scholarly journals Pre-existing medical conditions associated with Vibrio vulnificus septicaemia

2013 ◽  
Vol 142 (4) ◽  
pp. 878-881 ◽  
Author(s):  
M. P. MENON ◽  
P. A. YU ◽  
M. IWAMOTO ◽  
J. PAINTER
Keyword(s):  
Liver Disease ◽  
Vibrio Vulnificus ◽  
Severe Disease ◽  
Relative Importance ◽  
Medical Conditions ◽  
Life Threatening Illness ◽  
Serious Infection ◽  
Contaminated Food ◽  
Life Threatening

SUMMARYVibrio vulnificus (Vv) can result in severe disease. Although pre-existing liver disease is a recognized risk factor for serious infection, the relative importance of other comorbidities has not been fully assessed. We analysed reports of Vv infections submitted to CDC from January 1988 to September 2006 in order to assess the role of pre-existing conditions contributing to severe outcomes. A total of 1212 patients with Vv infection were reported. Only patients with liver disease [adjusted odds ratio (aOR) 5·1)] were more likely to become septic when exposure was due to contaminated food. Patients with liver disease (aOR 4·1), a haematological disease (aOR 3·2), or malignancy (aOR 3·2) were more likely to become septic when infection was acquired via a non-foodborne exposure. As such, patients with these pre-existing medical conditions should be advised of the risk of life-threatening illness after eating undercooked contaminated seafood or exposing broken skin to warm seawater.

Holding Secrets While Living With Life-Threatening Illness: Normalizing Patients’ Decisions to Reveal or Conceal

2019 ◽  
Vol 30 (5) ◽  
pp. 655-665 ◽  
Author(s):  
Anne Bruce ◽  
Rosanne Beuthin ◽  
Laurene Sheilds ◽  
Anita Molzahn ◽  
Kara Schick-Makaroff
Keyword(s):  
Health Care Providers ◽  
Narrative Analysis ◽  
Social Practice ◽  
Narrative Approach ◽  
Care Providers ◽  
Life Threatening Illness ◽  
Health And Illness ◽  
Life Threatening ◽  
Normative Practice

Communicating openly and directly about illness comes easily for some patients, whereas for others fear of disclosure keeps them silent. In this article, we discuss findings about the role of keeping secrets regarding health and illness. These findings were part of a larger project on how people with life-threatening illnesses re-story their lives. A narrative approach drawing on Frank’s dialogical narrative analysis and Riesman’s inductive approach was used. Interviews were conducted with 32 participants from three populations: chronic kidney disease, HIV/AIDS, and cancer. Findings include case exemplars which suggest keeping secrets is a social practice that acts along continuums of connecting–isolating, protecting–harming, and empowering–imprisoning. Keeping secrets about illness is a normative practice that is negotiated with each encounter. Findings call health-care providers to rethink the role of secrets for patients by considering patient privilege, a person’s right to take the lead in revealing or concealing their health and illness experience.

scholarly journals A Potential Role of the CD47/SIRPalpha Axis in COVID-19 Pathogenesis

2021 ◽  
Vol 43 (3) ◽  
pp. 1212-1225
Author(s):  
Katie-May McLaughlin ◽  
Denisa Bojkova ◽  
Joshua D. Kandler ◽  
Marco Bechtel ◽  
Philipp Reus ◽  
...  
Keyword(s):  
Immune Escape ◽  
Severe Disease ◽  
Kidney Injury ◽  
Bronchial Epithelial ◽  
Age Related ◽  
Literature Searches ◽  
Life Threatening ◽  
Infected Cells ◽  
Air Liquid Interface

