Hypoxic Brain Injury
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Wildland Firefighter Smoke Exposure
❑ United States Department of Agriculture Wildland Firefighter Smoke Exposure EST SERVIC FOR E Forest National Technology & 1351 1803 October 2013 D E E P R A U RTMENT OF AGRICULT Service Development Program 5100—Fire Management Wildland Firefighter Smoke Exposure By George Broyles Fire Project Leader Information contained in this document has been developed for the guidance of employees of the U.S. Department of Agriculture (USDA) Forest Service, its contractors, and cooperating Federal and State agencies. The USDA Forest Service assumes no responsibility for the interpretation or use of this information by other than its own employees. The use of trade, firm, or corporation names is for the information and convenience of the reader. Such use does not constitute an official evaluation, conclusion, recommendation, endorsement, or approval of any product or service to the exclusion of others that may be suitable. The U.S. Department of Agriculture (USDA) prohibits discrimination in all its programs and activities on the basis of race, color, national origin, age, disability, and where applicable, sex, marital status, familial status, parental status, religion, sexual orientation, genetic information, political beliefs, reprisal, or because all or part of an individual’s income is derived from any public assistance program. (Not all prohibited bases apply to all programs.) Persons with disabilities who require alternative means for communication of program information (Braille, large print, audiotape, etc.) should contact USDA’s TARGET Center at (202) 720-2600 (voice and TDD). To file a complaint of discrimination, write USDA, Director, Office of Civil Rights, 1400 Independence Avenue, S.W., Washington, D.C. -
Function and Biomarkers of the Blood-Brain Barrier in a Neonatal Germinal Matrix Haemorrhage Model
cells Article Function and Biomarkers of the Blood-Brain Barrier in a Neonatal Germinal Matrix Haemorrhage Model Erik Axel Andersson 1 , Eridan Rocha-Ferreira 2 , Henrik Hagberg 2, Carina Mallard 1 and Carl Joakim Ek 1,* 1 Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Medicinaregatan 11, 413 90 Gothenburg, Sweden; [email protected] (E.A.A.); [email protected] (C.M.) 2 Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 413 90 Gothenburg, Sweden; [email protected] (E.R.-F.); [email protected] (H.H.) * Correspondence: [email protected] Abstract: Germinal matrix haemorrhage (GMH), caused by rupturing blood vessels in the germinal matrix, is a prevalent driver of preterm brain injuries and death. Our group recently developed a model simulating GMH using intrastriatal injections of collagenase in 5-day-old rats, which corresponds to the brain development of human preterm infants. This study aimed to define changes to the blood-brain barrier (BBB) and to evaluate BBB proteins as biomarkers in this GMH model. Regional BBB functions were investigated using blood to brain 14C-sucrose uptake as well as using biotinylated BBB tracers. Blood plasma and cerebrospinal fluids were collected at various times after GMH and analysed with ELISA for OCLN and CLDN5. The immunoreactivity of BBB proteins was assessed in brain sections. Tracer experiments showed that GMH produced a defined region surrounding the hematoma where many vessels lost their integrity. This region expanded for at least 6 h following GMH, thereafter resolution of both hematoma and re-establishment of BBB Citation: Andersson, E.A.; Rocha- Ferreira, E.; Hagberg, H.; Mallard, C.; function occurred. -
Hypoxia in Alzheimer's Disease: Effects of Hypoxia Inducible Factors
