Search PubMed⌕ Search

Biomedical subjects

K Muraki

Publications and source records attributed to K Muraki.

At least 37 records · Page 2Linked to original sources
PubMed2001

Massive rhabdomyolysis and acute renal failure after acetonitrile exposure.

A case of systemic rhabomyolysis after acetonitrile exposure is reported. A 35-year-old previously healthy man suffered from vomiting, convulsion and consciousness loss 15 hours after exposure to acetonitrile. Since acetonitrile is known to be metabolized into cyanide, antidote therapy against cyanide poisoning was given. On admission, pain and all-over muscle swelling were marked. Although the initial therapy was effective, rhabdomyolysis and then acute renal failure developed. Renal function improved very slowly after six weeks of hemodialysis, but atrophy of the muscles remained. The rhabdomyolysis may have been caused by toxicity of the cyanide itself in combination with hypoxia and convulsion.

Acetonitriles↗
PubMed2000

Nifedipine and nisoldipine modulate membrane potential of vascular endothelium via a myo-endothelial pathway.

Effects of nifedipine (Nif) and nisoldipine (Nis), dihydropyridine Ca2+ channel blockers (DHPs) on membrane potential and currents of endothelial cells, which are enzymatically dispersed (dis-ECs) from or exist in arterial segments (seg-ECs) of rabbit and rat aorta, were examined. Outward currents induced by 1-10 microM acetylcholine (ACh) in dis-ECs were neither affected by a receptor operated Ca2+ channel blocker, SK&F 96365 (SKF), nor DHPs. ACh hyperpolarized dis-ECs and seg-ECs by 15-20 mV, whereas phenylephrine (Phe) elicited oscillatory depolarization in seg-ECs but not in dis-ECs. The Phe-induced response in seg-ECs was significantly inhibited by treatment with 18beta-glycyrrhetinic acid, a disrupter of gap junctions. Application of 0.3 microM Nif or Nis effectively inhibited the Phe-induced oscillatory depolarization, while these DHPs did not affect ACh-induced hyperpolarization in seg-ECs. The lack of effect on dis-ECs indicates that DHPs have little effect on dis-ECs themselves, nevertheless DHPs inhibit the Phe-induced endothelial potential oscillation which is conducted from smooth muscle cells via a myo-endothelial pathway.

Animals↗
PubMed2000

Cromakalim-induced membrane current in guinea-pig tracheal smooth muscle cells.

The characteristics of the cromakalim-induced membrane current were examined in single tracheal myocytes of the guinea-pig under voltage-clamp conditions. When K(+) concentrations in the pipette and bathing solutions were approximately 140 mM, cromakalim activated a membrane current (I(crom)) which was inward at -60 mV and reversed at -2 mV. I(crom) was blocked by 10 microM glibenclamide and potentiated when the ATP concentration in the pipette solution was decreased. The K(d) and Hill coefficient of glibenclamide for I(crom) block were 200 nM and 1.05, respectively. Application of the tyrosine kinase inhibitors, genistein and alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamid (ST638), reduced I(crom) in a concentration-dependent manner. Daidzein, which does not inhibit tyrosine kinase, was about 10 times less effective than genistein. Herbimycin A had no effect on I(crom). Internal application of these inhibitors from the pipette did not affect I(crom). In conclusion, cromakalim is a potent activator of the ATP-sensitive K(+) channel (K(ATP) channel) in guinea-pig tracheal myocytes. The inhibition of I(crom) by genistein and ST638 may be due to the direct block of the channel from outside.

Adenosine Triphosphate↗
PubMed2000

Two pathogenic point mutations exist in the authentic mitochondrial genome, not in the nuclear pseudogene.

Technical advancements in molecular genetics have shown various mitochondrial DNA (mtDNA) abnormalities in patients with mitochondrial myopathies. Recently, it has been revealed that, in these patients, the nuclear DNA carries sequences similar to those of the mtDNA (nuclear pseudogene) and it has several point mutations previously reported to be pathogenic. We verified the existence of the T3250C and T3291C mutations, which we have found in patients with mitochondrial myopathy, in the authentic mitochondrial genome. A long polymerase chain reaction provides a powerful tool for avoiding nuclear pseudogene amplification and for ruling out ambiguity in the detection of the mutation for diagnosis.

DNA, Mitochondrial↗
PubMed2000

4-Nonylphenols and 4-tert-octylphenol in water and fish from rivers flowing into Lake Biwa.

