Biomedical subjects
M Ichijo
Publications and source records attributed to M Ichijo.
[Current status of the clinic for comprehensive examinations for pregnant women at the Department of Gyneco-Obstetrics, Tohoku University Hospital].
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Tonic inhibition in the cat lateral geniculate nucleus maintained by retinal spontaneous discharge.
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Studies on electrohysterogram.
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[On laceration of the uterine cervix. Maternal factors contributing to the development].
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Characterization of human placental activity for transport of L-alanine, using brush border (microvillous) membrane vesicles.
To characterize the placental activity for the transport of amino acids, the uptake of L-alanine was investigated by rapid membrane filtration using brush border membrane vesicles separated from the human placenta of early pregnant (12-13 gestational weeks) and late pregnant (37-38 gestational weeks) women. The uptake of L-alanine into the brush border membrane vesicles at early and late stage of gestation showed a pattern of transport dependent on the intra- and extravesicular Na+ concentration gradient (extravesicular Na+ greater than intravesicular Na+). The Na+ concentration gradient-dependent uptake of L-alanine into the brush border membrane vesicles at early and late stage of gestation also showed a dependency on the potential difference of the internal and external membrane. The transport of L-alanine into the brush border membrane vesicles was markedly augmented at late stage of gestation. On the basis of the double reciprocal plotting of the L-alanine concentration and the Na(+)-dependent uptake of L-alanine into the vesicles, Km and Vmax were calculated as parameters of the Na(+)-dependent uptake of L-alanine into the vesicles. In the early stage of gestation Km was 0.78 mM, and in the late stage of gestation was 0.80 mM. In the early stage of gestation Vmax (nmol/mg protein/20 sec) was 0.62, and in the late stage of gestation was 3.53. From the results, it was considered that the placental active transport mechanism of L-alanine is the same in the early and late stages of gestation, and it was shown that its transport activity increases greatly in late stages compared to the early stages of gestation.
Studies on placental inhibition of platelet aggregation: a comparison of human syncytiotrophoblast brush border and basal plasma membranes.
We compared the platelet aggregation inhibiting activity of human placental syncytiotrophoblast brush border membrane vesicles (BBMV) and basal plasma membrane vesicles (BpMV), and obtained the following results. Strong platelet aggregation inhibiting activity is found in placental BBMV. BBMV inhibited platelet aggregation induced by ADP (adenosine diphosphate) and arachidonic acid in a way which depended on the protein concentration of BBMV added. In contrast, BpMV showed no detectable platelet aggregation inhibiting activity. Quite high ADP degrading activity (ADPase activity) was present in the placental BBMV. ADP was quickly degraded by BBMV. In contrast, BpMV did not degrade ADP so quickly. Platelet TXB2 production was almost completely abolished at the protein concentration of 40 micrograms/ml of BBMV. In contrast, BpMV did not significantly inhibit platelet TXA2 (TXB2) production. These results show that syncytiotrophoblast brush border and basal plasma membranes of the human placenta have markedly different properties with respect to platelet aggregation inhibiting activity.
Platelet aggregation inhibiting activity of human placental chorioepithelial brush border membrane vesicles.
We investigated the platelet aggregation inhibiting activity of human placental brush border membrane vesicles (BBMV) and obtained the following results. A strong platelet aggregation inhibiting activity existed in placental BBMV. The BBMV inhibited the platelet aggregation induced by ADP, arachidonic acid, collagen and ristocetin in a dose-dependent manner. The protein concentration of BBMV giving 50 per cent inhibition was 52 +/- 6 micrograms/ml for ADP-induced platelet aggregation, 21 +/- 2 micrograms/ml for arachidonic acid-induced platelet aggregation, 19 +/- 2 micrograms/ml for collagen-induced platelet aggregation and 107 +/- 9 micrograms/ml for ristocetin-induced platelet aggregation. There was a high level of ADP degrading activity (ADPase activity) in the placental BBMV. ADP degrading activity of the BBMV: 10.5 +/- 0.5 mumol/mg protein/min was 21 times greater than that of homogenate of the placental villi. The placental BBMV inhibited platelet TXA2 production. In the 40 micrograms/ml protein concentration of placental BBMV, platelet TXA2 production was almost completely inhibited.
Characterization of human placental activity for transport of taurocholate, using brush border (microvillous) membrane vesicles.