Perspective associated virus-HIF-1α inhibits neuronal Hypoxia in Alzheimer’s disease: apoptosis of the hippocampus induced by Aβ peptides. HIF-1 increases glycolysis and the hexose monophosphate shunt, maintains effects of hypoxia inducible factors the mitochondrial membrane potential and cytosolic accumulation of cytochrome C, thereby inactivating caspase-9 and caspase-3, * Halimatu Hassan, Ruoli Chen and thus prevents neuronal death in the AD brain. Oxidative damage, caused by Aβ peptide Alzheimer’s disease (AD), a common (Lall et al., 2019). Neuroinflammation plays induces mitochondrial dysfunction, which is neurodegenerative disease, afflicts 26 million a detrimental role in AD pathogenesis, as a major characteristic of neuronal apoptosis. people worldwide currently with projection of a microglia depletion by colony stimulating factor Additional pathological features of AD are fourfold increase in this figure by the year 2050 receptor 1 inhibitors improves AD symptoms in astrocyte activation and reduced glucose (Brookmeyer et al., 2018). The majority of AD in vivo (Rawlinson et al., 2020). metabolism in some selected brain areas. cases (95%) are sporadic, having the late-onset Cells respond to hypoxia by stabilizing hypoxia Maintenance of HIF-1α levels reverses Aβ affecting those over 65 years old. About 15% inducible factor (HIF), a key transcription factor peptide-induced glial activation and glycolytic among those 65 years and older suffer from regulating oxygen homeostasis. The HIF levels changes, thus mediating a neuroprotective AD, and the incidence of AD is close to 50% for in cells are directly regulated by four oxygen- response to Aβ peptide by maintaining those aged over 85 years (Brookmeyer et al., sensitive hydroxylases: 3 prolyl hydroxylases metabolic integrity. -
Hypoxic Brain Injury
Hypoxic brain injury Headway’s publications are all available to freely download from the information library on the charity’s website, while individuals and families can request hard copies of the booklets via the helpline. Please help us to continue to provide free information to people affected by brain injury by making a donation at www.headway.org.uk/donate. Thank you. Acknowledgements: Many thanks to Dr Steven White, Consultant Neurophysiologist at St. Mary’s Hospital, London, and Great Ormond Street Hospital, London, for co-authoring this factsheet. Introduction The brain needs a constant supply of oxygen to survive and function. Any interruption in this supply leads to a condition called hypoxia, which can cause brain injury. Hypoxic brain injuries can sometimes be overlooked due to the fact that the primary illness was unrelated to the brain, for example, a heart attack or smoke inhalation. This is especially true if the primary condition is successfully treated and the impact on the brain was relatively mild. It is very important to seek specialist support for the effects of the brain injury as soon as possible and to be aware that changes in functioning and behaviour after such an event may be related to brain injury. This factsheet is intended as an overview of the causes, effects, treatment and rehabilitation of hypoxic brain injury. The information will be particularly useful for the family members of people who have sustained such an injury and also provides a useful starting point for professionals who wish to improve their knowledge of the subject. What is hypoxic brain injury? The brain needs a continuous supply of oxygen to survive and it uses 20% of the body’s oxygen intake. -
Health Concerns from Smoke Released by Fires
Health Concerns from Smoke Released by Fires Key Points The materials released by a fire vary from one fire to another, depending on the items burning, the availability of oxygen and fresh air, and the temperature of the fire itself. Even within a fire covering a large area, the materials released may vary from location to location. Inhaling the smoke from a fire can cause injury from the heat of the smoke, the chemicals within the smoke, and the particles of soot. " The heat can cause burns to the nasal passages, airways and lungs. " The chemicals can poison the body, depending on the amount of carbon monoxide, cyanide, and other chemicals produced by the burning. " Soot particles and other substances can irritate the airways. Inhaling smoke can cause asthma and other lung conditions to worsen for hours to days after breathing the smoky air. The best course of action is to leave the smoky air as soon as possible. Staying indoors with closed windows is better than being outdoors when smoke is widespread. If symptoms occur after smoke inhalation, seek medical care for further evaluation and treatment as needed. Fire Chemistry and Toxicology The products of combustion from a fire are a complex mixture. Carbon monoxide is produced in every fire. In general, more carbon monoxide is produced from fires occurring indoors. Carbon monoxide is important to health because it interferes with a person’s ability to use oxygen to maintain body functions. As carbon monoxide levels rise, the amount of impairment also rises. Carbon monoxide levels above 10% typically cause symptoms. -
