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Purpose: Maximizing human comfort in design of medical environments depends immensely on specialized architects particularly critical care design; the study proposes Evidence-Based Design as an apparent analog to Evidence-Based Medicine. Healthcare facility designs are substantially based on the fin...

Cystic fibrosis transmembrane conductance regulator (CFTR) gene and sodium-independent Cl?/HCO₃? anion exchanger (AE) genes are expressed in a wide variety of mammalian tissues including cholangiocytes. They play an important role in the regulation of intracellular pH (pHi) as well as in transepithelial acid/base transport necessary for biliary bicarbonate secretion. The aim of this study was to examine the expression level of CFTR gene and AE genes (AE1, AE2 and AE3) in the cholangiocytes and the hepatocytes, and also measure AE2 gene expression level after bile duct ligation (BDL). As we previously described, isolated hepatocytes and cholangiocytes from the liver of normal and BDL rats were prepared and gene expression levels were measured by using RT-PCR. We found that AE1, AE2, and AE3 genes were expressed in both hepatocytes and cholangiocytes, but CFTR was only in cholangiocytes. AE2 gene expression level was higher in the BDL hepatocytes than normal hepatocytes, which was significantly different between two groups. AE2 gene expression level was lower in the BDL cholangiocytes than normal cholangiocytes. However, AE2 gene expression level in both hepatocytes and cholangiocytes were not changed with a longer duration of BDL. These results suggest that CFTR and AE2 may play an important role in the pathogenetic mechanism of biliary cholestatic liver disease.

BACKGROUND Bronchial asthma is a clinical syndrome characterized by reversibility of airway obstruction. However, many asthmatics have evidence of residual airway obstruction. It has become evident that the repair of the chronic inflammatory process can lead to various irreversible changes. It is generally accepted that the most common cause for the change is cigarette smoking but it is controversial whether asthma progresses to emphysema. High resolution computed tomography (HRCT) is more sensitive and more accurate than chest plain films in determining the type and extent of emphysema. This study was carried out to determine whether asthma can be a cause of emphysema without the effect of cigarette smoking and to evaluate clinical characteristics in asthmatics with emphysema. METHODS We studied 58 asthmatic patients with reversible airway obstruction and evaluated the presence of emphysema using HRCT and pulmonary function test. According to HRCT findings, they were divided into 2 groups: Asthmatics with emphysema and the ones without emphysema. RESULTS Of the 58 patients, 7 were revealed to have emphysema. (1) 6 asthmatics with emphysema were smokers, but one patient was a nonsmoker. (2) Highly significant differences between asthmatics with and without emphysema were found in cigarette smoking (p < 0.01) and smoking consumption (p < 0.01). (3) There were no significant differences in the duration of asthma, age or sex between patients with and without emphysema. (4) There were no significant differences in FEV1(%), FEV1/FVC (%), diffusing capacity for carbon monoxide (DLco) (%) and DLco/alveolar volume between patients with and without emphysema (5) Differences between asthma patients without emphysema and those with emphysema were found to be significant in bronchial wall thickness (p < 0.05) and in total Ig E levels (p = 0.07). CONCLUSION These results indicate that smoking is a main factor in causing emphysema in asthmatics.

Mast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell–deficient WBB6F1- W/Wv (W/Wv) and congenic normal (+/+) mice. Although a 5-min delay in shock signs and death were observed in W/Wv mice, 100% fatal reactions to penicillin V (Pen V) occurred in both +/+ and W/Wv mice. Administration of monoclonal anti–IL-4 antibody completely prevented the fatal reactions, and the effect of anti–IL-4 was associated with its suppressive activity on Pen V–specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/Wv mice, high levels of PAF in the circulation after challenge in both +/+ and W/Wv mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis.