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Biomedical subjects

R Kato

Publications and source records attributed to R Kato.

At least 361 records · Page 20Linked to original sources
PubMed1991

[Surgical results of small sized (less than 3 cm) advanced lung cancer].

We studied the surgical results in 31 patients with small sized but advanced lung cancer. Twenty-two patients had mediastinal lymph node metastasis, 6 had pulmonary metastasis, 3 had pleural dissemination. Histological type were adenocarcinoma in 21 patients, large cell carcinoma in 5 patients, small cell carcinoma in 4 patients. The 5-year survival rate in patients with mediastinal lymph node metastasis (pT1N2) was 24.1%. The 5-year survival rate in patients (pT1N2) for clinical N0, N1 was 34.6%, but no patient with clinical N2 disease survived more than 2 years after the operation. In the patients with pulmonary metastasis or pleural dissemination none survived more than 5 years after the operation.

Adenocarcinoma↗
PubMed1991

[A case of quadricuspid aortic valve associated with coronary arterial legion].

A case of quadricuspid aortic valve is reported in a patient with coronary artery disease and abdominal aortic aneurysms. A 54-year-old male who had undergone aortic replacement because of abdominal aortic aneurysms three years before presentation was readmitted due to complaints of angina pectoris and palpitations. Aortography and coronary arteriography revealed severe aortic regurgitation and proximal occlusion of LAD and RCA. Surgical correction consisted of aortic valve replacement with a Björk-Shilely valve and coronary revascularization of LAD. During the operation, a quadricuspid aortic valve with one smaller and three larger cusps that showed mild myxomatous degeneration without dystrophic calcification and normal coronary arterial orifices were noted. Accordingly, severe aortic regurgitation may have resulted from the dysfunction of congenital malformed cusps and acquired sclerotic coronary disease was the main cause of the chest pain.

Angina Pectoris↗
PubMed1991

[A case of acute myocardial infarction due to coronary spasm].

The patient was a 47 year-old man, who has been known to have effort angina since September 1989. His exercise stress ECG has revealed ST elevation in V2-V4 with maximum exercise. He experienced severe chest pain lasting for an hour on the way to his office in the early morning on November 16, 1989, and was admitted to our hospital. His ECG and laboratory findings indicated typical acute anteroseptal myocardial infarction, but the coronary arteriography (CAG) which was performed 7 hours after the onset showed no significant stenotic lesion. After administrating nitrate and calcium antagonist, he has had no attack of angina pectoris and his exercise stress test has revealed no ST-T changes on his ECG. 1 month later, while antianginal drugs were discontinued in order to perform an ergonovine stress test, the patient frequently complained of left anterior chest pain with remarkable ST elevation in precordial leads on his ECG. The CAG at chronic stage revealed that there was a 99% stenosis at Segment 6 of the left anterior descending artery (LAD) which was supplied with good collateral flow from the right coronary artery. The LAD was completely occluded at Segment 6 after intracoronary administration of ergonovine maleate 0.005 mg to the left coronary artery. After the intracoronary infusion of isosorbide dinitrate, there was no significant stenosis seen in the LAD except the minimum wall irregularity at Segment 6. These findings suggested that coronary spasm might play a major role of the occurrence of acute myocardial infarction in this case.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed1991

Surgical treatment of advanced thyroid carcinoma invading the trachea.

Operative methods, in relation to the completeness of resection and surgical results, and postoperative complications, in relation to operative methods, were discussed in 60 patients with advanced thyroid carcinoma in whom tumor invading the trachea was resected along with thyroid carcinoma. Laryngotracheal anastomosis was performed in 41 patients and tracheotracheal anastomosis in 19 patients. Complete resection was performed in 22 patients in the former group and in 12 patients in the latter group. Three-, 5-, and 10-year survival rates in patients undergoing complete resection were 87.0%, 78.1%, and 78.1%, respectively. Those for patients undergoing incomplete resection were 64.9%, 43.7%, and 24.3%, respectively. The locations of remaining tumor were the tracheal stump in patients in whom resection was incomplete. In four patients with esophageal invasion, the muscular layer of the esophagus was resected. Three of these patients had good postoperative results. Postoperative complications consisted of stenosis at the anastomosis in two patients, temporary mis-swallowing in three patients, temporary lower pharyngeal stenosis in one patient, temporary vocal cord edema in one patient, and tetany in two patients.

