1
40
4
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.jaci.2008.02.011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jaci.2008.02.011</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1140-1147
Issue
5
Volume
121
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Surfactant protein D alters allergic lung responses in mice and human subjects
Publisher
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Journal of Allergy and Clinical Immunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-05
Subject
The topic of the resource
inflammation; asthma; Immunology; polymorphism; lung; Allergy; endotoxin; Aspergillus; deficient mice; Allergy; aspergillus-fumigatus; d gene; emphysema; eosinophil; hygiene hypothesis; IL-13; sftpd gene; sp-a; surfactant protein D
Creator
An entity primarily responsible for making the resource
Brandt E B; Mingler M K; Stevenson M D; Wang N; Hershey G K K; Whitsett J A; Rothenberg M E
Description
An account of the resource
Background: Surfactant protein (SP) D has been proposed to be protective in allergic airway responses. Objective: We aimed to determine the effect of SP-D deficiency on murine and human airway allergy. Methods: Immunologic responses of SP-D gene-deficient mice (Sftpd(-/-)) at baseline and after 4 intranasal Aspergillus fumigatus exposures were assessed. In addition, the significance of a single nucleotide polymorphism (Met(11)Thr) in the human SP-D gene (known to decrease SP-D function) was investigated. Results: Macrophage and neutrophil bronchoalveolar lavage fluid levels and large airway mucus production were increased in naive Sftpd(-/-) mice in association with increased lung CCL17 levels and CD4(+) T cell numbers. T(H)2-associated antibody levels (IgG1 and IgE) were significantly lower in 4- to 5-week-old Sftpd(-/-) mice (P <.05). Accordingly, naive Sftpd(-/-) splenocytes released significantly less IL-4 and IL-13 on anti-CD3/CD28 stimulation (P <.01). After intranasal allergen exposures, a modest decrease in bronchoalveolar lavage fluid eosinophilia and IL-13 levels was observed in Sftpd(-/-) mice compared with values seen in wild-type mice in association with decreased airway resistance (P <.01). A single nucleotide polymorphism in the SFTPD gene, affecting SP-D levels and pathogen binding, was associated with decreased atopy in black subjects and potentially lower asthma susceptibility in white subjects. Conclusion: Sftpd(-/-) mice have an impaired systemic T(H)2 response at baseline and reduced inflammation and airway responses after allergen exposure. Translational studies revealed that a polymorphism in the SFTPD gene was associated with lower atopy and possibly asthma susceptibility. Taken together, these results support the hypothesis that SP-D-dependent innate immunity influences atopy and asthma.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jaci.2008.02.011" target="_blank" rel="noreferrer noopener">10.1016/j.jaci.2008.02.011</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2008
allergy
Aspergillus
aspergillus-fumigatus
asthma
Brandt E B
d gene
deficient mice
emphysema
endotoxin
eosinophil
Hershey G K K
hygiene hypothesis
IL-13
Immunology
Inflammation
Journal Article or Conference Abstract Publication
Journal of Allergy and Clinical Immunology
Lung
Mingler M K
Polymorphism
Rothenberg M E
sftpd gene
sp-a
Stevenson M D
surfactant protein D
Wang N
Whitsett J A
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1738-1746
Issue
11
Volume
22
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Title
A name given to the resource
INFLUENCE OF N-ACETYLCYSTEINE ON INDIRECT INDICATORS OF TISSUE OXYGENATION IN SEPTIC SHOCK PATIENTS - RESULTS FROM A PROSPECTIVE, RANDOMIZED, DOUBLE-BLIND-STUDY
Publisher
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Critical Care Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
1994
1994-11
Subject
The topic of the resource
blood gas analysis; critical illness; critically-ill patients; endotoxin; gastric mucosa; General & Internal Medicine; glutathione; intramural ph; l-arginine; multiple organ failure; n-acetylcysteine; nitric-oxide synthesis; organ failure; oxygen consumption; ph; relaxing factor; sepsis; septic; shock; skeletal-muscle; tissue oxygenation
Creator
An entity primarily responsible for making the resource
Spies C D; Reinhart K; Witt I; Meierhellmann A; Hannemann L; Bredle D L; Schaffartzik W
Description
An account of the resource
Objectives: Deactivation of endothelium-derived relaxing factor due to an increased oxygen radical load during sepsis may contribute to an impairment in microcirculatory blood flow. We investigated whether treatment with the sulfhydryl donor and oxygen radical scavenger, N-acetylcysteine, would improve whole-body oxygen consumption (Vo(2)), gastric intramucosal pH, and veno-arterial CO2 gradient (veno-arterial PCO2) during septic shock. Design: Prospective, randomized, double-blind study conducted over 2 yrs. Setting: Septic shock patients admitted to the intensive care unit. Patients: Fifty-eight patients requiring hemodynamic monitoring (radial and pulmonary artery catheters) due to septic shock, were included in this study. All patients were examined within 72 hrs after the onset of sepsis. They were optimally resuscitated by conventional means with volume and inotropic agents, and exhibited stable clinical conditions (hemodynamic values, body temperature, hemoglobin, FIO2). Interventions: A gastric tonometer was inserted to measure the gastric intramucosal pH. Subjects randomly received either 150 mg/kg of intravenous N-acetylcysteine or placebo over a 15-min period, then a continuous infusion of 12.5 mg/hr of N-acetylcysteine or placebo over similar to 90 mins. Measurements: Infusion measurements were begun 60 mins after the beginning of infusion and lasted similar to 30 