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Biomedical subjects

Y Hiasa

Publications and source records attributed to Y Hiasa.

At least 163 records · Page 9Linked to original sources

Morphology of ectopic ventricular beats and their relationship to ventricular tachycardia in acute myocardial ischemia.

The features of ventricular arrhythmia in coronary spasm induced by ergonovine were examined to elucidate the characteristics of ventricular arrhythmia in acute myocardial ischemia. The coupling intervals and configurations of the QRS wave of the premature ventricular beats (PVBs) were extremely variable, even in the same individual and at the closer time phases. The prematurity index (R-R'/QT) of PVBs with the right bundle branch block (RBBB) pattern was significantly smaller than with the left bundle branch block (LBBB) pattern. The vulnerability index (R-RX QT/R-R') of PVBs with the RBBB pattern was significantly larger than with the LBBB pattern. The incidence of PVBs with the RBBB pattern (50.4%) was slightly larger than with the LBBB pattern (40.5%). PVBs deteriorated into ventricular tachycardias (VTs) in 29 (24.8%) of 117 cases with the RBBB pattern and in 11 (11.7%) out of 94 cases with the LBBB pattern. Thus, PVBs with the RBBB pattern were more likely to progress to VT than with the LBBB pattern. But it is difficult to assess the clinical significance of PVBs from their QRS morphology alone, because 11 (27.5%) of 40 cases of VT were initiated by PVBs with the LBBB pattern.

Acute Disease↗

Trisodium nitriloacetate monohydrate: promoting effect in urinary bladder carcinogenesis in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine.

The effect of trisodium nitrilotriacetate monohydrate [(Na3NTA X H2O) CAS: 18662-53-8] on development of urinary bladder tumors in rats initiated with N-butyl-N-(4-hydroxybutyl)nitrosamine [(BBN) CAS: 3817-11-6] was studied. Twenty-one male inbred W rats 6 weeks of age were given drinking water containing 500 ppm of BBN for 4 weeks and then put on diet containing 10,000 ppm of Na3NTA X H2O for 28 weeks. Na3NTA X H2O promoted the development of urinary bladder tumors in rats treated with BBN. The incidences of papilloma and transitional cell carcinomas in the urinary bladder were 90% (18/20) and 25% (4/20), respectively, in rats treated with BBN and then Na3NTA X H2O and 0 in those treated with BBN or Na3NTA X H2O alone. The incidence of papillary or nodular hyperplasia in week 32 was 100% (20/20) in rats treated with BBN and then Na3NTA X H2O and 61% (13/21) in rats treated with BBN only.

Acetates↗

Dose-dependent promoting effect of trisodium nitrilotriacetate monohydrate on urinary bladder carcinogenesis in Wistar rats pretreated with N-butyl-N-(4-hydroxybutyl)nitrosamine.

The dose-dependent effect of trisodium nitrilotriacetate monohydrate (Na3.NTA.H2O) as a promoter in 2-stage carcinogenesis in the urinary bladder of male Wistar rats was investigated. Carcinogenesis was initiated by administration of 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in the drinking water for 4 weeks, then Na3.NTA.H2O was given at 1%, 0.5% and 0.3% in the diet for 28 weeks, and rats were killed in week 32. The incidences and numbers of preneoplastic lesions [papillary or nodular hyperplasia (PN hyperplasia)] in rats treated with 0.3% to 1% Na3.NTA.H2O increased progressively with increasing concentration of Na3.NTA.H2O. The incidences of papillomas in rats treated with 1% and 0.5% Na3.NTA.H20 in the diet and the incidence of transitional cell carcinoma (TCC) of the urinary bladder in the rats treated with 1% Na3.NTA.H2O (P less than 0.05) were significantly higher than those in rats treated with BBN only. Administration of various doses of Na3.NTA.H2O without BBN did not cause any histological changes (PN hyperplasia, papilloma or TCC) in the urinary bladder. These findings showed that Na3.NTA.H2O is a potent promoter of urinary bladder carcinogenesis initiated by BBN in rats, and that its effect is dose-dependent.

Acetates↗

Sex differential and dose dependence of phenobarbital-promoting activity in N-bis(2-hydroxypropyl)nitrosamine-initiated thyroid tumorigenesis in rats.

Studies were made on the dose and sex dependence of thyroid tumor development in rats pretreated with N-bis(2-hydroxypropyl)nitrosamine (DHPN) followed by exposure to various doses of phenobarbital (PB). A direct dose-response relationship in induction of thyroid tumors was found in both male and female rats. Upon feeding the DHPN-treated rats with basal diet containing 20, 100, 500, and 2500 ppm of PB, the incidences of follicular adenoma were, respectively, 8, 45, 70, and 66% in male rats and 12, 17, 50, and 58% in female rats. Development of papillary adenomas in male rats was observed only at the higher doses of PB, at incidences of 12 and 20% for doses of 500 and 2500 ppm. Follicular carcinoma was also seen at higher doses of PB, at 16 and 12%, respectively, for the 500- and 2500-ppm groups. Neither follicular nor papillary carcinomas were induced in female rats; only a low incidence of papillary adenoma (4%) was observed with a PB concentration as high as 2500 ppm. A single injection of DHPN resulted in production of approximately 1 tumor/female rat and 2.5 tumors/male rat. DHPN combined with posttreatment with PB at doses up to 500 ppm did not increase tumor yield in female rats, whereas a 3-fold increase was observed in male rats for the 500-ppm-treated groups. When PB was increased to 2500 ppm a marked increase (8-fold) in tumor yield in male rats was observed, in contrast to a less than 3-fold increase in similarly treated female rats.

