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Effect of Paternal Age on Aneuploidy Rates in First Trimester Pregnancy Loss
Journal of Medical Genetics and Genomics Vol. 2(3), pp. 38-43, August 2010 Available online at http://www.academicjournals.org/jmgg ©2010 Academic Journals Full Length Research Paper Effect of paternal age on aneuploidy rates in first trimester pregnancy loss Vitaly A. Kushnir, Richard T. Scott and John L. Frattarelli 1Department of Obstetrics, Gynecology and Women’s Health, New Jersey Medical School, MSB E-506, 185 South Orange Avenue, Newark, NJ, 07101-1709, USA. 2Department of Obstetrics, Gynecology and Reproductive Sciences, Robert Wood Johnson Medical School UMDNJ, Division of Reproductive Endocrinology and Infertility, New Brunswick, NJ. Reproductive Medicine Associates of New Jersey, Morristown NJ, USA. Accepted 16 July, 2010 A retrospective cohort analysis of patients undergoing IVF cycles at an academic IVF center was performed to test the hypothesis that male age may influence aneuploidy rates in first trimester pregnancy losses. All patients had a first trimester pregnancy loss followed by evacuation of the pregnancy and karyotyping of the abortus. Couples undergoing anonymous donor oocyte ART cycles (n = 50) and 23 couples with female age less than 30 years undergoing autologous oocyte ART cycles were included. The oocyte age was less than 30 in both groups; thereby allowing the focus to be on the reproductive potential of the aging male. The main outcome measure was the effect of paternal age on aneuploidy rate. No increase in aneuploidy rate was noted with increasing paternal age (<40 years = 25.0%; 40-50 years = 38.8%; >50 years = 25.0%). Although there was a significant difference in the male partner age between oocyte recipients and young patients using autologous oocytes (33.7 7.6 vs. -
The Endocrinology of Aging 329 (1989); J
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Erasmus University Digital Repository ARTICLES 37. T. Crook et al., Dev. Neuropsychol. 4, 261 (1986). 344 (1988); ibid. 281, 335 (1989); M. J. West, L. butions and advice, and W. G. M. Janssen, A. P. 38. M. S. Albert, Proc. Natl. Acad. Sci. U.S.A. 93, 13547 Slomianka, H. J. G. Gundersen, Anat. Rec. 231, 482 Leonard, and R. S. Woolley for expert technical as- (1996); iiii and M. B. Moss, in Handbook of (1991); M. J. West, Neurobiol. Aging 14, 275 (1993). sistance. Research in our laboratory was supported Biology of Aging, E. L. Schneider, J. W. Rowe, T. E. 56. We thank C. A. Barnes, C. Bouras, A. H. Gazzaley, by NIH grants AG05138 and AG06647, the Human Johnson, N. J. Holbrook, J. H. Morrison, Eds. (Aca- P. Giannakopoulos, C. V. Mobbs, E. A. Nimchinsky, Brain Project MHDA52145, the Charles A. Dana demic Press, San Diego, CA, ed. 4, 1996), pp. 217– P. R. Rapp, and J. C. Vickers for their crucial contri- Foundation, and the Brookdale Foundation. 233; R. Fama et al., Arch. Neurol. 54, 719 (1997); A. Convit et al., Neurobiol. Aging 18, 131 (1997); C. R. Jack Jr. et al., Neurology 49, 786 (1997). 39. J. W. Rowe and R. L. Kahn, Science 237, 143 (1987). 40. S. L. Vincent, A. Peters, J. Tigges, Anat. Rec. 223, The Endocrinology of Aging 329 (1989); J. Tigges, J. G. Herndon, A. Peters, Neurobiol. Aging 11, 201 (1990); J. Bachevalier et al., ibid. -
Human Physiology/The Male Reproductive System 1 Human Physiology/The Male Reproductive System
Human Physiology/The male reproductive system 1 Human Physiology/The male reproductive system ← The endocrine system — Human Physiology — The female reproductive system → Homeostasis — Cells — Integumentary — Nervous — Senses — Muscular — Blood — Cardiovascular — Immune — Urinary — Respiratory — Gastrointestinal — Nutrition — Endocrine — Reproduction (male) — Reproduction (female) — Pregnancy — Genetics — Development — Answers Introduction In simple terms, reproduction is the process by which organisms create descendants. This miracle is a characteristic that all living things have in common and sets them apart from nonliving things. But even though the reproductive system is essential to keeping a species alive, it is not essential to keeping an individual alive. In human reproduction, two kinds of sex cells or gametes are involved. Sperm, the male gamete, and an egg or ovum, the female gamete must meet in