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Ptvg-HP Vaccine Protocol
Version 10/7/2015 Randomized Phase II Trial of a DNA Vaccine Encoding Prostatic Acid Phosphatase (pTVG-HP) versus GM-CSF Adjuvant in Patients with Non-Metastatic Prostate Cancer CO 08801 Investigational Agent: BB IND 12109 - pTVG-HP DNA encoding human prostatic acid phosphatase Study Sponsors: 56 patients – treated at UWCCC and UCSF Department of Defense Prostate Cancer Research Program federal grant 50 patients in biomarker cohort – treated at UWCCC, UCSF and JHU Madison Vaccines Inc. (MVI) corporate sponsor STUDY SITE INFORMATION Study Sites: University of Wisconsin Carbone Cancer Center (UWCCC) 1111 Highland Avenue Madison, WI 53705 University of California San Francisco (UCSF) Johns Hopkins School of Medicine (JHU) Study Principal Investigator: Douglas G. McNeel, M.D., Ph.D. UWCCC 7007 Wisconsin Institutes for Medical Research 1111 Highland Ave. Madison, WI 53705 Tel: (608) 263-4198 Fax: (608) 265-0614 [email protected] UWCCC Local Principal Investigator : Glenn Liu, MD UWCCC 7051 Wisconsin Institutes for Medical Research 1111 Highland Ave. Madison, WI 53705 Tel : (608) 265-8689 Fax : (608) 265-5146 [email protected] Medical Monitor: Mark Albertini, M.D. UWCCC 600 Highland Ave. K6/5 CSC Madison, WI 53792 Tel: (608) 265-8131 Fax: (608) 265-8133 [email protected] Other UWCCC Investigators: Joshua Lang, M.D. – Clinical Investigator Christos Kyriakopolous, M.D. – Clinical Investigator Robert Jeraj, Ph.D. – Medical Physics, Quantitative Total Bone Imaging Scott Perlman, M.D. – Nuclear Medicine UCSF Principal Investigator: Lawrence Fong, M.D. JHU Principal Investigator: Emmanuel Antonarakis, MD Study Coordinator: Mary Jane Staab, R.N. B.S.N. UWCCC 600 Highland Ave. -
Endocrinology Resident Profile Jill Trinacty
Endocrinology Resident Profile Jill Trinacty July 2017 About me My name is Jill Trinacty, and I was raised in Berwick, Nova Scotia. I went completed my BSc. (Honours) at Saint Francis Xavier University in Antigonish, Nova Scotia. I spent a year as the Active Living Coordinator with the Town of Kentville then completed my MD at Dalhousie University. I moved to Ottawa, Ontario in 2013 for my residency in Internal Medicine at the University of Ottawa and am currently a PGY-5 in Endocrinology and Metabolism. Why I chose General Endocrinology In medical school I became interested in almost every area of medicine, but ultimately applied to internal medicine for a number of reasons. I have always been interested in Endocrinology, specifically diabetes. Diabetes affects so many people in our communities and can have significant morbidity and mortality. I liked the detail of internal medicine and the complexity of patients. Having some previous experience in public health, I knew that I wanted a career that would allow me to discuss lifestyle changes as an aspect of therapy – specifically nutrition and physical activity. I also wanted a career that would allow for work/life balance. Seeing the day-to-day lifestyle of each internal medicine subspecialty confirmed that Endocrinology was the right fit for me. Clinical Life What does a typical day of clinical duties involve? This is an example of my typical daily and weekly schedule: Endocrinology – A typical day 7:30 – 8:00 Clerical work / Chief resident duties. Review emails, follow up on patient results, approve vacation requests, make call schedule. -
Thursday 23 June 2016 – Morning A2 GCE HUMAN BIOLOGY F225/01 Genetics, Control and Ageing *5884237032* Candidates Answer on the Question Paper
Oxford Cambridge and RSA Thursday 23 June 2016 – Morning A2 GCE HUMAN BIOLOGY F225/01 Genetics, Control and Ageing *5884237032* Candidates answer on the Question Paper. OCR supplied materials: Duration: 2 hours None Other materials required: • Electronic calculator • Ruler (cm/mm) *F22501* INSTRUCTIONS TO CANDIDATES • Write your name, centre number and candidate number in the boxes above. Please write clearly and in capital letters. • Use black ink. HB pencil may be used for graphs and diagrams only. • Answer all the questions. • Read each question carefully. Make sure you know what you have to do before starting your answer. • Write your answer to each question in the space provided. If additional space is required, you should use the lined page(s) at the end of this booklet. The question number(s) must be clearly shown. • Do not write in the bar codes. INFORMATION FOR CANDIDATES • The number of marks is given in brackets [ ] at the end of each question or part question. • The total number of marks for this paper is 100. • Where you see this icon you will be awarded marks for the quality of written communication in your answer. • You may use an electronic calculator. • You are advised to show all the steps in any calculations. • This document consists of 24 pages. Any blank pages are indicated. © OCR 2016 [K/500/8502] OCR is an exempt Charity DC (NH/SW) 119808/4 Turn over 2 Answer all the questions. 1 Excretion is the removal of metabolic waste products from the body. The kidney is one of the organs involved in excretion. -