mins. The infusion was then discontinued and 2 hrs later the final measurements were taken. Main Results: Basic patient characteristics (age, sex, Acute Physiology and Chronic Health Evaluation [APACHE] II scores, Multiple Organ Failure scores) did not differ significantly, nor did pre- and 2-hr postinfusion measurements differ between any of the groups. Thirteen (45%) patients responded (i.e., showed an increase in Vo(2) >10%, reaching a mean of 19%) to the N-acetylcysteine infusion. The N-acetylcysteine responders also showed an increase in gastric intramucosal pH, a decrease in veno-arterial PCO2, an increase in oxygen delivery, cardiac index, stroke index, and left ventricular stroke work index, as well as a significant decrease in systemic vascular resistance in comparison to baseline. The N-acetylcysteine nonresponders, as well as the patients in the placebo group, did not show any significant changes in any of these variables. The N-acetylcysteine responders had a higher survival rate (69%) than the nonresponders (19%) and were studied earlier after onset of sepsis (37 hrs) than the nonresponders (61 hrs). The only significant difference between the entire N-acetylcysteine group (which included responders plus nonresponders) and the placebo group was an increased 30, in the entire N-acetylcysteine group during infusion measurements. Conclusions: N-acetylcysteine provided a transient improvement in tissue oxygenation in about half of the septic shock patients, as indicated by an increase in Vo(2) and gastric intramucosal pH and a decrease in veno-arterial PCO2. The higher survival rate in the N-acetylcysteine responders and the fact that half of the patients receiving N-acetylcysteine did not respond, suggests that, in some patients, sepsis irreversibly damages the microvasculature to the extent that N-acetylcysteine has no effect. If analyzed by intention to treat, the N-acetylcysteine did not produce effects that were significantly different from the placebo. Whether the N-acetylcysteine challenge was merely diagnostic or whether N-acetylcysteine can be effective in the treatment of sepsis deserves further investigation.
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
1994
Blood Gas Analysis
Bredle D L
Critical care medicine
Critical Illness
critically-ill patients
endotoxin
gastric mucosa
General & Internal Medicine
Glutathione
Hannemann L
intramural ph
Journal Article
l-arginine
Meierhellmann A
multiple organ failure
n-acetylcysteine
nitric-oxide synthesis
organ failure
Oxygen Consumption
ph
Reinhart K
relaxing factor
Schaffartzik W
sepsis
septic
Shock
skeletal-muscle
Spies C D
tissue oxygenation
Witt I
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
773-779
Issue
3
Volume
151
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Title
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N-ACETYLCYSTEINE PRESERVES OXYGEN-CONSUMPTION AND GASTRIC-MUCOSAL PH DURING HYPEROXIC VENTILATION
Publisher
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American Journal of Respiratory and Critical Care Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
1995
1995-03
Subject
The topic of the resource
cardiac-output; critically-ill patients; endotoxin; gas-exchange; General & Internal Medicine; l-arginine; nitric-oxide synthesis; relaxing factor; Respiratory System; septic patients; skeletal-muscle; superoxide
Creator
An entity primarily responsible for making the resource
Reinhart K; Spies C D; Meierhellmann A; Bredle D L; Hannemann L; Specht M; Schaffartzik W
Description
An account of the resource
Hyperoxic ventilation, used to prevent hypoxemia during potential periods of hypoventilation, has been reported to paradoxically decrease whole body oxygen consumption (Vo(2)). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigated whether pretreatment with the sulfhydryl group donor and O-2 radical scavenger N-acetylcysteine (NAG) would preserve whole body Vo(2) and prevent deterioration of oxygenation in gastric mucosal tissue during hyperoxia. Thirty-eight patients, requiring hemodynamic monitoring (radial and pulmonary artery catheters) due to sepsis syndrome, were included in this randomized experiment. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, Flo(2) < 0.5). A gastric tonometer was placed to measure the gastric intramucosal pH (pH(i)), which indirectly assesses nutritive blood flow to the mucosa. Cardiac output was determined by thermodilution and Vo(2) by cardiovascular Fick. After baseline measurements, patients randomly received either 150 mg . kg(-1) NAC (n = 19) or placebo (n = 19) in 250 ml 5% dextrose intravenously over a period of 15 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (Flo(2) = 1.0), and 60 min after resetting the original Flo(2). There were no significant differences between groups in any of the measurements before treatment and after the return to baseline Flo(2) at the end of the study. NAG, but not placebo infusion, caused a slight but significant increase in cardiac output and decrease in systemic vascular resistance. Significant differences between groups during hyperoxia were: Vo(2) (NAG: 114 +/- 9 mi min(-1) m(-2) versus placebo: 81 +/- 31 ml . min(-1) m(-2); p = 0.008) and oxygen extraction ratio (NAG: 21 +/- 6% versus placebo: 14 +/- 5%; p = 0.003). The mean decrease of Vo(2) was 11% in the NAC group versus 34% in the placebo group. The mean decrease of the oxygen extraction ratio was 12% in the NAC group versus 34% in the placebo group. NAC prevented a decrease in pH(i) in hyperoxia (NAG: 7.28 +/- 0.10 versus placebo: 7.14 +/- 0.18; p = 0.012). NAC helped preserve whole body oxygen uptake, oxygen extraction ratio, and pH(i) during brief hyperoxia in these septic patients. This suggests that pretreatment with NAC can attenuate impaired tissue oxygenation during hyperoxia.
