Acta Medica Okayama volume39 issue5

Levels of plasma cyclic AMP, serum immunoreactive insulin (IRI), serum c-peptide immunoreactivity (CPR) and blood sugar (BS) were determined 0, 15, 30, 45 and 60 min after a glucagon injection (0.01 mg per kg body weight) in normal controls, patients with acute hepatitis and liver cirrhosis. Plasma cyclic AMP responses to glucagon in liver disease patients varied widely in peak value, and only in patients with fulminant hepatitis and decompensated liver cirrhosis with poor prognosis was the response suppressed. The peak response of BS was found significantly later in liver cirrhosis patients than in normal controls. IRI and CPR responses to glucagon were lower in acute hepatitis patients than in normal controls and liver cirrhosis patients. IRI levels and their sum were also lower in acute hepatitis patients, although CPR levels were not significantly different. Thus, the ratio of the sum of CPR from 0 to 60 min to that of IRI was significantly higher in acute hepatitis, indicating impaired pancreatic secretion of insulin to glucagon stimulation as well as increased uptake of insulin by the liver in acute hepatitis.

In iron-induced epilepsy, partial section of the corpus callosum resulted in a decrease in rats showing dominant spike activity on the side of secondary focus and an increase in rats showing almost equal spike activity on the sides of primary and secondary focus in electrocorticograms (ECoGs). Changes in ECoG spike frequencies caused by sectioning the corpus callosum included an increase in unilateral spikes on the side of primary focus, a decrease in unilateral spikes on the side of secondary focus, and an increase in bilateral spikes appearing almost synchronously on both sides.

Polyamines have a close relationship with rapid cell proliferation. We measured polyamine levels in amniotic fluid, maternal plasma and urine during normal pregnancy. Plasma putrescine, spermidine and spermine gradually increased in the third trimester and reached the highest concentration at the end of pregnancy. There was a significant correlation between the level of these polyamines and the level of plasma estradiol and progesterone. In urine, putrescine and spermine increased with the progress of gestation and reached the highest level during the 8th to 10th months of gestation. In amniotic fluid, putrescine and spermidine concentrations were significantly high in the first trimester and decreased in the other trimesters, whereas spermine showed no significant change. Polyamine concentrations in maternal plasma and urine appear to reflect not only fetal metabolic changes but also the metabolic changes of the pregnant women, and to be influenced by several hormones which increase during pregnancy. Polyamines in amniotic fluid mainly reflect activated fetal metabolism and may be useful as biochemical indicators of fetal growth.

We examined the activity of peripheral blood monocytes in patients with autoimmune hemolytic anemia (AIHA) using an in vitro assay of monocyte-macrophage interaction with erythrocytes and an antibody-dependent cell-mediated cytotoxicity (ADCC) assay. The monocytes of AIHA patients in the hemolyzing period phagocytized autologous sensitized red cells and anti-D coated red cells more avidly than normal control monocytes. There was no significant relationship between phagocytic activity and ADCC activity. The activated monocytes phagocytized autologous sensitized red cells, but had no ADCC activity in a short time 51Cr release assay. Phagocytic activity of the patients' monocytes against autologous erythrocytes rapidly decreased after treatment with prednisolone even though the red cell sensitization with antibody remained almost the same as during the hemolyzing period. We postulated that the activation of monocytes in AIHA was due to the "arming" effect of anti-erythrocyte antibody, but we think that other mechanisms may also be involved in the activation of monocytes.

The effect of a lymphotoxin-like substance, OH-1, released by human acute lymphatic leukemia BALL-1 cells, on metastatic tumor proliferation was investigated in BDF1 mice with transplanted Lewis lung carcinoma cells. Mitomycin-C, cyclophosphamide and adriamycin were used as control agents. The effect of OH-1 on metastases, as determined by comparison of the numbers of pulmonary nodules and by 3H-thymidine labeling indices, was significant. Also, investigation of the effect of OH-1 on host immunity showed that, while the control preparations had considerable side effects, immunodepression and emaciation were not noted with OH-1. As to direct cytotoxicity, OH-1 is principally cytostatic in activity and effects cell progression delay in both the G1 and G2 phases.

The distribution of ferritin has been studied in many tissues, but has not yet been established on the cellular level. We investigated the cellular distribution of ferritin in the liver, spleen and bone marrow using the immunoperoxidase method, and compared it with that of hemosiderin. We also examined changes in the distribution of these proteins after phlebotomy and iron overload. In normal rats, ferritin was seen in centrilobular hepatocytes, Kupffer cells, macrophages in the red and white pulp of the spleen and central macrophages in bone marrow. Hemosiderin was observed almost exclusively in the red pulp and partly in tangible body macrophages of the white pulp. After phlebotomy, neither ferritin nor hemosiderin were detectable in these cells except for ferritin-positive cells in the white pulp, which showed little change after either phlebotomy or iron overload. In iron overloaded rats, both ferritin and hemosiderin increased in hepatocytes and reticulo-endothelial (RE) cells. Ferritin-positive cells in the liver were mainly located in the periportal area. These results indicated that hepatocytes and RE cells except for those in the white pulp may play an important role in iron storage, and that ferritin-positive cells in the white pulp may have a function other than iron reserve. They also suggested that the zonal distribution of ferritin-positive hepatocytes may be due to microcirculation in the hepatic lobules.

Twenty-five patients (30 hips) have had a total hip replacement using the cup supporter developed in our department. This report describes the follow-up findings on these patients. The mean period after hip replacement was 2 years and 8 months (range from 6 months to 6 years). The cup supporter was used in patients with rheumatoid arthritis with acetabular protrusions, central migration of the prosthesis after hemi-arthroplasty, revision operation for a defecting acetabular floor, primary acetabular protrusions (including osteoarthritis with acetabular protrusions) and traumatic fracture-dislocation of the hip. In five cases, autograft of bone was used in addition to the cup supporter for reinforcement of a thin acetabular floor. This combination appeared to provide good clinical results. The cup supporter was of value in revision operations due to loosening of the acetabular cup with severe acetabular protrusions.

Fulminant hepatic failure (FHF) was produced in rats with intraperitoneal injection of D-galactosamine. Control rats received only physiological saline. 15N-leucine (200 mg/kg of body weight) was injected into the rats via the tail vein. Arterial blood was drawn before and 5, 15, 30 and 60 min after the injection of 15N-leucine. 15N-amino acids were determined quantitatively by gas chromatography and mass spectrometry. The plasma 15N-leucine level decreased logarithmically in the same manner in both groups. This result suggests that leucine is mainly metabolized in extrahepatic tissues. The incorporation of 15N into plasma isoleucine and valine was not significantly different between the groups. Plasma alanine and glutamine concentrations increased in controls and decreased in FHF rates after the injection. The incorporation of 15N into plasma alanine in rats with FHF was significantly later than in controls. This result may suggest that undergoing hyperammonemia causes to form more glutamine from glutamate in extrahepatic sites as the same manner as for chronic hepatic failure. Additionally, insulin levels increased temporarily after the injection of leucine in both groups. This increase may play a role in the decrease in plasma isoleucine and valine concentrations after injection of leucine.