Few reports on a architecture and degneration of semilunar cartilage have been studied using scanning electron microscopy (SEM) .
The anther observed the architecture of the semilunar cartilage by its surface and cross section using SEM and studied about the change with aging, especially how degeneration progresses at each part of the semilunar cartilage.
Discoid, injuried, deformed and regenerated meniscuses were also studied with the aid of light microscopy.
These materials used in this experiment are 40 in total, ranging in age from 3 to 72 years.
Ten were obtained from the disturbed semilunar cartilages removed at operation and 18 from injuried.
Five were obtained from amputated legs, 4 from patients with arthropathy, 2 from autopsied legs and 1 from regenerated semilunar cartilage.
The results obtained from the observation are summarized as follows.
1) Three dimentional fibrous distribution was involved in the architecture of the semilunar cartilage. Main fibers were arranged in the horizontal direction. The fibers of the surface layer showed parallel arrangement which was thought to be a rational reason for the joint structure.
2) The surface layer of the semilunar cartilage from younger human showed round prominences arranged connectedly at the inner edge and covered with aging became remarkable over 30 years of age.
Physiological exhaustion was not related to the architecture of the semilunar cartilage, but non-physiological overweight influenced the progress of its degeneration.
3) The way how degeneration progresses at each part of the semilunar cartilage was related to the movement of the joint.
The degeneration of the semilunar cartilage facing the legs progressed more rapidly than that facing the thighs.
The outer part and the inner part were degenerated rapidly in the surface layer and in the middle layer, respectively.
In the inner part the middle to posterior segment and in the outer part the posterior segment were degenerated rapidly.
4) In the discoid meniscus, the degeneration was marked in the middle segment of incomplete discoid and in the center part of complete discoid, and degeneration was prominent in the middle layer rather than in the surface layer.
5) When the normal semilunar cartilage was injuried, the injury showed parallel running of fibers in many cases, and the degenration was limited to the fragmented parts and that by fragmentation.
6) Degeneration in arthropathy was most remarkable and its picture showed combined feature of physiological mechanical degeneration and inflammatory degeneration.
7) The structure of the surface layer in the regenerated semilunar cartilage was similar to the normal fibrous structure, but different from that of physiological semilunar cartilage.

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There have been many reports on multiplicity of monoamine oxidase (MAO) in many organs. It was reported that ethanol activated MAO activity in liver, but no concreted reports have been appeared on the effect of alcohol on MAO in brain. Male Wistar strain rats were used in this experiment. An intraperitoneal injection of ethanol (0.8 g/kg) resulted a transient increase in MAO activity 1 hour after administration with a peak of ethanol concentration in blood and at 48 hours after the injection the second increase was observed with no detection of ethanol in blood. Ethanol, at a concentration of 1 M, caused marked increase in MAO activity in vitro with serotonin and tyramine as substrates. The mechanism of the action of ethanol on MAO in brain mitochondria was studied by Lineweaver-Burk's double reciprocal plots. When serotonin used as substrate, both straight lines which obtained with and without 1 M ethanol, crossed on the abscissa, but when tyramine used as substrate, these two lines crossed on the ordinate.
Addition of 1 M ethanol in the reaction mixture did not show any changes in pS-activity curves and in pH-optima of MAO in brain mitochondria with serotonin and tyramine as substrates. The reversibility of activation of MAO activity with 1 M ethanol was studied by means of dialysis. It was found to be reversible. These results revealed three findings, such as, the first, there are two different types of MAO in rat brain, the second, initial activation of MAO might be caused by direct effect of ethanol and the third, the second activation of it might be caused by indirect effect of ethanol.

