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A case which presented with early cancer of the duodenal duplication in addition to a gallbladder defect is reported. This may be the first case of its kind reported in the literature.

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Antibody‐dependent cellular cytotoxicity (ADCC) and natural killer (NK) ativity were examined using MT‐2 cells persistently infected by HTLV‐1 as target cells, and mononuclear cells as effector cells, from helathy one‐week‐old newborn babies, infants, children and adults. More than 10% of ADCC was observed in 17 newborn babies out of 22 (77.3%) and in all 67 healthy one‐month‐old babies to adults, by adding serum from anti‐HTLV‐1 positive carriers. When anti‐HTLV‐1 negative serum was added, less than 10% of ADCC was observed. If infants without anti‐HTLV‐1 antibodies were breast‐fed they had the possibility of HTLV‐1 vertical transmission. There was no significant decrease in NK activity between 90 healthy newborn babies, infants, children, or adults. These results suggest that ADCC and NK activity protect against the transmission of HTLV‐1 from mother to child.

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To elucidate the mechanism of portal hypertension seen as a symptom of so-called Banti's syndrome (idiopathic portal hypertension), observation was made of rising of the portal pressure experimentally induced in sensitized rabbits. Intraintestinal injection of the same antigen as used for the sensitization resulted in elevation of the portal pressure. This phenomenon appears to be attributable to antigen-antibody reaction caused by the injected antigen absorbed from the intestine and entered thereby into the portal system while maintaining its antigenicity. From the phenomenon also, the site of the antigen-antibody reaction is estimated to be limited at least to the hepatic level. The portal pressure-rising phenomenon observed following intraintestinal introduction of antigen may suggest the possibility of entrance of the orally introduced antigen to the portal system, emphasizes importance of alimentary factors in the genesis of this syndrome.

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