DOCSLIB.ORG

A101.Full.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

COMPLICATIONS—HYPOGLYCEMIA COMPLICATIONS—HYPOGLYCEMIA ± 10 pg/ml; P < 0.01), and endogenous glucose production improved from baseline to 6 and 18 months (0.42 ± 0.08 to 0.47 ± 0.04 and 0.87 ± 0.20 mg/ kg/min; P < 0.05), albeit remaining less than normal (1.39 ± 0.11 mg/kg/min; Moderated Poster Discussion: Risks for and Consequences of Hypogly- P < 0.05); there was no improvement in epinephrine or the autonomic symp- cemia (Posters: 382-P to 387-P), see page 21. tom score. Real-time CGM can reduce the burden of problematic hypogly- cemia in patients with long standing T1D complicated by hypoglycemia & 382-P unawareness, which may in part be related to improvement in the endog- enous glucose production response to insulin-induced hypoglycemia that is Critical Hypoglycemia in Hospitalized Patients with Diabetes: Early POSTERS required to prevent or correct low blood glucose. Complications Outcomes of Standardized Reporting and Management Supported By: National Institutes of Health (R01 DK091331, UL1 TR000003, P30 Acute and Chronic KATHERINE A. ARAQUE, DEEPAK KADAYAKKARA, NINO GIGAURI, KASIA J. LIP- DK19525, T32 DK007314) SKA, GREGORY BULLER, CLARE A. FLANNERY, Bridgeport, CT, New Haven, CT Critical hypoglycemia (glucose <50 mg/dl) is associated with increased morbidity and mortality in hospitalized patients. We performed a root cause & 384-P analysis of critical hypoglycemia events (HGE) on two inpatient medical Risk of Cardiac Arrhythmias during Spontaneous Hypoglycemia in wards with the highest incidence of HGE. Pre-intervention, management Young People with Type 1 Diabetes and reporting of HGE were inconsistent, and time from HGE to documented PETER NOVODVORSKY, ALAN BERNJAK, ELAINE CHOW, AHMED IQBAL, LIANNE euglycemia (>100 mg/dl) was over 3 hours. To reduce HGE incidence and SELLORS, SCOTT WILLIAMS, ROBERT A. FAWDRY, RICHARD JACQUES, JEFFER- improve the time from HGE to euglycemia, we initiated several system- SON L.B. MARQUES, PAUL J. SHERIDAN, SIMON R. HELLER, Sheffi eld, United based changes. The EPIC EMR was programmed to provide a standardized Kingdom, Florianópolis, Brazil order set for basal-bolus insulin regimen, automated dextrose order for all Hypoglycemia has been strongly implicated in sudden nocturnal death in HGE (gel or IV), automated MD notifi cation, and recommendation for Endo- type 1 diabetes (T1DM) but the precise mechanism remains unclear. This crine consultation after 2 critical HGE. The Pyxis Med Station was pro- observational study evaluated spontaneous hypoglycemic episodes in 37 grammed to alert nurses to recheck blood glucose 15 minutes after dextrose. participants with T1DM (median age 34 years, 25th/75th centile 25.5 - 40.5) A card with the HGE management protocol was attached to each provider’s who underwent 4 days of simultaneous 12-lead ECG Holter and blinded con- ID badge, and educational seminars were given to all providers on the 2 tinuous interstitial glucose (IG) monitoring (CGM) while recording symptom- inpatient wards. Pre- and post-intervention events (Table 1) were analyzed atic hypoglycemic episodes. Altogether 3165 hours of CGM recordings were by 2-tailed Mann Whitney U and Chi-square tests. A marked improvement in analysed. Thirty-two participants (86.5%) experienced at least one episode the incidence of HGE and time to recovery demonstrate the positive impact of hypoglycemia (IG ɖ 3.5mmol/L, duration ɗ 20 min) and 23 participants of these system-based interventions. These interventions were expanded (62.2%) experienced at least one episode of nocturnal hypoglycemia (23.00- to the entire hospital and can be potentially applied to other hospitals to 7.00). Mean duration of nocturnal hypoglycemia (105 min ± 110 min) was lon- improve patient safety. ger compared to mean duration of daytime hypoglycaemia (59 min ± 48 min) (p = 0.011). Only 27% of nocturnal and 57% of daytime hypoglycemias were Table 1. Outcomes of HGE Management Pre- and Post Interventions. reported as symptomatic. Cardioacceleration was detected during daytime Pre-Intervention Post-Intervention p-value hypoglycemia (mean heart rate (HR) 80 ± 14bpm) vs. matched euglycemia (duration 3 months) (duration 6 months) (mean HR 77 ± 12bpm) (p = 0.021). Mean QTc was prolonged during nocturnal Co-Primary Outcome: Time from HGE to 225 ± 46 min 87 ± 26 min 0.03 hypoglycemia (405 ± 27msec) vs. euglycemia (400 ± 22msec) (p = 0.03) as euglycemia (median +/- SD) well as during daytime hypoglycemia (413 ± 29 msec) vs. euglycemia (401 Co-Primary outcome: Time from HGE to 76 ± 14 min 28 ± 10 min <0.001 ± 29 msec) (p < 0.001). We detected a higher incidence rate of bradycardia next fi ngerstick (median +/- SD) during nocturnal hypoglycemia compared to euglycemia (incidence rate ratio Secondary Outcome: Incidence of HGE (number 11 per 100 admissions 5.6 per 100 admissions <0.001 (IRR) 9.57 (95% CI 9.39 - 9.75), p < 0.001). During daytime hypoglycemia, of HGE per total ward admissions