The Role of Metabolism in Migraine Pathophysiology and Susceptibility
life Review The Role of Metabolism in Migraine Pathophysiology and Susceptibility Olivia Grech 1,2 , Susan P. Mollan 3 , Benjamin R. Wakerley 1,4, Daniel Fulton 5 , Gareth G. Lavery 1,2 and Alexandra J. Sinclair 1,2,4,* 1 Metabolic Neurology, Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK; [email protected] (O.G.); [email protected] (B.R.W.); [email protected] (G.G.L.) 2 Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham B15 2TH, UK 3 Birmingham Neuro-Ophthalmology Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham B15 2TH, UK; [email protected] 4 Department of Neurology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Trust, Birmingham B15 2TH, UK 5 Institute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2TT, UK; [email protected] * Correspondence: [email protected] Abstract: Migraine is a highly prevalent and disabling primary headache disorder, however its patho- physiology remains unclear, hindering successful treatment. A number of key secondary headache disorders have headaches that mimic migraine. Evidence has suggested a role of mitochondrial dysfunction and an imbalance between energetic supply and demand that may contribute towards Citation: Grech, O.; Mollan, S.P.; migraine susceptibility. Targeting these deficits with nutraceutical supplementation may provide an Wakerley, B.R.; Fulton, D.; Lavery, additional adjunctive therapy. Neuroimaging techniques have demonstrated a metabolic phenotype G.G.; Sinclair, A.J. The Role of in migraine similar to mitochondrial cytopathies, featuring reduced free energy availability and Metabolism in Migraine increased metabolic rate. -
Guidelines for the Management of Severe Traumatic Brain Injury 4Th Edition
Guidelines for the Management of Severe Traumatic Brain Injury 4th Edition Nancy Carney, PhD Oregon Health & Science University, Portland, OR Annette M. Totten, PhD Oregon Health & Science University, Portland, OR Cindy O'Reilly, BS Oregon Health & Science University, Portland, OR Jamie S. Ullman, MD Hofstra North Shore-LIJ School of Medicine, Hempstead, NY Gregory W. J. Hawryluk, MD, PhD University of Utah, Salt Lake City, UT Michael J. Bell, MD University of Pittsburgh, Pittsburgh, PA Susan L. Bratton, MD University of Utah, Salt Lake City, UT Randall Chesnut, MD University of Washington, Seattle, WA Odette A. Harris, MD, MPH Stanford University, Stanford, CA Niranjan Kissoon, MD University of British Columbia, Vancouver, BC Andres M. Rubiano, MD El Bosque University, Bogota, Colombia; MEDITECH Foundation, Neiva, Colombia Lori Shutter, MD University of Pittsburgh, Pittsburgh, PA Robert C. Tasker, MBBS, MD Harvard Medical School & Boston Children’s Hospital, Boston, MA Monica S. Vavilala, MD University of Washington, Seattle, WA Jack Wilberger, MD Drexel University, Pittsburgh, PA David W. Wright, MD Emory University, Atlanta, GA Jamshid Ghajar, MD, PhD Stanford University, Stanford, CA Reviewed for evidence-based integrity and endorsed by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. September 2016 TABLE OF CONTENTS PREFACE ...................................................................................................................................... 5 ACKNOWLEDGEMENTS ............................................................................................................................................. -
Studies on the Intracerebral Toxicity of Ammonia
Studies on the Intracerebral Toxicity of Ammonia Steven Schenker, … , Edward Brophy, Michael S. Lewis J Clin Invest. 