A case of seminoma in a black swan.
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Biomedical subjects
Publications and source records attributed to N Goto.
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Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.
A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. All 7 patients had a large gastro-renal or spleno-renal shunt, and a large proportion of superior mesenteric venous blood was being shunted as estimated from the diameter of the portal and the collateral vein, whereas in nonencephalopathic patients in whom part of the superior mesenteric venous blood was shunting this diversion was much less (P less than 0.001). Only one of the chronic portal-systemic encephalopathic patients had esophageal varices, insignificant in size, and the incidence of esophageal varices was significantly less compared to the 12 nonencephalopathic control patients with portal hypertension who had either a gastro-renal or spleno-renal shunt (P less than 0.05). It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices.
Hereditary hydronephrosis was detected in all of the male mice of DDD inbred strain maintained at the National Institute of Animal Health Japan, but in only a few of the females. From the standpoint that male hormones are related to the development of hydronephrosis in this strain, the incidence and severity of the disease were investigated in gonadectomized mice treated with testosterone. In the males, the incidence of hydronephrosis was 50% (7/14) in the control (gonadectomized) group, and 73.3% (11/15), 100% (13/13) and 100% (12/12) in the 0.1 mg, 3.3 mg and 10 mg treatment groups respectively. The same tendency was observed in the female animals, though the incidence in each group was not so high. In both sexes the degree of severity increased in proportion to the dose of testosterone administrated. Blood testosterone levels were higher in intact DDD mice than in C57BL/6 mice, which had normal kidneys in both sexes. These results suggest that male hormones play a significant role in the development of hydronephrosis.
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This is the report of a 50-year-old man with a more than 20-year history of chronic progressive portal-systemic encephalopathy. Liver tests were normal except for increased serum ammonia and indocyanine green plasma retention. The liver pathology was compatible with idiopathic portal hypertension or noncirrhotic portal fibrosis, demonstrating localized surface nodularity and portal fibrosis. Percutaneous transhepatic catheterization of the portal vein revealed near top normal portal vein pressure and a large shunt connecting the left gastric or superior mesenteric vein and the left renal vein. Presumably, the patient had portal hypertension in the past and formation of a short, large-caliber shunt between the portal system and the renal vein effectively decompressed the portal circulation.
A nonconjugative kanamycin-resistant (Kmr) recombinant plasmid, pNR5311, transferred at a low frequency from an Hfr or F' lac Escherichia coli donor to an F- lac- recipient. Among the transconjugants, two types of Kmr plasmids were found: one was indistinguishable from pNR5311 (type A), and the other was a recombinant between pNR5311 and the gamma delta sequence (type B). When the F' lac strain was used as a donor, 5% of lactose-fermenting (Lac+) and 75% of lactose-nonfermenting (Lac-) transconjugants had type A plasmids. A kinetic study revealed that type A plasmids were transferred more readily in short mating periods than were type B plasmids. Involvement of Tn903, which is present in pNR5311, in transfer of type A plasmids was unlikely since there was no discernible change in the F' lac molecule coexisting with the type A plasmid in the transconjugant cells. The non-gamma delta-associated conduction of pNR5311 by F' lac did not require the recA+ function of the donor. Conduction of pBR322 by F' lac was also carried out, and two types of plasmids with and without gamma delta were found, as with pNR5311. These findings suggest that the transfer of nonconjugative plasmids is conducted by a novel pathway which is not associated with translocation of transposable elements into either plasmid.
Chemoembolization by selective intra-arterial infusion of mitomycin C in microcapsule form exerts potential therapeutic effects through infarction and prolonged activity. Of 20 patients with inoperable hepatocellular carcinoma (HCC) treated with one or more courses via a hepatic arterial catheter, a change in tumor size could be measured in 16. Measurable tumor regression amounting to greater than 50% was shown in 6 patients (38%), 25-50% in 3 (19%), and less than or equal to 25% in 6 (38%), while tumor increased in 1. Serum alpha-fetoprotein, which was greater than 300 ng/ml before treatment in 13 patients, clearly fell after treatment in 10 (77%). The survival rate at 3, 6, and 12 months after treatment was 75%, 65%, and 24%, respectively, for all patients, and 92%, 85%, and 38% in 11 patients without a tumor cast in the portal vein or its major branches. Systemic toxicity was mild, and all patients tolerated treatment well. These results indicate that chemoembolization with mitomycin C microcapsules is a useful palliative measure for treatment of inoperable HCC.
The mode of inheritance of hydronephrosis was investigated by crossing inbred DDD mice having a high incidence of hydronephrosis and C57BL/6 mice having normal kidneys. In the males, incidences of hydronephrosis in F1 animals were intermediate between the two parental strains at a rate of 32.6% in (DDD x C57BL/6)F1 and 23.4% in reciprocal F1. The same tendency was observed in F2 male animals. In BCF1 males, the number of affected mice was higher in (C57BL/6 x DDD) F1 x DDD (72.4%) than in (DDD x C57BL/6)F1 x C57BL/6 (11.1%). A few affected mice were found among the females of hybrids F1, F2 and BCF1. These results suggested that hydronephrosis in the DDD strain of mice was controlled by polygenes, and that male hormones may have some effect on the occurrence of hydronephrosis.
10 inbred strains of mice including NOD and NON were identified by discriminant and canonical discriminant analysis of the mandible measurements. The number of erroneous discriminations was 0.5% (1/199) for the females and 0% for males (0/232). In canonical discriminant analysis (discriminant analysis with reduction of dimensionality), NOD and NON inbred strains were separately located on 2-dimensional planes, Z1-Z2, Z1-Z3, and Z2-Z3. These results clearly indicate that the genetic constitution of NOD and NON differs, although they have been established from a common ancestor ICR mouse. Causes of divergence between NOD and NON mice are discussed.
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