with DM) (35/320) (37/653) atrial ectopic activity was higher (IRR 2.50 (95% CI 1.35 - 4.66), p = 0.004), Recurrent HGE (glucose<50 mg/dl more than 37% (13/35) 24% (9/37) 0.09 but incidence of bradycardia was lower when compared to euglycemia (IRR once on a given patient) 0.025 (95% CI 0.002 - 0.26), p = 0.002). Our data suggest differences in car- diac electrophysiological responses during daytime vs. nocturnal hypogly- Documented Treatment of HGE 63% (22/35) 97% (36/37) <0.001 cemia. The increased risk of bradycardia during nocturnal hypoglycemia Physician Notifi cation 51.4% (18/35) 78% (29/37) <0.001 in susceptible individuals is clinically relevant and potentially amenable to therapeutic intervention. Supported By: Sheffi eld Teaching Hospitals & 383-P Effect of Real-Time Continuous Glucose Monitoring on Glucose & 385-P Counterregulation in Long-Standing Type 1 Diabetes: Preliminary Baseline Corrected QT Interval Is Associated with Prolongation of Results QTc during Severe Hypoglycemia in Patients with Type 2 Diabetes MICHAEL R. RICKELS, AMY PELECKIS, CORNELIA DALTON-BAKES, SHANNON SEON AH CHA, JAE-SEUNG YUN, HYUK-SANG KWON, JUNG-MIN LEE, YU-BAE O’BRIEN, NINA RAN, JOSEPH R. NAJI, HUONG-LAN NGUYEN, SANJIAN CHEN, AHN, SEUNG-HYUN KO, Suwon, Republic of Korea, Seoul, Republic of Korea INSUP LEE, MARK H. SCHUTTA, Philadelphia, PA We investigated an association between baseline heart rate−corrected Patients with long standing type 1 diabetes (T1D) are at increased risk QT (QTc) interval before severe hypoglycemia (SH) and prolongation of QTc for severe hypoglycemia due to defects in glucose counterregulation and interval during SH in patients with type 2 diabetes. hypoglycemia symptom recognition, in part mediated through exposure to Between January 2004 and June 2014, 208 patients with type 2 diabe- hypoglycemia. We sought to determine whether implementation of real- tes, who visited the emergency department for SH and conducted standard time continuous glucose monitoring (CGM) as a strategy for hypoglycemia 12−lead electrocardiography (ECG) within 6 months before SH (baseline avoidance could restore glucose counterregulation in response to insulin- ECG), were consecutively enrolled by retrospective medical record review. induced hypoglycemia in patients with long standing T1D complicated by The QT interval was corrected using Bazett’s formula (QTc), and the QTc hypoglycemia unawareness. Eleven subjects (age 44 ± 4, T1D duration 31 ± interval was analyzed during SH and 6 months before and after SH. QTc 4 years) completed paired hyperinsulinemic (1.0 mU/kg/min) euglycemic (90 intervals of 450 ms or longer in men and 460 ms or longer in women were mg/dl for 4 hours) and hypoglycemic (80, 65, 55 and 45 mg/dl each hour) considered abnormally prolonged. clamps at baseline and 6 months after initiation of CGM, with 9 subjects to The mean age and diabetes duration were 68.1 ± 12.1 and 14.1 ± 10.1 date having completed clamps after 18 months of CGM, and results com- years, respectively. The mean QTc intervals at baseline and SH episodes pared to a nondiabetic control group (n = 12). The T1D subjects experienced were 433 ± 33 ms and 460 ± 33 ms, respectively (P < 0.001). One hundred and improvement in hypoglycemia awareness (Clarke score 6.0 ± 0.3 to 4.6 ± 0.3 fourteen patients (54.8%) had a prolonged QTc interval during SH. There was and 2.9 ± 0.7; P < 0.01) and severity (HYPO score 1,884 ± 295 to 715 ± 135 and a signifi cant decrease in the prolonged QTc interval within 6 months after SH 354 ± 64; P < 0.01) without change in HbA1c (7.2 ± 0.2 to 7.0 ± 0.2 and 7.1 ± (QTc interval prolongation during SH vs. after recovery, 54.8% vs. 33.8%, P 0.3%). During the fi nal hour of clamped hypoglycemia, there was a trend for < 0.001). The prolonged QTc interval was signifi cantly associated with base- improvement in glucagon from baseline to 6 and 18 months post-interven- line QTc interval prolongation (odds ratio [OR] 2.92; 95% confi dence interval tion (41 ± 5 to 44 ± 5 and 50 ± 10 pg/ml; P = 0.08) still less than normal (96 [CI] 1.22−6.96; P = 0.016) after adjusting for age, sex, diabetes duration, body ADA-Supported Research & Moderated Poster Discussion For author disclosure information, see page A696. A101 COMPLICATIONS—HYPOGLYCEMIA mass index, smoking, presence of hypertension and chronic kidney disease, Table 1. Patient Characteristics and Economic Outcomes by Hypoglycemia previous SH, and use of insulin or sulfonylurea. Severity among Patients with T2DM Using Basal Insulin. In conclusion, a prolonged QTc interval at baseline was signifi cantly associated with prolongation of the QTc interval during SH in patients with type 2 diabetes. Therefore, this study suggests that we should pay attention to baseline QTc interval in patients with type 2 diabetes to avoid SH.
Recommended publications
  • Reactive Hypoglycemia from Metformin Immediate-Release Monotherapy Resolved by a Switch to Metformin Extended-Release: Conceptualizing Their Concentration-Time Curves