the female reproductive system to create a new individual. For reproduction to occur, both the female and male reproductive systems are essential. While both the female and male reproductive systems are involved with producing, nourishing and transporting either the egg or sperm, they are different in shape and structure. The male has reproductive organs, or genitals, that are both inside and outside the pelvis, while the female has reproductive organs entirely within the pelvis. The male reproductive system consists of the testes and a series of ducts and glands. Sperm are produced in the testes and are transported through the reproductive ducts. These ducts include the epididymis, ductus deferens, ejaculatory duct and urethra. The reproductive glands produce secretions that become part of semen, the fluid that is ejaculated from the urethra. These glands include the seminal vesicles, prostate gland, and bulbourethral glands. -
Cognition and Steroidogenesis in the Rhesus Macaque
Cognition and Steroidogenesis in the Rhesus Macaque Krystina G Sorwell A DISSERTATION Presented to the Department of Behavioral Neuroscience and the Oregon Health & Science University School of Medicine in partial fulfillment of the requirements for the degree of Doctor of Philosophy November 2013 School of Medicine Oregon Health & Science University CERTIFICATE OF APPROVAL This is to certify that the PhD dissertation of Krystina Gerette Sorwell has been approved Henryk Urbanski Mentor/Advisor Steven Kohama Member Kathleen Grant Member Cynthia Bethea Member Deb Finn Member 1 For Lily 2 TABLE OF CONTENTS Acknowledgments ......................................................................................................................................................... 4 List of Figures and Tables ............................................................................................................................................. 7 List of Abbreviations ................................................................................................................................................... 10 Abstract........................................................................................................................................................................ 13 Introduction ................................................................................................................................................................. 15 Part A: Central steroidogenesis and cognition ............................................................................................................ -
Reproductive DHEA-S
Reproductive DHEA-S Analyte Information - 1 - DHEA-S Introduction DHEA-S, DHEA sulfate or dehydroepiandrosterone sulfate, it is a metabolite of dehydroepiandrosterone (DHEA) resulting from the addition of a sulfate group. It is the sulfate form of aromatic C19 steroid with 10,13-dimethyl, 3-hydroxy group and 17-ketone. Its chemical name is 3β-hydroxy-5-androsten-17-one sulfate, its summary formula is C19H28O5S and its molecular weight (Mr) is 368.5 Da. The structural formula of DHEA-S is shown in (Fig.1). Fig.1: Structural formula of DHEA-S Other names used for DHEA-S include: Dehydroisoandrosterone sulfate, (3beta)-3- (sulfooxy), androst-5-en-17-one, 3beta-hydroxy-androst-5-en-17-one hydrogen sulfate, Prasterone sulfate and so on. As DHEA-S is very closely connected with DHEA, both hormones are mentioned together in the following text. Biosynthesis DHEA-S is the major C19 steroid and is a precursor in testosterone and estrogen biosynthesis. DHEA-S originates almost exclusively in the zona reticularis of the adrenal cortex (Fig.2). Some may be produced by the testes, none is produced by the ovaries. The adrenal gland is the sole source of this steroid in women, whereas in men the testes secrete 5% of DHEA-S and 10 – 20% of DHEA. The production of DHEA-S and DHEA is regulated by adrenocorticotropin (ACTH). Corticotropin-releasing hormone (CRH) and, to a lesser extent, arginine vasopressin (AVP) stimulate the release of adrenocorticotropin (ACTH) from the anterior pituitary gland (Fig.3). In turn, ACTH stimulates the adrenal cortex to secrete DHEA and DHEA-S, in addition to cortisol. -
Healthy Aging