The coronavirus SARS-CoV-2 is the cause of the ongoing COVID-19 pandemic. Most SARS-CoV-2 infections are mild or even asymptomatic. However, a small fraction of infected individuals develops severe, life-threatening disease, which is caused by an uncontrolled immune response resulting in hyperinflammation. However, the factors predisposing individuals to severe disease remain poorly understood. Here, we show that levels of CD47, which is known to mediate immune escape in cancer and virus-infected cells, are elevated in SARS-CoV-2-infected Caco-2 cells, Calu-3 cells, and air−liquid interface cultures of primary human bronchial epithelial cells. Moreover, SARS-CoV-2 infection increases SIRPalpha levels, the binding partner of CD47, on primary human monocytes. Systematic literature searches further indicated that known risk factors such as older age and diabetes are associated with increased CD47 levels. High CD47 levels contribute to vascular disease, vasoconstriction, and hypertension, conditions that may predispose SARS-CoV-2-infected individuals to COVID-19-related complications such as pulmonary hypertension, lung fibrosis, myocardial injury, stroke, and acute kidney injury. Hence, age-related and virus-induced CD47 expression is a candidate mechanism potentially contributing to severe COVID-19, as well as a therapeutic target, which may be addressed by antibodies and small molecules. Further research will be needed to investigate the potential involvement of CD47 and SIRPalpha in COVID-19 pathology. Our data should encourage other research groups to consider the potential relevance of the CD47/ SIRPalpha axis in their COVID-19 research.

scholarly journals ANGI — Anorexia Nervosa Genetics Initiative

2020 ◽  
Vol 23 (2) ◽  
pp. 135-136
Author(s):  
Cynthia Bulik ◽  
Martin Kennedy ◽  
Tracey Wade
Keyword(s):  
Anorexia Nervosa ◽  
Genetic Variants ◽  
Large Scale ◽  
Genome Wide Association Study ◽  
Genetic Correlations ◽  
Genome Wide Association ◽  
Life Threatening Illness ◽  
Genome Wide ◽  
Life Threatening

AbstractIdentification of genetic variants associated with eating disorders is underway. The Anorexia Nervosa Genetics Initiative, an initiative of the Klarman Family Foundation, has contributed to advancing the field, yielding a large-scale genome-wide association study published in Nature Genetics. Eight genetic variants significantly associated with anorexia nervosa were identified, along with patterns of genetic correlations that suggest both psychiatric and metabolic origins of this serious and life-threatening illness. This article details the role of Professor Nick Martin in contributing to this important collaboration.

scholarly journals ACE2: from protection of liver disease to propagation of COVID-19

2020 ◽  
Vol 134 (23) ◽  
pp. 3137-3158 ◽  
Author(s):  
Fiona J. Warner ◽  
Harinda Rajapaksha ◽  
Nicholas Shackel ◽  
Chandana B. Herath
Keyword(s):  
Liver Disease ◽  
Tissue Injury ◽  
Renin Angiotensin System ◽  
Protective Role ◽  
Alveolar Epithelial Cells ◽  
Cellular Receptor ◽  
Alveolar Epithelial ◽  
Key Enzyme ◽  
Life Threatening

Abstract Twenty years ago, the discovery of angiotensin-converting enzyme 2 (ACE2) was an important breakthrough dramatically enhancing our understanding of the renin–angiotensin system (RAS). The classical RAS is driven by its key enzyme ACE and is pivotal in the regulation of blood pressure and fluid homeostasis. More recently, it has been recognised that the protective RAS regulated by ACE2 counterbalances many of the deleterious effects of the classical RAS. Studies in murine models demonstrated that manipulating the protective RAS can dramatically alter many diseases including liver disease. Liver-specific overexpression of ACE2 in mice with liver fibrosis has proved to be highly effective in antagonising liver injury and fibrosis progression. Importantly, despite its highly protective role in disease pathogenesis, ACE2 is hijacked by SARS-CoV-2 as a cellular receptor to gain entry to alveolar epithelial cells, causing COVID-19, a severe respiratory disease in humans. COVID-19 is frequently life-threatening especially in elderly or people with other medical conditions. As an unprecedented number of COVID-19 patients have been affected globally, there is an urgent need to discover novel therapeutics targeting the interaction between the SARS-CoV-2 spike protein and ACE2. Understanding the role of ACE2 in physiology, pathobiology and as a cellular receptor for SARS-CoV-2 infection provides insight into potential new therapeutic strategies aiming to prevent SARS-CoV-2 infection related tissue injury. This review outlines the role of the RAS with a strong focus on ACE2-driven protective RAS in liver disease and provides therapeutic approaches to develop strategies to prevent SARS-CoV-2 infection in humans.

