New York Chapter American College of Physicians Annual
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VIEWS & REVIEWS Arterial ischemic stroke in HIV Defining and classifying etiology for research studies Laura A. Benjamin, ABSTRACT MRCP, PhD HIV infection, and potentially its treatment, increases the risk of an arterial ischemic stroke. Mul- Alan Bryer, FCN (SA), tiple etiologies and lack of clear case definitions inhibit progress in this field. Several etiologies, PhD many treatable, are relevant to HIV-related stroke. To fully understand the mechanisms and the Sebastian Lucas, FRCP, terminology used, a robust classification algorithm to help ascribe the various etiologies is FRCPath needed. This consensus paper considers the strengths and limitations of current case definitions Alan Stanley, FCN (SA) in the context of HIV infection. The case definitions for the major etiologies in HIV-related strokes Theresa J. Allain, FRCP, were refined (e.g., varicella zoster vasculopathy and antiphospholipid syndrome) and in some in- PhD stances new case definitions were described (e.g., HIV-associated vasculopathy). These case def- Elizabeth Joekes, FRCR initions provided a framework for an algorithm to help assign a final diagnosis, and help classify Hedley Emsley, FRCP, the subtypes of HIV etiology in ischemic stroke. Neurol Neuroimmunol Neuroinflamm 2016;3:e254; PhD doi: 10.1212/NXI.0000000000000254 Ian Turnbull, FRCR Colin Downey, MIBMS GLOSSARY Cheng-Hock Toh, FRCP, ACL 5 anticardiolipin antibodies; anti-b2GP1 5 anti–b2-glycoprotein I; APS 5 antiphospholipid syndrome; HSV 5 herpes PhD simplex virus; IgG 5 immunoglobulin G; LA 5 lupus anticoagulant; RPR 5 rapid plasma reagin; SVD 5 small vessel disease; 5 5 5 Kevin Brown, FRCPath, TB tuberculosis; TOAST Trial of Org 10172 in Acute Stroke Treatment; TTP thrombotic thrombocytopenic purpura; VDRL 5 Venereal Disease Research Laboratory; VZV 5 varicella zoster virus. -
Subclavian Vein Obstruction Without Thrombosis
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Subclavian vein obstruction without thrombosis Richard J. Sanders, MD,a and Sharon L. Hammond, MD,a,b Denver, Colo Background: Unilateral arm swelling caused by subclavian vein obstruction without thrombosis is an uncommon form of venous thoracic outlet syndrome (TOS). In 87 patients with venous TOS, only 21 patients had no thrombosis. We describe the diagnosis and treatment of these patients. Material and Methods: Twenty-one patients with arm swelling, cyanosis, and venograms demonstrating partial subclavian vein obstruction were treated with transaxillary first rib resection and venolysis. Results: Eighteen (86%) of 21 patients had good-to-excellent improvement of symptoms. There were two failures (9%). Conclusions: Unilateral arm swelling without thrombosis, when not caused by lymphatic obstruction, may be due to subclavian vein compression at the costoclavicular ligament because of compression either by that ligament or the subclavius tendon most often because of congenital close proximity of the vein to the ligament. Arm symptoms of neurogenic TOS, pain, and paresthesia often accompany venous TOS while neck pain and headache, other common symptoms of neurogenic TOS, are infrequent. Diagnosis was made by dynamic venography. First rib resection, which included the anterior portion of rib and cartilage plus division of the costoclavicular ligament and subclavius tendon, proved to be effective treatment. (J Vasc Surg 2005;41:285-90.) Unilateral arm swelling without thrombosis is uncom- system. Three separate injections were administered: one mon, and few papers have addressed this condition. The with the arm at the side, one with the arm abducted to 90 last article on this subject that we could find was published degrees; and one with the arm at 180 degrees. -
Radiculopathy Vs. Spinal Stenosis: Evocative Electrodiagnosis Identifies the Main Pain Generator
