[My suggestion on reorganization of the Japan Nursing Association. Organization based on the trust of the people].
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Biomedical subjects
Publications and source records attributed to T Kamimura.
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Electron microscopic observations in 30 cases of HBsAg positive liver disease and 12 asymptomatic carriers of HBsAg suggested the following mechanism of intracellular development of Dane particles: core particles migrated from the nucleus into the cytoplasm through the nuclear pores. Intracytoplasmic core particles protruded into the cisternae of endoplasmic reticulum by budding the outer coat of Dane particles being derived from the membrane of endoplasmic reticulum. Release of Dane particles into the blood stream by reversed pinocytosis was suggested by the finding of submembranous localization of endoplasmic reticulum containing these particles. No budding from the cell surface of the hepatocytes was encountered. Dane particles in the hepatocytes were detected in 14 of 15 cases positive for serum HBeAg while no particles were seen in 27 HBeAg negative cases, thus suggesting that serum HBeAg reflected ongoing replication of hepatitis B virus in the hepatocytes.
Electron microscopic observations were carried out on five HBsAg carrier chimpanzees infected with delta (delta) agent and two chimpanzees infected with human non-A, non-B hepatitis. The cytoplasmic tubular structures, which have been recognized in the liver of chimpanzees infected with human non-A, non-B hepatitis, were found also in the liver of HBsAg carrier chimpanzees infected with delta agent. The quantity of the cytoplasmic structures in serial studies was associated with SGPT elevation rather than with expression of delta antigen in sera and liver tissues. This indicates that the cytoplasmic structures reflect a pathologic change of the hepatocytes in chimpanzees infected with delta agent or human non-A, non-B hepatitis. These and other similarities between the two agents suggest a similar nature.
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Antibodies against a possible causative agent of non-A, non-B hepatitis, hepatitis C virus (HCV), in Japanese patients with hepatocellular carcinoma were analyzed using the enzyme-linked immunosorbent assay (ELISA) system from Ortho Diagnostic Systems, Japan. Fifty of 58 cases of hepatitis B virus surface antigen (HBsAg)-negative hepatocellular carcinoma were positive for the antibody (86%) and 8 of 42 cases of HBsAg-positive hepatocellular carcinoma were positive (19%). Among patients with HBsAg-negative hepatocellular carcinoma, the prevalence of the antibody was greater among those who had received a blood transfusion (97%) than among those with no history of transfusion (70%). Only 3 of 54 patients with cancers other than hepatocellular carcinoma were found to be antibody-positive (5.6%) and all three patients had a history of blood transfusion. These results show a close relationship between the presence of anti-HCV antibody and HBsAg-negative hepatocellular carcinoma in Japan.
A 69 year old female with a duodenal bulb obstruction due to direct invasion of common bile duct cancer who received total enteral nutrition through the route of percutaneous transhepatic internal drainage (PTID) was presented. The tip of PTID tube was placed over the duodeno-jejunal flexure. Jejunal infusion of all nutrients and the bile juice through this route kept her in good nutritional condition until the terminal stage of primary disease. This procedure did not cause the infection of the biliary system. Major problems, tube obstruction and diarrhoea, were easily resolved with the selection of an appropriate infusion schedule and nutrient concentration. We conclude that nutritional support through the PTID route is a beneficial means for compromised patients without laparotomy or hospitalization.
The pathogenesis of the increased number of megakaryocytes and thrombocytosis in essential thrombocythemia (ET) is still unknown. We examined the expression of c-mpl, a receptor of thrombopoietin (TPO), and its signaling molecules in a patient with ET. An 8-year-old girl showed a high platelet count and an increased number of bone marrow megakaryocytes. Neither chromosomal abnormalities nor myelofibrosis was observed. Following the diagnosis of ET, aspirin therapy was begun for the patient, with only modest improvement of symptoms. Her platelet count ranged from 1,200,000/microL to 2,200,000/microL for more than 2 years. In the analyses, the serum TPO level in the patient was 420 attomoles/mL (normal, 760 +/- 320). The level of c-mpl expression in bone marrow mononuclear cells was higher in the patient than in healthy children, while there was no difference in the level of c-mpl expression in CD34+ cells, indicating an expanded pool of megakaryocytic lineage cells. The level of Janus kinase 2 (Jak2) expression was lower in the patient than in a healthy child. These findings indicate that the signal pathway mediated by c-Mpl after binding to TPO may be impaired in ET. Further analysis is needed to clarify the mechanism underlying the development of thrombocytosis in ET patients.