Animals↗

Effect of propylthiouracil on the thyroid tumorigenesis induced by N-bis(2-hydroxypropyl)nitrosamine in rats.

The effect of 0.15% propylthiouracil (PTU) on thyroid tumorigenesis was studied in male Wistar rats given a single i.p. injection of 280 mg of N-bis(-2-hydroxypropyl)nitrosamine (DHPN) per 100 g body weight. The mean weights of the thyroid of rats treated with DHPN followed by PTU and with PTU alone were significantly higher than those of rats treated with DHPN only and control rats. The incidences of follicular adenoma at the end of week 20 of the experiment were 100% (21/21) in rats treated with DHPN followed by PTU, and 19% (4/21) in rats given DHPN alone. Papillary adenoma was observed in one rat treated with DHPN followed by PTU. The incidence of follicular carcinomas with invasive growth into the capsule, adipose tissues or blood vessels was 52% (11/21) in rats given DHPN and then PTU. No papillary carcinomas or solid tumors were found in any rats. Rats given PTU alone and untreated rats had no thyroid tumors. The serum concentration of T4 in rats treated with PTU alone was significantly lower than that in the control group. The serum concentration of T4 in rats treated with DHPN followed by PTU was slightly, but not significantly, lower than that in control rats. The serum concentrations of T3 in rats treated with DHPN followed by PTU, DHPN alone and PTU alone were also slightly, but not significantly, lower than that in controls.

Adenoma↗

Histopathological and biochemical analyses of transplantable renal adenocarcinoma in rats induced by N-ethyl-N-hydroxyethylnitrosamine.

Transplantable renal adenocarcinoma can be readily induced in Wistar strain male rats by initiation with N-ethyl-N-hydroxy-ethylnitrosamine followed by promotion with beta-cyclodextrin. The transplantability rates of the tumors by s.c. inoculation in newborn rats were 33 and 50%, respectively, for tumors of the first and second passages, and 100% for both third and fourth passages. The transplantability rates were affected by route of inoculation; rates of 50 and 100% were observed for s.c. and i.p. inoculations, respectively. The growth rate of tumors induced by i.p. inoculation was 3-fold higher than that induced by s.c. injection. Macroscopically, most of the tumors grew in the s.c. tissue of inoculation sites. However, invasive growth of tumors in spleen, liver, stomach, peritoneum, and intestine were seen in 50% of the animals inoculated i.p.; metastatic cancers to lung were seen in 16%. Histologically, the tumors were well-differentiated adenocarcinomas composed of uniform cells resembling kidney tubular cells and appeared to be derived from normal kidney tissues. A 5-fold decrease in gamma-glutamyl transferase activity in tumor tissues was found as compared with that of nontumorous kidney tissues. Electrophoretic analysis of cellular proteins in polyacrylamide gels revealed that tumor tissues exhibited five new polypeptides with molecular weights of 81,000, 64,000, 59,000, 50,000, and 36,000 which were either lacking or undetectable in the nontumourous area and control kidney. In addition, protein banding patterns of transplantable renal tumor appeared to be more heterogeneous than those of primary kidney tumor.

Adenocarcinoma↗

DL-Serine: promoting activity on renal tumorigenesis by N-ethyl-N-hydroxyethylnitrosamine in rats.

Subcutaneous injection of DL-serine increased the number and size of renal tubular cell tumors in male W rats treated with 500 or 1,000 ppm N-ethyl-N-hydroxyethylnitrosamine [(EHEN) CAS: 13147-25-6, 2-(ethylnitrosamino)ethanol]. At the end of the 32-week experiment, the incidences of renal tumors were 95% in rats treated with 1,000 ppm EHEN for 2 weeks and then given three sc injections of DL-serine every 2 weeks, 33% in rats treated with 1,000 ppm EHEN for 2 weeks, and 28% in rats treated with 500 ppm EHEN for 2 weeks and then given three sc injections of DL-serine every 2 weeks. No renal tumors were found in rats treated with 500 ppm EHEN alone or given three sc injections of DL-serine alone every 2 weeks.

Animals↗

Promoting effect of phenobarbital on N-bis (2-hydroxypropyl)nitrosamine thyroid tumorigenesis in rats. Effect of varying duration of exposure to phenobarbital.