Prenatal Growth Restriction, Retinal Dystrophy, Diabetes Insipidus and White Matter Disease: Expanding the Spectrum of PRPS1-Related Disorders
European Journal of Human Genetics (2015) 23, 310–316 & 2015 Macmillan Publishers Limited All rights reserved 1018-4813/15 www.nature.com/ejhg ARTICLE Prenatal growth restriction, retinal dystrophy, diabetes insipidus and white matter disease: expanding the spectrum of PRPS1-related disorders Almundher Al-Maawali1,2, Lucie Dupuis1, Susan Blaser3, Elise Heon4, Mark Tarnopolsky5, Fathiya Al-Murshedi2, Christian R Marshall6,7, Tara Paton6,7, Stephen W Scherer6,7 for the FORGE Canada Consortium9, Jeroen Roelofsen8, Andre´ BP van Kuilenburg8 and Roberto Mendoza-Londono*,1 PRPS1 codes for the enzyme phosphoribosyl pyrophosphate synthetase-1 (PRS-1). The spectrum of PRPS1-related disorders associated with reduced activity includes Arts syndrome, Charcot–Marie–Tooth disease-5 (CMTX5) and X-linked non-syndromic sensorineural deafness (DFN2). We describe a novel phenotype associated with decreased PRS-1 function in two affected male siblings. Using whole exome and Sanger sequencing techniques, we identified a novel missense mutation in PRPS1. The clinical phenotype in our patients is characterized by high prenatal maternal a-fetoprotein, intrauterine growth restriction, dysmorphic facial features, severe intellectual disability and spastic quadraparesis. Additional phenotypic features include macular coloboma-like lesions with retinal dystrophy, severe short stature and diabetes insipidus. Exome sequencing of the two affected male siblings identified a shared putative pathogenic mutation c.586C4T p.(Arg196Trp) in the PRPS1 gene that was maternally inherited. Follow-up testing showed normal levels of hypoxanthine in urine samples and uric acid levels in blood serum. The PRS activity was significantly reduced in erythrocytes of the two patients. Nucleotide analysis in erythrocytes revealed abnormally low guanosine triphosphate and guanosine diphosphate. -
Evaluation of Deficiency of 21 -Hydroxylation in Patients with Congenital Adrenal Hyperplasia 0
Arch Dis Child: first published as 10.1136/adc.43.230.410 on 1 August 1968. Downloaded from Arch. Dis. Childh., 1968, 43, 410. Evaluation of Deficiency of 21 -hydroxylation in Patients with Congenital Adrenal Hyperplasia 0. M. GALAL, B. T. RUDD, and N. M. DRAYER From the Institute of Child Health, University of Birmingham Congenital adrenal hyperplasia can manifest therapy in these 13 children started within the first 3 itself in a variety of clinical and biochemical weeks of life. abnormalities (Bongiovanni and Root, 1963). The In addition to the 18 patients with congenital adrenal salt-losing tendency in some of these patients can hyperplasia, 3 children with shortness of stature and 3 with early signs of puberty were given ACTH to be due to the absence of specific enzymes: dehydro- investigate their adrenal function. None of these genases or hydroxylases (Bongiovanni and Root, patients had received steroids and all had normal free 1963; Ulick et al., 1964; Visser and Cost, 1964). cortisol and 17-hydroxycorticosteroid urinary excretion In addition to the impaired production of certain rates. The age and sex of the patients in the 3 groups steroids, antagonism by steroids or other compounds and details of the steroid therapy are listed in Table I. could, theoretically, account for the salt-losing tendency (Neher, Meystre, and Wettstein, 1959; ACTH test. Twenty-four hour urine collections Jacobs et al., 1961). were obtained before and during ACTH stimulation. The purpose ofthis study was to discover whether, ACTH gel (Organon) was given intramuscularly at a copyright. despite the continuation of steroid therapy, stimula- dose of 20 I.U. -
Chronic Fatigue: Is It Endocrinology?