The uptake of taurocholate into brush border membrane vesicles prepared from human full term placenta was studied using a rapid filtration technique. The taurocholate uptake into brush border membrane vesicles was sensitive to extravesicular osmolarity, and pre-incubation of the brush border membrane vesicles with the taurocholate increased the uptake of taurocholate into the brush border membrane vesicles. These findings indicate that the uptake of taurocholate by brush border membrane vesicles represents transport into vesicles. The uptake of taurocholate into vesicles was not dependent on Na+ electrochemical gradient (extravesicular > intravesicular). But this uptake was markedly increased when the intravesicular space was rendered electrically more positive by the use of lowly permeant anions or valinomycin-induced K+ diffusion membrane potentials. These findings indicate that the taurocholate transport into brush border membrane vesicles was dependent on membrane potential. The initial rate of taurocholate transport into brush border membrane vesicles exhibited saturation kinetics with respect to the taurocholate concentration, an apparent Km of 67 microM and Vmax of 0.30 nmol/mg protein/20 sec were calculated.
Properties of ADP-degrading activity of human placental syncytiotrophoblast brush border membrane vesicles.
The enzymatic properties of ADP (adenosine diphosphate) degradation in human placental syncytiotrophoblast brush border membrane vesicles (BBMV) were explored and the following results were obtained. BBMV had high ADP degrading activity compared to homogenate of placental villi. ADP degrading activity of BBMV; 1.05 +/- 0.05 mumol/mg protein/min placental villi was 21 times higher than that of homogenate of placental villi. Hydrolysis of ADP by BBMV follows Michaelis-Menten saturation kinetics with an apparent Km of 10.9 +/- 0.8 microM and Vmax of 2.10 +/- 0.17 mumol/mg protein/min. The enzyme has a divalent cation requirement. EDTA (2 mM) was found to abolish ADP degrading activity but this could be restored by the addition of either magnesium or calcium ions. Maximum enzyme activity of ADP degradation in BBMV was observed at a pH close to 8.0. The enzyme was insensitive to vanadate, levamisole, oligomycin, ouabain and N-ethylmaleimide (NEM), omeprazole and adenosine (5') pentaphospho (5') adenosine.
A study of interferon-gamma and interleukin-2 production in premature neonates and neonates with intrauterine growth retardation.
Mononuclear cells from aborted fetuses, preterm infants, intrauterine growth retardation (IUGR) fetuses, and mature infants were stimulated with OK432 and PHA to study their effect on the production of interferon gamma (IFN-gamma) and interleukin-2 (IL-2), respectively. IFN-gamma production was reduced in the mature delivery group, while its production in preterm delivery and IUGR groups was markedly reduced compared to those in adults and the mature delivery group. Reduced IFN-gamma production in preterm delivery and IUGR groups was attributable neither to a decrease in T-cells nor to enhanced sensitivity of T-cells to prostaglandins. Unlike IFN-gamma production, IL-2 production in preterm delivery groups was higher than that in adults; its production in the IUGR group was comparable to that in adults. In addition, both IFN-gamma and IL-2 production in premature delivery cases was enhanced when these cases were exposed to the stress of infection.
Leukoaraiosis: correlation of MR and CT findings with blood flow, atrophy, and cognition.
Hypodense periventricular white-matter lesions detected by CT (leukoaraiosis) and high-intensity T2 signals detected by MR imaging were correlated with measurements of local cerebral blood flow (LCBF), cerebral atrophy, and cognitive performance. Subjects studied included elderly volunteers who were neurologically normal (n = 6), patients with chronic cerebral infarctions and intact cognition (n = 2), patients with multiinfarct dementia (n = 14), and patients with Alzheimer dementia (n = 9). Leukoaraiosis correlated with periventricular high-intensity lesions detected by MR, LCBF reductions, cognitive impairments, and cerebral atrophy. Moderate to severe leukoaraiosis was associated with LCBF reductions in the cortex, basal ganglia, and frontal white matter. Periventricular MR lesions correlated with cerebral atrophy but not with cognitive impairments or reductions in LCBF. The exquisite sensitivity of MR revealed small lesions that did not correlate with LCBF reductions and cognitive impairments. Remote subcortical white-matter lesions detected by MR did not correlate with periventricular MR lesions, leukoaraiosis, LCBF, cerebral atrophy, or cognitive performance, indicating little clinical relevance. We concluded that diffuse cerebral hypoperfusion, particularly in combination with the poor collateral circulation of white matter surrounding the lateral ventricles, is responsible for leukoaraiosis.