    Reactive Hypoglycemia from Metformin Immediate-Release Monotherapy Resolved by a Switch to Metformin Extended-Release: Conceptualizing Their Concentration-Time Curves

    Open Access Case Report DOI: 10.7759/cureus.16112 Reactive Hypoglycemia From Metformin Immediate-Release Monotherapy Resolved by a Switch to Metformin Extended-Release: Conceptualizing Their Concentration-Time Curves Ayesha Akram 1, 2 1. Internal Medicine, Combined Military Hospital, Rawalpindi, PAK 2. Internal Medicine, Rawalpindi Medical University, Rawalpindi, PAK Corresponding author: Ayesha Akram, [email protected] Abstract Metformin rarely, if ever, causes hypoglycemia when it is used as labeled. A 55-year-old woman presented to the medicine ward with an altered level of consciousness. She had been reviewed in an outpatient department three days earlier and prescribed 500 mg two times per day of metformin immediate-release (Met IR) for newly diagnosed type 2 diabetes mellitus (T2DM), to which she had been adherent; however, she had been experiencing intermittent episodes of hypoglycemia after taking the medication prescribed to treat her T2DM. On physical examination, she was diaphoretic and disoriented but responsive to sensory stimuli. In the ward, she received 25 ml of intravenous dextrose as the initial blood glucose reading was low at 54 mg/dl, and 4 ounces of apple juice additionally two hours later as her blood glucose level fell below 70 mg/dl again. She was no longer hypoglycemic a few hours later, and there was a significant neurological improvement. The remainder of the laboratory results, including serum renal and liver function tests, were normal. Met IR was discontinued, and metformin extended-release (Met XR) 500 mg/day was initiated at discharge. The patient's hypoglycemic episodes resolved within days after the initiation of Met XR.
  • Immunology, Immunity, Inflammation & Immunotherapies