HEALTHY AGING Presented by CONTINUING PSYCHOLOGY EDUCATION 8.4 CONTACT HOURS “The ability to prolong life is indeed within our grasp.” Marie-Francoise Schulz-Aellen (1997) Course Objective Learning Objectives The purpose of this course is to provide an Upon completion, the participant will be able to: understanding of the concept of healthy aging. 1. Discuss current biological theories regarding Major topics include current biological theories the causes of aging. of aging, physical factors, prevalent diseases 2. Explain physical factors associated with aging. and health strategies, Baltimore Longitudinal 3. Acknowledge common older adult diseases and Study of Aging, psychological factors, social their recommended preventative measures. factors, long-term care, and the nature of 4. Articulate findings from the Baltimore healthy aging. Longitudinal Study of Aging. 5. Expound upon psychological effects of aging. Accreditation 6. Understand social theories of aging, and the Provider approved by the California Board of value of social support systems. Registered Nursing, Provider # CEP 14008, for 7. Describe prevalent concerns in long-term care. 8.4 Contact Hours. 8. Discuss key characteristics which promote In accordance with the California Code of healthy aging. Regulations, Section 2540.2(b) for licensed vocational nurses and 2592.2(b) for psychiatric technicians, this course is accepted by the Board of Vocational Nursing and Psychiatric Technicians Faculty for 8.4 contact hours of continuing education Neil Eddington, Ph.D. credit. Richard Shuman, MFT Mission Statement Continuing Psychology Education provides the highest quality continuing education designed to fulfill the professional needs and interests of nurses. Resources are offered to improve professional competency, maintain knowledge of the latest advancements, and meet continuing education requirements mandated by the profession. -
Somatopause, Weaknesses of the Therapeutic Approaches and the Cautious Optimism Based on Experimental Ageing Studies with Soy Isoflavones
EXCLI Journal 2018;17:279-301 – ISSN 1611-2156 Received: November 06, 2017, accepted: March 10, 2018, published: March 21, 2018 Review article: SOMATOPAUSE, WEAKNESSES OF THE THERAPEUTIC APPROACHES AND THE CAUTIOUS OPTIMISM BASED ON EXPERIMENTAL AGEING STUDIES WITH SOY ISOFLAVONES Vladimir Ajdžanović1*, Svetlana Trifunović1, Dragana Miljić2, Branka Šošić-Jurjević1, Branko Filipović1, Marko Miler1, Nataša Ristić1, Milica Manojlović-Stojanoski1, Verica Milošević1 1 Department of Cytology, Institute for Biological Research “Siniša Stanković”, University of Belgrade, Belgrade, Serbia 2 Clinic for Endocrinology, Diabetes and Diseases of Metabolism, Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia * Corresponding author: Vladimir Z. Ajdžanović, PhD, Department of Cytology, Institute for Biological Research “Siniša Stanković”, University of Belgrade, Despot Stefan Blvd. 142, 11060 Belgrade, Serbia, Tel: +381-11-2078-321; Fax: +381-11-2761-433, E-mail: [email protected] http://dx.doi.org/10.17179/excli2017-956 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/). ABSTRACT The pathological phenomenon of somatopause, noticeable in hypogonadal ageing subjects, is based on the growth hormone (GH) production and secretion decrease along with the fall in GH binding protein and insulin-like growth factor 1 (IGF-1) levels, causing different musculoskeletal, metabolic and mental issues. From the perspective of safety and efficacy, GH treatment is considered to be highly controversial, while some other therapeutic ap- proaches (application of IGF-1, GH secretagogues, gonadal steroids, cholinesterase-inhibitors or various combi- nations) exhibit more or less pronounced weaknesses in this respect. -
Longitudinal Antimullerian Hormone and Its Correlation with Pubertal
