DOCSLIB.ORG

N E U R O P a T H O L O G Y 2009

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

N E U R O P A T H O L O G Y 2009 COLLEGE OF PHYSICIANS & SURGEONS COLUMBIA UNIVERSITY New York, New York 1 NEUROPATHOLOGY SYLLABUS CONTENTS PAGE Message from the Course Director 3 Neuropathology small-Group Schedule 4 Faculty 5 Cellular Neuropathology 6 Cerebral Edema, Intracranial Shifts & Herniations 12 Cerebrovascular Diseases 20 Infectious Diseases of Central Nervous System 30 Neuro-Radiology 44 Degenerative Diseases and Dementia 49 Metabolic Diseases 79 Developmental Disorders 89 Brain Tumors 99 Seizures and Epilepsy 108 Diseases of Myelin 113 Neuromuscular Diseases 126 Ophthalmology 144 Trauma 154 Image Guideline 167 Clinical Exercises 195 2 MESSAGE FROM THE COURSE DIRECTOR Welcome to the Neuropathology Course. We hope that you will find this to be a pleasurable and challenging introduction to diseases of the nervous system. During this phase of your medical school experience, you are expected to become familiar with the vocabulary, basic pathologic concepts and morphologic aspects of neurologic diseases. Traditionally, diseases of the nervous system have been classified or divided etiologically into vascular, metabolic, neoplastic, infectious, degenerative, demyelinative, traumatic and developmental categories. Diseases of the neuromuscular system have been segregated somewhat, but can be divided similarly. This approach is still considered to be the most effective and understandable way to present this myriad of afflictions, but it often seems disjointed to the novice. So, be patient and we believe that things will fall into place by the end of the course. We shall try to emphasize common entities in the lectures, the small groups and images reviews, but prototypes of rare diseases also will be presented to provide you with an overview and perspective. The main purpose of the formal lectures is the presentation of conceptual, nosological, or pathogenetic aspects of neuropathology. In the small groups, we will reinforce material from lectures largely through review of images. Additionally, we will illustrate the application of basic neuropathologic principles to problem solving and analysis in the clinical setting. To this end, we will discuss a series of clinical cases in the group sessions. We will enlist your help in generating differential diagnoses to give you a feel for how we approach neurological diseases. We have included a lecture on Neuroimaging since this area is currently expanding tremendously and a basic appreciation of techniques and the value, and limitations, of those techniques will assist you in many areas of your clinical training. The Course Syllabus will be used in lieu of the textbook. We have intentionally listed somewhat extensive chapters, too much to be used in a short course. These readings are for those of you who wish to explore material in more detail. Images for the small group sessions are online at the following website: www.columbia.edu/itc/hs/medical/pathology/pathoatlas. This will lead you to the site that contains images for all pathology courses (topic bar will say ‘General Pathology’). Scroll down to the ‘Neuropathology’ section to access images for this course. Access to this site is possible both on and off campus. A large number of additional websites are available that may enhance your learning, if you wish to investigate them. At www.neuropat.dote.hu/ you will find a large online resource with links to Neuroanatomy, Neuropathology and Neuroradiology. The website at University of Rochester (www.urmc.rochester.edu/neuroslides) is useful and contains neuroradiology along with pathologic images. If you want to review some normal neurohistology, there is an interesting “virtual slide box of histology” at www.medicine.uiowa.edu/pathology/nlm_histology. There are many others to explore. Finally, constructive criticism and comments are welcome and should be referred to the course director. Phone and office numbers are given for the preceptors and we encourage you to make use of this resource outside of our formal teaching plan. We hope and expect that this will be a good learning experience for you. 3 NEUROPATHOLOGY SMALL GROUP SCHEDULE - 2008-2009 Tues., 12/8 11:00-12:50 Prec.Rms. Introduction to Cellular Neuropathology/Cerebral Edema Cerebrovascular Diseases Review Weds., 12/9 11:00-12:50 Prec.Rms. Infectious Diseases Review Case 1: Cerebrovascular Diseases Thurs., 12/10 11:00-12:50 Prec.Rms. Dementia and Degenerative Diseases & Metabolic Diseases Review Case 2: Dementia Fri., 12/11 11:00-12:50 Prec.Rms. Developmental Disorders & Brain Tumors Review Case 3: Brain tumors Mon., 12/14 11:00-12:50 Prec.Rms. Diseases of Myelin Review Case 4: Myelin Tues., 12/15 11:00-12:50 Prec.Rms Diseases of Nerve & Muscle Review Case 5: Nerve/Muscle Weds., 12/16 11:00-12:50 Prec. Rms Trauma Review Review Session for exam 4 NEUROPATHOLOGY COURSE FACULTY Neuropathology Faculty Phyllis L. Faust, M.D., Ph.D. PH 15-124 5-7345 Andrew Dwork, M.D. New PI Bldg.Rm.2913 212 543-5563 James E. Goldman, M.D., Ph.D. P&S 15-420 5-3554 Arthur P. Hays, M.D. PH 15-124 2-3034 Jean Paul Vonsattel BHS T-8 5-5161 Peter Canoll, M.D. ICRC 10-01 