Anatomy, Histology and Embryology): Beyond Scientific Terms
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Cell Biology and Fundamentals in Histology - En-Cours-2018-Liepr1004 Liepr1004 Cell Biology and Fundamentals in 2018 Histology
Université catholique de Louvain - Cell biology and fundamentals in histology - en-cours-2018-liepr1004 liepr1004 Cell biology and fundamentals in 2018 histology 5 credits 45.0 h Q2 Teacher(s) Behets Wydemans Catherine ;Henriet Patrick ; Language : French Place of the course Louvain-la-Neuve Main themes The major themes are : - Characteristics common to all living species - The human cell, its functioning and division - Classical, evolutive and molecular genetics - Cellular bases in sexual reproduction - The differents cell types and their organisation in tissues - The major steps in human embryonic development Aims By the end of the module, students should understand the bases of unicity and diversity in the living world. They will know the structure and functioning of human cell and genome as well as the mechanisms of 1 cell division and embryonic development. Moreover, they will know the structure of the major types of human tissues. - - - - The contribution of this Teaching Unit to the development and command of the skills and learning outcomes of the programme(s) can be accessed at the end of this sheet, in the section entitled “Programmes/courses offering this Teaching Unit”. Content (auteurs - titulaires actuels) : P. Henriet and Ph. van den Bosch de Aguilar 1. UNICITY IN THE LIVING WORLD 2. THE HUMAN CELL 3. DIVERSITY IN THE LIVING WORLD 4. MOLECULAR GENETICS 5. CELL DIVISION 6. GAMETOGENESIS AND FERTILIZATION 7. INTRODUCTION TO HUMAN EMBRYOLOGY Histology 1. EPITHELIAL TISSUE 2. CONNECTIVE TISSUE 3. BLOOD TISSUE 4. MUSCLE TISSUE -
Immune Response and Histology of Humoral Rejection in Kidney
Document downloaded from http://www.elsevier.es, day 23/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited. n e f r o l o g i a 2 0 1 6;3 6(4):354–367 Revista de la Sociedad Española de Nefrología www.revistanefrologia.com Review Immune response and histology of humoral rejection in kidney transplantation a,∗ a b a Miguel González-Molina , Pedro Ruiz-Esteban , Abelardo Caballero , Dolores Burgos , a c a a Mercedes Cabello , Miriam Leon , Laura Fuentes , Domingo Hernandez a Nephrology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain b Immunology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain c Pathology Department, Regional University Hospital of Malaga, Malaga University, IBIMA, REDINREN RD12/0021/0015, Malaga, Spain a r t i c l e i n f o a b s t r a c t Article history: The adaptive immune response forms the basis of allograft rejection. Its weapons are direct Received 4 June 2015 cellular cytotoxicity, identified from the beginning of organ transplantation, and/or anti- Accepted 26 March 2016 bodies, limited to hyperacute rejection by preformed antibodies and not as an allogenic Available online 3 June 2016 response. This resulted in allogenic response being thought for decades to have just a cellu- lar origin. But the experimental studies by Gorer demonstrating tissue damage in allografts Keywords: due to antibodies secreted by B lymphocytes activated against polymorphic molecules were Immune response disregarded. -
Acute Liver Failure J G O’Grady
148 Postgrad Med J: first published as 10.1136/pgmj.2004.026005 on 4 March 2005. Downloaded from REVIEW Acute liver failure J G O’Grady ............................................................................................................................... Postgrad Med J 2005;81:148–154. doi: 10.1136/pgmj.2004.026005 Acute liver failure is a complex multisystemic illness that account for most cases, but a significant number of patients have no definable cause and are evolves quickly after a catastrophic insult to the liver classified as seronegative or of being of indeter- leading to the development of encephalopathy. The minate aetiology. Paracetamol is the commonest underlying aetiology and the pace of progression strongly cause in the UK and USA.2 Idiosyncratic reac- tions comprise another important group. influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and Viral seronegative hepatitis. The optimal care