Biomedical subjects

Hajime Togari

Publications and source records attributed to Hajime Togari.

43 records · Page 3Linked to original sources

PubMed2002

Association between sleep apnea and reactive astrocytes in brainstems of victims of SIDS and in control infants.

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age; 27 infants died from sudden infant death syndrome (SIDS), 5 from congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 with a prolonged seizure, and another with prolonged neonatal hypoxemia. The frequency and duration of sleep apneas recorded some 3-12 weeks prior to the infants' death were analyzed. Brainstem material was retrospectively collected from these 33 infants and studied in an attempt to elucidate the relationship between sleep apnea and hypoxic gliosis. The findings were compared between the SIDS victims and the control infants. Brainstem materials were immunohistochemically studied for quantitization of reactive astrocytes using an anti-glial fibrillary acidic protein (GFAP) antibody. The pathological materials were collected within 24h of death. This study focuses on the association between respiratory characteristics and pathology. Physiological and pathological data in the arousal pathway of the brainstem were linked for each infant and variant-covariant analyses were carried out using physiological data as dependent variables and pathological data and categorical data to evaluate the association with SIDS or non-SIDS as independent variables. The study failed to statistically support an association between hypoxic loads, reflected by the GFAP-positive reactive astrocytes in brainstems, the classification of being SIDS or non-SIDS infants, and the characteristics of sleep apnea.

Analysis of Variance↗

PubMed2002

Interaction between apnea, prone sleep position and gliosis in the brainstems of victims of SIDS.

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died suddenly and unexpectedly under 6 months of age. Of these, 26 died from sudden infant death syndrome (SIDS), 5 from congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 from a prolonged seizure, 1 from prolonged neonatal hypoxemia, and 1 from meningitis and brain infarction. The frequency and duration of apneas recorded some 3-12 weeks prior to the infants' death were analyzed. The brainstem materials were collected and studied in an attempt to elucidate the relationship between sleep apnea, and prone sleep position and gliosis in some nuclei associated with cardiorespiratory characteristics, such as nucleus ambiguus in the medulla oblongata and the solitary nucleus, as well as structures associated with arousal phenomenon, such as the reticular formation, the superior central nucleus and the nucleus raphe magnus in the pons, the dorsal raphe nuclei in the midbrain and medulla oblongata, periaqueductal gray matter in midbrain, and locus ceruleus. Gliosis was estimated as the density of glial fibrillary acidic protein (GFAP)-positive reactive astrocytes. Variant-covariant analyses were carried out using the characteristics of apnea as an independent variable and sleep position and gliosis as dependent variables. A significant association was found only in the frequency of obstructive apnea and prone position (P<0.001) and gliosis in the raphe nuclei in the midbrain (P<0.001). Although prone position is a well-known risk factor for SIDS, the frequency of obstructive apnea has not been associated with the prone sleep position. The observed relation between prone sleep and the density of gliosis does not relate to epidemiological findings. Further studies are needed to investigate the unexpected statistical association.

Analysis of Variance↗

PubMed2002

Developmental changes and localization of mouse brain serine proteinase mRNA and protein in mouse brain.

Serine proteases are known to be involved in neural development and various functions in the central nervous system. Mouse brain serine proteinase (mBSP) is expressed almost exclusively in the mouse brain and it has been characterized at the molecular and biochemical levels. In this study, we analyzed the developmental changes and localization of mBSP mRNA and protein in the mouse brain, using reverse transcription-polymerase chain reaction, Western blotting, and immunohistochemistry. Expression of mBSP was strong in the white matter and the nerve tracts after postnatal day 30, especially in the cerebellum and the medulla oblongata. These results suggest that mBSP contributes to development and sustaining the functions in the mouse brain.

Animals↗

PubMed2002

Arousal deficiency theory in sudden infant death syndrome with reference to neuronal plasticity.

OBJECTIVE: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age (including 26 infant victims of sudden infant death syndrome (SIDS), five with congenital cardiac abnormalities, two from infected pulmonary dysplasia, two from septic shock with multi-organ failure, one with a prolonged seizure, one from prolonged neonatal hypoxemia and one from meningitis and brain infarction). METHOD: The frequency and duration of sleep apnea events recorded some 3-12 weeks before the infants' deaths were analyzed. Brainstem material from these 38 infants was studied in an attempt to elucidate the relationship between sleep apnea and neuronal pathological changes in the arousal pathway. The histochemical analyses included Bielschowsky staining and the immunohistochemical analyses included the evaluation of growth-associated phosphoprotein 43 (GAP43) and of synaptophysin as markers for synaptic plasticity. Neurofibrae with positive pathological reactions were quantitatively analyzed. Pathological and physiological data were linked for each infant. RESULTS: The correlation between sleep apnea and neuronal plasticity in the arousal pathway of the SIDS victims was not seen in the control infants and the correlation between sleep apnea and neuronal plasticity in the arousal pathway found in the control infants was not seen in the SIDS victims. CONCLUSION: These findings suggest that neuronal plasticity in the brainstem arousal pathway is related with SIDS.

