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Biomedical subjects

M Yoshida

Publications and source records attributed to M Yoshida.

At least 1,369 records · Page 76Linked to original sources
PubMed1995

Active oxygen species generation by circulating leukocytes and gastric submucosal microcirculatory disturbances in the early period after thermal injury.

The purpose of the present study was to determine the pattern of microcirculatory disturbance to investigate the causes of gastric mucosal blood flow depression in the early period after thermal injury. Male Wistar rats were anesthetized and a 30% full skin-thickness dorsal burn was inflicted. Active oxygen species (AOS) generated by circulating leukocytes were measured by chemiluminescence. Contraction of arterioles and venules was observed by intravital microscopy, and rolling or sticking of leukocytes in venules was counted using fluorescence microscopy. AOS generation by circulating leukocytes was diminished and arteriolar contraction and increases in rolling or sticking leukocytes in venules were observed 15 min after thermal injury. Decreased AOS generation by circulating leukocytes, contractions of arterioles, and increased rolling or sticking of leukocytes in venules was observed in the early period after thermal injury. Arteriolar contraction may explain decreases in mucosal blood flow. Moreover, decreased AOS generation by circulating leukocytes does not obviate the potential participation of leukocytes in microcirculatory disturbances, because rolling or sticking leukocytes were increased significantly 15 min after thermal injury.

Animals↗
PubMed1995

The prevalence of diabetic complication of elderly diabetics in Himeji.

Diabetes mellitus has recently markedly increased among elderly patient's diseases. There are no recent epidemiological reports on the relative number of male and female diabetic patients. So, an epidemiological study was performed on 746 Non-Insulin-Dependent Diabetes Mellitus patients, whose data were obtained from members of the Himeji Internal Medicine Association, divided into six groups according to sex and duration of illness. The following results were obtained. 1) The number of male patients was greater by about 20% than that of female patients, while elderly patients accounted for a larger proportion, nd age at onset of disease was about ten years higher in female than in male patients. 2) All indicators of diabetes mellitus became worse with longer duration of illness. 3) There was a correlation between the prevalence of complications and the duration of illness: The prevalence of complications increased in parallel with increasing duration of illness, and this tendency was more marked in female than in male patients. 4) Female patients had a more marked tendency to develop hypertension, hyperlipidemia and obesity than male patients. 5) Microangiopathy generally manifested itself earlier than macroangiopathy, and the increase in the prevalence of angiopathy in accordance with prolonged duration of illness was more marked for microangiopathy than for macroangiopathy. Clinical features of Japanese diabetics are found to be similar to those of Europeans, especially dominant in females. This might be due to the changing life style in japan.

Aged↗
PubMed1995

Plasma endotoxin in typhoid fever.

Plasma endotoxin contents of the patients with sepsis or typhoid fever were measured by two sophisticated chromogenic limulus tests; Endospecy and Toxicolor tests. Endospecy test is the endotoxin-specific test and Toxicolor is responsible for both endotoxin and (1,3)-beta-D-glucan. Plasma was pretreated by our new PCA method which resolved the problem as to the detection of a lesser amount of plasma endotoxin when pretreated by the conventional PCA method. Although Toxicolor values have been reported to exceed more than the Endospecy value, under complicated pathophysiological situations, almost all specimens of these patients had a similar value, except in one expired septic shock case. In 18 typhoid fever cases, Salmonella typhi was isolated only from the bile in 5 cases, however endotoxemia occurred in 11 cases (61.1%). Within the first 4 days, the incidence of endotoxemia was higher (10/14, 71.4%). These results suggest that endotoxin assay seemed to be a useful tool for the diagnosis of typhoid fever.

Bacteremia↗
PubMed1995

Involvement of endothelin in peripheral circulatory change induced by hand-arm vibration.

