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K Nanba

Publications and source records attributed to K Nanba.

At least 109 records · Page 6Linked to original sources

Binding experiments of muscarinic acetylcholine and dopamine receptors in human brains with emphasis on a case of striatonigral degeneration.

In the regional distribution of I-3H-quinuclindinyl benzilate (3H-QNB) binding in human brains of neurologically unaffected cases, it was highest in the caudate nucleus which was followed by the putamen, amygdala, cerebral corteces and olfactory bulb and lowest in the substantia nigra. As to the regional distribution of 3H-spiroperidol binding in human control brains, it was highest in the caudate nucleus and was followed by the cerebral corteces, amygdala and lowest in the cerebellar cortex. In a case of striatonigral degeneration (SND), 3H-QNB binding in the putamen and thalamus was lowered and 3H-spiroperidol binding was decreased in the putamen, frontal and parietal corteces, Ammon's horn, amygdala and substantia nigra as compared to human brains of control cases. These results were noteworthy since no pathological changes were observed in the thalamus, cerebral corteces, amygdala and Ammon's horn in this case. The 3H-spiroperidol binding was increased by injection of 6-hydroxydopamine (6-OHDA) into the substantia nigra of rat brains by 17% as compared to the contralateral intact side. Conversely, 3H-spiroperidol binding was decreased by injection of kainic acid (KA) into the striatum of rat brains by 43% as compared to the contralateral intact side. This meant that dopamine receptors labelled by 3H-spiroperidol were at least partially localized at the postsynaptic site of the nigrostriatal dopamine neuron.

Animals↗

Recrudescence of infectious bovine rhinotracheitis virus and associated neural changes in calves treated with dexamethasone.

Reactivation of infection bovine rhinotracheitis (IBR) virus in calves administered dexamethasone (DM) was studied in 2 experiments. At 2, 3, 5, 15, or 30 months after inoculation of the Los Angeles strain of IBR virus, IV injections of DM were given for 5 consecutive days to induce a recurrent infection (experiment 1). Three months after the 1st treatment, a 2nd recurrent infection was induced, using DM with the same doses as used in experiment 1. The virus was excreted from nasal secretions from the 4th to the 10th day after initial treatment with DM, and from the 6th to the 9th day after the 2nd treatment. On pathologic examination, trigeminal ganglionitis, consisting of many proliferated microglia and inflammatory cells, was observed in all DM-treated calves. Moreover, degeneration of the ganglion cells and neuronophagia were prominent features in the calves after the 2nd recurrent infection. These observations indicated that the trigeminal ganglion may be one of the latent sites of IBR virus in calves after intranasal infection and that calves can develop a recrudescent infection after DM treatment several times during their lifetime.

Animals↗

Neural changes in vaccinated calves challenge exposed with virulent infectious bovine rhinotracheitis virus.

Recurrent infection in calves vaccinated with infectious bovine rhinotracheitis-(IBR) modified live virus was induced by dexamethasone (DM) treatment given 49 days after challenge exposure with virulent IBR virus. Nonchallenge-exposed IM and intranasally vaccinated calves did not excrete the virus after DM treatment; however, IM and intranasally vaccinated and subsequently challenge-exposed calves excreted the challenge-exposure virus into the nasal secretions 5 to 11 days and 6 to 10 days after the DM treatment, respectively. The calves were killed 15 to 18 days (experiment 1) and 14 days (experiment 2) and DM treatment was started and then were examined by histopathologic and fluorescent antibody techniques. All DM-treated calves that were inoculated with the vaccinal virus and challenge exposed with the virulent virus developed nonsuppurative trigeminal ganglionitis and encephalitis. On the contrary, the DM-treated nonchallenge-exposed vaccinated calves did not have lesions in the peripheral nervous system and CNS. Infectious bovine rhinotracheitis virus antigens were not observed in tissues of any of the calves examined (experiments 1 and 2) by fluorescent antibody techniques. These observations indicated that the modified live IBR virus neither produced lesions nor induced latent infection and that modified live IBR virus vaccination did not protect the calves against the establishment of a latent infection after their exposure to large doses of the virulent IBR virus.

Administration, Intranasal↗

Some problems on the histopathological diagnosis of non-Hodgkin's malignant lymphoma -- a proposal of a new type.

A new classification for non-Hodgkin's malignant lymphoma is proposed as the one suited for the Lymphomas in Japan, which is to provide a new subtype "pleomorphic" for those more or less rapid-growing lymphomas of peripheral T-cell nature, along with another subtype lymphoblastic, after Nathwani et al. for those of central T-cell nature. The proposal is based on the result of the investigation by the Study Group for Histopathological Diagnosis on Malignant Lymphoma that (1) the presence of a significant number of T-cell lymphomas with peculiar "pleomorphism" is responsible for the very low reproducibility rate of histopathological diagnosis on the diffuse, mixed L&H type of Rappaport classification, and (2) the relative incidence of lymphoms as peripheral T-cell nature including the so-called adult T-cell leukemia is much higher in Japan than in the Western countries.

B-Lymphocytes↗

Congenital abnormalities in newborn lambs following Akabane virus infection in pregnant ewes.

