Background-It has been reported that pranlukast reduces the antigen induced immediate and late phase asthmatic responses, airway hyperreactivity to acetylcholine, and pulmonary eosinophil accumulation in guinea pigs. A study was undertaken to test the hypothesis that pranlukast may reduce the number of inflammatory cells in the bronchial mucosa of patients with asthma. Methods-A double blind, placebo controlled study was performed in 17 mild to moderate asthmatic subjects to examine changes in inflammatory cell infiltration in response to pranlukast (225 mg orally twice per day for four weeks). Comparisons of the mean daily 2 agonist use, symptom score, FEV 1 percentage predicted, and airway methacholine responsiveness were made before and after treatment. Using fibreoptic bronchoscopy, bronchial biopsy specimens were obtained before and after treatment with either pranlukast (n = 10) or placebo (n = 7). Immunohistology was performed using monoclonal antibodies for CD3, CD4, CD8, CD68, NP57, AA1, EG1, EG2, GTP and CD19. Results-When the pranlukast and placebo treated groups were compared there were decreases in 2 agonist use, symptom score, and airway methacholine responsiveness after pranlukast but no increase in FEV 1 was seen. The clinical response in patients treated with pranlukast was accompanied by a reduction in CD3 (median diVerence -37, 95% confidence interval (CI) -69 to -1; p<0.05), CD4 (median diVerence -28, 95% CI -49 to -8; p<0.01), AA1 (median diVerence -15, 95% CI -26 to 0; p<0.05) and EG2 positive cells (95% CI -35 to 0; p<0.05), but not in EG1 positive eosinophils, GTP positive cells, and CD19 positive plasma cells. Conclusions-These results support the view that pranlukast may act by inhibition of bronchial inflammation in patients with asthma. (Thorax 1998;53:835-841)

. Dynamic interaction between T cell-mediated ␤-cell damage and ␤-cell repair in the run up to autoimmune diabetes of the NOD mouse.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the cause of novel coronavirus disease 2019 (COVID-19), was first reported in Wuhan, China, and now has spread across the world as a global pandemic. The propagation from asymptomatic polymerase chain reaction (PCR)-positive individuals represents a complicating factor in the efforts to control the COVID-19 pandemic. We examined the course of PCR assays and the duration of viral shedding in 23 asymptomatic or mild COVID-19 patients from the cruise ship who were admitted to our hospital. Among these 23 cases, the median duration of viral shedding was 19 days (range, 6-37 days) from initial viral detection. Eight cases (35%) had another positive PCR result after testing negative once. Although the duration of viral shedding was approximately three weeks, the infectivity and transmissibility period from asymptomatic and mild COVID-19 cases is unclear. Further studies are needed to determine how long such asymptomatic and mild COVID-19 cases have infectivity.

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