1967;46(5):838-848. https://doi.org/10.1172/JCI105583. Research Article Interference with cerebral energy metabolism due to excess ammonia has been postulated as a cause of hepatic encephalopathy. Furthermore, consideration of the neurologic basis of such features of hepatic encephalopathy as asterixis, decerebrate rigidity, hyperpnea, and coma suggests a malfunction of structures in the base of the brain and their cortical connections. The three major sources of intracerebral energy, adenosine triphosphate (ATP), phosphocreatine, and glucose, as well as glycogen, were assayed in brain cortex and base of rats given ammonium acetate with resultant drowsiness at 5 minutes and subsequent coma lasting at least 30 minutes. Cortical ATP and phosphocreatine remained unaltered during induction of coma. By contrast, basilar ATP, initially 1.28 ± 0.15 μmoles per g, was unchanged at 2.5 minutes but fell by 28.1, 27.3, and 26.6% (p < 0.001) at 5, 15, and 30 minutes after NH4Ac. At comparable times, basilar phosphocreatine fell more strikingly by 62.2, 96, 77.1, and 71.6% (p < 0.001) from a control level of 1.02 ± 0.38 μmoles per g. These basilar changes could not be induced by anesthesia, psychomotor stimulation, or moderate hypoxia and were not due to increased accumulation of ammonia in the base. Glucose and glycogen concentrations in both cortex and base fell significantly but comparably during development of stupor, and prevention of the cerebral glucose decline by pretreatment with […] Find the latest version: https://jci.me/105583/pdf Journal of Clinical Investigation Vol. -
Inhalation Injury
Emergency Files Inhalation injury Bryan Wise MD CCFP Zachary Levine MD CCFP(EM) Case description mask, and starting intravenous fluids as indicated by the Mr B. is a 46-year-old man who is brought to your patient’s circulatory status.2 emergency department one night after being rescued Once that is complete, a brief history should be from a fire in his apartment complex. He thinks he obtained from the patient or any witnesses. Details of might have briefly lost consciousness while he was the exposure, including the type and location of the fire, trapped in a smoke-filled room before firefighters the duration of smoke exposure, any loss of conscious- were able to free him. He is fully awake and breathing ness, and the condition of any other victims, can provide comfortably upon arrival. Measurement of his vital information about potential inhalation injury.3,4 signs reveals the following: heart rate of 85 beats/min, A targeted physical examination should evaluate for blood pressure of 124/76 mm Hg, respiratory rate of any signs suggestive of inhalation injury, such as face 20 breaths/min, oxygen saturation of 100% on room and neck burns, singed nasal hairs, carbonaceous spu- air, temperature of 36.8°C, and a glucose level of tum, soot in the upper airways, voice changes, or wheez- 6.5 mmol/L. A brief examination reveals only superfi- ing.3,4 It is important to note that the absence of these cial burns to his face and neck. He says that he feels signs does not rule out inhalation injury.2 Additionally, fine now and he wants to return home. -
Fire-Related Inhalation Injury
The new england journal of medicine Review Article Julie R. Ingelfinger, M.D., Editor Fire-Related Inhalation Injury Robert L. Sheridan, M.D. From the Burn Service, Shriners Hospital nhalation injury has been recognized as an important clinical for Children, the Division of Burns, Massa- problem among fire victims since the disastrous 1942 Cocoanut Grove night- chusetts General Hospital, and the Depart- 1 ment of Surgery, Harvard Medical School club fire. Despite the fact that we have had many years’ experience with treat- — all in Boston. Address reprint requests to: I ing injuries related to fires, the complex physiological process of inhalation injury Dr. Sheridan at the Burn Service, Shriners remains poorly understood, diagnostic criteria remain unclear, specific therapeutic Hospital for Children, 51 Blossom St., Boston, MA 02114, or at rsheridan@mgh interventions remain ineffective, the individual risk of death remains difficult to . harvard . edu. quantify, and the long-term implications for survivors remain ill defined. Central N Engl J Med 2016;375:464-9. to these uncertainties is the complex nature of the injuries, which include a varying DOI: 10.1056/NEJMra1601128 combination of thermal injury to the upper airway, bronchial and alveolar mucosal Copyright © 2016 Massachusetts Medical Society. irritation and inflammation from topical chemical exposure, systemic effects of absorbed toxins, loss of ciliated epithelium, accrual of endobronchial debris, sec- ondary systemic inflammatory effects on the lung, and subsequent pulmonary and systemic infection. Incidence, Prevention, and Implications of Inhalation Injury Data from the National Inpatient Sample and the National Burn Repository sug- gest that there are roughly 40,000 inpatient admissions for burns in the United States annually; at a conservative estimate, 2000 of these admissions (5%) involve concomitant inhalation injury.2 Structural fires are most common in developed environments, especially in impoverished communities. -