UC San Diego UC San Diego Previously Published Works Title Longitudinal antimüllerian hormone and its correlation with pubertal milestones. Permalink https://escholarship.org/uc/item/7rw4337d Journal F&S reports, 2(2) ISSN 2666-3341 Authors Smith, Meghan B Ho, Jacqueline Ma, Lihong et al. Publication Date 2021-06-01 DOI 10.1016/j.xfre.2021.02.001 Peer reviewed eScholarship.org Powered by the California Digital Library University of California ORIGINAL ARTICLE: REPRODUCTIVE ENDOCRINOLOGY Longitudinal antimullerian€ hormone and its correlation with pubertal milestones Meghan B. Smith, M.D.,a Jacqueline Ho, MD, M.S.,a Lihong Ma, M.D.,a Miryoung Lee, Ph.D.,b Stefan A. Czerwinski, Ph.D.,b Tanya L. Glenn, M.D.,c David R. Cool, Ph.D.,c Pascal Gagneux, Ph.D.,f Frank Z. Stanczyk, Ph.D.,a Lynda K. McGinnis, Ph.D.,a and Steven R. Lindheim, M.D., M.M.M.c,d,e a Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Southern California, Los Angeles, California; b Department of Epidemiology, Human Genetics and Environmental Sciences, University of Texas Health Science Center at Houston, School of Public Health, Brownsville, Texas; c Department of Obstetrics and Gynecology, Boonshoft School of Medicine, Wright State University, Dayton, Ohio; d Center for Reproductive Medicine Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People’s Republic of China; e Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, People’s Republic of China; and f Department of Pathology, Glycobiology Research and Training center (GRTC), University of California San Diego, California Objective: To examine the changes in AMH levels longitudinally over time and their relationship with both body composition, partic- ularly abdominal adiposity, and milestones of pubertal development in female children. -
Inside Front Cover October 7.Pmd
Early Female Puberty: A Review of Research on Etiology and Implications Eileen Daniel and Linda F. Balog Abstract Though the age of menarche has not decreased signifi cantly over the past 40 years, on average, girls began The age of female puberty appears to have decreased in to develop breasts one to two years earlier during the same the United States and western countries as child health time frame. African American girls typically begin thelarche and nutrition have improved and obesity has become more by age 9 compared to age 10 for White girls, though prevalent. Also, environmental contaminants, particularly approximately 15% of African American girls and 5% of endocrine disruptors, may also play a role in lowering the age White girls begin breast budding between the ages of 7 and of puberty. Puberty at an early age increases the risk of stress, 8 (Slyper, 2006). Currently, around 50% of all girls in the poor school performance, teen pregnancy, eating disorders, U.S. have begun to develop breasts by age 10 and 14% by substance abuse, and a variety of health issues which may ages 8 and 9. appear later in life including breast cancer and heart disease. The typical age range for the onset of puberty is between Articles for this literature review were located using a 8 and 14 years in girls while early puberty occurs between 7 computerized search of the databases Health Reference and 9, and precocious puberty generally takes place before Center, Medline, PsycINFO, and ScienceDirect from 2000 the age of 6 or 7 (Carel & Leger, 2008). -
Testosterone Deficiency in Men with Heart Failure: Pathophysiology and Its Clinical, Prognostic and Therapeutic Implications
Kardiologia Polska 2014; 72, 5: 403–409; DOI: 10.5603/KP.a2014.0025 ISSN 0022–9032 ARTYKUŁ SPECJALNY / STATE-OF-THE-ART REVIEW Testosterone deficiency in men with heart failure: pathophysiology and its clinical, prognostic and therapeutic implications Ewa A. Jankowska1, 2, 3, Michał Tkaczyszyn1, Elżbieta Kalicińska2, 4, Waldemar Banasiak2, Piotr Ponikowski2, 4 1Laboratory for Applied Research on Cardiovascular System, Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland 2Cardiology Department, Centre for Heart Diseases, Military Hospital, Wroclaw, Poland 3Institute of Anthropology, Polish Academy of Sciences, Wroclaw, Poland 4Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland HEART FAILURE: According to the data from the European Society of Cardio A CARDIOGERIATRIC SYNDROME logy (ESC) HFPilot registry [15], annual rehospitalisation Heart failure (HF) is a disease syndrome cha rate and mortality among outpatients with chronic HF has racterised by large incidence and prevalence, been estimated at 31.9% and 7.2%, respectively. Thus, new which has been estimated in the developed therapeutic approaches are needed to reverse these adverse countries at 5–10/1000 persons per year epidemiological trends. In the recent years, this search for and 1–2%, respectively [1], with a clear rise new therapies for HF has focused on pathogenetic concepts of these indices with age [2–4]. In the Bri related to noncardiac disturbances and abnormalities in HF tish Hillingdon study [2], the incidence of [16, 17]. In the current research on the pathophysiology and HF among subjects aged 25–34 years was natural history of HF, attention has been paid to renal dysfunc only 0.02/1000 persons per year, rising to tion [18–20], hepatic dysfunction [21, 22], immune activation 11.6/1000 persons per years among subjects [23], autonomic sympathetic/parasympathetic imbalance [24], aged ≥ 85 years. -