212 851-4632 Kurenai Tanji, M.D. PH 15-124 2-3035 John Crary, M.D., Ph.D. PH 15-124 5-7012 Andrew Teich, M.D., Ph.D. PH 15-124 5-7012 Neuroradiology Faculty Angela Lignelli. MH 3-101 5-2511 Neurology Faculty Hyunmi Choi, M.D. NI 1402 5-3049 Ophthalmology Faculty Steven Kane, M.D, Ph.D. EI Box 3 5/5400 or 212 927-8722 5 CELLULAR NEUROPATHOLOGY James E. Goldman, M.D., Ph.D. 6 CELLULAR NEUROPATHOLOGY At the beginning of this course, it is useful to consider each class of cells in the nervous system separately and to examine the diverse pathologies that may affect each of them. You will discover that these alterations are common to a variety of neuropathological disorders. NEURONS A. Cell body 1. Acute ischemic or hypoxic damage produces a shrinkage of the cell body and a hypereosinophilia. The nucleus becomes pyknotic. These are thought to be irreversible and lethal changes [CN-1]. 2. Atrophy, a non-eosinophilic shrinkage of the cell body [CN-2], is the hallmark of many neurodegenerative disorders (eg. Alzheimer, Parkinson, and Huntington diseases). The neuron may be involved directly or indirectly, through retrograde (via efferents) or anterograde (via afferents) transneuronal or transynaptic degeneration. 3. Chromatolysis results from axon damage (including axon transection). The cell body becomes hypertrophic and loses its Nissl substance (rough ER) [CN-3]. Chromatolysis may be followed by regrowth of the axon from the point of damage, a phenomenon more often seen in the peripheral than in the central nervous system. 4. In neuronal storage diseases, excessive amounts of lipids, carbohydrates, glycosaminoglycans, or glycoproteins accumulate within neurons, enlarging and distorting the normal geometry of the cell body and proximal processes. These are usually seen in the context of inherited disorders of lipid or glycosaminoglycan catabolism (eg. Tay Sachs disease, mucopolysaccharidoses). In many of these diseases, similar storage material accumulates in glial cells. 5. Inclusions represent abnormal nuclear or cytoplasmic structures. Some reflect the focal storage of metabolites, some the presence of viral proteins or nucleoproteins, and some the abnormal accumulation of structural proteins (eg. neurofibrillary tangles, Lewy bodies). 6. Lipofuscin is an insoluble mix of proteins, lipids, and minerals that accumulates in neurons and astrocytes during the normal aging process. 7. Neuronophagia is the phagocytosis of degenerating neurons, usually by macrophages. This is commonly seen after hypoxic or ischemic insults or during viral infections. 7 B. Axon 1. Wallerian degeneration is the loss of the axon (and its myelin sheath) distal to the point of axonal damage [CN-4]. 2. Dying back degeneration, a degeneration of the most distal axon, followed by the progressive loss of more and more proximal regions, is often seen in toxic peripheral neuropathies. 3. Demyelination refers to the primary loss of myelin with relative preservation of the axon (eg. as in multiple sclerosis) [CN-5]. 4. A spheroid is a focal enlargement of an axon due to damage, regardless of cause [CN-6]: trauma, local areas of necrosis, or toxic-metabolic insults. Spheroids contain mixtures of lysosomes, mitochondria, neurofilaments, and other cytoplasmic constituents. Slowing or cessation of axoplasmic transport at sites of damage presumably account for spheroids. C. Dendrite 1. Hypoplasia refers to an inadequate development of dendritic branches. This is seen in many types of mental retardation, including congenital hypothyroidism (cretinism). 2. Atrophy is a reduction in the volume and surface area of dendritic branches, commonly seen in neurodegenerative diseases. D. Neuropil 1. Neuritic plaques are collections of degenerating axons and dendrites, mixed with microglia and astrocytes and associated with the extracellular deposition of amyloid (beta-amyloid, see lecture on Neurodegenerative diseases). 2. Status spongiosis refers to a spongy state of the neuropil, the formation of fine to medium sized vacuoles representing swollen neuronal and astrocytic processes. This change is typical of transmissible spongiform encephalopathies, such as Creutzfeldt- Jacob disease. ASTROCYTES Astrocytes are found in all brain regions. They contact blood vessels, pial surfaces, and enfold synapses in their functions to maintain the concentration of ions, neurotransmitters, and other metabolites within normal levels in the extracellular space. They also play a fundamental role in inducing blood brain barrier functions in cerebral vessels [CN-7]. 8 1. Astrocytes undergo hypertrophy (enlargement) and hyperplasia (proliferation) in response to a great many pathological processes, including hypoxic-ischemic damage and trauma. Astrocytes form the majority of scars in the CNS (unlike other organs, in which scars are typically collagenous, formed by fibroblasts). Astrocytes develop abundant pink cytoplasm, either due to imbibing plasma proteins and fluid in the short-term (when the blood-brain-barrier is broken) or filling up with intermediate filaments (in long-term scarring).
Recommended publications
  • Neuropathology of Dementia in Patients with Parkinson's Disease: a Systematic Review of Autopsy Studies

