Enzymatic phosphorylation of fish phosvitin.
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Biomedical subjects
Publications and source records attributed to Y Mano.
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The hemoglobin vesicle (HbV) is a red cell substitute encapsulating purified concentrated Hb in a phospholipid vesicle. In order to suppress metHb formation or autoxidation, for the long-term maintenance of the oxygen transporting capability, a series of thiols (cysteine, Cys; glutathione, GSH; homocysteine, Hcy; and acetylcysteine, Acy) were studied as reductants of metHb. Hcy and GSH showed a good suppressive effect on metHb formation, while Cys adversely accelerates the metHb formation at a rate twice that of the Hb solution without any reductants and Acy showed no change. The significant suppression by the coaddition of superoxide dismutase (SOD) and catalase to Cys indicated that Cys was easily oxidized by oxygen and simultaneously generates a large amount of active oxygens. The effective suppression of metHb formation by SOD and catalase was not observed for HbV containing no reductants, indicating that the generation of active oxygens from Hb itself is not significant. The coencapsulation of Hcy with Hb resulted in a low rate of metHb formation in HbV (initial rate, 1%/h) in vitro at an oxygen partial pressure (Po2) of 142 Torr. The rate increased with decreasing Po2, showed a maximum (2.2%/h) around Po2 = 23 Torr, and then decreased to 0%/h at 0 Torr. From these results, it is suggested that the fast metHb formation rate in the blood circulation of Wistar rats injected with 20 vol % of the HbV solution would be mainly caused by the exposure of HbV to the low Po2.
A human myeloblastic leukemia cell line, ML-1, was induced to differentiate along the monocytic lineage following exposure to a 1,25-dihydroxyvitamin D3 analogue, 20-epi-22-oxa-24a,26a,27a-tri-homo-1,25-dihydroxyvitam in D3 (KH1060) or 12-O-tetradecanoylphorbol-13-acetate (TPA). The combination of KH1060 and TPA synergistically induced differentiation of ML-1 cells into mature macrophages with multinuclei. Maturation was also observed in other differentiation characteristics such as phagocytic activity, a-naphthyl acetate esterase activity, and expression of surface antigen CD14. Differentiated ML-1 cells showed attenuation of telomerase activity and cessation of proliferating activity based on evaluation of the expression of genes related to cell growth potential. Remarkable synergism was observed in TNF production. Treatment with TPA prior to KH1060 resulted in only slight production of TNF; however, treatment with KH1060 preceding TPA induced a substantial amount of TNF.
Telomerase, the enzyme that synthesizes telomeric DNA, is repressed in normal human somatic cells but is activated with in vitro immortalization or during tumorigenesis. In this study, we investigated telomerase activity and expression of genes involved in telomerase activity in human myeloblastic leukemia ML-1 cells, differentiated synergistically by treatment with all-trans retinoic acid (ATRA) and granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF alone was not effective in changing telomerase activity whilst ATRA alone slightly decreased the activity. A combination of ATRA and GM-CSF remarkably reduced telomerase activity. We also detected remarkable suppression of hTERT mRNA expression in ML-1 cells treated with ATRA and GM-CSF. These results indicate that a synergistic down-regulation of telomerase activity and hTERT mRNA expression is induced by treatment with ATRA and GM-CSF in ML-1 cells.
Repetitive breath-hold (BH) diving can lead to accumulation of nitrogen (N2) in blood and tissues, which may give rise to decompression illness (DCI). An unusual condition is "Taravana", the diving syndrome reported by Cross in the 1960s. That report generated wide discussion as to whether BH diving can cause DCI. Paulev was the first person to suggest the link between DCI and BH diving. He, a submarine medical officer developed symptoms of DCI after a series of BH dives, having proceeded the dives by spending time in a hyperbaric chamber at 20 meters for 8 minutes. Recently four professional Japanese BH divers (Ama) with histories of diving accidents were reported. Magnetic resonance imaging of these divers detected cerebral infarcts localized in the watershed areas of the brain. A survey conducted on their island revealed that many Ama divers had experienced stroke-like events. A clinical feature of DCI in BH diving is that the damage is limited to the brain. Although the mechanisms of brain damage in BH diving are unclear, N2 bubbles passing through the lungs or the heart so as to become arterialized are most likely to be the etiological factor.
Functional differentiation is found in the spinal cord. A unique set of neurological deficits follows a multi-focal injury. Clinically, sensory and motor disturbance present independently, often resulting in sensory and motor deficit dissociation. This study examined 103 spinal decompression illness (DCI) cases. The neurological deficit dissociation was classified as follows: 1) Cases with sensory impairment only, or motor dysfunction alone, were tagged as having "dissociation" (44 cases); when a case was with both sensory and motor dysfunction, the spinal level of the sensory impairment was determined and was matched with the spinal segments responsible for the motor dysfunction; 2) If the two spinal areas did not match (i.e. with no regional overlap), they were tagged as having "dissociation" for each motor dysfunction (32 cases). In total, dissociation was present in 76 out of 103 cases. We concluded that clinical neurological deficit dissociation is frequently observed in spinal DCI.
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