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Biomedical subjects

K Kanno

Publications and source records attributed to K Kanno.

At least 91 records · Page 5Linked to original sources

Comparative studies of carbohydrate-binding proteins from Xenopus laevis skin and eggs. Sugar-binding specificities and affinity purification.

Salt and detergent extracts of acetone-dried powder of Xenopus laevis skin and eggs were fractionated on sugar-Sepharose columns, to which lactose, melibiose, galactose, rhamnose and mannose had been covalently linked, by successive elution with chelating reagent and specific sugars, resulting in separation of the different Ca2(+)-dependent and Ca2(+)-independent carbohydrate-binding proteins. The skin of X. laevis contains a salt-extractable Ca2(+)-dependent lactose-binding lectin of 30 kilodalton (kDa) and the eggs a similar lectin of 43 kDa, but they both lack Ca2(+)-dependent galactose-binding lectins. The 30 kDa lactose-binding lectin which agglutinates human A erythrocytes was isolated by successive affinity chromatography on two linked sugar-Sepharose columns, i.e., a galactose-Sepharose-lactose-Sepharose (GL) column system. Since the 30 kDa lectin was not recovered in the Ca2(+)-dependent lactose-binding protein fraction from the GL column system under the dithiothreitol (DDT)-free conditions, it was concluded that the lectin requires the presence of DTT and calcium for binding to the lactose-Sepharose column.

Animals↗

Effect of endothelin-1 on release of arginine-vasopressin from perifused rat hypothalamus.

Endothelin-1 (ET-1) is an endothelium-derived vasoconstrictor peptide with potent pressor activity. We studied the effect of ET-1 on release of arginine-vasopressin (AVP) from perifused rat hypothalamus. ET-1 (10(-10) to 10(-8) M) significantly stimulated AVP release. The ET-1-induced AVP release was completely blocked in the presence of nicardipine. Our results suggest a possible involvement of ET in the regulation of AVP release.

Animals↗

Smooth muscle gelsolin and a Ca2+-sensitive contractile cell model.

Smooth muscle gelsolin, termed smooth muscle 90-kDa protein in our previous paper (Kanno et al. FEBS Lett. 1985; 184:202-206), was purified from bovine aorta. Antibody prepared against smooth muscle gelsolin was used to detect the presence of gelsolin in human lung fibroblast MRC-5 cells permeabilized with Triton X-100 (MRC-5 cell models). These cells contracted in the presence of MgATP and Ca2+ in doses over 1 microM. Immunofluorescence microscopy using phalloidin and antigelsolin antibody showed that gelsolin was distributed along the stress fibers, except for a marginal bundle of cells, when MRC-5 cells were growth-arrested in serum-depleted medium. Making use of immunoblotting and indirect immunofluorescence techniques, we demonstrated that gelsolin is not retained in the MRC-5 cell models. We used purified smooth muscle gelsolin as a specific agent to sever the actin filaments. Preincubation of MRC-5 cell models with gelsolin led to a destruction of stress fibers, in a dose- and Ca2+ -dependent manner. The contractility was also lost, in the same manner described above, thereby indicating that a continuous distribution of actin filaments within the stress fibers is required for cell contraction. Treatment of MRC-5 cells with the Ca2+ ionophore A23187 induced an extracellular Ca2+ -dependent contraction but not a massive destruction of stress fibers, thereby indicating that most of the endogenous gelsolin was inactive under these conditions. Our interpretation of these results is that increases in cytoplasmic Ca2+ concentrations are sufficient for the contraction but may be too transient to activate endogenous gelsolin and thereby disrupt the stress fibers. Indeed, the inhibition of contraction of the MRC-5 cell, as induced by smooth muscle gelsolin, required preincubation in the presence of Ca2+, before the addition of MgATP. These results suggest that destruction of the stress fibers by endogenous gelsolin, which leads to inhibition of cell contraction, may occur if the cytoplasmic Ca2+ is maintained at high concentrations for a few minutes.

Animals↗

[Quantitative evaluation of perspiration with equipment for continuous recording of local perspiration volume (II): Hyperhidrosis and hypohidrosis (or anhidrosis)].

