulation of MMP9 may play an important role in uterine tissue remodeling.

Biography:

Dr. Andrea M. P. Romani, MD, PhD, obtained his medical degree from the University of Siena, Italy and his PhD from the University of Turin, Italy. Upon completing his postdoctoral studies under Dr. Scarpa, he joined the faculty in the Department of Physiology and Biophysics, Case Western Reserve University, where he is currently Associate Professor. Dr. Romani has published almost 90 peer review articles in high profile journals together with numerous invited reviews and book chapters. He is currently serving as an Editorial Board Member for Archives of Biochemistry and Biophysics, Magnesium Research, World Journal of Gastro-Intestinal Physio-Pathology among others.

Abstract:

Tissue and serum Mg2+ deficiency have been observed in several endocrine pathologies including diabetes and metabolic syndrome, but it is still undefined to which extent an altered Mg2+ homeostasis contributes to the onset of these pathologies and/or their complications. In the present study, we report that Mg2+ deficient hepatocyte exhibit an increased entry of G6P into the endoplasmic reticulum, where the substrate is oxidized by the H6PD to generate NADPH. As H6PD operates in conjunction with 11β-HSD1, the increased level of NADPH is utilized by the latter enzyme to convert inactive cortisone to active cortisol. Administration of cortisone to Mg2+ deficient hepatocytes results in a marked production of cortisol, which in turn enhances gluconeogenesis and alters intrahepatic fatty acid synthesis, thus increasing intrahepatic triglyceride levels. Protein and mRNA expression of H6PD and 11β-HSD1 are both increased 3-4 fold in Mg2+ deficient cells. Mg2+ deficient hepatocytes also exhibit decreased insulin responsiveness, which is further compromised by cortisol production. Returning cellular Mg2+ content to its physiological levels, results in a dramatic decrease in cortisol production, and in the progressive renormalization of expression and activity of H6P, 11β-HSD1, and cortisol-responsive genes. Investigation into the underlying mechanism of action suggest that under Mg2+ deficient conditions 11β-HSD1 expression and activity increase as a consequence of increased nuclear translocation of NF-kB and increased expression of inflammatory cytokines (namely IL-1β and/or TNFα). Taken together, our results suggest that by increasing H6PD and 11β-HSD1 activity and expression, Mg2+ deficiency sets the conditions for an increased intrahepatic production of cortisol and decreased insulin responsiveness. This altered hormonal balance can play a major role in the onset and progression of the metabolic syndrome and its associated complications.

Biography:

Melissa Johnson received her PhD in Integrative Biosciences from Tuskegee University and currently serves as Assistant Professor in the Department of Food and Nutritional Sciences at Tuskegee University. She has published several papers in peer-reviewed journals, as well as served as co-author of chapters in edited books. Her research interests include cardiovascular and other chronic diseases, health promotion, disease prevention, and health disparities.

Abstract:

The relationship between diet and disease has long been established, with certain dietary patterns either enhancing or reducing inflammatory processes that mediate disease risk. Diets with lower omega-6/omega-3 fatty acid ratios as well as those rich in green, leafy vegetables (GLVs) are often associated with decreased risk. Indicators of inflammatory status such as adiponectin and highly sensitive C-reactive protein (hsCRP) are responsive to dietary modifications, with higher levels of adiponectin and lower levels of hsCRP indicating less inflammation. Two independent studies were conducted to determine the influence of GLVs (collard greens, purslane, sweet potato greens), incorporated into diets with a 25:1 or 1:3 omega-6/omega-3 fatty acid ratio on plasma adiponectin and hsCRP levels of the spontaneously hypertensive rat. Following 6-weeks consumption of the GLV diets with a 25:1 omega-6/omega-3 fatty acid ratio, plasma adiponectin levels were reduced; hsCRP levels were increased among rats consuming diets containing collard greens and purslane but not sweet potato greens. A desirable increase in plasma adiponectin and decrease in hsCRP were observed following the consumption of GLVs incorporated into diets containing a 1:3 omega-6/omega-3 fatty acid ratio. The findings of these studies suggest the ability of GLVs to influence levels of inflammatory biomarkers, with these vegetables favorably attenuating inflammation in the presence of a 1:3 omega-6/omega-3 fatty acid ratio. Based on their ability to serve as mediators in reducing inflammatory responses, it is expected that these GLVs have implications in reducing risk for both cardiovascular and endocrine diseases.

Biography:

Philip D. Houck, M.D. MSc. is a cardiologist associate professor of medicine Texas A&M University currently working at Baylor Scott & White Healthcare. He started his academic career in Engineering Science at Penn State University, received an MSc in Biomedical Engineering and MD from Northwestern University. He retired from the Air Force serving at the Aerospace Medical Research Laboratory, School of Aerospace Medicine, and Wilford Hall Medical Center. Research interests include weather and myocardial infarction, increasing circulating stem cells with EECP, electrical remodeling of the heart, peripartum immune disease, lymphatics role in decompensated heart failure, and fundamental laws of biology.

