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Biomedical subjects

M Ohshima

Publications and source records attributed to M Ohshima.

At least 109 records · Page 6Linked to original sources

[Analysis of left ventricular wall motion by computer image processing in patients with or without coronary artery involvement in Kawasaki disease].

Predicting myocardial infarction (MI) due to Kawasaki disease is quite difficult because it occurs exclusively in young infants without recognizable symptoms. This study was conducted to identify some clinical loading tests capable of evaluating cardiac reserve and predicting future occurrences of MI in children with Kawasaki disease. Two-dimensional left ventricular short-axis echocardiograms were processed by fast Fourier transformation (FFT) analysis, which yielded phase images and amplitude images, to evaluate objectively regional wall motion. The phase images obtained from five cases for each of normal coronary arteries, dilated coronary artery lesions, and stenosed arterial lesions had nearly homogeneous color levels of the lower scales, while those obtained from the cases with MI showed the areas composed of several different color levels, and the sites of these lesions corresponded to those of SPECT. The amplitude images obtained from five cases for each of the normal coronary arteries, dilated lesions, and dilated with stenosed lesions showed successive transformation of the color from inside to outside throughout the entire circumference. The cases with MI showed a decrease in the color change at the sites of lesion outlined by SPECT. Three-dimensional displays of MI also showed a decrease in the contraction ratios at the sites of infarction. It was concluded that analyses of color images processed by FFT in the three-dimensional display is helpful for objectively evaluating abnormal left ventricular wall motion.

Adolescent↗

Effects of trisodium nitrilotriacetate monohydrate, nitrilotriacetic acid and ammonium chloride on urinary bladder carcinogenesis in rats pretreated with N-bis(2-hydroxypropyl) nitrosamine.

The effects of trisodium nitrilotriacetate monohydrate (Na3 NTA.H2O) nitrilotriacetic acid (H3NTA) and ammonium chloride (NH4Cl) on two-stage urinary bladder carcinogenesis were examined. Carcinogenesis was initiated by administration of 0.2% N-bis (2-hydroxypropyl)-nitrosamine (DHPN) to male Wistar rats in the drinking water for 2 weeks, and then the animals were treated with basal diet containing Na3NTA.H2O, Na3NTA.H2O plus NH4Cl, H3NTA, H3NTA plus NH4Cl, or without these chemicals for 28 weeks. Na3NTA.H2O increased significantly the resultant incidence of neoplastic and preneoplastic lesions of the urinary bladder. Moreover, treatment with Na3NTA.H2O, without the initiation, itself induced papillary or nodular (PN)-hyperplasia. H3NTA produced only a slight increase in the incidence of preneoplastic urinary bladder lesions (PN-hyperplasia) in rats initiated by DHPN, and this was not statistically significant. Elevation of both pH and sodium ion concentration in the urine were correlated with promotion of tumor development. These data showed that Na3NTA.H2O was more effective than H3NTA with regard to promoting potential, and that changes in both urinary pH and concentration of sodium played important roles in enhancement of urinary bladder tumorigenesis by these chemicals.

Acetates↗

Promotive effect of 4,4'-methylenebis(N,N-dimethyl)benzenamine on N-bis(2-hydroxypropyl)nitrosamine-induced thyroid tumors in Wistar rats.

The promotive effect of 4,4'-methylenebis(N,N-dimethyl)benzenamine (MDBA) on 2-stage thyroid tumorigenesis induced by N-bis(2-hydroxypropyl)nitrosamine (DHPN) in Wistar male rats was investigated. Animals were given i.p. injections of DHPN, and then a basal diet containing 0.0375% MDBA for 19 weeks. In addition, localization of the thyroid-stimulating hormone (TSH) in the pituitary gland was investigated. Levels of TSH and T4 in serum were measured by radioimmunoassay (RIA). The addition of MDBA to the diet significantly increased the incidence and numbers of preneoplastic lesion (focal hyperplasia), adenoma and carcinoma of the thyroid. TSH was usually localized in the thyroidectomy-cell in the anterior lobe of the pituitary gland, and the number of TSH-positive cells increased in the group treated with MDBA. Mean circulating levels of TSH were elevated in all MDBA-treated groups, and mean T4 levels in groups treated with MDBA were significantly lower different (P less than 0.05) than those in control groups.