    Immunology, Immunity, Inflammation & Immunotherapies

    2231st Conference Immunology Summit & Immunity and Immunotherapies 2018 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA Poster Presentations Page 45 Daniel Horowitz et al., J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA The development of a novel 3D printed prototype device to simplify blood cell subset enrichment at clinical sites Daniel Horowitz, George Szabo, Rudolf Cedro Jr. and Ling-Yang Hao Janssen Pharmaceutical Companies of Johnson & Johnson, USA eripheral blood collection is a relatively non-invasive way to obtain biomarkers during clinical trials. Protein and gene Pexpression changes can be used to assess drug/target engagement and disease state changes. To avoid functional changes in blood cells during storage, cells need to be stored in appropriate buffers. For gene expression analysis, whole blood can be collected in buffers that lyse the cells and protect RNA from degradation, but this obscures changes that may be found only in specific cell types. The separation of specific subsets requires instrumentation and trained personnel not readily available at many clinical sites, and shipping to a processing lab may affect the results. Therefore, a way to enrich for and stabilize blood cell subsets at the site of collection is needed. We have developed a portable 3D printed prototype device that can be operated with minimal training. Blood is collected into a tube containing commercially available polystyrene spheres (PluriSelect) coupled to an antibody specific for a blood cell surface antigen.
  • Exendin-4 Peptide Analogues As Dual Glp-1/Gip Receptor Agonists

    Exendin-4 Peptide Analogues As Dual Glp-1/Gip Receptor Agonists

    (19) TZZ¥ZZ_Z_T (11) EP 3 080 150 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C07K 14/575 (2006.01) C07K 14/605 (2006.01) 01.08.2018 Bulletin 2018/31 (86) International application number: (21) Application number: 14828149.6 PCT/EP2014/077336 (22) Date of filing: 11.12.2014 (87) International publication number: WO 2015/086728 (18.06.2015 Gazette 2015/24) (54) EXENDIN-4 PEPTIDE ANALOGUES AS DUAL GLP-1/GIP RECEPTOR AGONISTS EXENDIN-4-PEPTIDANALOGA ALS DUALE GLP-1/GIP-REZEPTORAGONISTEN ANALOGUES PEPTIDIQUES D’EXENDINE-4 EN TANT QU’AGONISTES DU RÉCEPTEUR GIP/GLP-1 DOUBLE (84) Designated Contracting States: (74) Representative: Weickmann & Weickmann AL AT BE BG CH CY CZ DE DK EE ES FI FR GB PartmbB GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO Postfach 860 820 PL PT RO RS SE SI SK SM TR 81635 München (DE) (30) Priority: 13.12.2013 EP 13306712 (56) References cited: WO-A1-2012/167744 WO-A2-2009/035540 (43) Date of publication of application: US-A1- 2011 166 062 US-A1- 2012 196 802 19.10.2016 Bulletin 2016/42 • JOHN L. KRSTENANSKY ET AL: "Importance of (73) Proprietor: SANOFI the 10-13 region of glucagon for its receptor 75008 Paris (FR) interactionsand activation of adenylate cyclase", BIOCHEMISTRY, vol. 25, no. 13, 1 July 1986 (72) Inventors: (1986-07-01), pages 3833-3839, XP055117918, • KADEREIT, Dieter ISSN: 0006-2960, DOI: 10.1021/bi00361a014 65926 Frankfurt am Main (DE) • VICTOR A.
  • Renato Wilberto Zilli Eficácia Em Longo Prazo Das