is multidisciplinary ALF is an uncommon complication of viral and up to half of the cases receive liver transplants, with hepatitis, occurring in 0.2%–4% of cases depend- ing on the underlying aetiology.3 The risk is survival rates around 75%–90%. Artificial liver support lowest with hepatitis A, but it increases with the devices remain unproven in efficacy in acute liver failure. age at time of exposure. Hepatitis B can be associated with ALF through a number of ........................................................................... scenarios (table 2). The commonest are de novo infection and spontaneous surges in viral repli- cation, while the incidence of the delta virus cute liver failure (ALF) is a complex infection seems to be decreasing rapidly. multisystemic illness that evolves after a Vaccination should reduce the incidence of Acatastrophic insult to the liver manifesting hepatitis A and B, while antiviral drugs should in the development of a coagulopathy and ameliorate replication of hepatitis B. -
Satellitosis, a Crosstalk Between Neurons, Vascular Structures and Neoplastic Cells in Brain Tumours; Early Manifestation of Invasive Behaviour
cancers Review Satellitosis, a Crosstalk between Neurons, Vascular Structures and Neoplastic Cells in Brain Tumours; Early Manifestation of Invasive Behaviour Prospero Civita 1,2,* , Ortenzi Valerio 3 , Antonio Giuseppe Naccarato 3 , Mark Gumbleton 2 and Geoffrey J. Pilkington 1,2,4,* 1 Brain Tumour Research Centre, Institute of Biological and Biomedical Sciences (IBBS), School of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth PO1 2DT, UK 2 School of Pharmacy and Pharmaceutical Sciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff CF10 3NB, UK; gumbleton@cardiff.ac.uk 3 Department of Translational Research and New Technologies in Medicine and Surgery, Pisa University Hospital, 56100 Pisa, Italy; [email protected] (O.V.); [email protected] (A.G.N.) 4 Division of Neuroscience, Department of Basic and Clinical Neuroscience, Institute of Psychiatry & Neurology, King’s College London, London SE5 9RX, UK * Correspondence: CivitaP@cardiff.ac.uk (P.C.); geoff[email protected] (G.J.P.) Received: 9 November 2020; Accepted: 4 December 2020; Published: 11 December 2020 Simple Summary: This article reviews the concept of cellular satellitosis as originally described histologically by Santiago Ramón y Cajal in 1899 and Hans Joachim Scherer, more specifically in the context of glioblastoma invasiveness, during the early part of the 20th century. With the advent of new and emerging molecular technologies in the 21st century, the significance of both vascular and neuronal satellitosis by neoplastic cells offers intriguing possibilities into further clarifying the development, pathobiology and therapy of malignant glioma through closer investigation into the nature of these histological hallmarks. -
Differential Metabolism of Alprazolam by Liver and Brain Cytochrome (P4503A) to Pharmacologically Active Metabolite
The Pharmacogenomics Journal (2002) 2, 243–258 2002 Nature Publishing Group All rights reserved 1470-269X/02 $25.00 www.nature.com/tpj ORIGINAL ARTICLE Differential metabolism of alprazolam by liver and brain cytochrome (P4503A) to pharmacologically active metabolite HV Pai1,2* ABSTRACT SC Upadhya1,2* Cytochrome P450 (P450) is a superfamily of enzymes which mediates metab- 1 olism of xenobiotics including drugs. Alprazolam, an anti-anxiety agent, is SJ Chinta * metabolized in rat and human liver by P4503A1 and P4503A4 respectively, SN Hegde1 to 4-hydroxy alprazolam (4-OHALP, pharmacologically less active) and ␣- V Ravindranath1,2 hydroxy alprazolam (␣-OHALP, pharmacologically more active). We exam- ined P450 mediated metabolism of alprazolam by rat and human brain 1Department of Neurochemistry, National microsomes and observed that the relative amount of ␣-OHALP formed in Institute of Mental Health & Neurosciences, brain was higher than liver. This biotransformation was mediated by a P450 Bangalore, India; 2National Brain Research Centre, ICGEB Campus, Aruna Asaf Ali Marg, isoform belonging to P4503A subfamily, which is constitutively expressed in New Delhi , India neuronal cells in rat and human brain. The formation of larger amounts of ␣-OHALP in neurons points to local modulation of pharmacological activity Correspondence: in brain, at the site of action of the anti-anxiety drug. Since hydroxy metab- V Ravindranath, National Brain Research olites of alprazolam are hydrophilic and not easily cleared through blood- Centre, ICGEB Campus, Aruna Asaf Ali ␣ Marg, New Delhi - 110 067, India CSF barrier, -OHALP would potentially have a longer half-life in brain. Tel: +91 124 630 8317 The Pharmacogenomics Journal (2002) 2, 243–258. -
