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

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.