An in vitro system of mitochondrial protein synthesis was studied. The system was reconstructed with pH 5 and polyribosomal fractions, both of which were prepared from the isolated liver mitochondria of tadpole, Rana catesbeiana. The activity of the reconstructed system was assayed by incorporation of L-[4, 5-³H] leucine into hot trichloroacetic acid insoluble fraction and by immunochemical determination of cytochrome c oxidase subunit I .
The results obtained are as follows:
1) The activity which is measured in the presence of cycloheximide is inhibited by puromycin, chloramphenicol and erythromycin. The pH and temperature for full activity of the system are 7.1 and 27°, respectively.
2) The system prepared from the liver mitochondria of tadpole at metamorphic climax has higher activity than that from the tadpole at premetamorphic stage.
3) Cytochrome c oxidase subunit I is synthesized by the reconstructed system. The relative rate of synthesis is higher in the system from the tadpole at metamorphic climax than that from the tadpole at premetamorphosis. A high capability of the system to synthesize cytochrome c oxidase subunit I is ascribed at least in part to an increase in the amount of mRNA coding for the subunit I.

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1) The rabbit was anesthetized with Nembutal and immobilized with D-tubocurarine, and tone burst evoked potentials were recorded from the dosal cochlear nucleus.
2) Neither supramaximal electrical stimulation of the optic chiasma, nor that of the perioral skin affected tone burst evoked potentials in either direction.
3) Pinching the perioral skin resulted in the appearance of a continuous theta rhythm activity in the hippocampus and low voltage fast activity in the neocortex. Nevertheless, the tone burst evoked potentials exhibited no changes.
4) Taken all these results together, it may be concluded that the neural mechanism which could possibly subserve attention does not exist at the level of the dorsal cochlear nucleus.

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It is well recognized that the iron absorption is increased during iron deficiency state and many substantial evidences support a view that the regulatory mechanism is taken place in the duodenal mucosal cells. To clarify the role of the mucosal iron binding proteins in the regulatory process of iron absorption, the author has isolated and characterized iron binding proteins from the rat intestinal mucosa and observed their biochemical features during iron absorption.
Male Wistar rats fed on low iron containing diet for a week were used throught the investigation. The rats were sacrificed at 3 hours after ⁵⁹Fe administration and then the piece of upper small intestinal loop was excised. The homogenate of the mucosa was then centrifuged at 20, 000 g for 30 min at 4°C. Two iron containing fractions (peak 1 and peak 2) were obtained respectively by Sepharose 6 B gel filtration of the 20, 000 g supernatant and the extract of the precipitate with Triton X-100 (Triton extract). The nature of these fractions has been analysed.
Based on the studies of the molecular weight, isoelectric point and pattern of the immuno-precipitin reaction, it was justified that the peak 2 represent the mucosal ferritin. No significant difference in biochemical characterization between mucosal ferritin purified from the supernatant and that of the Triton extract was confirmed. Incidentally the iron content of the mucosal ferritin was much less than that of the liver ferritin. The quantitation of the protein concentration of the mucosal ferritin was made in virtue of the highly sensitive 2-site immunoradiometric assay (IRMA) in supernatant and Triton extracted ferritin. The concentration of ferritin in superna-tant was 12.8μg/mucosa g and that in Triton extracted one was 0.19μg/g.
Moreover, the interrelationship between iron absorption and concentration of the mucosal ferritin was also investigated. Rats were given ⁵⁹Fe-iron solution by gastric intubation and sacrificed chronologically from 1 to 72 hours after iron administration. Contents of mucosal ferritin in supernatant and Triton extract were quantitatively investigated by the method of IRMA or immunoprecipitin reaction. In supernatant, the incorporation of the ⁵⁹Fe into ferritin reached to the maximum value at 5 hours and gradually decreased. Contents of the ferritin protein showed wavy-shaped curve and maximum values were observed at 0, 10 and 72 hours after the iron administration. The observation may support a view that the simultaneous occurrences of ferritin synthesis as well as degradation and mucosal denudation in the time course of ⁵⁹Fe administration is taken place. The iron administration may cause the biosynthesis of the mucosal ferritin, however, a possibility that the increased amount of the ferritin may act as the inducing factor (trigger) of the degradation mechanism of the ferritin per se in the mucosal cells.
The radioactivity study of the Triton extracted ferritin disclosed essentially identical tendency with the ferritin in supernatant.

