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T Oba

Publications and source records attributed to T Oba.

At least 19 recordsLinked to original sources
PubMed2001

Pure and scrambled self-aggregates prepared with zinc analogues of bacteriochlorophylls c and d.

Zinc analogues of bacteriochlorophylls c and d self-assembled in aqueous media with phospholipids. A methanol solution of zinc chlorin and alpha-lecithin was put in a cellulose tube and the inner methanol solvent was gradually replaced with water by dialysis to form the self-assembled oligomers. Visible absorption spectra of the aqueous solution showed that zinc chlorins formed J-aggregates within the hydrophobic core of alpha-lecithin assemblies and that the supramolecular structure of the aggregates depended upon the stereochemistry at the 3(1)-position and the alkyl substituents at the 8-, 12-, and 17(4)-positions of the zinc chlorin. When the aqueous aggregates were prepared with a mixture of 3(1)-epimers and/or 8-, 12-, or 17(4)-homologues of zinc 3(1)-hydroxy-13(1)-oxochlorins, the structurally distinct components coaggregated to make scrambled oligomers. However, during the dialysis, zinc 3(1)-hydroxy- and 7(1)-hydroxy-13(1)-oxochlorins slowly individually aggregated to give two structurally different oligomer units in the cellulose tube. In contrast, if the two zinc chlorin components rapidly self-assembled in an aqueous medium, these components coaggregated to form scrambled oligomers. The present study shows that both the molecular structure of the pigments and the speed of the oligomerization determine the molecular arrangement in chlorosome-type self-assembled oligomers.

Bacterial Proteins↗
PubMed2001

Tubular aggregates observed in spindle muscle fiber of horse lumbrical muscle.

Tubular aggregates (TAs) originate from the sarcoplasmic reticulum (SR) and form polymorphic double (or single) -walled structures in cross section. TAs are involved in various human skeletal muscle disorders including periodic paralysis, congenital myasthenic syndromes, inflammatory myopathies, and malignant hyperthermias. Horse lumbrical muscle (LM) is a slender fusiform muscle that shows varying degrees of regression due to its limited activity in the limb. Double-walled TAs were found in degenerating spindle fibers and with a range of 80-116 nm (average 92 nm, n=135) for outer layer and 50-78 nm (average 59 nm, n=135) for the inner layer. TAs exhibit degradation of myofibrillar proteins, disruption of mitochondria with cristae lost, glycogen accumulation, electron-dense metabolic products, blebbing appearance of sarcolemma, and presence of various vacuoles. LM fibers also show a similarly degenerative state. The disassembly of the SR structure probably produces a large accumulation of SR proteins which remain as molecules without being further degraded and which could aggregate to form the orderly structure of TAs. We believe that TA formation may be an adaptation to store unbalanced extra proteins by forming ordered aggregates in degeneration caused by stress in cells.

Animals↗
PubMed2001

A semi-immobilization of a partial auricle induces hypertrophy and ultrastructural alteration of cardiomyocytes.

Semi-immobilization of a partial area of the ventral edge, lateral epicardium of the left auricle (ventrolateral of left auricle), by using quick adhesion glue induces moderate hypertrophy of myocytes with an average increase of 34% in cross-sectional area. Intercellular connective tissues increased, and cellular sizes varied markedly. The ultrastructure of immobilized (semi-immobilized) myocytes commonly exhibited degenerating features in myofibrils, various cytoplasmic organelles including mitochondrial cristae and sarcoplasmic reticulum (SR) were disrupted, and T-tubules disappeared. Z-line streaming and widening (hypertrophic Z-line, rod bodies) and increase of metabolic particle deposition are typical phenomena in addition to intercalated disc (Id) disorganization. The results suggest that semi-immobilization of the auricle induces hypertrophy of myocytes in association with degeneration and disruption of myofibrils and other cytoplasmic organelles, and an increase of intercellular connective tissues, rather than increase of myofibril mass. This is the first study to immobilize only a part of the heart rather than the whole animal. Our results using artificial immobilization of cardiac myocytes were extremely significant since the structural alterations obtained were similar to that observed in cardiomyopathies. This suggests that myocytes progressing to heart failure are also subjected to inhibition of movement. Therefore, this experiment may prove very useful as a model for studying the functional effect of heart failure observed in cardiomyopathy.