Abstract:

 Biology must be consistent with the fundamental laws of physics and chemistry. 2. Life, as opposed to non-living, exhibits negative entropy; developing order out of chaos. (The energy to support negative entropy is yet to be defined.) 3. The cell is the fundamental unit of biology 4. The cell must be in homeostasis with its environment. (This property allows for evolution. The environment changes life.) 5. There must be a distinction between self and the environment. (Immunity and inflammation are the defenses against invaders from the environment and responsible for repair of damaged and senile cells) 6. Electromagnetic information transfer is necessary for development and regeneration. (Life, regeneration of tissue will not exist in a non-electromagnetic environment, denervation) A new model of disease is health exists when degeneration and regeneration are in balance. Inflammation is the fulcrum between the two, being both beneficial in repair and detrimental by promoting degeneration. 1. Insulin in excess (insulin resistance) is a proliferative hormone that promotes abdominal obesity, lipid infiltration of blood vessels, hypertension, and is a precursor to cardiovascular events. 2. Allostasis, the innate drive for energy storage, introduces noise into the metabolic control loops resulting in obesity, and inflammation from excess fat. 3. The microcosm of bacteria influenced by dietary intake mainly carbohydrates is one of the inflammatory triggers that promotes insulin resistance. This model suggests a low inflammatory diet, exercise, and weight loss decreases the proliferative effects of insulin, increases circulating stem cells, and decreases inflammation to maintain health.

Biography:

Dr. Jose Mario Franco de Oliveira is an Associate Professor of Medicine in the Department of Medicine of Universidade Federal Fluminense, in the State of Rio de Janeiro, Brazil. He is also one of the Deputy Editors for Diabetes of The British Medical Journal. He has published a number of papers and served as a reviewer or author&co-author for many prestigious medical journals like “Hypertension”, “The American Journal of Hypertension”, “The Journal of the American Society of Nephrology”, “The British Medical Journal”, and the “New England Journal of Medicine. His main interests are in the clinical research of diabetes and hypertension. He is a Certified Preventive Cardiologist, Nephrologist, and Adult Intensive Care Unit Physician,. Finally, Prof de Oliveira, was a Post-Doctoral Clinical&Research Fellow at the Endocrinology-Hypertension-Diabetes Division of the Brigham&Women,s Hospital at Harvard Medical School, in Boston, USA, and is one of the two authors of the recent electronic Diabetes e-book published and edited by the British Medical Journal for All Doctors World-Wide.

Abstract:

In both type 1 and type 2 diabetes, cardiovascular diseaseas are the leading causes of morbi-mortality in both infancy, adolescense, and adulthood. And this is proved nowaday by a increasing number of new epidemiological data which shows an increase in the risk of cardiovascular events. The evidence from earlier trials have demonstrated that improvement in glycated haemoglobin will reduce the risk of micro vascular disease but there is lack of robust evidence to suggest whether improvement in glycaemic control will have similar beneficial outcomes on macro vascular disease. Also, despite all controversies surrounding the etiology, pathogenesis, and therapeutic role for hyperglycaemia in the mostly common form of diabetes, type 2 diabetes mellitus, newer anti-hyperglycaemic drugs are still getting onto the market at a high speed, due to the confidence in HbA1c as a surrogate outcome for microvascular complications; albeit all large recent randomised clinical trials and meta-analysis have shown that trying to achieve glycaemic levels close to the normal range did not reduce the most clinically important microvascular or macrovascular hard endpoints as end-stage renal disease, vision loss, amputations, strokes, fatal myocardial infarctions, heart failure, cardiovascular and total mortalities, with the added harm of substantial increase in the number of hypoglycaemic episodes. In summary, cardiovascular diseases are stil the number one cause of mortality for both type 1 and type 2 diabetes, independent of blood glycaemic levels of control, and wwe do not know the reasons for that, being probably multifactorial.

Biography:

Beatriz is doing her PhD at the Hospital Irmandade Santa Casa de São Paulo, in Brazil, and will do part of her research at Joslin Center Diabetes. She is endocrinologist at Hospital Samaritano, researcher at Endoclinica, and have been presented a few paper at many congress, as well as having been awarded.

