What is the role of neonatal organ dysfunction and illness severity scores in therapeutic studies in sepsis?

2005 ◽  
Vol 6 (Supplement) ◽  
pp. S135-S137 ◽  
Author(s):  
William O. Tarnow-Mordi
Critical Care ◽  
2012 ◽  
Vol 16 (S1) ◽  
Author(s):  
G Argyriou ◽  
J Terrovitis ◽  
G Sainis ◽  
V Papas ◽  
C Marvaki ◽  
...  

2003 ◽  
Vol 197 (10) ◽  
pp. 1297-1302 ◽  
Author(s):  
Martin Hegen ◽  
Linhong Sun ◽  
Naonori Uozumi ◽  
Kazuhiko Kume ◽  
Mary E. Goad ◽  
...  

Pathogenic mechanisms relevant to rheumatoid arthritis occur in the mouse model of collagen-induced arthritis (CIA). Cytosolic phospholipase A2α (cPLA2α) releases arachidonic acid from cell membranes to initiate the production of prostaglandins and leukotrienes. These inflammatory mediators have been implicated in the development of CIA. To test the hypothesis that cPLA2α plays a key role in the development of CIA, we backcrossed cPLA2α-deficient mice on the DBA/1LacJ background that is susceptible to CIA. The disease severity scores and the incidence of disease were markedly reduced in cPLA2α-deficient mice compared with wild-type littermates. At completion of the study, >90% of the wild-type mice had developed disease whereas none of the cPLA2α-deficient mice had more than one digit inflamed. Furthermore, visual disease scores correlated with severity of disease determined histologically. Pannus formation, articular fibrillation, and ankylosis were all dramatically reduced in the cPLA2α-deficient mice. Although the disease scores differed significantly between cPLA2α mutant and wild-type mice, anti-collagen antibody levels were similar in the wild-type mice and mutant littermates. These data demonstrate the critical role of cPLA2α in the pathogenesis of CIA.


2016 ◽  
Vol 28 (1) ◽  
pp. 57 ◽  
Author(s):  
Ehsan Bolvardi ◽  
Jafar Malmir ◽  
Hamidreza Reihani ◽  
Amir Hashemian ◽  
Mehran Bahramian ◽  
...  

2016 ◽  
pp. 21-24
Author(s):  
Şule Yıldırım ◽  
Nazan Kaymaz ◽  
Naci Topaloğlu ◽  
Fatih Köksal Binnetoğlu ◽  
Mustafa Tekin ◽  
...  

Objective: The goal was to establish the role of intravenous hydration therapy on mild bronchiolitis. Methods: This was a retrospective case control study. Infants between 1 month and 2 years of age admitted to our general pediatrics ward between June 2012 and June 2013 with a diagnosis of uncomplicated acute bronchiolitis were enrolled to the study. Hospital medical files were reviewed to get information about children personal history, symptoms of the disease, disease severity scores and their management. Patients were classified into 4 groups according to the management; nebulized short-acting β2-agonist (salbutamol) +hydration; nebulized short-acting β2-agonist (salbutamol); hydration and neither bronchodilator nor hydration. We examined length of stay in the hospital as an outcome measure. Results: A total of 94 infants were studied. There was no significant difference between groups in terms of length of stay in hospital. Conclusions: IV hydration is not effective on length of stay in hospital in mild acute bronchiolitis patients.


Critical Care ◽  
10.1186/cc961 ◽  
2000 ◽  
Vol 4 (Suppl 1) ◽  
pp. P242 ◽  
Author(s):  
R Matos ◽  
R Moreno ◽  
T Fevereiro

2002 ◽  
Vol 88 (10) ◽  
pp. 663-667 ◽  
Author(s):  
Mariko Okudaira ◽  
Tomotaka Yoshida ◽  
Yasuo Ontachi ◽  
Masahide Yamazaki ◽  
Eriko Morishita ◽  
...  

SummaryWe have investigated the role of two vasoactive substances, nitric oxide (NO) and endothelin (ET), in the pathophysiology of disseminated intravascular coagulation (DIC), using two types of DIC models. Experimental DIC was induced by sustained infusion of 0.1, 1, 10, or 50 mg/kg lipopolysaccharide (LPS), or 3.75 U/kg thromboplastin (TF), for 4 h via the rat tail vein. Plasma levels of both NOX (metabolites of NO) and ET were significantly increased following infusion of 0.1 mg/kg or greater of LPS in the LPS-induced DIC rat model. In contrast, although a marked increase in the plasma levels of NOX was observed, only a slight increase in plasma ET levels was seen in the TF-induced DIC rat model. No significant differences in the plasma levels of platelets or thrombin-ATIII complex were observed among the TF-induced and LPS (50 mg/dl)-induced DIC models. However, plasma NOX levels rose significantly higher in the TF-induced model, relative to the LPS-induced model (p <0.01). Conversely, plasma ET levels were significantly greater after LPS-induction, compared to TF-induction, of DIC (p <0.01). Vasoconstriction, as well as depressed fibrinolytic activity, may be additional factors leading to severe organ dysfunction in the LPS-induced DIC rat model. Moreover, vasodilatation, as well as enhanced fibrinolytic activity, may help to prevent rats from severe organ dysfunction in the TF-induced DIC model. Our results suggest that modulator of vasoactive substances should be examined in the treatment of DIC.


10.5772/65348 ◽  
2016 ◽  
Author(s):  
Mariana Conceição de Souza ◽  
Tatiana Almeida Pádua ◽  
Maria das Graças Henriques

2012 ◽  
Vol 78 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Donald E. Fry

Human sepsis is thought to be systemic inflammatory response syndrome (SIRS) that is activated by invasive infection. The multiple organ dysfunction syndrome (MODS) is the identified failure of critical organ function in patients that have sustained SIRS. Because SIRS and MODS are consequences of the excessive activation of inflammation, extensive research and numerous clinical trials have pursued treatments that would modify the inflammatory response. This presentation reviews the normal local mechanisms of inflammation and provides a theoretical framework for the transition of the inflammatory process to a systemic level. Clinical trials with biomodulators to block or inhibit inflammation have generally failed to improve the outcomes in patients with severe sepsis, septic shock, and MODS. The role of counter-inflammatory signaling and the newer concept of the cholinergic anti-inflammatory pathway are being investigated, and newer hypotheses are focusing upon the balancing of proinflammatory and counter-inflammatory mechanisms as important directions for newer therapies. It is concluded that failure to define novel and effective treatments reflects fundamental gaps in our understanding of inflammation and its regulation.


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