Cystic fibrosis (CF) is an inherited disorder associated with severe inflammation and repeated bacterial infection and colonization in the lung. Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro‐inflammatory cytokines can stimulate the expression of inducible nitric oxide synthase (iNOS), an enzyme generating nitric oxide, which functions as an important mediator in host defence mechanisms. To understand better the poor resistance to infections in the CF lung, the expression of the iNOS gene was investigated in explanted lungs from patients with cystic fibrosis (n‐13), bronchiectasis (n‐3), emphysema (n‐14), and in normal lungs (n‐8). In addition, bronchial epithelial cell lines were examined to study iNOS gene expression in vitro. Strong immunoreactivity for iNOS was seen in inflammatory cells and bronchial epithelium in all the diseased lungs, except for bronchial epithelium in CF. Quantitative analysis showed a significant reduction in the area of epithelium immunostained in CF [CF 6·8±1·6 (%±SEM); emphysema 18·2±2·8; normal 9·6±0·8, P<0·01], regardless of steroid treatment. These results were supported by in situ hybridization of iNOS mRNA, which showed a pattern of gene expression in CF, emphysema, and normal lung which paralleled that of protein immunoreactivity. Stimulation with cytokines (IL‐1β, TNF‐α, and IFN‐γ) increased the expression of iNOS mRNA detected by reverse transcriptase‐polymerase chain reaction (RT‐PCR) in cultures of normal (16HBE14o−), but not CF (CFBE41o−, with ΔF508 CFTR mutation) epithelial cells. Expression of iNOS in inflammatory cells suggests that the gene is normal in CF. Absence of iNOS from bronchial epithelium may be due to low expression of the gene resulting from abnormalities in the signalling system that normally causes induction, such as cytokine receptors, second messengers or transcription factors. The resulting deficiency of the nitric oxide defence system may be relevant to the susceptibility of CF patients to pulmonary bacterial colonization. © 1998 John Wiley & Sons, Ltd.

The primary and secondary patency rates of endovascular repair of PAA are equivalent to the reported outcome of open repair. Reintervention and limb salvage rate appears better than open repair. With improved long-term outcomes, endovascular repair can be considered a credible treatment strategy for routine uncomplicated PAA.

The aim of this study is to quantify myocardial perfusion during coronary CT angiography using data from a modified timing test-bolus acquisition. Institutional review board approval and informed consent were obtained. Nineteen patients with suspected coronary artery disease underwent combined coronary CT angiography and cardiac (82)Rubidium-PET perfusion. Prior to the CT angiogram a retrospectively ECG-gated dynamic test bolus was obtained following 25 mls of IV contrast medium injected at 5 ml/s. Images were acquired every 1.5 s for 30 s using 4 x 1.25-mm slices at 120 kV, 35 mAs. Regions of interest were drawn to delineate the myocardium and aorta on the resulting transaxial images. Time density curves were created and perfusion calculated using two simple approaches: maximum-slope method and peak method. In patients with normal PET myocardial perfusion, the mean (SD) resting myocardial perfusion estimated by CT using the maximum-slope method was 0.89 (+/-0.27) ml/min/g and 0.93 (+/-0.21) ml/min/g at end-systole and end-diastole, respectively, and 0.69 (+/-0.11) ml/min/g and 0.79 (+/-0.19) at end-systole and end-diastole, respectively, for the peak method. Thus quantification of myocardial perfusion from a routine coronary CT angiography test bolus is possible. CT-derived myocardial perfusion values are consistent with published values derived from other techniques.