Abstract:

Introdution: The glycated hemoglobin (HbA1c) has a key role in monitoring of glycemic control for reporting the retrospective index of plasma glucose. Studies show that HbA1c can serve as a parameter for risk evolution to DM complications, but little is known of statistical data in relation to the prognosis of other pathologies. Objective: The objective is to analyze the HbA1c as prognostic and predictive marker for necessity of hospitalization in patients with other diseases. Method: The study was performed in a hospital having a solicitation protocol of HbA1c for all patients with hyperglycemia in the moment of hospitalization. The study carried out in the five years period HbA1c analyzes by HPLC method, outpatient and hospitalized for clinical pathologies unrelated to DM patients. Parameters were set to analyze glycosylated hemoglobin equal to or less than 6.9%, 7 to 9%, and greater than 9%. Statistical differences were considered significant at p <0.05. Results: Evaluated a total of HbA1c in 2433 patients who hospitalization required and 48,164 outpatients in a period of five years. We found greater adherence to the solicitation protocol HbA1c up to date, starting with 300 requests until the last year with 656.The median of HbA1c in the first group were: less than or equal to 6.9%: 57% of patients, between 7-9%: 25.55% and higher than 9%: 17.02%. In outpatients were: less than or equal to 6.9%: 90.58% of patients, between 7-9%: 7.72%, higher than 9%: 1.70%. Discussion: The Diabetes Control and Complications Trial (DCCT) and United Kingdom Prospective Diabetes Study (UKPDS), determined the use of HbA1c as a laboratory parameter for DM control. In our study, the HbA1c showed significant importance in relation to patients requiring hospitalization or not, demonstrating that can also be used as an independent prognostic tool of the patient's pathology. Conclusion: Patients with high HbA1c have greater need for hospitalization regardless of pathology, having this method as an important marker prognostic of need for hospitalization.

Biography:

May.1978-Dec.1982, Zhejiang Medical University, major in clinical medicine with B.Sc. Sep.1985-Jul.1988, Suzhou Medical College, major in medical genetics with M.Sc. Sep.1990-Jun.1991, Visiting scholar at Obstetrics and gynecology in the faculty of medicine, the University of Hong Kong,, research in the prenatal genetic diagnosis, a CMB-HKU scholar. Oct.1997-Nov.1998, Visiting scholar at Obstetrics and gynecology, the University of Adelaide, Australian. Research in the Comparative genomic hybridization (CGH) in preimplantation genetic diagnosis. Nov.2002- Nov.2003,Jan.2005-Aug.2005 and Oct.2008-Feb.2009, Visiting scholar at Institute of Endocrinology and Obstetrics and gynecology at MAYO Clinic, America, research in reproductive endocrinology.

Abstract:

Since the birth of Louise Brown, the world’s first in vitro fertilisation (IVF) baby 30 years ago, more than 6 million children have been born worldwide with assisted reproductive technology (ART), and in some countries ART infants account for more than 1% of the birth cohorts (Pinborg et al., 2013). However, the health of the offspring conceived by ART has been a big concern with the increasing application of ART to solving infertility problems for its unnatural conception procedures. The incidences of low birth weight (?) and birth defects (Hansen et al., 2005; Lie et al., 2005) have been found more often among infants conceived by ART. Interference of ART to the gametogenesis and preimplantation embryo development resulted in the alteration of epigenetic reprogramming (Manipalviratn et al., 2009) or genomic stability (Manipalviratn et al., 2009; Feng et al., 2008) , which was deduced to be the causes of abnormalities in ART children. However, the association of ART with de novo genetic aberrations is still in dispute (Caperton et al., 2007; Riccaboni et al., 2008). Dynamic mutation is one type of DNA alteration, distinguished by unstable trinucleotide repeat expansion or contraction (Rosales-Reynoso et al., 2009). Compared with other gene loci, the frequency of dynamic mutation is much higher because its copy number alteration of trinucleotide repeats within a certain range of these genes will not result in any phenotypic change. Thus, the frequencies of dynamic mutations are a relatively sensitive index DNA instability analysis. To determine the stability degree of the dynamic mutation genes in ART offspring, seven common dynamic mutation genes were selected, which include Dentatorubral-pallidoluysian atrophy (DRPLA), Huntington disease (HD), Spinobulbar muscular atrophy (SBMA), Dystrophia myotonica-protein kinase （DMPK）, Myotonic dystrophy 1 (DM1) and Fragile X syndrome (Fra X). The peripheral blood and umbilical blood were collected from 75 IVF families (75 couples and 100 babies), 72 ICSI families (72 couples and 91 babies) and 99 natural conceived families ( 99 couples and 100 babies). The ratios of dynamic mutation were screened in the IVF and ICSI babies with the naturally conceived babies as the control. 2,466 transmissions were identified in ART offspring, with 2.11% (n=52/2,466) of alleles being unstable. In the control group, the frequency of dynamic mutation was 0.77% (n=10/1,300). Statistical significance was found between the ART group and the control group (P <0.01). The unstable transmission alleles were detected in 32of 1,288 alleles (2.48%) in IVF offspring and 20 of 1,178 alleles (1.70%) in ICSI offspring, both of which were significantly different from naturally conceived babies (P<0.01 and P<0.05, respectively). However, there were no significant differences in the size of mutational repeats, the rates of expansion or contraction among the three groups (P>0.05). The repeat copy numbers of the examined genes in all parents and their babies were found to be within the normal ranges. To further investigate how ART affects the genome instability in the offspring, 52 ART conceived singleton placentas (32 IVF and 20 ICSI) and 32 comparative naturally conceived placentas were collected, and the DNA damage repair associated genes were analysed. Results showed that gene expressions of PMS2, RPA1, XPA, MSH2 and MSH6 were significantly higher in the IVF and ICSI groups than in the control group. Both IVF and ICSI groups showed significant different DNA methylation rate of OGG1, RPA1, PMS2, MSH6 and XPA compared with the natural group. Meantime, the protein expressions of PMS2, MSH6 and MLH1 in the ICSI group were also significantly higher than in the IVF and control groups. Therefore, ART procedures and infertile background could result in mild genomic instability, which could result from the alteration of epigenetic modification like DNA methylation of DNA damage repair associated genes.

Biography:

Okeke Chukubike U, obtained Ph.D and M.Sc degrees in chemical pathology from Rivers State University of Science and Technology, Port Harcourt, Rivers State, Nigeria. He obtained Fellow of Institute of Medical Laboratory Sciences in Hematology and Blood Group Serology in 1999. He have publications in reputable journals. He is currently working as a lecturer in department of Prosthesis and Orthopedic Technology, School of Health Technology, Federal University of Technology Owerri, Imo State, Nigeria. He has been collaborating with my professional colleagues in laboratory medicine researches. His research interests are endocrinology, metabolic diseases, heamatology and molecular biology.

Abstract:

Background: Pregnancy in HIV-positive women might be associated with at least small increases in risk of adverse maternal outcomes, and these are spontaneous abortion, still birth, foetal abnormality, perinatal mortality, low birth weight, pre-term delivery. These adverse eff ects might be as a result of endocrine abnormalities in HIV patients. This study was carried out to investigate the possible changes in pregnancy hormones of the HIV infected women within the few weeks of pregnancy prior to antiretroviral therapy. Materials & Methods: A total of 120 pregnant women with 28 weeks of pregnancy participated in the study. 60 of them were HIV seropositive, while the rest 60 were HIV sero positive were not or had not commenced antiretroviral therapy before the sample collection. Their serum prolactin, estrodiol, progesterone, beta-human chorionic gonadotropin, was estimated using Enzyme Linked Immunosorbent Assay method. Result: It was observed that prolactin and estradiol levels of non-infected pregnant women were signifi cantly higher (p<0.05) than the seropositive pregnant women. The human chorionic gonadotropin and progesterone of the two groups showed no signifi cant change (p>0.05). Conclusion: HIV infection has no eff ect on human chorionic gonadotropin and progesterone but has reducing eff ect on estradiol and prolactin production/metabolism in infected pregnant women. Th is eff ect may aff ect development of the foetus or breast milk production in these women if commencement of antiretroviral therapy is delayed.

Biography:

Maryam Barzin is a general physician and PhD candidate working as a senior researcher for the in Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran since 2008. She has been under the supervision of Prof. Fereidoun Azizi and Prof. Farhad Hosseinpanah for 7 years. She is expert in advanced research methodology and statistical software including SPSS, STATA, SAS and Nodixcel). Her field of interest fields abdominal obesity, childhood obesity, cardiovascular outcomes and bariatric surgery. As she has put a lot of passion, effort and time into my work, she can claim it to be another one of her children for whom she has written more than 20 papers. She has brought the title of the articles below: “Natural course of metabolically healthy abdominal obese adults after 10 years of follow-up: Tehran Lipid and Glucose Study” Int J Obes (Lond). 2014 Oct. “Changes in waist circumference and incidence of chronic kidney disease.” Eur J Clin Invest. 2014 May;44(5):470 “Metabolic aspects of different phenotypes of polycystic ovary syndrome: Iranian PCOS Prevalence Study” Clin Endocrinol (Oxf). 2014 Jul “Adolescence metabolic syndrome or adiposity and early adult metabolic syndrome” J Pediatr. 2013 Dec.

Abstract:

Objective: Obesity is a heterogeneous condition and risk of related health outcomes in different obesity phenotypes is a controversial subject. In this study, we aimed to evaluate the risk of cardiovascular disease (CVD) in different abdominal obesity phenotypes during a decade-long follow-up. Methods: In this large population-based cohort, 7122 participants (42.7% men), aged _30 years, from the Tehran Lipid and Glucose Study (TLGS) were enrolled. Abdominal obesity was defined using national waist circumference cut-off points of ≥89 cm for men and ≥91 cm for women. Metabolic health was defined as<=1 components of metabolic syndrome (excluding waist circumference), using the Joint Interim Statement (JIS) definition. Results: At baseline, 3745 individuals (52.7%) were abdominal obese and 23.5% (n = 881) of these were categorized as “metabolically healthy abdominal obese” (MHAO). A total of 638 CVD events occurred during a median follow-up of 10 years (1999-2011). “Metabolically healthy non-abdominal obese” was considered as the reference group. After adjustment for various variables, MHAO individuals were at increased risk for CVD events compared with the reference group (HR: 1.64, CI: 1.09 -2.47). Both the metabolically unhealthy phenotypes (with and without abdominal obesity) were also at increased risk. We also observed the same pattern using insulin resistance data for categorizing abdominal obesity phenotypes. Conclusion: Abdominal obesity and presence of metabolic derangements are both important risk factors for future CVD. MHAO may not be a benign condition regarding future CVD events, which highlights the importance of prevention and treatment of abdominal obesity, even in the absence of metabolic derangements.

