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April 15, 2011

asthma; +42 new citations

42 new pubmed citations were retrieved for your search.
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asthma

These pubmed results were generated on 2011/04/15

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April 6, 2011

asthma; +86 new citations

86 new pubmed citations were retrieved for your search.
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asthma

These pubmed results were generated on 2011/04/06

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April 1, 2011

Grape Seed Proanthocyanidin Extract Attenuates Airway Inflammation and Hyperresponsiveness in a Murine Model of Asthma by Downregulating Inducible Nitric Oxide Synthase.

Grape Seed Proanthocyanidin Extract Attenuates Airway Inflammation and Hyperresponsiveness in a Murine Model of Asthma by Downregulating Inducible Nitric Oxide Synthase.

Planta Med. 2011 Mar 30;

Authors: Zhou DY, Du Q, Li RR, Huang M, Zhang Q, Wei GZ

Allergic asthma is characterized by hyperresponsiveness and inflammation of the airway with increased expression of inducible nitric oxide synthase (iNOS) and overproduction of nitric oxide (NO). Grape seed proanthocyanidin extract (GSPE) has been proved to have antioxidant, antitumor, anti-inflammatory, and other pharmacological effects. The purpose of this study was to examine the role of GSPE on airway inflammation and hyperresponsiveness in a mouse model of allergic asthma. BALB/c mice, sensitized and challenged with ovalbumin (OVA), were intraperitoneally injected with GSPE. Administration of GSPE remarkably suppressed airway resistance and reduced the total inflammatory cell and eosinophil counts in BALF. Treatment with GSPE significantly enhanced the interferon (IFN)- ? level and decreased interleukin (IL)-4 and IL-13 levels in BALF and total IgE levels in serum. GSPE also attenuated allergen-induced lung eosinophilic inflammation and mucus-producing goblet cells in the airway. The elevated iNOS expression observed in the OVA mice was significantly inhibited by GSPE. In conclusion, GSPE decreases the progression of airway inflammation and hyperresponsiveness by downregulating the iNOS expression, promising to have a potential in the treatment of allergic asthma.

PMID: 21452107 [PubMed – as supplied by publisher]

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March 31, 2011

asthma; +71 new citations

71 new pubmed citations were retrieved for your search.
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March 26, 2011

asthma; +20 new citations

20 new pubmed citations were retrieved for your search.
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March 25, 2011

asthma; +91 new citations

91 new pubmed citations were retrieved for your search.
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March 24, 2011

The Effect of Second Hand Smoke Exposure on Markers of Elastin Degradation.

The Effect of Second Hand Smoke Exposure on Markers of Elastin Degradation.

Chest. 2011 Mar 17;

Authors: Slowik N, Ma S, He J, Lin YY, Soldin OP, Robbins RA, Turino GM

ABSTRACT Tobacco smoke is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). Second-hand smoke exposure is a known risk factor in asthma, bronchitis and coronary artery disease. Elastin is a recognized target for injury in COPD and amino acids desmosine and isodesmosine (D/l), which are specific for elastin degradation are elevated in COPD. This study determined whether exposure to second-hand smoke affects elastin degradation in asymptomatic individuals. Two cohorts of asymptomatic individuals without evidence of respiratory or circulatory disease, exposed to second hand smoke were studied. Both cohorts comprised normal non-smokers, active smokers and second-hand smoke exposed. D/I were measured in plasma. D/I were quantified by HPLC and tandem mass spectrometry by published methods. Plasma cotinine, a metabolite of nicotine, was also measured. In each cohort, the levels of D/l in plasma were statistically significantly higher in second-hand smoke exposed subjects than in the normal non-exposed subjects. Smokers had the highest levels of D/l but their levels were not statistically significantly higher than those of the second-hand smoke exposed. Cotinine levels were elevated in the second-hand smoke exposed subjects and active smokers but not in most non-smoking controls. Results indicate a tissue matrix effect for the first time of degradation of body elastin from second-hand smoke exposure and possible lung structure injury which may result in COPD. Long term studies of individuals exposed to second-hand smoke for the development of COPD are warranted.

PMID: 21415130 [PubMed – as supplied by publisher]

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March 23, 2011

Grading the Severity of Obstruction in Mixed Obstructive-Restrictive Lung Disease.

Grading the Severity of Obstruction in Mixed Obstructive-Restrictive Lung Disease.