Journal Article↗

PubMed2002

Human leucocyte antigen-Cw-specific cytotoxic T lymphocytes generated from naive cord blood used for cord blood stem cell transplantation.

Human leucocyte antigen (HLA)-Cw-reactive cytotoxic T lymphocytes (CTL) were generated from cord blood (CB) lymphocytes of two cases used for cord blood stem cell transplantation (CBSCT). In both cases, the CTL were cytotoxic against the patient's leukaemic cells, as well as the patient's Epstein-Barr virus (EBV)-lymphoblastoid cell line (EBV-LCL) and phytohaemagglutinin blasts, and the cytotoxicity was blocked by anti-HLA-class I monoclonal antibodies. In the first case, the CTL recognized Cw 3 (Cw 9 and Cw 10)-positive EBV-LCL, while in the second case, the CTL recognized Cw1 and/or Cw7. These cases suggest that CB T cells may be competent enough for generating CTL to induce a graft-versus-leukaemia effect and/or graft-versus-host disease in patients with CBSCT and that the mismatching of Cw antigens between patient and CB may be related to the outcome of CBSCT.

Acute Disease↗

PubMed2002

Nitric oxide further attenuates pulmonary hypertension in magnesium-treated piglets.

BACKGROUND: Persistent pulmonary hypertension of the newborn (PPHN) commonly appears as a complication of several pulmonary and non-pulmonary diseases. The hypoxia possibly inhibits Ca2+ +/- dependent K+ channels, thus resulting in membrane depolarization of pulmonary smooth muscle cells, which leads to the opening of Ca2+ channels and Ca2+ entry, resulting in contraction of the vascular smooth muscle. However, magnesium (Mg2+) is an antagonist of Ca2+. We studied the effect of magnesium sulfate on the treatment of hypoxia-induced pulmonary hypertension and compared to the site of action of nitric oxide (NO). METHODS: Zero-day-old piglets were used in each experiment. The effects of Mg2+ were tested in each hypoxic, normoxic and hyperoxic states. Once the desired physical state was achieved, Mg2+ was administered at a dose of 100 mg/kg approximately every 10 min. In order to determine the exact mechanism of the Mg2+, Nw-nitro-l-arginine (LNNA), a NO synthase-inhibitor, was administered simultaneously with Mg2+ in some of the experiments. RESULTS: There was a significant correlation between the percent reduction of the pulmonary arterial pressure (PAP) caused by magnesium and the level of oxygen (O2) present in the pulmonary artery. The greatest amount of reduction was seen in the hypoxic condition where the least amount of O2 is found. A further reduction in the PAP was seen when NO was given at the end of the Mg2+ trials. There was no significant reduction seen in the systemic arterial pressure. CONCLUSIONS: Inhaled NO further reduced the PAP in piglets already treated with Mg2+.

Animals↗

PubMed2002

ACTH(1-24) down-regulates expression of ciliary neurotrophic factor mRNA in cultured rat astrocyte.

We examined the effects on astrocytes of ACTH, which is used to treat West syndrome. We stimulated cultured rat astrocytes with ACTH(1-24), corticotropin-releasing factor, and dexamethasone, and examined changes in neurotrophic factor mRNAs by reverse transcription-PCR. Down-regulation of ciliary neurotrophic factor mRNA expression was observed by stimulation with ACTH(1-24), but the expression of nerve growth factor, brain-derived neurotrophic factor, and nerotrophin-3 mRNAs was unaffected. Northern blot analysis revealed that the decrease in ciliary neurotrophic factor mRNA occurred 4 h after stimulation with more than 10 nM of ACTH(1-24). Up-regulation of nerotrophin-3 mRNA expression was found after stimulation with 1 mM dexamethasone. These results suggest that ACTH(1-24) administrated in West syndrome may influence the expression of neurotrophic factors in astrocytes in vivo.

Animals↗