Aniline Compounds↗

Biorhythm of core temperature in depressive and non-depressive alcoholics.

Core temperature was longitudinally evaluated during the day- and nighttime in six non-depressive and in four depressive alcoholics who had been abstaining from alcoholic beverages. The least squares spectrum method was employed for detecting the periods and acrophase of the circadian rhythm of core temperature. Although normal periods were observed in all the patients throughout the study, an abnormal acrophase was found in many patients, especially in depressive alcoholics. On the 3rd and 4th days after alcohol withdrawal, all of the four depressive alcoholics showed a phase advance of the circadian rhythm, and three patients of the six non-depressive alcoholics exhibited an abnormal acrophase. On the 21st and 22nd days after alcohol withdrawal, a normal acrophase was observed in two patients of the four depressives and in four of the six non-depressives. The mean core temperature was higher in the depressives than in the non-depressives on the third and fourth days after alcohol withdrawal.

Adult↗

The promoting effects of food dyes, erythrosine (Red 3) and rose bengal B (Red 105), on thyroid tumors in partially thyroidectomized N-bis(2-hydroxypropyl)-nitrosamine-treated rats.

The effects of erythrosine (Red 3), rose bengal B (Red 105) and thyroidectomy on the development of thyroid tumor were examined in male Wistar rats treated with N-bis(2-hydroxypropyl)nitrosamine (DHPN). Red 3 and Red 105 were used at 4% in the basal diet and were administered for 19 weeks from week 2 to 20. Thyroidectomy was performed by resection of the left lobe at week 4. Single injection of DHPN was performed intraperitoneally at 280 mg per 100 g body weight at the beginning of the experiment. Red 3 and Red 105 significantly promoted the development of thyroid tumors in thyroidectomized rats given DHPN, but had no significant effect in non-thyroidectomized rats. The incidence of thyroid tumors was 91% in rats with partial thyroidectomy, Red 3 and DHPN, 100% in rats with partial thyroidectomy, Red 105 and DHPN, and 64% in rats with partial thyroidectomy and DHPN. Serum TSH was 5.5 +/- 3.1 ng/ml in rats with partial thyroidectomy, Red 3 and DHPN, 2.1 +/- 2.2 ng/ml in rats with partial thyroidectomy, Red 105 and DHPN, and 1.5 +/- 0.5 ng/ml in rats with partial thyroidectomy and DHPN.

Animals↗

Nucleotide sequence of the PR-1 gene of Nicotiana tabacum.

A gene encoding one of the pathogenesis-related proteins, PR1a, and two related pseudogenes were isolated from Nicotiana tabacum. The cloned PR1a gene (pPR-gamma) and one of the pseudogenes (pPR-alpha) were sequenced and found to have similar structures. The sequence of pPR-gamma was quite similar to that of the cDNA clone of PR1a. The plasmid pPR-gamma did not contain an intron and had a typical promoter sequence in the 5'-flanking region.

Base Sequence↗

Comparative metabolism of fenitrothion in aquatic organisms. I. Metabolism in the euryhaline fish, Oryzias latipes and Mugil cephalus.

[14C]Fenitrothion at 0.1 ppm in running water is more rapidly absorbed in the killifish (Oryzias latipes) at 25 than at 15 degrees C to a similar plateau level, and bioaccumulation ratios of fenitrothion are 235 and 339, respectively. Water of higher salinity (23%) resulted in slightly higher accumulation ratios of fenitrothion in both killifish (303) and mullet, Mugil cephalus (179), than fresh water (235 and 30, respectively), but the half-lives are independent of temperature and salinity, with values of 0.24-0.36 day. Fenitrothion was metabolized primarily through hydrolysis by the killifish, demethylation by the mullet, and conjugation of the liberated phenol with glucuronic acid by both species. Although metabolism of the compound was not affected by the different salinities and temperatures in both fish, the glucuronide conjugate was more directly excreted into water under lower temperature and higher salinity conditions. 14C-labeled compounds are distributed primarily in the gall bladder as shown by whole-body radioautography.

Animals↗

Comparative metabolism of fenitrothion in aquatic organisms. II. Metabolism in the freshwater snails, Cipangopaludina japonica and Physa acuta.

