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Biomedical subjects

N Goto

Publications and source records attributed to N Goto.

At least 361 records · Page 20Linked to original sources

Coronary circulatory failure and thromboxane A2 release during coronary occlusion and reperfusion in anaesthetised dogs.

Attempts were made to demonstrate release of vasoactive substances from the heart during coronary occlusion (for 60 min) and reperfusion (for 60 min), and to clarify the pathophysiological significance of them. Vasoactive substances were detected by superfusion of rabbit aortic and dog coronary arterial strips with great coronary venous blood. Plasma thromboxane (TX) B2 was radioimmunologically assayed. Gradually developing, sustained contraction of both vascular strips was noted during coronary occlusion and reperfusion, while a transient contraction in rabbit aortic and relaxation in dog coronary arterial strips were seen immediately after reperfusion. The TXB2 released into the great coronary venous blood significantly increased during occlusion and reperfusion. Indomethacin treatment of the dog abolished the sustained contraction of both vascular strips and TXB2 release. The transient contraction of rabbit aorta after reperfusion was inhibited by phenoxybenzamine. Reactive hyperaemia following a 60 min occlusion was significantly depressed, as compared with that following 30 s to 30 min occlusion, and the depression was alleviated by indomethacin and imidazole. These results suggest that catecholamine(s) and TXA2 are released during coronary occlusion and reperfusion, and that the latter might be responsible for the coronary circulatory failure during reperfusion of irreversibly damaged myocardium.

Animals↗

Histopathological studies of reactions in mice injected with aluminum-adsorbed tetanus toxoid.

Histopathological observations of changes at the injection site in mice were made for 20 weeks after a single intramuscular (im) injection of aluminum hydroxide-adsorbed tetanus toxoid (Alum-TT), plain tetanus toxoid (TT), or aluminum adjuvant (Alum alone). Marked injury to muscle fibers and infiltration of neutrophils around the aluminum remnants were observed, and some microabscesses were occasionally formed, after im injection of Alum-TT. Some mature alum-granulomas were seen in the Alum-TT group, while the Alum alone group had only a few immature alum-granulomas. The TT group showed only slight injury to muscle fibers and acute inflammation at an early stage. In the Alum-TT group, well-developed lymphold tissues and granulomatous lesions were still observable even 20 weeks after the injection; however, these changes had already diminished in the Alum alone group by that time. These findings could serve as good models for undesirable local reactions to aluminum-adjuvanted vaccines.

Adjuvants, Immunologic↗

Genetic relationships among 5 inbred strains established from common ancestor, dd mouse, as assessed by mandible analysis.

By multivariate analysis using mandible measurements genetic relationships were investigated among 5 inbred strains, DDD, DDK, DSD, DD/Tbr and DDY, derived from the common ancestor, dd mouse. (1) In canonical discriminant analysis (discriminant analysis with reduction of dimensionality), 3 DD strains, DDD, DSD, and DDY, were closer to one another than to any control strain on planes Z1-Z2, Z1-Z3, and Z2-Z3. Only the DDK strain was quite far from those 3 strains. (2) In the discriminant analysis, however, the 5 inbred strains could be classified correctly at the rate of 100%. They were genetically different from one another. (3) The causes for this genetical difference seemed to be the genetic heterogeneity of the ancestor dd mouse and the method of inbreeding which had been independent since the separation.

Analysis of Variance↗

[Effects of 2,3-dimethoxy-5-methyl-6-(10'-hydroxydecyl)-1,4-benzoquinone (CV-2619) on the energy metabolism of red blood cells of rats].

Effects of CV-2619 and ubiquinone-10 (Q-10) on the energy metabolism of red blood cells (RBC) of Sprague Dawley rats were studied in the presence or absence of NaF. NaF (0.3--10 mM) dose-dependently decreased the ATP and lactate contents of the RBC. In the presence of NaF (1.5 mM), ATP content decreased to about 30% of the control. Phosphofructokinase (PFK) was markedly activated, while glyceraldehydephosphate dehydrogenase (GAPDH) and enolase were inhibited by NaF. Thus, the decrease in ATP by NaF might be attributed to retarded glycolysis due to inhibition of the latter two enzymes. The decrease in ATP by NaF (1.5 mM) was dose-dependently inhibited by CV-2619 (0.3--30 microM). Inhibition of enolase and activation of PFK by NaF were still noted even in the presence of CV-2619. Inhibition of GAPDH by NaF, however, was released by CV-2619. Q-10 (1--100 microM) did not affect the ATP levels decreased by NaF. It could be concluded that CV-2619 counteracted the NaF-induced decrease in the ATP level by accelerating the glycolytic flux through the GAPDH step, which was a rate-limiting one in the presence of NaF. Q-10, however, had no effect on the glycolytic flux.

Adenosine Triphosphate↗

Persistent infection with mouse hepatitis virus, JHM strain in DBT cell culture.

After inoculation with JHM strain into DBT cell monolayers, a persistently infected DBT cell culture was established without producing typical cytopathic changes after about 15th passages. By immunofluorescence virus specific antigen was demonstrated in 10 to 15% DBT cells. This persistently infected culture (JHM-CC) was resistant to superinfection with parental JHM, but such resistance was not shown against vesicular stomatitis virus. JHM-CC virus produced small plaques on DBT cell monolayers. Temperature sensitive (TS) mutant, defective interfering (DI) particle or interferon was not detected in the JHM-CC. To intracerebral inoculation with JHM-CC virus, cortisone treated ICR mice survived without showing clinical signs, however, demyelinating lesions were produced in the brain and spinal cord of them.