Biography:

Joshua Barzilay, MD, is an endocrinologist in Atlanta GA who works for the Kaiser Permanente of Georgia. He is a professor of medicine in the division of endocrinology at the Emory University School of Medicine. He has published approximately 150 peer-reviewed papers.

Abstract:

The microcirculation plays an important role in bone formation during the ante-natal period. It is not known whether microvascular disease in post-natal life plays a role in impaired bone health, such as osteoporosis. Here we review several epidemiological studies that we have conducted in recent years showing that hip fractures – one the most serious manifestations of osteoporosis - are associated with several markers of microvascular disease: (1) retinal vascular disease, (2) albuminuria, and (3) abnormal white matter volume on a brain MRI. We further show that the presence of albuminuria mediates the association of dementia (a brain disorder related in part to small vessel disease of the brain) with hip fracture risk. These findings, plus recent reports that specialized cells in the osseous microvasculature play an important role in post-natal bone formation, support the hypothesis that extra-osseous microvascular disease may signify the presence of osseous microvascular disease that leads to osteoporotic fractures. Finally, we review radiological studies that show diminished bone perfusion in association with osteoporosis.

Biography:

Mary Cataletto M.D. is Professor of Clinical Pediatrics at SUNY at Stony Brook and a member of the clinical staff at Winthrop University Hospital in Mineola, New York. She serves as chair of the Asthma Coalition of Long Island and as a member of the Children’s Asthma Leadership Coalition. Dr. Cataletto has published and presented on this topic at regional, national and international venues. Dr. Cataletto is editor in chief of Pediatric Allergy, Immunology and Pulmonology, an international and peer reviewed publication of the Mary Anne Liebert Publishers , Inc.

Abstract:

Asthma is one of the most common serious chronic diseases of childhood and the third most common cause of hospitalization among children. This session will review the risk factors for severe asthma and the emergency department management of acute asthma episodes. The EPR-3 treatment algorithm will be discussed and interactive case based scenarios will be incorporated to highlight key messages, including the importance of a team based approach to management of acute asthma episodes.

Biography:

Dr. Gragnoli is a MD/PhD, who has been working in the genetics of type 2 diabetes and associated phenotypes. She became MD and endocrinologist at the U. La Sapienza of Rome; she obtained her PhD at the U. Tor Vergata of Rome. She is double-board-certified by the American Board of Internal Medicine in Internal Medicine, Endocrinology, Diabetes, and Metabolism. She was a JDFI Fellow at U. of Chicago, NIH Training Fellow at Mass General Hospital and Instructor in Medicine at Harvard Medical School in Boston. She was Assistant Professor in Medicine, Molecular & Cellular Physiology and Public Health Sciences at Penn State. She is an Associate Professor in Medicine at the U. of Florida and Adjunct Associate Professor in Public Health Sciences at Penn State.

Abstract:

Schizophrenia (SCZ) and type-2 diabetes (T2D) are clinically associated, and common knowledge attributes this association to side effects of antipsychotic treatment. However, even drug-naïve patients with SCZ are at increased risk for T2D. Dopamine dysfunction plays a central role in SCZ. It is well-known that dopamine constitutively inhibits prolactin (PRL) secretion via the dopamine receptor 2 (DR2D). If dopamine is increased or dopamine receptors hyper-function, PRL may be reduced. During the first SCZ episode, low PRL levels are associated with worse symptoms. PRL is essential in human and social bonding as well as it is implicated in glucose homeostasis. Dopamine dysfunction, beyond contributing to SCZ symptoms, may lead to altered appetite and T2D. To our knowledge, there are no studies of the genetics of the SCZ-T2D comorbidity focusing jointly on the dopamine and PRL pathway in the attempt to capture molecular heterogeneity correlated to possible disease manifestation heterogeneity. We propose new studies to establish the genetic role of PRL and dopamine pathway in SCZ-T2D co-morbidity.

