Search PubMed⌕ Search

Biomedical subjects

A Sakai

Publications and source records attributed to A Sakai.

At least 307 records · Page 17Linked to original sources

[Atrial septal defect with tricuspid valve regurgitation and heart failure in early childhood: report of a case with successful surgical management consisting of special patch closure technique and use of polydioxanone suture for the tricuspid annuloplasty].

A management of surgery for infant having a small left ventricular cavity associated with atrial septal defect and tricuspid valve regurgitation was presented. A right upper part of the defect was remained in open during a patch closure of ASD and this portion was temporarily sutured by prolene stayed extracardialy through Waterston's groove. During 20 minutes after weaning from the cardiopulmonary bypass, left heart failure did not appear and then it was completely closed. DeVega's method was employed for the tricuspid valve regurgitation using a absorbale Polydioxanone suture, because of a growth of the sutured annulus. Postoperative course was uneventful and trivial tricuspid valve regurgitation was recognized in angiocardiographic studies performed in 2 weeks and 6 months after operation.

Child, Preschool↗

Comparison of P+-active and -inactive pro-1 homologues from human nasopharyngeal carcinoma cells.

Eleven pro-1 homologous clones from human nasopharyngeal carcinoma cell line CNE2 were studied with respect to their ability to transfer sensitivity to tumor promoter-induced neoplastic transformation (P+ activity), their molecular structure, and their homology to both mouse pro-1 and each other. Restriction mapping and Southern analysis of CNE2 pro-1 homologous clones revealed three structural classes, all of which showed P+ activity. The approximate limits of mouse pro-1 hybridizing sequences within CNE2 clones from each structural class were identified, and some of these minimum homologous sequences were tested for P+ activity by transfection into P- cells. For all classes, a strong association between P+ activity and pro-1 homology was observed. This finding implies that, for CNE2 clones to be P+-active, structural homology to mouse pro-1 is required. The minimum P+-active sequence thus far identified was a 2.6-kbp EcoRI-SstI fragment. One clone was inactive, even though it was indistinguishable from active clones of the same class by restriction mapping, Southern analysis, and electron microscope examination of heteroduplexes formed by an active and an inactive clone. This raises the possibility that discrete changes, involving a few nucleotides rather than gross rearrangement, may determine the P+ activation of these pro-1-homologous sequences.

Blotting, Southern↗

Dibutyryl cyclic adenosine monophosphate inhibits pulmonary vasoconstriction.

The effects of the cell-permeable dibutyryl derivative of cyclic AMP on the vascular reactivity of isolated perfused rat lungs were examined. In lungs perfused with homologous blood, pulmonary arterial infusion of db-cAMP (30 micrograms/min) inhibited hypoxia-induced vasoconstriction (IC50 = 6.3 X 10(-5) M) and vasoconstriction due to bolus injection of angiotensin II (IC50 = 8.2 X 10(-5) M). Cyclic AMP phosphodiesterase inhibition by aminophylline acted synergistically with db-cAMP in the reduction of hypoxia-induced vasoconstriction. Somatostatin, an inhibitor of adenylate cyclase, prevented the decay of hypoxic vasoconstriction typically observed in isolated lungs, suggesting that a rise in intracellular cAMP may occur during hypoxic vasoconstriction as a consequence of activation of the adenylate cyclase. In lungs perfused with cell and protein-free salt solution, db-cAMP inhibited both initial and prolonged vasoconstriction following bolus injection of 2 microgram leukotriene C4. Thus, db-cAMP inhibited pulmonary vascular reactivity nonspecifically.

Aminophylline↗

Tumor induction in mice administered neonatally with 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole or 2-amino-dipyrido[1,2-a:3',2'-d]imidazole.

The tumorigenic effects of 2 L-glutamic acid pyrolysates to ICR mice were studied. The newborn animals received subcutaneously either 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) or 2-amino-dipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2). The mice were observed for 1 year. The tumors of the lung and liver were induced. Statistical analysis revealed that the incidences of the lung tumor in the mice given Glu-P-1 or Glu-P-2 and that of liver tumor in the male mice given Glu-P-2 25 mg/kg body wt were significantly higher than those of controls.

Animals↗

Role of red blood cells in the coronary microcirculation during cold blood cardioplegia.

