The changes in local cerebral glucose utilization (LCGU) following a fluid-percussion injury were studied in 23 rats using the 2-deoxyglucose (2-DG) technique in order to determine the critical period for neuronal damage.
Three rats were used as controls. All the rats received a moderate impact of 4.8-5.6 atm from a fluidpercussion device using the University of California, San Francisco, method. LCGU was studied at 15, 30, 45, 60, and 120 min and 24 hours after injury. The optical density on autoradiographs was measured at the site of the brain contusion, in the rim around the contused brain, and in the bilateral cerebral cortex, hippocampus, and thalamus.
Decreased 2-DG uptake was observed in the contused brain. However, increased 2-DG uptake was seen in the rim around the contused brain from 15-60 min after injury.
The changes in 2-DG uptake noted in this study were very similar to those caused by permanent focal ischemia in a previous study, which suggests that the pathophysiologic phenomena occurring after fluidpercussion injury in the rat brain are based on ischemic changes.

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High affinity binding sites for endothelin (ET) -1 were identified on mouse parenchymal hepatocytes. The binding of ¹²⁵I-ET-1 at its site was specific, saturable, and time dependent, but dissociation of the receptor-bound ligand was minimal. Scatchard analysis of the binding data revealed the presence of a non-interacting, single class of high-affinity binding sites on hepatocytes. The dissociation binding constant (K_d) and the maximal binding capacity (B_max) were determined as 2.1×10^-10 M and 3.0×10² sites/cell, respectively. Unlabeled ET-1 competitively inhibited the binding of ¹²⁵I-ET-1 to primary cultured mouse hepatocytes with a concentration for half-maximal inhibition (IC₅₀) of 2.0×10^-10 M.
ET-1 apparently enhanced total protein synthesis in primary cultured mouse hepatocytes concentration ranging from 3×10^-11 M to 3×10^-8 M in a dosedependent manner.
These data indicate that specific receptor for ET-1 is present in the mouse liver and suggest for the first time that hepatocyte protein synthesis is involved in its direct, agonistic effect.

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Glycerol and mannitol are used clinically as hyperosmolar agents for the treatment of brain edema. In the present study the effects of pre-ischemic treatment with glycerol or mannitol on delayed neuronal death in the gerbil hippocampal CA1 region were examined. In addition, the effects of post-ischemic treatment with glycerol were studied.
Male Mongolian gerbils were subjected to transient forebrain ischemia by bilateral common carotid artery occlusion for 5 min. Skull and rectal temperatures were maintained at 36.5 ±0.5°C from 30 min prior to occlusion through 60 min post-ischemia. In the pre-treatment study, glycerol (650mg/kg or 1, 300mg/kg), mannitol (650mg/kg or 1, 300mg/kg), or saline were administered intraperitoneally to the gerbils 30 min before ischemia. In the post-treatment study, 1, 300mg/kg glycerol was given immediately or 60 min after ischemia. Seven days after the ischemic episode, the brains were fixed and stained for histopathological analysis. Normal pyramidal cell counts per 1 mm length in CA1 (neuronal density, ND) were then assessed under a light microscope.
ND in the sham-operated normal control group was 275.3±16.7 (mean ±SD). In the pre-treatment study, ND in ischemic gerbils treated with saline was 14.8±5.0. ND in ischemic animals treated with glycerol (650 or 1, 300mg/kg) or mannitol (650 or 1, 300mg/kg) were 29.0 ±15.7, 68.2±56.7, 88.9±79.8 and 52.8±54.4 respectively. Both glycerol and mannitol, at either dose, significantly ameliorated ND.
In the post-treatment study, ND in gerbils treated with saline or glycerol immediately after ischemia were 10.3±3.4 and 43.1±78.4, respectively, and 60 min after ischemia, 13.1±9.5 and 68.9±68.9, respectively. The ND in both post-treatment groups were not ameliorated significantly.
These results indicate that pre-treatment with glycerol or mannitol has protective effects on delayed neuronal death in the gerbil hippocampal CA1 region, while post-treatment with glycerol does not produce any significant protection of CA1 neurons from transient ischemia.

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A forty-nine-year-old female patient, complaining of swallowing difficulties and general fatigue, was admitted to the first hospital of Nippon Medical School.
At the age of 32, she was operated on for the removal of a well encapsulated non-invasive thymoma. Since then, she had been well till the age of 46, when chest X-ray films showed a recurrent thymoma which was excised together with the complete thymic tissues.
One year later, she developed myasthenia gravis (MG) with a ptotic right upper eyelid and general fatigue. Subsequently, she was placed on medication. After 21 months, however, she died of myathenic crisis in spite of vigorous respiratory and nutritional support. The autopsy revealed a small residual thymoma on the left lung, and systemic atrophy of the skeletal muscles.
In this paper, the mechanism of post-thymectomy MG and the recurrence of non-invasive thymoma are discussed.

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