Okayama University Medical School

Caryophyllaeidae Claus, 1879 1. Glaridacris limnodrili Yamaguti, 1934 Bothriocephalidae Blanchard, 1849 2. Bothriocephalus fluviatilis n. sp. 3. B. lateolabracis n. sp. 4. B. branchiostegi n. sp. 5. B. acheilognathi Yamaguti, 1934 6. B. brotulae n. sp. 7. B. apogonis n. sp. 8. Oncodiscus sauridae Yamaguti, 1934 9. Glossobothrium nipponicum n. g., n. sp. Amphicotylidae Ariola, 1899 10. Amphicotyle quinquarii n. sp. 11. Eubothrioides lamellatus n. g., n. sp. Phyllobothriidae Braun, 1900 12. Phyllobothrium triacis n. sp. 13. P. filiforme n. sp. 14. P. serratum n. sp. 15. P. laciniatum (Linton, 1889) 16. P. loculatum n. sp. 17. P. squali n. sp. 18. P. lactuca van Beneden, 1850 19. Anthobothrium rajae n. sp. 20. A. pteroplateae n. sp. 21. A. bifidum n. sp. 22. A. parvum Stossich, 1895 23. Orygmatobothrium musteli (van Beneden, 1850) 24. O. versatile Die3ing, 1854 25. Monorygma megacotyla n. sp. 26. Pithophorus vulpeculae n. sp. 27. Echeneibothrium bifidum n. sp. 28. E. tobijei Yamaguti, 1934 29. Marsupiobothrium alopias n. g ., n. sp. 30. Dinobothrium spinulosum n. sp. 31. Gastrolecithus planus (Linton, 1922) n. g. Onchobothriidae Braun, 1900 32. Acanthobothrium triads n. sp. 33. A. micracantha n. sp. 34. A. latum n. sp. 35. A. gracile n. sp. 36. A. dasybati Yamaguti, 1934 37. A. ijimai Yoshida, 1917 38. A. grandiceps n. sp. 39. Calliobothrium verticillatum (Rud., 1819) van Bened., 1850 40. Platybothrium auriculatum n. sp. 41. P. musteli n. sp. Aberrant Tetraphyllidea 42. Pelichnibothrium speciosum Montic., 1889 43. Discobothrium japonicum Yamaguti, 1934 Tentaculariidae Poche, 1926 44. Nyelinia manazo n. sp. 45. N. sphyrnae n. sp. Floricipitidae Dollfus, 1929 46. Floriceps uncinatus (Linton, 1924) Tetrarhynchidean larvae 47. Pintneriella musculicola Yamaguti. 1934 48. Microbothriorhynchus coelorhynchi n. g., n. sp. 49. Oncomegas wageneri (Linton, 1890) 50. Pterobothrium chaeturichthydis n. sp. 51. P. hira n. sp. 52. Callotetrarhynchus speciosus (Linton, 1897) 53. Symbothriorhynchus uranoscopi n. g., n. sp. 54. Nybelinia anguillae n. sp. 55. N. nipponica n. sp. 56. Otobothrium dipsacum Linton, 1897

1) I designed a new micro-method for complement fixation test by means of a capillary pipette. 2) By this method, the complement-fixing antibodies in an individual mouse could be tested without taking its life. 3} The complement fixation titers in mice immunized with Japanese B encephalitis had a considerable individuality. 4) An adjuvant containing anhydrous lanoline and paraffin-oil, when mixed with Japanese B encephalitis vaccine, was effective to potent complement-fixing antibody productions in mice to this antigen.

1. In normal adults and in patients of non-hepatic diseases a transient hyperbilirubinemia occurs after peroral administration of hemolysed blood. 2. In cases of severe anchylostomiasis the serum bilirubin displays a remarkable decrease, and on imposition of hemolysed blood, no hyperbilirubinemia occurs but a relative one may be seen. 3. In patients with highly impaired functions of the parenchymal cells of the liver, neither absolute nor relative hyperbilirubinemia occurs on similar imposition of hemolysed blood. 4. Imposed blood or hemoglobin seems primarily to be phagocytosed by the reticulo-endothelial system. 5. A similar transient hyperbilirubinemia is also seen in rabbits after peroral imposition of hemohsed blood. 6. When the functions of the reticulo-endothelial system are accelerated by administration of "Koha", even incases of nonimposition of blood a hyperbilirubinemia occurs, but when hemolysed blood is imposed an additional transient increase in the hyperbilirubinemia may be detected. 7. In cases of blockage of the reticulo- endothelial system, this degree in the occurrence of hyperbilirubinemia is somewhat lower. 8. In cases of impaired liver cells by carbon tetrachloride, this decline is especially remarkable, and only a tendency of occurence can be dected. Since it is very difficult to explain this fact only by the co-existing impairment in the reticulo-endothelial system, the decline in the functions of the parenchymal cells of the liver must be placed under consideration. 9. By absorption tests of the intestines and by serological procedures, it is apparent that the perorally administerred hemoglobin may be readily absorbed from the jejunum, under any of these conditions. 10. Consequently, as for the cause of the hyperbilirubinemia occurring after peroral administration of hemolysed blood, most naturaly the reticulo-endothelial system participates, but it is impossible to neglect the part payed by the parenchymal cells of the liver.