Surveys of 4-nonylphenols (NOs) and 4-tert-octylphenol (OC) were performed for water and fish samples obtained from eight rivers flowing into Lake Biwa once every two months from April 1998 to March 1999. For water samples, NOs were detected all the year round (0.11-3.08 ng ml(-1)) at high frequency (48/48) in the eight rivers. OC was detected at lower concentrations (ND approximately 0.09 ng ml(-1)) and at lower frequency (23/48). The concentrations of NOs in the river water always showed minimum values at 5-8 degrees C in winter. It was presumed that the formation of NOs by the biotransformation of nonylphenol polyethoxylates decreased much in the sludge treatment of nonionic surfactants at the low temperature (5-8 degrees C) in winter. Average BCF values of NOs and OC in the six kinds of fish were calculated from the field data. The field BCF values of NOs 15-31 in the six kinds of fish were lower than the laboratory BCF values of 167 in Killifish and 282 in Salmon. For OC, the field BCF values 129-297 for the three kinds of fish were nearly equal to the laboratory BCF value, 261, in Killifish.

Animals↗
PubMed2000

Two cases of non-Hodgkin's lymphoma in first degree relatives.

Two cases of non-Hodgkin's lymphoma (NHL) generated within 6 months in first degree relatives, a father and a son, are presented. The NHL was a diffuse large B-cell type in the father and a small cleaved follicular type in the son. Cytogenetic and molecular studies of the lymphoma cells revealed the rearrangement of the immunoglobulin heavy chain (JH) gene in both patients, the mutation of p53 gene in the father and t(14; 18) (q32; q21) in the son. Both patients had low serum immunoglobulin levels. It is not known whether the occurrence of NHL in this family was incidental or pathogenetically related, since there was no clear common molecular abnormality between the father and the son. The pathogenetic mechanism of this familial occurrence of NHL is discussed.

Adult↗
PubMed2000

Conserved smooth muscle contractility and blood pressure increase in response to high-salt diet in mice lacking the beta3 subunit of the voltage-dependent calcium channel.

Voltage-dependent calcium channels are crucially important for calcium influx and the following smooth muscle contraction. Beta subunits of these channels are known to modify calcium currents through pore-forming alpha subunits. Among the four reported independent beta subunits, the beta3 subunit is expressed in smooth muscle cells and thought to compose L-type calcium channels in the tissue. To determine the role of the beta3 subunit in the cardiovascular system, we have analyzed beta3-null mice. Electrophysiological examinations proved the existence of dihydropyridine (DHP)-sensitive. L-type calcium channels in the smooth muscle cells. Beta3-null mice show no apparent changes in smooth muscle contraction and sensitivity to DHP, and normal blood pressure when they are raised on a normal diet, but the 13 subunit deficient mice show elevated blood pressure in response to a high-salt diet, with significant reductions in plasma catecholamine concentrations. Our finding strongly suggests a close relationship between voltage-dependent channels and high blood pressure.

Animals↗
PubMed2000

Protective effect of benidipine against the abnormal electrical activity in single ventricular myocytes of the guinea pig under simulated ischemic conditions and reperfusion.

Induction of electrical abnormalities (EAs) under simulated ischemic conditions and after reperfusion was measured from single cardiac myocytes isolated from guinea pig ventricle using whole-cell voltage or current clamp with perforated patch variation. Conditions of simulated ischemia were produced by the exchange of medium from the standard one oxygenated with 95% O2-5% CO2 gas (pH 7.4) to the modified one, which contained no glucose, 8 mM K+ and 30 mM sodium-D,L-lactate and was gassed with 90% argon-10% CO2 (pH 6.6). Under the simulated ischemia for 20 min, EAs such as delayed afterdepolarization, early afterdepolarization, automatic activity or transient inward current were observed in about 37% of myocytes driven electrically at 1 Hz. Irreversible hypercontracture occurred in myocytes of 10% or less. Upon reperfusion with the standard solution, EAs and hypercontracture were observed in about 43% and 22% of cells, respectively. Glibenclamide-sensitive current was detected during ischemia, but tended to be enhanced during reperfusion. Amplitude of Ca2+ current and ATP-sensitive K+ current after reperfusion varied widely with time and from cell to cell. When myocytes were pretreated for 10 min with 10 nM benidipine, a 1,4-dihydropyridine derivative Ca2+ blocker, the incidence of EAs and hypercontracture was markedly reduced, suggesting the protective effect of benidipine against cardiac cell injury during ischemia and reperfusion.

Action Potentials↗
PubMed2000

SK4 encodes intermediate conductance Ca2+-activated K+ channels in mouse urinary bladder smooth muscle cells.

The single channel current of intermediate conductance Ca2 +-activated K+ channel (IK channel) was measured in mouse urinary bladder myocytes (MBM), and the molecular basis of the channel was suggested to be the SK4 subtype by RT-PCR. Among Ca2+-activated K+ channel subtypes (SK2, SK3, SK4 and BK), the mRNAs of SK4 and BK were predominantly expressed in MBM. IK channel currents recorded from MBM showed: 38.7 pS slope conductance under symmetrical 140 mM K+ conditions, Ca2+-dependent activation, and blockade by charybdotoxin and econazole. These results strongly suggest that SK4 encodes IK channels in MBM.

