Thirty-six different normal tissues and 13 different malignant epithelial tumours, were examined immunohistochemically for the presence of protein 1 (P1) and Clara cell 10-kDa protein (CC10). Adenocarcinomas of the lung were also examined for the expression of pulmonary surfactant apoprotein using a monoclonal antibody (PE-10). The staining results of P1 and CC10 were almost identical both in normal tissues and in malignant tumours. In normal lung, Clara cells were strongly positive for both P1 and CC10. In addition, some goblet cells and non-ciliated non-mucus cells in the upper airways were moderately positive for both proteins. In the malignant tumours, some lung cancers were positive for P1 and CC10, both of which were positive in the same tumour cells on sequential sections. In 117 lung cancers, P1 and CC10 were positive in 10.2% of adenocarcinomas, 20.5% of squamous cell carcinomas, and 12.5% of large cell carcinomas. PE-10 stained positively in 65.3% of adenocarcinomas, a frequency significantly higher than that of P1 and CC10 (P < 0.01). These results suggest that P1 and CC10 are nearly identical proteins, that both are useful markers of Clara cells, and that many pulmonary adenocarcinomas express surfactant apoprotein rather than Clara cell proteins.

It is well known that lymphocytic infiltration of pancreatic islets, a condition referred to as "insulitis," is seen in acute-onset type 1 diabetes at autopsy and in biopsy specimens. However, there have been no proven cases of insulitis in type 1 diabetes with residual beta-cell function. We believe that this is the first type 1 diabetic patient with residual beta-cell function who was proven to have T-cell insulitis. This novel evidence will contribute to the proper classification and treatment of diabetes and to a better understanding of the pathophysiology of type 1 diabetes.

No abstract

Serum levels of surfactant protein A (SP-A) were studied in 237 healthy subjects in relation to sex, age, and smoking habits. SP-A values in male smokers were significantly higher than those in male nonsmokers (p < 0.001). The amount of cigarette smoking did not correlate significantly with SP-A values, however. SP-A values in young nonsmoking males and females were somewhat lower than those in older, but without significant difference. No significant difference in values was found between the sexes. We conclude that (1) smoking increases serum levels of SP-A, and (2) SP-A serum levels are not affected by age and sex.

No abstract