CD16+ and CD56+ cells as markers of necrotizing and crescentic glomerulonephritis and active IgA glomerulonephropathy.
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Biomedical subjects
Publications and source records attributed to A Shimoda.
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The clonal origins of 20 multifocal hepatocellular carcinomas (HCCs) in four woodchucks were analyzed by the Southern blot hybridization technique. The woodchucks were divided into two groups according to the morphological classification of multifocal tumors: 1) three woodchucks had multifocal tumors that were widely separated and similar in size, which suggests a multiclonal origin of the tumors; and 2) one woodchuck had ten small multifocal tumors surrounding two large main tumors, which indicated intrahepatic metastasis from an original tumor. Results from the first group demonstrated that the number of integrated woodchuck hepatitis virus (WHV) DNAs differed from tumor to tumor, and none of the bands were the same size. In the second group, eight of the ten small tumors surrounding the two large tumors showed the same pattern of WHV DNA integration. One demonstrated an additional band and also shared the same bands with the other tumors, and one small tumor had a different pattern of integration from the others. It was concluded that the clone dissimilarity demonstrated by hybridization patterns does not necessarily mean that HCCs originate independently from different clones, because genetic changes may occur after or at the time of metastasis.
In the hepadnavirus enhancer region, a 33 bp DNA sequence is strongly conserved among mammalian hepadnavirus genomes. To elucidate the role of the sequence, we tested enhancer activities and capability to form DNA-protein complex of several synthetic DNAs. Not only two tandem copies of a 46 bp DNA covering the sequence but also two tandem copies of a 23 bp in the sequence exhibit enhancer activity. Also the activity was augmented by treatment of a tumor promoter, TPA. DNA binding proteins complexes with the 23 bp DNA were augmented in extracts of HepG2 or HeLa cells stimulated with TPA. These results imply that the conserved sequence of hepadnavirus enhancer is a TPA-inducible enhancer which is transactivated by ubiquitous DNA-binding proteins. We presented results showing that DNA-protein complexes with a 23 bp DNA are similar to but distinct from those with a TPA-responsive element DNA, the recognition site for c-jun/fos products. We also presented results suggesting that hepadnavirus X protein may not directly or indirectly affect DNA-protein complex formation with the conserved sequence in the hepadnavirus enhancer.
Unilateral transient cerebral ischemia was produced in Mongolian gerbils by clipping the left common carotid artery for 1 h. About 60% of the gerbils with neurological symptoms had post-ischemic seizures. The majority of those that had seizures died within a few days, and sections of their cerebral cortices contained many dark and shrunken neurons. However, the gerbils that did not have seizures survived without any severe complications. In the cerebral cortex of the latter, the neurons with diffuse or peripheral pallor of the perikarya were seen along with a small number of dark and shrunken neurons. Diffuse pallor occurred within a few hours following ischemia in layers III, V, and VI, and disappeared 1 or 2 days after recirculation. Electron microscopically, these neurons showed dispersion of ribosomes, simple and elongated profiles of rough endoplasmic reticulum (r-ER), clustered vacuoles, and mild to moderate mitochondrial swelling. Occasional net-like tubulomembranous structures, probably derived from r-ER, were observed. On the other hand, peripheral pallor became apparent after 5 days following ischemia, usually involving layer II first and gradually extending to the deeper layers. Concomitantly, the amount of neuropil decreased and the dendrites exhibited tortuosity and irregularity in layer II. Electron microscopically, these neurons showed marked swelling of peripheral perikarya and polyribosomes and organelles were located peripherally to the nuclei. In addition, numerous degenerated axon terminals and distended dendrites were observed around the neurons. These observations indicate that diffuse pallor represents damage directly induced by ischemia and subsequent recirculation, while peripheral pallor is the delayed and remote effect of ischemia, probably due to degeneration of neuronal processes.
Mice inoculated intravenously with trehalose-6,6'-dimycolate (TDM), a glycolipid component of the cell wall of Mycobacterium, in an oil-in-water emulsion (TDM emulsion) acquired a high resistance to intranasal infection by influenza virus. Athymic nude mice inoculated with TDM emulsion could not acquire such an augmented resistance to influenza virus infection. The augmented antiviral resistance of TDM emulsion-treated mice was diminished by prior intravenous inoculation of silica particles, which selectively impair macrophage functions. In vitro experiments showed that macrophage cultures treated with TDM emulsion released an activator(s) of T lymphocytes. Histological studies of the lung of TDM emulsion-inoculated mice revealed that a typical granuloma and severe perivascular lymphocyte infiltration appeared, though no such histological change was observed in the lung of control emulsion-inoculated mice. The lungs from TDM emulsion-treated athymic nude mice and the lungs from silica particle- and TDM emulsion-treated mice showed fewer and smaller granulomata and milder perivascular lymphocyte infiltration than a typical granuloma and lymphocyte infiltration in the lungs of TDM emulsion-treated mice. These and earlier results suggest that an acquired antiviral resistance of TDM emulsion-treated mice was caused by elicitation of macrophages with TDM, then activation of T lymphocytes, leading to granuloma formation and an amplified earlier interferon production in response to influenza virus infection.