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Effects of tricyclic antidepressants and MAO inhibitors on mitochondrial MAO activities in dog brain and liver with tyramine and serotonin as substrates and effects of oxygen in gas phase on these actions were studied. The pH optimum for tyramine oxidation was pH 8.0 and for serotonin oxidation was pH 8.8 in dog brain MAO activity. Tyramine and serotonin oxidation by dog brain MAO were inhibited by concentrations more than 10^-4 M of imipramine, desipramine, amitriptyline and nortriptyline, and pI₅₀ values with both substrates were 10^-3 M for these four antidepressants. The same results were obtained either 20% or 100% oxygen used as gas phase. Concentrations of 10^-8 M or more of tranylcypromine and pheniprazine inhibited brain MAO activity with both concentrations of oxygen and pI₅₀ values were approximately 5 × 10^-7 M in all cases. These inhibitory effects were 1, 000 times more potent than those of antidepressants. With 20% oxygen as gas phase, pI₅₀ values of the dog brain MAO by harmine were 10^-5 M for tyramine and 10^-7 M for serotonin oxidation, and with 100% oxygen as gas phase, they were 10^-4 M for tyramine and 10^-7 M for serotonin oxidation.
Tyramine and serotonin oxidation by dog liver MAO were inhibited by concentrations more than 10^-4 M of imipramine, desipramine, amitriptyline and nortriptyline, and pI₅₀ values were 10^-3 M with both substrates for these four antidepressants. Concentrations of 10^-7 M or more of tranylcypromine and pheniprazine inhibited liver MAO activity with both substrates and with both concentrations of oxygen and pI₅₀ values were approximately 10^-6 M in all cases. With 20% oxygen as gas phase, pI₅₀ values of liver MAO by harmine were 2 × 10^-4 M for tyramine and 3 × 10^-6 M for serotonin oxidation, and with 100% oxygen as gas phase, they were 3 × 10^-4 M for tyramine and 5 × 10^-8 M for serotonin oxidation. Distinct differences of pI₅₀ values between tricyclic antidepressants and MAO inhibitors were observed, but correlation between MAO inhibitory effects and antidepressive effects was not found. It is suggesting that pharmacological effects of antidepressants are not caused only by inhibition of MAO activity in brain. From the result obtained the differences of inhibitory effects of harmine on oxygen consumption and of Km values when dog brain and liver MAO used as enzyme, it is also suggesting that there are multiple formes of MAO which shows different enzymatic characteristics in brain and liver.

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The time courses of reaction rate, effect of oxygen concentration and effect of various reagents on human placental MAO were studied. Homogenate of human placenta was used as an enzyme source and MAO activity was measured by Warburg's manometer. Human placental MAO activity with β-phenylethylamine as substrate did not show any changes in activity for a long time from the start of reaction, but with serotonin, tryptamine, and tyramine as substrate it decreased markedly in the course of reaction time. MAO activity with β-phenylethylamine as substrate in 100% O₂ concentration as gas phase was three times higher than that of in 20% O₂ concentration. However, MAO activity with serotonin as substraet in 100% O₂ concentration as gas phase was only 1.5 times higher than that of in 20% O₂ concentration. MAO activity with β-phenylethylamine as substrate increased with the increase in O₂ concentration as gas phase almost linearly, while MAO activity with serotonin as substrate increased rapidly at 10-20% O₂ concentration and reached almost maximum velocity at 40% O₂ concentration. MAO activity with β-phenylethylamine as substrate was inhibited by catron more strongly than by harmaline, while MAO activity with serotonin as substrate was inhibited more strongly by catron. Catron showed a noncompetitive inhibition of MAO against O₂ when serotonin was used as substrate, but it showed a competitive inhibition of MAO against O₂ when β-phenylethylamine was used as substrate.

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The substrate specificity of MAO in dog stomach was investigated manometrically. The MAO activities in total stomach homogenate with tyramine, serotonin, 3-phenylethylamine and benzylamine as substrates were found to be 111, 98, 32 and 21μl O₂/3 hr/2.0 ml homogenate, respectively. Almost the same results in specific activity were obtained in the three parts of stomach, such as lesser curvature, greater curvature and pylorus. However, in cardia the specific activity with tyramine as substrate was clearly decreased to 71 compared with 111 in total stomach, and the specific activity with serotonin as substrate in cardia was decreased to 36 compared with 98 in total stomach. Moreover, different MAO activities with serotonin as substrate were found in these four parts of stomach. According to the method of Cox and Perhach, the contents of serotonin in these four parts of dog stomach were studied. It was found that the greater curvature contained about twice of serotonin (12.74 μg/g tissue) as much as that in the other three parts. Clorgyline and harmine, which are specific inhibitors of type A MAO, inhibited MAO activity in stomach with serotonin as substrates. On the other hand, these two inhibitors showed a slight inhibition of MAO activity with β-phenylethylamine as substrates which are specific substrates for type B MAO. Deprenyl and pargyline which are the specific inhibitors for type B MAO did not showed any marked inhibition of MAO activity with any of the four substrates. The inhibitors of hydrazine type, such as semicarbazide, iproniazid and pheniprazine showed a slight inhibition of MAO activity with serotonin and tyramine as substrates. On the other hand, marked inhibition of MAO activity with β-phenylethylamine and benzylamine as substrates were observed. Any marked inhibition of MAO activity was not obtained in the case of isoniazid, cuprizone and KCN were used as inhibitor.
From these results, it was suggested that there might be three types of MAO in dog stomach and among them, type A MAO would have a special role in serotonin metabolism.