Anatomy, Cross-Sectional↗
PubMed2001

Soluble osteopontin and vascular calcification in hemodialysis patients.

BACKGROUND: Vascular calcification often occurs in patients with uremia. As osteopontin (OPN) is not only involved in the physiological but also the pathological calcification of tissues, OPN may be associated with the pathogenesis of aortic calcification in hemodialysis (HD) patients. METHODS: We examined the expression of OPN in atherosclerotic aortas of HD patients. In addition, we performed a prospective longitudinal study by using CT scans to detect aortic calcifications and by measuring the plasma OPN concentration by ELISA in HD patients (20 men, 16 women; mean age 55.2 +/- 21.3 years) and in healthy volunteers (18 men, 17 women; mean age 54.0 +/- 13.2 years). RESULTS: By immunohistochemical staining, OPN was abundantly localized in atherosclerotic plaques of HD patients. The macrophages surrounding the atheromatous plaques were identified as the OPN-expressing cells. We furthermore found that the concentration of soluble plasma OPN was significantly higher in HD patients as compared with the concentrations in age-matched healthy volunteers (837.3 +/- 443.2 vs. 315.1 +/- 117.4 ng/ml, p < 0.01). The OPN concentration was positively correlated with the aortic calcification index in HD patients (r = 0.749, p < 0.01). CONCLUSION: These data suggest that OPN, secreted by macrophages, plays a role in the calcification of atheromatous plaques in HD patients.

Adult↗
PubMed2000

Hydrogen peroxide decelerates recovery of action potential after high-frequency fatigue in skeletal muscle.

Effects of reactive oxygen species (ROS), especially hydrogen peroxide (H(2)O(2)), on recovery of action potential by resting for 30 min after high-frequency fatigue were studied using frog skeletal muscle fibers. After stimulation at a frequency of 50 HZ for 2 min, the action potential amplitude was decreased by 14.5 mV from controls, and resting membrane was depolarized by 15.4 mV. Action potential duration was also prolonged by high-frequency stimulation (1.5 ms in controls to 2.6 ms). The high-frequency stimulation used here caused no muscle damage. The action potential was partially improved after a 30-min rest. Addition of catalase at 500 units/ml or H(2)O(2) at 0.5 mM to sartorius muscle did not alter any of the parameters of the action potential after high-frequency stimulation. Treatment with catalase accelerated post-fatigue recovery of the action potential. Application of H(2)O(2) delayed post-fatigue recovery of resting and action potentials. When added to detubulated toe muscle fibers, catalase no longer improved the attenuation of action potential induced by high-frequency stimulation, even after a 30-min rest. These findings suggest that removal of H(2)O(2) from transverse tubules is effective for post-fatigue recovery of action potential in skeletal muscle.

Action Potentials↗
PubMed2000

H(2)O(2) and ethanol act synergistically to gate ryanodine receptor/calcium-release channel.

We examined the effect of low concentrations of H(2)O(2) on the Ca(2+)-release channel/ryanodine receptor (RyR) to determine if H(2)O(2) plays a physiological role in skeletal muscle function. Sarcoplasmic reticulum vesicles from frog skeletal muscle and type 1 RyRs (RyR1) purified from rabbit skeletal muscle were incorporated into lipid bilayers. Channel activity of the frog RyR was not affected by application of 4.4 mM (0.02%) ethanol. Open probability (P(o)) of such ethanol-treated RyR channels was markedly increased on subsequent addition of 10 microM H(2)O(2). Increase of H(2)O(2) to 100 microM caused a further increase in channel activity. Application of 4.4 mM ethanol to 10 microM H(2)O(2)-treated RyRs activated channel activity. Exposure to 10 or 100 microM H(2)O(2) alone, however, failed to increase P(o). Synergistic action of ethanol and H(2)O(2) was also observed on the purified RyR1 channel, which was free from FK506 binding protein (FKBP12). H(2)O(2) at 100-500 microM had no effect on purified channel activity. Application of FKBP12 to the purified RyR1 drastically decreased channel activity but did not alter the effects of ethanol and H(2)O(2). These results suggest that H(2)O(2) may play a pathophysiological, but probably not a physiological, role by directly acting on skeletal muscle RyRs in the presence of ethanol.

