Biomedical subjects

K Oiwa

Publications and source records attributed to K Oiwa.

At least 37 records · Page 2Linked to original sources

PubMed1997

Control of actin moving trajectory by patterned poly(methylmethacrylate) tracks.

Poly(methylmethacrylate) (PMMA), a photoresist polymer, was found to be useful for immobilizing heavy meromyosin (HMM) molecules while retaining their abilities to support the movement of actin filaments. PMMA substrate was spin-coated on a coverslip, and various shapes of PMMA tracks, such as straight lines, concentric circles, and alphabetical letters, were fabricated by UV photolithography. An observation by a Tapping mode atomic force microscope (AFM) shows that the typical circular tracks were 1-2 microns wide and about 200 nm high. In in vitro motility assay, a solution of HMM molecules was applied to immobilize the molecules on the tracks by adsorption, and movement of actin filaments labeled with tetramethylrhodamine-phalloidin were observed in the presence of ATP by using an epifluorescence microscope and an image-intensified CCD camera. Actin filaments were seen to move precisely only on the PMMA tracks, and their traces drew the exact shapes of the tracks. The mean velocity of actin movement on the PMMA was 4.5 mm/s at 25 degrees C, and it was comparable to that on a conventionally used nitrocellulose film.

Actins↗

PubMed1997

[Bilateral vertebral artery occlusion].

We studied 9 patients with bilateral vertebral artery occlusion (BVAO). BVAO was confirmed using angiography in order to clarify its clinical feature, mechanism, and long term prognosis. Three patients showed bilateral intra-cranial occlusion, 3 bilateral extra-cranial occlusion, and 3 intra and extra-cranial occlusion. The basilar artery was fed by the posterior communicating artery in 8 out of 9 patients. In one of the 8, reconstitution of the thyrocervical artery was seen. We divided the patients into 4 groups according to MRI findings, as follows: Group 1 with no abnormal finding on MRI (N = 2); Group 2 with deep pontine infarcts and non-territorial small cerebellar infarcts (N = 2); Group 3 with extended pontine infarcts (N = 3); and Group 4 with cerebellar cortical artery infarcts, deep pontine infarcts, and non-territorial small cerebellar infarcts (N = 2). Transient episodes were seen in all patients, 8 patients out of 9 had vertigo/dizziness, 3 tinnitus, 2 diplopia, 2 headache, 2 numbness, and 1 hearing disturbance. These episodes preceded a final attack or complete stroke 2 days to 5 months, and those who had a longer period of episodes in the preceding term tended to have less severe deficits. Six of the patients had vertebro-basiler symptoms after being in the upright position, including all the patients in Groups 2 and 4, which had cerebellar border zone/terminal zone infarcts. These results indicate that the hemodynamic mechanism plays an important role in BVAO. The prognosis was not always grave. Four of the patients could walk independently, 2 could walk with a cane, and 3 were bed ridden (2 of which died). Long-term follow-up data (a mean of 5 years) were obtained in all patients. In the patients who could walk, one had asymptomatic cerebellar infarcts, and one had TIAs frequently. Patients with BVAO often also have TIAs and/or preceding episode and show cerebellar border zone/terminal zone infarcts. This research strongly suggests that hemodynamic mechanism might play an important role in BVAO, and that paying attention to border zone infarction in MRI and transient episodes can lead to earlier diagnosis and treatment.

Activities of Daily Living↗

PubMed1997

[Bilateral caudate head infarcts].

We reported a 67-year-old woman with bilateral caudate head infarcts. She developed sudden mutism followed by abulia. She was admitted to our hospital 2 months after ictus for further examination. She showed prominent abulia and was inactive, slow and apathetic. Spontaneous activity and speech, immediate response to queries, spontaneous word recall and attention and persistence to complex programs were disturbed. Apparent motor disturbance, gait disturbance, motor aphasia, apraxia and remote memory disturbance were not identified. She seemed to be depressed but not sad. Brain CT and MRI revealed bilateral caudate head hemorrhagic infarcts including bilateral anterior internal capsules, in which the left lesion was more extensive than right one and involved the part of the left putamen. These infarct locations were thought to be supplied by the area around the medial striate artery including Heubner's arteries and the A1 perforator. Digital subtraction angiography showed asymptomatic right internal carotid artery occlusion. She bad had hypertension, diabetes mellitus and atrial fibrillation and also had a left atrium with a large diameter. The infarcts were thought to be caused by cardioembolic occlusion to the distal portion of the left internal carotid artery. Although some variations of vasculature at the anterior communicating artery might contribute to bilateral medial striate artery infarcts, we could not demonstrate such abnormalities by angiography. Bilateral caudate head infarcts involving the anterior internal capsule may cause prominent abulia. The patient did not improve by drug and rehabilitation therapy and died suddenly a year after discharge.