When freshwater snails, Cipangopaludina japonica and Physa acuta, were exposed to 0.1 ppm [14C]fenitrothion in a dynamic flow system, the concentrations of fenitrothion and 14C in the body reached equilibrium on Day 1 of exposure. The maximum bioaccumulation ratios of fenitrothion were 18 and 53 in C. japonica and P. acuta, respectively. These snails metabolized the compound primarily by demethylation, hydrolysis, and reduction. The liberated phenol moiety was found to be conjugated with sulfate in C. japonica and mainly with glucose in P. acuta. When the snails were transferred to a freshwater stream, fenitrothion and its metabolites were rapidly excreted, and the half-life of the parent compound was less than 0.5 day in both snails. Fenitrothion and its decomposition products were mainly distributed in liver of P. acuta, as evidenced by whole-body radioautography.

Animals↗

Comparative metabolism of fenitrothion in aquatic organisms. III. Metabolism in the crustaceans, Daphnia pulex and Palaemon paucidens.

When the waterflea Daphnia pulex and the shrimp Palaemon paucidens were exposed to 1.0 ppb [14C]fenitrothion in a flowthrough system, the concentrations of fenitrothion and 14C in the body reached equilibrium, and the maximum bioaccumulation ratios of fenitrothion were 71 and 6 in the daphnia and shrimp, respectively. These crustaceans primarily metabolized the compound by oxidation of P = S to P = O, hydrolysis of P-O-aryl linkage, and demethylation. The liberated phenol was found to be conjugated with sulfate in the daphnia and with glucose in the shrimp. When the organisms were transferred to a freshwater stream, fenitrothion and its metabolites were rapidly excreted from their bodies, and the half-life of the parent compound was less than 0.2 day in both species.

Animals↗

Vaginal agenesis: classification by MR imaging.

Vaginal agenesis was studied by magnetic resonance (MR) imaging lin a 15-year-old girl, a 19-year-old woman, and a 21-year-old woman. In each case MR studies demonstrated the presence or absence of a normal cervix and functioning endometrium. This information was useful in planning surgical management. MR imaging assisted in the classification of the abnormality by noninvasively demonstrating the details of pelvic anatomy-and the uterine morphologic characteristics.

Adolescent↗

Potassium perchlorate, potassium iodide, and propylthiouracil: promoting effect on the development of thyroid tumors in rats treated with N-bis(2-hydroxypropyl)-nitrosamine.

The effect of 1000 ppm potassium perchlorate (KClO4), 1000 ppm potassium iodide (KI) or 1000 ppm propylthiouracil (PTU) in the diet on the development of thyroid tumors was studied histologically and biochemically in Wistar rats given a single ip injection of 280 mg of N-bis(2-hydroxypropyl)nitrosamine (DHPN) per 100 g body weight. Basal diet containing 100 ppm KClO4, 1000 ppm KI or 1000 ppm PTU was given for 19 weeks from week 2 to week 20. The incidence of thyroid adenomas at the end of week 20 of the experiment was 100% (20/20) in rats treated with DHPN followed by KClO4, 85% (17/20) in rats given DHPN followed by KI, 95% (19/20) in rats given DHPN followed by PTU, and 5% (1/20) in rats given DHPN alone. The incidence of thyroid cancers was 100% (20/20) in rats treated with DHPN followed by KClO4, 65% (13/20) in rats treated with DHPN followed by KI and 0% (0/20) in rats treated with DHPN followed by or not followed by PTU. Rats given KClO4, KI or PTU alone and untreated rats had no thyroid tumors. The mean values of TSH in serum were 2.94 +/- 0.79 ng/ml in rats treated with DHPN followed by KClO4, 9.40 +/- 16.0 ng/ml in rats treated with DHPN followed by KI and 60.94 +/- 20.60 ng/ml in rats treated with DHPN followed by PTU. It was confirmed that (1) KClO4, PTU and KI promote the development of thyroid tumor in rats treated with DHPN, (2) the promoting effect of KClO4 or KI is stronger than that of PTU and (3) the value of TSH in serum is not parallel to the promoting effect on the development of thyroid tumor.