Anastomosis, Surgical↗
PubMed1991

[Tracheal surgery to preserve or improve pulmonary and laryngeal functions].

One hundred and two patients underwent tracheal surgery to preserve or improve pulmonary and laryngeal functions. For pre- and post-operative functional examinations of tracheal stenotic patients, the flow volume curve and frequency analysis of tracheal stenotic sounds were very useful. As a results of tracheal surgery in 76 malignant cases, vocal cord stenosis due to bilateral laryngeal nerve paralysis was occurred in 21 patients. For vocal cord stenosis, T tube insertion was very effective and we were able to close the orifice of tracheostomy in 11 out of 15 cases by this method.

Adolescent↗
PubMed1991

[Reconstruction and its prognosis in patients undergoing resection of tracheal bifurcation].

Seventeen resections of tracheal bifurcation were performed: 12 for bronchogenic carcinoma, 2 for primary neoplasm of the trachea, one each for pulmonary sarcoma, inflammatory lesion and metastatic thyroid carcinoma. We performed carinal reconstruction in eight patients, sleeve pneumonectomy in eight patients and wedge pneumonectomy in one. In patients undergoing carinal reconstruction, there were 2 operative deaths and six patients survived over five years after the operation. However, in patients undergoing sleeve (wedge) pneumonectomy, there were 3 operative deaths, four patients died from 3 months to 7 months, and only two patients survived 5 years after the operation. Carinal resection with pneumonectomy had poorer prognosis than carinal reconstruction.

Adult↗
PubMed1991

Difference in the susceptibility of two phenobarbital-inducible forms, P450IIB1 and P450IIB2, to thyroid hormone- and growth hormone-induced suppression in rat liver: phenobarbital-inducible P450IIB2 suppression by thyroid hormone acting directly, but not through the pituitary system.

Suppression of two major phenobarbital-inducible cytochrome P-450s, P450IIB1 and P450IIB2, by thyroid hormone was studied and compared with growth hormone (GH)-induced suppression in rats in vivo and hepatocytes in primary culture in vitro. Treatment of adult male rats with 50 micrograms/kg triiodothyronine (T3) reduced the constitutively expressed amounts of P450IIB1 (up to 1 pmol/mg of protein) and P450IIB2 (2-5 pmol/mg of protein) to 42% and 3% of their levels in nontreated controls. Thyroidectomy increased the hepatic contents of P450IIB2 (to levels of 50-80 pmol/mg of protein) and, to a lesser extent, P450IIB1 (1-5 pmol/mg of protein) in male and female rats. Supplement of T3 to thyroidectomized rats reversed the increased contents to levels similar to those observed in normal rats. Hypophysectomy also increased both P450IIB1 and P450IIB2 protein, and their levels in both sexes were similar to that of P450IIB2 in thyroidectomized rats. Treatment of hypophysectomized rats with T3 as well as human GH suppressed hepatic contents of P450IIB1 and P450IIB2. In a hepatocyte culture including 2 mM phenobarbital, T3 and GH suppressed both P450IIB1 and P450IIB2. Other thyroid hormone derivatives, including thyroxine, D-T3, and reversed T3, also showed suppressive effects, in parallel with the potencies for their stimulatory action that have been reported. These results indicate that thyroid hormone may suppress both P450IIB1 and P450IIB2 by a direct effect on the liver, but not by an indirect effect through the modulation of pituitary GH synthesis. The high susceptibility of hepatic P450IIB2 to thyroid hormone-induced suppression also indicates that constitutive and phenobarbital-induced levels of P450IIB2 are suppressively regulated preferentially by thyroid hormone, in contrast to the high susceptibility to GH of P450IIB1 in rat liver. In addition, a difference in the suppressive mechanisms of thyroid hormone and GH was suggested by the difference in susceptibility to cycloheximide.

Animals↗
PubMed1990

Inhibition by nitric oxide and nitric oxide-producing vasodilators of DNA synthesis in vascular smooth muscle cells.

