It has been postulated that prostaglandin (PG) _s affect the pituitary-thyroid axis in man and experimental animals. However, the role of endogenous PG_s in mediating the effect of thyrotropin (TSH) is unclear. Thus, the present investigation was designed to determine the effect of indomethacin (Ind) and aspirin, PG synthesis inhibitors, on the thyroid and TSH-secretory mechanism in the rat. Animals were injected sc daily with Ind (1. 5mg/100g bw) or aspirin (8mg/100g bw) for 3 days.
The plasma T₄, and T₃ levels, determined by radio-immunoassay, were consistently lower in the Ind or aspirin treated groups than in the controls. Both thyroid ¹³¹I uptake and numbers of intracellular colloid droplet formation in the thyroid after TSH stimulation were also reduced by the Ind treatment. The basal TSH levels appeared to decrease in the Ind or aspirin treated groups, with significant decreases in plasma T₄ and T₃. However, Ind treatment significantly potentiated the TSH response to synthetic thyrotropin-releasing hormone (TRH) in intact rats. The pituitary TSH content was higher in the Ind group than in the controls. In contrast, aspirin inhibited the TSH response to TRH, when the pituitary TSH content decreased significantly.
On the other hand, the compensatory rise in plasma TSH following thyroidectomy was inhibited by the Ind treatment. Nevertheless, the higher plasma TSH response to TRH was observed in thyroidectomized rats treated with Ind than in the controls. The pituitary TSH content was markedly increased by the Ind, while the hypothalamic TRH content in the two groups was not different.
The increased sensitivity of plasma TSH response to exogenous TRH in the Ind treated group is presumably due to higher pituitary TSH content than in the controls. The action of Ind appears to be mediated, at least in part, at the pituitary level. In addition, there is a dissociation between the action of Ind and aspirin in the TSH response to TRH.

View full abstract

In comparison among health center districts in Gunma prefecture for the years 1971-1974, an area was revealed to have significantly high mortality rate for the malignant neoplasm of the stomach in male (Report 1). Then, the aim of the present study is to investigate the mortality in the area covering a period of 10 years (1965-1974).
The age adjusted mortality rates for the malignant neoplasm of the stomach were calculated for the two composing communities of the area for the two five year periods 1965-1969 and 1970-1974. The rates for the male were considerably high and no difference was observed between those of the two communities.
The distribution of the occupational types of the households of the deaths from the malignant neoplasm of the stomach was compared with those from the other malignant neoplasms, the ischemic heart diseases, and the cerebro-vascular diseases, under the correction for age. The test statistic is a usual x² quantity, except that the expectation was calculated separately for each age group and the separate expectations added together to provide a total expectation standardized for age. Then, these expected numbers are calculated on the assumption that within one age group, each death group has a same distribution of the occupational types of the households. The statistically significant difference was observed between the distribution of the deaths from the malignant neoplasm of the stomach and from the cerebro-vascular diseases in male, and it was shown that there were more households of “employee (white collar)” and less households of “agriculture only” in the former than the latter.

View full abstract

1) Loss of blood group A activity produced by N-deacetylase from Clostridium tertium O (H), Le^a was restored and A_deac activity with human anti-A_deac serum was disappeared by acetylation of enzyme treated blood group A red cells and water soluble A substances.
2) Loss of A_deac activity of A_deac red cells and substances by the treatment of α-galactosaminidase from Cl. tertium A was accompanied by an increase in blood group H activity.
3) All human adult sera agglutinated blood group O red cells coated with O-antigenic lipopolysaccharides from E. coli O₈₆ and S. milwaukee which had blood group B activity. Not all sera from cord blood agglutinated the corted cells. Dolichos biflorus and Arachis hypogaea extracts which contained panagglutinin did not agglutinate the lipopolysaccharide coated cells.
4) Antibodies in human sera against A_deac red cells and red cells coated with E. coli O₈₆ lipopolysaccharide were absorbed with heat killed E. coli and Salmonella, wheather the bacterium had blood group activities or not.
5) Agglutination of E. coli O₈₆ coated cells was inhibited by N-acetyl-D-galactosamine and slightly by N-acetyl-D-glucosamine.

View full abstract

The inhibitory effect of aspirin (ASA) on platelet function has been well known, but the inhibitory mechanism has not been known yet. In this study, the effects of ASA on the aggregation and release reaction of rabbit platelets and the inhibitory site of ASA were investigated, and the following results were obtained :
1) In a series of in vitro experiment, the addition of 10^-6 M of ASA to normal citrated platelet-rich plasma prolonged_ lag time and suppressed the maximum rate of the platelet aggregation induced by collagen. The addition of more than 10^-4 M of ASA completely inhibited collagen-induced platelet aggregation. No significant inhibition of primary aggregation induced by ADP was observed.
2) ASA inhibited collagen-or ADP-induced release of both platelet factor 3 and serotonin from platelets.
3) Significant inhibition of the collagen-induced platelet aggregation become evident as early as 1 to 2 hrs and was maintained till 48 hrs, following the single dose of more than 0.05g of ASA. Increase in oral dose of ASA ingested to 1.0g did not enhance the inhibitory effect. Ingestion of 0.01g of ASA resulted in lesser and transient inhibition in the collagen-induced platelet aggregation.
4) Coagulation parameters were not influenced by ingestion of ASA except for a slight decrease in plasma concentration of fibrinogen.
5) In vitro study with washed or gel-filtered platelet revealed that the inhibitory effect of ASA on collagen-induced aggregation of platelets is mainly due to the direct modification of the platelet itself rather than to change of a plasma cofactor.

View full abstract

1) Gastric cancer antigen was detected with rabbit anti-gastric cancer serum which was absorbed with pooled normal human plasma and pooled normal gastric mucosal extracts. The precipitation reaction was inhibited by D-galactosamine and cancer patient's sera. The gastric cancer antigenic substance was a glycoprotein and appeared on immunoelectrophoresis as a single line in the y-region. The gastric cancer antigen was not detected in normal gastric mucosal extracts and other normal organ extracts.
2) Gastric mucosal antigens were detected with rabbit anti-normal gastric mucosa serum which was absorbed with pooled normal human plasma and duodenum, jejunum, ileum and colon extracts. The precipitation reaction was inhibited by D-galactosamine. One of gastric mucosal antigenic substances was a glycoprotein and appeared on immunoelectrophoresis as a single line in the α₂-region. It was detected in gastric cancer extracts.

View full abstract