I ORIGINAL PAPERS Chronic fatigue: is it endocrinology? Kate M Evans, Daniel E Flanagan and Terence J Wilkin Kate M Evans ABSTRACT – Fatigue and stress-related illnesses imal physical signs where initial investigations are MRCP, Consultant often become diagnoses of exclusion after exten- normal. It is possible to reassure the individual that Physician sive investigation. ‘Tired all the time’ is a frequent there is no significant disease at that point but there Daniel E reason for referral to the endocrine clinic, the are no clear data to address the question of whether Flanagan implicit question being – is there a subtle overt pathology will develop in the future. This paper FRCP, Consultant endocrine pathology contributing to the patient’s reports audit findings for a cohort of patients seen Physician symptoms? Often initial assessment suggests not in an endocrinology clinic with fatigue, including but there are no clear data to address the ques- Terence J Wilkin outcome data at five or more years later. FRCP, Professor of tion of whether overt pathology will develop in the Medicine future. This study observed outcomes after five Subjects and methods years in 101 consecutive and unselected referrals Department of to secondary care for ‘fatigue?cause’, where initial Consecutive and unselected referrals from primary Endocrinology and assessment did not suggest treatable endocrine care to the endocrinology service over a four-year Metabolism, Peninsula Medical pathology. The findings suggest that the clinical period (1995–99) were identified from the clinic School, Plymouth diagnosis of fatigue, based on history and tests to database. Referrals were included in the dataset if the and Derriford exclude anaemia, hypothyroidism and diabetes, is primary reason for referral or primary symptom was Hospital, Plymouth secure: these patients do not subsequently fatigue. -
400 We Have Studied Six Infants and Young Children with Hyper
400 ABSTRACTS We have studied six infants and young children with hyper- ml plasma sample has been evaluated for the rapid (4—6 hr) diag- thyroidism whose clinical course differs from the few reports of nosis of CAH. Pet ether, benzene and methylene chloride extracts others. Neonatal and early childhood hyperthyroidism are usually of plasma are quantitated by competitive protein binding using thought of as separate, rare, and transient disorders seldom re- 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol (cmpd S), quiring long term treatment. 1) Our cases have not been tran- and cortisol standards, respectively, for comparison. The observed sient: 2) they have occurred in families with a high incidence of plasma steroid concentrations are expressed as a ratio of adult Graves disease. "17-OHP" + "cmpd S" to "cortisol" since comparison of ratios, Four were born with Graves disease. Three continue to be rather than absolute values, has been found to differentiate nor- hyperthyroid at ages 1, 5, and 6 years. Two developed Graves mals from patients more clearly. disease at ages 3 and 8 years and continue on anti-thyroid medi- Plasma samples have been obtained from six normal children cation. Graves disease occurred in five of the six mothers and aged 4 days-7 yrs following administration of ACTH, from six was apparent during gestation in four. The sixth mother, mother adults with 11-hydroxylation impaired by the administration of of a neonatal case, has never had overt Graves disease, but female metyrapone, and from three children aged 11 mos, 6 yrs and 8 members of four generations have had Graves disease. -
Tumor Markers