    Neuropathology of Dementia in Patients with Parkinson's Disease: a Systematic Review of Autopsy Studies

    Neurodegeneration J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp-2019-321111 on 23 August 2019. Downloaded from REVIEW Neuropathology of dementia in patients with Parkinson’s disease: a systematic review of autopsy studies Callum Smith ,1 Naveed Malek,2 Katherine Grosset,1 Breda Cullen ,3 Steve Gentleman,4 Donald G Grosset1 ► Additional material is ABSTRact have other causes of cognitive impairment and published online only. To view Background Dementia is a common, debilitating dementia, such as comorbid Alzheimer’s disease please visit the journal online (http:// dx. doi. org/ 10. 1136/ feature of late Parkinson’s disease (PD). PD dementia (AD) or cerebrovascular disease. These pathologies jnnp- 2019- 321111). (PDD) is associated with α-synuclein propagation, but may be difficult to identify in vivo, as the clinical coexistent Alzheimer’s disease (AD) pathology may features often overlap with those of PDD, and there 1 Department of Neurology, coexist. Other pathologies (cerebrovascular, transactive are no definitive biomarkers. The differentiation Institute of Neurosciences, response DNA-binding protein 43 (TDP-43)) may of dementia type is an important consideration in Queen Elizabeth University Hospital, Glasgow, UK also influence cognition.W e aimed to describe the clinical research, as treatments under development 2Department of Neurology, neuropathology underlying dementia in PD. are specifically targeted against abnormal accumu- Ipswich Hospital NHS Trust, Methods Systematic review of autopsy studies lation of α-synuclein, which is the pathological Ipswich, UK 3 3 published in English involving PD cases with dementia. hallmark of PDD and DLB, or tau or amyloid-β, Institute of Health and 4 5 Wellbeing, College of Medical, Comparison groups included PD without dementia, AD, which underlie AD.
  • Section 8: Hematology CHAPTER 47: ANEMIA