Aged↗

PubMed1995

Force-velocity relations of rat cardiac myosin isozymes sliding on algal cell actin cables in vitro.

The difference in kinetic properties between two myosin isozymes (V1 and V3) in rat ventricular myocardium was studied by determining the steady-state force-velocity (P-V) relations in the ATP-dependent movement of V1 and V3-coated polystyrene beads on actin cables of giant algal cells mounted on a centrifuge microscope. The maximum unloaded velocity of bead movement was larger for V1 than for V3. The velocity of bead movement decreased with increasing external load applied by the centrifuge microscope, and eventually reached zero when the load was equal to the maximum isometric force (P0) generated by the myosin heads. The maximum isometric force P0 was less than 10 pN, and did not differ significantly between V1 and V3. The P-V curves consisted of a hyperbolic part in the low force range and a non-hyperbolic part in the high force range. The critical force above which the curve deviated from the hyperbola was much smaller for V1 than for V3. An analysis using a model with an extremely small number of myosin heads involved in the bead movement suggested a marked difference in kinetic properties between V1 and V3.

Actins↗

PubMed1995

Diminished nocturnal blood pressure decline and lesion site in cerebrovascular disease.

BACKGROUND AND PURPOSE: Many studies have suggested that diminished nocturnal blood pressure decline in hypertensive cardiovascular disease is associated with the extent of hypertensive vascular disease. In our previous observation of cerebrovascular disease, however, we found reduced nocturnal blood pressure decline to be associated not only with the extent of hypertensive vascular disease but also with the specific location of cerebrovascular lesions. The purpose of this study was to elucidate the mechanism of nocturnal blood pressure decline in cerebrovascular disease. Moreover, to clarify whether reduced nocturnal blood pressure decline occurs before cerebrovascular disease, we examined patients with recurring episodes. METHODS: Ambulatory blood pressure monitoring was carried out every 30 minutes in 14 control subjects, 15 hypertensive subjects, 90 patients with cerebrovascular disease (16 single lacunar infarctions, 15 multiple lacunar infarctions, 10 putaminal hemorrhages, 14 thalamic hemorrhages, 11 pontine base infarctions, 15 pontine tegmentum infarctions, 8 pontine hemorrhages, 13 wide cortical infarctions), and 7 patients with recurring stroke episodes. The percentage of nocturnal blood pressure decline and the correlations for systolic blood pressure and heart rate were calculated. RESULTS: The percentage of nocturnal blood pressure decline was significantly smaller in the groups with multiple lacunar infarction (systolic, P < .001; diastolic, P < .01), thalamic hemorrhage (P < .01, P < .05), pontine tegmentum infarction (P < .01, P < .05), and pontine hemorrhage (both P < .05). The correlation between systolic blood pressure and heart rate was not significant for almost all the groups with diminished blood pressure decline. CONCLUSIONS: Diminished nocturnal blood pressure decline in cerebrovascular disease is thought to be caused by specific injury to the central autonomic nervous system such as the striatum, diencephalon, midbrain, and pontine tegmentum and their connecting fibers.

Aged↗

PubMed1995

The mode of ATP-dependent microtubule-kinesin sliding in the auxotonic condition.

Kinesin is a motor protein that converts chemical energy derived from ATP hydrolysis into mechanical work to transport cellular components along microtubules. We studied the properties of ATP-dependent microtubule-kinesin sliding with two different in vitro assay systems. In one assay system, a kinesin-coated glass microneedle (elastic coefficient, 1-2.5 pN microns -1) was made to slide along an axoneme. Using this system, we obtained the relationship between the force (= load) on the microneedle and the velocity of microneedle-kinesin sliding in the auxotonic condition, in which the load on the microtubule-kinesin contacts increased as sliding progressed. The force-velocity curve was upwardly convex (maximum velocity Vmax, 0.58 +/- 0.15 microns s-1; maximum isometric force P0, 5.0 +/- 1.6 pN) and was similar to that of in vitro actin-myosin sliding in the auxotonic condition, suggesting that the two motor protein systems have fundamental kinetic properties in common. In the other assay system, an axoneme attached to a glass microneedle (elastic coefficient, 4-5 pN microns -1) was made to slide on a kinesin-coated glass surface (Vmax, 0.68 +/- 0.17 microns s-1; P0, 46.1 +/- 18.6 pN). The change in shape of the axoneme indicated an enormous flexibility of randomly oriented kinesin molecules.