    Renato Wilberto Zilli Eficácia Em Longo Prazo Das

    RENATO WILBERTO ZILLI EFICÁCIA EM LONGO PRAZO DAS GLIFLOZINAS VERSUS GLIPTINAS NO TRATAMENTO DO DIABETES MELLITUS TIPO 2 APÓS FALÊNCIA DA METFORMINA COMO MONOTERAPIA: REVISÃO SISTEMÁTICA E METANÁLISE EM REDE Tese apresentada ao Programa de Ciências Médicas da Faculdade de Medicina da Universidade de São Paulo para obtenção do título de Doutor em Ciências. Área de Concentração: Processos Imunes e Infecciosos Orientador: Prof. Dr. Fabiano Pinheiro da Silva (Versão corrigida. Resolução CoPGr 6018/11, de 13 de outubro de 2011. A versão original está disponível na Biblioteca da FMUSP) São Paulo 2017 Dados Internacionais de Catalogação na Publicação (CIP) Preparada pela Biblioteca da Faculdade de Medicina da Universidade de São Paulo ©reprodução autorizada pelo autor Zilli, Renato Wilberto Eficácia em longo prazo das gliflozinas versus gliptinas no tratamento do diabetes mellitus tipo 2 após falência da metformina como monoterapia : revisão sistemática e metanálise em rede / Renato Wilberto Zilli ‐‐ São Paulo, 2017. Tese(doutorado)--Faculdade de Medicina da Universidade de São Paulo. Programa de Ciências Médicas. Área de concentração: Processos Imunes e Infecciosos. Orientador: Fabiano Pinheiro da Silva. Descritores: 1.Diabetes mellitus tipo 2 2.Metanálise 3.Terapia combinada 4.Falha de tratamento 5.Metformina 6.Inibidores da dipeptidil peptidase IV 7.Transportador 2 de glucose‐sódio/inibidores 8.Empagliflozina 9.Dapagliflozina 10.Saxagliptina USP/FM/DBD ‐302/17 Esta tese de doutorado está de acordo com as seguintes normas, em vigor no momento desta publicação: Referências: adaptado de International Committee of Medical Journals Editors (Vancouver). Guia de apresentação e dissertações, teses e monografias. Elaborado por Anneliese Cordeiro da Cunha, Maria Julia de A.L.
  • Table of Contents

    Table of Contents

    DISCLAIMER The information contained within this document is restricted to and intended for professional use by licensed health care providers. The statements made should not be construed as a claim, nor does it represent any particular product procedure or advice as constituting a specific cure, whether palliative or ameliorative. Procedures and products mentioned are designed to support the client’s health and may be considered as support for other procedures deemed necessary by the practitioner. Although specific manufacturers make the supplements, herbs and homeopathies referenced in this document, the opinions expressed are those of the author and are not those of any of the manufacturers. This document is not designed to replace medical advice or medical treatments, but to be used adjunctively in the care and support of health and vitality. 9 © Copyright 2005 Return to Table of Contents . CHAPTER II: SUGAR HANDLING BLOOD SUGAR STABILIZATION RELATED CONDITIONS • Hypoglycemia PROTOCOL AT A GLANCE • Reactive Hypoglycemia • Low blood sugar Primary Supplemental Support • Syndrome X Bio-Glycozyme Forte • Triglycerides high Biomega-3 • Carbohydrate sensitivity Secondary Supplemental Support • Pre-diabetic Whey Protein Isolate • B vitamin deficiency Amino Acid Quick Sorb • Sugar sensitivity Beta-TCP • Food cravings ADHS Cytozyme-PAN • Carbohydrate cravings Cytozyme-LV Cytozyme-AD PHYSIOLOGIC CONSIDERATIONS Tri-Chol Blood sugar problems begin in childhood with excess use of sugary snacks and drinks. This is extremely common today. The U.S. Department of Agriculture estimates that the average American consumes from 150 to 180 pounds of sugar each year––an unbelievable amount compared to two or three hundred years ago when normal sugar consumption was one to five pounds per year.
  • Antidiabetic Therapy in the Treatment of Nonalcoholic Steatohepatitis