Basic Histology (23 Questions): Oral Histology (16 Questions
Board Question Breakdown (Anatomic Sciences section) The Anatomic Sciences portion of part I of the Dental Board exams consists of 100 test items. They are broken up into the following distribution: Gross Anatomy (50 questions): Head - 28 questions broken down in this fashion: - Oral cavity - 6 questions - Extraoral structures - 12 questions - Osteology - 6 questions - TMJ and muscles of mastication - 4 questions Neck - 5 questions Upper Limb - 3 questions Thoracic cavity - 5 questions Abdominopelvic cavity - 2 questions Neuroanatomy (CNS, ANS +) - 7 questions Basic Histology (23 questions): Ultrastructure (cell organelles) - 4 questions Basic tissues - 4 questions Bone, cartilage & joints - 3 questions Lymphatic & circulatory systems - 3 questions Endocrine system - 2 questions Respiratory system - 1 question Gastrointestinal system - 3 questions Genitouirinary systems - (reproductive & urinary) 2 questions Integument - 1 question Oral Histology (16 questions): Tooth & supporting structures - 9 questions Soft oral tissues (including dentin) - 5 questions Temporomandibular joint - 2 questions Developmental Biology (11 questions): Osteogenesis (bone formation) - 2 questions Tooth development, eruption & movement - 4 questions General embryology - 2 questions 2 National Board Part 1: Review questions for histology/oral histology (Answers follow at the end) 1. Normally most of the circulating white blood cells are a. basophilic leukocytes b. monocytes c. lymphocytes d. eosinophilic leukocytes e. neutrophilic leukocytes 2. Blood platelets are products of a. osteoclasts b. basophils c. red blood cells d. plasma cells e. megakaryocytes 3. Bacteria are frequently ingested by a. neutrophilic leukocytes b. basophilic leukocytes c. mast cells d. small lymphocytes e. fibrocytes 4. It is believed that worn out red cells are normally destroyed in the spleen by a. neutrophils b. -
Fact Sheet - Symptoms of Pancreatic Cancer
Fact Sheet - Symptoms of Pancreatic Cancer Diagnosis Pancreatic cancer is often difficult to diagnose, because the pancreas lies deep in the abdomen, behind the stomach, so tumors are not felt during a physical exam. Pancreatic cancer is often called the “silent” cancer because the tumor can grow for many years before it causes pressure, pain, or other signs of illness. When symptoms do appear, they can vary depending on the size of the tumor and where it is located on the pancreas. For these reasons, the symptoms of pancreatic cancer are seldom recognized until the cancer has progressed to an advanced stage and often spread to other areas of the body. General Symptoms Pain The first symptom of pancreatic cancer is often pain, because the tumors invade nerve clusters. Pain can be felt in the stomach area and/or in the back. The pain is generally worse after eating and when lying down, and is sometimes relieved by bending forward. Pain is more common in cancers of the body and tail of the pancreas. The abdomen may also be generally tender or painful if the liver, pancreas or gall bladder are inflamed or enlarged. It is important to keep in mind that there are many other causes of abdominal and back pain! Jaundice More than half of pancreatic cancer sufferers have jaundice, a yellowing of the skin and whites of the eyes. Jaundice is caused by a build-up bilirubin, a substance which is made in the liver and a component of bile. Bilirubin contains a lot of yellow pigment, and gives bile it’s color. -
Hepatitis B? HEPATITIS B Hepatitis B Is a Contagious Liver Disease That Results from Infection with the Hepatitis B Virus