Acetaldehyde↗
PubMed1999

Different effects of two gold compounds on muscle contraction, membrane potential and ryanodine receptor.

Effects of gold sodium thiomalate and NaAuCl4 on skeletal muscle function were studied using intact single fibres of frog skeletal muscle and fragmented sarcoplasmic reticulum prepared from frog and rabbit skeletal muscles. Gold sodium thiomalate at a concentration of 500 microM decreased tension amplitude by 27% and resting membrane potential by 5.3% after 30 and 22 min, respectively. The duration of tetanus tension was markedly shortened by 500 microM gold sodium thiomalate. When 10 microM NaAuCl4 was applied to gold sodium thiomalate-pretreated fibres, the fibres lost the ability to contract upon electrical stimulation, similar to the effects of 10 microM NaAuCl4 alone. In the presence of thiomalic acid, on the other hand, NaAuCl4 did not completely block tetanus tension even at 50 microM. Thiomalic acid also inhibited NaAuCl4-induced membrane depolarization. These findings suggest that thiomalate masks the effects of gold ion on muscle function. When sarcoplasmic reticulum vesicles were incorporated into lipid bilayers, exposure of the cis side of the Ca2+-release channel to 100 microM gold sodium thiomalate rapidly increased the open probability of the channel 3.3-fold, from 0.032 in controls to 0.105, with an increase in number of open events and a decrease in mean closed time. The ability of NaAuCl4 to activate the Ca2+-release channel was much stronger than that of gold sodium thiomalate. Only 1 microM NaAuCl4 was enough to activate the channel and this gold was effective from either side of the channel. These results suggest that gold sodium thiomalate could be used as an antirheumatic drug without considering severe side-effects on skeletal muscle. Coexistent thiomalate probably contributes to protection of muscle function from side-effects of gold ion.

Action Potentials↗
PubMed1999

Further characterization of the type 3 ryanodine receptor (RyR3) purified from rabbit diaphragm.

We characterized type 3 ryanodine receptor (RyR3) purified from rabbit diaphragm by immunoaffinity chromatography using a specific antibody. The purified receptor was free from 12-kDa FK506-binding protein, although it retained the ability to bind 12-kDa FK506-binding protein. Negatively stained images of RyR3 show a characteristic rectangular structure that was indistinguishable from RyR1. The location of the D2 segment, which exists uniquely in the RyR1 isoform, was determined as the region around domain 9 close to the corner of the square-shaped assembly, with use of D2-directed antibody as a probe. The RyR3 homotetramer had a single class of high affinity [3H]ryanodine-binding sites with a stoichiometry of 1 mol/mol. In planar lipid bilayers, RyR3 displayed cation channel activity that was modulated by several ligands including Ca2+, Mg2+, caffeine, and ATP, which is consistent with [3H]ryanodine binding activity. RyR3 showed a slightly larger unit conductance and a longer mean open time than RyR1. Whereas RyR1 showed two classes of channel activity with distinct open probabilities (Po), RyR3 displayed a homogeneous and steeply Ca2+-dependent activity with Po approximately 1. RyR3 was more steeply affected in the channel activity by sulfhydryl-oxidizing and -reducing reagents than RyR1, suggesting that the channel activity of RyR3 may be transformed more precipitously by the redox state. This is also a likely explanation for the difference in the Ca2+ dependence of RyR3 between [3H]ryanodine binding and channel activity.

Animals↗
PubMed1999

Identification of biosynthetic intermediates of the extracellular polysaccharide viilian in Lactococcus lactis subspecies cremoris SBT 0495.