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A rare case of carcinoid tumor of the uterine cervix associated with adenocarcinoma was reported. The carcinoid tumor was composed of round to polygonal cells showing solid or trabecular proliferation. Most of these cells and a small number of isolated cells wedged in neoplastic glands were positive with either Grimelius or Fontana-Masson stains, and also positive for serotonin by immunostain (PAP method). Positively stained cells were thus considered to have the same histochemical nature as enterochromaffin cell. The carcinoid tumor was minute, about 2 X 2 mm and the adenocarcinoma was a microinvasive one. In some parts, smooth transition between both tumor components was observed. From these findings, it is suggested that both the carcinoid tumor and the adenocarcinoma in the present case were derived from a primitive precursor cell of common mesodermal origin.
In order to ascertain the mode of anti-inflammatory action of a topical non-steroidal anti-inflammatory drug, etofenamate which is a diethylene glycol ester of flufenamic acid, the in vitro test for the mechanism of the action were carried out. Etofenamate (3 microM) was hydrolysed to flufenamic acid at a rate of 39.5% and 57.0% of the dose during 30 and 60 min incubation, respectively, when incubated with rat peritoneal macrophages stimulated with starch and bacto peptone in phosphate-buffered saline. PGE2 generation by these cells in MEM medium was dose-relatedly inhibited with etofenamate as well as flufenamic acid at the dosage range of 1 to 30 microM. This suggests that unchanged etofenamate is active, since the highest conversion rate of etofenamate to flufenamic acid was 15% of the dose during the incubation. Etofenamate produced a dose-related inhibition against lipoxygenase prepared from peritoneal polymorphonuclear leucocytes of guinea pigs, and its activity (IC50 = 5.3 X 10(-5) M) was stronger than that of caffeic acid; flufenamic acid was inactive. Inhibitory activity of etofenamate was one-third or less that of flufenamic acid against the hypotonic-hyperthermic lysis of rat erythrocytes and heat-denaturation of bovine serum albumin. From these results, it was suggested that topically applied etofenamate produces its anti-inflammatory action through prostaglandin synthesis inhibition by flufenamic acid produced in the inflammatory tissue and inhibition of prostaglandin synthesis by macrophages and lipoxygenase inhibition by unchanged etofenamate.
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The site of the analgesic action of non-acidic (basic), non-steroidal anti-inflammatory drugs (NSAIDs) was investigated in the acetic acid writhing test. In rats the anti-writhing potency ratio of i.p. to i.v. administered aminopyrine, tiaramide HCl or mepirizole was 4.96, 1.87 and approximately 4, respectively, suggesting an involvement of both central and peripheral mechanisms of their anti-writhing action. In mice the ratio of intracisternally (i.c.) to i.v. administered aminopyrine, tiaramide HCl or mepirizole was approximately 5.8, approximately 50 and approximately 7, respectively. Since the above ratio for morphine and methadone was higher than 10 and tolmetin sodium, an acidic NSAID, did not produce any anti-writhing effect when given i.c., it could be assumed that the anti-writhing action of these non-acidic NSAIDs was at least partially mediated via the central nervous system. In common with tolmetin sodium, aminopyrine showed more of anti-inflammatory potency when administered i.p. than i.v. and it did not reduce vascular permeability in mice when administered i.c. These results suggest that non-acidic NSAIDs produce their anti-writhing action through both central and peripheral mechanisms.
A rare case of plasma cell granuloma of the lung in a 5-year-old girl showing extrapulmonal extension to the adjoining thoracic wall was reported. Intrapulmonal and thoracic wall granulomas revealed the same histopathologic features; proliferation of plasma cells and fibrous connective tissue. Although slightly atypical plasma cells were observed among many mature ones, immunohistochemical examination revealed polyclonal proliferation, confirming their inflammatory nature. Cellular components of fibrous connective tissue were identified as fibroblastic cells and myofibroblasts by electron microscopy. The present case and literature suggested the importance of the fact that "infiltrative" plasma cell granuloma had a tendency to occur in children.
A congenital anaplastic infratentorial ependymoma, occurring in a female infant whose sister also died of brain tumor, is described. The tumor, located in the cerebellum and the fourth ventricle, is characterized by predominantly undifferentiated neuroepithelial cells associated with numerous mitoses, and partially of the cells demonstrating differentiation into ependymal cells and astrocytes. Of special interest is the fact that the elder sister of the patient had also died of a congenital glioma located in the cerebellum and the fourth ventricle, which leads to the discussion about the influences of genetic factors in the development of the familial gliomas as well as about the histogenesis of the tumor examined.
A case of congenital cerebellar tumor is reported. The tumor is composed of a few incomplete tubular structures analogous to the neural tube, and of neuroblastic, mature ganglionic, astrocytic, ependymal and undetermined neuroepithelial cells. A tentative diagnosis of congenital cerebellar neuroepithelial tumor with multiple divergent differentiations is made: the histogenesis is discussed. From a histogenetic point of view this tumor is given the provisional name of matrix cell tumor.
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