U.S. National Library of Medicine (NIH) Archives - Page 53 of 55

January 13, 2011

asthma; +16 new citations

16 new pubmed citations were retrieved for your search.
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asthma

These pubmed results were generated on 2011/01/13

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January 13, 2011

asthma; +16 new citations

16 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

asthma

These pubmed results were generated on 2011/01/13

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January 12, 2011

Terminal Signal: Anti-Inflammatory Effects of ?-Melanocyte-Stimulating Hormone Related Peptides Beyond the Pharmacophore.

Terminal Signal: Anti-Inflammatory Effects of ?-Melanocyte-Stimulating Hormone Related Peptides Beyond the Pharmacophore.

Adv Exp Med Biol. 2010;681:107-16

Authors: Brzoska T, Böhm M, Lügering A, Loser K, Luger TA

During the last two decades a significant number of investigations has established the fact that ?-Melanocyte-stimulating hormone (?-MSH) is a potent anti-inflammatory mediator. The anti-inflammatory effects of ?-MSH can be elicited via melanocortin receptors (MC-Rs) broadly expressed in a number of tissues ranging from the central nervous system to cells of the immune system and on resident somatic cells of peripheral tissues. ?-MSH affects various pathways regulating inflammatory responses such as NF-?B activation, expression of adhesion molecules, inflammatory cytokines, chemokine receptors, T-cell proliferation and activity and inflammatory cell migration. In vivo ?-MSH has been shown to be anti-inflammatory as well in animal models of fever, irritant and allergic contact dermatitis, cutaneous vasculitis, fibrosis, in ocular, gastrointestinal, brain and allergic airway inflammation and arthritis. A broad range of effects of ?-MSH exerted beyond the field of inflammation, its pigmentory capacity being only the most visible aspect, has been one of the major impediments limiting the use of ?-MSH in human inflammatory disorders. Interestingly KPV, C-terminal tripeptide of ?-MSH, which lacks the entire sequence motif required for binding to any of the known MC-Rs, retains almost all of the anti-inflammatory capacity of the full hormone, but in its activities display a lack of any pigmentory action. While the exact signaling mechanism utilized by KPV and related peptides currently is unknown it has been demonstrated already that significant similarities between anti-inflammatory signaling of ?-MSH and those short peptides exist. These ?-MSH related tripeptides thus may be useful alternatives for anti-inflammatory peptide therapy. KdPT, a derivative of KPV corresponding to IL-1?(193-195), currently is emerging as another tripeptide with potent anti-inflammatory effects. A more limited spectrum of biologic activities, potentially advantageous physicochemical, pharmacokinetic and pharmacodynamic properties as well as the expectation of low costs for pharmaceutical production make these agents interesting candidates for the treatment of immune-mediated inflammatory skin and bowel diseases, allergic asthma and arthritis.

PMID: 21222263 [PubMed – in process]

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January 11, 2011

asthma; +36 new citations

36 new pubmed citations were retrieved for your search.
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asthma

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January 10, 2011

asthma; +153 new citations

153 new pubmed citations were retrieved for your search.
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asthma

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January 2, 2011

asthma; +23 new citations

23 new pubmed citations were retrieved for your search.
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asthma

These pubmed results were generated on 2011/01/02

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January 1, 2011

Environmental risk factors for respiratory symptoms and childhood asthma.

Environmental risk factors for respiratory symptoms and childhood asthma.

Ann Agric Environ Med. 2010 Dec;17(2):221-9

Authors: Kasznia-Kocot J, Kowalska M, Gorny R, Niesler A, Wypych-Slusarska A

The presented cross-sectional study, comprised a group of 1,130 children from 13-15 years of age living in Upper Silesia, Poland, was undertaken to ascertain the role of environmental factors in the development of adverse respiratory health outcomes. To estimate the prevalence of these effects, the ISAAC questionnaire supplemented by questions related to risk factors was used. Bronchial asthma was identified in 4.5 percent of the children, asthma diagnosed by physicians in 8.7 percent, and prevalence of wheezing in the previous 12 months in 12.6 percent. The highest probability of wheezing was found in children with maternal genetic propensity (such as asthma, allergy), exposed to maternal smoking, or was connected with household risk factors such as the presence of dampness/mould or living in 50-year-old building. Female gender and attendance at nursery school were shown to be protective factors against wheezing. The probability of asthma was nearly twice as high in children residing in damp/mouldy dwellings, heated by coal-fired furnaces and living in the immediate vicinity of a road with heavy traffic. This study revealed that exposure to indoor (tobacco smoke, coal stove emission, mould or dampness in dwelling) and outdoor (traffic pollution) air contaminants are major environmental factors responsible for adverse respiratory health effects in children.

PMID: 21186763 [PubMed – in process]

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December 31, 2010

Cord-Blood 25-Hydroxyvitamin D Levels and Risk of Respiratory Infection, Wheezing, and Asthma.

