Search PubMed⌕ Search

Biomedical subjects

T Sugano

Publications and source records attributed to T Sugano.

At least 55 records · Page 3Linked to original sources

Genetic analysis in Japanese kindreds of congenital type I antithrombin deficiency causing thrombosis.

We have identified two novel minor deletions (case 1; -TA or -AT at nucleotide 9831-3 in exon 5 and case 2; -A at nucleotide 7640-1 in exon 4), one novel nonsense mutation (case 3; TAT to TAA at nucleotide 7491 in exon 4), and one recurrent nonsense mutation (case 4; CGA to TGA at nucleotide 5381 in exon 3A) in Japanese kindreds with congenital type I antithrombin deficiency. The deletion detected in case 1 represented a symmetric element (CTCTGTCTC) and possessed a direct repeat (CTCTATGTCTC). The deletion in case 2 was recognized in a consensus sequence (TGAAT) and possessed a direct repeat (GATGAA). The nonsense mutation in case 3 formed a palindrome (CCGTTAACGG) and that in case 4 was caused by a CpG dinucleotide mutation. These results confirm that the mutations of congenital type I antithrombin deficiency are not random events but are influenced strongly by DNA sequences.

Adult↗

Angiotensin II increases plasminogen activator inhibitor-1 and tissue factor mRNA expression without changing that of tissue type plasminogen activator or tissue factor pathway inhibitor in cultured rat aortic endothelial cells.

Angiotensin converting enzyme inhibitors (ACE-I) have been reported to prevent the recurrence of cardiovascular events. The mechanism of this decrease, however, can not be completely explained by anti-hypertensive and anti-hypertrophic effects of ACE-I. To investigate the mechanism of this decrease, we studied the regulation of plasminogen activator inhibitor-1 (PAI-1), tissue type plasminogen activator (TPA), tissue factor (TF), and tissue factor pathway inhibitor (TFPI) by angiotensin II (Ang II) in cultured rat aortic endothelial cells. Ang II increased PAI-1 and TF mRNA expression without affecting that of TPA or TFPI. These inductions were accompanied by increases in PAI-1 and TF activities and were inhibited by a type I Ang II receptor antagonist. The results suggest that Ang II decreases the antithrombotic properties of endothelial cells which increases the chance of thrombosis. Thus, inhibition of the renin-angiotensin system may be beneficial to prevent thrombus formation in treatment of ischemic heart disease.

Angiotensin II↗

[Hemodynamic effects of right ventricular outflow pacing].

The effects of right ventricular outflow pacing were studied in 13 patients (mean [+/-SD] 69.8 +/- 8.2 years old). All patients received DDD pacemakers except two patients with implanted VVI pacemakers who had chronic atrial fibrillation. Cardiac output and pulmonary capillary wedge pressure were measured by Swan-Ganz catheter. Pacing rate was fixed at 70-80/min and atrioventricular delay was fixed at 165 msec. When the pacing site was changed from the right ventricular apex to the right ventricular outflow during right ventricular pacing in 11 patients, cardiac output increased from 3.3 +/- 0.6 to 3.4 +/- 0.5 l/min (p < 0.001), and wedge pressure decreased from 9.3 +/- 1.9 to 8.8 +/- 2.0 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow during atrioventricular pacing in eight patients, cardiac output increased from 3.9 +/- 0.4 to 4.0 +/- 0.4 l/min (p < 0.05), and wedge pressure decreased from 7.1 +/- 2.3 to 6.6 +/- 2.1 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow in seven patients with ejection fraction (EF) greater than 55%, cardiac output increased from 3.6 +/- 0.5 to 3.7 +/- 0.4 l/min (p < 0.05), and in four patients with EF less than 55%, it increased from 2.9 +/- 0.4 to 3.0 +/- 0.4 l/min (p < 0.01). Cardiac function was improved by right ventricular outflow pacing compared to right ventricular apex pacing regardless of the pacing mode or cardiac function.

Aged↗

Reserpine-induced immunocytochemical change of neuropeptide Y in the hypothalamic arcuate nucleus.

