Airway remodeling measured by multidetector CT is increased in severe asthma and correlates with pathology.

Background: To prospectively apply an automated, quantitative three-dimensional approach to imaging and airway analysis to assess airway remodeling in asthma patients.

Methods: Using quantitative software (Pulmonary Workstation, version 0.139; VIDA Diagnostics; Iowa City, IA) that enables quantitative airway segment measurements of low-dose, thin-section (0.

Epithelial cell proliferation contributes to airway remodeling in severe asthma.

Rationale: Despite long-term therapy with corticosteroids, patients with severe asthma develop irreversible airway obstruction.

Objectives: To evaluate if there are structural and functional differences in the airway epithelium in severe asthma associated with airway remodeling.

Methods: In bronchial biopsies from 21 normal subjects, 11 subjects with chronic bronchitis, 9 subjects with mild asthma, and 31 subjects with severe asthma, we evaluated epithelial cell morphology: epithelial thickness, lamina reticularis (LR) thickness, and epithelial desquamation.

Alterations in thigh subcutaneous adipose tissue gene expression in protease inhibitor-based highly active antiretroviral therapy.

Use of protease inhibitor (PI)-based highly active antiretroviral therapy (HAART) has been associated with altered regional fat distribution, insulin resistance, and dyslipidemias. To assess how PI-based HAART affects adipocyte gene expression in male HIV-1-infected patients, reverse transcription-polymerase chain reaction was used to quantify messenger RNA expression of adipocyte transcription factors and adipocytokines in thigh and abdominal subcutaneous adipose tissue from male (1) HIV-1 seronegative subjects (control, n = 9), (2) asymptomatic treatment-naive HIV-1-infected patients (naive, n = 6), (3) HIV-1-infected patients who were receiving antiretroviral agents but never received PIs (PI naive, n = 5), (4) HIV-1-infected patients who were receiving PI-based HAART (PI, n = 7), and (5) HIV-1-infected patients who discontinued the PI component of their antiviral therapy more than 6 months before enrollment (past PI, n =7). In the PI group, the messenger RNA expression levels of the CCAAT/enhancer-binding protein alpha , leptin, and adiponectin (18%, P < .

Increased neonatal mortality in mice lacking cellular retinol-binding protein II.

Cellular retinol-binding protein II (CRBP II) is a member of the cellular retinol-binding protein family, which is expressed primarily in the small intestine. To investigate the physiological role of CRBP II, the gene encoding CRBP II was inactivated. The saturable component of intestinal retinol uptake is impaired in CRBP II(-/-) mice.

Analysis of human cellular retinol-binding protein II promoter during enterocyte differentiation.

Cellular retinol binding protein II (CRBP II) is a vitamin A-binding protein that is expressed specifically in small intestinal villus absorptive cells. Previous studies have shown that retinoic acid upregulates endogenous human CRBP II gene expression in differentiated Caco-2 cells. To better characterize the regulation of human CRBP II expression, we analyzed the ability of receptor-selective agonists to enhance transcription from the 5'-upstream flanking region of the human CRBP II gene.