The following results were obtained through the experiments on the cytochrome c oxidase activities and the analysis of the glycolysis and high energy phosphorus compounds in the normal bacteria and those fast to penicillin, sulfathiazol, 2.4-dimethylthiazdl, and macramin. 1. In the normal bacteria, the cytochrome c oxidase activities, glycolysis and high energy phosphorylated cycles increase accordto the order of S.57 s-type<S.57 r-type<staphylococcus aureus F. D. A. strain <staphylococcus aureus Terazima strain. 2. In the bacteria fast to penicillin originated these normal bacterial strain, the cytochrome c oxidase activities, glycolysis and high energy phosphorylated cycles increase, especially glycolysis. 3. In the bacteria fast to sulfathiazol, there are shown the same results as in the case of penicillin. 4. In the bacteria fast to 2.4-dimethylthiazol, the cytochrome c oxidase activities decrease, glycolysis increases markedly and high energy phosphorylated cycle decreases. 5. In the bacteria fast to macramin, these activities and cycles show no specific changes.

1. When hemolysed blood is administered orally to rabbits, in cases of healthy and those with blocked reticulo-endothelial systems, a transient increase in the verdohemoglobin (M. Engel) is seen in circulating blood, while in that of rabbits with impaired parenchymal liver cells, no such increase occurs. 2. On irrigation of hemolysed blood through rabbit livers, in healthy rabbits production of indirect bilirubin may be demonstrated while in that with blockage of the reticulo-endothelial system or with impaired liver parenchymal cells, this may not be seen. Moreover, in this case of blockade of the reticulo-endothelial system. production of verdohemoglobin may be demonstrated. while none whatsoever may be demonstrated in cases of impaired liver parenchmal. On the other hand on irrigation of verdohemoglobin and biliverdin solutions, in healthy and in impaired liver parenchymal cell cases, production of bilirubin may be observed while absolutely none was detected in cases of blocked reticulo-endothelial systems, 3. Concluding from the results stated above and those of clinical experiments stated elsewhere, the following process is assumed: when blood is imposed on the organism it is primarily phagocytosed by the reticulo-endothelial system, next dissolved to verdohemoglobin {M. Engel) in the parenchymal cells of the liver, and then dissolved into globin, iron, and biliverdin in the reticulo-endothelial system, of which biliverdin is further reduced to bilirubin. A portion of this remains in the circulating blood as indirect bilirubin, while the majority of it is esterized in the parenchymal cells of the liver, and proceeds to the bile ducts as direct bilirubin.

While I was on duty with the Naval Institute of Tropical Hygiene at Macassar, Celebes, during World War Ⅱ, I had the opportunity to examine various wild and domestic animals for parasites, these animals being taken mainly from Celebes. Since the parasitic worms of this island had not yet been worked out at any length, an opportunity for collecting in this part of the world yielded much interesting material. I collected a fairly large amount of material from monkeys, buffaloes, birds, lizards, snakes and fishes, the latter being examined very carefully from the stand-point of prevention of parasitic infections transmitted from fish to man. Domestic fowl and small wild birds were also examined for intestinal parasites during my study on avian malaria carried out at the institute. Unfortunately I managed to bring back to Japan by air only a part of the collection before the termination of the war. The greater part of the collection shipped to me subsequently by air mail suffered serious damage in transit, and for this reason description and illustrations are based almost exclusively on mounted slides.

1. The proteolytic action of papayotin is activated by X-ray irradiation with 60 r and 1000 r, and inhibited with 200 r and 400 r. 2. The influences of X-rays upon papayotin are direct and remain unchanged for definite periods of time. 3. The proteolytic action of papayotin show wavy phenomena which correspond to the time and dose of the X-ray irradiation. 4. The proteolytic action of papayotin is considered to be inhibited by the decomposition products (polypeptides) of substrate only in the presence of some other factors.