Biography:

Jose Figueiredo is working in the State University of Ceara

Abstract:

In vitro culture of preantral follicles provides a valuable tool to study early folliculogenesis including the the critical and complex interactions regulating follicle and oocyte development and may also have implications for fertility preservation. Goats are considered suitable models for human. In fact, follicular development in the adult goat (i.e. ,10 weeks) was the closest to that observed in adult women. The aim of this study was to establish a culture system that improves the in vitro development of isolated caprine preantral follicles. In a first experiment we determined the optimal concentration of alginate (ALG). In a subsequent experiment we investigated the effects of the multiple follicle culture and the type of hydrogel (ALG, fibrin-alginate [FA] and hyaluronate [HA]) on the in vitro follicular development. For this, secondary follicles (200µm) were encapsulated or not (control) in ALG (0.25%, 0.5% or 1%) and cultured for 18 days and the recovered oocytes were destined for in vitro maturation. Estradiol and progesterone were measured and the mRNA levels of CYP19A1 and 3βHSD were quantified. Yet, follicles were cultured individually or in group (n=5), in multiple ALG beads or in the same bead, for 18 days. Next, follicles were encapsulated or not (control) in ALG, FA or HA and cultured for 18 days. Estradiol and progesterone were measured and the mRNA levels of CYP19A1, 3βHSD, Cx43, Cx37, MMP-9 and TIMP-2 were quantified. Finally, groups of 5 follicles were encapsulated in FA and cultured for 30 days. The in vitro matured oocytes were parthenogenetically activated. ALG 0.25% improved the antrum formation, growth, hormone production, gene expression of CYP19A1 and 3βHSD and the meiotic resumption compared to the others ALG concentrations (P<0.05). The culture of 5 follicles in the same ALG bead significantly enhanced follicular diameter compared to the individual culture, and antrum formation and meiotic resumption in relation to the culture in group in individual ALG beads. Follicles cultured in FA grew progressively until day 18 and generated mature oocytes. The hormone secretion was higher in follicles encapsulated in hydrogels (P<0.05). mRNA levels for all genes evaluated, except for CYP19A1, were similar between the FA group and uncultured antral follicles. 8-cell embryos were obtained after parthenogenetic activation of oocytes from follicles cultured in FA for 30 days. In conclusion, ALG 0.25% improved the in vitro development of goat preantral follicles. The encapsulation of 5 follicles in the same FA bead improved oocyte maturation which, after parthenogenetic activation, resulted in an 8-cell embryos.

Biography:

Leonardo Romano Torres MD : Assistant General and Endocrine Surgeon. General Hospital Puebla (México). Post Graduate Studies in Endocrine surgery (Masters degree) at the Catholic University of Rome- Agostino Gemelli in Rome Italy at the age of 35 years, continuing The Same at The Hospital Universitario del Mar in Barcelona Spain (fellowship degree)

Abstract:

Surgery for thyroid and thyroid has changed in recent years. Since the study published by Lahey 1938, the rate of disphonia decreased considerably. Multiple studies support this technique like the Study of Hermann in 2002 with more than 27 thousand nerves studied, as the Ridell ,s in the 50, s decade ; however this technical direction has not been enough to Prevent Damage to the RLN (recurrent laryngeal nerve) , And Avoid Causing Dysphonia that decrease Quality of Life of Patients. Dysphonia is the cause of More Frequent medical Lawsuits in thyroid and para thyroid surgery. The rate of temporary RLN injuries ranging between 5 -10%, and The Permanent Between 1-2%. There are several factors That may condition NLR mayor Exposure and Risk for Injury Patients As For example: Giant goiter, Lymphadenectomy, hyperthyroidism, Thyroid Carcinoma, Re-operations. Exist Other Circumstances as the anatomical variants RLN which exposed a mayor injury rate Such as: bifurcations, trifurcations (extra-laryngeal branches). As the Study of Sitges Serra and J. Sancho (BJS Published in 2006) is based. The neuro-monitoring has proven useful Significant decreasing rate of RLN injury in some Studies. Also has great help in other aspects of thyroid and para thyroid surgery. Neuromonitoring of the RNL is a technique that brings Benefits Such as: • Aid Identification of the RLN. • Aid RLN dissection. • Decreased post-operative dysphonia Rate in Patients with higher risk. • Diagnosis intraoperative of RLN injury. • Legal -Medical support. • Neurophysiological nerve support during surgery.

Biography:

Sofia Guerreiro is a in General Surgery Chief Resident in Setúbal Medical Center, Portugal and is a member of Portuguese Endocrinology Society (SPEDM) and Portuguese Surgery Society (SPCIR). She works in Setúbal Medical Center, in General Surgery Department – Endocrine Surgery Unit which is mainly focused in thyroid, parathyroid and adrenal diseases and also neuroendocrine tumors.

Abstract:

The existence of anatomic variants in the path of the inferior laryngeal nerve (ILN) is an additional reason to enhance their preoperative identification. One of these variants is the nonrecurrent inferior laryngeal nerve (NRILN) whose incidence ranges from 0.3% to 1.6% for the right and it is approximately 0.04% for the left. Its presence on the right is a consequence of a right subclavian artery variant that arises directly from the aortic arch behind the esophagus. Therefore, the absence of recurrence of the inferior laryngeal nerve results from an embryological variant. NRILN incidence is very rare, but when present, increases the risk of damage during thyroidectomy. Preoperative imagiologic diagnosis of arteria lusoria and dysphagia lusoria may suggest its presence. We describe a patient without dysphagia but with NRILN which was an incidental discovery through CT scan. We present this case because it highlights this anatomical variant. There are auxiliary methods that allow intra-operatory identification, as intraoperative neuro-monitoring (IONM). The knowledge of NRILN presence and a correct surgical technique minimize morbidity.