Functional Electromyography Loren M. Fishman · Allen N. Wilkins Functional Electromyography Provocative Maneuvers in Electrodiagnosis 123 Loren M. Fishman, MD Allen N. Wilkins, MD College of Physicians & Surgeons Manhattan Physical Medicine Columbia University and Rehabilitation New York, NY 10028, USA New York, NY 10013, USA [email protected] ISBN 978-1-60761-019-9 e-ISBN 978-1-60761-020-5 DOI 10.1007/978-1-60761-020-5 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2010935087 © Springer Science+Business Media, LLC 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. -
ANGIOGRAPHY of the UPPER EXTREMITY Printed in the Netherlands by Koninklijke Drukkerij G.J.Thieme Bv, Nijmegen ANGIOGRAPHY of the UPPER EXTREMITY
1 f - h-' ^^ ANGIOGRAPHY OF THE UPPER EXTREMITY Printed in The Netherlands by Koninklijke drukkerij G.J.Thieme bv, Nijmegen ANGIOGRAPHY OF THE UPPER EXTREMITY PROEFSCHRIFT ter verkrijging van de graad van Doctor in de Geneeskunde aan de Rijksuniversiteit te Leiden, op gezag van de Rector Magni- ficus Dr. A. A. H. Kassenaar, Hoogleraar in de faculteit der Geneeskunde, volgens besluit van het college van dekanen te verdedigen op donderdag 6 mei 1982 te klokke 15.15 uur DOOR BLAGOJA K. JANEVSKI geborcn 8 februari 1934 te Gradsko, Joegoslavie MARTINUS NIJHOFF PUBLISHERS THE HAGUE - BOSTON - LONDON 1982 PROMOTOR: Prof. Dr. A. E. van Voorthuisen REPERENTEN: Prof. Dr. J. M. F. LandLandsmees r 1 Prof. Dr. J. L. Terpstra ! I Copyright © 1982 by Martinus Nijhoff Publishers, The Hague All rights reserved. No part of this publication may be repro- duced, stored in a retrieval system, or transmitted in any form or by any means, mechanical, photocopying, recording, or otherwise, without the prior written permission of the pub- lishers, Martinus Nijhoff Publishers,P.O. Box 566,2501 CN The Hague, The Netherlands if ••»• 7b w^ wife Charlotte To Lucienne, Lidia and Dejan h {, ,;T1 ii-"*1 ™ ffiffp"!»3^>»'*!W^iyJiMBiaMMrar^ ACKNOWLEDGEMENTS This thesis was produced in the Department of Radiology, Sirit Annadal Hospital, Maastricht. i Case material: Prof. Dr. H. A. J. Lemmens, surgeon. Technical assistence: Miss J. Crijns, Mrs. A. Rousie-Panis, Miss A. Mordant and Miss H. Nelissen. Secretarial help: Mrs. M. Finders-Velraad and Miss Y. Bessems. Photography: Mr. C. Evers. Graphical illustrations: Mr. C. Voskamp. Correction English text: Dr. -
Thoracic Outlet and Pectoralis Minor Syndromes
S EMINARS IN V ASCULAR S URGERY 27 (2014) 86– 117 Available online at www.sciencedirect.com www.elsevier.com/locate/semvascsurg Thoracic outlet and pectoralis minor syndromes n Richard J. Sanders, MD , and Stephen J. Annest, MD Presbyterian/St. Luke's Medical Center, 1719 Gilpin, Denver, CO 80218 article info abstract Compression of the neurovascular bundle to the upper extremity can occur above or below the clavicle; thoracic outlet syndrome (TOS) is above the clavicle and pectoralis minor syndrome is below. More than 90% of cases involve the brachial plexus, 5% involve venous obstruction, and 1% are associate with arterial obstruction. The clinical presentation, including symptoms, physical examination, pathology, etiology, and treatment differences among neurogenic, venous, and arterial TOS syndromes. This review details the diagnostic testing required to differentiate among the associated conditions and recommends appropriate medical or surgical treatment for each compression syndrome. The long- term outcomes of patients with TOS and pectoralis minor syndrome also vary and depend on duration of symptoms before initiation of physical therapy and surgical intervention. Overall, it can be expected that 480% of patients with these compression syndromes can experience functional improvement of their upper extremity; higher for arterial and venous TOS than for neurogenic compression. & 2015 Published by Elsevier Inc. 1. Introduction compression giving rise to neurogenic TOS (NTOS) and/or neurogenic PMS (NPMS). Much less common is subclavian Compression of the neurovascular bundle of the upper and axillary vein obstruction giving rise to venous TOS (VTOS) extremity can occur above or below the clavicle. Above the or venous PMS (VPMS). -
Herpesviruses