scholarly journals Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk

2021 ◽  
Vol 22 (9) ◽  
pp. 4459
Author(s):  
Siarhei A. Dabravolski ◽  
Evgeny E. Bezsonov ◽  
Mirza S. Baig ◽  
Tatyana V. Popkova ◽  
Ludmila V. Nedosugova ◽  
...  
Keyword(s):  
Liver Disease ◽  
Causative Role ◽  
Nucleotide Polymorphisms ◽  
Mitochondrial Mutations ◽  
Single Nucleotide ◽  
Alcoholic Fatty Liver ◽  
Dna Mutations ◽  
Life Threatening ◽  
Mitochondria Dna

NAFLD (non-alcoholic fatty liver disease) is a widespread liver disease that is often linked with other life-threatening ailments (metabolic syndrome, insulin resistance, diabetes, cardiovascular disease, atherosclerosis, obesity, and others) and canprogress to more severe forms, such as NASH (non-alcoholic steatohepatitis), cirrhosis, and HCC (hepatocellular carcinoma). In this review, we summarized and analyzed data about single nucleotide polymorphism sites, identified in genes related to NAFLD development and progression. Additionally, the causative role of mitochondrial mutations and mitophagy malfunctions in NAFLD is discussed. The role of mitochondria-related metabolites of the urea cycle as a new non-invasive NAFLD biomarker is discussed. While mitochondria DNA mutations and SNPs (single nucleotide polymorphisms) canbe used as effective diagnostic markers and target for treatments, age and ethnic specificity should be taken into account.

Role of GacA in virulence of Vibrio vulnificus

Microbiology ◽  
2010 ◽  
Vol 156 (12) ◽  
pp. 3722-3733 ◽  
Author(s):  
Julie D. Gauthier ◽  
Melissa K. Jones ◽  
Patrick Thiaville ◽  
Jennifer L. Joseph ◽  
Rick A. Swain ◽  
...  
Keyword(s):  
Capsular Polysaccharide ◽  
Vibrio Vulnificus ◽  
Phase Variation ◽  
Dependent Manner ◽  
Wild Type ◽  
Significant Impairment ◽  
Life Threatening ◽  
Two Component Signal Transduction ◽  
Systemic Infections

The GacS/GacA two-component signal transduction system regulates virulence, biofilm formation and symbiosis in Vibrio species. The present study investigated this regulatory pathway in Vibrio vulnificus, a human pathogen that causes life-threatening disease associated with the consumption of raw oysters and wound infections. Small non-coding RNAs (csrB1, csrB2, csrB3 and csrC) commonly regulated by the GacS/GacA pathway were decreased (P<0.0003) in a V. vulnificus CMCP6 ΔgacA : : aph mutant compared with the wild-type parent, and expression was restored by complementation of the gacA deletion mutation in trans. Of the 20 genes examined by RT-PCR, significant reductions in the transcript levels of the mutant in comparison with the wild-type strain were observed only for genes related to motility (flaA), stationary phase (rpoS) and protease (vvpE) (P=0.04, 0.01 and 0.002, respectively). Swimming motility, flagellation and opaque colony morphology indicative of capsular polysaccharide (CPS) were unchanged in the mutant, while cytotoxicity, protease activity, CPS phase variation and the ability to acquire iron were decreased compared with the wild-type (P<0.01). The role of gacA in virulence of V. vulnificus was also demonstrated by significant impairment in the ability of the mutant strain to cause either skin (P<0.0005) or systemic infections (P<0.02) in subcutaneously inoculated, non-iron-treated mice. However, the virulence of the mutant was equivalent to that of the wild-type in iron-treated mice, demonstrating that the GacA pathway in V. vulnificus regulates the virulence of this organism in an iron-dependent manner.

Role of Dance Therapy in Coping with Life Threatening Illness

2008 ◽  
Author(s):  
Eleanor M. DiPalma ◽  
Martha Hines ◽  
Marcia B. Leventhal ◽  
Iris Rifkin-Gainer
Keyword(s):  
Dance Therapy ◽  
Life Threatening Illness ◽  
Life Threatening
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