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Biomedical subjects

A Masood

Publications and source records attributed to A Masood.

10 recordsLinked to original sources
PubMed2001

Radiofrequency ablation for sleep-disordered breathing.

Radiofrequency volumetric tissue reduction (RFVTR) has been applied to the nose, palate, and tongue as a treatment for sleep-disordered breathing. Data on the outcome of this procedure are very scant. When applied to the palate, RFVTR seems to be moderately effective for simple snoring. It has not been shown to be effective treatment for significant sleep apnea. Application of RFVTR to the tongue and turbinates has not been studied thoroughly enough to assess its efficacy at present.

Catheter Ablation↗
PubMed2000

Sleep apnea.

Progress continues in the refinement of historical and physical examination findings predictive of sleep-disordered breathing. Home monitoring is becoming more widely accepted and validated. The most significant development in the diagnosis of sleep-disordered breathing this year was the American Academy of Sleep Medicine's report on "Recommendations for syndrome definition and measurement techniques in clinical research." In this report, hypopnea and respiratory effort related arousal are defined, and the term obstructive sleep apnea is appropriately changed to obstructive sleep apnea-hypopnea syndrome. Because of the importance of this report, we discuss the recommendations in detail.

Body Mass Index↗
PubMed1999

Expression of PKA inhibitor (PKI) gene abolishes cAMP-mediated protection to endothelial barrier dysfunction.

We investigated the hypothesis that cAMP-dependent protein kinase (PKA) protects against endothelial barrier dysfunction in response to proinflammatory mediators. An E1-, E3-, replication-deficient adenovirus (Ad) vector was constructed containing the complete sequence of PKA inhibitor (PKI) gene (AdPKI). Infection of human microvascular endothelial cells (HMEC) with AdPKI resulted in overexpression of PKI. Treatment with 0.5 microM thrombin increased transendothelial albumin clearance rate (0.012 +/- 0.003 and 0.035 +/- 0.005 microl/min for control and thrombin, respectively); the increase was prevented with forskolin + 3-isobutyl-1-methylxanthine (F + I) treatment. Overexpression of PKI resulted in abrogation of the F + I-induced inhibition of the permeability increase. However, with HMEC infected with ultraviolet-inactivated AdPKI, the F + I-induced inhibition was present. Also, F + I treatment of HMEC transfected with reporter plasmid containing the cAMP response element-directed transcription of the luciferase gene resulted in an almost threefold increase in luciferase activity. Overexpression of PKI inhibited this induction of luciferase activity. The results show that Ad-mediated overexpression of PKI in endothelial cells abrogated the cAMP-mediated protection against increased endothelial permeability, providing direct evidence that cAMP-dependent protein kinase promotes endothelial barrier function.

Adenoviridae↗