Increases in serum concentrations of immunoreactive gastrin in patients with hyperthyroidism have been reported by several investigators. However, no detailed information is available about the mechanism responsible for the high gastrin levels. The present study was undertaken to elucidate the mechanism of abnormal secretion of gastrin in hyperthyroidism.
The results obtained herein were as follows :
1. The mean fasting serum gastrin concentration for the patients with untreated hyperthyroidism was significantly higher than in normal subjects.
2. No significant correlation was observed between the basal serum gastrin levels and any of the thyroid function tests determined.
3. The high gastrin levels in hyperthyroid patients appeared to be lowered after treatment with antithyroid drug. However, serum gastrin levels in some treated patients were still higher than that of normal subjects, even when they became euthyroid after therapy.
4. No rise in serum gastrin levels occurred when normal subjects were treated with daily dose of 75 pig triiodothyronine for 8 days.
5. Decreased gastric acidity, as determined by BAO, MAO, BSVR and MSVR, was observed in patients with hyperthyroidism as compared with normal subjects : Such decreased gastric acidity tended to be elevated by antithyroid drug therapy.
6. Histologic examination of gastric mucosa in hyperthyroid patients showed superficial or atrophic gastritis, associated with lower gastric acidity.
7. No difference in serum calcium concentrations was observed between hyperthyroid patients and normal subjects.
8. Serum gastrin rose significantly from the basal levels in hyperthyroidism during arginine drip infusion. However, no difference in the per cent of the increase in gastrin levels was observed between hyperthyroid patients and normal subjects.
The present findings provide evidence that chronic stimulation of excess thyroid hormone is an important determinant in inducing hypergastrinemia, associated with decreased gastric acid secretion.

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The purpose of the study is to investigate the association or the disassociation of the tuberculosis to the lung cancer. From all the death certificates, for the years 1971-1975 in “N” health center (in Gunma prefecture), every one of those specified malignant neoplasms (B 19) was selected. Those were retrospectively collated with the tuberculosis registry made by the health center since 1960, and the cases died from the malignant neoplasms were confirmed whether they had been listed in the registry.
The deaths from malignant neoplasms observed in the term were 242 for male and 186 for female in number, and 11 (4.5%) in male and 6 (3.2%) in female were listed in the tuberculosis registry.
The number of the deaths from lung cancer (B19. e) was 21 in male and 17 in female and 19.0% male (4 cases) and 23.5% female (4 cases) were found in the registry; these rates were compared with those of stomach cancer deaths (B19.b) and with those of deaths from the all malignant neoplasms except lung cancer, under the correction for age. Compared with the rate of stomach cancer death, one of lung cancer deaths was high (but not statistically significant) in male (0.05<p<0.10) and was significantly high in female (p<0.05). And the rates were significantly higher than those for the deaths from malignant neoplasms except lung cancer deaths both in male (p<0.05) and in female (p<0.01).
The observation of the period, from the time that the deceased ones were listed in tuberculosis registry, to the time of their deaths, revealed that all those for lung cancer cases were shorter than 2 years except one case, whose term was 8 years. And all of those for the cases from the other malignant neoplasms were longer than 5 years but one exception.
From the observation above, it is considered that some of the lung cancer cases might be erroneously registered as tuberculosis, and this may be the reason that the rate of registered in lung cancer cases was high. Then the conclusion about the association or the disassociation between tuberculosis and lung cancer could not be obtained.

