It has been assumed that many blood-group factors may be involved in the cause of hemolytic disease in newborn pigs. This experiment was carried out to clarify whether the interaction between blood-group factor Ea and anti-Ea induced the disease or not. A litter of pigs born from a sow possessing a high titer of anti-Ea was studied. The results of serological and hematological observations are as follows. 1. The titers of anti-Ea in the serum and colostrum of the sow at parturition were 128 and 256, respectively, when determined by a tube-centrifuge technique. Of seven pigs of the same litter born healthy, four were Ea-positive and three Ea-negative. Shortly after the start of nursing, the antibody was detected from the sera of Ea-negative pigs and its titer reached a maximum level 12 hours after the start of nursing and then decreased gradually. No free anti-Ea was found in the serum of any Ea-positive pig. 2. The osmotic fragility of red blood cells in the Ea-positive pigs after nursing was very different from that in the Ea-negative pigs, due to the sensitization of red blood cells with anti-Ea transferred from the colostrum into the circulating blood. There was no remarkable difference in clinical sign, hematocrit value, or the pattern of the serum fracitons between the two groups of pigs. 3. Anti-Ea in the serum was found to be fairly common among the sow population. However, when the titer in the Colostrum was less than 256, no acute hemolytic anemia nor any clinical symptom was observed in the newborn, except some Changes in the osmotic fragility of red blood cells.

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The acetylcholine (ACh) release by carbachol was studied in relation to the pattern of bound ACh in the brain, and its pharmacological significance. It was shown in preliminary experiments for the bioassay of ACh on the rectus abdominis muscle of frog that heating at pH 9.5 for 10 minutes selectively hydrolysed the ACh without causing any loss of carbachol in its mixture. Therefore, it was possible to estimate the ACh and carbachol content separately. The equivalent amounts of sample hydrolysed by such treatment were added to the ACh standard solutions for estimation of ACh. When rabbit-brain slices were incubated in an eserinized Krebs Ringer solution at 0°C for 60minutes, an addition of carbachol (10^-8∼10^-4g/ml) caused an increased reduction in the amount of bound ACh in them. When these slices were treated with 10^-4g/ml of carbachol, their ACh contents were reduced to about 20% of the initial content. When the nerve-ending particle fractions from the rabbit whole brain were incubated in 0.32 M sucrose, addition of carbachol did also show an effect corresponding to the results obtained from slices of the same brain. When the bound ACh was assayed and divided into two types, a labile and a stable fraction, by means of the French press method, ACh release from the former fraction was shown at a relatively low concentration of carbachol, but that from the latter was a little. The ACh contents in both fractions decreased significantly at a relatively high concentration of carbachol. From these results it was suggested that carbachol might have a direct ACh-releasing effect on bound ACh, that this effect might be more remarkable upon the labile fraction of the bound ACh than upon the stable one. If carbachol tremor depends upon the ACh-releasing action of this drug, the main source of ACh released will be the labile fraction, rather than the stable one, of the bound ACh.

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