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Biomedical subjects

Y Sei

Publications and source records attributed to Y Sei.

89 records · Page 5Linked to original sources
PubMed1984

Partial characterization of the extracellular keratinase from Microsporum canis.

The extracellular keratinase of Microsporum canis released peptides from alpha-type fibrous protein and the membranous fraction isolated from human stratum corneum. Inhibition of the enzyme by phenylmethyl-sulfonylfluoride and its weak inhibition by N-ethylmaleimide and etheneglycol tetra-acetic acid indicated that it is probably a serine proteinase.

Egtazic Acid↗
PubMed1982

Histological identification of prolonged survival of a skin allograft on an extensively burned patient.

We applied skin allografts obtained from 38 unrelated volunteers to a very extensively burned female patient. Seven months after skin transplantation, one allograft from a male still survived clinically. In order to ascertain that the graft site resulted from growth of the male donor skin, the allografted area and patient's own unburned normal area were examined by the fluorescent staining of Y-body (Y-chromosomal fluorescence). Y-body was detected in 57 per cent and 65 per cent of cells from the grafted area, whereas no fluorescence was detected in the patient's own unburned normal area. These observations suggest that one allograft from an unrelated donor survived for 221 days on a very extensively burned subject.

Adult↗
PubMed1982

Isolation of an extracellular proteinase (keratinase) from Microsporum canis.

Proteolytic activity was demonstrated when a strain of Microsporum canis was cultured in broth with human hair, but not in the medium without hair. The extracellular proteinase (keratinase) was isolated and purified by chromatography. Disc electrophoresis showed one protein band of extracellular proteinase, and the antibody against this enzyme gave a single precipitin line in agar diffusion. The IgG fraction completely neutralized the proteinase activity. The proteinase of M. canis may play a role in infection caused by this fungus, by affecting keratinized tissue such as stratum corneum and hair.

Chromatography, Gel↗
PubMedDate not supplied

Evidence of neuronal degeneration in C57B1/6 mice infected with the LP-BM5 leukemia retrovirus mixture.

Mice infected with LP-BM5 develop a severe immunodeficiency accompanied by learning and memory deficits, gliosis, and neurotransmitter abnormalities. The neurochemical alterations are consistent with elevated excitotoxin levels, suggesting that infected mice may incur neuronal damage. Although the number of neocortical neurons was unchanged in mice 12 wk after LP-BM5 infection, the expression of cytoskeletal proteins declined, particularly in the frontal and parietal cortex as indicated by MAP2, NF-200, and synaptophysin immunoreactivity. In contrast, the number of striatal neurons decreased 19%. The remaining neurons were smaller, with fewer synaptic boutons, and showed decreased synaptophysin and NF-200, immunoreactivity. Immunoblots of cortex and striatum confirmed decreases in MAP2, NF-200 and synaptophysin expression. Finally, although NCAM expression decreased in the striatum, it increased in the cortex. These results indicate that LP-BM5-infected mice sustain significant neuronal damage, which may contribute to their behavioral deficits. Moreover, the increase in cortical NCAM expression suggests active synaptic remodeling to compensate for the persistent excitotoxic environment in these mice, whereas striatal neurons degenerate. These concurrent degenerative and compensatory processes may also occur in the brains of patients with AIDS dementia complex (ADC), who suffer extensive degeneration of the basal ganglia and cerebral cortex.

AIDS Dementia Complex↗
PubMedDate not supplied

Cytokines in the central nervous system: regulatory roles in neuronal function, cell death and repair.

Recent evidence suggests that neurons and glia can synthesize and secrete cytokines, which play critical roles in maintaining homeostasis in the central nervous system (CNS) by mediating the interaction between cells via autocrine or paracrine mechanisms. Circulating cytokines and soluble receptors also regulate neuronal function via endocrine mechanisms. Disturbance of the cytokine-mediated interaction between cells may lead to neuronal dysfunction and/or cell death and contribute to the pathogenesis of the CNS diseases (e.g., ischemia, Alzheimer's disease and HIV encephalopathy). Defining the molecular pathways of cytokine dysregulation and neurotoxicity may help to elucidate potential therapeutic interventions for many devastating CNS diseases.

Animals↗
PubMedDate not supplied

Strain variation in immune response and behavior following the death of cage cohorts.

Strain differences in both immune function and behavior were observed following exposure of mice to the death of cage-cohorts. AKR/J, BALB/cN, and C3H/HeJ mice were exposed to a dead cohort for two hours at 48 hour intervals for 30 days. During this two hour period, AKR/J mice displayed intense fighting and mounting behavior. In addition, these mice attacked, cannibalized, and buried carcasses. Neither C3H/HeJ nor BALB/cN mice exhibited the complete repertoire of behaviors directed at either carcasses or cage-cohorts observed in AKR/J mice. After 15 exposures to the death of cage-cohorts, allogeneic cytotoxic T-lymphocyte (CTL) response was suppressed in AKR/J mice, but was enhanced or unchanged in C3H/HeJ and BALB/cN mice, respectively. Other immune parameters including natural killer (NK) cell activity, and lipopolysaccharide-stimulated B cell proliferation were unchanged in AKR/J mice but increased in BALB/cN mice exposed to the death of cage-cohorts for thirty days. These results suggest: 1) that both suppression of the CTL response and behaviors indicative of defensive burying in AKR/J mice may specifically be due to the loss of cage-cohorts, since they were not observed following exposure of these mice to the death of contraspecific animals; and 2) that both the behavioral repertoire and immune responses following exposure to the death of cage-cohorts may be strain dependent. This strain dependence may reflect differences in the ability to cope with the intermittent presentation of a stressor, and may explain, at least in part, variability in stress-induced changes in immune functions.

Agonistic Behavior↗