The turnover of plasma urea was studied in goats fed rations with differentprotein contents by using "C- and "N-urea as tracers. The biological half-life time ofurea determined with "N-urea was always longer than that determined with "C-urea, reflecting the difference in the metabolic pathway between the urea hydrolysates, ammoniaand carbon dioxide. It was roughly estimated from the turnover studies that more thana half the quantity of urea synthesized might be transferred to the alimentary canal, including the rumen, where it underwent dissociation. With a decrease in the proteincontent of the ration, the percentage of transfer and dissociation increased. The "C-ureadischarged into the urine was less than 57% of the administered dose. It decreased to3.9% in goats fed rations with a low protein content.The rate of urea turnover determined with "N-urea was nearly consistent with the rateof urea discharge into the urine in goats fed higher protein rations. In goats fed lowerprotein rations, on the other hand, the rate of urea discharge decreased and its consistencywith the rate of turnover determined with "N-urea was upset. This was caused byassimilation of urea-nitrogen in rumen microorganisms, as was convinced by studying theincorporation of urea-"N into the fraction of rumen microorganisms. It was assumedthat in goats fed lower protein rations the bulk of urea synthesized might have enteredthe endogenous recycling system within the body and assimilated by rumen micro-organusms.

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Characteristic symptoms due to hemostatic disorders were produced in agroup of 3 calves fed approximately 2kg of bracken fronds per head per day. Fourclinical stages, subclinical, initial, hemorrhagic and serious, were classified according tosymptoms. The circulating anticoagulant test, plasma recalcification time, thrombin titra-tion test, protamine neutralization test, tissue thromboplastin neutralization test, andanti-plasma thromboplastin test were performed on blood samples collected in each stage.Edema or hyperemia in the conjunctiva preceded a fever and bleeding. The initialstage was accompanied by a tendency for platelets to decrease. The thrombin titrationtest and protamine neutralization test showed that blood heparin was concerned with theincreasing curve of the circulating anti-coagulant test both in the hemorrhagic and theserious stages. In these stages, the anti-thromboplastin activity of heparin and the anti-plasma thromboplastin activity were stimulated alike.

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Quantitative determination of the blood level of a heparin-like substancewas made using a group of three calves with experimentally-induced bracken poisoning.The average blood level of the heparin-like substance in eight normal calves was 3.2+0.95 jtg / mZ (mdhn -4- s.d.). The blond level 61 the hepaririLIikc substance exceeded 6.0 7tg /mZ in all the affected animals in the hemorrhagic stage. It did not increase in the initialstage, when the clotting time prolonged mildly. This was due to the effect of a decreasein the platelet count observed in this stage. It was very likely that the prolonged clottingtime in the hemorrhagic stage might have been caused by the synergistic etrect of anincrease in the blood level of the heparin-like substance and the stimulated sensitivity ofthe affected blood to the heparin-like substance as a result of the decrease in the plateletcount.

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The development and structure of the perianal gland were studied his-tologically in 74 dogs of age 0 day to 16 years. The gland was seen already in 14-day-oldpuppies of both sexes, and in dogs younger than 9 months old it opened to the hairfollicle through an excretory duct. The glandular tissues of adult dogs developed flourish-ingly around semi-closed duct-like structures which fused with each other forming a"tortoise-shell" lobules without connection to hair follicles. In electron microscopy, theglandular cells were divided into two types, light and dark cells, and the former typeof cells had well-developed vacuoles. No secretory granules were contained in both typesof cells. In larger lobules of adult male dogs, intralobular cysts developed occasionallyshowing sometimes a central necrosis. This might result from a rapid and successiveconversion of tubular cells to glandular cells. Some glandular tissues comparable to theperianal gland were detected also at the loin, the prepuce, the dorsal and ventral partsof the tail, and the groin. Administration of testosterone propionate to 60-day-old pup-pies induced a significant developmernt of the glandular tissues which became to havesize and structure comparable to those in adult dogs.

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A field survey on the drug resistance of chicken coccidia found in Japanesebroilers was performed by the chicken inoculation test with 30 fecal samples collectedfrom 29 prefectures in June, 1973. A strain was judged as a resistant one when it showedoocyst production with or without symptoms of coccidiosis in an experimental birdmedicated with twice as much as tlae recommended dose of a coccidiostat.As a result, 93% and 97% of the strains of Eimeria acervulina studied were foundresistant to clopidol and decoquinate, respectively. A considerable percentage of thestrains of E. tenella and E. necatrix studied were found resistant to amprolium, clopidol anddecoquinate. Only a small percentage of these strains was resistant to sulfadimethoxine.Moreover, multiple drug-resistant strains were found very commonly in E. tetzella, E.necatrix. E. maxintct and E. acervulina.Distribution of the resistant coccidia was variable over seven geographical districts inJapan.A large number of E. acervulina strains were found resistant to eight times the recom-mended dose of amprolium and/or decoquinate. Many strains of E. tenella and E. necatrixwere highly resistant to amprolium and decoquinate. Development of resistance to clopi-dol was variable among these species.