Animals↗

Effects of castration before and after treatment with N-bis (2-hydroxypropyl)-nitrosamine (DHPN) on the development of thyroid tumors in rats treated with DHPN followed by phenobarbital.

The effect of castration on the development of thyroid tumors was studied histologically and biochemically in Wistar rats given a single ip injection of 210 mg of N-bis (2-hydroxypropyl)-nitrosamine (DHPN) followed by phenobarbital (Pb). Castration was performed one week after, or one week before the injection of DHPN. The injection of DHPN was given at the end of the first week, and the rats were fed 500 ppm Pb in the basal diet for 38 weeks from week 3 to week 40. The incidence of thyroid adenomas and cancers was 20% (4/20) and 10% (2/20) in rats treated with DHPN alone. It was 75% (15/20) and 40% (8/20) in rats treated with DHPN and Pb; 30% (6/20) and 15% (3/20) in rats treated with DHPN and Pb, and castrated after DHPN; 20% (4/20) and 0% in rats treated with DHPN and Pb, and castrated before DHPN and Pb; and 0% and 0% in rats castrated either before or after receiving DHPN. Castration thus inhibited the development of thyroid tumor in rats treated with DHPN. The inhibition of tumor development in rats treated with DHPN and Pb, and castrated before receiving DHPN, was greater than in the rats castrated after receiving DHPN. Castration inhibited the secretion of TSH in rats treated with DHPN and Pb.

Animals↗

Epithelial lesions of the urinary bladder in three hundred and thirteen autopsy cases.

Urinary bladders that appeared normal macroscopically were obtained from 313 autopsy cases of both sexes and examined microscopically. Proliferative lesions such as Brunn's nests and cystitis glandularis were frequent in cases of all ages and both sexes. Metaplastic lesions such as columnar or cuboidal metaplasia and squamous metaplasia were less frequent. These two types of lesions were not related to age, but squamous metaplasia was more common in females than in males. The sites of predilection for these 4 types of lesions were the trigone and anterior wall. Hyperplasia was observed in 16.3% of the male and 10.6% of the female cases, and dysplasia in 6.8% of the male and 5.7% of the female cases. Both types of lesions were more frequent in older than younger cases. Neither type of lesions was related to chronic inflammation. One case of carcinoma in situ was found in a male. These data and mapping of the bladders indicated that none of these benign proliferative and metaplastic lesions were related with the development of dysplasia or carcinoma in situ.

Adult↗

The role of iodine in carcinogenesis.

Iodine is an essential nutrient for the normal growth and development of humans and animals and is necessary for normal metabolism and regulation of thyroid hormones. Iodine excess can produce thyrotoxicosis but not cancer. However, radioiodine is carcinogenic for the thyroid gland. Dietary iodine deficiency is associated with goiter in humans and animals. The goiter develops because of a feedback system between thyroid hormones, the pituitary gland, and the hypothalamus, and it regulates the synthesis and release of thyroid-stimulating hormone. Chronic hypersecretion of thyroid-stimulating hormone causes profound goiter (diffuse thyroid hyperplasia), which appears to be related to carcinogenesis. Chronic dietary iodine deficiency in rats leads to thyroid follicular adenomas by 12 months and follicular carcinomas by 18 months. An increased risk of thyroid cancer has been reported in humans with goiter and those living in some iodine-deficient areas of the world. In very recent animal studies, iodine deficiency, chemical goitrogens, and thyroid toxins have been shown to have potent tumor-promoting effects. In rats, iodine deficiency is a much more effective tumor promoter than it is a carcinogen, suggesting that a similar relationship may exist in human populations. These studies suggest that a major role of iodine is to prevent the formation of thyroid tumors in humans and animals.

Animals↗

Interstrain differences in susceptibility to liver carcinogenesis initiated by N-nitrosodiethylamine and its promotion by phenobarbital in C57BL/6NCr, C3H/HeNCrMTV- and DBA/2NCr mice.