Biography:

I'm a Pediatric Endocrinologist, trained in Mexico City and Barcelona. My area is growth and development, diabetes in children, thyroid diseases, puberty, obesity, bone metabolism and everything related to hormones in children. My practice is located in the American British Cowdray Medical Center and inthe northern part of Mexico City

Abstract:

We acquire most of the bone mineral density before we reach the 30 years of age and then it starts declining at different rates for different people but almost inevitably. Most of the bone accrual actually takes place during the pediatric age and many factors may alter it, with consequences not evident until many years later. Therefore during recent years the focus of osteoporosis study has widened not only to prevent bone loss but to promote bone health during infancy, puberty and young adult ages. As the knowledge on pediatric bone density has widened, the definition of osteoporosis in such population has changed from the WHO description for adults and its measure is made as a Z-score instead of a T-score, with different considerations taken into account. Several tools have been used for this matter, including the widely used Dual-Energy X-ray Absortiometry (DXA) as well as central and peripheral tomography and ultrasound, to name a the better known. Using them, a number of countries have developed curves of normality in their pediatric population in order to have reference data to compare such cases in which a lower density is suspected due to disease, nutrition or some other risk factors. Among these, low consumption or absorption of calcium and vitamin D are the most frequent and relatively easy to prevent in one end, congenital severe diseases altering the bone on the other and chronic diseases and treatment of oncologic diseases in the middle of the range of possible skeletal alterations. New tools have been developed to have a better look not only of the mineral contents of the bone, but also to have a better insight of the trabecular and cortical structure of the bone while trying to minimize the radiation exposure of this, a particularly susceptible group. Peripheral quantitative computerized tomography (pQCT) for long bones and Trabecular Bone Score (TBS) for vertebrae using conventional DXA have found great acceptance and are gathering data which may lead during the following years to improve general bone health during childhood and prevent osteoporosis from an earlier age.

Biography:

Kiran V. Sandhu has completed PhD in 2015 from Department of Genetics and Molecular Neuroscience, from Otto-von-Guericke University Germany and currently working carrying own research in the same Department . She is working extensively on the endocrine aspect of psychiatric disorders and role of phytoestrogen as a treatment to ablate psychiatric symptoms. She is working extensively to promote science to kids.

Abstract:

Dietary phytoestrogens affects spectrum of social, emotional and cognitive behavior with beneficial effects towards anxiety and affective disorders. Here, I reported the effect of phytoestrogens in the regulation of social and emotional behavior which is often known to be affected in psychiatric condition. Additionally, the role of phytoestrogens in the regulation of Glutamic acid decarboxylase (GAD), a rate-limiting enzyme which is often associated with various psychiatric disorders. Phytoestrogens were dietary administered post-weaning through commercial diet consisting each of 150 mg/kg Daidzein and Genistein. Male mice showed disturbance in social and emotional behavior when phytoestrogen was removed from their diet for a period of 6 weeks. These animals showed disrupted social behavior, aggression and altered urine marking pattern. They also displayed reduced sensitivity to both social and non-social odors. In the fear-memory-paradigm the male mice showed altered freezing response to the contextual paradigm. Further, I investigated the role of phytoestrogens in the regulation of GAD. High resolution microdissection showed increase in GAD67 and 65 expression with phytoestrogens. GAD67-GFP quantification showed a similar increase in gene activity in different subregions of amygdala with phytoestrogens in GAD67+/- male mice. Thus the output therefore suggests, phytoestrogens as a possible treatment for various psychiatric disorders like Schizophrenia, Autism and Bipolar disorders with altered social and emotional behaviors.

Biography:

I'm a Pediatric Endocrinologist, trained in Mexico City and Barcelona. My area is growth and development, diabetes in children, thyroid diseases, puberty, obesity, bone metabolism and everything related to hormones in children. My practice is located in the American British Cowdray Medical Center and inthe northern part of Mexico City

Abstract:

Exposure to environmental chemicals starts already in the prenatal period, as chemicals present in the body of the mother may pass the placenta. Endocrine disrupting chemicals (EDCs) are of particular concern as hormones are involved in many processes during development. We examined if there were associations between early life exposure to EDCs and growth in early childhood (birth weight, and growth during the first year after birth), as well as with thyroxine (T4) levels at birth, in a newly recruited prospective mother-child cohort in the Netherlands. High perfluorooctanesulfonic acid (PFOS) and high dichlorodiphenyldichloroethylene (DDE) exposure were associated with higher birth weight, although for DDE this was only observed in male children. For mono(2-ethyl-5-carboxypentyl)phthalate (MECPP) on the other hand, low exposures in particular were associated with higher birth weights in girls. Low exposure to MECPP was furthermore associated with a higher BMI during the first year, both in boys and in girls. Similar effects were observed for low mono(2-ethyl-5-oxohexyl)phthalate (MEOHP) exposure in boys. Moreover, for most compounds boys showed an increase in BMI between six and eleven months of age. Exposure levels of DDE which were associated with both a relatively high birth weight and BMI later in life, also showed a relatively high T4 level, independent of gender. Furthermore exposure to perfluorooctanoic acid (PFOA) was positively associated with T4 levels in girls. We conclude that for various EDCs effects on all studied health outcomes were apparent, and that associations were non-monotonic as well as gender-specific. Follow-up is required to assess long-term effects and to face the challenge of mixture-effects.

Biography:

Ming-Sheng Zhou, M.D. & Ph. D., FAHA, is professor and chairman at department of physiology in Liaoning Medical University, China. He has completed his Ph. D. from Kagawa Medical University Japan and postdoctoral training from University of Minnesota and University of Miami. He was the faculty member of Miller School of Medicine University of Miami. His research interest focuses on the cellular and molecular mechanisms of vascular injury in hypertensive and metabolic diseases. He has published more than 50 papers in peer-reviewed journals in cardiovascular medicine and has been serving as an editorial board member of several medical journals.

Abstract:

Insulin resistance is highly prevalent in patients with essential hypertension, particularly those with salt-sensitivity (SS), and frequently progress to type II diabetes and cardiovascular diseases (CVD). However, there are still critical gaps in our knowledge of the mechanisms that lead to the development of insulin resistance in SS hypertension. Recent studies have underscored the importance of heightened activation of the renin-angiotensin system, oxidative stress and inflammation in promoting insulin resistance and CVD. Using Dahl SS rat, a paradigm of human SS hypertension characterized by CVD and insulin resistance, we have demonstrated that in SS hypertension, despite low plasma renin levels, there is an upregulation of local Ang II action that contributes to increased NADPH oxidase-derived ROS production and activation of NFB associated with impaired insulin activation of phosphatidylinositol 3-kinase (PI3K) signaling pathway in the vasculature and skeletal muscle. Furthermore, we have shown that treatment with angiotensin receptor 1 blocker candesartan, antioxidant tempol or NFB inhibitor PTDC improved endothelial function, vascular injury and insulin signaling molecules through PI3K pathway, reduced ROS production and NFB activation in the vasculature and skeletal muscle. PCR array showed that eight genes among 84 target genes related to obesity, insulin resistance and inflammation were altered in the soleus muscle of hypertensive rats, which were reversed by specific peptide inhibitor of NFB SN50. These results suggest that activation of the NFB inflammatory pathway by endogenous Ang II-ROS plays critical role in the development of endothelial dysfunction, skeletal muscle insulin resistance in SS hypertension.

Biography:

Dr. June-Woo Park has completed his PhD from Michigan State University and postdoctoral studies from University of Tennessee, Knoxville. He is a senior scientist of Korea Institute of Toxicology, a national research institute of toxicological studies. He has published more than 28 papers in reputed journals and has been serving as an editorial board member of New Journal of Science: Toxicology.

Abstract:

Bisphenol A (BPA) is an applied chemical that is used in many industrial fields and is a potential endocrine disruption chemical (EDC) that is found in the environment. Bisphenol S (BPS) and polyethersulfone (PES) have been suggested as putative BPA alternatives. In this study, the estrogenic potency induced by the binding of 17-beta-estradiol (E2), BPA, BPS, PES and their metabolites formed by the rat liver S9 fraction to the human estrogen receptor (ER) was estimated. We used an in vitro bioassay based on the luciferase reporter assay in MVLN cells to evaluate the estrogenic activity of 17-beta-estradiol (E2), BPA, BPS, PES (E2: 0.001 to 0.3 nM; BPA, BPS and PES: 0.0001 to 5 microM) and their metabolites (E2: 0.05 microM; BPA, BPS and PES: 0.1 mM) according to incubation times (0, 20 and 40 min). After chemical treatment to MVLN cells for 72 hrs, and the cell viability and luciferase intensity induced were estimated, from which the estrogenic activity of the chemicals tested was evaluated. BPA and BPS induced estrogenic activity whereas PES did not show any estrogenic activity in the concentrations tested. In an in vitro assay of metabolites, BPA metabolites displayed comparable estrogenic activity with BPA and metabolites of both BPS and PES showed increasing estrogenic activity. The results suggest that the metabolites of BPS and PES have estrogenic potential and the need for the assessment of both chemicals and their metabolites in other EDC evaluation studies. The estrogenic potency of PES and its metabolites is the first report in our best knowledge.