    Antidiabetic Therapy in the Treatment of Nonalcoholic Steatohepatitis

    International Journal of Molecular Sciences Review Antidiabetic Therapy in the Treatment of Nonalcoholic Steatohepatitis Yoshio Sumida 1,* , Masashi Yoneda 1, Katsutoshi Tokushige 2, Miwa Kawanaka 3, Hideki Fujii 4, Masato Yoneda 5, Kento Imajo 5 , Hirokazu Takahashi 6, Yuichiro Eguchi 7, Masafumi Ono 8, Yuichi Nozaki 9 , Hideyuki Hyogo 10, Masahiro Koseki 11, Yuichi Yoshida 12, Takumi Kawaguchi 13 , Yoshihiro Kamada 14, Takeshi Okanoue 15, Atsushi Nakajima 5 and Japan Study Group of NAFLD (JSG-NAFLD) y 1 Division of Hepatology and Pancreatology, Department of Internal Medicine, Aichi Medical University, Nagakute, Aichi 480-1195, Japan; [email protected] 2 Department of Internal Medicine, Institute of Gastroenterology, Tokyo Women’s Medical University, Tokyo 162-8666, Japan; [email protected] 3 Department of General Internal Medicine2, Kawasaki Medical School, Okayama 700-8505, Japan; [email protected] 4 Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka 558-8585, Japan; [email protected] 5 Department of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan; [email protected] (M.Y.); [email protected] (K.I.); [email protected] (A.N.) 6 Department of Metabolism and Endocrinology, Faculty of Medicine, Saga University, Saga 840-8502, Japan; [email protected] 7 Liver Center, Saga University Hospital, Saga 840-8502, Japan; [email protected] 8 Division of Gastroenterology and Hepatology,
  • Neurologic Manifestations of Hypoglycemia

    Neurologic Manifestations of Hypoglycemia

    13 Neurologic Manifestations of Hypoglycemia William P. Neil and Thomas M. Hemmen University of California, San Diego United States of America (USA) 1. Introduction Unlike most other body tissues, the brain requires a continuous supply of glucose. It has very limited endogenous glycogen stores, and does not produce glucose intrinsically.1 Although it accounts for 2% of body weight, the brain utilizes 25% of the body’s glucose due to its high metabolic rate.2, 3 Evidence for the brains sole reliance on glucose came from obtaining a respiratory quotient of one after measuring differences between arterial and venous content of oxygen and carbon dioxide in blood traveling through the brain.4 In the past, neurons were thought to directly metabolize glucose, however, more recent studies suggest astrocytes may play an important role in glucose metabolism.5 Astrocytic foot processes surround brain capillaries, which deliver glucose to the brain. With this, they form the first cellular barrier for entering glucose.5 Astrocytes contain the non-insulin dependent GLUT1 transporter, as well as the insulin dependent GLUT4 transporter, suggesting a possible role for astrocytes in regulating and storing brain glucose in an insulin dependent and independent manner (see figure 1).6-8 In addition to glucose, the brain contains a very limited store of glycogen, (between 0.5 and 1.5 g, or about 0.1% of total brain weight). Unlike peripheral tissue, where glycogen is readily mobilized during hypoglycemia, the brain can only function normally for a limited duration. Glycogen content seems to fall in areas of highest brain metabolic rate, suggesting at least some, albeit limited role as fuel during hypoglycemia.7 Although the brain relies primarily on glucose during normal conditions, it can use ketone bodies during starvation.
  • 1 Jasvinder Chawla, MD, MBA Chief Neurology, Hines Veterans Affairs