The effect of reserpine on neuropeptide Y immunoreactive (NPY-IR) neurons in the rat hypothalamic arcuate nucleus was examined by immunocytochemical techniques. Although only NPY-IR fibers and terminals were distributed in this nucleus in untreated and saline treated rats, single treatment of reserpine (10 mg/kg, i.p.) visualized abundant NPY-IR neuronal cell bodies: the increase began at 12 h of postinjection, reached its maximal level at 48 h, and returned to its normal level at 96 h. Pretreatment of nialamide, a monoamine oxidase inhibitor, prevented these acute reserpine-induced changes, suggesting reserpine acts on NPY neurons through monoaminergic mechanism. Chronic treatment of haloperidol (5 mg/kg, once daily for 5 days) a dopamine receptor antagonist, could induce the similar increase of NPY immunoreactivity. However, interruption of adrenergic and serotonergic neurotransmissions by chronic treatment of propranorol and methysergide, or chemical lesions of ascending noradrenergic and serotonergic pathways by 6-hydroxydopamine and 5,6-dihydroxytryptamine, could not induce any immunoreactive increase of NPY in arcuate neurons. These findings strongly suggest that reserpine-induced NPY increase occurs through dopaminergic afferents in hypothalamic arcuate neurons.

Animals↗

Simplified technique for hemi-arch replacement during open distal anastomosis: the "calla" method.

During open distal anastomosis for type A dissecting aneurysm, the beveled end of the graft was rolled back like a bract of the Calla flower and inserted into the aortic lumen. The inverted graft was anastomosed using forehand continuous sutures. After completion of the distal anastomosis, the inverted graft was pulled out and then the proximal anastomosis was completed. This "Calla flower" deformation facilitates the hemostatic distal anastomosis in hemi-arch replacement during open distal anastomosis.

Aged↗

Primary culture of chicken hepatocytes in serum-free medium (pH 7.8) secreted albumin and transferrin for a long period in free gas exchange with atmosphere.

To study liver functions of chicken, we examined the primary culture of chicken hepatocytes, and found an easy method of long-term culture with free atmosphere exchange. Chicken hepatocytes were obtained by collagenase perfusion and cultured at 37 degrees C as a monolayer without substratum in serum-free L-15 medium (pH 7.8) with free atmosphere exchange. The amounts of albumin and transferrin in medium were assayed by ELISA. The culture of chicken hepatocytes was maintained in the serum-free L15-medium )pH 7.) and 37 degrees C with free atmosphere exchange for 20 days. The amount of albumin secreted in the medium decreased to low levels early in culture; however, this was followed by marked increase from day 9 to day 17 of culture. The amount of transferrin was constant until day 6, then it too increased with further culture. We reported an easy method for the simple monolayer culture of chicken hepatocytes in serum-free L12 medium (pH 7.8) with free atmosphere exchange over an extended period. Expression of liver-specific functions, viz. albumin and transferrin synthesis, was observed after 1 week of culture.

Air↗

Decreased ureagenesis from alanine, but not from ammonia and glutamine, in the perfused rat liver after partial hepatectomy.

Ureagenesis from ammonia, alanine, and glutamine in the liver after partial hepatectomy (PH) was determined by using the liver-perfusion system. The maximum rate of ureagenesis from ammonium chloride (10 mmol/L) in hepatectomized (HX) rats at 24 hours after surgery was obtained in the presence of ornithine, lactate, and pyruvate, and it was almost identical to that in sham-operated (SO) rats. The rate of urea production from glutamine (1 mmol/L or 10 mmol/L) in HX rats was significantly lower than that of SO rats with a concomitant decrease in hepatic glutaminase activities. However, the rate of urea synthesis from glutamine (1 mmol/L) in the presence of added ammonia (0.5 mmol/L) was accelerated approximately 10-fold, and the significant difference in the rate of urea formation between HX and SO rats was abolished. This result indicates that there is enough glutaminase to generate ammonia from glutamine in the liver of HX rats. The rate of urea production from alanine (1 mmol/L or 10 mmol/L) in HX rats was significantly decreased at 24 hours following surgery, while that of SO rats was increased. The decreased formation of urea from alanine was not seen at 72 and 120 hours after the operation. These results suggest that during the proliferation phase of liver regeneration, a reduction of ureagenesis from alanine facilitates the remnant liver to make nonessential amino acids such as aspartate. This metabolic alteration might be related to the proliferation of liver cells.

Alanine↗

Population of hepatic macrophages and response of perfused liver to platelet-activating factor during production of thioacetamide-induced cirrhosis in rats.