Effects of nitric oxide (NO) and NO-producing vasodilators such as glyceryl trinitrate and sodium nitroprusside were tested on DNA synthesis in the clonal rat aortic smooth muscle cells, RACS-1. DNA synthesis was estimated by [3H]thymidine incorporation to DNA. NO and NO-producing vasodilators inhibited the DNA synthesis that was induced by 10% fetal calf serum. NO and NO-producing vasodilators also inhibited the basal level of DNA synthesis that occurred possibly as a result of autocrine mechanisms. NO-producing vasodilators also inhibited the fetal calf serum-induced proliferation of cells. Sodium nitroprusside inhibited the endothelin-mediated DNA synthesis. In another mesenchymal cell line, Chinese hamster fibroblast V79 cells, NO and NO-producing vasodilators failed to inhibit DNA synthesis, excluding the possibility of general cell toxicity. An exposure to NO and NO-producing vasodilators resulted in an increase of cyclic GMP (cGMP) content in the RACS-1 cells. A cGMP analog, 8-bromo-cGMP, inhibited DNA synthesis in the RACS-1 cells. These results suggest that EDRF/nitric oxide released from endothelium possibly contributes to inhibition of the DNA synthesis in vascular smooth muscle cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Stimulus-responsive and rapid formation of inositol pentakisphosphate in cultured adrenal chromaffin cells.

When [3H]inositol-prelabeled cultured bovine adrenal chromaffin cells were stimulated with high K+ (56 mM) and nicotine (10 microM), a large and transient increase in [3H]inositol 1,3,4,5,6-pentakisphosphate (InsP5) accumulation was observed. The accumulation reached the maximum level at 15 s and then declined to the basal level at 2 min. The time course of accumulation of InsP5 was parallel to that of [3H]inositol 1,4,5-trisphosphate (Ins(1,4,5)P3). Angiotensin II (Ang II) (10 microM) rapidly accumulated InsP5, but the level was sustained for 2 min. With a slower time course and a lesser amount than InsP5, high K+, nicotine, and Ang II caused an accumulation of [3H]inositol 1,3,4,5-tetrakisphosphate and [3H]inositol hexakisphosphate. Veratridine (100 microM), maitotoxin (10 ng/ml), ATP (30 microM), platelet-derived growth factor (10 ng/ml), and endothelin (10 ng/ml) also induced the InsP5 accumulation. High K+, nicotine, veratridine, and maitotoxin induced an increase in 45Ca2+ uptake, whereas Ang II, ATP, platelet-derived growth factor, and endothelin did not cause 45Ca2+ uptake. Nifedipine, a calcium channel antagonist, inhibited the high K(+)-induced InsP5 accumulation but failed to affect the Ang II-induced InsP5 accumulation. In an EGTA-containing and Ca2(+)-depleted medium, the high K(+)-induced InsP5 accumulation was completely inhibited, whereas the InsP5 accumulation induced by Ang II was not significantly inhibited. 12-O-tetradecanoylphorbol-13-acetate inhibited partially the Ang II-induced InsP5 accumulation but failed to inhibit the high K(+)-induced accumulation. In those experiments, the changes of InsP5 accumulation were closely correlated to those of Ins(1,4,5)P3. In the chromaffin cell homogenate, [3H] Ins(1,4,5)P3 was converted eventually to [3H]InsP5 through [3H]inositol 1,3,4,6-tetrakisphosphate. Taken together, the above results suggest that InsP5 is rapidly formed by a variety of stimulants and that the formation of InsP5 may occur through two mechanisms, i.e. Ca2+ uptake-dependent and Ca2+ uptake-independent ones in cultured adrenal chromaffin cells.

Adrenal Medulla↗
PubMed1990

Differential effects of various skin tumor-promoting agents on prostaglandin E2 release from primary cultures of mouse epidermal cells.

Prostaglandin E2 (PGE2) release from primary cultures of mouse epidermal cells was markedly stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA), mezerein and 1-oleoyl-2-acetyl-glycerol but not by 4 alpha-phorbol-12,13-di-decanoate in low Ca2+ (50 microM) medium. TPA-evoked PGE2 release was inhibited by mepacrine, indomethacin and H-7 but not by HA1004. These findings suggest that TPA stimulates PGE2 release through activation of protein kinase C, phospholipase A2 and the cyclooxygenase pathway. Of the non-TPA type of tumor promoting agents, i.e. anthralin, chrysarobin, 7-bromomethylbenz[a]anthracene, benzoylperoxide, okadaic acid and palytoxin, only anthralin stimulated PGE2 release. Anthralin-evoked PGE2 release was not inhibited by H-7. In normal Ca2+ (1.8 mM) medium, PGE2 release increased markedly compared to the release in low Ca2+ medium. In normal Ca2+ medium, PGE2 release was stimulated by TPA, anthralin and okadaic acid but not by other tumor promoting agents. In mouse peritoneal macrophages, TPA, palytoxin and okadaic acid stimulated PGE2 release, but other tumor-promoting agents failed to stimulate it. These results suggest that skin tumor promoting agents are not necessarily effective stimulators of prostaglandin production either in macrophages or in epidermal cells, the target cells of skin tumor promotion.