    1 Jasvinder Chawla, MD, MBA Chief Neurology, Hines Veterans Affairs

    Jasvinder Chawla, MD, MBA Chief Neurology, Hines Veterans Affairs Hospital, Professor of Neurology, Loyola University Medical Medical Center Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjuct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Editor-in-Chief, Medscape Drug Reference Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine, Director, Vanderbilt Stroke Center, Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital, Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center. Chief Editor Helmi L Letsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine, Associate Director, OHSU Stoke Center Additional Contributors Pitchaiah Mandava, MD, PhD Assistant Professor, Department of Neurology, Baylor College of Medicine, Consulting Staff, Department of Neurology, Michael E DeBakey Veterans Affairs Medical Center. Richard M Zweifler, MD Chief of Neurosciences, Sentara Healthcare, Professor and Chair of Neurology, Eastern Virginia Medical School. 1 Thomas A Kent, MD Professor and Director of Stroke Research and Education, Department
  • Blood Sugar the Hidden Factor in Health

    Blood Sugar the Hidden Factor in Health

    Blood Sugar The Hidden Factor in Health Disorders in blood sugar balance disrupt all aspects of human physiology. To understand this, we must keep in mind that our bodies primarily produce their energy from converting glucose (blood sugar) into ATP. If this system is not working properly, health cannot be achieved. Blood sugar disorders are extraordinarily common in the U.S. today. Much (but not all) of the prob- lem can be placed on the Standard American Diet that is high in saturated fats and sugars while being low in essential fatty acids and fiber. In the past decade, there has been an explosion in the number of cases of diabetes, which only figures to grow in the decades ahead. Insulin Insulin is a protein hormone secreted by the pancreas. Its primary job is to stimulate the uptake of glucose from our blood into our cells. Cell membranes have a lipid layer thru which glucose cannot pass on its own. It has to be carried across with the assistance of insulin. Once inside the cells, glu- cose can be used for energy. All foods are ultimately converted into glucose. An increase of glucose in the bloodstream stimulates the release of more insulin. Insulin promotes the production of glycogen, which is the form that glucose is stored in, for later use. Insulin also promotes the formation of lipids, triglyceride and protein. Alterations in insulin are responsible for causing metabolic disorders such as hypoglycemia and diabetes. Hypoglycemia If the pancreas overreacts to a sudden surge in glucose, it will release excess insulin which will subsequently cause a drop in blood sugar.
  • Arun Chauhan, Ph.D. Assistant Research Professor University Of

    Arun Chauhan, Ph.D. Assistant Research Professor University Of

    Arun Chauhan, Ph.D. Assistant Research Professor University of North Dakota, Grand Forks, ND, 58202 Phone: (701) 215-2044 Email: [email protected] (US Permanent Resident) SUMMARY OF QUALIFICATIONS Wide-ranging experience in Immunology, Oncology, Molecular Biology and infectious disease with strong expertise in disease Model. Experience in immune cell isolation, innate cell purification, co-culture assays, cytokine (ELISA, CBA) and cell proliferation, Cytotoxic assay. Extensive experience in molecular biology techniques such as, RT-PCR, western blot, Nucleic acid Extraction, Quantitative PCR, DNA footprinting assay, and recombinant DNA technology). Strong expertise in cell based immunological assays (ELISPOT), Reporter assay, transplantation, multiparametric flow cytometry, FACS, Intracellular Cytokine staining. Experience in mammalian primary cell Culture, & primary human lymphocyte (T cells, B cells, DCs and macrophages) from blood, si/shRNA transfection, CRISPR/Cas9. Successfully initiated, managed and completed multiple projects simultaneously and published research in peer-reviewed journals. Competent to work independently and in team-based projects as evident from more than 20 publications. Ability to critically analyze and troubleshoot data, interpret results and effectively present findings in meetings. Excellent organizational, and written, oral and interpersonal communication skills. PROFILE Interdisciplinary immunology, Molecular, Epigenetics-scientist with an in-depth expertise in in vitro and in vivo cell-based assays (murine and human), involving macrophages, Neutrophils and T- cells. Development of murine models to investigate the role of macrophage plasticity and T-cell functionality in Sjogren’s Syndrome and Pneumonic Sepsis (2° Infection) in fate mapping mice. Proven expertise in genome molecular biology (RNA-Seq, ChIP Seq, ATAC seq & short capped RNA-seq). Proven ability to complete projects in time-bound manner.
  • Jack L. Snitzer,D.O

