Search PubMed⌕ Search

Biomedical subjects

S Shida

Publications and source records attributed to S Shida.

At least 19 recordsLinked to original sources
PubMed1996

Familial occurrence of electrocardiographic abnormalities of the Brugada-type.

Electrocardiographic abnormalities were pointed out in a 51-year-old Japanese male whose major complaint was dizziness. His electrocardiogram showed a complete right bundle branch block, and a prolonged His bundle-ventricle (HV) interval of 100 msec. Two members of his family died of heart disease and 3 members, including a case of sudden death, presented an abnormal electrocardiogram of the Brugada-type with persistent ST segment elevation in the right precordial leads and right bundle branch block. The signal-averaged examination was made in the children of cases that died with the diagnosis of sudden death. Four cases showed a tendency of delay in the HV interval and a positive finding in the late potential. Further studies are necessary to clarify the relationship between electrocardiographic abnormalities of the Brugada-type and atrioventricular conduction disorder as well as to clarify the genetic basis of this disorder.

Adolescent↗
PubMed1994

Beta 1 adrenoceptor mediated decrease in pHi in quiescent ventricular myocardium.

OBJECTIVE: The aims were to examine the effect of beta adrenergic stimulation on the intracellular pH (pHi) and to compare it with that of alpha adrenergic stimulation in ventricular myocardium. METHODS: Using conventional and ion selective electrodes membrane potential and pHi were measured simultaneously in quiescent papillary muscles of guinea pigs in HEPES or bicarbonate buffered solution. Isoprenaline and propranolol (1 microM) plus phenylephrine (30 microM) were used to stimulate beta and alpha adrenoceptors, respectively. In order to evaluate underlying mechanism(s) of beta adrenoceptor mediated pHi change, effects of Na(+)-H+ exchange, Cl(-)-HCO3- exchange, Na(+)-HCO3- symport, and glycolysis blockers on the pHi change were examined. RESULTS: Isoprenaline (1 microM) produced a decrease in pHi of 0.08(SEM 0.01) pH units and a transient depolarisation of the resting membrane. The isoprenaline induced intracellular acidosis was blocked by the beta 1 blocker atenolol (10 microM) but not by the beta 2 blocker ICI 118,551 (0.1 microM). Forskolin also produced a decrease in pHi of 0.06(0.03) pH units. In contrast, alpha adrenergic stimulation produced an increase in pHi, which was abolished by 1 mM amiloride, an Na(+)-H+ exchange blocker. In the presence of amiloride, the isoprenaline induced decrease in pHi was rather enhanced. 4,4'-Diisothiocyanostilbene-2,2'-disulphonic acid (DIDS, 1 mM), a blocker of Cl(-)-HCO3- exchange and the Na(+)-HCO3- symport system, failed to affect the isoprenaline induced pHi decrease in bicarbonate buffered solution. However, pretreatment with 2-deoxyglucose or iodoacetic acid abolished the isoprenaline induced pHi decrease. CONCLUSIONS: beta 1 Adrenoceptor stimulation causes intracellular acidosis via the enhanced glycolysis, and the Na(+)-H+ exchange system appears to play a compensatory role. The beta 1 adrenoceptor mediated intracellular acidosis may modulate inotropic response to adrenergic stimulation in ventricular myocardium.

Adrenergic beta-Antagonists↗
PubMed1994

[Adenocarcinoma].

Explore the source record for details and available documents.

Adenocarcinoma↗
PubMed1994

[Adenocarcinoma].

Explore the source record for details and available documents.

Adenocarcinoma↗
PubMed1994

[Beta 1-adrenoceptor-mediated changes in intracellular Na+, K+, Cl- activities and pHi in guinea-pig ventricular myocardium].

Effects of beta-adrenergic stimulation on the membrane potential and intracellular Na+, K+, Cl- activities and pH (pHi) were examined in isolated guinea-pig ventricular muscles using conventional and ion-selective microelectrodes. Isoproterenol (1 microM) produced a transient membrane depolarization followed by a slight hyperpolarization in quiescent papillary muscles. Although the isoproterenol (1 microM)-induced depolarization was not blocked by tetrodotoxin (10 microM), nifedipine (10 microM), Cs+ (5 mM), Ba2+ (0.3 mM), amiloride (1 mM) or ouabain (10 microM), it was significantly attenuated by anthracene-9-carboxylic acid (9 AC, 1 mM), a Cl(-)-channel blocker. Intracellular K+ activity increased, whereas intracellular Na+ activity slightly decreased during beta-adrenergic stimulation. Intracellular Cl- activity significantly decreased during the isoproterenol-induced depolarization of the resting membrane potential, which was attenuated by 9 AC. Isoproterenol significantly decreased pHi, which was enhanced by amiloride. 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid(DIDS, 1 mM), a stilbene derivative possessing blocking action on Cl-/HCO3- exchange system and Na+/HCO3- symport system, failed to affect the isoproterenol-induced acidosis, but pretreatment with 2-deoxyglucose (2-DG, 5.5 mM) or iodoacetic acid(IAA, 0.3 mM) abolished the isoproterenol-induced pHi decrease. Thus, beta-adrenergic stimulation decreased aiCl, aiNa and pHi, and increased aiK. The decrease in aiCl may be ascribed to the activation of Cl- channels, and opposite changes in aiNa and aiK appear to be due to the beta-adrenoceptor mediated activation of Na+/K+ pump. Acceleration of glycolysis during beta-adrenergic stimulation may be responsible for the intracellular acidosis. These changes in intracellular ionic activities may play a role in the modulation of electromechanical response to beta-adrenergic stimulation.

Animals↗
PubMed1992

Effects of Cl- channel blockers on beta-adrenoceptor-mediated decreases in resting potential and intracellular Cl- activity in guinea-pig heart.

