In order to investigate the role played by the different organs of chicken red blood cell (for example, Nucleus, Mitochondria, Microsome, etc.) in hemoglobin formation, several experiments were carried out.
The results were as follows :
1) The biosyntheses of porphyrin and heme were observed in each fraction of chicken red blood cell, however, concerning the ability of biosynthesis of protoporphyrin in the supernatant fraction, a conclusion was suspended.
2) In 1000g fraction of chicken red blood cell uroporphyrin and coproporphyrin were formed at first and then protoporphyrin : in 10000g fraction uroporphyrin only was produced at first : in 20000g fraction and the supernatant fraction, the three porphyrins were simultaneously obtained from the onset.
3) KCN (10^-4M, 10^-3M) remarkably inhibited porphyrin and hem formation in 1000g and 10000g fractions respectively, and RNA ase (0.5mg/ml) prevented porphyrin and heme formation only in 10000g fraction. Pb, (CH₃COO) ₂ (10^-4M, 10^-3M) obstructed protoporphyrin formation and incorporation of iron into heme, especially in 1000g fraction and CoCl₂ (10^-4M, 10^-3M) inhibited porphyrin and hem formation remarkably, having no direct erythropoietic faculty. Folic acid (15mg/10ml) accelerated porphyrin formation especially in 1000g and 20000g fractions, while it inhibited heme formation conversely, VB₁₂ (30γ/10ml) stimulated porphyrin synthesis only in 1000g fraction, having no effect on heme synthesis. ATP (10^-2M), orotic acid (10^-2M) thioctic acid (10^-2 M), ACTH (25^I.U./10ml) etc, did more harm than good.
4) The X-Ray inhibited the biosynthesis of porphyrin in all the fractions, especially at above 1000γ and protoplasmas were more influenced in heme biosynthesis.

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In order to study the morphogenesis of atherosclerosis, human aortas at various ages from embryo to 86 years were investigated pathologically, pathohistologically and histochemically. At the same time, experimental atherosclerosis in cholesterol-fed rabbits which were bred in normal stock diet for 18 months afier cessation of cholesterol feeding were compared with those of human subjects. Further in order to examine the thrombogenic theory concerning genesis of atherosclerosis, reduplicate observation was made by Duguid method.
1) Intirnal thickening of the human aorta with ageing was observed from embryonal stage.
2) Arteriosclerosis of the aorta was remarkable in the abdominal aorta which showed great development of intima with ageing, and was mild in the ascending aorta which showed weak one. Consequently it is considered that a common factor may be involved both in diffuse intimal thickening with ageing and development of atherosclerosis.
3) Atherosclerosis is observed approximately at age above 50, but it appears ten years earlier in the hypertensives.
4) The early lesion of arteriosclerosis is intimal edema; atherosclerosis develops from it by insudation of blood plasma rich in lipid and fibrous plaque is produced from it when is is poor in lipid.
5) The precursor of atherosclerosis is intimal lipoidosis (fatty streaks or fatty spots). Lipid accumulated in the intima consists of lipid insudated directly from the circulating blood and of cellular lipids (foam cells and smooth muscle cells).
6) Pathohistologically, there are two types of atherosclerosis-type α which mainly consists in fatty swelling of collagen fiber and type β which mainly consists in tissue debris. The type α develops when intima contains poor lipids and rich collagen fibers and the type β is produced when it contains rich lipids and few collagen fibers. Foam cells play a very important role in the formation of type β atherosclerosis.
7) In order to investigate the significance of thrombi in the morphogenesis of atherosclerosis, the aortas of 50 autopsy cases ranging in age from 10 to 81 were studied. There were, however, no findings which indicate that thrombus played a principal role in the morphogenesis of atherosclerosis.
8) The rabbit which was first raised on 1 per cent cholesterol diet for 14-17 weeks and then on normal stock diet for 61 weeks at the longest, showed the closely slmilar change-to human atherosclerosis, especially of type β.
9) In the rabbit raised by the daily administration of the diet containing 6 g lard for a year, atherosclerosis does not appear. Therefore neutral fat is not involved in the formation of atherosclerosis, but the participation of cholesterol has an important significance.