Animals↗
PubMed1990

Rapid increase in inositol pentakisphosphate accumulation by nicotine in cultured adrenal chromaffin cells.

When [3H]inositol-prelabeled cultured bovine adrenal chromaffin cells were stimulated with nicotine (10 microM), a large and transient increase in [3H]inositol pentakisphosphate (InsP5) accumulation was observed. The accumulation reached the maximum level at 15 s, then declined to the basal level at 2 min. Nicotine also induced [3H]inositol tetrakisphosphate (InsP4) and [3H]inositol hexakisphosphate (InsP6) accumulation with a slower time course and a lesser magnitude than [3H]InsP5. The peaks of [3H]InsP4, [3H]InsP5 and [3H]InsP6 coincided with those of 32P radioactivity, when cells were doubly labeled with [3H]inositol and inorganic 32P. These results suggest that inositol pentakisphosphate is rapidly increased by nicotine, a cholinergic agonist, in cultured adrenal chromaffin cells.

Adrenal Medulla↗
PubMed1990

cDNA cloning of the hydroxysteroid sulfotransferase STa sharing a strong homology in amino acid sequence with the senescence marker protein SMP-2 in rat livers.

A cDNA encoding hydroxysteroid sulfotransferase a (STa), which catalyzes activation of carcinogenic polycyclic hydroxymethyl-arenes, was isolated from a lambda gtll cDNA expression library constructed from poly(A)+RNA of a female Sprague-Dawley (SD) rat liver. The cDNA, designated as ST-40, consisted of 1,015 base pairs which had an open reading frame of 852 base pairs encoding the entire rat STa subunit of 284 amino acids. The nucleotide base sequence of the ST-40 cDNA shared a strong homology of 94.4% with that of ST-20 cDNA encoding a hydroxysteroid ST which had been reported by us. The deduced amino acid sequence of STa had a homology of 73.7% with that of an SD rat liver senescence marker protein (SMP-2) consisting of 282 amino acid residues. However, STa was found to share a much stronger homology of 92% on the average with SMP-2 in their four specific regions corresponding to about 60% of the total sequences, indicating SMP-2 to be an isozyme of hydroxysteroid ST.

Amino Acid Sequence↗
PubMed1990

Effect of growth hormone on rat hepatic cytochrome P-450f mRNA: a new mode of regulation.

Growth hormone (GH) is known to be involved in the control of rat hepatic drug and steroid metabolism through its action on cytochrome P-450s. To examine the role of GH in the regulation of cytochrome P-450f (P-450f), a full-length cDNA clone corresponding to P-450f was isolated and the 3'-non-coding region was utilized for Northern and slot-blot analyses. P-450f mRNA levels were low in neonates, increased after age 4 weeks in male and female rats, and were approximately 3 times higher in the liver of adult female rats than male rats. Hypophysectomy caused a significant decrease in P-450f mRNA levels in male and female rats. Intermittent injection with human growth hormone (hGH) to mimic the male secretory pattern of GH caused a 9-fold increase in P-450f mRNA in hypophysectomized male rats to levels near male control levels, whereas continuous administration of hGH to mimic the female secretory pattern caused a greater increase in P-450f mRNA levels in male and female hypophysectomized rats (25-fold and 9-fold respectively) to levels nearer female control levels. The responses of the other GH-stimulated P-450s, P-450-male and P-450-female, to the different modes of hGH treatment were different from that of P-450f. Since sex hormones are known to affect the regulation of other P-450s, the effect of sex hormones on P-450f mRNA was studied. Ovariectomy caused a 2.4-fold reduction in P-450f mRNA which was partially reversed by estradiol treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