J Clin Pathol: first published as 10.1136/jcp.32.9.859 on 1 September 1979. Downloaded from Journal of Clinical Pathology, 1979, 32, 859-881 Herpesviruses MORAG C. TIMBURY' AND ELIZABETH EDMOND2 From the 'Department of Bacteriology, Royal Infirmary, Glasgow and the 2Regional Virus Laboratory, City Hospital, Greenbank Drive, Edinburgh, UK Herpesviruses are ubiquitous in both human and tion (Plummer et al., 1970) or microneutralisation animal populations (Plummer, 1967). The four tests (Pauls and Dowdle, 1967) are often used for human herpesviruses are herpes simplex (HSV), this, but differentiating the two types of virus today varicella-zoster (VZ), cytomegalovirus (CMV), and can probably be done more easily by biochemical Epstein-Barr (EBV) viruses, and all exhibit the prop- methods. Thus the DNA of the viruses can be dis- erty, rare among human pathogenic viruses, of tinguished by restriction enzyme analysis (Skare et remaining latent within the body after primary infec- al., 1975). Similarly, many of the virus polypeptides tion. Latent virus persists for many years-probably produced in infected cells by the two types of virus throughout life-and in some patients reactivates to can be distinguished by polyacrylamide gel electro- cause secondary or recurrent infections. Human phoresis (Courtney and Powell, 1975). herpesviruses can almost be regarded as part of the commensal flora, and certainly HSV is present in LABORATORY DIAGNOSIS the saliva of healthy people from time to time HSV-1 infections are most rapidly diagnosed by (Douglas and Couch, 1970). The viruses exhibit a isolation of the virus in cell cultures such as BHK21 remarkably successful parasitism since the upset to or RK1 3 cells (Grist et al., 1979). -
Role of Cornification and Triglyceride Synthesis Genes
Gillespie et al. BMC Genomics 2013, 14:169 http://www.biomedcentral.com/1471-2164/14/169 RESEARCH ARTICLE Open Access Transcriptome analysis of pigeon milk production – role of cornification and triglyceride synthesis genes Meagan J Gillespie1,2*, Tamsyn M Crowley1,3, Volker R Haring1, Susanne L Wilson1, Jennifer A Harper1, Jean S Payne1, Diane Green1, Paul Monaghan1, John A Donald2, Kevin R Nicholas3 and Robert J Moore1 Abstract Background: The pigeon crop is specially adapted to produce milk that is fed to newly hatched young. The process of pigeon milk production begins when the germinal cell layer of the crop rapidly proliferates in response to prolactin, which results in a mass of epithelial cells that are sloughed from the crop and regurgitated to the young. We proposed that the evolution of pigeon milk built upon the ability of avian keratinocytes to accumulate intracellular neutral lipids during the cornification of the epidermis. However, this cornification process in the pigeon crop has not been characterised. Results: We identified the epidermal differentiation complex in the draft pigeon genome scaffold and found that, like the chicken, it contained beta-keratin genes. These beta-keratin genes can be classified, based on sequence similarity, into several clusters including feather, scale and claw keratins. The cornified cells of the pigeon crop express several cornification-associated genes including cornulin, S100-A9 and A16-like, transglutaminase 6-like and the pigeon ‘lactating’ crop-specific annexin cp35. Beta-keratins play an important role in ‘lactating’ crop, with several claw and scale keratins up-regulated. Additionally, transglutaminase 5 and differential splice variants of transglutaminase 4 are up-regulated along with S100-A10. -
Lumbosacral Plexus Entrapment Syndrome. Part One: a Common Yet Little-Known Cause of Chronic Pelvic and Lower Extremity Pain