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1. The blood group A-decomposing enzyme preparation from Clostridium tertium A which had been adsorbed on a DEAE-Sephadex column was eluted in two portions which had A-decomposing activity. The fast eluted fraction (Fr. 4) had activity of N-deacetylase, and when incubated with A substance, it abolished the A-activity, which was restored by N-acetylation. It did not abolish the reactivity of A substance to anti-A+B agglutinin of group O serum or of plant seed, nor it affected the O (H) -activity. The slow eluted fractions (Fr. 31- 34), acting on A substance, destroyed its A-activity and reactivity to anti-A+B agglutinin, and enhanced O (H) -activity. In this case, the lost A-activity of the ènzyme treated substance did not restore by N-acetylation.
2. Antiserum, prepared by immnizing the rabbit or chicken with Fr. 4-treated A substance, contained an antibody which reacted with Fr. 4 -treated blood group A red cells but not with untreated blood group A or B red cells and blood group substances, and which was specifically inhibited by D-galactosarnine. When incubated with Fr. 31-34 enzyme, the Fr. 4- treated A substance or red cells lost reactivity to this antiserum, while the O (H) -activity was enhanced.
3. Fr. 4 of A-decomposing enzyme did not liberate reducing sugar from A substance or blood group A red cells, whereas Fr. 31-34 of A-decomposing enzyme freed galactosamine (and a small amount of N-acetylgalactosainine) from them. These results show that Fr. 4 exerts N-deacetylase action on N-acetylgalactosaminoyl residue, which is determinant of the A specificity, and that Fr. 31-34 possesses the activity of galactosaminidase and/or partially of N-acetylgalactosaminidase as well as the activity of N-deacetylase.

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抗生剤.化学療法剤の進歩によって.細菌感染症の治療及び外科領域においては大きい変革がもたらされた。しかしこれらの薬剤の広汎な, 時には不必要な使用によって, 薬剤耐性菌が出現し, 細菌感染症の場合, 分離された細菌の薬剤耐性を知ることなしに抗生剤を使用することは困難な状況になっている。
グラム陽性菌の中ではブドウ球菌が多剤耐性菌の代表をなし, その伝染性, 定着性の高いことと相俟ってこれらの菌が病巣から分離される頻度は極めて高く, 病原性の低いグラム陰性桿菌と共に, 病巣由来菌の大きいパーセントを占めているのが現状である。
ブドウ球菌の薬剤耐性, そのファージ型については多くの報告がなされている。
本報においては, 著者が外科領域において病巣から分離したブドウ球菌を集め, ペニシリンG (PC) 耐性とペニシリナーゼ (PCase) の関係について研究した結果について報告する。

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ブドウ球菌の薬剤耐性の中, (CM.SM.SA.PC) 耐性の多いことは前報で述べた。クロラムフェニュール (CM) 耐性は必ずしも目立って多くない吾が国での病巣分離株の9%, 米国では12%, ヨーロッパでは20%という報告がある。
試験管内で上昇せしめたCM耐性の機構については多くの研究が発表されているが, 結論的なことはでていない。
今回病巣から分離されるCM耐性ブドウ球菌を集めて, その耐性機構を検討したのでその結果について報告する。

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全身エリテマトーデス (SLE) は, 1942年Klempererらによって膠原病 (CoUagen disease) の範疇にとりあげられて以来, 急激にその報告例数も増加してきた。しかし膠原病が重合する際, 常に一方はSLEであるという奇妙な事実などから, いまだその病因はもちろん, SLEの膠原病における位置づけさえも明確になされていない。さらに最近, ステロイドホルモンによる病変の修飾も問題となっており, SLEの病変はいっそう複雑化している。
最近われわれは, 臨床的ならびに病理解剖学的に典型的SLEと思われるものに, 強い血管 (動脈) 変化をみた一例を経験したので, 病理組織学的に検索し, その血管病変を中心に若干の考察を加えて, ここに報告する。

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1966年7月, 桐生市に於て温泉地に旅行した子供会の会員中に原因不明の集団下痢症が発生し, 各種調査の結果細菌によるものは否定され, ウイルス学的検査の結果, コクサツキーA9ウイルス (以下A9と略) が分離されたほか, 血清学的にも同ウィルス感染を裏付ける結果を得た。従来A9がこのような疾患を起すことは極めて稀れであるとされていたが, 国立予防衛生研究所の調査によれば, たまたま同時期に東京都に於ても同様なA9による集団下痢症が2件発生しており, 今後詳細な検討をする必要があると思われるので概要を報告する。

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