Tumor Markers Alan H.B. Wu, Ph.D. Professor, Laboratory Medicine, UCSF Section Chief, Clinical Chemistry, Toxicology, Pharmacogenomics Laboratory, SFGH Learning objectives • Know the ideal characteristics of a tumor marker • Understand the role of tumor markers for diagnosis and management of patients with cancer. • Know the emerging technologies for tumor markers • Understand the role of tumor markers for therapeutic selection How do we diagnose cancer today? Physical Examination Blood tests CT scans Biopsy Human Prostate Cancer Normal Blood Smear Chronic Myeloid Leukemia Death rates for cancer vs. heart disease New cancer cases per year Cancer Site or Type New Cases Prostate 218,000 Lung 222,500 Breast 207,500 Colorectal 149,000 Urinary system 131,500 Skin 68,770 Pancreas 43,100 Ovarian 22,000 Myeloma 20,200 Thyroid 44,700 Germ Cell 9,000 Types of Tumor Markers • Hormones (hCG; calcitonin; gastrin; prolactin;) • Enzymes (acid phosphatase; alkaline phosphatase; PSA) • Cancer antigen proteins & glycoproteins (CA125; CA 15.3; CA19.9) • Metabolites (norepinephrine, epinephrine) • Normal proteins (thyroglobulin) • Oncofetal antigens (CEA, AFP) • Receptors (ER, PR, EGFR) • Genetic changes (mutations/translocations, etc.) Characteristics of an ideal tumor marker • Specificity for a single type of cancer • High sensitivity and specificity for cancerous growth • Correlation of marker level with tumor size • Homogeneous (i.e., minimal post-translational modifications) • Short half-life in circulation Roles for tumor markers • Determine risk (PSA) -
LEUKOCYTE SURFACE ORIGIN of HUMAN At-ACID GLYCOPROTEIN (OROSOMUCOID)*
LEUKOCYTE SURFACE ORIGIN OF HUMAN at-ACID GLYCOPROTEIN (OROSOMUCOID)* BY CARL G. GAHMBERG AND LEIF C. ANDERSSON (From the Department of Bacteriology and Immunology, and the Transplantation Laboratory, Department of Surgery IV, University of Helsinki, Helsinki 29, Finland) Human al-acid glycoprotein (orosomucoid) (o~I-AG)1 constitutes the main component of the seromucoid fraction of human plasma. It belongs to the acute phase proteins, which increase under conditions such as inflammation, pregnancy, and cancer (1, 2). al-AG has previously been found to be synthesized in liver (3), and after removal of terminal sialic acids, it is cleared from the circulation by binding to a receptor protein on liver cell plasma membranes (4). The structure of al-AG is well known. It is composed of a single polypeptide chain and contains 245% carbohydrate including a large amount of sialic acid. The carbohydrate is located in the first half of the peptide chain linked to asparagine residues (5, 6). The function of al-AG is unclear. However, Schmid et al. (5) and Ikenaka et al. (7) and reported that the amino acid sequence of the protein shows a significant homology with human IgG. This finding and the striking increase in inflammatory and lymphopro- liferative disorders made us consider the possibility that leukocytes could be directly involved in the synthesis and release of a~-AG. We report here the presence of a membrane form of al-AG, with an apparent tool wt of 52,000, on normal human lymphocytes, granulocytes, and monocytes. By the use of internal labeling with [3H]leucine in vitro, we demonstrate that the membrane protein is synthesized by lymphocytes. -
Diabetes Insipidus
Your feelings about Infertility conditions series: › Diabetes insipidus The Pituitary Foundation Information Booklets Working to support pituitary patients, their carers & families The Pituitary Foundation is a charity working About this booklet in the United Kingdom and Republic of The aim of this booklet is to provide information Ireland supporting patients with pituitary about diabetes insipidus. conditions, their carers, family and friends. You may find that not all of the information Our aims are to offer support through the applies to you in particular, but we hope it helps pituitary journey, provide information to the you to understand your condition better and community, and act as the patient voice to raise offers you a basis for discussion with your GP awareness and improve services. and endocrinologist. What is diabetes insipidus and why do we get it? 3 The two forms of diabetes insipidus 5 How is DI diagnosed and treated? 7 How is DI diagnosed? 7 What tests are carried out and how will they feel? 7 How is DI treated? 7 Aftercare 9 How will diabetes insipidus affect my life? 10 Prescriptions 10 Driving 10 Employment problems 10 Insurance & pensions 10 Personal medical identification 11 Toilet facilities card 11 National key scheme 11 Common questions 12-13 What DI means to me - a patient's story 14 Membership & donation information 15 2 Diabetes insipidus What is diabetes insipidus (DI) and why do we get it? Diabetes insipidus (DI) is caused by a problem with either the production, or action, of the hormone vasopressin (AVP). If you have DI your kidneys are unable to retain water. -