    Section 8: Hematology CHAPTER 47: ANEMIA

    Section 8: Hematology CHAPTER 47: ANEMIA Q.1. A 56-year-old man presents with symptoms of severe dyspnea on exertion and fatigue. His laboratory values are as follows: Hemoglobin 6.0 g/dL (normal: 12–15 g/dL) Hematocrit 18% (normal: 36%–46%) RBC count 2 million/L (normal: 4–5.2 million/L) Reticulocyte count 3% (normal: 0.5%–1.5%) Which of the following caused this man’s anemia? A. Decreased red cell production B. Increased red cell destruction C. Acute blood loss (hemorrhage) D. There is insufficient information to make a determination Answer: A. This man presents with anemia and an elevated reticulocyte count which seems to suggest a hemolytic process. His reticulocyte count, however, has not been corrected for the degree of anemia he displays. This can be done by calculating his corrected reticulocyte count ([3% × (18%/45%)] = 1.2%), which is less than 2 and thus suggestive of a hypoproliferative process (decreased red cell production). Q.2. A 25-year-old man with pancytopenia undergoes bone marrow aspiration and biopsy, which reveals profound hypocellularity and virtual absence of hematopoietic cells. Cytogenetic analysis of the bone marrow does not reveal any abnormalities. Despite red blood cell and platelet transfusions, his pancytopenia worsens. Histocompatibility testing of his only sister fails to reveal a match. What would be the most appropriate course of therapy? A. Antithymocyte globulin, cyclosporine, and prednisone B. Prednisone alone C. Supportive therapy with chronic blood and platelet transfusions only D. Methotrexate and prednisone E. Bone marrow transplant Answer: A. Although supportive care with transfusions is necessary for treating this patient with aplastic anemia, most cases are not self-limited.
  • Nongenetic Reactivation and Is Caused by the Action of the Uncoating Protein

    Nongenetic Reactivation and Is Caused by the Action of the Uncoating Protein

    Poxviruses Dr. Ali Hashemi Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran Introduction Structure and Composition Poxviruses are the largest and most complex of viruses infecting humans. Poxviruses are large enough to be seen as featureless particles by light microscopy. By electron microscopy, they appear to be brick-shaped or ellipsoid particles. An outer lipoprotein membrane,or envelope, encloses a core and two structures of unknown function called lateral bodies Cont…. The core contains the large viral genome of linear double- stranded DNA. The DNA contains inverted terminal repeats of variable length, and the strands are connected at the ends by terminal hairpin loops. The chemical composition of a poxvirus resembles that of a bacterium. Vaccinia virus is composed predominantly of protein (90%), lipid (5%), and DNA (3%). Classification Poxviruses are divided into two subfamilies based on whether they infect vertebrate or insect hosts. Most of the poxviruses that can cause disease in humans are contained in the genera Orthopoxvirus and Parapoxvirus; there are also several that are classified in the genera Yatapoxvirus and Molluscipoxvirus. Cont… Cont… The orthopoxviruses have a broad host range affecting several vertebrates. They include ectromelia (mousepox), camelpox, cowpox, monkeypox, vaccinia, and variola (smallpox) viruses. Some poxviruses have a restricted host range and infect only rabbits (fibroma and myxoma) or only birds. Others infect mainly sheep and goats (sheeppox, goatpox) or cattle (pseudocowpox, or milker’s nodule). Poxvirus replication Poxviruses are unique among DNA viruses in that the entire multiplication cycle takes place in the cytoplasm of infected cells. Poxviruses are further distinguished from all other animal viruses by the fact that the uncoating step requires a newly synthesized, virus-encoded protein.
  • The Nature of Storage Iron in Idiopathic Hemochromatosis and in Hemosiderosis