To objectively evaluate perspiration volume, we tried to measure the perspiration volume from 6 cases of hyperhidrosis and 4 cases of hypo-(or an-) hidrosis using recently developed equipment for continuous recording of local perspiration volume. Patients with hyperhidrosis were loaded with various factors to possibly influence the perspiration volume, and the effects were compared. The results revealed: 1) The measurement of local perspiration volume with this equipment provides objective data useful for the diagnosis of hyperhidrosis and hypo-(or an-) hidrosis and for the judgement of its grade; 2) in case of palmar hyperhidrosis, mental stimuli most strongly induced perspiration; and 3) the responses to mental arithmetic or hand grasping and the base-line stable time are reliable parameters for measurement of perspiration volume.

Adolescent↗

[Evaluation of a measurement method for perspiration volume using newly developed equipment for continuous recording of local perspiration volume (Kenz-Perspiro) (I)].

Using newly developed equipment for continuous recording of local perspiration volume, we have tried to standardize the measurement of perspiration volume and evaluate it. This equipment enables continuous determination of local perspiration volume more easily and accurately than the ventilation method ordinarily used. Induced perspiration was measured on the inner surface of the right thumbs of 20 healthy male and female volunteers. Four inducing factors, grasping the hand with warm and cold hand mental arithmetic, and deep breathing, were used as stimulations. Perspiration induced by each factor was compared and evaluated. As a result it was concluded that the stimulation of mental arithmetic was the most stable and reliable factor. Another measurement factor, base line stable time from mounting the equipment, was also a considerably reliable measurement basis for evaluating the perspiration volume and mental state.

Adolescent↗

Disorganization by calcium antagonists of actin microfilament in aortic smooth muscle cells.

To assess the physiological role of intracellular Ca2+ in the organization of actin microfilaments in smooth muscle cells, we employed several types of Ca2+ antagonists. The rabbit aortic smooth muscle cells treated with the putative intracellular Ca2+ antagonist 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB 8) at 5-100 microM showed a loss or a decrease in size and length of the actin-containing microfilament structure in a dose-dependent manner. Similar disorganization of actin structure was observed in the smooth muscle cells treated with 1-(5-isoquinolinesulfonyl)-homopiperazine (HA 1077) at 5-100 microM, which is a new type of Ca2+ antagonist different from Ca2+ entry blocker. In contrast, 100 microM verapamil and diltiazem induced no reorganization of the actin microfilament structure. Antimycin A decreased the ATP levels in smooth muscle cells and disorganized the actin-containing structure. Unlike antimycin A, TMB 8 and HA 1077 did not lower the ATP level below the threshold needed to maintain the actin filament structure. Both TMB 8 and HA 1077 directly interacted with neither the actin monomer nor F-actin in a viscometrical assay system. Thus these reagents may induce the disorganization of actin microfilament structure in smooth muscle cells through the indirect reaction(s) with the actin, suggesting that an appropriate level of ATP and Ca2+ and/or its involving reactions may be essential for maintenance of the actin structure.

Actin Cytoskeleton↗

A Ca2+-sensitive actin regulatory protein from smooth muscle.

Using a procedure involving DNase I affinity chromatography and Sephadex G-200 gel filtration, we partially purified a Ca2+-sensitive actin regulatory 90-kDa protein from bovine aorta. The 90-kDa protein existed in the form of a complex with actin on a DNase I column even in the presence of 5 mM EGTA, indicating that the 90-kDa protein binds tightly to actin in a Ca2+-insensitive manner. The isolation procedure described above indicates that the 90-kDa protein is present in smooth muscles including aorta, uterus and bladder, but not in skeletal and heart muscles. When added to G-actin before polymerization, the 90-kDa protein increases the initial rate of actin polymerization and lowers the final viscosity at Ca2+ concentrations greater than 10(-7) M. This decrease in viscosity is due to the generation of filaments which cannot be readily sedimented.

Actin Depolymerizing Factors↗

[Factors influencing the development of low output state in patients with right ventricular infarction].

