[A study of the expression of CD(44) in pneumocytes in pulmonary sarcoidosis].

Objective: To study the expression of CD(44) in pneumocytes in pulmonary sarcoidosis.

Methods: CD(44) and AE(1)/AE(3) were detected by immunostaining in lung tissues from 21 cases of pulmonary sarcoidosis, 5 cases of tuberculosis, 4 cases of idiopathic interstitial fibrosis, 3 cases of Wegener's granulomatosis and 8 normal controls. The numbers of CD(44) positive cells and AE(1)/AE(3) positive cells (total alveolar epithelial cells) per three high-power fields were counted, and the ratio of CD(44) cells to AE(1)/AE(3) cells (84 +/- 6) were calculated.

Intervention by azithromycin on bleomycin-induced lung injury in rats and its mechanisms.

Objective: To study the role of Th1/Th2 balance in the pathogenesis of pulmonary fibrosis and to investigate the therapeutic mechanisms of azithromycin.

Methods: Male wistar rats were randomly divided into three experimental groups: the bleomycin A(5) (BLM) group (BLM group), the azithromycin (AZI) group (AZI group) and the control group. Quantitative analysis of the histopathologic changes was performed by computer gray scan.

Effective dosing regimen of 1-aminobenzotriazole for inhibition of antipyrine clearance in rats, dogs, and monkeys.

1-Aminobenzotriazole (ABT) has been extensively used as a nonspecific inhibitor of cytochromes p450 (p450s) in animals for mechanistic studies, and antipyrine (AP) has been used as a probe for hepatic oxidative metabolic capacity determination in vivo. The method of use of ABT has been variable from lab to lab due largely to unknown pharmacokinetics of ABT itself and incomplete information on various p450s inhibited. The oral pharmacokinetic profiles of ABT were generated in rats, dogs, and monkeys in the dose range of 5 to 200 mg/kg.

[Therapeutic effects of pulmonary surfactant on smoking-induced lung injury in rats, an experimental study].

Objective: To investigate the therapeutic effects of pulmonary surfactant (PS) on smoking-induced lung injury in rats.

Methods: Thirty male Wistar rats were randomly divided into four groups: normal control group (n = 8, killed by the end of the 7th week), 3-week smoking group (n = 8, in haling mainstream smoke of cigarette for 3 weeks and killed by the end of the 3rd week), 7-week smoking group (n = 8, in haling mainstream smoke of cigarette for 7 weeks and killed by the end of the 7th week), and PS treatment group (n = 6, inhaling mainstream smoke of cigarette for 7 weeks and given PS 25 mg/kg via trachea per week for 4 weeks since the end of the 3rd week of smoking, totally 5 times, and then killed by the end of the 7th week). The histological changes of respiratory bronchioles were observed by light microscopy and transmission electron microscopy.

DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL.

Immunoglobulin (Ig) class-switch DNA recombination (CSR) is thought to be highly dependent upon engagement of CD40 on B cells by CD40 ligand on T cells. We show here that dendritic cells up-regulate BLyS and APRIL upon exposure to interferon-alpha, interferon-gamma or CD40 ligand. In the presence of interleukin 10 (IL-10) or transforming growth factor-beta, BLyS and APRIL induce CSR from C(mu) to C(gamma) and/or C(alpha) genes in B cells, whereas CSR to C(epsilon) requires IL-4.

[Electroencephalogram spectral power analysis of obstructive sleep apnea syndrome patients before and during continuous positive airway pressure therapy].

Objective: To investigate the instant effects of continuous positive airway pressure (CPAP) on EEG spectral power changes in obstructive sleep apnea syndrome (OSAS) patients.

Methods: 26 OSAS patients were included. The diagnosis was made by polysomnography (PSG).

Sharing of a conserved haplotype suggests a susceptibility gene for multiple sclerosis at chromosome 17p11.

Multiple sclerosis (MS) is a chronic inflammatory disease resulting in demyelination in the central nervous system (CNS). Increasing evidence supports that genetic factors confer susceptibility to MS. One locus, the HLA complex (6p21), has been identified as important in MS, but no other loci have been clearly implicated, neither by a candidate gene approach, nor by a genomic screen strategy.