To clarify the pathogenicity of Akabane virus for ovine embryos, pregnant ewes were inoculated intravenously with the virus. As a result, all of them were affected with viremia and showed an increase in neutralizing antibody 2 weeks after inoculation. The virus was recovered from many organs of embryos which were inoculated with it at 29--45 days of pregnancy and sacrificed 9--30 days later. In particular, some of these embryos which were sacrificed 15 days after inoculation were found suffering from systemic infection. A large quantity of virus was recovered from the organs all over the body of them. No virus, however was recovered from any organ of embryos which were inoculated with the virus at 81 days of pregnancy and sacrificed 30 days later. Abnormal changes were observed in neonatal lambs born from ewes inoculated with the virus at 30--50 days of pregnancy. They were especially severe when the virus was inoculated at 30 days of pregnancy. They consisted of ankylosis of the limbs, scoliosis, hydranencephaly, porencephaly, stillbirth with dwarfism, and death after birth with dwarfism and weakness. Nothing abnormal was found in any neonatal lambs born from ewes inoculated with the virus at 91--101 days of pregnancy. When embryos exceeded 64 days of intra-uterine life more than 29 days after virus inoculation, it was possible to detect immunoglobulin, IgM or IgG or both, and antibody from the serum. Attempts failed to detect either immunoglobulin from embryos less than 59 days of intrauterine life. No IgA was detected from the serum of any embryo. In almost all the neonatal lambs born from ewes inoculated with the virus at 28--101 days of pregnancy, neutralizing antibody was detected from the serum at the time of birth.

Animals↗

Immunologic aspects and pathology of the malignant lymphomas.

Malignant lymphomas have traditionally been classified on solely morphologic grounds. With new immunologic and cytochemical techniques, it has been possible to characterize normal cells of the T-lymphocytic, B-lymphocytic, and monocyte-macrophage systems. Application of these methodologies to malignant lymphomas has established their nature as neoplasmas of the immune system. Within the B-lymphocytic system it is possible to identify subpopulations responsible for Burkitt's tumor, follicular (nodular) lymphomas, lymphocytic lymphomas of intermediate differentiation and well differentiated lymphocytic lymphomas. The T-lymphocytic system includes lymphoblastic lymphomas, mycosis fungoides, and Sezary's syndrome. Large cell lymphomas are diverse but the majority are tumors of transformed lymphocytes, usually of the B-lymphocytic system. The precise nature of the neoplastic cells of Hodgkin's disease, i.e., Reed-Sternberg cells and their mononuclear counterparts, has not yet been established. Despite previous suggestions of a B-lymphocytic or T-lymphocytic origin, recent studies utilizing in vivo cultivation have strongly suggested derivation from the monocyte-macrophage system.

Adolescent↗

Antibody forming cell precursors among glass-adherent peritoneal exudate cells.

Among glass-adherent peritoneal exudate cells (gaPEC), induced by an inoculation of 1% glycogen solution, about 4.5% were classified as antibody-forming cell precursors (AFCP) on the first day of culture by means of anti-mouse B-cell antibody (anti-B-Ab). They proliferated and differentiated into IgG-forming plasma cells when cultured with antigen and thymic RNA in vitro. Pretreatment of PEC with anti-B-Ab and complement suppressed the formation of plasma cells. AFCP had receptors for IgM-antigen complexes and for complement, both of which were independent of Ca++ and MG++ and resistant to treatment by pronase or phospholipase C. Cells bearing detectable receptors for EA (IgM) an EAC diminished by the 6th day when gaPEC were cultured with thymic RNA, but persisted longer in cultures without thymic RNA. The same percentages of cells demonstrated tartrate-resistant acid phosphatase activities but were devoid of esterase. Twenty to thirty percent of anti-B-Ab sensitive cells ingested latex particles. The proliferation kinetics of IgG-forming cells were studied through the 21st day of culture by means of peroxidase-labeled antibody staining methods.

Animals↗

Bovine virus diarrhea-mucosal disease. II. Isolation and characterization of a cytopathogenic virus and experimental production of the disease.

A disease broke out in calves in the Tokachi district of Hokkaido. It induced pyrexia, respiratory symptoms, diarrhea, bloody feces, leukopenia, and sometimes erosion of the oral mucous membrane and muzzle. Its morbidity rate was 90% and its fatality rate 50%. Bovine virus diarrhea (BVD) virus was isolated from organs of dead calves and blood and feces of affected calves. It exhibited a cytopathic effect on calf kidney cell culture. Antisera against the Nose and the Oregon C24V strains of BVD virus showed an antibody titer of the same order against the homologous virus and the isolated strain. Antiserum against the isolated strain, however, showed much lower antibody titers against the Nose and the Oregon C24V strains than against the homologous virus. When inoculated with the isolated virus, two calves manifested acute symptoms, but recovered at any rate. One of them, however, suffered again from clinical infection and died eventually 37 days after inoculation. It presented pathological changes closely resembling those of the case of spontaneous infection. Virus was recovered from its principal organs, intestinal canal, and lymph nodes of various regions of the body.

Animals↗