Lactococcus lactis subspecies cremoris SBT 0495 produces the phosphopolysaccharide viilian, which consists of the repeating unit beta-D-glucosyl-(1-->4)-(alpha-L-rhamnosyl-(1-->2))-(alpha-D-galac tose-1- phosphoryl-(-->3)-beta-galactosyl-(1-->4)-beta-D-glucose. A lipid extract was prepared from cells in the late exponential phase of growth and was hydrolyzed by hydrochloric acid under mild conditions to split lipid-linked intermediates in the extract into lipid and sugar moieties. Both moieties were purified by chromatographic techniques and were characterized to identify intermediates of the viilian biosynthetic pathway. A polyisoprenoid isolated from the chloroform-soluble fraction of the hydrolyzed lipid extract was identified by mass spectrometry as undecaprenol. Saccharides isolated from the water-soluble fraction of the hydrolyzed lipid extract by anion-exchange chromatography, were characterized by glycosidic linkage analysis to discriminate sugar moieties of intermediates of viilian biosynthesis from compounds liberated from cell wall components. Some oligosaccharide analogues contain a glycerol residue, suggesting that these are fragments of glycosylglycerides and/or lipoteichoic acid. Three fragments were identified to be glucose, galactosyl-(1-->4)-glucose, and rhamnosyl-(1-->2)-galactosyl-(1-->4)-glucose, which are in agreement with the structure of the repeating unit of viilian. These saccharides most likely represent the first three steps of the sequential assembly of the repeating unit of the undecaprenol assembly.

Carbohydrates↗
PubMed1999

Z-line structural diversity in frog single muscle fiber in the passive state.

The structural changes of the Z-line between small square net (ss) and basket weave (bw) cross-sectional patterns were examined using intact single fibers and mechanically skinned fibers in the passive state to determine if the pattern is related to the sarcomere length (SL) and if the pattern undergoes a reversible transition in low- and high-osmotic medium. Frog single fibers were isolated from the anterior tibial muscle in Ringer's solution. Entirely or partially skinned single fibers were prepared in relaxing solution (also called low-osmotic medium). The high osmotic medium contained 10% polyvinylpyrrolidone (PVP) in relaxing solution. The sarcomere length (SL) of each fiber was measured directly by use of a laser beam or indirectly from electron micrographs with use of a correction factor. The ss and bw forms in cross sections were quantified by analysis of electron micrographs. The results show that the structural change of Z-line occurs around bw << 2.3-2.4 microns << ss (n = 25) and bw << 3.1-3.2 microns << ss (n = 13) in intact single fibers and skinned fibers, respectively. With the quick freeze-freeze substitution method, an intact single fiber with a SL of 2.35 microns showed almost 100% of ss form. The structural transition in cross section was also confirmed in four partially skinned fibers, where patterns went from mostly ss form (intact portion) to mostly bw form (skinned portion) at the SL between 2.40 to 3.20 microns. The reversibility of the change between ss and bw was proved by using low- and high-osmotic medium. The transition and reversion of cross-sectional patterns both occur in the passive state.

Animals↗
PubMed1999

Polymerase chain reaction screening of immunoglobulin heavy chain and T cell receptor gamma gene rearrangements: a practical approach to molecular DNA analysis of non-Hodgkin's lymphoma in a surgical pathology laboratory.

Characterization of the clonality of non-Hodgkin's lymphoma (NHL) by the rearranged segments of immunoglobulin heavy chain (Ig(H)) or T cell receptor (TCR) genes is not only useful in the confirmation of the diagnosis but also for the future assessment of how a secondary lymphoma, such as a recurrence or another primary lymphoma, occurs. As a practical approach to obtaining and registering this information in a surgical pathology laboratory, FR3 and FR1 regions of Ig(H) gene and TCRgamma gene were concurrently amplified by polymerase chain reaction (PCR) using each pair of consensus primers and the same PCR protocol. Examined samples consisted of 134 primary NHL (phenotypically, 108 B cell and 26 T cell NHL), 19 reactive lymphadenopathies, as well as five secondary lymphomas whose primary lesions were included in this study. Among the primary NHL, the combined PCR analysis disclosed the clonality in 103 of 134 NHL (77%), by FR3 PCR in 77 B cell and two T cell NHL, by FR1 PCR in 59 B cell and one T cell NHL, and by TCRgamma PCR in 11 B cell and 17 of 26 T cell NHL, but in none of the reactive lymphadenopathies. Among the secondary lymphomas, the same pattern of PCR analysis was obtained in two cases (the durations between first and second lymphomas; 6 and 10 months), which suggested recurrence. In contrast, different results were obtained in three cases (17-37 months), which indicated another primary or emergence of the subclones. The results of Southern blot analysis were concordant with the PCR results of the first and the secondary lymphomas. Although the combined PCR analysis cannot replace Southern blot hybridization because of its lower detection rate, it can select those cases suitable for further Southern blot analysis thus reducing the number of unnecessary examinations by nearly 75%. This approach may also be useful in the comparative evaluation of primary and secondary lymphomas.