Hypoxic-Ischemic Brain Injury After Perinatal Asphyxia As a Possible Factor in the Pathology of Alzheimer's Disease
Hypoxic-Ischemic Brain Injury after Perinatal Asphyxia as a Possible Factor in the Pathology of Alzheimer's Disease Agata Tarkowska, MD, PhD Department of Neonate and Infant Pathology, Medical University of Lublin, Lublin, Poland Author for correspondence: Agata Tarkowska, Department of Neonate and Infant Pathology, Medical University of Lublin, Lublin, Poland. Email: [email protected] Cite this chapter as: Tarkowska A. Hypoxic-Ischemic Brain Injury after Perinatal Asphyxia as a Possible Factor in the Pathology of Alzheimer's Disease. In: Pluta R, editor. Cerebral Ischemia. Brisbane (AU): Exon Publications; 2021. Online first Aug 31. Doi: https://doi.org/10.36255/exonpublications.cerebralischemia.2021.perinatalasphyxia Note to the user: This chapter has been peer reviewed and accepted for publication in the book Cerebral Ischemia, but not yet copyedited or typeset. Abstract Perinatal asphyxia is a common pathological condition occurring worldwide in approximately 4 million newborns annually. The result of this phenomenon is multi-organ damage and the development of chronic hypoxic encephalopathy. It is currently believed that an episode of cerebral hypoxia/ischemia may be one of the major factors responsible for the development of Alzheimer's disease-type dementia and/or Alzheimer's disease. It cannot be ruled out that hypoxia in the perinatal period may be a trigger factor for the development of Alzheimer's disease in adulthood. The data from scientific research indicate a possible relationship between hypoxia in the earliest stages of life and the occurrence of long-lasting genetic and biochemical changes leading to the development of neurodegeneration in Alzheimer’s disease-type. Keywords: Alzheimer’s disease; brain ischemia; genes; hypoxic-ischemic encephalopathy; perinatal asphyxia Running title: Perinatal Asphyxia and Alzheimer's Disease 1 INTRODUCTION Perinatal asphyxia (PA) is a condition resulting from insufficient availability of oxygen to various organs and tissues of the fetus and newborn in the antenatal and intranatal periods. -
Addressing Toxic Smoke Particulates in Fire Restoration
Addressing Toxic Smoke Particulates in Fire Restoration By: Sean M. Scott In the restoration industry today, a lot of attention testing laboratory or industrial hygienist provides an is given to the testing and abatement of air clearance test to certify that the abatement or microscopic hazardous materials. These include remediation process was successful. Upon receipt asbestos, lead, mold, bacteria, bloodborne of the clearance, people can then reenter the pathogens, and all sorts of bio-hazards fall into this remediated area, rooms, or building. However, category. If these contaminants are disturbed, when the structural repairs are completed after a treated, or handled improperly, all of them can fire, an air clearance test is rarely ever performed. cause property damage and serious harm to the How then can consumers be assured or restoration health and welfare of those living or working in or companies guarantee that the billions of toxic near the areas where they’re present. However, particulates and VOC’s generated by the fire have there are other hazardous toxins that commonly been removed? Is there cause for concern or is a present themselves in restoration projects, that simple “sniff” test or wiping a surface with a Chem- seem to go unnoticed. These are the toxic smoke sponge sufficient? Why is it so common to hear particulates and volatile organic compounds customers complain of smelling reoccurring smoke (VOC’s) created during structure fires. odor long after the restoration is completed? What measures are being taken to protect workers and When a building is abated from asbestos, lead, or their families from toxic ultra-fine particulate matter mold, special care is given to be sure every or VOC’s? microscopic fiber, spore, and bacteria is removed.