Cord-Blood 25-Hydroxyvitamin D Levels and Risk of Respiratory Infection, Wheezing, and Asthma.

Pediatrics. 2010 Dec 27;

Authors: Camargo CA, Ingham T, Wickens K, Thadhani R, Silvers KM, Epton MJ, Town GI, Pattemore PK, Espinola JA, Crane J,

Objective: Higher maternal intake of vitamin D during pregnancy is associated with a lower risk of wheezing in offspring. The relationship between cord-blood levels of 25-hydroxyvitamin D (25[OH]D) and childhood wheezing is unknown. We hypothesized that cord-blood levels would be inversely associated with risk of respiratory infection, wheezing, and asthma. Patients and Methods: Cord blood from 922 newborns was tested for 25(OH)D. Parents were asked if their child had a history of respiratory infection at 3 months of age or a history of wheezing at 15 months of age and then annually thereafter. Incident asthma was defined as doctor-diagnosed asthma by the time the child was 5 years old and reported inhaler use or wheezing since the age of 4 years. Results: The median cord-blood level of 25(OH)D was 44 nmol/L (interquartile range: 29-78). Follow-up was 89% at the age of 5 years. Adjusting for the season of birth, 25(OH)D had an inverse association with risk of respiratory infection by 3 months of age (odds ratio: 1.00 [reference] for ?75 nmol/L, 1.39 for 25-74 nmol/L, and 2.16 [95% confidence interval: 1.35-3.46] for <25 nmol/L). Likewise, cord-blood 25(OH)D levels were inversely associated with risk of wheezing by 15 months, 3 years, and 5 years of age (all P < .05). Additional adjustment for more than 12 potential confounders did not materially change these results. In contrast, we found no association between 25(OH)D levels and incident asthma by the age of 5 years. Conclusions: Cord-blood levels of 25(OH)D had inverse associations with risk of respiratory infection and childhood wheezing but no association with incident asthma.

PMID: 21187313 [PubMed – as supplied by publisher]

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December 30, 2010

Gene Expression Patterns of Th2 Inflammation and Intercellular Communication in Asthmatic Airways.

Gene Expression Patterns of Th2 Inflammation and Intercellular Communication in Asthmatic Airways.

J Immunol. 2010 Dec 27;

Authors: Choy DF, Modrek B, Abbas AR, Kummerfeld S, Clark HF, Wu LC, Fedorowicz G, Modrusan Z, Fahy JV, Woodruff PG, Arron JR

Asthma is canonically thought of as a disorder of excessive Th2-driven inflammation in the airway, although recent studies have described heterogeneity with respect to asthma pathophysiology. We have previously described distinct phenotypes of asthma based on the presence or absence of a three-gene “Th2 signature” in bronchial epithelium, which differ in terms of eosinophilic inflammation, mucin composition, subepithelial fibrosis, and corticosteroid responsiveness. In the present analysis, we sought to describe Th2 inflammation in human asthmatic airways quantitatively with respect to known mediators of inflammation and intercellular communication. Using whole-genome microarray and quantitative real-time PCR analysis of endobronchial biopsies from 27 mild-to-moderate asthmatics and 13 healthy controls with associated clinical and demographic data, we found that asthmatic Th2 inflammation is expressed over a variable continuum, correlating significantly with local and systemic measures of allergy and eosinophilia. We evaluated a composite metric describing 79 coexpressed genes associated with Th2 inflammation against the biological space comprising cytokines, chemokines, and growth factors, identifying distinctive patterns of inflammatory mediators as well as Wnt, TGF-?, and platelet-derived growth factor family members. This integrated description of the factors regulating inflammation, cell migration, and tissue remodeling in asthmatic airways has important consequences for the pathophysiological and clinical impacts of emerging asthma therapeutics targeting Th2 inflammation.

PMID: 21187436 [PubMed – as supplied by publisher]

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December 29, 2010

Comorbidities of migraine.

Comorbidities of migraine.

Front Neurol. 2010;1:16

Authors: Wang SJ, Chen PK, Fuh JL

Migraine is a common neurological disorder and can be severely disabling during attacks. The highest prevalence occurs between the ages of 25 and 55?years, potentially the most productive period of life. Migraine leads to a burden not only for the individual, but also for the family and society in general. Prior studies have found that migraine occurs together with other illnesses at a greater coincidental rate than is seen in the general population. These occurrences are called “comorbidities,” which means that these disorders are interrelated with migraine. To delineate the comorbidities of migraine is important, because it can help improve treatment strategies and the understanding of the possible pathophysiology of migraine. The comorbid illnesses in patients with migraine include stroke, sub-clinical vascular brain lesions, coronary heart disease, hypertension, patent foramen ovale, psychiatric diseases (depression, anxiety, bipolar disorder, panic disorder, and suicide), restless legs syndrome, epilepsy and asthma. In this paper, we review the existing epidemiological and hospital-based studies, and illustrate the connections between these illnesses and migraine.

PMID: 21188255 [PubMed – in process]

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