Animals↗
PubMed2000

Morphological and cytogenetic changes in therapy-related leukemia developed in a t(8;21)-acute myeloid leukemia (M2) patient: sequential cytogenetic and molecular analyses.

A patient with acute myeloid leukemia (AML)-M2 with t(8;21)(q22;q22) achieved complete remission with remission-induction chemotherapy followed by consolidation and intensification chemotherapies. T(8;21)(q22;q22) disappeared, but chimeric AML1/MTG8 was continuously detected in bone marrow cells. Following the development of therapy-related leukemia after 1 year, evolution of therapy-related AML-M4 with t(11;17)(q23;q25) and the rearrangement of the MLL gene were observed, while AML/MTG8 disappeared. After reinduction and following intermittent chemotherapies, a subsequent alternative transformation to AML-M2 occurred after detection of t(3;21)(q21;q22), with a break in the AML1 gene shown by interphase fluorescence in situ hybridization analysis. This leukemia transformed to AML-M4 after t(9;22)(q34;q11), with a minor BCR/ABL rearrangement, and then finally to AML-M2. This therapy-related leukemia was resistant to chemotherapy. These findings indicate that alterations in cytogenetic and molecular events caused by chemotherapeutic agents contribute to the sequential evolution of new leukemic clones with different morphology.

Adult↗
PubMed1999

Gas chromatographic-mass spectrometric determination of 4-nonylphenols and 4-tert-octylphenol in biological samples.

A simple and rapid method is described for the GC-MS determination of 4-nonylphenols (NOs) and 4-tert-octylphenol (OC) in biological samples. The NOs and OC in the sample are extracted with acetonitrile and the lipid in the sample extract is eliminated by partitioning between hexane and acetonitrile. After Florisil PR column clean-up, the sample extract is analyzed by GC-MS in the selected ion monitoring (SIM) mode. Average recoveries in pale chub (fish) and corbicula (shellfish) are 86.0 and 93.4% for NOs, and 95.8 and 96.4% for OC, respectively, spiked at the levels of 1.0 microg of NOs and 0.1 microg of OC per 5 g of fish and shellfish samples. The detection limits are 20 ng/g for NOs and 2 ng/g for OC.

Animals↗
PubMed1999

Mechanisms of the palmitoylcarnitine-induced response in vascular endothelial cells.

The mechanisms of Ca2+ mobilization induced by palmitoylcarnitine (Palcar) in rabbit aortic endothelial cells (ETCs) were examined using electrophysiological techniques. The results obtained were compared with those induced by acetylcholine (ACh). When a rabbit aortic muscle preparation with an intact endothelium was treated with 10 microM Palcar, the ACh-induced relaxation was markedly attenuated, whereas endothelium-independent relaxation caused by sodium nitroprusside was not affected. Under perforated-patch whole-cell-clamp conditions, the application of Palcar over the concentration range 0.3 and 10 microM elicited a slowly activating outward current (IPalcar-out), whereas ACh induced a rapidly activating outward current (IACh). A potassium channel blocker, 4-aminopyridine, significantly inhibited both IPalcar-out and IACh. Removal of external Ca2+ almost abolished IPalcar-out. Under the same conditions, however, IACh remained transient. Addition of cation channel blockers SK&F96365 and La3+ inhibited IPalcar-out more effectively than IACh. Application of staurosporine, an inhibitor of protein kinase C, affected neither IACh nor IPalcar-out. In contrast, treatment of ETCs with pertussis toxin (PTX) reduced IACh and almost abolished IPalcar-out. These findings demonstrate that, in ETCs, Palcar induces Ca2+ influx via the activation of PTX-sensitive GTP-binding protein, leading to the activation of Ca(2+)-dependent K+ current and hyperpolarization of the cell.

Acetylcholine↗
PubMed1999

Disodium cromoglycate use in children and adolescents with asthma: correlation between plasma concentrations and protective effects for various inhalation methods.

BACKGROUND: Few studies have addressed the association between the plasma concentration of disodium cromoglycate and its protective effects on patients with bronchial asthma. OBJECTIVE: We measured plasma concentrations of disodium cromoglycate for various asthmatic treatments in children and adolescents and estimated plasma concentrations and protective effects. METHOD: Disodium cromoglycate as a 2-mg aerosol (n = 12), 4-mg aerosol (n = 5), or 20-mg nebulizer solution (n = 13) was inhaled by patients in remission. RESULTS: The plasma concentrations of disodium cromoglycate after 5 minutes of inhalation were 3.04 +/- 2.72 ng/mL in the 2-mg aerosol group, 2.95 +/- 0.86 ng/mL in the 4-mg aerosol group, and 7.72 +/- 4.65 ng/mL in the nebulizer solution group. Subjects who used the nebulizer exhibited markedly higher plasma concentrations of disodium cromoglycate. There was a significant correlation between the concentration of disodium cromoglycate at 5 minutes and the protective effect determined by a ratio of the difference in the asthma score between baseline and treatment periods to the baseline asthma score. CONCLUSION: When the plasma concentration of disodium cromoglycate is low, administration of larger aerosol dose or nebulization might be necessary.