The role of red blood cells during cold blood cardioplegia was studied using an intravital microscope in 13 isolated canine hearts perfused with diluted blood containing potassium chloride. The coronary microcirculation on the left ventricular epicardial surface was observed while the perfusate temperature was varied between 37 degrees C and 10 degrees C. Considerable sludging of red blood cells occurred during hypothermia. The percentage of capillaries perfused by red blood cells (percentage change) significantly decreased as perfusate temperature was reduced (100, 56, and 31% at 37, 20, and 10 degrees C respectively). This was caused by occlusion of microvessels due to sludging and by functional closure due to hypothermia. There was incomplete recovery of perfusion of capillaries at the end of rewarming (60%). The diameters of venules were reduced to 76% of control value at 10 degrees C because of the decrease in the numbers of feeding capillaries, but this value returned to 91% at the end of rewarming. Coronary vascular resistance (mmHg.ml-1.min-1 (kPa.s.litre-1] significantly decreased from 2.0(0.2) at 37 degrees C to 1.2(0.12) at 10 degrees C, but it increased to 2.4(0.24) at the end of rewarming. The finding in this study that sludging occurred which was slow to clear is a definite disadvantage of perfusion with red blood cells during hypothermia.

Animals↗

Isolation and characterization of mutants which show an oversecretion phenotype in Saccharomyces cerevisiae.

We have isolated mutants responsible for an oversecretion phenotype in Saccharomyces cerevisiae, using a promoter of SUC2 and the gene coding for alpha-amylase from mouse as a marker of secretion. These mutations defined two complementation groups, designated as ose1 (over secretion) and rgr1 (resistant to glucose repression). The ose1 mutant produced an oversecretion of amylase by 12- to 15-fold under derepressing conditions; however, the amylase mRNA was present at nearly the same amount as it was in the parent cells. No expression of the amylase gene was detected under repressing conditions. The rgr1 mutant oversecreted amylase by 11- to 13-fold under repressing conditions by 15- to 18-fold under derepressing conditions. The rgr1 mutant showed pleiotropic effects on the following cellular functions: (1) resistance to glucose repression, (2) temperature-sensitive lethality, (3) sporulation deficieny in homozygous diploid cells, and (4) abnormal cell morphology. The rgr1 mutation was not allelic with ssn6 and cyc9, and failed to suppress snf1.

Genes, Fungal↗

Morphological differences in hearts of rats well adapted and poorly adapted to chronic hypoxia.

We carried out an experiment to analyze morphological differences in hearts of rats well adapted and poorly adapted to chronic hypoxia. Male and female Wistar rats, 1 week, 4 weeks and 9 weeks old, were employed on the assumption that adaptive ability was dependent on age and sex. These rats were raised at an altitude of 2,400 m and were kept for 7 to 9 weeks. Control groups were maintained at an altitude of 600 m during the same period of time. Each group consisted of 4 to 6 rats. At the end of the experiment, body weight, heart weight, ratio of heart weight to body weight and hematocrit were measured, and ventricular wall thickness, myocardial fiber diameter, capillary supply and mitochondria were morphometrically studied. Of the 6 experimental groups, the 4-week-old male rats (M2) had the highest body weight, as compared with the other experimental groups. In addition, relative to these other experimental groups, the following features were found for M2. Heart weight was intermediate, heart weight/body weight ratio was low and hematocrit was also low. Ventricular wall thickness was intermediate in the right ventricle (RV) and interventricular septum (IVS) but was thin in the left ventricle (LV). Myocardial fiber diameter was intermediate in the RV, large in the IVS and small in the LV. Capillary supply was intermediate in the RV and dense in the IVS and LV. Mitochondria were small but cristal density and percentage area, estimated from electron micrographs, were found to be high.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Dibutyryl cyclic AMP inhibits acute hypoxic pulmonary vasoconstriction in conscious sheep.