The cause of the death due to the atomic-bomb radiation is yet unknown definitely and the same can be said of shock brought about by the atomic-bomb. It cannot be said with certainity that infection of pathogenic bacteria concerns in the mortality, for even minor injuries did not often escape bacterial invasion from any part of the whole body. In this case the progress was same to a symptom of agranulocytosis, namely collapse, chill, fever, red throat or ulcerative stomatitis and from the reason of the heavily infected tonsils, although cultures were not made, there are reasons to consider it as agranulocytosis angina. The interpretation of the histologic changes observed in this patient, is rendered difficult not only by the factor of infection, but by the possible influence of one damaged organ upon another. From the histological changes there were the destruction of the epithelium of the gastro-intestinal organs, the atrophy of the testis and the necrosis of the tonsils, but the most noteworthy was the changes in the bone-marrow. The hyperplasia of the reticulum cells, the disappearance of the hematopoetic foci, and the great quantity of mitotic figures in the myeloid cells observecl in this case are found in many of the atomic-bomb victims died approximately one month after the exposure. This is a case of the death caused by aplastic anemia with infective complication or in orther words symptomatic agranulocytosis caused by the atomic-bomb radiation with sepsis.

1. In the bile of rabbits, the metabolisms of biliverdin and bilirubin are in a solucible state, and which have a ratio of 2: 1 in normal animals. 2. In the production of biliverdin, the liver, especially the parenchyma of the liver has a very important role, while that of the reticulo-endothelial system is rather minor. However, in the case of glucose administration, the reduction of bilirubin from biliverdin is performed in the reticulo-endothelial system, thus conferring an important part of this system. 3. The production of bilirubin is performed primarily extrahepatically, and the participation of the extrahepatical reticuloendothelial system is of a conservative nature, thus denying us any willingness to agree to the theory of bilirubin production in the reticulo-endothelial system. 4. On administration of hemolysed blood, bile pigments in bile demonstrate a remarkable increase, while as compared when injected into the auricle veins in cases of administration through the portal vein a decline in the functions of the liver reticulo-endothelial system is seen, causing a decrease in biliverdin amount. In the former modus of administration, an occasional stimulation of the liver reticulo- endothelial system is seen, causing reduction of biliverdin to bilirubin. 5. Concluding from these facts, biliverdin in rabbit bile occupies the role of an intermediate product in the production and metabolism of bilirubin.

It has long been a clinically and experimentally well recognized fact that the hearing organs of man and animal would be impaired by the excessive sound stimuli. It has also been pointed out that the hearing organ of each man is not always impaired in the same degree by the same noise, and their impairments show the individual variation in a considerable range. It is indeed not too difficult to imagine, that, under the same acoustic condition, such individual variation of the acoustic impairment owes to the inherent disposition of each man. But at the same time, this individual variation may more or less owe to the patency of the ear tube; the normal tube having a physiological function to control the unnecessary acoustic stimuli, and on the contrary, the stenosed tube being devoid of this function, induces more impairment of the hearing organ. This latter suggestion, which occured to the author, led him to attempt the following experiment.

Bucephalidae Poche, 1907 1. Prosorhynchus longicollis n. sp. 2. Rhipidocotyle khalili Nagaty, 1937 Allocreadiidae Stossich, 1904 3. Helicometra epinepheli Yamaguti, 1934 4. Opeehona scombri Yamaguti, 1938 5. Pseudopecoeloides tenuis Yamaguti, 1940 Schistorchiidae Yamaguti, 1942 6. Schistorchis sigani Yamaguti, 1942 7. Apocreadium synagris n. sp. Fellodistomidae Nicoll. 1913 8. Symmetrovesicula ehaetodontis Yamaguti, 1938 Monorchiidae Odhner, 1911 9. Lasiotocus lethrini n. sp. Heterophyidae Odhner, 1911 10. Paracryptogonimus aeanthostomus Yamaguti, 1934 Gyliauchenidae Ozaki, 1933 11. Gyliauchen nahaensis Ozaki, 1937 12. Gyliauehen papillatus (Goto et Matsudaira, 1918) Hemiuridae Luhe, 1901 13. Parahemiurus clupeae n. sp. 14. Aphanurus harengulae Yamaguti, 1938 15. Aphanurus dorosomatis n. sp. 16. Aponurus laguncula Looss, 1907 17. Aponurus synagris n. sp. 18. Lecithochirium priacanthi n. sp. 19. Lecithochirium longicaudatum n. sp. 20. Lecithocladium parviovum n. sp. 21. Lecithocladium megalaspis n. sp. 22. Lecithocladium angustiovum n. sp. 23. Lecithocladium scombri n. sp. 24. Tubulovesicula angusticauda (Nicoli, 1915) 25. Magnacetabulum leiognathi n. sp. 26. Hysterolecitha nahaensis Yamaguti, 1942 27. Hysterolecithoides epinepheli Yamaguti, 1934 28. Lecithaster stellatus Looss, 1907 Angiodictyidae Looss, 1902 29. Hexangium sigani Goto et Ozaki, 1929 Didymozoidae Poche, 1907 30. Didymozoon spirale Yamaguti, 1938 31. Didymozoon brevicolle Yamaguti, 1938 32. Unitubulotestis carangis n. g., n. sp.