    The Nature of Storage Iron in Idiopathic Hemochromatosis and in Hemosiderosis

    THE NATURE OF STORAGE IRON IN IDIOPATHIC HEMOCHROMATOSIS AND IN HEMOSIDEROSIS ELECTRON OPTICAL, CHEMICAL, AND SEROLOGIC STUDIES ON ISOLATED HEMOSIDERIN GRANULES* BY GOETZ W. RICHTER, M.D. (From the Department of Pathology, Cornell University Medical College, New York) PLATES 47 TO 51 (Received for publication, April 21, 1960) Although ferritin has long been recognized as an important iron storage compound and as an intermediary in normal iron metabolism, its role in idiopathic hemochromatosis and in secondary hemosiderosis is still unkuown. Diverse means have been employed to gain more knowledge on the pathway of iron in these conditions, and numerous publications attest the difficulties inherent in trying to distinguish between normal and abnormal storage of iron in cells of various sorts. Histochemical studies have provided evidence that inorganic compounds of iron stored in cells as hemosiderin are combined with an organic carrier substance that contains variable quantities of protein, lipid, and carbohydrate (1, 2). Results of chemical analyses led Ludewig to emphasize the heterogeneity of hemosiderin granules (3); his findings have provided qualitative and quantitative data on the carbohydrate, lipid, protein, and iron content of various hemosiderin preparations. The term "hemosiderin" has been used rather loosely; generally it refers to granules that are visible in the light micro- scope, brown when unstained, and give a positive Prussian blue test. Iron that gives a positive Prussian blue test with potassium ferrocyanide without the previous application of oxidizing agents must be in the trivalent (ferric) state. This is true of the bulk of iron in hemosiderin granules; it is also true of the iron hydroxide present in ferritin (4, 5, 7).
  • Visualization of Microbleeds with Optical Histology in Mouse Model of Cerebral Amyloid Angiopathy

    Visualization of Microbleeds with Optical Histology in Mouse Model of Cerebral Amyloid Angiopathy

    Microvascular Research 105 (2016) 109–113 Contents lists available at ScienceDirect Microvascular Research journal homepage: www.elsevier.com/locate/ymvre Visualization of microbleeds with optical histology in mouse model of cerebral amyloid angiopathy Patrick Lo a,b, Christian Crouzet a,b, Vitaly Vasilevko c,1,BernardChoia,b,d,⁎,1 a Beckman Laser Institute and Medical Clinic, University of California, Irvine, 1002 Health Sciences Road East, Irvine, CA 92612, USA b Department of Biomedical Engineering, University of California, Irvine, 3120 Natural Sciences II, Irvine, CA 92697, USA c Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 1207 Gillespie NRF, Irvine, CA 92697-4540, USA d Edwards Lifesciences Center for Advanced Cardiovascular Technology, University of California, Irvine, 2400 Engineering Hall, Irvine, CA 92697, USA article info abstract Article history: Cerebral amyloid angiopathy (CAA) is a neurovascular disease that is strongly associated with an increase in the Received 14 May 2015 number and size of spontaneous microbleeds. Conventional methods of magnetic resonance imaging for detec- Revised 3 February 2016 tion of microbleeds, and positron emission tomography with Pittsburgh Compound B imaging for amyloid Accepted 4 February 2016 deposits, can separately demonstrate the presence of microbleeds and CAA in affected brains in vivo;however, Available online 10 February 2016 there still is a critical need for strong evidence that shows involvement of CAA in microbleed formation. Here, we show in a Tg2576 mouse model of Alzheimer's disease, that the combination of histochemical staining and Keywords: Intracerebral hemorrhage an optical clearing method called optical histology, enables simultaneous, co-registered three-dimensional visu- DiI alization of cerebral microvasculature, microbleeds, and amyloid deposits.
  • CBME TIME TABLE – II MBBS BLOCK 1: March to June-2021