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
1995
American journal of respiratory and critical care medicine
Bredle D L
cardiac-output
critically-ill patients
endotoxin
gas-exchange
General & Internal Medicine
Hannemann L
Journal Article
l-arginine
Meierhellmann A
nitric-oxide synthesis
Reinhart K
relaxing factor
Respiratory System
Schaffartzik W
septic patients
skeletal-muscle
Specht M
Spies C D
superoxide
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1046/j.1469-7580.1998.19210013.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1046/j.1469-7580.1998.19210013.x</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
13-23
Volume
192
Search for Full-text
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Title
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Ultrastructural and cytochemical evaluation of sepsis-induced changes in the rat pulmonary intravascular mononuclear phagocytes
Publisher
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Journal of Anatomy
Date
A point or period of time associated with an event in the lifecycle of the resource
1998
1998-01
Subject
The topic of the resource
acid-phosphatase; Anatomy & Morphology; Blood; cells; coagulation; differentiation; endotoxin; expression; host defence; human macrophage; lung uptake; monocytes; mononuclear phagocyte system; surface-coat
Creator
An entity primarily responsible for making the resource
Singh B; Doane K J; Niehaus G D
Description
An account of the resource
Sepsis stimulates an increase in the number and activity of mononuclear phagocytes in systemic host-defence organs. The present study was conducted to define the ultrastructural and cytochemical characteristics of the mononuclear phagocytes that sequester in the lung microvasculature of septic rats, Fourteen rats were challenged with a single intraperitoneal injection of saline (0.5 ml/100 g), E. coli (2 x 10(7)/100 g) or glucan (4 mg/100 g), and euthanased 2, 4, or 7 d later. The lungs were inflation fixed and processed for transmission electron microscopy. Cellular morphology was used to identify the intravascular mononuclear phagocytes and acid phosphatase (AcPase) expression was monitored as an index of cellular differentiation and activation. Control rats contained a limited number of monocytes in the pulmonary vasculature. In contrast, large numbers of activated mononuclear phagocytes were seen in the microvasculature within 48 h of treatment with either microbial product. The recruited pulmonary intravascular mononuclear phagocytes (PIMP) exhibited AcPase-reactive Golgi complexes, accumulation of secretory vesicles and other features of cell activation consistent with enhanced biosynthetic activity. Subsequent electron microscopy, conducted 4 and 7 d posttreatment, suggested that a progressive decline in the number and activity of PIMPs then occurred. In order to quantify the sepsis-induced accumulation of AcPase-positive PIMP, the experimental challenges were repeated in 11 rats and, 48 h later, tissue samples were evaluated by light microscopy for tartrate-insensitive acid phosphatase. Control rats exhibited 0.148 +/- 0.107 AcPase-positive PIMP/alveoli. E. coli and glucan challenged animals exhibited significant (P < 0.01) increases in AcPase-positive mononuclear phagocytes, with 0.782+/-0.073 and 0.636+/-0.170 PIMP/alveoli respectively, The results demonstrate that focal sepsis stimulates a significant, but transient, recruitment of activated mononuclear phagocytes into the rat pulmonary microvasculature.
Identifier
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<a href="http://doi.org/10.1046/j.1469-7580.1998.19210013.x" target="_blank" rel="noreferrer noopener">10.1046/j.1469-7580.1998.19210013.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
1998
acid-phosphatase
Anatomy & Morphology
Blood
Cells
coagulation
differentiation
Doane K J
endotoxin
expression
host defence
human macrophage
Journal Article
Journal of anatomy
lung uptake
monocytes
mononuclear phagocyte system
Niehaus G D
Singh B
surface-coat