Admiral Nelson’s illnesses and injuries

2020 ◽  
Vol 32 (3) ◽  
pp. 736-742
Author(s):  
Fleur Mason ◽  
Robert Mason
Keyword(s):  
Lung Injury ◽  
Blood Loss ◽  
Yellow Fever ◽  
Professional Performance ◽  
Spinal Shock ◽  
Arm Amputation ◽  
Recurrent Malaria ◽  
Trafalgar Square ◽  
Battle Injuries

Horatio Nelson is one of the greatest English heroes. His key exploits at the battles of the Nile and Trafalgar, which led to Britain’s maritime supremacy, are well known and celebrated in the 5.5m statue at the summit of Nelson’s column in Trafalgar Square, London. The statue also showcases his most famous injuries, the injury to his right eye and arm amputation. However, as well as these he had a number of other battle injuries and afflictions including recurrent malaria, yellow fever, scurvy, tuberculosis and dysentery, which, although he bore with stoicism, may have affected his professional performance at different times in his career. The exact cause of his death was probably a combination of blood loss, lung injury and spinal shock.

HMGB1 contributes to the development of acute lung injury after hemorrhage

2005 ◽  
Vol 288 (5) ◽  
pp. L958-L965 ◽  
Author(s):  
Jae Yeol Kim ◽  
Jong Sung Park ◽  
Derek Strassheim ◽  
Ivor Douglas ◽  
Fernando Diaz del Valle ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Blood Loss ◽  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Plasma Concentrations ◽  
High Mobility ◽  
Pulmonary Endothelial Cells ◽  
Hmgb1 Expression

High mobility group box 1 (HMGB1) is a novel late mediator of inflammatory responses that contributes to endotoxin-induced acute lung injury and sepsis-associated lethality. Although acute lung injury is a frequent complication of severe blood loss, the contribution of HMGB1 to organ system dysfunction in this setting has not been investigated. In this study, HMGB1 was detected in pulmonary endothelial cells and macrophages under baseline conditions. After hemorrhage, in addition to positively staining endothelial cells and macrophages, neutrophils expressing HMGB1 were present in the lungs. HMGB1 expression in the lung was found to be increased within 4 h of hemorrhage and then remained elevated for more than 72 h after blood loss. Neutrophils appeared to contribute to the increase in posthemorrhage pulmonary HMGB1 expression since no change in lung HMGB1 levels was found after hemorrhage in mice made neutropenic with cyclophosphamide. Plasma concentrations of HMGB1 also increased after hemorrhage. Blockade of HMGB1 by administration of anti-HMGB1 antibodies prevented hemorrhage-induced increases in nuclear translocation of NF-κB in the lungs and pulmonary levels of proinflammatory cytokines, including keratinocyte-derived chemokine, IL-6, and IL-1β. Similarly, both the accumulation of neutrophils in the lung as well as enhanced lung permeability were reduced when anti-HMGB1 antibodies were injected after hemorrhage. These results demonstrate that hemorrhage results in increased HMGB1 expression in the lungs, primarily through neutrophil sources, and that HMGB1 participates in hemorrhage-induced acute lung injury.

Yellow Fever–induced Acute Lung Injury

2019 ◽  
Vol 200 (2) ◽  
pp. 250-252 ◽  
Author(s):  
Alexandre Todorovic Fabro ◽  
Gustavo Gonçalves Engelman ◽  
Natasha Nicos Ferreira ◽  
Júlia Maranhão Fagundes Velloni ◽  
Danillo Lucas Alves Espósito ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Yellow Fever

Microthrombus Formation May Trigger Lung Injury After Acute Blood Loss

Shock ◽  
2010 ◽  
Vol 34 (6) ◽  
pp. 601-607 ◽  
Author(s):  
Robert L. Conhaim ◽  
Martin J. Mangino ◽  
William F. Dovi ◽  
Kal E. Watson ◽  
Thomas F. Warner ◽  
...  
Keyword(s):  
Lung Injury ◽  
Blood Loss ◽  
Acute Blood Loss

Systemic blood loss affects NF-kappa B regulatory mechanisms in the lungs

1997 ◽  
Vol 273 (1) ◽  
pp. L185-L192 ◽  
Author(s):  
P. Moine ◽  
R. Shenkar ◽  
D. Kaneko ◽  
Y. Le Tulzo ◽  
E. Abraham
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Blood Loss ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Mononuclear Cells ◽  
Nf Kappa B ◽  
I Kappa B Alpha ◽  
Xanthine Oxidase Activity ◽  
Proinflammatory Mediators