What is Hepatitis B? HEPATITIS B Hepatitis B is a contagious liver disease that results from infection with the Hepatitis B virus. When first infected, a person can develop Are you at risk? an “acute” infection, which can range in severity from a very mild illness with few or no symptoms to a serious condition requiring hospitalization. Acute Hepatitis B refers to the first 6 months after someone is exposed to the Hepatitis B virus. Some people are able to fight the infection and clear the virus. For others, the infection remains and leads to a “chronic,” or lifelong, illness. Chronic Hepatitis B refers to the illness that occurs when the Hepatitis B virus remains in a person’s body. Over time, the infection can cause serious health problems. How is Hepatitis B spread? Hepatitis B is usually spread when blood, semen, or other body fluids from a person infected with the Hepatitis B virus enter the body of someone who is not infected. This can happen through having sex with an infected partner; sharing needles, syringes, or other injection drug equipment; or from direct contact with the blood or open sores of an infected person. Hepatitis B can also be passed from an infected mother to her baby at birth. Who should be tested for Hepatitis B? Approximately 1.2 million people in the United States and 350 million people worldwide have Hepatitis B. Testing for Hepatitis B is recommended for certain groups of people, including: Most are unaware of their infection. ■ People born in Asia, Africa, and other regions with moderate or high rates Is Hepatitis B common? of Hepatitis B (see map) Yes. -
Hepatitis A, B, and C: Learn the Differences
Hepatitis A, B, and C: Learn the Differences Hepatitis A Hepatitis B Hepatitis C caused by the hepatitis A virus (HAV) caused by the hepatitis B virus (HBV) caused by the hepatitis C virus (HCV) HAV is found in the feces (poop) of people with hepa- HBV is found in blood and certain body fluids. The virus is spread HCV is found in blood and certain body fluids. The titis A and is usually spread by close personal contact when blood or body fluid from an infected person enters the body virus is spread when blood or body fluid from an HCV- (including sex or living in the same household). It of a person who is not immune. HBV is spread through having infected person enters another person’s body. HCV can also be spread by eating food or drinking water unprotected sex with an infected person, sharing needles or is spread through sharing needles or “works” when contaminated with HAV. “works” when shooting drugs, exposure to needlesticks or sharps shooting drugs, through exposure to needlesticks on the job, or from an infected mother to her baby during birth. or sharps on the job, or sometimes from an infected How is it spread? Exposure to infected blood in ANY situation can be a risk for mother to her baby during birth. It is possible to trans- transmission. mit HCV during sex, but it is not common. • People who wish to be protected from HAV infection • All infants, children, and teens ages 0 through 18 years There is no vaccine to prevent HCV. -
The Histology of the Neuromuscular Junction In
75 THE HISTOLOGY OF THE NEUROMUSCULAR JUNCTION Downloaded from https://academic.oup.com/brain/article/84/1/75/372729 by guest on 27 September 2021 IN DYSTROPHIA MYOTONICA BY VIOLET MACDERMOT Department of Neurology, St. Thomas' Hospital, London, S.E.I (1) INTRODUCTION DYSTROPJHC MYOTONICA is a familial disease affecting males and females, usually presenting in adult life, characterized by muscular wasting and weakness together with certain other features. The muscles mainly in- volved are the temporal, masseter, facial, sternomastoid and limb muscles, in the latter those mainly affected being peripheral in distribution. A widespread disorder of muscular contraction, myotonia, is also present but is noticed chiefly in the tongue and in the muscles involved in grasping. The other features of the condition are some degree of mental defect, dysphonia, cataracts, frontal baldness, sparse body hair and testicular atrophy. Any of the manifestations of the disease may be absent and the order of presentation of symptoms is variable. The myotonia may precede muscular wasting by many years or may occur independently. In those muscles which are severely wasted the myotonia tends to disappear. The interest of dystrophia myotonica lies in the peculiar distribution of muscle involvement and in the combination of a disorder of muscle function with endocrine and other dysplasic features. The results of histological examination of biopsy and post-mortem material have been described and reviewed by numerous workers, notably Steinert (1909), Adie and Greenfield (1923), Keschner and Davison (1933), Hassin and Kesert (1948), Wohlfart (1951), Adams, Denny-Brown and Pearson (1953), Greenfield, Shy, Alvord and Berg (1957). -