I. Dactylogyridae Bychowsky, 1933 1. Ancyrocephalus macrogaster n. sp. 2. Ancyrocephalus bilobatus n. sp. 3. Ancyrocephalus spinicirrus n. sp. 4. Ancyrocephalus platycephali n. sp. 5. Haliotrema alatum Yamaguti, 1942 6. Haliotrema lutiani n. sp. 7. Haliotrema caesionis n. sp. 8. Haliotrema upenei n. sp. 9. Metahaliotrema scatophagi n. g., n. sp. 10. Metahaliotrema arii n. sp. 11. Pseudohaliotrema (Pseudohaliotrema) sphincteroporus n. g., n. sp. 12. Pseudohaliotrema (Pseudohaliotrema) sigani n. sp. 13. Pseudohaliotrema (Pseudohaliotrematoides) fusiforme n. subg., n. sp. 14. Hamatopeduncularia arii n. g., n. sp. 15. Diplectanum serrani n. sp. 16. Pseudolamellodiscus sphyraenae n. g., n. sp. 17. Lamellodiscus flexuosus n. sp. 18. Lamellodiscus convolutus n. sp. 19. Lamellodiscus difficilis n. sp. 20. Lamellodiscus duplicostatus n. sp. 21. Diplectanocotyla gracilis n. g., n. sp. II. Capsalidae Baird, 1853 22. Benedenia synagris n. sp. III. Mazocraeidae Price, 1936 23. Kuhnia scombri (Kuhn, 1829) Sproston, 1945 24. Kuhnia otolithis n. sp. IV. Discocotylidae Price, 1936 25. Allodiscocotyla chorinemi n. g., n. sp. 26. Vallisia chorinemi n. sp. 27. Protomicrocotyle celebesensis n. sp. V. Microcotylidae Taschenberg, 1879 28. Metamicrocotyla bora n. g., n. sp. 29. Metamicrocotyla filiformis n. sp. 30. Heteromicrocotyla carangis n. g., n. sp. 31. Gotocotyla mesercei n. sp.

Das oben erwahnte Verfahren hat vor den anderen Methoden besonders die Vorzuge, 1) daβ man dadurch zu einem sicheren Resultat gelangen und gleichzeitig auch jedes Datum mit exakten Ziffern zum Ausdruck bringen kann, 2) daβ bei diesem Verfahren keineswegs erforderlich ist, eine bestimmte Anzahl von Keimen einschlieβende Bakterienaufschwemmung herzusteHen und auch Kontrollversuch anzustellen, 3) daβ es von den Fehlern des Mischverhaltnisses zwischen der Bakterienlosung und dem Blut nicht so erheblich beeinfluβt wird, und 4) daβ man durch dieses Verfahren gleichzeitig mehrere bakterientotende Faktoren untersuchen kann. Ferner hat dieses Verfahren auch den Vorzug, daβ es praktisch sehr einfach auszufuhren ist und nur 6 Stunden nach der Blutentnahme bereits das Ergebnis liefert. Es gestattet ferner, die bakterizide Kraft des Blutes gleichzeitig bei 6 - 8 Menschen zu untersuchen, was mich zur Uberzeugung fuhrt, daβ es in der Klinik hochgeschatzt werden wird. Auch das Verfahren und die ebenfalls vom mir aufgestellte Formel zur zusammenfassenden Beurteilung kann man nach meinem Erachten durch entsprechende Veranderungen einiger Faktoren ohne jede Schwierigkeiten auch fur andere Bakterienarten anwenden. Man wird wohl gegen eine einzige Lucke dieses Verfahrens, daβ die mikroskopische Untersuchung und die Berechnung allzu verwickelt zu sein scheint, Einwand erheben, eine Lucke, zu deren Schluβ jedoch nur eine kurzfristige Ubung erfordert wird, durch welche die mikroskopische Untersuchung innerhalb 30 Minuten, die Berechnung nur in 5 Minuten vollendet werden kann. (Zur Berechnung bedarf es einer Gauss'schen Logarithmentafel.) Obgleich das geschilderte Verfahren noch viele, genauere Prufungen erheischende Punkte in sich einschlieβt, muβ es hier, wenn auch in Grundzugen, jetzt schon angefuhrt werden,. da ich der festen Uberzeugung bin, daβ es im Vergleich zu den bisherigen Methoden ein dem wirklichen Wert der Bakterizidie des Vollblutes im lebenden Organismus viel naheres Resultat liefert.