Physiologic mechanisms involving local vasoregulating factor, endothelium-derived relaxing factor (EDRF) and endothelium-derived constricting factors (EDCF) have been postulated to play a role in VWF. Recent evidence that endothelin is a potent vasoconstrictor peptide indicates that it may play a role in vasoregulation during vibration exposure through the local actions of EDRF or EDCF. Therefore, we examined the effects of grasping (50 N) and hand-arm vibration with an unweighted acceleration of 50 m/s2 rms at a frequency of 120 Hz in the direction of X-axis on digital blood flow (DBF) and on the level of plasma endothelin in 7 healthy male office workers. DBF was measured by an apparatus based on the thermal diffusion method where the thermal diffusion flow probe was incorporated in the Peltier's stack. In the grasping test, DBF decreased by about 40% from resting level within 1 minute after the grasping was begun, and was maintained at almost the same level during grasping, but increased immediately after cessation of grasping. In the vibration exposure test, initial decrease in DBF due to grasping was the same as that observed in the grasping test, but DBF gradually increased when exposure to vibration was performed simultaneously. No significant change in plasma endothelin level was induced by grasping. Endothelin was significantly lower after exposure to vibration than at rest and after grasping. The grasping-induced decrease in DBF seemed to be due to mechanical compression of the vessels. The negative correlation between DBF and endothelin during vibration exposure suggests that a reduction in release of endothelin from smooth muscle into the vessel cavity during vibration leads to vasodilatation, possibly attributable to the local axon reflex.

Blood Flow Velocity↗
PubMed1994

Stimulation of transcription in cultured cells by high mobility group protein 1: essential role of the acidic carboxyl-terminal region.

Several in vitro studies have suggested that high mobility group (HMG) protein 1 has a role in gene regulation as a trans activator or quasi-transcription factor. However, data on the molecular functions of HMG1 protein in these reactions are contradictory or obscure. In order to assess whether HMG1 protein does, in fact, have transcriptional activation potential, two assay systems in cultured cells were employed. HMG1 protein introduced into COS-1 cells as a complex with a reporter plasmid carrying the lacZ gene enhanced the level of the gene expression. Cotransfection of an expression plasmid carrying HMG1 cDNA into the cells with the reporter plasmid enhanced the activity of beta-galactosidase 2-3-fold in comparison with that of the control effector plasmid. The enhancement was proved to be dependent not on the replication but on the transcription of the reporter plasmid. In the cotransfection experiments, an expression plasmid the HMG1 molecule lacking the acidic carboxyl terminus repressed the expression of the reporter gene. The binding of an HMG1 protein variant lacking the acidic carboxyl terminus to DNA gave an extremely large shift of gel retardation in comparison with the complete HMG1 molecule. Together, these results indicate that HMG1 protein can enhance expression in cells in culture at the step of gene transcription and that the DNA binding domains comprising two-thirds of the HMG1 protein molecule are responsible for the inhibition property. Also, the acidic terminus of the HMG1 molecule is essential for the enhancement of gene expression in addition to elimination of the repression caused by the DNA binding. (ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1994

Catalytic cooperativity of beef heart mitochondrial F1-ATPase revealed by using 2',3'-O-(2,4,6-trinitrophenyl)-ATP as a substrate; an indication of mutually activating catalytic sites.

The interaction of 2',3'-O-(2,4,6-trinitrophenyl)ATP (TNP-ATP) with bovine mitochondrial F1-ATPase (MF1) was examined under substoichiometric and stoichiometric conditions to investigate the relationship between the amount of bound TNP-AT(D)P and extent of inhibition on steady state ATP hydrolysis. The hydrolysis of bound TNP-ATP under substoichiometric condition proceeded slowly, with a first order rate constant of 0.014 s-1. However, hydrolysis was greatly accelerated by addition of excess ATP. The hydrolyzed product, TNP-ADP, did not dissociate from the enzyme even after the addition of excess ATP. These properties were the same for both native and nucleotide depleted enzyme. The difference spectrum induced by binding TNP-ATP to MF1 had a distinct peak at 410 nm and a deep trough at 395 nm, which were similar to those induced when TNP-ATP bound to the isolated beta subunit of the thermophilic F1-ATPase. The magnitude of difference spectra as a function of TNP-ATP concentration suggested the presence of at least two types of binding sites on the MF1 molecule. The first site, where substoichiometric TNP-ATP was hydrolyzed, had a very high affinity for TNP-ATP. TNP-AT(D)P bound to this site did not dissociate even in the presence of excess ATP. TNP-AT(D)P bound to the second site dissociated slowly when excess ATP was added. The steady state ATPase activity at 100 microM ATP was linearly suppressed as pre-loaded TNP-ATP increased. The binding of 2 mol of TNP-ATP per mol of MF1 was required to abolish ATPase activity. A model which assumes mutually-activating two catalytic sites is presented to explain these results.

Adenosine Triphosphate↗
PubMed1994

Benign schwannoma of the liver: a case report.

Neurogenic tumors of the liver are very rare, irrespective of associated neurofibromatosis. We report here a well-documented case of benign schwannoma in a 56-year-old woman without neurofibromatosis, including imaging and pathological examinations.

Cystadenocarcinoma↗
PubMed1994

Amantadine increases the extracellular dopamine levels in the striatum by re-uptake inhibition and by N-methyl-D-aspartate antagonism.

This study was performed to investigate the mechanism how amantadine increases the extracellular dopamine (DA) levels in the striatum in vivo. Local application of amantadine (1 mM, 40 min) to the striatum through the dialysis membrane significantly increased the extracellular DA levels. Coadministration of nomifensine (10 mM, 120 min), an inhibitor of neuronal DA uptake, into the perfusion fluid attenuated the amantadine-induced increase in DA outflow. The amantadine-induced increases in the extracellular DA levels were also inhibited by co-perfusion with Ringer containing high Mg2+ (15 mM, 120 min) or with MK-801 (1 microM, 80 min). These findings suggest that amantadine increases the extracellular DA levels in the striatum by inhibiting the re-uptake of DA and/or by blocking the channel in the N-methyl-D-aspartate (NMDA) receptor, which results in antagonism of NMDA receptor function.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Isolation of the stable hexameric DnaK.DnaJ complex from Thermus thermophilus.

A DnaK homolog (T.DnaK) has been purified as a stable complex with a DnaJ homolog (T.DnaJ) from a thermophilic bacterium, Thermus thermophilus. This complex has an approximate molecular size of 300 kDa and appears to contain three copies of each of T.DnaK and T.DnaJ molecules. Consistently, trigonal ring structures with a diameter (trigonal apex-to-apex) of about 11 nm were observed with electron microscopy. The complex has no endogenously bound AT(D)P and is stable in the presence of Mg-AT(D)P. It possesses a weak ATPase activity and retains about 3 mol of ADP/mole of the complex when incubated with Mg-ATP. This complex is able to interact with the reduced carboxymethylated alpha-lactalbumin which we used as a model unfolded protein.

Adenosine Triphosphatases↗
PubMed1994

Human adhalin is alternatively spliced and the gene is located on chromosome 17q21.

Mutations in the dystrophin gene cause the X chromosome-linked, recessive Duchenne and Becker muscular dystrophies. Dystrophin, a large cytoskeletal protein, copurifies with a complex of dystrophin-associated proteins which serve to anchor dystrophin to the sarcolemma. One of these associated proteins, adhalin, has been implicated as a candidate for severe childhood autosomal recessive muscular dystrophy (SCARMD) due to absence of anti-adhalin staining in muscle biopsy samples taken from SCARMD patients. Furthermore, the Duchenne-like dystrophic phenotype seen in the SCARMD families was shown to be tightly linked to chromosome 13 markers. To determine the genetic mutation responsible for autosomal dystrophy, we characterized the human adhalin gene. Contrary to our expectation, human adhalin was mapped to chromosome 17q21, excluding adhalin as the gene causing chromosome 13-associated SCARMD. Additionally, a splice form of adhalin message was found that predicts a 35-kDa nontransmembrane adhalin. The expression of both adhalin splice forms is exclusively restricted to striated muscle, unlike other components of the dystrophin-glycoprotein complex.