We examined the effects of cell-permeable dibutyryl cyclic AMP (DBcAMP) on acute hypoxic pulmonary vasoconstriction (HPV) in conscious sheep. Mean left and right atrial, pulmonary, and systemic pressures (Pla, Pra, Ppa, and Psa, mm Hg), cardiac output (CO, L/min), and heart rate were measured continuously. Systemic (SVR) and pulmonary vascular resistances (PVR) were calculated by (Psa-Pra)/CO and (Ppa-Pla)/CO, respectively. Five groups of experiments were performed using the same sheep (n = 6). After a 30-min baseline period, sheep inhaled a hypoxic gas mixture (O2:N2 = 1:9) for 40 min. Pretreatment with DBcAMP (200 micrograms/kg/min) inhibited HPV (Ppa, 12.0 +/- 2.3 to 20.0 +/- 2.3 versus 13.2 +/- 2.5 to 14.3 +/- 1.4 mm Hg, p less than 0.01; PVR, 2.61 +/- 0.81 to 4.15 +/- 1.14 versus 2.30 +/- 0.87 to 2.52 +/- 0.59 mm Hg/L/min, p less than 0.01). DBcAMP treatment (200 micrograms/kg/min) after induction of HPV also significantly attenuated hypoxic pulmonary response (Ppa, 19.0 +/- 1.7 to 14.2 +/- 2.3 mm Hg, p less than 0.01; PVR, 3.92 +/- 0.39 to 2.34 +/- 0.34 mm Hg/L/min, p less than 0.01) without significant decreases in Psa and SVR. Pretreatment with DBcAMP (200 micrograms/kg/min) did not significantly alter pulmonary pressor responses to bolus injections of prostaglandin F2 alpha (PGF2 alpha) (10 micrograms/kg) and norepinephrine (4 micrograms/kg). These results may suggest that intracellular augmentation of cyclic AMP plays a crucial role in modulating HPV.

Acute Disease↗

Histochemical demonstration of carbonic anhydrase activity in the odontogenic cells of the rat incisor.

Aldehyde-fixed, EDTA-demineralized frozen sections of the rat maxillary incisor were histochemically stained for carbonic anhydrase activity, by use of Hansson's method. Intense staining was observed in the odontoblasts, all types of epithelial cells of enamel organ in the maturation zone, cementoblasts, and the cells of the lingual dental sac. Less intense but consistent staining was observed in all types of epithelial cells of odontogenic origin directly facing the pulp and pulp cells adjacent to the odontoblast cell layer in the apical part of the pulp, and was considered due to the carbonic anhydrase-catalyzed reaction. Staining of these cells was completely inhibited by heat pretreatment (120 degrees C, 30 min), 10(-6) mol/L acetazolamide in the incubation medium, incubation by continuous immersion under the liquid surface, and omission of the substrate, NaHCO3. The dentin also exhibited heavy staining which was inhibited by the heat pre-treatment. However, this dentinal staining resisted the inhibition by 10(-3) mol/L acetazolamide and was not inhibited by incubation by continuous immersion or incubation without the substrate NaHCO3. The dentinal staining was thus judged to have been due to non-enzymatic cobalt precipitation.

Animals↗

Thromboxane synthetase inhibition and pulmonary response to hypoxia in conscious adult sheep.

This study investigated the effects of a thromboxane synthetase inhibitor (OKY-046) and a cyclooxygenase inhibitor (ketoprofen) on hypoxic pulmonary vasoconstriction in conscious adult sheep in order to evaluate the physiological role of thromboxane and other cyclooxygenase products. In addition, we studied the effects of histamine H1 (chlorpheniramine) and H2 antagonists (cimetidine) on hypoxic pulmonary vascular tone. Hypoxia caused a 37% rise in pulmonary arterial pressure (p less than 0.05) and a 36% increase in pulmonary vascular resistance (p less than 0.05). Pretreatment with intravenous OKY-046 10 mg/kg or ketoprofen 2 mg/kg had no effect on normoxic pulmonary vascular tone and inhibited the increase in plasma TXB2 concentration during hypoxia without affecting the pulmonary pressor response to hypoxia. Cimetidine produced an increase in hypoxic pulmonary vascular tone when individual members of the group were compared, but there was no statistically significant difference when the group was compared to the control study. Chlorpheniramine had no effect on hypoxic pulmonary tone. These data suggest that hypoxic pulmonary vasoconstriction is not mediated by release of TXA2, that hypoxic vascular tone is not modulated by cyclooxygenase products, and that the histamine H2 receptor may play a modulating role in hypoxic pulmonary vasoconstriction in conscious adult sheep.

Acrylates↗

Two human papillomavirus DNAs molecularly cloned from a patient with epidermodysplasia verruciformis: restriction maps.

Two distinct human papillomavirus (HPV) DNAs (MY-1 and MY-2) were molecularly cloned from the benign skin lesions of a patient with epidermodysplasia verruciformis. The restriction map of MY-1 was the same as that of HPV 3a. The map of MY-2 appeared to be different from those of any HPVs reported in the literature. MY-2 did not cross-hybridize with MY-1 or the DNAs of HPV types 1, 2 and 4 under stringent conditions.

DNA, Viral↗

[Studies on the metabolic fate of 14C-rokitamycin. Absorption, distribution, metabolism and excretion in infant rats].

