We screened 1,200 living heart, lung, liver, and kidney transplant recipients for hepatitis E virus infection by reverse transcription PCR. In 12 (1%) patients, hepatitis E virus infection was identified; in 11 patients, chronic infection developed. This immunocompromised population is at risk for hepatitis E virus infection.

1 We have examined the e ects of 12 glucocorticoids as inhibitors of A549 cell growth. 2 Other than cortisone and prednisone, all the glucocorticoids inhibited cell growth and this was strongly correlated (r=0.91) with inhibition of prostaglandin (PG)E 2 formation. 3 The molecular mechanism by which the active steroids prevented PGE 2 synthesis was examined and three groups were identi®ed. Group A drugs did not inhibit arachidonic acid release but inhibited the induction of COX2. Group B drugs were not able to inhibit the induction of COX2 but inhibited arachidonic acid release through suppression of cPLA 2 activation. Group C drugs were apparently able to bring about both e ects. 4 The inhibitory actions of all steroids was dependent upon glucocorticoid receptor occupation since RU486 reversed their e ects. However, group A acted through the NF-kB pathway to inhibit COX2 as the response was blocked by the inhibitor geldanamycin which prevents dissociation of GR and the e ect was blocked by APDC, the NF-kB inhibitor. On the other hand, the group B drugs were not inhibited by NF-kB inhibitors or geldanamycin but their e ect was abolished by the src inhibitor PP2. Group C drugs depended on both pathways. 5 In terms of PGE 2 generation, there is clear evidence of two entirely separate mechanisms of glucocorticoid action, one of which correlates with NF-kB mediated genomic actions whilst the other, depends upon rapid e ects on a cell signalling system which does not require dissociation of GR. The implications for these ®ndings are discussed.

Rationale: In cystic fibrosis (CF), lung disease is the predominant cause of morbidity and mortality. Little is known about the spectrum of structural abnormalities on CT scans from patients with CF with severe advanced lung disease (SALD). No specific CT scoring system for SALD is available. Objectives: To design a quantitative CT scoring system for SALD, to determine the spectrum of structural abnormalities in patients with SALD and to correlate the SALD system with an existing scoring system for mild CF lung disease and pulmonary function tests (PFTs). Methods: 57 patients with CF contributed one CT made during screening for lung transplantation. For the SALD system, lung tissue was divided into four components: infection/inflammation (including bronchiectasis, airway wall thickening, mucus and consolidations), air trapping/ hypoperfusion, bulla/cysts and normal/hyperperfused tissue. The volume proportion of the components was estimated on a 0-100% scale; mean volumes for the whole lung were computed. Scores were correlated with Brody-II scores and PFTs. Results: The SALD system identified a wide spectrum of structural abnormalities ranging from predominantly infection/inflammation to predominantly air trapping/ hypoperfusion. SALD infection/inflammation scores correlated with Brody-II scores (r s = 0.36-0.64) and SALD normal/hyperperfusion scores correlated with forced expiratory volume in 1 s (FEV 1 ; r s = 0.37). Reproducibility for both systems was good. Conclusions: A CT scoring system was developed to characterise the structural abnormalities in patients with SALD. A wide spectrum was observed in SALD, ranging from predominantly air trapping to predominantly infection/inflammation-related changes. This spectrum may have clinical implications for patients with SALD.

This study clarifies the epidemiology of SSc in The Netherlands and confirms the frequent occurrence of pulmonary complications, based on 654 cases. This can and will be studied further in the ongoing POEMAS study.

CT score INF correlates with survival, and adds to the predictive value of LAS.