Alternative Splicing↗
PubMed1994

Crystallization of mutant beta subunit of F1-ATPase from thermophilic Bacillus PS3.

The mutant beta subunit of F1-ATPase from a thermophilic Bacillus strain, PS3, in which tyrosine at position 341 is replaced by leucine (beta Y341L) was expressed in Escherichia coli and crystallized by the vapor-diffusion procedure. Small needle-like crystals were obtained using ammonium sulfate as a precipitant and grown by the stepwise seeding method. The crystals obtained by this procedure diffracted X-rays to about 3 A resolution. The diffraction patterns indicated that the crystals belong to the orthorhombic system and the space group I222 or I2(1)2(1)2(1) with unit-cell dimensions of a = 232 A, b = 66 A, and c = 80 A. It is thought that the asymmetric unit comprises one beta Y341L molecule.

Bacillus↗
PubMed1994

Selective defect of sarcoglycan complex in severe childhood autosomal recessive muscular dystrophy muscle.

Dystrophin-associated glycoprotein complex is classified into two subcomplexes: the dystroglycan complex (156DAG and 43DAG) and the sarcoglycan complex (50DAG, A3b, and 35DAG). Severe childhood autosomal recessive muscular dystrophy (SCARMD) was first reported to result from a deficiency of 50DAG. We examined muscles from five SCARMD patients and found that dystrophin and 43DAG were present in almost normal levels while 35DAG and the newly-identified protein A3b in addition to 50DAG were absent or greatly reduced. Therefore, SCARMD is the disease with a selective defect of the sarcoglycan complex.

Child↗
PubMed1994

Relationship between core histone acetylation and histone H1(0) gene activity.

In this study we show a striking correlation between histone H1(0) gene expression and histone acetylation. Trichostatin A, a highly specific inhibitor of histone deacetylase, efficiently induces H1(0) gene expression. Moreover, using a cell line sensitive to trichostatin A (FM3A) and a derived cell line selected for its resistance to this inhibitor (TR303), it is shown that the level of H1(0) gene expression is related to the extent of chromatin acetylation. After showing the S-phase-dependent activation of H1(0) gene expression, we demonstrate that hyperacetylation has a dominant effect on H1(0) gene expression, since it enhances the expression of the gene independent of the position of cells in the cell cycle. This response to deacetylase inhibitors is specific to H1(0), since it is not shared by other cell-cycle-dependent histone genes (H1 and H4). Finally, by transfection of trichostatin-A-resistant and trichostatin-A-sensitive cells with a plasmid containing a H1(0) promoter, we show that the exogenous H1(0) promoter is also highly sensitive to trichostatin A treatment and that activation of transcription follows exactly the same pattern as activation of the endogenous gene. These data show that histone acetylation may be used to modulate H1(0) gene activity and offers insight into a possible mechanism in which the developmentally regulated chromatin acetylation acts to potentiate H1(0) gene expression.

Acetylation↗
PubMed1994

Axial ligands and alicyclic ring size modulate the activity and biochemical pharmacology of ammine/cycloalkylamine-platinum(IV) complexes in tumor cells resistant to cis-diamminedichloroplatinum(II) or trans-1R,2R-1S,2S-diaminocyclohexanetetrachloroplatinum(IV).

