Biomedical subjects

Satoshi Matsuoka

Publications and source records attributed to Satoshi Matsuoka.

23 records · Page 2Linked to original sources

PubMed2002

Stoichiometry of the Na+/Ca2+ exchanger: models and implications.

We reevaluated the exchange stoichiometry of the Na(+)/Ca(2+) exchange current by measuring its reversal potential. The exchange current was measured from the inside-out macropatch excised from intact sarcolemma of guinea pig ventricular myocytes. This method provides more accurate control of extracellular and cytoplasmic ion concentrations and of membrane potential than is possible with a whole-cell clamped preparation. The exchange current was isolated as exchanger inhibitory peptide (XIP)-sensitive current or as cytoplasmic Na(+)- and Ca(2+)-induced current. The reversal potential of the Na(+)/Ca(2+) exchange current was, for the most part, close to the equilibrium potential of the 4Na(+):1Ca(2+) exchange, although it tended to get closer to that of 3Na(+): 1Ca(2+) exchange at lower Na(+) concentrations. We concluded that the stoichiometry is 4 or that it may vary depending on the cytoplasmic Na(+). The 4Na(+):1Ca(2+) exchange was further studied with computer modeling. A consecutive 4Na(+):1Ca(2+) exchange model with two active states and two inactive states (E2 model) could not well reconstruct the current-voltage relation of the exchanger. However, a consecutive 4Na(+):1Ca(2+) exchange model with 10 active states and 2 inactive states (E10 model), which included voltage-dependent Na(+) and Ca(2+) occlusions, well simulated the current-voltage relation. Implications of 4Na(+):1Ca(2+) exchange is also discussed.

Animals↗

PubMed2002

Molecular organization of intrinsic restriction and modification genes BsuM of Bacillus subtilis Marburg.

Transcriptional analysis and disruption of five open reading frames (ORFs), ydiO, ydiP, ydiR, ydiS, and ydjA, in the prophage 3 region of the chromosome of Bacillus subtilis Marburg revealed that they are component genes of the intrinsic BsuM restriction and modification system of this organism. The classical mutant strain RM125, which lacks the restriction and modification system of B. subtilis Marburg, lacks the prophage 3 region carrying these five ORFs. These ORFs constitute two operons, the ydiO-ydiP operon and the ydiR-ydiS-ydjA operon, both of which are expressed during the logarithmic phase of growth. The predicted gene products YdiO and YdiP are the orthologues of cytosine DNA methyltransferases. The predicted YdiS product is an orthologue of restriction nucleases, while the predicted YdiR and YdjA products have no apparent paralogues and orthologues whose functions are known. Disruption of the ydiR-ydiS-ydjA operon resulted in enhanced transformation by plasmid DNA carrying multiple BsuM target sequences. Disruption of ydiO or ydiP function requires disruption of at least one of the following genes on the chromosome: ydiR, ydiS, and ydjA. The degrees of methylation of the BsuM target sequences on chromosomal DNAs were estimated indirectly by determining the susceptibility to digestion with XhoI (an isoschizomer of BsuM) of DNAs extracted from the disruptant strains. Six XhoI (BsuM) sites were examined. XhoI digested at the XhoI sites in the DNAs from disruptants with disruptions in both operons, while XhoI did not digest at the XhoI sites in the DNAs from the wild-type strain or from the disruptants with disruptions in the ydiR-ydiS-ydjA operon. Therefore, the ydiO-ydiP operon and the ydiR-ydiS-ydjA operon are considered operons that are responsible for BsuM modification and BsuM restriction, respectively.

Bacillus subtilis↗

PubMed2002

Nonuniformity of sarcomere shortenings in the isolated rat ventricular myocyte.

By projecting the image of a single ventricular myocyte upon a linear image sensor, the striation pattern was analyzed during resting and contracting states. During rest, the individual cycle length (ICL) of the striation pattern varied from 1.8 to 2.0 microm within a given cell. ICL measured every 2 ms fluctuated approximately 0.05 microm around the mean. The variance of temporal fluctuations was decreased by chelating the extracellular Ca(2+) and increased by the Ca(2+) overload. Blocking the Ca(2+) release channels with 10 micromol/l ryanodine reversed this increase. In the power spectral density, an increase in the power occurred in the frequency range below 10 Hz. This increase should reflect overall kinetics of both intracellular Ca(2+) handling and responses of contractile filaments, because the same pattern was observed when spontaneous contractions occurred as well as when contractions were evoked by activating the L-type Ca(2+) channels. It is suggested that the temporal fluctuations of ICL in the resting state are caused by spontaneous Ca(2+) release from ryanodine receptors on the sarcoplasmic reticulum. Furthermore, under evoked contractions the shortenings of ICL were spatially inhomogeneous. These findings of nonuniform sarcomere shortenings are consistent with the temporal and spatial inhomogeneity of Ca(2+) transients.

Animals↗

PubMed2002

First paralytic shellfish poison (PSP) infestation of bivalves due to toxic dinoflagellate Alexandrium tamiyavanichii, in the southeast coasts of the Seto Inland Sea, Japan.

The mussel Mytilus edulis and the cultured ark shell Anadara broughtonii in the southeast coasts of the Seto Inland Sea were contaminated with paralytic shellfish poison (PSP) following the appearance of the dinoflagellate Alexandrium tamiyavanichii in early December 1999. A. tamiyavanichii plankton collected around the Straits of Naruto on December 3, 1999 showed PSP toxicity, of which 83 mol% was accounted for by GTX2, GTX3 and GTX4. Its specific toxicity was 112.5 fmol/cell, and one MU was equivalent to 7,200 cells. Toxicity values at the beginning of toxification were 4.7 MU/g for the ark shell and 7.3 MU/g for the mussel. In the former, the value remained at almost 4 MU/g, resulting in prohibition of marketing for about two months. In the latter, it sharply decreased to less than 4 MU/g. These bivalves collected during the toxification period were dissected into five tissues, mantle, adductor muscle, hepatopancreas, gills and "others", and submitted to high-performance liquid chromatography (HPLC). The cultured ark shell accumulated GTX2, GTX3 and STX as major components and GTX1, GTX4, GTX5, neoSTX, dcSTX and PX1-3 (C1-C3) as minor ones. The amount of GTX3 decreased with time, while STX tended to increase. At the early stage of PSP toxification, toxins were accumulated in the gills and "others", most of which were quickly detoxified. On the other hand, PSP of the toxified mussel consisted of GTX4 as a main component, and GTX1, GTX2, GTX3, GTX5, STX and PX1-2 (C1-C2) as minor ones. Its toxin composition pattern was similar to that of the ingested causative plankton. Its total toxin decreased soon after disappearance of the dinoflagellate. During the decrease of toxicity, PSP tended to be retained in the hepatopancreas, resulting in accumulation of 50 mol% of total toxin.

Animals↗

PubMedDate not supplied

Simulation of ATP metabolism in cardiac excitation-contraction coupling.

To obtain insights into the mechanisms underlying the membrane excitation and contraction of cardiac myocytes, we developed a computer model of excitation-contraction coupling (Kyoto model: Jpn. J. Physiol. 53 (2003) 105). This model was further expanded by incorporating pivotal reactions of ATP metabolism; the model of mitochondrial oxidative phosphorylation by Korzeniewski and Zoladz (Biophys. Chem. 92 (2001) 17). The ATP-dependence of contraction, and creatine kinase and adenylate kinase were also incorporated. After minor modifications, the steady-state condition was well established for all the variables, including the membrane potential, contraction, and the ion and metabolite concentrations in sarcoplasmic reticulum, mitochondria and cytoplasm. Concentrations of major metabolites were close to the experimental data. Responses of the new model to anoxia were similar to experimental results of the P-31 NMR study in whole heart. This model serves as a prototype for developing a more comprehensive model of excitation-contraction-metabolism coupling.

Adenosine Triphosphate↗