3-A Running head: ANAESTHESIA, PAIN & INTENSIVE CARE www.apicareonline.com ORIGINAL ARTICLE Lumbosacral plexus entrapment syndrome. Part one: A common yet little-known cause of chronic pelvic and lower extremity pain Kjetil Larsen, CES, George C. Chang Chien, D O2 ABSTRACT Corrective exercise specialist, Training & Rehabilitation, Oslo Lumbosacral plexus entrapment syndrome (LPES) is a little-known but common cause Norway of chronic lumbopelvic and lower extremity pain. The lumbar plexus, including the 2 Director of pain management, lumbosacral tunks emerge through the fibers of the psoas major, and the proximal Ventura County Medical Center, sciatic nerve beneath the piriformis muscles. Severe weakness of these muscles may Ventura, CA 93003, USA. lead to entrapment plexopathy, resulting in diffuse and non-specific pain patterns Correspondence: Kjetil Larsen, CES, Corrective throughout the lumbopelvic complex and lower extremities (LPLE), easily mimicking Exercise Specialist, Training & other diagnoses and is therefore likely to mislead the interpreting clinician. It is a Rehabilitation, Oslo Norway; pathology very similar to that of thoracic outlet syndrome, but for the lower body. This Kjetil@trainingandrehabilitation. two part manuscript series was written in an attempt to demonstrate the existence, com; pathophysiology, diagnostic protocol as well as interventional strategy for LPES, and Tel.: +47 975 45 192 its efficacy. Received: 23 November 2018, Reviewed & Accepted: 28 Key words: Pelvic girdle; Pain, Pelvic girdle; Lumbosacral plexus entrapment syndrome; February 2019 Piriformis syndrome; Nerve entrapment; Double-crush; Pain, Chronic; Fibromyalgia Citation: Larsen K, Chien GCC. Lumbosacral plexus entrapment syndrome. Part one: A common yet little-known cause of chronic pelvic and lower extremity pain. -
Anti-Inflammatory Role of Curcumin in LPS Treated A549 Cells at Global Proteome Level and on Mycobacterial Infection
Anti-inflammatory Role of Curcumin in LPS Treated A549 cells at Global Proteome level and on Mycobacterial infection. Suchita Singh1,+, Rakesh Arya2,3,+, Rhishikesh R Bargaje1, Mrinal Kumar Das2,4, Subia Akram2, Hossain Md. Faruquee2,5, Rajendra Kumar Behera3, Ranjan Kumar Nanda2,*, Anurag Agrawal1 1Center of Excellence for Translational Research in Asthma and Lung Disease, CSIR- Institute of Genomics and Integrative Biology, New Delhi, 110025, India. 2Translational Health Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India. 3School of Life Sciences, Sambalpur University, Jyoti Vihar, Sambalpur, Orissa, 768019, India. 4Department of Respiratory Sciences, #211, Maurice Shock Building, University of Leicester, LE1 9HN 5Department of Biotechnology and Genetic Engineering, Islamic University, Kushtia- 7003, Bangladesh. +Contributed equally for this work. S-1 70 G1 S 60 G2/M 50 40 30 % of cells 20 10 0 CURI LPSI LPSCUR Figure S1: Effect of curcumin and/or LPS treatment on A549 cell viability A549 cells were treated with curcumin (10 µM) and/or LPS or 1 µg/ml for the indicated times and after fixation were stained with propidium iodide and Annexin V-FITC. The DNA contents were determined by flow cytometry to calculate percentage of cells present in each phase of the cell cycle (G1, S and G2/M) using Flowing analysis software. S-2 Figure S2: Total proteins identified in all the three experiments and their distribution betwee curcumin and/or LPS treated conditions. The proteins showing differential expressions (log2 fold change≥2) in these experiments were presented in the venn diagram and certain number of proteins are common in all three experiments. -
Computational and Experimental Approaches for Evaluating the Genetic Basis of Mitochondrial Disorders
Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Lieber, Daniel Solomon. 2013. Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders. Doctoral dissertation, Harvard University. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11158264 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders A dissertation presented by Daniel Solomon Lieber to The Committee on Higher Degrees in Systems Biology in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Systems Biology Harvard University Cambridge, Massachusetts April 2013 © 2013 - Daniel Solomon Lieber All rights reserved. Dissertation Adviser: Professor Vamsi K. Mootha Daniel Solomon Lieber Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders Abstract Mitochondria are responsible for some of the cell’s most fundamental biological pathways and metabolic processes, including aerobic ATP production by the mitochondrial respiratory chain. In humans, mitochondrial dysfunction can lead to severe disorders of energy metabolism, which are collectively referred to as mitochondrial disorders and affect approximately 1:5,000 individuals. These disorders are clinically heterogeneous and can affect multiple organ systems, often within a single individual. Symptoms can include myopathy, exercise intolerance, hearing loss, blindness, stroke, seizures, diabetes, and GI dysmotility. -