Right ventricular infarction is frequently accompanied by a low output state, but the factors influencing the development of this state remain unknown. To elucidate these factors, clinical findings, hemodynamic findings and left ventricular infarct size (T1-score) calculated from thallium-201 myocardial scintigrams by a circumferential profile method were evaluated in 147 consecutive patients with acute transmural inferior myocardial infarction. They were divided into two groups: 44 patients with right ventricular involvement (RVI group) and 103 patients without right ventricular involvement (IMI group). A low cardiac output state was defined when the cardiac index was less than 2.2 L/min/M2. There was a good correlation between T1-score and any of peak value of serum creatine phosphokinase (CPKmax), total released CPK (CPKr) and left ventricular ejection fraction (LVEF) (r = 0.66, 0.74 and -0.54, respectively), indicating the usefulness of T1-score as an index of left ventricular damage. Compared to the IMI group, the RVI group showed a higher average of age (p less than 0.01), lower systemic blood pressure (p less than 0.01), higher right atrial pressure (p less than 0.001) and lower cardiac index (p less than 0.01). Furthermore, the incidence of a low output state (RVI group : 47.7% vs IMI group : 14.6%, p less than 0.001) and mortality (25.0% vs 7.8%, p less than 0.01) were higher in the RVI group. However, CPKmax, CPKr, LVEF and T1-score, which were considered to reflect the severity of left ventricular damage, were not different between the two groups. T1-score was inversely correlated with cardiac index in the RVI group (r = -0.49, p less than 0.05), and with left ventricular stroke work index in the both groups (RVI group; r = -0.46, p less than 0.01, IMI group; r = -0.64, p less than 0.01). Additionally, age as well as heart rate was correlated significantly with cardiac index (r = -0.45, p less than 0.001 and r = 0.35, p less than 0.001, respectively), and the percentage of elderly patients (age greater than 60 years) and the incidence of bradycardia (heart rate less than 60/min) were both higher in the RVI group than the IMI group (either p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗

Interaction of psychotropic drugs with phospholipids.

The interactions of psychotropic drugs with phospholipids, including lysophosphatidylcholine, phosphatidylinositol, and lysophosphatidylserine, were studied using calmodulin-dependent cyclic nucleotide phosphodiesterase partially purified from the cortex of hog brain. All the compounds used inhibited both calmodulin- and phospholipid-stimulated phosphodiesterase activity but not the basal activity. Fluphenazine was confirmed by kinetic analysis to be a competitive inhibitor, with both calmodulin and phospholipid. Using fluphenazine-Sepharose affinity chromatography, it was demonstrated that fluphenazine did not interact with the enzyme. The potencies of antipsychotics such as fluphenazine in inhibiting the various phospholipid-dependent activations decreased in the following order: lysophosphatidylcholine-, phosphatidylinositol-, and lysophosphatidylserine-dependent activation. On the other hand, antidepressant drugs exhibited similar inhibitory potencies towards lysophosphatidylcholine- and phosphatidylinositol-dependent activation. Antipsychotic and antidepressant drugs appear to have different characteristics with regard to lipid-drug interaction.

3',5'-Cyclic-AMP Phosphodiesterases↗

Disturbance of serum lipid metabolism in acute renal failure.

Serial studies of serum lipids were performed on five patients with acute renal failure (ARF) due to five different causes (Of five patients one did not achieve complete recovery.). There were striking alterations in serum lipid levels at the period of oliguria in all patients, characterized by an increase in triglycerides (TG) and an extreme decrease in HDL-cholesterol (HDL-C). These conditions gradually returned to normal as the patients improved. The restoration to normal of the altered lipid levels were preceded by normalization of serum creatinine (S-Cr) and followed by creatinine clearance (Ccr). These fluctuational patterns of the lipid levels in the course of illness were observed similarly in all patients who recovered, despite the difference in the cause of their diseases. Improvement of the lipid metabolism was not observed in the one patient who did not recover. These results suggest that the alteration in lipid metabolism of ARF is due to renal impairment and not related to uremic state per se.

Acute Kidney Injury↗