    CBME TIME TABLE – II MBBS BLOCK 1: March to June-2021

    SRI ADICHUNCHANAGIRI SHIKSHANA TRUST (R.) BGS GLOBAL INSTITUTE OF MEDICAL SCIENCES (Affiliated to Rajiv Gandhi University of Health Sciences, Bangalore) No. 67, BGS Health & Education City, Uttarahalli Road, Kengeri, Bangalore- 560060, Karnataka CBME TIME TABLE – II MBBS BLOCK 1: March TO June-2021 WEEK 1 DAY 8-11 11.30-12.30 12.30-1.30 2.00-4.00 4.00-5.00 Monday Postings L1 –PH: 1.1 OBG-LL1: OG 1.1: Integration: PH-A: PH: 1.1 MIC SDL 1 PSM: Birth rate, maternal 08/03/21 Batch A - Principles of mortality rate and morbidity Source of drug , drug information , Integration with Physiology and Gen Med pharmacology & drug compendia ,essential medicine, Pathology pharmacotherapeutics Formative Assessment: counterfeit drug , orphan drug. Batch B - Written/ Viva Assessment: Written/ viva Gen Sur Formative Assessment: MI 1.7.2 immune system Written/ Viva Batch C - Assessment: Written/ OBG Pharmacology –PH: 1.2: Therapeutic drug Monitoring & Clinical Trials Viva/MCQs Assessment: Short Notes Error! Not a valid embedded object. CM - B CM 7.2 - SGD-1: Cold chain system and its uses Assessment: Skill demo CM 7.3 - SGD-2: Integration Biochemistry Immunizing agents, national immunization schedule and vaccination strategies including vaccine development and implementation Assessment: MCQ/Viva Tuesday Postings L2 –PH: 1.3 & 1.11 FM: L1: SGD -1: FM- A: SGD-1 09/03/21 Batch A - Routes of Drug FM 1.1: Basics of Forensic PA 1.1 - Describe the role of a Gen Med administration medicine, Definition of FMT, pathologist in diagnosis and and its Sub Specialities management of disease Batch B - Formative Assessment: FM 2.8: Post Mortem Changes - ASSESSMENT: (written,viva-voce) Gen Sur Written/ Viva FM 1.2: History and Immediate & Early changes.
  • Brain Metastasis from Unknown Primary Tumour: Moving from Old Retrospective Studies to Clinical Trials on Targeted Agents

    Brain Metastasis from Unknown Primary Tumour: Moving from Old Retrospective Studies to Clinical Trials on Targeted Agents

    cancers Review Brain Metastasis from Unknown Primary Tumour: Moving from Old Retrospective Studies to Clinical Trials on Targeted Agents Roberta Balestrino 1,* , Roberta Rudà 2,3 and Riccardo Soffietti 3 1 Department of Neuroscience, University of Turin, Via Cherasco 15, 10121 Turin, Italy 2 Department of Neurology, Castelfranco Veneto/Treviso Hospital, Via dei Carpani, 16/Z, 31033 Castelfranco Veneto, Italy; [email protected] 3 Department of Neuro-Oncology, University of Turin, Via Cherasco 15, 10121 Turin, Italy; riccardo.soffi[email protected] * Correspondence: [email protected] Received: 13 October 2020; Accepted: 9 November 2020; Published: 12 November 2020 Simple Summary: Brain metastases (BMs) are the most common intracranial tumours in adults and occur up to 3–10 times more frequently than primary brain tumours. In up to 15% of patients with BM, the primary tumour cannot be identified. These cases are known as BM of cancer of unknown primary (CUP) (BM-CUP). The understanding of BM-CUP, despite its relative frequency and unfavourable outcome, is still incomplete and clear indications on management are missing. The aim of this review is to summarize current evidence on the diagnosis and treatment of BM-CUP. Abstract: Brain metastases (BMs) are the most common intracranial tumours in adults and occur up to 3–10 times more frequently than primary brain tumours. BMs may be the cause of the neurological presenting symptoms in patients with otherwise previously undiagnosed cancer. In up to 15% of patients with BMs, the primary tumour cannot be identified. These cases are known as BM of cancer of unknown primary (CUP) (BM-CUP).
  • Internet Resources for Neurosurgeons and Neuropathologists S Thomson, N Phillips