14C-Rokitamycin (RKM) at the dose of 200 mg/kg was administered orally to fasted infant rats to study the absorption, distribution, metabolism and excretion in infant animals. The mean blood level of 14C-RKM reached its peak of 20.25 micrograms/ml in 30 minutes. The mean area under the curve was 93.23 micrograms.hr/ml. In vivo plasma protein binding rates of 14C-RKM were about 30% in both infant and adult rats. 14C-RKM was distributed at high concentrations into liver, kidney, lung, spleen, pancreas, bone marrow, submaxillary gland and some other tissues. Major metabolites detected in plasma, urine and bile were 10"-OH-RKM, leucomycin A7, leucomycin V and 14-OH-leucomycin V. In excretion studies, about 97% of the administered radioactivity was recovered in urine and feces within 144 hours. After intraduodenal administration to rats with cannulated bile ducts, 7.42% and 25.66% of the radioactivity were excreted within 24 hours in the urine and bile, respectively.

Absorption↗

[Studies on the absorption and excretion of rokitamycin in infant beagle dogs. Comparison with adult beagle dogs].

Absorption and excretion of rokitamycin (RKM) were studied after oral administration of 50 mg/kg to fasted infant and adult Beagle dogs. In infant Beagle dogs, the mean plasma level of RKM reached its peak of 6.53 micrograms/ml in 15 minutes after administration. The area under the curve (AUC) value was 11.04 micrograms.hr/ml. In adult Beagle dogs, the mean plasma level of RKM reached its peak of 8.62 micrograms/ml in 30 minutes after administration. The AUC value was 18.25 micrograms.hr/ml. Ratios of Cmax and AUC value in infant Beagle dogs to those in adults were about 75% and 60%, respectively. In infant Beagle dogs, urinary excretion of RKM was 2.55% of the dose within 24 hours. In adult Beagle dogs, urinary excretion of RKM was 3.03% of the dose within the same period. The excretion ratio of RKM in infant Beagle dogs was about 85% of the adults' value.

Absorption↗

[Studies on absorption and excretion of rokitamycin dry syrup in healthy volunteers].

The absorption and excretion of rokitamycin (RKM) in dry syrup form for children were studied following oral administration to fasted healthy volunteers with high gastric acidity as a suitable model to estimate bioavailability of RKM in children. In a comparative study on tablet and dry syrup forms, peak plasma concentrations of RKM and areas under plasma concentration-time curve (AUC) values were calculated using the trapezoidal rule. RKM dry syrup gave about 84 and 86% of these values for RKM tablet. Urinary recovery of RKM in 8 hours with the administration of dry syrup was also about 80% of the value obtained with tablet. Judging from these results, the bioavailability of RKM administered as dry syrup, was fairly close to that obtained with RKM tablet. The AUC values were dose dependent when examined with dose levels of 300, 500 and 800 mg administered as RKM dry syrup. The AUC value and urinary recovery of RKM administered as dry syrup were 3-4 times higher than these values for midecamycin acetate administered also as dry syrup.

Absorption↗

[Studies on concentrations in body fluids of 16-membered ring macrolide antibiotics upon oral administration to healthy volunteers. Effects of their metabolites on bioassay values].

Plasma and urinary antibiotic concentrations measured by 3 different bioassay methods were compared to each other in vitro, after oral administrations of rokitamycin (RKM) tablet, midecamycin acetate (MOM) tablet or josamycin (JM) tablet at a dose of a potency of 600 mg to each of nine healthy volunteers. Method I (RKM bioassay method) was an agar-well method using the agar medium described in the Minimum Requirements for Antibiotic Products of Japan (MRAPJ medium, pH 6.5), method II (MOM bioassay method) was an agar-well method using mycin-assay agar (pH 8.0) and method III (JM bioassay method) was an agar-well method using nutrient agar (pH 7.8). Micrococcus luteus ATCC 9341 was used as the test organism in all the assay method. With any of the bioassay methods tested, plasma concentrations of RKM were determined to be higher than those of MOM or JM. When the three different bioassay methods were compared, method II and III gave consistently higher values than method I for plasma concentrations of any of the drugs tested. These higher values obtained by method II and III appeared to be due to their inability to correctly assay potencies of metabolites of these antibiotics. Using in vitro assay method, potencies of metabolites were found to be estimated higher than they should when method II and III were used. Method I, on the other hand, determined relative potencies of these antibiotics and their metabolites correctly, reflecting differences in MIC values of original antibiotics and their metabolites. Method I, therefore, should be used as the method of preference to determine concentrations of these drugs in body fluids.

Administration, Oral↗