In order to investigate the actions of ovarian hormones in initiating the induction of mammary cancer by 7,12-Dimethylbenz(a)anthracene,85 young adult female JCLSprague-Dawley rats were divided to 3 main experimental groups: non-operated control group, ovariectomized control group and the groups administered with exogeneous ovarian hormones immediately after the ovariectomy. Daily examinations on the vaginal smears of all experimental rats were done aroun 9.00am frcm the age of 45 days, when their vaginas opened already, to the time of autopsy. Ovariectomy was performed around the age of 48-50 days. In the 1st experiment, the ovariectomized, hormone-injected groups were received by daily subcutaneous injections of oily solution of Estradio1-17p (E)0.4μg, E 20 fig, Progesterone (P) 4 mg, E 0.4μg + P 4 mg, and E 20μg + P 4 mg, respectively, from the age of 52 days to 70 days. All ovariectomized rats of the 1st experiment were injected daily by E 0.4μg P 4 rug from the age of 71 days to the time of autopsy. In the 2nd experiment, the ovariectomized rats started to be treated every 6 days with the implantation of pellet of cholesterol, E 1μg, P 4 mg, and E 1μg P 4mg, respectively, on the age of 48 days, and they exchanged on the age of 72days and continued through the experiment to be implanted weekly by the pellet of E 1μg + P 4 mg. All experimental animals were injected intravenously by 3 nag of 7,12-DMBA twice around the age of 60 days, and they were sacrificed to observe the induction of mammary tumors 3 months after the 1st intravenous injection. On this carcinogenesis, a half month after the administration of carcinogen might be speculated to be the initiation stage, and the following process would be the growthpromotion stage. Biopsy on thesmammary tissue was performed on the time of carcinogenadministration and of sacrifice. Morphological appearances of the glands and tumors were observed histochemically and electron-microscopically.
The non-operated controls of both experiments showed a regular sex cycle throughout the experiment. All ovariectomized control and progesterone-treated rats did never reveal an estrous stage, but the estrogen-treated rats did a continious estrus. E and Pinjected rats showed no estrous stages, but E and P-implanted rats did estrous cycles of 6-7 days throughout the experiment. The vaginal smears and the autopsy findings might suggest that the E and P-implantation in the promotion stage did compensate more to ovariectomy than the E and P-injection. The morphologic findings on the mammary tissue were different from each other groups, reflecting the hormonal conditions of each groups. All induced mammary tumors revealed moderately anaplastic pictures of adenocarcinoma, and no any histologic patterns were paticular to the each groups. The induction rate of mammary cancer was as follows: non-operated controls 80%, ovariectomized controls 0%, ovariectomized and estrogen-treated groups; 0.4μg. -injected 0%,1pg-implanted 30%,20μg-injected 17%, ovariectomized and progesterone-tr eated groups; 4mg-injected 38%,4mg-implanted 10%, and ovariectomized and E and P-treated groups; E 0.4μg +P 4. mg-injected 38%, E 1pg + P 4 mg-implanted 22%, E 20μg P 4 mg-injected 0%. In summary, D MBA-carcinogenesis on the mammary ducts in 3 months after the carcinogenadministration were suppressed completely by ovariectomy, provocated by moderate stimuli of estrogen or progesterone sole at the initiation stage, and inhibited by strong stimuli of estrogen during the initiation process. The role of exogeneous ovarian hormones in initiating the induction of mammary cancer on the ovariectomized and DMBA-injected animals were discussed.

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The present investigation was undertaken to demonstrate the distribution of fluorescein sodium in the choroid and retina after the dye was given intravenously. It has been thought that it is difficult to ascertain the exact location of the dye in histologic sections on account of the diffusion properties of apueous fluorescein. I could clearly demonstrate the distribution of the dye in the choroid and retina.
Under Nembutal anesthesia, rhesus monkeyes and albino rabittes weighing 2 kg were given intravenously 0.5m1 of 5 % fluorescein sodium. Also pigmented rabbittes after the photocoagulation were examined. The bulbus was removed 8,9,10,30 seconds and 2,4,10,20 and 60 minutes after the dye injection.10μ thick frozen-dried sections were made and examined with fluorescence microscope.
The results obtained are as follows: The blood vessels, large or small, of retina and optic disc are impermeable to fluorescein. Although fluorescein diffuses rapidly throughout the choroid, none passes the pigment epithelium to enter the retina. In contrast, at the posterior scleral foramen some fluorescein enters the optic disc by diffusion from neighbouring choroid. At the optic disc retina is protected from fluorescein by the intermediary tissue of Kuhnt. In the optic nerve fluorescein diffuses from the vessels to connective septa, but never enters the nerve fivers. After the photocoagulation the dye diffuses to retina.