    Internet Resources for Neurosurgeons and Neuropathologists S Thomson, N Phillips

    154 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.2.154 on 1 February 2003. Downloaded from REVIEW Internet resources for neurosurgeons and neuropathologists S Thomson, N Phillips ............................................................................................................................. J Neurol Neurosurg Psychiatry 2003;74:154–157 Neurosurgical and neuropathological resources on the Neurosurgery://On-call has an “image bank” internet are rapidly developing. Some excellent clinical, section, which has an excellent downloadable collection of radiographs. There are also some patient information, professional, academic, and photographic images. This is a rapidly developing teaching web sites are available. This review database, easy to search, and likely to have images summarises the most useful online sites for relevant to most neurosurgical and neuropatho- logical conditions. neurosurgeons and neuropathologists in the United Neuroanatomy and Neuropathology on the Kingdom and beyond. More general internet resources Internet provides a very comprehensive collection of pathological images within the online neu- have been covered in the first article in this series. ropathology atlas. The neuroanatomy structures .......................................................................... subsection shows the locations of anatomical structures within normal pathological specimens. ver the past 10 years the internet has The functional neuroanatomy tables are also expanded rapidly. While potential ben- highly
  • Formation of Hirano Bodies in Cell Culture 1941

    Formation of Hirano Bodies in Cell Culture 1941

    Research Article 1939 Formation of Hirano bodies in Dictyostelium and mammalian cells induced by expression of a modified form of an actin-crosslinking protein Andrew G. Maselli, Richard Davis, Ruth Furukawa and Marcus Fechheimer* Department of Cellular Biology, University of Georgia, Athens, Georgia 30602, USA *Author for correspondence (e-mail: [email protected]) Accepted 26 February 2002 Journal of Cell Science 115, 1939-1952 (2002) © The Company of Biologists Ltd Summary We report the serendipitous development of the first pathological conditions. Furthermore, expression of the cultured cell models of Hirano bodies. Myc-epitope-tagged CT fragment in murine L cells results in F-actin forms of the 34 kDa actin bundling protein (amino acids 1- rearrangements characterized by loss of stress fibers, 295) and the CT fragment (amino acids 124-295) of the 34 accumulation of numerous punctate foci, and large kDa protein that exhibits activated actin binding and perinuclear aggregates, the Hirano bodies. Thus, failure to calcium-insensitive actin filament crosslinking activity regulate the activity and/or affinity of an actin crosslinking were expressed in Dictyostelium and mammalian cells to protein can provide a signal for formation of Hirano bodies. assess the behavior of these modified forms in vivo. More generally, formation of Hirano bodies is a cellular Dictyostelium cells expressing the CT-myc fragment: (1) response to or a consequence of aberrant function of the form ellipsoidal regions that contain ordered assemblies of actin cytoskeleton. The results reveal that formation of F-actin, CT-myc, myosin II, cofilin and α-actinin; (2) grow Hirano bodies is not necessarily related to cell death.
  • Theory, Practicals Block

    Theory, Practicals Block

    MVJ Medical College And Research Hospital Integrated and Aligned Time table Block -2 Teaching Program - Theory, Practicals Block - 2 01/07/2021 to 30/09/2021 8.30 - Time 11.30 - 12.30 12.30 - 1.30 1.30 - 2.00 2.00 - 4.00 2 TO 3 3 TO 4 4 TO 5 11.30 Lecture/ SGD Date Day clinicals Lecture/SGD class lunch Practicals /SGD/SDL OBG AETCOM SDL SPRTS /ECA class Microbiology Pathology Pharmacology Community Medicine SPORTS /ECA PA18.2 Acute PH 1.20 - Alcohol PH CM 1 PQLI, HDI calculation 1/7/21 THURS Leukemia (L) 1.23 - Drug Deaddiction (L) SGD Ph.1.24.1 physiology of Nephron MI3.1.1 (LECTURE ((SGD 1 )MI3.1.2 01) Introduction to Diarrheagenic E.coli PA 18.1 Non Leukemic 2/7/21 FRI gastrointestinal PA18.2 Chronic Leukemia (L) MI3.1.5 Viral Leucocyte disoreder Pandemic 2.4 infections diarhhea (SGD) IM22.1:- Enumerate the causes of hpercalcemia and distinguish the features of PTH us non PTH mediated hypercalcemia. IM22.2:- Describe the OG14.1 Maternal SU5.1 - Describe normal wound actiology, clinical pelvis: Diameters 3/7/21 SAT healing and factors affecting AETCOM2.4 manifestations, (Clinical pelvimetry healing diagnosis and clinical & Types of pelvis) approach to primary hyperthroidism. IM22.3:- Describe the approach to the management to ypercalcemia 4/7/21 SUN MI3.1.2 ,3,5 AE -3(BATCH A) Diarrheagenic E.coli, cholera,food PH 1.19.58 - 1.19.65 - PA 19.4 Hodgkins Lymphoma & poisoning Hanging drop preperation 5/7/21 MON NEURODEGENERATIVE PA 14 15 MHA & Dimorphic ( Pracs B) MICRO SDL Non Hodgkins Lymphoma (L) MI3.1.7 ,8,9 DOAP: Stool examination DISORDERS
  • Genetic and Phenotypic Characterization of a Rabies Virus Strain Isolated from a Dog in Tokyo, Japan in the 1940S