Animals↗

Olivary enlargement: chronological and morphometric analyses.

Chronologic and morphometric changes in the inferior olivary nucleus of the human medulla oblongata were studied in eight cases of primary pontine hemorrhage with different survival periods. To measure the olivary areas and analyze the neuronal and glial components, an optic electronic planimeter was used. A desk-top computer was also used for the calculation of the obtained data. The olivary enlargement was observed in cases with survival periods ranging from 3 weeks after the onset to 9.5 months. A morphometric analysis revealed six different stages of olivary changes after the destruction of the central tegmental tract in the pons: (1) no olivary changes, (2) olivary amiculum degeneration, (3) olivary hypertrophy, (4) culminant olivary enlargement, (5) olivary pseudohypertrophy, and (6) olivary atrophy. In stage (3) - noticed here for the first time -, neuronal cellular hypertrophy and sclerotic neurons with "insect-bite appearance" were observed. In stages (4) and (5), we also found the presence of prominent gemistocytic astrocytes in the characteristically enlarged inferior olivary nuclei. However, no proliferation of astrocytes during the olivary enlargement was confirmed in the morphometric analysis.

Aged↗

Acute demyelination in mice inoculated intraspinally with mouse hepatitis virus, JHM strain.

After intracerebral or intralumbar inoculation of mouse hepatitis virus, JHM strain, into weanling mice, viral growth and lesions in the central nervous system were comparatively studied for 5 days postinoculation. In the intralumbar group the virus titer of the spinal cord exceeded that of the brain until 24 hr postinoculation, and declined later. In the intracerebral group the brain virus titer was always higher, and the cord titer attained the same level as that of intralumbar group at 72 hr. Demyelinating lesions in the spinal cord appeared 48 hr after intralumbar inoculation, that is, 36 hr earlier than after intracerebral inoculation. Virus-specific fluorescence was detected within glia cells in the cord white matter 48 hr intralumbar inoculation. Electron microscopy revealed a number of virions within oligodendroglia cells, suggesting that the acute phase demyelination might be due to viral growth within this type of cells.

Animals↗

Electron microscopy of massive cerebrocortical necrosis in suckling rats inoculated intracerebrally with mouse hepatitis virus, A59 strain.

Cerebrocortical lesions produced in suckling rats by intracerebral inoculation with MHV-A59 was studied by electron microscopy. Many cytoplasmic vesicles and irregular patterns of the nuclear membrane were observed in infected neurons at 48 h post-inoculation (p.i.). The abnormally electron-lucent or -dense neurons were seen at 72 h p.i., and in the formers, many virions were detected between the outer and inner nuclear membranes as well as in the dilated endoplasmic reticulum cisternae. Both reticular and tubular inclusion bodies appeared in the cytoplasm and some virions seemed to be associated with an end of the latter. Many virions were also seen in the intercellular spaces. At 96 h p.i. many virions were present not only in the cytoplasm of degenerated neurons but also in astrocytes appearing in the spongy lesions. There was also degeneration of oligodendrocytes while having no virions. In rats which survived the acute phase of infection and were killed at 8 days or 14 days p.i., many macrophages and fibroblasts were accumulated in the thickened leptomeninges and submeningeal area. At 22 days p.i., atrophied electron-dense neurons having no virions were scattered throughout the cerebral cortex.

Animals↗

Genetic relationships between sublines of inbred strains of mice as assessed by mandible analysis.

Genetic relationships between sublines of inbred strains of mice were investigated by using mandible measurements. (1) Canonical discriminant analysis (discriminant analysis with reduction of dimensionality) was applied to the investigation of genetic relationships between sublines on two kinds of dimensionality. As a result, it was made clear that all the sublines of the same strains mapped closer to each other than they were to other strains on the plane of z1--z2, except the sublines of strain AA. (2) According to the result of discriminant analysis, misclassification among the sublines of the other strains was only 0 head/302 head, or 0%, for the male mice and 6 head/302 head, or 1.99%, for the female mice. Misidentification between the sublines of the same strain was also of low rate; that is, 28/302, or 9.27%, or the males and 9/302, or 2.98%, for the females. These results suggested that the mice of the sublines of the same strain might be genetically different from one another. (3) The cause for the occurrence of such subline divergence as this seemed to be mainly due to the spontaneous mutation of each colony after the separation of mice. It appeared that the subline divergence of strain AA might be due to the genetic heterozygosity of an original stock before the separation of mice.

Animals↗

Hydrocephalus in suckling rats infected intracerebrally with mouse hepatitis virus, MHV-A59.

After intracerebral inoculation of mouse hepatitis virus, MHV-A59 strain, into 3- to 5-day-old Wistar rats, some survivors at 14 days postinoculation (p.i.) were found to lack the cerebral cortex and to have an accumulation of considerable amount of cerebrospinal fluid. The virus titer in the brain increased exponentially after inoculation, reaching a maximum 4 to 6 days p.i. when immunofluorescence revealed virus-specific antigen within neurons in the cerebral cortex. A small amount of infectious virus was also detectable 14 days p.i. when the cerebral anomaly was evident. This brain malformation causing hydrocephalus was due to cerebral damage by viral infection.

Age Factors↗