Adenosine Triphosphate↗

PubMed1995

Distinct effect of G-CSF on the growth and differentiation of myeloid progenitor cells from chronic idiopathic neutropenia.

Chronic idiopathic neutropenia (CIN) is a disorder characterized by severe neutropenia and a maturational arrest of the neutrophil precursors in the bone marrow. We examined the effect of recombinant human granulocyte-colony stimulating factor (rhG-CSF) on the growth and maturation of the myeloid progenitor cells from a patient with CIN. The patient's marrow cells showed poor colony forming activity, but a normal differentiating capacity to the stimulation with rhG-CSF, although they displayed a normal colony forming capacity in the presence of GM-CSF. Our observation indicates the distinct effect of rhG-CSF on the growth and maturation of the myeloid progenitors from a CIN patient.

Aged↗

PubMed1993

Dependence of the work done by ATP-induced actin-myosin sliding on the initial baseline force: its implications for kinetic properties of myosin heads in muscle contraction.

The properties of the ATP-dependent actin-myosin sliding responsible for muscle contraction was studied using an in vitro force-movement assay system, in which a myosin-coated glass microneedle was made to slide on actin filament arrays (actin cables) in the giant algal cell with iontophoretic application of ATP. With a constant amount of ATP application, the amount of work done by the actin-myosin sliding increased with increasing baseline force from zero to 0.4-0.6 Po, and then decreased with further increasing baseline force, thus giving a bell-shaped work versus baseline force relation. The result that the maximum actin-myosin sliding velocity did not change appreciably with increasing baseline force up to 0.4-0.6 Po implies, together with the limited number of myosin heads involved, that (1) the rate of power output of actin-myosin sliding is determined primarily by the amount of external load rather than the velocity of actin-myosin sliding, and (2) the bell shaped work versus baseline force relation (and also the hyperbolic force-velocity relation) results from the kinetic properties of individual myosin head rather than the change in the number of myosin heads involved.

Actins↗

PubMed1993

Unitary distance of ATP-induced actin-myosin sliding studied with an in vitro force-movement assay system.

We studied the unitary distance of ATP-induced actin-myosin sliding using an in vitro force-movement assay system consisting of a myosin-coated glass microneedle and well organized actin filament arrays (actin cables) in the internodal cell of an alga Nitellopsis obtusa. The number of myosin heads interacting with actin cables was reduced to about 100, as judged from the isometric force of about 100 pN attained in the presence of 2 mM ATP. When the amount of iontophoretically applied ATP was reduced by decreasing the amount of charge passed through the ATP electrode from 80 to 2 nC, the distance of the ATP-induced actin-myosin sliding decreased almost linearly from about 100 to about 10 nm, no detectable sliding being observed with further reduction of charge through the electrode. The sliding distances with small amounts of ATP (7-16 nC) distributed around integral multiples of 10 nm, suggesting the unitary distance of actin-myosin sliding of about 10 nm.

Actins↗

PubMed1993

Kinetic properties of the ATP-dependent actin-myosin sliding as revealed by the force-movement assay system with a centrifuge microscope.

To study the kinetic properties of the ATP-dependent actin-myosin sliding responsible for muscle contraction, we developed an in vitro force-movement assay system, in which centrifugal forces were applied to myosin-coated polystyrene beads sliding along actin cables of giant algal cells in the presence of ATP. Under constant centrifugal forces directed opposite to the bead movement ("positive" loads), the beads moved with constant velocities. The steady-state force-velocity (P-V) curve thus obtained was double-hyperbolic in shape, being analogous to the P-V curve of single muscle fibers. Under constant centrifugal forces in the direction of the bead movement ("negative" loads), on the other hand, the beads also moved with constant velocities. Unexpectedly, the velocity of bead movement did not increase with increasing negative loads, but decreased markedly (by 20-60%). We also studied the effect of centrifugal forces at right angles with actin cables on the bead movement.