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In order to clarify gastrointestinal involvement in PSS, 59 patients were investigated roentgenologically.
The results were as follows :
1) Esophageal abnormalities were observed in 36 out of 59 cases (61.0%), which consisted of diminished peristalsis, aperistalsis, diffuse dilatation, reflux esophagitis and stricture, particularly the last change was observed in 4 cases (6.7%). Colon was involved in 5 out of 18 cases (27.7%), which consisted of diminution or disappearance of haustration, and dilatation. Small intestine showed abnormalities in 7 out of 29 cases (24.1%), which consisted of dilatation, retained barium, sacculation in 1 case and haustration as colon in 2 cases. Duodenal changes were observed in 6 out of 59 cases (10.1%), which consisted of dilatation in 4 cases and ulcer in 2 cases.
2) Gastrointestinal symptoms those of heartburn, dysphagia, abdominal pain, diarrhea, constipation, anorexia, etc. were observed in 26 out of 59 cases (44.0%). Among 9 cases with dysphagia, 7 cases (77.7%) showed roentgenologic esophageal abnormality, whereas among 50 cases without dysphagia, only 29 cases (58.0%) showed esophageal change.
3) To clarify the relation between skin change and esophageal change, sclerosis of the skin was classified into first, second and third degree, and also roentgenologic esophageal change was classified into 0, I, II, and III stage. In the first degree, 3 out of 10 (30.0%), in the second degree, 26 out of 41 (63.4%), and in the third degree, 7 out of 8 (87.5%), showed esophageal abnormalities respectively.
4) Long term observation from 1 to 4 years revealed no improvement of esophageal involvement in 20 cases, namely about a half (11 cases, 55.0%) showed progression, and the rest (9 cases, 45.0%) remained stationary.

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Two cases of the simple nonspecific ulcer of cecum and sigmoid colon were reported. A literature review of their pathological aspects was added. Cecum was the most frequent site of the ulcer, next the sigmoid colon. The ulcer was undermined near the Bauhin's valve of cecum and opposite to the mesenteric side of the sigmoid colon.
Histologically they were similar to the gastric peptic ulcer. Granulation tissue was more commonly seen in the ulcer of the sigmoid colon than the cecum.

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Anti-Le^a and anti-Le^b agglutinins and precipitins were produced in chicken sera immunized with human Le (a + b-) non-secretor and Le (a-b +) secretor saliva respectively. The chicken anti-Lewis agglutinins reacted with enzyme treated red cells. The results of the agglutination and precipitation inhibition tests with mono-and oligosaccharides indicated that the chicken anti-Le^a antibodies had stronger affinity for nonreducing end β-galactosyl residue joined by a (1→3) linkage to N-acetylglucosamine than a (1→4) linked α-fucosyl residue. The chicken anti-Leb antibodies were specifically inhibited by lacto-N-difucohexaose I. Therefore chicken anti-Leb had potent affinity for adjacent nonreducing end α-fucosylresiduesioined by (1→2) and (1→4) linkage.

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It is well known that the dominant pacemaker in the heart exists in a faster beating site rather than a slowly beating one. In this experiment we found that the dominant pacemaker site in the frog's sinus venosus was not always subject to the above law, when the pacemaker shift was arising from vagus stimulation. In all experiments the heart was excised together with the vagosympathetic nerve. The ventricle and large part of the auricles were cut away. A vagosympathetic nerve-sinus preparation was perfused with Ringer's solution saturated with 95% O₂ + 5% CO₂.
Intracellularly were recorded changes of pacemaker potential just during and after the stimulation of the vagus nerve. When the stimulation was applied with a certain strength and frequency, the normal pacemaker potential was separated from the prepotential and it showed a shift of dominant pacemaker site where an ectopic pacemaker was generated in a same sinus. In this case the rhythm of the sinus was under control of a new shifting site, but the intrinsic pacemaker was still remained underground. The new dominant pacemaker was generally a more slowly beating rate than the intrinsic, once a while, faster than the intrinsic. If the stimulation was removed, the intrinsic pacemaker was gradually recovered and dominated the sinus again.
In conclussion the presented results suggest that under abnormal circumstance ectopic pacemaker action can develop, compete with the normal pacemaker, and the ectopic pacemaker begins to drive the sinus temporarily, but finally it is replaced by the intrinsic pacemaker after destruction of abnormal circumstance. The abilities which dominate the rythm of pacemaker cell are dependent not only on beating rate but also on other many factors, that is, size, number, combination of true cell groups and conjunction with the nerve terminals.

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