Biomarkers, Tumor↗
PubMed1998

Hypocalcemic induced increase in creatine kinase in rats.

Calcium plays an important role in various myopathies. We report on an animal model with increased plasma creatine kinase (CK) resulting from hypocalcemia that will provide clues for studying human hypocalcemic myopathy. Male Wistar rats were pair-fed either a control or a calcium- and vitamin D3-deficient diet for 1, 2, 3, 4, or 5-6 weeks after weaning (3 weeks old). In the deficient diet-fed rats, plasma creatine kinase was increased and was accompanied by marked hypocalcemia. The omission of calcium and vitamin D3 from the diet for 1 or 2 weeks was enough to cause increased plasma creatine kinase; the creatine kinase ratio of deficient diet-fed rats to controls was 4.84 (1,777 IU L(-1)/367 IU L(-1)), and the calcium ion ratio was 0.41 (1.8 mg dL(-1)/4.4 mg dL(-1)) after 2 weeks. These values returned to control levels on treatment of the rats with the control diet and 1alpha-OH-vitamin D3 for 1 week.

Animals↗
PubMed1998

Sulfhydryls associated with H2O2-induced channel activation are on luminal side of ryanodine receptors.

The mechanism underlying H2O2-induced activation of frog skeletal muscle ryanodine receptors was studied using skinned fibers and by measuring single Ca(2+)-release channel current. Exposure of skinned fibers to 3-10 mM H2O2 elicited spontaneous contractures. H2O2 at 1 mM potentiated caffeine contracture. When the Ca(2+)-release channels were incorporated into lipid bilayers, open probability (Po) and open time constants were increased on intraluminal addition of H2O2 in the presence of cis catalase, but unitary conductance and reversal potential were not affected. Exposure to cis H2O2 at 1.5 mM failed to activate the channel in the presence of trans catalase. Application of 1.5 mM H2O2 to the trans side of a channel that had been oxidized by cis p-chloromercuriphenylsulfonic acid (pCMPS; 50 microM) still led to an increase in Po, comparable to that elicited by trans 1.5 mM H2O2 without pCMPS. Addition of cis pCMPS to channels that had been treated with or without trans H2O2 rapidly resulted in high Po followed by closure of the channel. These results suggest that oxidation of luminal sulfhydryls in the Ca(2+)-release channel may contribute to H2O2-induced channel activation and muscle contracture.

4-Chloromercuribenzenesulfonate↗
PubMed1998

Plasma concentration of brain natriuretic peptide as an indicator of cardiac ventricular function in patients on hemodialysis.

The plasma concentration of human brain natriuretic peptide (BNP) was measured by immunoradiometric assay in patients on maintenance hemodialysis (HD) to assess the possible relationship between the plasma levels of this peptide and cardiac ventricular function, as judged by M-mode echocardiography. The plasma BNP levels in the pre-HD state were significantly higher (688.5 +/- 154.5 pg/ml) than those of healthy subjects (<40 pg/ml). In addition, the plasma BNP levels were slightly decreased during HD (post-HD, 617.3 +/- 157.1 pg/ml). There was no correlation between the plasma levels of BNP and body weight changes during HD. The mean plasma BNP level was significantly higher in the group of patients with a low left ventricular ejection fraction (EF < 60%) than in the group with a normal EF. In the patients as a whole, there was an inverse correlation between plasma BNP levels and EF. Moreover, a positive correlation was found between plasma BNP levels and left ventricular mass index (r = 0.57, p < 0.05). These results suggest that plasma BNP levels increase in response to chronic stimulation in accordance with increased cardiac load, and that they may be a possible indicator of reduced ventricular function in HD patients.