Chest. 2011 Mar 17;

Authors: Gardner ZS, Ruppel GL, Kaminsky DA

ABSTRACT BACKGROUND: The severity of obstructive pulmonary disease is determined by the percent predicted FEV(1) based on ATS/ERS guidelines. In patients with coexisting restrictive lung disease, the decrease in FEV(1) can overestimate the degree of obstruction. We hypothesize that adjusting the FEV(1) for the decrease in TLC results in a more appropriate grading of the severity of obstruction. METHODS: We examined a large PFT database and identified patients with both restrictive (TLC < 80% predicted) and obstructive (FEV(1)/FVC < the lower limit of normal) lung disease. FEV(1) percent predicted was adjusted for the degree of restriction by dividing it by percent predicted TLC. We compared the distribution of severity grading between adjusted and unadjusted values according to ATS/ERS criteria, and determined how the distribution of severity would change based on asthma and COPD guidelines. RESULTS: We identified 199 patients with coexisting restrictive and obstructive lung disease. By ATS/ERS grading, the unadjusted data categorized 76% of patients as having severe or very severe obstruction, and 11% as having mild or moderate obstruction. The adjusted data classified 33% with severe or very severe obstruction, and 44% with mild or moderate obstruction. Of the corrected values, 83% resulted in a change to less severe obstruction by ATS/ERS guidelines, and 44% and 70% of patients, respectively, would be reclassified as having less severe obstruction by current asthma and COPD guidelines. CONCLUSIONS: This method results in a more appropriate distribution of severity of obstruction, which should lead to more accurate treatment of obstruction in these patients.

PMID: 21415132 [PubMed – as supplied by publisher]

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March 22, 2011

OBESITY IS A DETERMINANT OF ASTHMA CONTROL, INDEPENDENT OF INFLAMMATION AND LUNG MECHANICS.

OBESITY IS A DETERMINANT OF ASTHMA CONTROL, INDEPENDENT OF INFLAMMATION AND LUNG MECHANICS.

Chest. 2011 Mar 17;

Authors: Farah CS, Kermode JA, Downie SR, Brown NJ, Hardaker KM, Berend N, King GG, Salome CM

ABSTRACT BACKGROUND: It is unclear why obesity is associated with worse asthma control. We hypothesized that: (1) obesity affects asthma control independent of spirometry, airway inflammation and airway hyperresponsiveness (AHR); and (2) residual symptoms after resolution of inflammation are due to obesity-related changes in lung mechanics METHODS: 49 asthmatic subjects performed the following, before and after 3 months high-dose inhaled corticosteroid (ICS) treatment: asthma control questionnaire (ACQ-5), spirometry, exhaled nitric oxide (F(E)NO), methacholine challenge and the forced oscillation technique (FOT), which allows for the calculation of respiratory system resistance (Rrs) and reactance (Xrs) as indicators of airway calibre and elastic load, respectively. The effects of treatment were assessed by BMI group (18.5-24.9, 25-29.9, ?30 kg.m(-2)) using ANOVA. Multiple regression analyses determined the independent predictors of ACQ-5. RESULTS: At baseline, the independent predictors of ACQ-5 were FEV(1), F(E)NO and BMI (model r(2) = 0.38, p < 0.001). After treatment, asthma control, spirometry, airway inflammation and AHR improved similarly across BMI groups. The independent predictors of ACQ-5 after treatment were Rrs and BMI (model r(2) = 0.42, p < 0.001). CONCLUSIONS: BMI is a determinant of asthma control independent of airway inflammation, lung function and AHR. After ICS treatment, BMI again predicts ACQ-5, but independent of obesity-related changes in lung mechanics.

PMID: 21415135 [PubMed – as supplied by publisher]

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March 21, 2011

Alveolar macrophages modulate allergic inflammation in a murine model of asthma.

Alveolar macrophages modulate allergic inflammation in a murine model of asthma.

Exp Mol Med. 2011 Mar 18;

Authors: Bang BR, Chun E, Shim EJ, Lee HS, Lee SY, Cho SH, Min KU, Kim YY, Park HW

The role of alveolar macrophages (AMs) in the pathogenesis of asthma is still unknown. The aim of the present study was to investigate the effects of AM in the murine model of asthma. AMs were selectively depleted by liposomes containing clodronate just before allergen challenges, and changes in inflammatory cells and cytokine concentrations in bronchoalveolar lavage (BAL) fluid were measured. AMs were then adoptively transferred to AM-depleted sensitized mice and changes were measured. Phenotypic changes in AMs were evaluated after in vitro allergen stimulation. AM-depletion after sensitization significantly increased the number of eosinophils and lymphocytes and the concentrations of IL-4, IL-5 and GM-CSF in BAL fluid. These changes were significantly ameliorated only by adoptive transfer of unsensitized AMs, not by sensitized AMs. In addition, in vitro allergen stimulation of AMs resulted in their gaining the ability to produce inflammatory cytokines, such as IL-1b, IL-6 and TNF-?, and losing the ability to suppress GM-CSF concentrations in BAL fluid. These findings suggested that AMs worked probably through GM-CSF-dependent mechanisms, although further confirmatory experiments are needed. Our results indicate that the role of AMs in the context of airway inflammation should be re-examined.

PMID: 21415590 [PubMed – as supplied by publisher]

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