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Secretory component (SC) and carcinoembryonic antigen (CEA) were localized by the peroxidase-labeled antibody method after Nakane in human gastric mucosa with intestinal metaplasia, adenocarcinoma and polyps, and their cellular and ultrastructural localization sites were compared in these disorders.
In histologically intact gastric mucosa, little or no SC and CEA were found in the epithelial cells, but in intestinal metaplasia both glycoproteins were present. SC was localized on the baso-lateral plasma membrane (BLM) to the level of the intercellular tight junctions and in the peri-nuclear spaces, the cisternae of endoplasmic reticulum and Golgi complex, but not observed along the microvillous surface and apical plasma membrane. In contrast to the SC localization, CEA was found on the microvilli of metaplastic cells but only rarely present along the BLM. In adenocarcinoma, this polar distribution of SC and CEA was absent and both were distributed all over the surface of cancer cells, i.e., on basolateral surfaces as well as the apical surface of cancer cells. This abnormal distribution of both glycoproteins appeared to be present in atypical cells in tubular adenoma. In hyperplastic polyp, neither SC nor CEA was evident except for the metaplastic foci, in which their polar distribution was preserved. These findings, together with ultrastructural observations previously made in colonic and gastric carcinoma, suggest that the abnormalities on localization SC and CEA on the cell surface were correlated with the histologic abnormalities, and intestinal metaplasia and atypia of the gastric mucosa might be a disorder related to certain varieties of adenocarcinoma per se.

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Sixty-four cases of intracranial AVM were examined by angiography and CT scan. Their clinical symptoms, CT findings, operative results and pathological findings were then studied. There were 64 patients with AVM of the brain who were admitted to the Department of Neurosurgery of Nippon Medical School from 1974 to 1983. Fifty-nine cases were confirmed by angiography and five cases were diagnosed by histological examination. There were 38 males and 26 females. The ratio of males to females was 1.5 : 1. Age at the onset of the symptoms ranged from 2 months to 48 years, median age was 26.2 years. Symptoms due to intracranial hemorrhage were the in 38 cases (59.3%), epileptic attack in 13 cases (20.3%), and headache in 6 cases (9.3%). The median age of the hemorrhage group was 26.9 years and the median age of the seizure group was 16.0 years. Ten cases of the non hemorrhage group suffered the hemorrhage afterward, so 48 out of the 64 cases (75.0%) had a single or a recurrent hemorrhage. The AVMs were located as follows : frontal (37.5%), parietal (20.3%), temporal (9.3%), occipital (15.6%), diffuse type (1.56%), corpus callosum (7.8%), thalamus (3.12%), brain stem (3.12%), cerebellum (15.6%). AVMs occurred about equally in the right and the left hemisphere (right 24, left 29). In 8 cases (12.5%) AVMs were in the midline and in 3 cases they occupied both cerebral hemispheres. Four cases were dural, and supplied by the external carotid artery. Three patients had 4 associated aneurysms, 2 occurring in one patient. Smaller and deeply located AVMs had bleeding tendency, while larger ones had a tendency to have a seizure. Smaller AVMs were more often situated superficially, while larger AVMs were situated deeply.
The 12 cases of non ruptured AVM were classified into two categories on the basis of the plain CT. Eleven cases (9.6%) exhibited a mixed density (M type), and one case (8.4%) showed a normal density (N type). Contrast enhancements were obtained in all cases. Hetero-geneous patterns were obtained in 11 cases, and a homogeneous pattern in 1 case. Of the 26 cases of ruptured AVM, M type was seen in 8 cases (30.7%) and N type in 18 cases. Contrast enhancements were obtained in 16 cases (61.5%). Heterogeneous pattern was obtained in 12 cases, curvilinear pattern in 4 cases. The CT scan was carried out for 34 cases with ruptured AVM. Intracerebral hematomas were noted in 27 cases (75.0%), intraventricular extension of hemorrhages was seen in 20 cases (55.8%), and no case showed subarachnoid hemorrhage. Five cases were not demonstrated by angiography but they were diagnosed by histological examination. Two of them were small AVM. The pathological examination revealed features of an AVM, and they also showed the telangiectatic features in parts. Three cases of them were thrombosed AVM. Pathological examination revealed various degree of thrombosis in abnormal vessels and depositions of hematoidin and hemosiderin adjacent to the AVM. Forty-seven cases (73.400) were treated surgically. Thirty cases (63.8%) had totally extirpated, seven cases had partially extirpated, seven cases had clipped afferent vessels, three cases had removed hematoma only. Thirteen cases were treated conservatively. Two of totally extirpated cases, one of partially extirpated case, two drainaged cases, and one of conservatively treated case expired. All patients who died or completely incapacitated suffered intracranial hemorrhage, so it is important to protect against hemorrhage from AVM.

