Although it has been considered for a long time that the secretion of growth hormone from the pituitary gland may have a some causative role of pathogenesis of diabetes mellitus, the insulin-induced hypoglycemia and arginine infusion can not be employed to ascess whether or not there might be a deficiency of the pituitary gland to secrete the growth hormone in the diabetic, because the diabetes mellitus has been recognized by many clinicians as one of typical metabolic diseases. However, recently it was found that dopamine was the drug to stimulate only the growth hormone secretion from the pituitary without any changes of blood sugar levels, serum fatty acids and amino acids metabolism.
In the present study, in order to clarify how the growth hormone was secreted by several stresses from the pituitary in the diabetic, tolbutamide, arginine and L-dopa methods were compared both in normal subjects and in diabetics without obesity. In normal subjects, the pituitary secretion of growth hormone was clearly stimulated by all of three methods. However, the tolbutamide and the arginine methods were not reasonable to ascertain the ability of pituitary gland to secrete the growth hormone in the diabetic as well known. On the other hand, L-dopa, which is well known to be a precursor of the dopamine, stimulated the secretion of growth hormone from the pituitary with no influence on blood sugar and IRI in both normal subjects and diabetics. The serum concentrations of growth hormone of normal subjects and diabetics at the fasting time before the infusion of 200 ml of physiological saline containing 200 mg L-dopa for 30 min were between 2 and 4 ng/ml. Maximum concentration of serum growth hormone, approximately 30 ng/ml, were observed at 60 min after the beginning of starting of 30 min infusion of L-dopa in the normal subject. In contrast, this value of diabetics was only nearly 6ng/ml which was also observed at 60 min after the L-dopa infusion was started. The fact indicated strongly that the ability of pituitary gland to secrete the growth hormone was clearly impaired in the diabetes mellitus when it was compared with that of normal subject.

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There has not been elucidated the conclusive mechanism of high resistance mutant on R factor. In this studies, we have examined that the demonstration of R factor mutant capable of hypersynthesis of penicillinase and genetic studies of the mutant.
When the strains of E. coli W3630 harboring R_M201 factor (TC.CM.SM.SA.APC) were inoculated on plates containing various concentration of APC, mutants carrying various levels of APC resistance were due to a quantitative increase in the formation of penicillinase. By conjugation experiments and transduction analysis, the mutation was found to affect the gene (amp) governing APC resistance on the R factor. The R-factor mutnats carrying high and stable APC resistance were conjugally transferred at the same frequency as their parent R factors, and the level of their resistance to drugs other than APC was not distinct from that conferred by their parents. Such R-factor mutants could easily be obtained from wild-type R factors carrying low APC resistance. The hypersynthesis of penicillinase by such R-factor mutants was considered to be due to the replication of the amp gene on the R factor at hyper-rates and the integration of multiple copies of the amp gene (amp-hyper) in the R-factor genome.
The physical characteristics of a mutant R_M201-2 capable of conferring high and stable APC-resistance was analysed. The R_M201-2 and its parent R factor DNA could be isolated as an extrachromosomal and covalently closed circular form, their buoyant densities both 1.712 g/cm³ and the molecular weight were about 8.2× 10⁷ and 6.4 × 10⁷ daltons respectively when measured by CsCl and sucrose density gradient analyses. The contour lengths under electromicroscope were 35.9±0.6μm and 31±0.6μm, respectively. Using the extracted R factor DNA, the mutant and parent characters were transformable to another E. coli strain, respectively. The mutant R factor showed an increased amount of DNA even after conjugaltransfer to Protues. Increase in the size of R factor DNA was thus considered to be the cause for the high level of APC resistance.

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From the observation on palatal region of human embryos aged 5-11 weeks, the author summarised the results as follows.
1) In the tip of palatal process and the lower surface of nasal septum during the secondary palate formation, hypertrophy of the covering, disarrangement of the epithelial cells and disappearance or discontinuity of the basement membrane were observed.
2) PAS positive substances (chiefly consisting of flycogen) were already present in primary oral mucous membrane of fetus at the stage of five weeks. Covering flat epithelium appeared as the palatal processes took horizontal position.
3) At the critical period of palatal formation, following two points were significant.
a. The epithelium at the tip of palatal process invaginated into mesenchymal tissue prior to contact, and the invaginated cell mass was resemble to the form of epithelial peal.
b. In the median portion of lower surface of nasal septum, covering flat epithelial cell appeared and the previous epithelial cells were replaced by them.
4) Though the covering flat epithelium might take part during formation of epithelial pearl in the region of fusion, these cells could not be clearly found in the epithelial pearl.
5) The epithelium at the tip of palatal process was composed of oral and nasal epithelium. The two epithelium assumed to be overlapped. The superficial layer was derived from that of oral epithelium and deep layer from that of nasal epithelium.
6) From the findings mentioned above, it may be possible to say that the specific eptihelial cell changes in the region of fusion bring about not only in the rodents, but in the human embryos.

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A case of congenital atresia of the duodenum in the five-day-old female infant was presented. The means of clinical and roentgen evaluation are outlined. A plain x-ray film of the abdomen is regarded as the most reliable single diagnostic measure.
The experience with 11 patients of the duodenal atresia (excluding stenosis) treated by duodenojejunostomy with or without the transanastomotic feeding tube during the past 10 years is briefly given. Nine of the infants recovered (82 per cent) and two died.

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²⁰³HgCl₂ was given to mice, and its retention, excretion and distribution were investigated, Furthermore various drugs were examined for ²⁰³ Hg-expelling effect.
1. Retention : The retention after the s.c., i.p. and p.o. administration were daily explored for 3 days. The retention after s.c. administration was highest, and next in order were i.p. and p.o. administration.
2. Distribution : The distribution of ²⁰³ HgCl₂ was determined times daily for 3 days after i.p. administration. The radioactivity was highest in the kidney already at 1 hour, and attained the peak at 4 hours.
The subcellular distribution of ²⁰³ HgCl₂ in the liver and kidney at 24 hours after i.p. administration was greater in the supernatant fraction from both organs than in the other fractions.
3. Effects of administration of various drugs : 3-day experiments on the whole body : The retention of ²⁰³ HgCl₂ after its i.p. administration was decreased by BAL and D-Penicillamine. ²⁰³ Hg Activity was lowered in the kidney, liver, pancreas, spleen, brain and blood by BAL, in the kidney, pancreas and spleen by D-Penicillamine, in the brain by L-CySH·Gly, in the brain and blood by L-CySH, in the kidney by 2-Mercatopropiony glycine and also by Pyridonine-4SH, in the spleen, brain and blood by Mercaptoacetic acid (though it increased ²⁰³ Hg concentration in the kidney), and in the kidney be EDTA and DTPA (though increased in the pancreas and brain).
4. Effect of starvation : The fecal excretion of ²⁰³ HgCl₂was decrease and its retention was increased by the starvation. The absorption of ²⁰³ HgCl₂ was increased by the starvation.

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