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Y Katoh

Publications and source records attributed to Y Katoh.

At least 235 records · Page 13Linked to original sources
PubMed1987

[The changes in EPH gestosis placental amino acid transport activity (using human placental microvillous membrane vesicles)].

To elucidate the change in EPH gestosis placental amino acid transport activity, we investigated the uptake of L-alanine into microvillous membrane vesicles prepared from EPH gestosis placenta and from normal placenta by using a rapid filtration technique. 1. Alkaline phosphatase (ALP) was the marker enzyme of microvillous membrane vesicles (MMV). The ALP activity of mild EPH gestosis placental MMV didn't differ from that of normal placental MMV. On the other hand, the ALP activity of severe EPH gestosis placental MMV decreased compared to that of normal placental MMV. 2. The uptake of L-alanine into human placental MMV was dependent on the Na+ electrochemical gradient, so the transport across human placental MMV was a secondarily active one. The L-alanine transport activity of mild EPH gestosis placental MMV didn't differ from that of normal placental MMV. On the other hand, the L-alanine transport activity of severe EPH gestosis placental MMV decreased prominently compared to that of normal placental MMV.

Alanine↗
PubMed1987

[The effect of antibiotics (gentamicin) on placental amino acid transport activity (using human placental microvillous membrane vesicles)].

In order to elucidate the effect of antibiotics (gentamicin) on placental amino acids transport, we investigated L-alanine transport using microvillous membrane vesicles prepared from full-term human placental by a rapid filtration technique. 1. The active transport of L-alanine into microvillous membrane vesicles was dependent on Na+ electrochemical gradient (extravesicular greater than intravesicular). And the double reciprocal plot of this Na+ dependent initial uptake rate versus L-alanine concentration exhibited an apparent Km of 0.79 + 0.23mM and a Vmax of 3.56 + 0.70n mol/mg protein/20 sec. 2. Gentamicin did not affect the Km value of this Na+ dependent L-alanine transport kinetics (0.77 + 0.19 mM [lmM gentamicin], 0.79 + 0.21mM [10mM gentamicin]). On the other hand, gentamicin apparently decreased, the Vmax value of this transport kinetics (1.99 + 0.48n mol/mg protein/20 sec [1mM gentamicin], 1.12 + 0.32n mol/mg protein/20 sec [10mM gentamicin]).

Alanine↗
PubMed1987

The study of placental L-ascorbate (vitamin C) transport mechanism (using microvillous membrane vesicles).

To investigate the placental L-ascorbate (Vitamin C) transport mechanism, the uptake of L-ascorbate into microvillous membrane vesicles prepared from human term placenta was studied using the rapid filtration technique. The uptake of L-ascorbate into microvillous membrane vesicles was osmotically sensitive. This finding indicated that the uptake of L-ascorbate into microvillous membrane vesicles represented transport into the vesicles. The uptake of L-ascorbate into microvillous membrane vesicles was not dependent on sodium electrochemical gradient. The initial rate of uptake was not changed when the intravesicular space was rendered electrically more negative by membrane diffusion potential induced by the use of highly permeant anions. The initial rate of L-ascorbate transport exhibited saturation kinetics with respect to the L-ascorbate concentration; an apparent Km of 1.33 mM and Vmax of 47p mol/mg protein/20 sec was calculated. The uptake of L-ascorbate into microvillous membrane vesicles was competitively inhibited by D-isoascorbate. These results indicated that transport of L-ascorbate across the placental microvillous membrane vesicles was carrier mediated and was passive transport.

Ascorbic Acid↗
PubMed1987

[The character of human placental glucose and amino acid transport activity (using microvillous membrane vesicles)].

To elucidate the character of human placental D-glucose and L-alanine transport activity, we investigated the uptake of D-glucose and L-alanine into microvillous membrane vesicles prepared from human early and term placenta using the rapid filtration technique. 1. The uptake of D-glucose into microvillous membrane vesicles did not depend on the Na+ gradient (extravesicular greater than intravesicular). The uptake of D-glucose into vesicles was three times as great as that of L-glucose. And phloretin prominently inhibited the uptake of D-glucose into vesicles. So, it was indicated that the transport mechanism of D-glucose across microvillous membrane was facilitated diffusion. 2. The uptake of L-alanine into microvillous membrane vesicles depended on Na+ gradient (extravesicular greater than intravesicular), so that the transport mechanism of L-alanine across microvillous membrane was a secondary active one. The transport of L-alanine into vesicles prepared from term placenta increased prominently compared to that of early placenta. On the other hand, the transport activity of D-glucose into vesicles prepared from term placenta did not differ from that of early placenta.

