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.

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1971～1974年についての群馬県内の保健所管内別死亡率の比較において, 男の胃の悪性新生物死亡が特に高率であった安中保健所管内をとりあげ, 1965～1974年の10年間の管内の胃の悪性新生物死亡についての観察を行なった.男の胃の悪性新生物死亡はこの期間においても高率あり, また管内の安中市と松井田町との間に差は認められなかった.世帯のおもな仕事についての比較では, 男で, 脳血管疾患死亡者の群よりも, 胃の悪性新生物死亡者の群に, 常用勤労者世帯(I)の者が多く専業農家世帯の者が少なかった.

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先の報告で, Gerbal らのA型血球に対する細菌性の deacetylase の作用と acquired B に関する報告をもとに, clostridium tertium O (H), Le^a の培養濾液から精製した N-deacetylaseをA型血球に作用させ, deacetylase 処理A型血球 (A_deac) と特異的に反応する抗体及びB型血球とも交差反応性を示す抗体がヒト血清中に含まれていることを見出した.また水溶性A型物質も N-deacetylase の作用によって, 血球と同じ抗原活性を持つようになることを証明した.ここでは, A_deac血球及び型物質のN-アセチル化とgalactosarninidase作用による反応性の変化及びacquired Bに関連して, Springerらによって報告されたB型活性を持つ腸内細菌の菌体多糖体吸着血球と A_deac血球との反応性を調べたので報告する.

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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.

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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.

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