A platinum(II) and 3 platinum(IV) ammine/cycloalkylamine homologous series were evaluated for cytotoxicity and biochemical pharmacology in murine leukemia L1210/0, cis-diamminedichloroplatinum(II)- resistant L1210/DDP, and diaminocyclohexaneplatinum-resistant L1210/1,2-diaminocyclohexane (DACH) cells. Within each series, which contained 4 homologues with differing alicyclic (cycloalkyl) ring size (cyclopropane, cyclobutane, cyclopentane, or cyclohexane), cytotoxicity increased with increasing ring size. This appeared to be due to an increase in partition coefficient, and the resulting increase in drug accumulation and intracellular DNA adducts in ascending each of the series. There were exceptions to this generalization, predominantly in L1210/DACH cells, where the biochemical pharmacology was not entirely consistent with the cytotoxic response and suggested that other factors may be at play. The relationship between structure and ability to circumvent cis-diamminedichloroplatinum(II) and/or trans-1R,2R-1S,2S- diaminocyclohexanetetrachloroplatinum(IV) resistance was complex. Ascending the platinum(II) series caused resistance factors to decrease in L1210/DDP cells but increase in L1210/DACH cells. An increase in resistance factors was also observed in ascending the axial chloroplatinum(IV) series in the L1210/DACH line. In contrast, ascending the axial chloroplatinum(IV) series in the L1210/DDP line and axial acetatoplatinum(IV) and axial hydroxoplatinum(IV) series in both cell lines resulted in increases in resistance factors for the first stepwise increase in the cycloalkylamine ring size, but resistance factors then decreased progressively with further increases in ring size. Reduction of the platinum(IV) analogues to the platinum(II) congener appears to be necessary for binding to DNA. The similarity in biological actions between the platinum(II) and axial chloroplatinum(IV) series is likely due to the rapid reduction of tetravalent members to platinum(II) forms. The axial acetatoplatinum(IV) and axial hydroxoplatinum(IV) complexes were reduced more slowly, which may explain their lower potency, but not the ability of the higher member to circumvent both cis-diamminedichloroplatinum(II) and trans-1R,2R-1S,2S- diaminocyclohexanetetrachloroplatinum(IV) resistances. Explanation for this will require additional studies. The results have demonstrated high dependencies on ring size of the carrier amine ligand, valence state of platinum, and the nature of the axial ligand for modulation of potency, cross-resistance property, and biochemical pharmacology of ammine/cycloalkylamine complexes.

Animals↗
PubMed1994

Structural model of the ATP-binding domain of the F1-beta subunit based on analogy to the RecA protein.

In contrast to the previous topological model of the ATP binding domain of the F1-ATPase beta subunit based on analogies to those of ras p21 and adenylate kinase, a more consistent model can be constructed with the known structure of the recA protein as a reference. The secondary structure of the F1-ATPase beta subunit predicted from the primary structure agrees well with that of the recA protein. The topology includes a repetitive beta alpha c beta alpha beta alpha beta alpha beta structure where all beta strands are parallel and surround the central alpha c helix above which bound ATP is located. Several residues thought to be located at catalytic site as reported in genetic and chemical labeling work can be consistently positioned in this model.

Adenosine Triphosphate↗
PubMed1994

Correlation of total and interstrand DNA adducts in tumor and kidney with antitumor efficacies and differential nephrotoxicities of cis-ammine/cyclohexylamine-dichloroplatinum(II) and cisplatin.

Mixed amine platinum complexes have been identified as a new class of antitumor agents with activity in some cisplatin-resistant tumor models. cis-Ammine/cyclohexylamine-dichloroplatinum(II) is one such analog that we have evaluated in vivo and found it to have antitumor activity that was comparable to that of cisplatin in a solid murine fibrosarcoma tumor model. In contrast to the nephrotoxicity observed with cisplatin, the analog was free from inducing this side-effect. Pharmacokinetics of the two compounds administered i.v. at equitoxic dose levels to tumor-bearing mice indicated similar decay kinetics of total platinum in plasma, kidney and the tumor. Furthermore, DNA-platinum adducts of the two agents were similar in the tumor. Total adduct levels in the kidney, on the other hand, were significantly greater (P < 0.5) by up to 4-fold for cisplatin compared with the mixed amine analog. Likewise, the levels of interstrand cross-links of the two platinum complexes were comparable in the tumor, but significantly greater (P < 0.05) in the kidney for cisplatin. The data indicate that the greater renal levels of total and interstrand DNA-platinum adducts formed by cisplatin correlate with renal damage associated with this agent, and suggest that adduct levels, and not total tissue platinum levels, provide a more useful correlation with pharmacodynamic observations.

Animals↗