Actins↗

PubMed1993

Relation between magnetically-applied force and velocity in beads coated with rabbit myosin, sliding on actin cables in Nitellopsis cells.

We have succeeded in controlling the sliding movement of myosin-coated magnetizable beads on actin cables in Nitellopsis cells by the inhomogeneous magnetic field adjacent to a small, strong permanent magnet. The relation between magnetic force acting on the bead and the bead velocity was, in many respects, similar to that obtained from the same system by the use of centrifugal force (Oiwa et al., 1990). In particular, force favouring the motion (negative load) had little effect on the velocity until it was sufficient to pull the bead off the actin, whereas a relatively small positive load caused a reduction in velocity to a plateau value. Although the present method does not allow a good control of force direction, it demonstrates the promise of magnetic force in studying in vitro motility.

Actins↗

PubMed1993

Unitary distance of actin-myosin sliding studied using an in vitro force-movement assay system combined with ATP iontophoresis.

To obtain information about the mechanism of ATP-dependent actin-myosin sliding responsible for muscle contraction, we studied the "unitary" distance of sliding between a myosin-coated glass microneedle and actin filament arrays (actin cables) in a giant algal cell induced by iontophoretic application of ATP, attention being focused on the minimum distance of ATP-induced sliding when the amount of applied ATP was gradually decreased in the presence of hexokinase and D-glucose. The number of myosin heads interacting with actin cables was reduced to less than 100, as judged from the maximal force Po (approximately 100 pN) generated by myosin heads on the needle in the presence of 2 mM ATP. When the amount of iontophoretically applied ATP was decreased by reducing the amount of charge passed through the ATP electrode from 80 to 2 nC, the distance of ATP-induced actin-myosin sliding decreased almost linearly from approximately 100 to approximately 10 nm, no detectable actin-myosin sliding being observed with further reduction of the charge passed through the electrode. The amount of external load exerted by the bent microneedle was less than 1% of Po for the sliding distance < 50 nm. The actin-myosin sliding distances with a small amount of ATP slightly above the amount required to induce the minimum sliding distance were distributed around integral multiples of 10 nm, suggesting that the unitary distance of actin-myosin sliding coupled with ATP hydrolysis is of the order of 10 nm.

Actins↗

PubMed1993

Impaired G-CSF production at post-transcriptional level in a patient with chronic idiopathic neutropenia.

Chronic idiopathic neutropenia (CIN) is a disorder characterized by severe neutropenia and a maturational arrest of the neutrophil precursors in the bone marrow. The pathogenesis of this disorder has been obscure. We examined the production of endogenous G-CSF and the expression of G-CSFmRNA in a patient with adult type CIN. The G-CSF production by the patient's mononuclear cells was deficient in spite of the adequate accumulation of G-CSFmRNA. Our data suggests that the defect in the endogenous G-CSF production at the post-transcriptional level is likely to be an aetiological factor in CIN.

Aged↗

PubMed1993

Scanning electron microscopy of the myosin-coated surface of polystyrene beads in a force-movement assay system for ATP-dependent actin-myosin sliding.

We examined the myosin-coated surface of polystyrene beads, which slide on actin filaments in the presence of ATP with characteristics essentially similar to those of contracting muscle, using a high-resolution scanning electron microscope (JSM-890, JEOL). The bead surface was mostly covered with myosin filaments (diameter, 15-45 nm) with helically arranged myosin heads. Considering the amount of force generated by the myosin heads on the bead (approximately 10 pN), this result indicates that the bead movement may be caused by about 10 myosin heads within a short myosin filament segment, but not by randomly oriented myosin heads.

Actins↗

PubMed1991

Measurement of work done by ATP-induced sliding between rabbit muscle myosin and algal cell actin cables in vitro.

1. The basic properties of the ATP-dependent actin-myosin interaction responsible for muscle contraction were studied using an in vitro force-movement assay system, in which a glass microneedle coated with rabbit skeletal muscle myosin was made to slide on the actin filament arrays (actin cables) in the internodal cell of an alga Nitellopsis obtusa with ionophoretic application of ATP. 2. In response to an ATP current pulse (intensity, 5-85 nA; duration, 0.5-10 s), the myosin-coated needle moved for a distance and eventually stopped, indicating reformation of rigor actin-myosin linkages to prevent elastic recoil of the bent needle. A subsequent ATP current pulse again produced the needle movement starting from the baseline force attained by the preceding needle movement. 3. With a constant amount of ATP application, the amount of work done by the ATP-induced actin-myosin sliding first increased with increasing baseline force from zero to 0.4-0.6P0, and then decreased with further increasing baseline force, thus giving a bell-shaped work versus baseline force relation. 4. With increasing amount of ATP application, the amount of work done by the actin-myosin sliding increased more steeply as the baseline force was increased from zero to 0.4-0.6P0. 5. These results are discussed in connection with the basic properties of the actin-myosin sliding in muscle contraction.