1. Ceramide: the Center of Sphingolipid Biosynthesis
Introduction 1. Ceramide: the center of sphingolipid biosynthesis 1.1. Introducing the sphingolipid family The cell membrane contains three main classes of lipids: glycerolipids, sphingolipids and sterols (Futerman and Hannun 2004; Gulbins and Li 2006; Grassme et al. 2007). First discovered by J.L. W. Thudichum in 1876, sphingolipids were considered to play primarily structural roles in membrane formation (Zheng et al. 2006; Bartke and Hannun 2009). However, by the end of the twentieth century, sphingolipids were described as effector molecules which are involved in the regulation of apoptosis, cell proliferation, cell migration, senescence, and inflammation (Hannun 1996; Perry and Hannun 1998; Hannun and Obeid 2002; Futerman and Hannun 2004; Ogretmen and Hannun 2004; Reynolds et al. 2004; Fox et al. 2006; Modrak et al. 2006; Saddoughi et al. 2008). Sphingolipid metabolism pathways have a unique metabolic entry point, serine palmitoyl transferase (SPT) which forms 3-ketosphinganine, the first sphingolipid in the de novo pathway and a unique exit point, sphingosine-1-phosphate (S1P) lyase, which breaks down S1P into non-sphingolipid molecules. In this network, ceramide can be considered to be a metabolic hub because it occupies a central position in sphingolipid biosynthesis and catabolism (Hannun and Obeid 2008) (Figure 1). 1.2. Ceramide structure and metabolism Ceramide (Cer) from mammalian membranes is composed of sphingosine, which is an amide linked to a fatty acyl chain, varying in length from 14 to 26 carbon atoms (Mimeault 2002; Pettus et al. 2002; Ogretmen and Hannun 2004; Zheng et al. 2006) (Figure 1). Ceramide constitutes the metabolic and structural precursor for complex sphingolipids, which are composed of hydrophilic head groups, such as sphingomyelin, ceramide 1-phosphate, and glucosylceramide (Saddoughi et al. -
Thoracic Outlet Syndrome: Evaluation and Management
nalytic A al & B y i tr o s c i h e Kocyigi and Kuyucu, Biochem Anal Biochem 2016, m m Biochemistry & e i h s c t 5:2 r o i y B DOI: 10.4172/2161-1009.1000274 ISSN: 2161-1009 Analytical Biochemistry Review Article Open Access Thoracic Outlet Syndrome: Evaluation and Management Figen Kocyigi T1* and Ersin Kuyucu2 1School of Physical Therapy and Rehabilitation, Pamukkale University, Turkey 2Department of Orthopaedics and Traumatology, Istanbul Medipol University, Faculty of Medicine, Istanbul, Turkey *Corresponding author: Figen Kocyigi T, School of Physical Therapy and Rehabilitation, Pamukkale University, 20070, Denizli, Turkey, Tel: +90-258-4444295; Fax: +90-258-2964494; E-mail: [email protected] Rec date: March 04, 2016; Acc date: May 21, 2016; Pub date: May 24, 2016 Copyright: © 2016 Kocyıgı T et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Thoracic outlet syndrome is an umbrella term that describes the potential compression of the brachial plexus, subclavian vein or subclavian artery by different clinical disorders. This review covers the classification, clinical findings, physical examination findings and management of this challenging syndrome under the light of recent scientific research. Various medical specialties can encounter TOS within their field of expertise. TOS should not be viewed as a single clinical entity that simply manifests variations from one patient to another. TOS is composed of three very discrete subgroups, and treatment should be individualized after diagnosis is definite.