Alanine↗
PubMed1986

Polyclonal B cell activation by a B cell differentiation factor, B151-TRF2. II. Evidence for interaction of B151-TRF2 with glycoprotein on B cell membrane via recognition of terminal N-acetyl-D-glucosamine residue(s).

We investigated the role of carbohydrates in the interaction of a B cell differentiation factor designated as B151-TRF2 derived from B151K12 T cell hybridoma with the corresponding receptor on B cells. Induction of polyclonal differentiation of unprimed B cells into IgM-secreting cells by B151-TRF2 was specifically inhibited by addition of N-acetyl-D-glucosamine (GlcNAc) but not by structurally unrelated monosaccharides such as D-galactose, D-glucose, and N-acetyl-D-galactosamine (GalNAc). Absorption of B151-TRF2 activity with spleen cells was specifically inhibited by the presence of GlcNAc. These results indicate that GlcNAc residues are involved in the interaction of B151-TRF2 with the receptor on B cells. To gain insight into mechanism by which GlcNAc inhibits B151-TRF2-mediated B cell responses, the existence of GlcNAc residues was examined on the B151-TRF2 molecule and the corresponding receptor on the B cell surface. The results revealed that B151-TRF2 molecule was not bound to various lectin-coupled agarose beads so far tested, suggesting absence of carbohydrate moieties on the B151-TRF2 molecule. By contrast, pretreatment of spleen cells with trypsin or glycosidase mixture abolished their ability to absorb B151-TRF2 activity. Moreover, B151-TRF2-absorbing ability of spleen cells disappeared by the pretreatment with beta-N-acetylglucosaminidase, which cleaves terminal GlcNAc. The fact that pnitrophenyl (PNP)-GlcNAc specifically inhibited such enzyme activity on target cells indicates that terminal GlcNAc on the B cell surface plays a crucial role in the interaction with B151-TRF2 molecule. Interestingly, it was also found that B151-TRF2 activity was trapped and eluted from GlcNAc-coupled agarose beads. Taken collectively, these results strongly suggest that B cell membrane receptors for B151-TRF2 comprise glycoproteins with a terminal GlcNAc residue(s), and that binding of B151-TRF2 with terminal GlcNAc on the receptor is important for the subsequent activation of B cells.

Acetylglucosamine↗
PubMed1986

Identification of two distinct factors, B151-TRF1 and B151-TRF2, inducing differentiation of activated B cells and small resting B cells into antibody-producing cells.

We demonstrated previously that cellfree supernatant of the B151K12 T cell hybridoma (B151-CFS) contained T cell-replacing factor (here in after referred to as B151-TRF1) capable of inducing growth and differentiation of antigen-activated B cells into antigen-specific plaque-forming cells (PFC). In the present study, we have identified in B151-CFS another unique lymphokine activity (referred to as B151-TRF2), which induces polyclonal differentiation of unstimulated B cells into IgM-secreting cells without concomitant stimulation of antigen, mitogen, or anti-Ig antibody. The B151-TRF2 activity induced polyclonal IgM PFC responses via the action on surface Ig-positive small resting B cells from normal unprimed mice. This activation was effective across an H-2 barrier, and apparently independent of the presence of T cells and accessory cells. Interestingly, the B151-TRF2 activity notably stimulated B cells of neonatal and mutant DBA/2Ha mice, which are nonresponders to B151-TRF1, whereas it failed to activate the xid B cells from CBA/N mice. To substantiate that B151-TRF1 and B151-TRF2 activities are mediated by mutually distinguishable molecules, an absorption experiment of B151-CFS was performed by utilizing DBA/2Ha B cells which are lacking in B151-TRF1 receptor. It was found that DBA/2Ha B cells could absorb B151-TRF2 activity but not B151-TRF1 activity. In contrast, murine chronic B cell leukemia BCL1 cells, which were shown to differentiate into IgM-secreting cells by stimulation with B151-CFS, selectively removed B151-TRF1 activity but not B151-TRF2 activity. Furthermore, biochemical analysis revealed that the B151-TRF2 was a heat (56 degrees C for 30 min)-sensitive protein with an apparent m.w. of 30,000 by gel filtration, whereas B151-TRF1 was a heat-resistant glycoprotein with m.w. of 50,000. In addition, it was shown that prostaglandin E2 selectively inhibited B151-TRF2-mediated B cell responses. These results demonstrate clearly that B151-TRF1 and B151-TRF2 are distinct B cell differentiation factors involved in the different activation pathways of distinct B cell subpopulations. The immunologic implication of B151-TRF2 activity in B cell differentiation is discussed in comparison with other lymphokines so far reported to activate small resting B cells.

