PubMed Health⌕ Search

Biomedical subjects

F Stenbäck

Publications and source records attributed to F Stenbäck.

At least 127 records · Page 7Linked to original sources
PubMed1976

Benign cartilagenous tumour of the temporomandibular joint.

An unusual case of a benign cartilagenous tumour of the temporomandibular joint is presented. The difficulties encountered in histological diagnosis, the benign behaviour of the tumour and the need for restraint in treatment are emphasized.

Adult↗
PubMed1976

Intratracheal instillation studies with 7H-dibenzo(c,g)carbazole in the Syrian hamster.

The morphologic effects and the retention and distribution times of single and multiple intratracheal instillations in Syrian hamsters of 7H-dibenzo[c,g]carbazole (DBC) and benzo[a]pyrene (BP) were compared. A single instillation of DBC induced slight changes in the hamster respiratory tract; however, five treatments caused tracheobronchial epithelial proliferation, cell hyperplasia, and occasionally, squamous metaplasia. The particle size of both carcinogens was approximately the same. BP in saline remained longer in the lungs than did DBC in saline. The shortest retention time was recorded when DBC was administered in aqueous solution, whereas multiple doses of DBC in aqueous solution did not markedly affect retention time. DBC passed from the lungs to the intestinal tract and was mainly excreted in the feces.

Animals↗
PubMed1976

Carcinogenicity of Benzo(a)pyrene and dusts in the hamster lung (instilled intratracheally with titanium oxide, aluminum oxide, carbon and ferric oxide).

The possible carcinogenic or fibrogenic effects of intratracheal instillation of a polycyclic hydrocarbon, benzo(a) pyrene (B(a)P), alone or in combination with several dusts - titanium dioxide (TiO2), aluminum oxide (Al2O3), carbon (C), and ferric oxide (Fe3O3) - were investigated in hamsters. When administered alone, the dusts induced interstitial cell proliferation, bronchial epithelial alterations and a few granulomatous changes in the pulmonary system, but no tumors. B(a)P alone induced only two tracheal papillomas. However, combined treatment with B(a)P and the dusts caused a number of tumors, dependent upon the dust used. B(a)P plus TiO2 in a small particle size (below 0.5mu) induced papillomas, squamous cell carcinomas and a few adenomas and adenocarcinomas of the larynx, trachea and lungs. These were morpholoigcally similar to neoplasms found after B(a)P and Fe2O3 treatment. B(a)P, combined with C or Al2O3, induced mainly laryngeal and tracheal papillomas. B(a)P- and C-treated hamsters also showed a few lung adenocarcinomas.

Adenocarcinoma↗
PubMed1975

Hexachlorophene in mice. Effects after long-term percutaneous applications.

The toxicity and carcinogenicity of life-time applications of hexachlorophene on the skin of Swiss mice were studied. Twice weekly applications of 0.02 ml of a 50% or 25% solution produced necrosis and ulceration of the skin as well as neurological symptoms and a mortality of up to 22% within two weeks. At autopsy, edema and cystic lesions were seen in the white matter of the central nervous system. The neurological symptoms were reversible, though a proportion of the cystic lesions persisted. Only one skin tumor was seen and the number of tumors of other organs, lymphomas, lung adenomas, liver hemangiomas, and other tumors, was not higher than in the controls. It is concluded from this study that percutaneous application of hexachlorophene has toxic local and systemic effects in mice, but no carcinogenic effects.

Animals↗
PubMed1975

Cellular injury and cell proliferation in skin carcinogenesis by UV light.

The effects on mouse skin of varying doses of light from a high-voltage mercury lamp were compared to the alterations occurring after repeated light applications from a carbon-arc xenon sunlamp. A single dose of UV light at a carcinogenic wavelength caused necrosis and ulceration, followed by scarring, but failed to produce tumors. In the case of repeated small doses, the neoplastic response was predominantly epithelial, resulting in formation of papillomas and squamous cell carcinomas. Increasing the dose caused formation of fibromas and fibrosarcomas of the ear. However, repeated applications of UV light having a spectrum similar to sunlight failed to induce tumors. In these studies, only animals showing initially destructive lesions ultimately presented tumor formation, while the hyperplasia induced by UV irradiation showed no relationship to neoplastic transformation. The results emphasize the significance of dose and wavelength in evaluating effects of UV-light skin carcinogenesis.

Animals↗
PubMed1975

Species-specific neoplastic progression by ultraviolet light on the skin of rats, guinea pigs, hamsters and mice.

Repeated ultraviolet light (UV) irradiation on the skin of rats caused ulceration, scarring and epithelial tumors; 38% of the animals had ear tumors and 5% skin tumors. Guinea pigs presented minimal evidence of neoplastic transformation; only two tumors were seen while hamsters displayed localized epidermal hyperplasia, and 35% of the animals had papillomas and keratoacanthomas of the dorsal skin. In Swiss mice UV irradiation caused ulceration, necrosis and hyperplasia; moreover, fibromas and fibrosarcomas occurred in 17 of 20 tumor-bearing mice. Epithelial tumors originated from the proliferation of benign epidermal cells, through dysplastic changes in the surface epithelium, or from the borders of skin ulcers (in rats). These tumors were local and circumscribed in the hamsters, while covering the entire ear tip in rats. Dermal tumors, consisting of fibroblastic 'light' and 'dark' cells, occurred in mice previously showing extensive ulceration and scarring.

Animals↗
PubMed1975

Initiation-promotion skin carcinogenesis and immunological competence.

The immune competence of mice during initiation-promotion skin carcinogenesis was determined by skin allograft rejection and lymphocyte mitogenesis. The carcinogen 7, 12-dimethylbenzanthracene inhibited the cellular immune competence of mice while lymphocytes from croton oil treated mice had enhanced PWM response. Chlorphenesin, a stimulator of cellular immunity, was found to inhibit tumorigenesis in initiation-promotion skin carcinogenesis when injected during promotion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

Magnesium oxide as carrier dust in benzo(a)pyrene-induced lung carcino-genesis in Syrian hamsters.

The neoplastic progression induced by intratracheal instillation of benzo[a]pyrene (BP) and magnesium oxide (MgO) was compared with that induced by intratracheal instillation of BP and ferric oxide (Fe2O3). BP and MgO produced squamous cell carcinomas and papillomas in the larynx with a latent period as shor as 9 weeks. They also induced many papillomas as well as squamous cell carcinomas and adenocarcinomas in the trachea and a papilloma, squamous cell carcinomas, adenocarcinomas, adenosquamous lesions, and peripheral adenomatoid lesions in the bronchi. They rarely caused tumors in other organs; only a few forestomach papillomas, one melanoma on the dorsal skin, and one ovarian carconoma were seen BP, with Fe2O3 as the carrier, induced a comparable number of histologically similar tumors; however, tumors developed more frequently in the main bronchi. Thus MgO strongly facilitated the tumor-inducing effects of BP, causing tumors in different areas of the respiratory tract, and was as effective as Fe2O3 as a carrier agent in the experimental induction of respiratory tumors.

Animals↗