The response of hepatic macrophages and the effects of platelet-activating factor (PAF) in perfused liver were studied during production of experimental cirrhosis induced by thioacetamide (TAA) in female Sprague-Dawley rats. Within 4 weeks of TAA administration (300 mg/L drinking water), an increase in hepatic macrophage population and enlargement in cell size preceded the alterations characteristic of cirrhosis. During 12 weeks of TAA administration, the changes in hepatic macrophages were maintained and cirrhosis of the micronodular type developed with a marked increase in hydroxyproline content. Although TAA treatment for 4 weeks had no effect on oxygen consumption or hepatic portal pressure in the perfused liver, the increment in hepatic portal pressure and decrement in oxygen consumption induced by PAF in TAA-treated rats were double those in control rats. The amounts of prostaglandin D2 (PGD2) and thromboxane B2 (TxB2) in perfusate induced by PAF were seven- and fivefold greater, respectively, in TAA-treated rats than in control rats. Zymosan mimicked the effects of PAF. These results are consistent with the hypothesis that hepatic macrophages and PAF play important roles in the development of cirrhosis induced by TAA.

Animals↗

Phorbol ester, but not endotoxin, desensitizes mannan-induced glycogenolysis in the perfused rat liver.

Mannan, a ligand for the mannose/N-acetylglucosamine (GlcNAc) receptor, induces suppression of oxygen consumption and increases glucose production in the perfused rat liver, and repeated infusion of mannan causes desensitization of the responses. In this study, we examined whether activation of Kupffer cells by endotoxin and phorbol ester alters the glycogenolytic responses to mannan. Infusion of lipopolysaccharide (LPS, 10 micrograms/ ml) in the perfusate failed to inhibit the responses to mannan. Intravenous administration of LPS (1 mg/kg) 6 and 24 h before perfusion did not desensitize the responses to mannan, suggesting that the responses through mannose/GlcNAc receptors in the liver are retained even after activation of Kupffer cells by LPS. In contrast, prior infusion of phorbol 12-myristate 13-acetate (PMA, 100 nM) in vitro abolished the glycogenolytic responses to subsequently infused mannan, but not that to norepinephrine (100 nM), while prior infusions of 4-alpha-phorbol 12,13-didecanoate (100 nM), A23187 (50 nM), or forskolin (1 microM) had no effect on the mannan-induced responses. H-7, an inhibitor of protein kinase C, reduced the glycogenolytic responses to mannan, while it failed to restore the desensitization. These results suggest that protein kinase C may be involved in the process of glycogenolysis by mannan, but is unlikely to be involved in the homologous desensitization of the responses.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Vertebral bone mineral density in postpartum women.

The purpose of this study was to measure the bone mineral density of the lumbar spine (L2-L4) in healthy postpartum women following term delivery, and to evaluate factors associated with bone mineral density. Using dual energy X-ray absorptiometry, the bone mineral density of the lumbar spine was determined during 1 year in 123 healthy postpartum Japanese women following term delivery. The mean bone mineral density of the lumbar spine was 1.007 +/- 0.108 g/cm2 (range 0.731-1.252 g/cm2). Thus, there were wide inter-individual differences. Also, this result was in agreement with the peak bone mass previously reported for other Japanese women. Multiple regression analysis and linear regression analysis showed that weight and body mass index were each significantly correlated with bone mineral density of the lumbar spine. Age, parity, height, and baby's birth weight were not contributory.

Absorptiometry, Photon↗

[Mitral reconstruction in patients with infective endocarditis].

Between June 1992 and October 1993, 5 patients with infective endocarditis in native mitral valve underwent open heart surgery. The patients ranged in age from 51 to 64 years and were all males. According to NYHA functional classification, 4 patients were class II and one was class III. Surgery was indicated because of hemodynamic deterioration (2 pts), echocardiographic mobile vegetation with or without previous emboli (2 pts) and both condition (1 pt). Before surgery the patients were afebrile and had negative serum CRP and negative blood cultures for at least one week after adequate medical treatment. The leaflet lesions found in the 5 patients were vegetation (2 pts), perforation (1 pt), calcification (1 pt) and thickening (2 pts). The chordal lesions found were rupture (5 pts) and thickening (1 pt). The infective lesions did not extend to the annulus. The mitral leaflets, including all apparently infectious lesions, were resected in a V-shaped fashion and then valve reconstruction was performed. The resected parts were sutured together with anchoring chordae. The annuloplasty with Teflon-tapes was also added. Postoperatively, all 5 patients showed a dramatic improvement in hemodynamics and endocarditis did not recur during 22 to 38 months of follow-up. The patients who received the repair did not require Warfarin. This study shows that mitral valve repair is an acceptable operation in patients with infective endocarditis, giving the patients better quality of life than mitral valve replacement when (1) infectious lesion are limited to mitral leaflet and chordae, (2) there is no severe calcification of the mitral valve, (3) the infection is healed by the adequate antibiotic therapy.

Endocarditis, Bacterial↗