Animals↗
PubMed1986

Cortical and tectal afferent terminals in the suprageniculate nucleus of the cat.

The suprageniculate nucleus (Sg) of the cat was observed electron microscopically after wheat germ agglutinin-horseradish peroxidase (WGA-HRP) injection into the anterior ectosylvian visual cortical area (AEV) and superior colliculus (SC). Small axon terminals filled with round synaptic (RS) vesicles were labeled with HRP injected into the AEV and SC, whereas large axon terminals containing round synaptic (RL) vesicles were labeled after HRP injection in the SC. After producing a lesion in the AEV and adjoining orbito-insular cortex and injecting WGA-HRP into the SC, degenerated terminals and HRP-labeled RS terminals were occasionally found to make synaptic contacts with a single dendritic profile of Sg neurons.

Animals↗
PubMed1986

Connections of the anterior ectosylvian visual area (AEV).

We have previously described a visual area situated in the cortex surrounding the deep infolding of the anterior ectosylvian sulcus of the cat (Mucke et al. 1982). Using orthograde and retrograde transport methods we now report anatomical evidence that this anterior ectosylvian visual area (AEV) is connected with a substantial number of both cortical and subcortical regions. The connections between AEV and other cortical areas are reciprocal and, at least in part, topographically organized: the rostral AEV is connected with the bottom region of the presylvian sulcus, the lower bank of the cruciate sulcus, the rostral part of the ventral bank of the splenial sulcus, the rostral portion of the lateral suprasylvian visual area (LS) and the lateral bank of the posterior rhinal sulcus; the caudal AEV is connected with the bottom region of the presylvian sulcus, the caudal part of LS, the ventral part of area 20 and the lateral bank of the posterior rhinal sulcus. Subcortically, AEV has reciprocal connections with the ventral medial thalamic nucleus (VM), with the medial part of the lateralis posterior nucleus (LPm), as well as with the lateralis medialis-suprageniculate nuclear (LM-Sg) complex. These connections are also topographically organized with more rostral parts of AEV being related to more ventral portions of the LPm and LM-Sg complex. AEV also projects to the caudate nucleus, the putamen, the lateral amygdaloid nucleus, the superior colliculus, and the pontine nuclei. It is concluded that AEV is a visual association area which functionally relates the visual with both the motor and the limbic system and that it might play a role in the animal's orienting and alerting behavior.

Afferent Pathways↗
PubMed1986

Ethyl 2-cyanoacrylate as an embolic agent for cranial arteriovenous malformations. An experimental study.

Physical properties of ethyl 2-cyanoacrylate (Aron Alpha) were studied in comparison with isobutyl 2-cyanoacrylate (IBCA). Aron Alpha is characterized by high viscosity, a short polymerization time, low spreadability and low fragmentability. On the other hand, IBCA had low viscosity, a relatively long polymerization time, high spreadability and high fragmentability. Based on these findings, it is suggested that IBCA is suitable for transcatheter embolization, and Aron Alpha for intraoperative embolization. Mixture of IBCA with 5% Aron Alpha suppressed the spreadability and the fragmentability of IBCA, resulting in reduction of distal migration of IBCA into the venous system.

Adhesives↗
PubMed1986

[Morphologic and metabolic studies on the effect of ethane-1-hydroxy-1, 1-diphosphonate (EHDP) on the epiphyseal plate and metaphysis of the rat].

Ethane-1-hydroxy-1, 1-diphosphonate (EHDP) has been widely used in recent clinical and laboratory investigations. The author examined epiphyseal and metaphyseal morphology as well as cartilage matrix and calcium metabolism during EHDP administration and after drug discontinuation by 35S, 45Ca and 3H-thymidine autoradiographic study. The effect of low-dose EHDP was limited to osteoclast dysfunction of the metaphysis with resultant widening of trabeculae. High dose administration of EHDP induces a variety of disorders with a manifestation of marked widening of the epiphyseal growth plate. This process is probably derived from a reduction in matrix calcification that relates an inhibition of chondrocyte metabolism with a resultant decreased rate of chondroitin sulfate turnover. Furthermore, high dose EHDP causes a metaphysis which exhibits rickets+-like changes with little calcification and a decrease in the normal rate of osteoprogenitor cell differentiation to osteoblasts and osteocytes.

Animals↗