Cerebral NIRS Profiles During Premedication for Neonatal Intubation

Conditions:   Premedication;   Endotracheal Intubation;   Cerebral Hypoperfusion
Interventions:   Drug: atropine+ propofol;   Drug: atropine + atracurium + sufentanil
Sponsors:   Centre Hospitalier Intercommunal Creteil;   Association Clinique et Thérapeutique du Val de Marne;   Centre de Recherche Clinique du CHIC
Not yet recruiting – verified March 2016

View full post on ClinicalTrials.gov: asthma | received in the last 14 days

Transcriptome analysis of controlled and therapy-resistant childhood asthma reveals distinct gene expression profiles.

Related Articles

Transcriptome analysis of controlled and therapy-resistant childhood asthma reveals distinct gene expression profiles.

J Allergy Clin Immunol. 2015 Apr 9;

Authors: Persson H, Kwon AT, Ramilowski JA, Silberberg G, Söderhäll C, Orsmark-Pietras C, Nordlund B, Konradsen JR, de Hoon MJ, Melén E, Hayashizaki Y, Hedlin G, Kere J, Daub CO

Abstract
BACKGROUND: Children with problematic severe asthma have poor disease control despite high doses of inhaled corticosteroids and additional therapy, leading to personal suffering, early deterioration of lung function, and significant consumption of health care resources. If no exacerbating factors, such as smoking or allergies, are found after extensive investigation, these children are given a diagnosis of therapy-resistant (or therapy-refractory) asthma (SA).
OBJECTIVE: We sought to deepen our understanding of childhood SA by analyzing gene expression and modeling the underlying regulatory transcription factor networks in peripheral blood leukocytes.
METHODS: Gene expression was analyzed by using Cap Analysis of Gene Expression in children with SA (n = 13), children with controlled persistent asthma (n = 15), and age-matched healthy control subjects (n = 9). Cap Analysis of Gene Expression sequencing detects the transcription start sites of known and novel mRNAs and noncoding RNAs.
RESULTS: Sample groups could be separated by hierarchical clustering on 1305 differentially expressed transcription start sites, including 816 known genes and several novel transcripts. Ten of 13 tested novel transcripts were validated by means of RT-PCR and Sanger sequencing. Expression of RAR-related orphan receptor A (RORA), which has been linked to asthma in genome-wide association studies, was significantly upregulated in patients with SA. Gene network modeling revealed decreased glucocorticoid receptor signaling and increased activity of the mitogen-activated protein kinase and Jun kinase cascades in patients with SA.
CONCLUSION: Circulating leukocytes from children with controlled asthma and those with SA have distinct gene expression profiles, demonstrating the possible development of specific molecular biomarkers and supporting the need for novel therapeutic approaches.

PMID: 25863981 [PubMed – as supplied by publisher]

View full post on pubmed: asthma

Comparison of temporal transcriptomic profiles from immature lungs of two rat strains reveals a viral response signature associated with chronic lung dysfunction.

Comparison of temporal transcriptomic profiles from immature lungs of two rat strains reveals a viral response signature associated with chronic lung dysfunction.

PLoS One. 2014;9(12):e112997

Authors: Hines EA, Szakaly RJ, Leng N, Webster AT, Verheyden JM, Lashua AJ, Kendziorski C, Rosenthal LA, Gern JE, Sorkness RL, Sun X, Lemanske RF

Abstract
Early life respiratory viral infections and atopic characteristics are significant risk factors for the development of childhood asthma. It is hypothesized that repeated respiratory viral infections might induce structural remodeling by interfering with the normal process of lung maturation; however, the specific molecular processes that underlie these pathological changes are not understood. To investigate the molecular basis for these changes, we used an established Sendai virus infection model in weanling rats to compare the post-infection transcriptomes of an atopic asthma susceptible strain, Brown Norway, and a non-atopic asthma resistant strain, Fischer 344. Specific to this weanling infection model and not described in adult infection models, Sendai virus in the susceptible, but not the resistant strain, results in morphological abnormalities in distal airways that persist into adulthood. Gene expression data from infected and control lungs across five time points indicated that specific features of the immune response following viral infection were heightened and prolonged in lungs from Brown Norway rats compared with Fischer 344 rats. These features included an increase in macrophage cell number and related gene expression, which then transitioned to an increase in mast cell number and related gene expression. In contrast, infected Fischer F344 lungs exhibited more efficient restoration of the airway epithelial morphology, with transient appearance of basal cell pods near distal airways. Together, these findings indicate that the pronounced macrophage and mast cell responses and abnormal re-epithelialization precede the structural defects that developed and persisted in Brown Norway, but not Fischer 344 lungs.

PMID: 25437859 [PubMed – in process]

View full post on pubmed: asthma