I. Trematodes of reptiles 1. Cyathocotyle crocodili n. sp. 2. Pseudoneodiplostomum (Pseudoneodiplostomoides) crocodili n. subg. n. sp. 3. Acanthostomum crocodili n. sp. II. Trematodes of birds 4. Plagiorchis maculosus (Rud., 1ε02) 5. Echinochasmus bagulai Verma, 1935

In 1951 the junior author reported two unnamed species of the genus Aedes from Mt. Hakusan, Ishikawa Prefecture, suggesting the first species to be related to Aedes (Ochlerotatus) punctor. An examination made by the senior author on large numbers of additional specimens collected at the same locality in 1952 and 1953 has revealed that each of the two represents a new species, so that Aedes (Ochlerotatus) hakusanensis is proposed for the first species, and Aedes (Aedes) pseudoesoensis for the second species.

Anoplocephalidae Kholodk., 1902 1. Oochoristica celebesensis n. sp. Dilepididae Fuhrmann, 1907 2. Ophiovalipora micracantha n. sp. Proteocephalidae La Rue, 1911 3. Acanthotaenia shipleyi von Linstow, 1903

Lecithodendriidae Odhner, 1910 1. Phaneropsolus simiae n. sp. Heterophyidae Odhner, 1914 2. Galactosomum canis n. sp. Paramphistomidae Fischoeder, 1901 3. Explanatum explanatum (Creplin, 1857) 4. Paramphistomum cervi (Schrank, 1790) 5. Calicophoron cauliorchis (Stiles et Goldberger, 1900) 6. Ceylonocotyle εcoliocoelium (Fischoeder, 1901) 7. Fischoederius elongatus (Poirier, 1883) Fasciolidae Railliet, 1895 8. Fasciola hepatica Linne, 1758

In such animals not having any organic changes in their brains during the initial stage showed a descendence of convulsive threshold. abnormal findings in their electroencephalogram and ascending activity of ChE. But what is the cause of these functional changes? First, from the fact that though there was no organic changes, they were sensitized and reiniected by a known antigen, which is obviously an antigen-antibody reaction. Second, from the fact that we got a histological.change, which was acknowledged as C.L.A. changes by increasing the concentration of these solution and the number of injections, it could be thought that these functional changes were caused by what I called latent C.L.A.. That is, it seems it could be thought that it would give functionally a permanent hypersensitivity, which is called convulsive arrangement. Furthermore, a similar histological findings as seen in old epileptics were made experimentally after prolonged and repeated injections of very diluted antigens. I believe it can be said, also from this histological point that they are experimental epileptics. But I am not trying to say that idiopathic epilepsy is the same allergic disease as asthma. If it was so, it should offer clinically a problem of eosinophilia in the blood of epileptics. But actually there is no eosinophilia in epileptics. Also, in adult epileptics, convulsive attacks is not often seen soon after introduction of antigens. Consequently, my theory that epilepsy is allergic, does not mean that allergy is the direct cause of epileptic attacks. What I mean is, the causal genesis of idiopathic epilepsy is hypersensitivity of nerve cells in the brain. This hypersensitivity was attained as a tissue reaction by some allergic mechanism without any organic changes. This functional change gives the nerve cell a hypersensitive state, which becomes the base of the beginnihg of convulsion. Its inducement of attack could be water stagnation in the body, anemic state of the brain, alkalosis, or introduction of allergens. In short, the cause of attack does not always come from allergic reactions.