    Genetic and Phenotypic Characterization of a Rabies Virus Strain Isolated from a Dog in Tokyo, Japan in the 1940S

    viruses Article Genetic and Phenotypic Characterization of a Rabies Virus Strain Isolated from a Dog in Tokyo, Japan in the 1940s Tatsuki Takahashi 1, Maho Inukai 2, Michihito Sasaki 3 , Madlin Potratz 4, Supasiri Jarusombuti 5 , Yuji Fujii 6, Shoko Nishiyama 2, Stefan Finke 4 , Kentaro Yamada 7, Hiroki Sakai 1,6,8,9, Hirofumi Sawa 3, Akira Nishizono 7, Makoto Sugiyama 1,2,6 and Naoto Ito 1,2,6,9,* 1 The United Graduate School of Veterinary Sciences, Gifu University, Gifu 501-1193, Japan; [email protected] (T.T.); [email protected] (H.S.); [email protected] (M.S.) 2 Laboratory of Zoonotic Disease, Faculty of Applied Biological Sciences, Gifu University, Gifu 501-1193, Japan; [email protected] (M.I.); [email protected] (S.N.) 3 Division of Molecular Pathobiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo 001-0020, Japan; [email protected] (M.S.); [email protected] (H.S.) 4 Institute of Molecular Virology and Cell Biology, Federal Research Institute for Animal Health, Friedrich-Loeffler-Institut, 17493 Greifswald, Germany; madlin.potratz@fli.de (M.P.); stefan.finke@fli.de (S.F.) 5 Graduate School of Bioagricultural Science, Nagoya University, Nagoya 464-8601, Japan; [email protected] 6 Joint Graduate School of Veterinary Sciences, Gifu University, Gifu 501-1193, Japan; [email protected] 7 Department of Microbiology, Faculty of Medicine, Oita University, Oita 879-5593, Japan; [email protected] (K.Y.); [email protected] (A.N.) 8 Laboratory of Veterinary
  • Neuromuscular Medicine Core Competencies Outline

    Neuromuscular Medicine Core Competencies Outline

    The American Board of Psychiatry and Neurology Neuromuscular Medicine Core Competencies Outline I. Neuromuscular Patient Care Core Competencies A. GENERAL: Neuromuscular Medicine Specialists shall demonstrate the following abilities: 1. To perform and document relevant history and examination of culturally diverse patient to include as appropriate: a. Chief complaint b. History of present illness c. Past medical history d. Developmental history (especially for children) e. Comprehensive review of both neurologic and general systems f. Biological family history g. Sociocultural history h. Neurological examination and a germane general examination as appropriate to the present illness 2. Delineate appropriate differential diagnoses 3. Formulate, assess and recommend effective management B. FOR NEUROMUSCULAR MEDICINE: Based on comprehensive neurological assessments, Neuromuscular Specialists shall demonstrate the following abilities: 1. To determine: a. If a patient’s symptoms are the result of a disease affecting the central and/or peripheral nervous system or are of another origin (e.g., of a systemic, psychiatric, or psychogenic illness) by performing appropriate neuromuscular evaluation b. An initial diagnostic formulation with differential diagnosis c. Appropriate diagnostic modalities to include laboratory blood, urine, and cerebrospinal fluid analyses, electrodiagnostic, imaging, genetic, and pathologic investigations to evaluate and manage such patients d. Management plan 2. To develop and maintain the technical skills to: a. Perform