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Male mice were fed a diet containing various concentrations of 3, 5-diethoxycarbonly-1, 4-dihyd-rocollidine (DDC) for 20 to 95 days. The livers of the mice were examined by light, electron and fluorescent microscopy. The following results were obtained :
1) Mice fed daily a diet containing more than 0.1% DDC developed Mallory bodies (MBs) after 40 days regardless of the DDC concentration in the diet. After 60 days, MBs were more numerous in the mice fed higher concentrations of DDC. Some of the mice fed 0.05% DDC for 40 to 60 days developed MBs following an additional treatment of 2.5% DDC for 3 days. These results suggest that the formation of MBs in this animal model may involve two successive processes of cellular alteration which are termed priming and induction. Priming is the initial state which is time-dependent, whereas induction is the second stage which appears to be dose-dependent. During the priming stage marked hepatomegaly was observed and by light microscopy pale swollen hepatocytes were noted. In this stage the electron microscopic and immunofluorescent studies revealed that intermediate filaments (IFs) were increased in the hepatocytes. In the induction stage hepatomegaly was not as marked as that in the priming stage. At this stage MBs were observed in grossly misshapen hepatocytes. By immunofluorescent microscopy, MBs strongly reacted with anti-prekeratin antibody. However, the cytoplasmic stains of MB-containing hepatocytes were markedly decreased or totally absent. These observations suggest that the induction of MBs is caused by the aggregation of IFs, which are increased during the priming stage.
2) MBs in the livers of mice fed DDC completely disappeared after the withdrawal of DDC from the diet for about 10 weeks. MBs reappeared in this group of mice following rechallenge of a higher concentration of DDC for one week.
3) These events in the animal model might be analogus to the development of alcoholic hepatitis in patients with a history of heavey drinking for many years (priming) whose admission to the hospital was immediately preceded by a binge drinking (induction).
4) It is probable that cytoskeletal changes similar to those observed in this animal model also occur in patients with alcoholic hepatitis and that those changes may constitute a major pathogenic factor of cell injury and necrosis in alcoholic liver disease.

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The ability of the liver to metabolise ¹²⁵I-insulin was studied in regard to a varying insulin level within a physiological concentration, age and fasted state in the cyclically perfused rat liver. High performance liquid chromatography was used to measure ¹²⁵I-insulin and its radioactive degradation products. Insulin disappearance from perfusates followed first-order kinetics in all experiments. The half life was 10.7±1.1 min and clearance was 6.5±0.6 ml/min/liver at 100 μU/ml ¹²⁵I-insulin level and these remained almost unchanged at 200, 400 and 800 μU/ml. In 7-, 12- and 21-old-day rats, clearances per g wet liver (0.39±0.09, 0.34±0.06 and 0.33±0.05 ml/ min/g wet liver) was significantly smaller than that of adult rats at 100 μU/ml ; however, there existed no significant difference between 30-day-old rats and 8-9-week-old rats. Clearances per liver increased after becoming 12-day-old with an increasing liver weight. Clearances in adult and 21-day-old rats having fasted for 96 hours were significantly reduced and the half life was 2.2 times longer as in each control group. Radioactive degradation products were free-¹²⁵I ¹²⁵I-Tyr and substances of three different molecular weights (78, 000, 48, 000 and 26, 000). The amount of these degradation products changed with insulin clearance : the amount of degradation products was equal to that of reduced ¹²⁵I-insulin in perfusates. These results suggest that metabolic states, i.e. age and fasting, rather than insulin concentration influence removal and degradation of insulin by the liver.

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Hydatid disease of the liver is a common endemic parasitic condition which prevails in areas of the world where pastoral industry is well developed, and allegealy affects both animals and man. It is commonly found in northwestern provinces of China. A total of nine hundred patients with unilocular hydatid disease had been treated by surgical operation in our hospital between 1953. and 1982, of these, 650 were cases with hydatid cysts in the liver. The diagnosis and treatment of the series of 650 cases is briefly described as follows.

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Six hundred and fifty patients with hydatid disease of the liver had been treated by surgical operation in our hospital between 1953 and 1982, of these 220 developed various complications (38.8%). In this paper, a preliminary analysis is presented of the forms of the manifestations.

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