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Biomedical subjects

W L Morison

Publications and source records attributed to W L Morison.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effects of ultraviolet radiation on the immune system in humans.

In experimental animals, exposure to UV-B radiation produces selective alterations of immune function which are mainly in the form of suppression of normal immune responses. This immune suppression is important in the development of nonmelanoma skin cancer, may influence the development and course of infectious disease and possibly protects against autoimmune reactions. The evidence that this form of immune suppression occurs in humans is less compelling and very incomplete. The wavelengths of radiation most affected by a depletion of the stratospheric ozone layer are those known to be most immunosuppressive in animals and it is likely that such depletion will increase any suppressive effect of sunlight on immunity in humans. In addition to establishing whether or not UV-B radiation can cause suppression of immune function in humans, studies are required to determine if melanin can provide protection against such suppression, the role of this suppression in the pathogenesis of skin cancer, the development of infectious disease and vaccine effectiveness, and the capacity for humans to develop adaptive, protective mechanisms which may limit damage from continued exposure to UV-B radiation.

Animals↗
PubMed1988

Skin cancer and artificial sources of UV radiation.

Exposure of people to indoor ultraviolet (UV) radiation has vastly increased in the past one or two decades, mainly due to increased recreational exposure and partly as a result of therapy for skin disease. This trend will result in an increased incidence of skin cancer, but the magnitude of the increase is speculative at present because of a lack of information about the extent and nature of the recreational UV exposure.

Body Surface Area↗
PubMed1987

Ultraviolet carcinogenesis in athymic nude mice.

We have investigated the development of skin cancer from exposure to ultraviolet (UV) radiation in C3H- nu/nu nude mice. Nude mice, nude mice reconstituted with thymuses, and nude mouse skin grafted onto normal haired mice had similar tumor incidences and rates of tumor development. All tumors were squamous cell carcinomas and both well-differentiated and poorly differentiated lesions occurred in each of the groups. Transplants of the tumors that developed in nude skin grew preferentially in immunosuppressed mice as compared with normal mice, indicating that tumors from each treatment group were antigenic. These results indicate that the presence or absence of a functioning thymus does not seem to influence UV carcinogenesis.

Animals↗
PubMed1987

A novel model for testing enhancers of pigmentation.

Mouse skin, unlike human skin, does not contain active epidermal melanocytes, with the exception of the ear and tail skin in some pigmented strains. We have investigated enhancement of pigmentation in inbred C3H- mice using tail skin as a model for testing the effects of phosphorylated DOPA (DP) and ultraviolet radiation. Mice were restrained by cage dividers and treated with various doses of DP in dimethylsulphoxide (DMSO) or DMSO alone with or without the addition of UV radiation. Each tail served as its own control since only the dorsal surface was treated and irradiated. Pigmentation was graded blindly on histologic sections stained with Fontana-Masson. UV radiation caused a marked increase in epidermal and dermal pigmentation and this was enhanced in a dose-dependent manner by DP. However, there was minimal effect from DP alone.

Animals↗
PubMed1986

Studies on the mechanism of systemic suppression of contact hypersensitivity by UVB radiation. II. Differences in the suppression of delayed and contact hypersensitivity in mice.

Exposing mice to UV radiation in the UVB range (280-320 nm) causes a selective immune suppression that contributes to the development of UVB-induced skin cancers. Among the immune responses suppressed by UVB irradiation are contact and delayed hypersensitivity reactions to haptens administered at unexposed sites. In these studies we provide evidence that delayed and contact hypersensitivity to the same hapten are not equivalent reactions and that they are suppressed in UVB-irradiated mice by 2 different mechanisms. This conclusion is based on the findings that: suppression of contact hypersensitivity could not be overcome by immunizing UVB-irradiated mice with hapten-coupled antigen-presenting cells derived from normal donors; and treatment of UVB-irradiated mice with methylprednisolone before immunization prevented the suppression of delayed hypersensitivity but had no effect on the suppression of contact hypersensitivity. The decreased ability to induce contact hypersensitivity in UVB-irradiated mice could be transferred to x-irradiated mice by reconstituting them with spleen cells from UVB-irradiated donors. The induction of hapten-specific suppressor cells, however, required both UVB irradiation and priming with hapten. Based on these results, we postulate that UVB irradiation induces a population of suppressor-inducer cells with specificity for a modified skin antigen and that this antigen serves as a carrier molecule for haptens that induce contact hypersensitivity and for tumor-specific transplantation antigens on UVB-induced tumors.

Animals↗
PubMed1986

Photoageing: the role of UVB, solar-simulated UVB, visible and psoralen UVA radiation.