The nuclear regulatory factor (NF)-kappa B is activated in the lungs of patients with acute respiratory distress syndrome (ARDS). In experimental models of acute lung injury, activation of NF-kappa B contributes to the increased expression of immunoregulatory cytokines and other proinflammatory mediators in the lungs. Because of the important role that NF-kappa B activation appears to play in the development of acute lung injury, we examined cytoplasmic and nuclear NF-kappa B counterregulatory mechanisms in lung mononuclear cells, using a murine model in which inflammatory lung injury develops after blood loss. Sustained activation of NF-kappa B was present in lung mononuclear cells over the 4-h period after blood loss. The activation of NF-kappa B after hemorrhage was accompanied by alterations in levels of the NF-kappa B regulatory proteins I kappa B alpha and Bcl-3. Cytoplasmic and nuclear I kappa B alpha were increased and nuclear Bcl-3 was decreased during the first hour after blood loss, but, by 4 h posthemorrhage, cytoplasmic and nuclear I kappa B alpha levels were decreased and nuclear levels of Bcl-3 were increased. Inhibition of xanthine oxidase activity in otherwise unmanipulated unhemorrhaged mice resulted in increased levels of I kappa B alpha and decreased amounts of Bcl-3 in nuclear extracts from lung mononuclear cells. No changes in the levels of nuclear I kappa B alpha or Bcl-3 occurred after hemorrhage when xanthine oxidase activity was inhibited. These results demonstrate that blood loss, at least partly through xanthine oxidase-dependent mechanisms, produces alterations in the levels of both I kappa B alpha and Bcl-3 in lung mononuclear cell populations. The effects of hemorrhage on proteins that regulate activation of NF-kappa B may contribute to the frequent development of inflammatory lung injury in this setting.

scholarly journals Phosphatidic acid signaling mediates lung cytokine expression and lung inflammatory injury after hemorrhage in mice.

1995 ◽  
Vol 181 (2) ◽  
pp. 569-575 ◽  
Author(s):  
E Abraham ◽  
S Bursten ◽  
R Shenkar ◽  
J Allbee ◽  
R Tuder ◽  
...  
Keyword(s):  
Lung Injury ◽  
Blood Loss ◽  
Phosphatidic Acid ◽  
Lysophosphatidic Acid ◽  
Protein Production ◽  
Human Neutrophils ◽  
Mrna Levels ◽  
Neutrophil Accumulation

Because phosphatidic acid (PA) pathway signaling may mediate many basic reactions involving cytokine-dependent responses, we investigated the effects of CT1501R, a functional inhibitor of the enzyme lysophosphatidic acid acyltransferase (LPAAT) which converts lysophosphatidic acid (Lyso-PA) to PA. We found that CT1501R treatment not only prevented hypoxia-induced PA increases and lyso-PA consumption in human neutrophils, but also prevented neutrophil chemotaxis and adherence in vitro, and lung injury and lung neutrophil accumulation in mice subjected to hemorrhage and resuscitation. In addition, CT1501R treatment prevented increases in mRNA levels and protein production of a variety of proinflammatory cytokines in multiple lung cell populations after blood loss and resuscitation. Our results indicate the fundamental role of PA metabolism in the development of acute inflammatory lung injury after blood loss.

scholarly journals Risk Factors of Acute Lung Injury in Cancer Patients after Operations Accompanied by Excessive Blood Loss

2008 ◽  
Vol 4 (3) ◽  
pp. 14
Author(s):  
S. V. Lomidze ◽  
I. V. Nekhayev ◽  
A. V Sytov ◽  
O. V. Zhuzhginova ◽  
S. P. Sviridova
Keyword(s):  
Risk Factors ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Blood Loss ◽  
Cancer Patients ◽  
Excessive Blood Loss

Success Strategies: Implementing the Professional Performance Review Process for School-Based Speech-Language Pathologists

2009 ◽  
Vol 19 (1) ◽  
pp. 4-9
Author(s):  
Jill Parmenter ◽  
Sheryl Amaral ◽  
Julia Jackson
Keyword(s):  
Review Process ◽  
Successful Implementation ◽  
Speech Language Pathologists ◽  
Self Advocacy ◽  
Professional Performance ◽  
Performance Review ◽  
Roles And Responsibilities ◽  
Speech Language Pathologist ◽  
School Based ◽  
Review Management

Abstract The Professional Performance Review Process for School-Based Speech-Language Pathologists (PPRP) (ASHA, 2006) was developed in response to the need for a performance review tool that fits school district requirements for performance review management while addressing the specific roles and responsibilities of a school-based speech-language pathologist (ASHA, 2006). This article will examine the purpose and components of the PPRP. A description of its use as a tool for self-advocacy will be discussed. Strategies for successful implementation of the PPRP will be explained using insight from speech-language pathologists and other professionals familiar with the PPRP.

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