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It is needless to say that chemotherapy is playing a very important role in the treatment of tumor. However, at present we must admit that no ideal drug specifically killing tumor cells without ill effects on normal cells is available. We therefore must devise some method to make present anti-tumor drugs manifest their effect maximally. Side effects, the sensitivity of tumor cells to the drugs and lack of penetration of drugs into tumor masses and cells are given as factors preventing presently available antitumor drugs from manifesting their maximum effect. Mentioning only the last factor, the route of administration of anti-tumor drugs is very important; for example, injection directly into the blood vessels controling the tumor. Tumor bearing hosts are generaly characterized by a tendency toward coagulability and reduced tendency toward fibrinolytic activity. Fibrin deposition and thrombus formation are apt to occur in tumor masses in relation to these host change s and a barrier is made by fibrin deposition around tumor masses. For such reasons, the anti-tumor drugs in use are thought to be prevented from penetrating tumor masses. Accordingly the skilful manipulation of fibrinolytic phenomena and anticoagulants may be regarded as promising measures. It is desirable to activate fibrinolytic ability as well as to suppress hypercoagulability so that antitumor drugs may penetrate tumor masses easily. We examined the ability of fibrinolytic enzyme to potentiate penetration of anti-tumor drugs into tumor masses. Two interesting findings are presented below: 1) The fibrinolytic enzyme was able to potentiate penetration of the anti-tumor drugs into tumor masses.2) The incorporation of 125I-fibrinogen into tumor masses was greater than in healthy tissues and this could be reduced by fibrinolytic enzyme.

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In part 1, We demonstrated that fibrinolytic enzyme promoted penetration of an antitumor agent into tumors by changing the fibrin barrier of a tumor mass. Next meas ures are needed to faciliate the penetration of the anti-tumor drugs into individua l tumor cells. Reliable manifestation of their anti-tumor effect in cells should be arran ged. In this respect Kimura, Niitani and others at the National Cancer Center pr oposed a very reasonable method using lysosome labilizers. We also carried out FAMT therapy us i ng urokinase in cases of relapsed, metastasized or advanced tumor with excellent results in several cases, and recognized the effectiveness of chemotherapy combined with lysosome labilizers. Accordingly, in part 2, We examined the abilit y of fibrinolytic enzyme to potentiate penetration of anti-tumor drugs into tumor cells. The results are as follows:
1) The fibrinolytic enzyme p romoted the release of hydrolytic enzymes (Acid phosphatase and β-glucuronidase) into the surrounding medium from lysosomes in tumo r cells. The fibrinolytic enzyme also may produce changes in permeability of the cell membrane.
2) Under fluorescent microscopy using acridine orange in Yoshida sarcoma cells, lysosomes began to appear in cells about 30 minutes after urokinase administrati on, increased in size and number an hour later and began to decrease 3 hours later, when intracellular particles stained with orange were still found in cells. Then cha n ges in acid-phosphatase and β-glucuronidase activity were pursued in Yoshida s a rcoma cells by histochemical techniques after urokinase administration. In view of the above results urokinase is regarded as a lysosome labilizer and one of the promisin g agents potentiating the effect of anti-tumor drugs in tumor cells.
3) The incorporation of³H-5Fu into DNA and RNA of Yos hida sarcoma cells was potentiated by the fibrinolytic enzyme.

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Characteristics of the Wiener filter technique proposed by D.O Walter are investigated with the aid of a simple numerical simulation. The discussion is focussed upon the difference between the Wiener filtering and the conventional averaging and upon the applicability of these methods to estimations of average evoked potentials. It is explained that, in contrast to the conventional averaging, the Wiener filtering can effectively remove periodic components of the noise; even when their amplitudes are large if their frequency components are in random phases among samples. Furthermore, it is pointed out that, in order to obtain qualitative l y reasonable average evoked potentials for a single stimulus, aperiodic presentation of stimuli is effective in reducing possible interferences with background activities, such as the prominent alpha. Finally, several remarks on evoked potential measurements are presented.