Male Wistar rats were injected subcutaneously with a single dose of 280 mg N-bis(2-hydroxypropyl)nitrosamine (DHPN) per 100 g body weight and then given a diet containing 500 mg/kg phenobarbital (PB) for 6, 12 and 19 weeks. Exposure to PB for 12 or 19 weeks enhanced the development of thyroid tumours in rats treated with DHPN. The incidences of thyroid tumours at the end of the experiment were 87% in rats given DHPN and then PB for 19 weeks, 83% in rats given DHPN and then PB for 12 weeks, 42% in rats given DHPN and then PB for 6 weeks, and 37% in rats given DHPN. The incidence of thyroid cancer was 12% in rats given DHPN and then PB for 19 weeks. The total numbers of thyroid tumours were: 241 in rats given DHPN and then PB for 19 weeks, 125 in rats given DHPN and then PB for 12 weeks, 65 in rats given DHPN and then PB for 6 weeks, and 23 in rats given DHPN alone. The total numbers of thyroid tumours were proportional to the period of exposure to PB.

Animals↗

4,4'-Diaminodiphenylmethane: promoting effect on the development of thyroid tumors in rats treated with N-bis(2-hydroxypropyl)nitrosamine.

4,4'-Diaminodiphenylmethane (4,4'-methylenedianiline) (DDPM) promoted the development of thyroid tumors in rats treated with a subeffective dose of N-bis(2-hydroxypropyl)nitrosamine (2,2'-dihydroxy-N-nitrosodipropylamine) (DHPN) for thyroid tumorigenesis. Male inbred W rats were given a single ip injection of 280 mg DHPN/100 g body weight and fed diets with or without 1,000 ppm DDPM. Thyroid tumor incidences at the end of week 20 of the experiment were 90% (19/21) in rats given DHPN and then DDPM and 28% (6/21) in rats given DHPN alone. The incidence of thyroid cancers was 9.5% (2/21) in rats first given DHPN and then DDPM. Untreated rats and rats given DDPM alone had no thyroid tumors after 20 weeks. Incidences of kidney tumors were 38% (8/21) in rats given DHPN and then DDPM and 28% (6/21) in rats given DHPN alone. No tumors were found in the kidneys and lungs of rats given DDPM alone and in those of control rats. Treatment with DDPM alone slightly but not significantly decreased the serum concentrations of thyroxine and triiodothyronine; treatment with DHPN plus DDPM had no such effect.

Aniline Compounds↗

Trisodium nitrilotriacetate monohydrate: promoting effects on the development of renal tubular cell tumors in rats treated with N-ethyl-N-hydroxyethylnitrosamine.

The effect of trisodium nitrilotriacetate monohydrate [N,N-bis(carboxymethyl)glycine trisodium salt] (Na3NTA X H2O) on development of renal tubular cell tumors induced with N-ethyl-N-hydroxyethylnitrosamine [CAS:13147-25-6; 2-(ethylnitrosamino)-ethanol] (EHEN) was studied. Six-week-old male inbred W rats were given a diet containing 1,000 ppm of EHEN for 2 weeks and then a diet containing a high (10,000 ppm) or low (500 ppm) concentration of Na3NTA X H2O for 30 weeks. The rats were killed during week 32. The higher concentration of Na3NTA X H2O enhanced the development of renal tubular cell tumors and increased the number and size of tumors in rats treated with EHEN, but the lower concentration of Na3NTA X H2O did not. The incidence of renal tubular cell tumors in week 32 was 33% in rats treated with 1,000 ppm EHEN for 2 weeks, 100% in rats treated with 1,000 ppm EHEN for 2 weeks plus high Na3NTA X H2O diet for 30 weeks, and 39% in rats treated with 1,000 ppm EHEN for 2 weeks and then given low Na3NTA X H2O diet for 30 weeks. Numbers of atypical cell foci per kidney area (No./cm2) were 17.0 +/- 7.6 in rats treated with EHEN and high Na3NTA X H2O, 7.3 +/- 2.2 in rats treated with EHEN and low Na3NTA X H2O, 3.7 +/- 1.4 in rats treated with EHEN alone, and 1.0 +/- 2.4 in rats treated with high Na3NTA X H2O diet alone. Atypical cell foci retained a tubular pattern and consisted of basophilic cells with a large nucleus or clear cells with a small nucleus.

Acetates↗

Effect of varying the duration of exposure to phenobarbital on its enhancement of N-bis(2-hydroxypropyl)nitrosamine-induced thyroid tumorigenesis in male Wistar rats.

Male Wistar rats were injected s.c. with a single dose of 280 mg N-bis(2-hydroxypropyl)nitrosamine (DHPN) per 100 g body weight and the effect of subsequent exposure to 500 p.p.m. phenobarbitone (PB) for 6, 12 and 19 weeks on development of thyroid tumors was studied. Exposure to PB for 12 or 19 weeks enhanced the development of thyroid tumors in the rats. The incidences of thyroid tumors in DHPN-treated rats at the end of the experiment for 20 weeks were 87%, 83%, 42% and 37%, respectively, in rats given PB for 19 weeks, 12 weeks, and 6 weeks, and in those given no PB. The incidence of thyroid cancers was 12% in rats given DHPN and then PB for 19 weeks. The total numbers of thyroid tumors were 241, 125, 65 and 23, respectively, in DHPN-treated rats given PB for 19 weeks, 12 weeks, and 6 weeks, and in those given no PB. Thus, the total numbers of thyroid tumors were correlated with the period of PB treatment.

Animals↗