In order to find a more specific blocker of the cardiac Cl- channel, we examined the effects of anthracene-9-carboxylic acid (9AC) and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) on the beta-adrenoceptor-mediated decreases in resting potential and intracellular chloride ion activity (aiCl) in guinea-pig papillary muscles by using Cl- ion selective microelectrodes. 9AC (1 mM) significantly inhibited the isoproterenol (1 microM)-induced decreases in resting potential and aiCl in quiescent preparations. However, 1 mM DIDS did not significantly affect the changes in aiCl and resting potential during beta-adrenergic stimulation. Thus, in cardiac cells, 9AC is a more potent blocker of the Cl- channels activated by beta-adrenergic stimulation than DIDS.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Amplification and overexpression of the c-erbB-2 protooncogene in human gastric cancer.

The c-erbB-2 protooncogene encodes a possible growth factor receptor. This gene has been studied as to whether it can be regarded as a prognostic indicator in human breast carcinoma. As amplification and overexpression of the gene have been reported in several adenocarcinomas, 24 specimens of human gastric cancers were examined by immunohistochemical staining (24 cases), by Southern blotting (23/24) and by Northern blotting (16/24). Amplification of the gene was detected in two moderately differentiated tubular adenocarcinomas (8.7%), and overexpression of c-erbB-2 mRNA was detected in three moderately differentiated tubular adenocarcinomas (18.8%). By immunohistochemical staining of paraffin-embedded tissues using a polyclonal antibody to c-erbB-2 gene products, the cell membrane was stained positively in three cases of gastric cancers which overexpressed c-erbB-2 mRNA. Peritoneal metastases were found in six gastric cancers, including two moderately differentiated tubular adenocarcinomas in which amplification of c-erbB-2 occurred. These results suggest that amplification and overexpression of c-erbB-2 may be correlated with metastases in differentiated adenocarcinoma of the stomach.

Adenocarcinoma↗
PubMed1992

Dependence of endocochlear potential on basolateral Na+ and Cl- concentration: a study using vascular and perilymph perfusion.

Inside-positive endocochlear potential (EP) and high potassium concentration in the endocochlear duct are generated by transepithelial K+ transport in marginal cells of the stria vascularis. In order to estimate the degree of involvement of Na+ and Cl- in K+ transport in marginal cells, EP in guinea pigs was measured under artificial vascular and perilymphatic perfusion in situ. Na+ depletion due to both vascular and perilymphatic perfusion decreased EP by -10.0 +/- 4.1 mV (delta EP = -86 +/- 5.2 mV, n = 5) from the control value of 78 +/- 4.3 mV (p < 0.01). Cl- depletion due to vascular and perilymphatic perfusion also decreased EP by -10.0 +/- 4.9 mV (delta EP = 8.5 +/- 4.8 mV, n = 6) from the control value of 77 +/- 5.1 mV (p < 0.01). However, under either vascular or perilymphatic perfusion, even lowering of Na+ or Cl- concentration in the perfusate decreased EP only slightly compared to the results under both vascular and perilymphatic perfusion. Furosemide, a blocker of Na+/K+/2Cl- symport, decreased EP under vascular perfusion. This dependency of EP on basolateral Na+ and Cl- concentration strongly suggests that K+ transport by the marginal cell is dependent on the basolateral Na+ and Cl- concentration, and that Na+/K+/2Cl- symport is raised as a possible mechanism for Na+ and Cl- dependency of EP.

Animals↗
PubMed1992

[Clinical assessment of urinary free L-fucose levels].

We measured urinary levels of free L-fucose in healthy subjects, patients with benign diseases, and patients with cancer using an automated analyzer and a newly isolated L-fucose dehydrogenase, and evaluated the clinical usefulness of the results. The values obtained were corrected for urinary creatinine as micromoles per gram of creatinine. The cutoff value, set at the mean + 2SD for the healthy subjects, was 250 mumol/g.Cr. Patients with gallbladder cancer, bile-duct cancer, liver cancer, pancreatic cancer, or cirrhosis of the liver had significantly higher levels of L-fucose than the healthy subjects. The diagnostic sensitivity for these five diseases, taken together, was 68% (144/213). Specificity for the detection of cancer was calculated by use of false positives for patients with cholelithiasis, hepatitis, and pancreatitis: it was 73% (76/104). Diagnostic accuracy for these seven diseases taken together was therefore 69% (220/317). We compared the positive ratio of the L-fucose level with that of the tumor markers AFD and CA19-9. The positive ratio of an L-fucose value above the cutoff was higher than the positive ratio of either marker in bile-duct cancer, gallbladder cancer, liver cancer, and pancreatic cancer. The results suggested that the urinary levels of free L-fucose reflected the metabolism of sugar chains of glycoconjugates, and may be usefully clinically as a tumor marker.

Biomarkers, Tumor↗
PubMed1992

[Application of image cytometry to cytological diagnosis of breast tumors].

Computerized morphological analysis of the cell nuclei was performed on 66 cases (2222 nuclei) of aspirated materials from breast tumors: 25 benign cases (302 nuclei), 41 malignant cases (1420 nuclei). Its diagnostic significance and the correlation between nuclear analysis and clinical staging were studied. Nuclear diagram and intranuclear chromatin distribution pattern were evaluated using computer system named 6400. The malignant tumor had larger, more round-shaped nuclei and less uniform chromatin distribution. Under tnm classification, stage IV tumors had larger, more flattened nuclei and more irregular chromatin distribution pattern than the others. Computerized morphological analysis of breast tumors may give a quantitative aspect to classical diagnostic process. Furthermore, this analytical method provides information on clinical stage of breast cancer.

Adult↗