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A study of monoamine oxidase (MAO) has been made on homogenate of adult dog thoracic aorta and some characteristic properties of MAO in dog aorta were compared to that of MAO in dog serum and of MAO in dog liver.
The pH-activity curve of MAO in dog aorta showed a typical bell shape and its optimum pH was found to be 7.5 when MAO activity was measured by a slight modification of McEwen and Cohen's benzylamine method.
The maximum activity in pS-activity curve of dog aorta MAO was obtained at the concentration of 0.1 mM of benzylamine as substrate and it was found this value to be very low when compared to that of 10 mM obtained from dog liver MAO. The MAO in dog aorta and in dog serum were inhibited by KCN while MAO in dog liver was not inhibited at all.
Pargyline did not inhibited both MAO in dog aorta and in dog serum but strongly inhibited MAO in liver. Tris (hydroxymethyl) aminomethane showed strong inhibition against MAO in dog serum but did not show any effect on MAO in dog aorta and in dog liver. Moreover, marsilid and catron inhibited all three of MAO in dog serum, aorta and liver. From these results, it was suggested that MAO in dog aorta was a different enzyme from MAO in serum and in liver.

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The ultrastructural demonstration of monoamine oxidase (MAO) activity in rat liver was studied by the ferricyanide method. The modification of the ferricyanide method by Hanker et al. were as follows : the fixing time in situ with 2% paraformaldehyde (PFA) was 10 minutes, the volume of dimethylsulfoxide was 1/4 of the method of Hanker et al. and the fixed tissues in incubation medium were immersed at 25°C for 18 hours.
The effect of perfused PFA on MAO activity in rat liver mitochondria was studied. When 1, 2, 4, 8 and 10% PFA solution were perf used, MAO activities with tyramine as substrate were 98, 90, 70, 55 and 43% of the control values, respectively. The substrate specificities of MAO in rat liver mitochondria fixed with 2% PFA were shown as the same pattern as the control rat, nevertheless these activities were lower than those of the control. By means of this modified method, the ultrastructural demonstration of MAO activity in rat liver cells was studied. The strong MAO activity was observed as electron dense area, both in the inner and the outer mitochondrial membrane. However, the main localization of MAO on which inner or outer membrane was not recognized. While, slight MAO activities were also observed in the other ultrastructural parts, such as mitochondrial cristae, endoplasmic reticulum and nuclear membrane. When rat liver was immersed in the incubation medium without tryptamine or pretreated with 10^-3 M pargyline, MAO activity could not detected. On the other hand, at 6 hours after administration of pargyline 25 mg/kg i.p. a slight MAO activity was observed in mitochondrial membrane, but at 12 hours after the administration no MAO activity was observed.

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we have carried out 208 cases of endoscopic retrograde cholangio-pancreatography (abv. ERCP) since 1976, corresponding 112 cases for biliary diseases, 23 cases for pancreatic diseases, 3 cases of papillary diseases, 5 cases of miscellaneous and 55 cases of no pathological findings.
The purpose of this study was to estimate the selective cannulation of major papilla in order to visualize the biliary and pancreatic ducts, according with clinical symptoms.
The main point of this technique is the insertion of the scope which reccomend the pushing method for pancreatogram and straight for cholangiogram. Furthermore the changing position of the patient, that means from left lateral to prone position aids for this purpose, because it allows the frontal view of the major papilla.
Bending of the distal end of the cannula either right or left makes easier the selective cannulation of the pancreatic and biliary tract respectively.
By this procedure we obtained a succesfull rate of 95, 9% for biliary duct and 93, 5% for pancreatic duct.

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We autopsied infantile polycystic kidney generally showed in brothers. No abnormal findings in family by intraveuous pyelography and genic examination were found. Pathologically, cysts were found in bilateral kidneys and liver.

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A-60-year-old male suffering from endotoxin shock due to infection of the bilary duct underwent cholecystectomy under modified NLA.
After the operation, he developed severe respiratory failure and DIC.
Controlled ventilation with PEEP, using the volume limited respirator and nebulization, was continued for respiratory failure. DIC was treated with intravenous administration of heparin, fresh blood and thrombocyte, and antibiotics and steroid were administered for sepsis.
But all treatment failed, and we lost the patient 87 hours after the operation.

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