Comprehensive Urinary Hormone Assessments
ENDOCRINOLOGY Complete Hormones – Analytes Comprehensive Urinary Hormone Assessments Urinary Pregesterones Urinary Glucocorticoids Urinary Androgens Urinary Estrogens Pregnanediol Cortisol, Free Testosterone Estrone Pregnanetriol Total 17-Hydroxy-corticosteroids Dehydroepiandrosterone (DHEA) Estradiol allo-Tetrahydrocortisol, a-THF Total 17-Ketosteroids Estriol Tetrahydrodeoxycortisol Androsterone 2-Hydroxyestrone Tetrahydrocortisol, THF Etiocholanolone 2-Methoxyestrone Tetrahydrocortisone, THE 11-Keto-androsterone 4-Hydroxyestrone 17-Hydroxysteriods, Total 11-Keto-etiocholanolone 4-Methoxyestrone Pregnanetriol 11-Hydroxy-androsterone 16α-Hydroxyestrone 11-Hydroxy-etiocholanolone 2-Hydroxy-estrone:16α-Hydroxyestrone ratio 2-Methoxyestrone:2-Hydroxyestrone ratio CLINICIAN INFORMATION 4-Methoxyestrone:4-Hydroxyestrone ratio ADVANCING THE CLINICAL UTILITY OF URINARY HORMONE ASSESSMENT Specimen Requirements Complete Hormones™ is Genova’s most comprehensive • 120 ml aliquot, refrigerated until shipped, urinary hormone profile, and is designed to assist with the from either First Morning Urine or 24-Hour clinical management of hormone-related symptoms. This profile Collection Why Use Complete Hormones? assesses parent hormones and their metabolites as well as key metabolic pathways, and provides insight into the contribution Hormone testing is an effective tool for assessing Related Profiles: that sex hormones may have in patients presenting with and managing patients with hormone- related symptoms. This profile supports: • Male Hormonal Health™ -
Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes
Tohoku J. Exp. Med., 2011,Differential 223, 161-176 Gene Expression in OPCs, Oligodendrocytes and Type II Astrocytes 161 Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes Jian-Guo Hu,1,2,* Yan-Xia Wang,3,* Jian-Sheng Zhou,2 Chang-Jie Chen,4 Feng-Chao Wang,1 Xing-Wu Li1 and He-Zuo Lü1,2 1Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, P.R. China 2Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical College, Bengbu, P.R. China 3Department of Neurobiology, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China 4Department of Laboratory Medicine, Bengbu Medical College, Bengbu, P.R. China Oligodendrocyte precursor cells (OPCs) are bipotential progenitor cells that can differentiate into myelin-forming oligodendrocytes or functionally undetermined type II astrocytes. Transplantation of OPCs is an attractive therapy for demyelinating diseases. However, due to their bipotential differentiation potential, the majority of OPCs differentiate into astrocytes at transplanted sites. It is therefore important to understand the molecular mechanisms that regulate the transition from OPCs to oligodendrocytes or astrocytes. In this study, we isolated OPCs from the spinal cords of rat embryos (16 days old) and induced them to differentiate into oligodendrocytes or type II astrocytes in the absence or presence of 10% fetal bovine serum, respectively. RNAs were extracted from each cell population and hybridized to GeneChip with 28,700 rat genes. Using the criterion of fold change > 4 in the expression level, we identified 83 genes that were up-regulated and 89 genes that were down-regulated in oligodendrocytes, and 92 genes that were up-regulated and 86 that were down-regulated in type II astrocytes compared with OPCs.