Selected inbred strains of mice were compared with respect to their susceptibility to two-stage liver carcinogenesis. Five-week-old male mice of strains C57BL/6NCr (C57), C3H/HeNCrMTV- (C3H) and DBA/2NCr (DBA) were given a single i.p. injection of N-nitrosodiethylamine (DEN, 90 mg/kg body weight) or the solvent tricaprylin (10 ml/kg). Beginning 2 weeks later, half of the DEN-treated and half of the control mice were given drinking water containing 0.05% phenobarbital (PB). Ten mice from each treatment group were killed at 12, 24, 36 and 52 weeks of age (5, 17, 29 and 45 weeks exposure to PB). PB significantly increased both the number of hepatocellular foci/cm2 and the incidence of hepatocellular tumors after 17 weeks of treatment in 24-week-old DEN-initiated mice of strains C3H (0.11 +/- 0.07 versus 2.9 +/- 0.3 foci/cm2 and 20 versus 70% incidence of hepatocellular tumors) and DBA (0.09 +/- 0.09 versus 3.72 +/- 0.6 foci/cm2 and 0 versus 90% incidence of hepatocellular tumors) but was ineffective in C57 mice (0.04 +/- 0.04 versus 0.07 +/- 0.07 foci/cm2). At 36 weeks of age the incidence of liver cell tumors in mice given DEN but not PB was 10 (DBA), 10 (C57) and 50% (C3H); the incidence was increased by PB to 90% in DBA and 100% in C3H mice, but there was no increase in C57 mice. Even at 52 weeks, the low incidence of hepatocellular tumors in C57 mice given DEN only (20%) was not significantly increased by subsequent exposure to PB. Serum PB levels observed at 12, 24 and 36 weeks of age were significantly higher in DBA mice than in C57 or C3H mice. Similar results were observed in a separate study in which PB was administered in drinking water to 7-week-old male mice of these three strains for 20 days, during which period serum PB levels were measured at shorter intervals. DBA mice thus appear to be unable to metabolize PB, which itself rather than its metabolites is probably responsible for tumor-promoting effects. DBA mice were especially sensitive, while C57 mice were refractory to promotion of hepatocarcinogenesis by PB. These two strains, which differ with respect to other significant parameters for chemical carcinogenesis including inducibility for aryl hydrocarbon hydroxylase and susceptibility to promotion of hydrocarbon-initiated skin tumors by 12-O-tetradecanoylphorbol-13-acetate, thus also provide a means for analysis of the pharmacogenetics of susceptibility to hepatocellular tumor promotion.

Animals↗

Tumor-initiating and promoting activities of di(2-ethylhexyl) phthalate in vivo and in vitro.

The carcinogenic effects of di(2-ethylhexyl) phthalate (DEHP), including its potential as an initiator and as a promoter of carcinogenesis, were studied in mouse liver and skin and in rat liver in vivo, and in mouse epidermis-derived JB6 cells in vitro. A mouse model for liver initiation and promotion involved initiation by injection of N-nitrosodiethylamine (DEN) intraperitoneally into male B6C3F1 mice at 4 weeks of age, followed by exposure to either DEHP in the diet (3000, 6000, or 12,000 ppm) or phenobarbital in the drinking water (500 ppm), beginning 1 to 2 weeks later and continuing for periods of from 1 day to 18 months. Female F344/NCr rats were subjected to a similar protocol in which promotion continued for 14 weeks. DEHP promoted focal hepatocellular proliferative lesions (FHPL), including hyperplastic foci and neoplasms initiated by DEN in mice but not in rats. Skin-painting studies in female CD-1 or SENCAR mice involved initiation by a single topical exposure to 7,12-dimethylbenz[a]-anthracene (DMBA) applied to the dorsal skin, followed by repeated percutaneous exposure to a tumor promoter, either DEHP or 12-O-tetradecanoylphorbol-13-acetate (TPA). To test for two-stage skin tumor promotion, SENCAR mice were initiated with DMBA and then TPA was administered for only 2 weeks, after which DEHP was subsequently administered for 26 weeks. DEHP displayed very weak complete promoting activity and definite second stage promoting activity in SENCAR mouse skin, but was inactive under our conditions on CD-1 mouse skin. In vitro promoting activity of DEHP and its hydrolysis products, mono(2-ethylhexyl) phthalate (MEHP) and 2-ethylhexanol (EH), was studied by using promotable mouse epidermis-derived JB6 cells. DEHP and MEHP promoted JB6 cells to anchorage independence, while EH did not.

Adenoma↗