動物の組織には広く亜鉛が存在し, その代謝に関して多くの研究がなされている。また癌組織と亜鉛との関係についてもいくつかの研究がある。しかしながらin vitroにおけるEhrlich腹水癌細胞の亜鉛代謝の実験は少く, われわれの研究以外には, Palら, 黒田らの報告が見られるにすぎない。
さきに著者は, in vitroにおけるEhrlich腹水癌細胞のZn65摂取について実験を行い, 特に代謝阻害剤, アミノ酸, 抗癌剤および金属イオンの影響について報告した。
今回はさらにこの実験を補足し, incubateする場合の温度, mediumのpHやcarfier, キレート剤および金属イオン添加などの影響について, 実験を行ったので, その結果を報告する。

抄録全体を表示

Antisera were prepared by injecting Salmonella F⁺ and Escherichia coli F⁺ respectively into rabbits, and absorbed with F^-, having the same phenotype with F⁺, to obtain anti-f⁺ sera, which react with F' strain and Hfr strain. And in this way immunochemical properties of f+ antigens in F' and Hfr strains of Salmonella and Escherichia coli were investigated.
1. Anti-S. f⁺ antibody reacted with both Escherichia coli Hfr and Salmonella F', but after absorption with the former, remained an antibody which reacted only with latter.
Anti-E. coli f⁺ antibody reacted with both Salmonella F' and Escherichia coli Hfr, but after absorption with the former, remained an antibody which reacted only with the latter. It is therefore considered that f⁺ antigens of Salmonella and Escherichia coli contain a common antigen as well as specific antigens, respectively.
2. Bacterial suspensions of Salmonella F' and Escherichia coli Hfr, after treatment with a blendor or a sonicator, were each cetrifuged at 10, 000 r. p. m. and the supernatants were further subjected to ultracentrifugation at 38, 000 r. p. m. The sediments were found to have the highest activity of f+ antigen. This fraction contained about 2% sugar. The f⁺ antigens found in the living bacterial cells and the ultracetrifuged fraction lost the antigenicity either on heating at 100°C for 60 minutes or on treatment with proteinase such as trypsin, ficin and bromelin. It is subsequently assumed that f⁺ antigen may have chiefly properties of protein.

抄録全体を表示

Experimental typhoid was produced with Salmonella enteritidis in mice, immunized with the killed vaccine, and the histological picture was investigated chiefly with relation to the killed cells. Besides chrome-alum vaccine, azo-labelled killed vaccine were used to trace their fates easily.
Injection of chrome-alum vaccine started diffusive swelling and proliferation of Kupffer's stellate cells and formation of epithelioid cells, which subsequently bacame focal to produce the so-called killed veccine nodules. These nodules displayed proliferation of reticulin fibers and severe accumulation of fatty droplets, and were conspicuously different in morphology from living vaccine nodules (typhoma).
In the group, given the azo-labelled killed cells, only stellate cells contained them immediately after the injection, but by and by they aggregated together with epithelioid cells to form nodules. These nodules were morphologically same with those in the chiome-alum vaccine group. Cellular reaction and appearance of the bacterial cells in the Glisson's capsule was far delayed compared with those in the sinusoid. It is therefore considered that the killed vaccine nodules will be formed by stellate cell derived from epithelioid cells, in which the discharge and ingestion of the killedd cells will be repeated.

抄録全体を表示

In 31 cases of cerebral infarction (24 cases of the infarction of the thalamus and the basal ganglia and 7 cases of that of the cerebral cortex), the cerebral arteries, especially those supplying the infarcts were investigated histologically in order to elucidate arterial lesions which are considered to be the cause of the infarction. Further, morphogenesis of these arterial lesions were discussed.
1) Out of 84 infarcts in the thalamus and the basal ganglia, 62 (74%) were resulted from stenosed cerebral arteries owing to arteriosclerosis and 22 (26%) were derived from thrombosis at the site of angionecrosis (fibrinoid degeneration of cerebral arteries), or from the so-called “nodular lesions of the arteries”.On the other hand, 5 of 8 infarcts in the cerebral cortex were resulted from occlusion by thrombi which were formed on atherosclerotic plaques of meningeal arteries, and the remaining 3 (38%) were caused by arteriosclerotic stenosis without thrombosis.
2) Cerebral arteriosclerosis (atherosclerosis, intimal lipoidosis and intimal fibrosis) in arteries with diameters of above 150μ were resulted from insudation of plasma protein and lipid into cellulofibrous intimal thickening at the bifurcation (bifurcation-pad). In smaller arteries with diameters of below 150μ, arteriosclerosis was started by insudation of plasma into the intima without predilection either for the bifurcation or for other. That is the development of arteriosis, which was followed by the secondary prolifelation of subendothelial cells and became to be arteriosclerosis.
3) Atherosclerosis of the cerebral arteries were classified into two types, α and β. In the former, the atheroma was formed as the result of destruction of increased intimal collagenous fibers showing fatty swelling, while in the latter it was resulted from necrosis and destruction of aggregated intimal form cells. The β type atherosclerosis was predominant in the cerebral arteries.
4) Pseudocalcification in the wall, especially in the media of the arteries running through the globus pallidus, induced or enhanced intimal lesions (intimal edema, intimal fibrosis and atherosclerosis), and was the common cause of the infarction of the globus pallidus.
5) Angionecrosis of the cerebral arteries, which is the cause of hypertensive intracerebral hemorrhage, was seen in the 91. 7% of the cases of infarction of the thalamus and of the basal ganglia. There was multiple occurrence of this lesion in the lenticulostriate arteries and the thalamic arteries.
6) The angionecrosis was commonly found in the intracerebral arteriosclerotic arteries about 150μ in diameter, and when the change was severe, the arteries exhibited aneurysmal dilatation with hemorrhage into the arterial walls. This suggests that in the course of cerebral infarction, cerebral hemorrhage is apt to be induced.
7) The so-called k nodular lesions of the arteries were produced when the thrombi formed on the angionecrotic walls were organized together with fibrinoid substance in the arterial walls.
8) Multiple occurrence of angionecrosis was seen not only in cerebral infarction cases with hypertension but also in those without hypertension (27%). Because arterial lumina were stenosed by arteriosclerotic changes at many bifurcations on the proximal side of the angionecrotic arteries, it is considered that not only hypertension but also hypoxidosis resulting from decreased blood flow would participate in the morphogenesis of the angionecrosis in cerebral infarction.

抄録全体を表示