Quiescent Satellite Glial Cells of the Adult Trigeminal Ganglion
Cent. Eur. J. Med. • 9(3) • 2014 • 500-504 DOI: 10.2478/s11536-013-0285-z Central European Journal of Medicine Quiescent satellite glial cells of the adult trigeminal ganglion Research Article Mugurel C. Rusu*1,2,3, Valentina M. Mănoiu4, Nicolae Mirancea3, Gheorghe Nini5 1 „Carol Davila” University of Medicine and Pharmacy, 050511 Bucharest, Romania. 2 MEDCENTER - Center of Excellence in Laboratory Medicine and Pathology 013594 Bucharest, Romania 3 Institute of Biology of Bucharest – The Romanian Academy, , 060031 Bucharest, Romania 4 Faculty of Geography, University of Bucharest, 050107 Bucharest, Romania 5 Faculty of Medicine, Pharmacy and Dental Medicine, “Vasile Goldiş” Western University, 310045 Arad, Romania Received 18 August 2013; Accepted 27 November 2013 Abstract: Sensory ganglia comprise functional units built up by neurons and satellite glial cells (SGCs). In animal species there was proven the presence of neuronoglial progenitor cells in adult samples. Such neural crest-derived progenitors were found in immunohistochemistry (IHC). These fi ndings were not previously documented in transmission electron microscopy (TEM). It was thus aimed to assess in TEM if cells of the human adult trigeminal ganglion indeed have ultrastructural features to qualify for a progenitor, or quiescent phenotype. Trigeminal ganglia were obtained from fi fteen adult donor cadavers. In TEM, cells with heterochromatic nuclei, a pancytoplasmic content of free ribosomes, few perinuclear mitochondria, poor developed endoplasmic reticulum, lack of Golgi complexes and membrane traffi cking specializations, were found included in the neuronal envelopes built-up by SGCs. The ultrastructural pattern was strongly suggestive for these cells being quiescent progenitors. However, further experiments should correlate the morphologic and immune phenotypes of such cells. -
How Is Alcohol Metabolized by the Body?
Overview: How Is Alcohol Metabolized by the Body? Samir Zakhari, Ph.D. Alcohol is eliminated from the body by various metabolic mechanisms. The primary enzymes involved are aldehyde dehydrogenase (ALDH), alcohol dehydrogenase (ADH), cytochrome P450 (CYP2E1), and catalase. Variations in the genes for these enzymes have been found to influence alcohol consumption, alcohol-related tissue damage, and alcohol dependence. The consequences of alcohol metabolism include oxygen deficits (i.e., hypoxia) in the liver; interaction between alcohol metabolism byproducts and other cell components, resulting in the formation of harmful compounds (i.e., adducts); formation of highly reactive oxygen-containing molecules (i.e., reactive oxygen species [ROS]) that can damage other cell components; changes in the ratio of NADH to NAD+ (i.e., the cell’s redox state); tissue damage; fetal damage; impairment of other metabolic processes; cancer; and medication interactions. Several issues related to alcohol metabolism require further research. KEY WORDS: Ethanol-to acetaldehyde metabolism; alcohol dehydrogenase (ADH); aldehyde dehydrogenase (ALDH); acetaldehyde; acetate; cytochrome P450 2E1 (CYP2E1); catalase; reactive oxygen species (ROS); blood alcohol concentration (BAC); liver; stomach; brain; fetal alcohol effects; genetics and heredity; ethnic group; hypoxia The alcohol elimination rate varies state of liver cells. Chronic alcohol con- he effects of alcohol (i.e., ethanol) widely (i.e., three-fold) among individ- sumption and alcohol metabolism are on various tissues depend on its uals and is influenced by factors such as strongly linked to several pathological concentration in the blood T chronic alcohol consumption, diet, age, consequences and tissue damage. (blood alcohol concentration [BAC]) smoking, and time of day (Bennion and Understanding the balance of alcohol’s over time.