Administration, Inhalation↗
PubMed1999

Levcromakalim causes indirect endothelial hyperpolarization via a myo-endothelial pathway.

1. Effects of K+ channel opener, levcromakalim, on vascular endothelial cells were examined. Under voltage- and current-clamp conditions, application of acetylcholine to dispersed endothelial cells isolated from rabbit superior mesenteric artery (dispersed RMAECs) produced hyperpolarization and outward currents. On the other hand, dispersed RMAECs did not respond to levcromakalim. 2. When membrane potential was recorded from endothelium in a mesenteric arterial segment, exposure to levcromakalim in a concentration range of 0.1 to 3 microM caused concentration-dependent hyperpolarization. The hyperpolarization was observed in the absence of external Ca2+ and was inhibited by 10 microM glibenclamide. 3. The presence of 1 mM heptanol did not affect the levcromakalin-induced hyperpolarization, whereas treatment of the mesenteric arterial segment with 20 microM 18 beta-glycyrrhetinic acid significantly reduced the hyperpolarization. The response to acetylcholine of RMAECs in an arterial segment with 18 beta-glycyrrhetinic acid was, however, similar to that without 18 beta-glycyrrhetinic acid. 4. These suggest that although RMAECs themselves are functionally insensitive to levcromakalim, those in an arterial segment are hyperpolarized by levcromakalim via myo-endothelial electrical communication.

Animals↗
PubMed1999

Plasma concentrations of disodium cromoglycate after various inhalation methods in healthy subjects.

AIMS: To compare the plasma concentrations of disodium cromoglycate (DSCG) following various inhalation procedures in healthy volunteers. METHODS: Nine healthy subjects inhaled 2 mg of aerosol, 20 mg of nebuliser solution only, 20 mg of nebuliser solution mixed with isotonic saline, or 20 mg of nebuliser solution mixed with saline and procaterol, a beta2-adenoceptor agonist, on separate occasions 2-3 weeks apart. Plasma concentrations of DSCG were determined by high-performance liquid chromatography (h.p.l.c.). RESULTS: The peak plasma concentrations of DSCG were 1.5+/-0.7 (range 0.4-2.4) ng ml-1 in the aerosol group, 8.8+/-6.2 (range 5.3-19.9) ng ml-1 in the nebuliser solution only group, 17.2+/-16.3 (range 5.0-38.6) ng ml-1 in the nebuliser solution plus isotonic saline group, and 24.5+/-11. 9 (range 10.2-44.9) ng ml-1 in the nebuliser solution plus saline and procaterol group. Thus subjects who used the nebuliser had markedly higher plasma concentrations of DSCG than subjects who used the aerosol inhaler. CONCLUSIONS: These findings may have important implications for the evaluation of inhalation treatment with DSCG for bronchial asthma.

Administration, Inhalation↗
PubMed1999

Ca2+ spark as a regulator of ion channel activity.

Ca2+ spark is a local and transient Ca2+ release from sarcoplasmic reticulum (SR) through the ryanodine receptor Ca2+-releasing channel (RyR). In cardiac myocytes, Ca2+ spark is an elementary unit of Ca2+-induced Ca2+ release (CICR) by opening of RyR(s) in junctional SR (jSR), which is triggered by Ca2+-influx through L-type Ca2+ channels to the narrow space between a transverse tubule and jSR. Ca2+ spark has, therefore, been described as the evidence for "the local control of excitation-contraction coupling". In contrast, Ca2+ sparks in smooth muscle have been reported in relation to Ca2+-dependent K+ (K(Ca)) channel activation and muscle relaxation. A spontaneous Ca2+ spark in a superficial area activates 10-100 K(Ca) channels nearby and induces membrane hyperpolarization, which reduces Ca2+ channel activity. In several types of smooth muscle cells, which have relatively high membrane excitability, an action potential (AP) elicits 5-20 Ca2+ hot spots (evoked sparks with long life) in the early stage via CICR in discrete superficial SR elements and activates K(Ca)-channel current highly responsible for AP repolarization and afterhyperpolarization. CICR available for contraction may occur more slowly by the propagation of CICR from superficial SR to deeper ones. The regulatory mechanism of ion channel activity on plasma membrane by superficial SR via Ca2+ spark generation in smooth muscle cells may be analogously common in several types of cells including neurons.

Action Potentials↗