We have studied the morphological and histological effects of chronic exposure of two strains of haired mice (albino Balb/c and pigmented C3H-) to various types of radiation. UVB (280-320 nm) radiation from unfiltered sunlamp bulbs for 20 and 30 weeks produced marked epidermal acanthosis and dyskeratosis which was reversible in mice exposed for 20 weeks followed by a 20-week rest. In the dermis the elastic fibres were altered and in the pigmented mice these changes had almost completely reversed 29 weeks after cessation of exposure. Cellulose acetate-filtered sunlamp bulbs (greater than 289 nm) produced similar but less marked changes. Chronic exposure to UVA (320-400 nm) radiation produced minimal alterations in the dermis while the epidermis was normal. Visible (greater than 400 nm) radiation in large doses produced no degenerative changes. Methoxsalen/UVA radiation produced epidermal acanthosis, dermal sclerosis, and alteration of elastic fibres, which was prominent in both strains at 40 weeks. These findings suggest that the UVB component of sunlight is largely responsible for photoageing of the skin. Furthermore, chronic exposure to methoxsalen/UVA therapy is likely to potentiate solar-induced photoageing.

Aging↗
PubMed1986

Histopathologic findings in papulovesicular light eruption.

Papulovesicular light eruption (PVLE) is a distinct clinical and histological subset of polymorphous light eruption. Biopsies from 16 patients with PVLE showed prominent epidermal and dermal changes consisting of intercellular edema, papillary dermal edema and a perivascular and interstitial infiltrate in the upper dermis.

Adult↗
PubMed1986

UV radiation-induced tumors in haired mice: identification as squamous cell carcinomas.

The most common tumor induced by UV radiation in haired mice is considered to be a fibrosarcoma on the basis of its presentation as a nodule in the skin and on the basis of a spindled appearance upon light microscopic examination. A squamous cell carcinoma is thought to be a much less common tumor. In the present report this concept was reevaluated in mammary tumor virus-free C3H/HeNCr (C3H-) mice. From first appearance, almost all lesions upon gross morphologic examination have an epidermal component and initially are similar to solar keratoses in humans. The lesions then become nodular and eventually develop central ulceration, often with a rolled border characteristic of squamous cell carcinomas. The morphology upon light microscopic examination ranged from well-differentiated squamous cell carcinoma to a poorly differentiated spindle cell neoplasm. Occasionally, variable patterns of squamous differentiation were seen in the same lesion. Immunoperoxidase examination with a polyclonal antikeratin serum demonstrated the presence of keratin in 84 of 87 tumors. Frequent, poorly formed desmosomes were found on ultrastructural examination. These tumors usually had a regressor phenotype upon transplantation into recipients. In conclusion, almost all UV radiation-induced tumors in C3H- mice are squamous cell carcinomas, and these tumors are usually antigenic.

Animals↗
PubMed1986

Studies on the mechanism of systemic suppression of contact hypersensitivity by ultraviolet B radiation.

Exposure of mice to ultraviolet (UV) B radiation (280-320 nm) induces suppressor T lymphocytes (Ts) that prevent the rejection of primary skin cancers. A model for understanding how UVB radiation activates the suppressor cell pathway is based on the finding that UVB irradiation of mice also induces hapten-specific Ts following application of a contact sensitizing agent to unirradiated skin. Studies presented here address the mechanism by which the Ts pathway is activated in UV-irradiated mice. The hypothesis tested is that the induction of Ts results from a direct alteration of circulating antigen-presenting cells (monocytes) by the radiation. This hypothesis predicts that the UV-induced suppression of contact hypersensitivity will be reversed by replacing the antigen-presenting cells (monocytes or macrophages) after irradiation. To test this prediction, UVB-irradiated mice were given normal bone marrow cells, spleen fragments, splenic antigen-presenting cells, or stimulants of endogenous bone marrow cells. None of these procedures reversed the effects of the irradiation. Furthermore, immunization of UVB-irradiated mice with hapten-coupled splenic macrophages also failed to restore the contact hypersensitivity reaction. Therefore, direct inactivation of circulating monocytes does not appear to be the mechanism by which UVB radiation induces Ts. Experiments are also presented indicating that passive accumulation of inflammatory cells in the skin does not explain the UVB-induced systemic suppression of contact hypersensitivity. Collectively, these results support the hypothesis that a soluble mediator, induced by exposure of the skin to UVB radiation, is involved in UVB-induced systemic immunosuppression.

Animals↗
PubMed1986

Possible mechanism of piroxicam-induced photosensitivity.

The therapeutic use of piroxicam as a nonsteroidal anti-inflammatory agent is associated with the development of photosensitivity in less than 1% of patients. The eruption usually occurs within a few days of commencing treatment with the medication. This time course suggests a phototoxic reaction. Attempts to demonstrate the phototoxic effects of piroxicam in humans, laboratory animals, and in in vitro cell assays were unsuccessful. At high concentration, however, one metabolite of piroxicam was phototoxic in animal studies and in in vitro assays. A second metabolite was mildly phototoxic in laboratory animals. These results suggest a mechanism whereby piroxicam photosensitivity may be due to a metabolite preferentially formed or accumulated in affected patients.

Animals↗