Adrenopause Andropause Growth Hormone Somatopause
All “HRT” is not Alike! The Necessity and Safety of Menopause is a hormone-deficiency state with known deleterious Bioidentical Sex-Steroid Restoration consequences for quality of life and health. in Menopause Estradiol-progesterone-testosterone (EPT) replacement for menopause is medically necessary. Estradiol replacement is safe when transdermal and accompanied Henry Lindner, MD by sufficient progesterone and testosterone. Hormonerestoration.com Bioidentical EPT therapy does not have the cardiovascular or breast cancer risks seen with PremPro . This presentation is available on the CD, handout How to provide EPT therapy to menopausal women Adrenopause Not Just “Sex Hormones” DHEA DHEA-S Converted into estradiol and testosterone within tissues Estradiol, progesterone, and testosterone are required for the growth, function and maintenance of all tissues in both sexes! Maintain brain function and health—vital neurosteroids Maintain tissue health/strength: skin, hair, bone, muscle, heart Improve insulin sensitivity: belly fat, risk of diabetes Reduce blood pressure: improve endothelial function Prevent atherosclerosis: reduce risk of MI, stroke What about the loss of hormones with aging? J Clin Endocrinol Metab. 1997 Aug;82(8):2396-402 Andropause Somatopause Testosterone in Men Growth Hormone Baltimore Longitudinal Study of Aging (BLSA). Harman et al., 2001 Clinical Chemistry 48, No. 12, 2002 1 Thyropause Menopause 8000 Men Women Testosterone Progesterone 7000 average 6000 5000 pg/ml Estradiol Estradiol T Endocr Rev. 1995 HP response to low T4 (2.7-3.2g/dL) Dec;16(6):686-715 4000 25-55 pg/ml 0-20 pg/ml 120 P 100 80% 3000 80 E decline 2000 60 TSH 40 1000 20 0 Carle, Thyroid. -
From Adrenarche to Aging of Adrenal Zona Reticularis: Precocious Female Adrenopause Onset
ID: 20-0416 9 12 E Nunes-Souza et al. Precocious female 9:12 1212–1220 adrenopause onset RESEARCH From adrenarche to aging of adrenal zona reticularis: precocious female adrenopause onset Emanuelle Nunes-Souza1,2,3, Mônica Evelise Silveira4, Monalisa Castilho Mendes1,2,3, Seigo Nagashima5,6, Caroline Busatta Vaz de Paula5,6, Guilherme Vieira Cavalcante da Silva5,6, Giovanna Silva Barbosa5,6, Julia Belgrowicz Martins1,2, Lúcia de Noronha5,6, Luana Lenzi7, José Renato Sales Barbosa1,3, Rayssa Danilow Fachin Donin3, Juliana Ferreira de Moura8, Gislaine Custódio2,4, Cleber Machado-Souza1,2,3, Enzo Lalli9 and Bonald Cavalcante de Figueiredo1,2,3,10 1Pelé Pequeno Príncipe Research Institute, Água Verde, Curitiba, Parana, Brazil 2Faculdades Pequeno Príncipe, Rebouças, Curitiba, Parana, Brazil 3Centro de Genética Molecular e Pesquisa do Câncer em Crianças (CEGEMPAC) at Universidade Federal do Paraná, Agostinho Leão Jr., Glória, Curitiba, Parana, Brazil 4Laboratório Central de Análises Clínicas, Hospital de Clínicas, Universidade Federal do Paraná, Centro, Curitiba, Paraná, Brazil 5Serviço de Anatomia Patológica, Hospital de Clínicas, Universidade Federal do Paraná, General Carneiro, Alto da Glória, Curitiba, Parana, Brazil 6Departamento de Medicina, PUC-PR, Prado Velho, Curitiba, Parana, Brazil 7Departamento de Análises Clínicas, Universidade Federal do Paraná, Curitiba, Paraná, Brazil 8Pós Graduação em Microbiologia, Parasitologia e Patologia, Departamento de Patologia Básica – UFPR, Curitiba, Brazil 9Institut de Pharmacologie Moléculaire et Cellulaire CNRS, Sophia Antipolis, Valbonne, France 100Departamento de Saúde Coletiva, Universidade Federal do Paraná, Curitiba, Paraná, Brazil Correspondence should be addressed to B C de Figueiredo: [email protected] Abstract Objective: Adaptive changes in DHEA and sulfated-DHEA (DHEAS) production from adrenal zona reticularis (ZR) have been observed in normal and pathological conditions.