[Anesthetic management of tracheal surgery.--A case of problematic aspirated foreign body (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Hirose.
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The effects of the sequential administration of 0.01% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), 0.15% N-(4-(5-nitro-2-furyl)-2-thiazoly)formamide (FANFT), 0.025% N-2-fluorenylacetamide (2-FAA), and 0.3% 3.3'-dichlorobenzidine (3,3'-DCB) on urinary bladder carcinogenesis were examined in male Wistar rats. Each chemical was administered for 4 weeks in various combinations. BBN for 4 weeks resulted in no histopathological changes, mild diffuse cell growth, and/or focal hyperplasia after 4, 8, 12, or 16 weeks of observation. No bladder carcinomas were present in rats given only BBN or any one of the other 3 chemicals. Statistically significant incidences of bladder carcinomas occurred with the sequential administration of all 4 chemicals or the first 3 chemicals without 3,3'-DCB. Bladder cancer was also present in rats administered the sequence of FANFT, 2-FAA, and 3,3'-DCB. No antagonistic effects between chemicals were observed.
The kinetics of initiation of in vitro RNA synthesis by Escherichia coli RNA polymerase on the chromatin template of chick oviduct was examined and compared to initiation on the template of deproteinized chick DNA. The formation of rapidly starting, highly stable binary complexes (RS complexes) between RNA polymerase and chromatin was an apparent first order process with a half-time (t1/2) of 9.4 min. By contrast, the t1/2 of formation of RS complex on chick DNA was 1.3 min. The apparent first order rate constants of RNA chain initiation from performed RS complexes were 0.57 s-1 for chromatin and 0.98 s-1 for DNA. Thus, although the formation of RS complex on chromatin was much slower than on DNA, the actual rate of RNA chain initiation on chromatin was similar to that on DNA. The effects of temperature on the formation of RS complex were examined. On chick DNA, both the rate of formation and the amount of RS complex formed decreased as the temperature of preincubation was lowered from 37 degrees to 0 degrees. On chromatin, the t1/2 of formation of RS complex was independent of temperature, and the amount of complex formed was only slightly affected at changing, temperatures. The kinetics of initiation on chromatin is consistent with the hypothesis that the rate-limiting step in the formation of RS complex is dissociation of RNA polymerase from nonspecific interaction with chromosomal proteins. Furthermore, chromosomal proteins seem to interact with initiation sites to facilitate the opening of the DNA strands required for RS complex formation.
Six groups of female outbred Wistar rats were subjected to the following treatments: 2,500 ppm 3-amino-1H-1,2,4-triazole (amitrole) administered in the drinking water (group I); partial thyroidectomy and administration of amitrole in the drinking water (group II); partial thyroidectomy plus autoimplantation of resected thyroid tissue plus administration of amitrole in the drinking water (group III); no treatment (control of group I) (group IV); partial thyroidectomy without amitrole administration (control of group II) (group V); or partial thyroidectomy plus autoimplantation of resected thyroid tissue without amitrole administration (control of group III) (group VI). Goiters developed in all rats given amitrole (groups I-III). Invasive growth of the proliferating follicular tissue through the capsule into adjacent fatty tissue and of pericapsular blood vessels was frequent in these groups (P less than 0.001); invasive lesions were more frequent in the lobectomized thyroid glands of rats (groups II and III). Seven papillary adenomas composed of atypical cells with hyperchromatic nuclei and many mitoses were found in the thyroid glands and grafts in amitrole-treated groups I-II. No invasive growth or adenomas appeared in the control rats of groups IV-VI. Cholangiofibrosis developed in 5 of 100 rats in groups I-III.
A follow-up study has been made of 25 cases with infantile spasms, all of whom were six years old or more at review. Only four (16%) out of 25 cases made a full recovery and attended normal school. Spasms ceased in 96% of all cases, but fits other than spasms (grand mal, tonic seizure, atonic seizure, myoclonic seizure, atypical absence and psychomotor seizure) occurred subsequently in 11 cases (44%). The EEG became normal in two cases (8%), but still showed modified hypsarhythmia in three cases (12%), "epileptic non-hypsarhythmic" discharges in 17 cases (68%) and non-specific abnormalities in three cases (12%). The important factors associated with good prognosis were normal development before the onset of spasms, late onset (seven months old or over) and short duration of spasms, the absence of other types of fit following spasms and lack of neurological abnormality. A bad prognosis was associated with abnormal development prior to the onset of spasms, early onset and long duration of spasms, the presence of other types of fit following spasms and evidence of any neyrological abnormality This follow-up may confirm that the therapy with ACTH-A has no significant effect on final mental state.
The effect of ulcers induced by iodoacetamine on the development of gastric tumors by N-methyl-N'-nitro-N-nitrosoguanidine was studied in male Wistar rats. The ulcerative lesions induced by iodoacetamide were confined symmetrically to the fundic region along the limiting ridge in the stomach and the pyloric region was unaffected. Animals treated with iodoacetamide and N-methyl-N'-nitro-N-nitrosoguanidine produced a high incidence of tumors including adenocarcinoma in the fundic region. The incidence of tumors in the pyloric region in the control group was 80% but there were no tumors in the fundic region. The tumors in the fundic region were most frequently found in the same areas that ulcers had previously been induced. These findings suggest that ulceration and regeneration of the mucosa are important factors in gastric carcinogenesis induced in rats by N-methyl-N'-nitro-N-nitrosoguanidine.