    Jack L. Snitzer,D.O

    JACK L. SNITZER,D.O. Internal Medicine Board Review Course 2019 ENDOCRINE PANCREAS JACK L. SNITZER, D.O. Peninsula Regional Endocrinology 1415 S. Division Street Salisbury, MD 21804 Phone:410-572-8848 Fax:410-572-6890 E-Mail: [email protected] Endocrine Pancreas n Alpha Cells: Glucagon n Beta Cells: Insulin n Delta Cells: Somatostatin n D1 Cells: Vasoactive intestinal Polypeptide (VIP) n F Cells: Pancreatic Polypeptide (PP) n G Cells: Gastrin GLUCAGONOMA -Glucagonoma Causes increased glucose production. Rare, often malignant tumors. Classic Rash: Necrolytic Migratory Erythema Painful glossitis, angular stomatitis. Tx: Surgery, Octreotide INSULINOMA -Insulinoma Spontaneous hypoglycemia. 80% are benign. Usually very small tumors. Second most common pancreatic tumor found in MEN 1. INSULINOMA -Insulinoma Dx: elevated insulin and C-peptide level with simultaneously low glucose and symptoms. -Fasting glucose <50 mg/dl. Tx: Surgery. Octreotide to palliate. Hypoglycemia: other causes in non- diabetics • Reactive hypoglycemia (generally in obese patient with metabolic syndrome) • Malnutrition (celiac disease, eating disorder, etc.) • Cortisol insufficiency (adrenal or pituitary cause) • Nesidioblastosis (for instance: post-gastric bypass: islet cell hyperplasia) Hypoglycemia: other causes in non- diabetics • Liver disease • Surreptitious, malicious or inadvertent use of insulin. In this case, when the BG is low, insulin level will be high and C-peptide level will be low. Need to obtain these levels before treating with glucose or glucagon. • Surreptitious use of insulin secretagogue. Insulin and c- peptide levels will be high when BG is low. • Glucometer error (glucose meters are inaccurate when the BG is low); or hypoperfusion of the fingers Hypoglycemia: other causes in non- diabetics • Remember: early hypoglycemia symptoms (shakes, sweats, anxiety, hunger) are due to catecholamine release.
  • Cancer Immunology and Immunotherapy

    Cancer Immunology and Immunotherapy

    UC Irvine UC Irvine Previously Published Works Title Cancer Immunology and Immunotherapy. Permalink https://escholarship.org/uc/item/67q1k6k3 Authors Owais, Mohammad Zubair, Swaleha Agrawal, Anshu et al. Publication Date 2015 DOI 10.1155/2015/393454 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Hindawi Publishing Corporation BioMed Research International Volume 2015, Article ID 393454, 2 pages http://dx.doi.org/10.1155/2015/393454 Editorial Cancer Immunology and Immunotherapy Mohammad Owais,1 Swaleha Zubair,1 Anshu Agrawal,2 and Yung-Fu Chang3 1 AligarhMuslimUniversity,Aligarh,India 2University of California, Irvine, USA 3Cornell University, Ithaca, USA Correspondence should be addressed to Mohammad Owais; owais [email protected] Received 10 May 2015; Accepted 10 May 2015 Copyright © 2015 Mohammad Owais et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The study of molecular and cellular interplays between of the newly introduced method with various published immune system and cancerous cells is gaining tremen- protocols to underline its effectiveness thereof. In the arena dous momentum across the globe. Concomitantly, with the of NK cell based immunotherapies, the article “NKG2D and better insight into the intricacies of cancer immunology, DNAM-1 Ligands: Molecular Targets for NK Cell-Mediated immunotherapeutic approaches to deal with cancer have Immunotherapeutic Intervention in Multiple Myeloma” by garnered tremendous boost in the recent past; reckoning C. Fionda et al. has come up with satisfactory results to with these, it is timely to analyse their potentialities either further potentiate NK cell based immunotherapies.