Infection with Pneumocystis carinii was demonstrated immunohistochemically in the lungs of pigs 15 to 75 days of age from a herd with epidemic pneumonia due to the organism. The distribution of the organism was centered on the airways, and extended progressively with age from the alveolar ducts to the alveoli. In a retrospective immunohistochemical study of 245 newborn to adult pigs which were necropsied between 1988 and 1995, P carinii infection was found in 87 pigs (35.5 per cent) aged between 17 days to seven months. In the pigs aged between one and three months the infection rate was 63.1 per cent. Pigs from herds in which suckler and weaner pigs shared the same air space were more heavily infected than those from the herds in which they were reared separately. There were no regional or seasonal variations in the level of infection, and the infection was not associated with any single disease.

Type 2 diabetes caused by chronic obesity is a major lifestyle-related disease. The present study aimed to determine the pathological changes in hepatocytes in chronic obesity. To develop our type 2 diabetes mouse model, we induced chronic obesity to mice by monosodium glutamate. By overeating, the mice signiˆcantly increased their body weight compared with age-matched healthy animals. To analyze the pathological changes in hepatocytes of chronic obesity before preclinical stage of type 2 diabetes, the mice were analyzed by hematoxylin-eosin staining of tissue sections at 15 w of age. In these mice, we observed eosin-negative accumulations of hepatocytes around central veins in the hepatic lobule. By Oil-Red O staining, the eosin-negative granules were identiˆed in the lipid droplets. We then ascertained whether these lipid droplets of hepatocytes in the obese mice could be modiˆed by diet. After 24 h of diet restriction, the lipid droplets of hepatocytes in the obese mice were swollen. Furthermore, after 48 h of the diet restriction, the lipid droplets continued swelling and the autophagy-like structures that were found in the healthy mice under the same condition in the obese mice were not observed. These results suggest that the obese mice might have delayed energy metabolism, which might have in‰uenced the mechanisms of hepatocytes. Theseˆndings provide new insight into the functional changes in chronic obesity-induced type 2 diabetes and it is possible that the pathological feature make a contribution to promise the target of pharmacological therapy.Key words-centrolobular fatty degeneration; hepatocyte; obesity-induced type 2 diabetes; pathological change; scanning electron microscopy; transmission electron microscopy 緒 言

b-cryptoxanthin is a common carotenoid pigment found in fruit, especially in Satsuma mandarins and in persimmons. After ingestion, b-cryptoxanthin is distributed to and accumulates in organs, such as the liver, lung, and kidney. Recent studies have reported that because of its antioxidant defense, b-cryptoxanthin performs several important functions in the preservation of human health and in the prevention of several diseases, including cancer and osteoporosis. The present study aims to determine whether b-cryptoxanthin has a protective eŠect on renal glomeruli during acute nephritis. To develop our acute nephritis mouse model, we induced kidney in‰ammation in mice using lipopolysaccharide. To analyze pathological changes in the renal glomeruli of these mice, tissue sections of the kidney were analyzed by hematoxylin eosin and periodic acid-SchiŠ staining. In mice with acute nephritis, we observed a thickening of the basal membrane in the renal glomeruli. By ultrastructural analysis, abnormalities in the foot cells were also identiˆed. In the bcryptoxanthin-ingested mice, these pathological changes were decreased. Migration of urinal proteins occurred in mice with acute nephritis, but this was decreased in b-cryptoxanthin-ingested mice, such that it correlated with the blood concentration of b-cryptoxanthin. Furthermore, in b-cryptoxanthin-ingested mice, both the accumulation and activation of in‰ammatory cells were decreased in the renal glomeruli. These results suggest that b-cryptoxanthin ingestion may produce great improvement in acute nephritis. Theseˆndings provide new insights into b-cryptoxanthin and its protective eŠect, and provide a new target for pharmacological therapy in human disease.

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