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A total of 69 fowls were examined to describe and illustrate the renal portaland venous systems. The kidney of the fowl receives venous blood from the V. iliacaexterna, V.ischiadica and V.iliaca interna. These three vessels anastomose with theV. portae renalis media et caudalis and form the renal venous circulation (Fig. 1). By wayof this circulation the kidney receives venous blood from the portal veins. The newnomenclature Circulus venosus renis is proposed.The V. portae renalis cranialis courses cranialward, giving branches to all the directionsin the Divisio renalis cranialis, and anastomoses with the vertebral vein or sinus at twopoints. In the Divisio renalis media the V. portae renalis media has large branches whichrun dorsolaterad. In the Divisio renalis caudalis, the V. portae renalis caudalis has brancheswhich run in all the directions.The ramifications of the V.intervertebra1is in the Divisio renalis media et caudalisanastomose with the V. vertebralis at several points. They contribute to the formation ofthe Circulus venosus renis.The lobules of the kidney are divided into two types, Japanese fan-shaped and fig-shapedlobules. In the former type, the V. intralobalis run parallel with the kidney surface inthe Lobulus corticalis, giving off the V. centralis at an interval. In the latter type, theV.centra1is is derived directly from the V.interloba1is or from the V. intralobalis andenters the lobulus from its basis.The directions of arterial and venous blood flows in the parezuchyma of the kidney aresummarized in the following table.

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Two cases of parasitic embolism of the cerebral arteries in the dog causedby Dirofilaria immitis were recorded by Olson (1970) and Patton and Garner (1970) inthe United States. No such cases had been reported in Japan where canine heart wormdisease is enzootic most prominently in the world. Recently, the authors had an oppor-tunity of examining three dogs with the cerebral arteries affected with D. immitis em-bolism, showing such sudden nervous signs as unstable gait, circling, tumble, roaring, visual disorders, disturbed swallowing, cloudiness of consciousness and coma. The resultsof pathological examination of these dogs are summarized as follows.l. In each dog, severe obstruction was established in the cerebral arteries by a singleworm of D. immitis. The parasite was so large and long in size that it filled the vesselalmost completely, extending from the left middle cerebral artery to the left posteriorcommunicating artery and the left posterior cerebral artery in dog No. 1, from the leftanterior cerebral artery to the left middle cerebral artery in dog No. 2, and from the leftposterior cerebral artery to the cerebral arterial circle and the basilar artery in dog No. 3(Fig. l).2. In each case, the size and severity of cerebral infarct corresponded generally to thedistribution of arteries occluded by v. immitis, as shown in rigs. 2 to 4; that is, theaffected areas of the cerebrum were the left temporal and occipital lobes in dog No. 1, the left frontal, parietal and temporal Robes in dog No. 2, and almost all the lobes ofthe right hemisphere and the left-side portions of the thalamus and hippocampus in dogNo. 3. It was confirmed microscopically that these affected cerebral areas were stillrecognized in the early stage of encepholomalacia.3. Worms recovered from the cerebral arteries of the three dogs were morphologicallyidentified as adult forms of D. immitis.

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Eleven Macaca monkeys were infected experimentally with 20 to 800 meta-cercariae of the "Japanese species" of the liver fluke, Fasciola sp. They consisted of twomonkeys of Macaca irus, one of M. mulatta, three of M. nemestrina, three of M. cyclopisand two of M. fuscata. All of them were highly susceptible to infection with Fasciola sp.When infected with 8.8 or more metacercariae per kg of body weight, six monkeys diedwithin 48 to 80 days after infection. The percentage of worm recovery averaged 36.4%, ranging from 16.0 to 62.O7.. Adult flukes recovered from the monkeys after infectiondecreased in number as the duration of infection was prolonged. The recovery rate ofadult worms from the monkeys was comparable with that from very susceptible hostspecies, such as mice, rabbits and sheep.The major clinical signs observed were rough hair coat, pallor of the face, inappetence, emaciation, prostration, abdominal pain, and ascites with scrotal hydrocele. A prominentchange in white blood cell picture was eosinophilia which appeared soon after infection, increased in intensity during the migratory phase of flukes, and subsided gradually afterflukes had entered the bile passages.Almost all the monkeys that died during the parenchymal phase of migration of theparasite presented a decrease in the erythrocyte count, the hemoglobin content, and thehematocrit level shortly before death. The main gross pathological findings in thesemonkeys were numerous hemorrhagic tracts in the liver and a large volume of blood-stained fluid in the peritoneal cavity. Death occurred to these animals as a result ofevident internal hemorrhage affecting the erythrocyte count.

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