Actins↗

PubMed1991

Expression of terminal deoxynucleotidyltransferase gene in a case of adult T-cell leukemia.

A 37-year-old male from Kagoshima Prefecture was admitted with adult T-cell leukemia (ATL). Monoclonal integration of HTLV-1 proviral DNA was found, but the integration site was different from that of terminal deoxynucleotidyltransferase (TdT)-positive MT-1 cells (an ATL cell line). The ATL cells expressed enzymatically active TdT and exhibited 2100 b TdT mRNA, which corresponds to the thymus type of TdT mRNA. The same size of TdT mRNA was also detected in MT-1. Southern blot analyses revealed no differences in the gene structure of the promoter region of TdT genes between this ATL case and TdT-positive lymphoblastic leukemia cells. There is little possibility that cis-acting viral elements promote TdT gene expression by proviral integration. The activation of TdT gene in ATL may be mediated by other trans-acting factors.

Adult↗

PubMed1990

A case of infantile acute monocytic leukemia caused by vertical transmission of the mother's leukemic cells.

A case of infantile acute monocytic leukemia (AMoL), which was probably transmitted from a pregnant woman with leukemia to her unborn infant, is presented. A woman had AMoL when her third infant was born. This infant, who was a boy, also suffered from AMoL when he was 20 months of age. The infant's leukemic cells had the same cytochemical and immunophenotypic patterns as the mother's leukemic cells. By cytogenetic analysis, the majority of the infant's leukemic marrow cells had the 46,XX karyotype and showed no Y body by quinacrine staining. Moreover, the phenotype for human major histocompatibility system, HLA-A, HLA-B, and HLA-DR of the infant's leukemic cells was consistent with that of the mother's lymphocytes. Thus, the infant's leukemic clone was found to be identical to the mother's leukemic clone. His lymphocytes could not react with the mother's leukemic cells or his own leukemic cells in mixed lymphocyte culture, suggesting that the HLA homozygosity of the mother may have played a role in inducing immunologic tolerance to the immigrated leukemic cells in the infant. This is the first report of an infantile leukemia transmitted from a mother with leukemia, supposedly through the placenta.

Adult↗

PubMed1990

Steady-state force-velocity relation in the ATP-dependent sliding movement of myosin-coated beads on actin cables in vitro studied with a centrifuge microscope.

To eliminate the gap between the biochemistry of actomyosin in solution and the physiology of contracting muscle, we developed an in vitro force-movement assay system in which the steady-state force-velocity relation in the actin-myosin interaction can be studied. The assay system consists of the internodal cells of an alga, Nitellopsis obtusa, containing well-organized actin filament arrays (actin cables); tosyl-activated polystyrene beads (diameter, 2.8 microns; specific gravity, 1.3) coated with skeletal muscle myosin; and a centrifuge microscope equipped with a stroboscopic light source and a video system. The internodal cell preparation was mounted on the rotor of the centrifuge microscope, so that centrifugal forces were applied to the myosin-coated beads moving along the actin cables in the presence of ATP. Under constant centrifugal forces directed opposite to the bead movement ("positive" loads), the beads continued to move with constant velocities, which decreased with increasing centrifugal forces. The steady-state force-velocity curve thus obtained was analogous to the double-hyperbolic force-velocity curve of single muscle fibers. The unloaded velocity of bead movement was 1.6-3.6 microns/s (20-23 degrees C), while the maximum "isometric" force generated by the myosin molecules on the bead was 1.9-39 pN. If, on the other hand, the beads were subjected to constant centrifugal forces in the direction of bead movement ("negative" loads), the bead also moved with constant velocities. Unexpectedly, the velocity of bead movement did not increase with increasing negative loads but first decreased by 20-60% and then increased towards the initial unloaded velocity until the beads were eventually detached from the actin cables.

Actins↗