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Plasma ADH levels were studied in 19 patients with liver cirrhosis,2 patients with chronic hepatitis and 5 patients with malignant liver tumors after fluid deprivation for 13 hours. Liver functions, serum and urinary osmolality, circulating blood volume and serum electrolytes were studied simultaneously. ADH was extracted from plasma by Yoshida 's method and bioassay was carried out using experimental diabetes insipidus rats according to Yamane and Kunishige's method.
Results obtained were as follows:
1) Plasma ADH levels were slight ly elevated in about 24% of patients with liver diseases. But no correlation was found between plasma ADH level and the degree of ascites.
2) There were no statistically significant correlations between plasma ADH level and liver functions, serum protein fractions, serum and urinary osmolality, TCH20serum sodium and circulating blood volume respectively.
3) In some cases plasma ADH levels in creased in order to maintain homeostasis after forced diuresis by diuretics or anti-aldosterone agents.
4) At least in one case SIADH was suspected. Thus ADH seems not to be a primary cause of fluid retention in liver diseases and therefore other factors causing sodium and water retention would appear important. But in some cases ADH will increase secondary to body fluid disarrangement, and in others some still unknown factors will be responsible for inappropriate secretion of ADH. The problem of osmoreceptor in liver still remains unsolved.

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Part I. Actions on the vas deferens preparation
1) Trimetazidine gave scarcely any influence on the tension of the vas deferens preparation, when the drug was given to it independently.
2) Noradrenaline induced the contraction of the preparation and this contraction was potentiated by the pre-addition of trimetazidine.
3) When the tension of the preparat i on had been increased by the noradrenaline addition, the succeeding addition of trimetazidine could induce the contraction as if the more noradrenaline was added there.
4) The vas deferens response to noradrenaline reduced in the calcium-free Locke's solution when the preparation had been kept in this medium for a fairly long time.
5) In high calcium media, the potentiation of the noradrenaline contracti on by trimetazidine in the preparation was more remarkable than that seen in a Locke's solution, but the effect of trimetazidine was not so remarkable in low calcium media.
6) In high or low potassium media, this kind of effect of trimetazidine was as much as that seen in a Locke's solution.
7) In low sodium media, this effect of trimetazidine was much more remarkable than that seen in a Locke's solution, while it was scarcely seen in high sodium media. From these results, it was assumed that the potentiation of the noradren aline contraction by trimetazidine was caused by its action that can increase the available calcium ions released from the tissue, and that this action was manifested in low sodium or high calcium media while suppressed in high sodium media.
Part II. The actions on the small intestine preparation
1) Trimetazidine in high concentrations dec reased the smooth muscular tone and suppressed its spontaneous contractions.
2) Trimetazidine in high concentrations suppressed the actions of barium chloride, nicotine, acetylcholine, serotonin, and histamine on the smooth muscle tone of the small intestine. From these results, it was assumed that trimetazidine has the anti-nicotinic action, and that the drug can suppressed the spontaneous contraction of the smooth muscle in the small intestine through its action suppressing the permeability of calcium or barium ions in the muscle membrane, in a different manner from that seen in the smooth muscle of the vas deferens.

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無菌マウスと普通マウスの急性X線死に関する研究から松沢はその死因を造血系障害と腸壁障害に区別した.造血系障害死は両マウスとともに照射後1-12日前後に認められ,腸壁障害死は無菌マウスの場合7日前後に認められるという.普通マウスの腸上皮の寿命は2-3日である(QuasUer)に比べて,無菌マウスでは腺窩細胞が絨毛に移行する日時が普通マウスより長く(Sherman),且つ腸内感染のないことを考えれば,腸壁障害死が7日前後になつたことも理解される.無菌マウスによる松沢の実験成績をみると,照射後4日間は外見上の異常はほとんどなく,5日間を過ぎると運動減少し,下痢を始める,そしてシヨツク死するに至るという.著者はMethyhnethionine sulfonium chloride(以下,MMSCと略記する)をマウスに注射した場合,X線照射死に対して,防禦的効果を示すかどうかを検討したが,考慮すべき影響を有することを見出したので報告する.

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