Atrial Natriuretic Factor↗
PubMed1997

BAY K 8644 and ClO4- potentiate caffeine contracture without Ca2+ release channel activation.

Effects of perchlorate (ClO4-) and BAY K 8644 on caffeine contracture and Ca2+ release channel current were studied in frog skeletal muscle. Single fibers produced a small transient contracture on addition of 2.2 mM caffeine. ClO4 at 10 mM enhanced caffeine contracture 3.7-fold. This effect was inhibited by 10 microM nifedipine pretreatment. An increase in caffeine contracture was also obtained after exposure to 0.1 microM BAY K 8644 for 1 h. At 20 mM, external K+ potentiated caffeine contracture 2.2-fold. ClO4- (< 10 mM) and BAY K 8644 (0.1-1 microM) did not affect open probability (Po), unitary conductance, and open and closed time constants of the Ca2+ release channel current. BAY K 8644 at 0.1 microM did not further enhance the channel that had been activated by 2 mM caffeine. However, 20-30 mM ClO4 increased Po significantly and led the channel to a long open state by increasing the slow open time constant and decreasing the fast closed time constant. These results suggest that binding of ClO4 and BAY K 8644 to dihydropyridine receptors elicits a further increase in Ca2+ release from the sarcoplasmic reticulum.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Ethanol enhances caffeine-induced Ca2+-release channel activation in skeletal muscle sarcoplasmic reticulum.

When sarcoplasmic reticulum (SR) vesicles prepared from frog skeletal muscles were actively loaded with Ca2+, pretreatment of the SR with 2.2 mM (0.01%) ethanol for 30 s significantly potentiated 5 mM caffeine-induced release of Ca2+ from 16.7 +/- 3.7 nmol/mg protein in control without ethanol to 28.0 +/- 2.6 nmol/mg (P < 0.05, n = 5). Ethanol alone caused no release of Ca2+ from the SR. Exposure of the Ca2+-release channel, incorporated into planar lipid bilayers, to 2 mM caffeine significantly increased open probability (Po) and mean open time, but unitary conductance was not affected. Ethanol (2.2 mM) enhanced caffeine-induced Ca2+-release channel activity, with Po reaching 3.02-fold and mean open time 2.85-fold the values in the absence of ethanol. However, ethanol alone did not affect electrical parameters of single-channel current, over a concentration range of 2.2 mM (0.01%) to 217 mM (1%). The synergistic action of ethanol and caffeine on the channel activity could be attributable to enhancement of caffeine-induced release of Ca2+ from the SR vesicles in the presence of ethanol.

Animals↗
PubMed1997

Niflumic acid differentially modulates two types of skeletal ryanodine-sensitive Ca(2+)-release channels.

The effects of niflumic acid on ryanodine receptors (RyRs) of frog skeletal muscle were studied by incorporating sarcoplasmic reticulum (SR) vesicles into planar lipid bilayers. Frog muscle had two distinct types of RyRs in the SR: one showed a bell-shaped channel activation curve against cytoplasmic Ca2+ or niflumic acid, and its mean open probability (Po) was increased by perchlorate at 20-30 mM (termed "alpha-like" RyR); the other showed a sigmoidal activation curve against Ca2+ or niflumic acid, with no effect on perchlorate (termed "beta-like" RyR). The unitary conductance and reversal potential of both channel types were unaffected after exposure to niflumic acid when clamped at 0 mV. When clamped at more positive potentials, the beta-like RyR channel rectified this, increasing the unitary current. Treatment with niflumic acid did not inhibit the response of both channels to Ca2+ release channel modulators such as caffeine, ryanodine, and ruthenium red. The different effects of niflumic acid on Po and the unitary current amplitude in both types of channels may be attributable to the lack or the presence of inactivation sites and/or distinct responses to agonists.

Animals↗