Histological types and grades of 613 urinary bladder cancers induced in rats by N-butyl-N-(4-hydroxybutyl) nitrosamine(BBN) were analyzed. Most of them (95.1%) were transitional cell carcinomas, the remainder being squamous cell carcinomas (3.3%), undifferentiated carcinomas (2.5%), and carcinosarcomas (0.3%). Among the transitional cell carcinomas, 23.3% were Grade I anaplasia, 55.2% Grade II, and 21.5% Grade III. Among the squamous cell carcinomas, 20% each were Grade I and II, and 60% Grade III. Most of the undifferentiated carcinomas were Grade III. Some of the cases of transitional cell carcinoma had areas of squamous metaplasia and/or glandular metaplasia, and the incidence of metaplasia increased with the grade of anaplasia. Approximately 36% of the cases of transitional cell carcinoma were of the invasive type. Invasive types were twice as numerous among cases of squamous cell carcinoma as among those of transitional cell carcinoma and all of undifferentiated carcinomas were invasive. The incidence of invasive type was closely related to the grade of anaplasia. These results show that the morphological characteristics of urinary bladder carcinomas induced by BBN in rats are similar to those seen clinically in humans.
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Seven of 35 male Wistar rats developed well-differentiated adenocarcinoma of the glandular stomach on combined treatment with N-methyl-N'-nitro-N-nitro soguanidine and 4-nitroquinolin 1-oxide. One of the tumors was successfully transplanted into newborn Wistar rats by subcutaneous inoculation. The latent period after inoculation was less than one month and the growth of the transplanted tumor was slow throughout 10 transplant generations. The tumor appeared nodular or cystic in subcutaneous tissues of rats and often caused ulceration of the skin. The histology of transplanted tumors was very similar to that of the primary tumor. Metastasis to both lungs was observed in one rat of the first transplant generation.
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Differences in the susceptibilities of the urinary bladder epithelium of Wistar rats, ICR mice, Syrian golden hamsters, and Hartley guinea pigs to three N-nitroso compounds, N-butyl-N-(4-hydroxybutyl)nitrosamine, N-ethyl-N-(4-hydroxybutyl)nitrosamine, and N-butyl-N-(3-carboxypropyl)nitrosamine, were examined histologically. The urinary bladder epithelium of rats was the most susceptible to all three compounds, and especially to N-ethyl-N-(4-hydroxybutyl)nitrosamine, and bladder cancers developed in all the rats given this compound. The bladder epithelium of mice was less susceptible than that of rats but, although the incidence of cancer was lower than in rats, that of cancer with invasion was higher. Hamsters were far less susceptible than mice, and cancer developed only in 3 of 41 animals given N-ethyl-N-(4-hydroxybutyl)nitrosamine. Guinea pigs were the least susceptible of the 4 species and no tumors were found. Hisotlogically, most of the tumors induced in rats and mice were transtitional cell carcinomas. The incidence of undifferentiated carcinoma was higher in mice than in rats and cellular or structural atypism of the cancer was also greater in mice. Cancers induced in hamsters were all transitional cell carcinomas showing invasion.
Experiments were made on induction of cancer of the glandular stomach of rats by a combination of oral administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and insertion of a plastic bead into the gastric lumen. The incidence of cancer with this combination of treatments was greater than by administration of MNNG alone. Fluoroscopic examination showed that barium sulfate remained in the stomach longer when a bead had been inserted into the gastric lumen. This indicates that after insertion of a bead, MNNG must have remained in the stomach longer, and so the period of exposure of the gastric mucosa to the carcinogen must have increased.
Studies were made on the effect of mucin on the induction of gastric carcinomas by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), with or without sodium chloride, in male Wistar rats. Seven groups of rats were treated as follows: Group 4 was given continuously 50 mg MNNG/liter solution to drink and 1 ml of saturated sodium chloride once a week and fed on stock diet supplemented with 4% mucin. Group 2 was given 50 mg MNNG/liter solution and fed on stock diet supplemented with 4% mucin. Group 3 received 1 ml of saturated sodium chloride once a week and 50 mg MNNG/liter solution to drink. Group 1 was treated with MNNG only. Group 5 was fed on stock diet supplemented with 4% mucin. Group 6 was given sodium chloride only. Group 7 was untreated. The incidence of gastric cancer in Group 3 was significantly higher than that in Group 4 (P less than 0.05) or in Group 1 (P less than 0.05). The difference in the incidence of gastric cancer in Groups 2 and 4, and of intestinal tumors in Groups 1 to 4 were not statistically significant. No malignant tumors were seen in Groups 5, 6, and 7. Thus mucin reduced the high incidence of gastric cancer induced by MNNG and sodium chloride to the level induced by MNNG alone, but it had no effect on the incidence of intestinal tumors. The effect of mucin in preventing destruction of the gastric mucosal barrier by sodium chloride and so reducing the induction of gastric cancer is discussed.
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