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L K Roberts

Publications and source records attributed to L K Roberts.

48 records · Page 3Linked to original sources
PubMed1981

The effect of various sunscreen agents on skin damage and the induction of tumor susceptibility in mice subjected to ultraviolet irradiation.

Sunscreen preparations containing various chemical UV absorbers, para-aminobenzoic acid (PABA), 2 PABA derivatives, benzophenone or a combination of these were topically applied to the backs of C3H/HeN mice prior to their being irradiated with ultraviolet light in the UVB range. In all cases this treatment was effective in preventing the pathological skin changes associated with UVB irradiation. Histological evaluation of skin biopsies from mice treated with the sunscreen preparations and UVB irradiation showed little or no difference from normals in amount of hyperplasia, melanization or parakeratosis present. These histologic changes were observed in animals receiving UVB irradation in the absence of any sunscreen agent. Pretreatment with the various sunscreen agents did not, however, prevent the induction of tumor susceptibility as measured by the sustained growth of a UV-induced tumor which is immunologically rejected in normal syngeneic mice. These data show a clear distinction between the effects of UVB irradiation leading to histological changes in the epidermis and those leading to the state of tumor susceptibility in mice. The distinction was further corroborated by the finding that epidermal hyperplasia induced by repeated applications of croton oil had no significant enhancing or inducing effects on the induction of tumor susceptibility. In addition, the induction of tumor susceptibility. In addition, the induction of tumor susceptiblity is not due to wavelengths of light less than 320 nm since this effect was abrogated when the UVB radiation was filtered through glass. Possible mechanistic differences between the tumor susceptiblity generated in UVB and photoprotected UVB irradiated animals were observed, however, when we attempted to adoptively transfer the state of tumor susceptibility to normal animals. While it was readily transferable with splenic lymphoid cells from UVB irradiated animals, all attempts to transfer the tumor susceptibility from photoprotected animals have, to date, been unsuccessful.

Animals↗
PubMed1981

Gastric angiodysplasia.

Gastric angiodysplasias may be more common than previously described, and should be considered when barium studies and endoscopy do not reveal the source of chronic or recurrent upper gastrointestinal hemorrhage. Since these lesions are generally submucosal, angiography is the ideal method to diagnose and show the extent of an angiodysplasia. Magnification angiography and gastric air insufflation aid in making the lesions more apparent and in confirming the diagnosis, but prominent early draining veins can be identified by high-quality nonmagnified selective angiography.

Aged↗
PubMed1979

Tumor-susceptibility generated in mice treated with subcarcinogenic doses of 8-methoxypsoralen and long-wave ultraviolet light.

Evidence is presented to show that mice treated with various regimens of 8-methoxypsoralen followed by exposure to long-wave ultraviolet light (PUVA) are rendered tumor-susceptible when challenged with short-wave ultraviolet light (UVB) induced regressor tumors. These same tumors are readily rejected when implanted into normal syngeneic animals. Similar observations have been made in mice treated with subcarcinogenic doses of UVB, where it was shown that the tumor-susceptible state is mediated by suppressor T lymphocytes. These suppressor T-cells may be generated in response to antigens expressed by UVB damaged skin cells. It is now known that suppressor T-cells generated in mice treated with UVB are Ia-positive and have specificities for cross-reacting tumor antigens shared by all UVB-induced tumors, which have been tested to date. Our data suggest that, like UVB treated mice, treatment of mice with PUVA results in tumor-susceptibility mediated through the generation of Ia+ suppressor cells. Since PUVA treatments appear to generate a suppressor cell response in mice, a possible mechanism by which these treatments act to manage autoimmune type skin diseases, such as vitiligo, is discussed.

Animals↗
PubMedDate not supplied

Commercial sunscreen lotions prevent ultraviolet radiation-induced depletion of epidermal Langerhans cells in Skh-1 and C3H mice.

There is much controversy regarding the ability of sunscreens to prevent ultraviolet (UV)-induced immune suppression. Epidermal Langerhans cells (LC) play a key antigen-presenting role in the afferent limb of the immune system's response to antigens introduced through the skin. It has been suggested that depletion of LC in UV-exposed skin is a critical step toward the induction of immunosuppression by UV radiation. There are a number of disparate reports with inconsistent results concerning the ability of sunscreens to prevent UV-induced depletion of LC. The purpose of this study was to systematically evaluate the ability of sunscreens to prevent UV-induced LC depletion in mice. Epidermal sheets obtained from skin biopsies taken from mice exposed to UV radiation from Kodacel-filtered FS20 sunlamps, which do not emit UV power at wavelengths < 290 nm, were immunoperoxidase stained for LC using a rat monoclonal antibody against mouse Ia (major histocompatibility complex class II antigen). Time course and dose-response curves for LC depletion were generated for Skh-1 and C3H mice. Dose-response curves for acute UV exposure induced depletion of LC in Skh-1 and C3H mice were similar, but not identical. LC density in the skin of Skh-1 mice that received chronic UV exposure (3 days/week for 8 weeks) was reduced by 62% after 2 weeks of exposure, but returned to normal levels by 6 weeks. Five commercial sunscreen lotions with labeled sun protection factors (SPF) of 4, 8, 15, 30 and 45 were tested for their capacity to block UV-induced depletion of LC. LC were depleted approximately 75% in the skin of unprotected or placebo lotion treated Skh-1 mice exposed to UV given on two consecutive days. Conversely, LC depletion was prevented in similarly UV exposed Skh-1 mice protected with a SPF 30 sunscreen. In C3H mice the levels of protection against LC depletion provided by the five sunscreens were proportional to the level of protection predicted by their labeled SPF. Comparisons of dose-response curves showed that significantly higher doses of UV were required for LC depletion and induction of skin edema than for the induction of local suppression of contact hypersensitivity. Thus, at UV doses where sunscreens provide complete protection against immunosuppression of contact hypersensitivity, prevention of LC depletion and skin edema would be expected.

Animals↗
PubMedDate not supplied

Splenic contribution to the recovery of ATPase/Ia+ epidermal cells in the skin of mice after exposure to ultraviolet radiation.

The density of Langerhans cells (LC) is significantly decreased in skin sites exposed to ultraviolet radiation (UVR). This results in reduced antigen-presenting cell (APC) activity in UVR-exposed skin. We have previously reported that the recovery in the density of ATPase/Ia+ epidermal cells (EC) parallels the restoration of APC function in the UVR-exposed skin of mice. The present study was designed to determine whether the spleen might serve as a source of ATPase/Ia+ cells to restore APC function to the skin after UVR exposure. ATPase/Ia+ EC densities were calculated from skin biopsies taken from BALB/c mice at various time points after low dose UVR treatment (2000 J/m2 protracted over 4 days). The recovery rate of ATPase/Ia+ EC in splenectomized mice after UVR exposure was similar, although delayed, compared to that of sham-operated mice. For example, 3 days after UVR exposure the density of ATPase/Ia+ EC in sham controls was 90% of normal and exceeded normal values by 5 days. In contrast, ATPase/Ia+ EC density in splenectomized mice was 60% of normal at 3 days and did not exceed normal values until 7 days after UVR exposure. Normal recovery of ATPase/Ia+ EC was restored to splenectomized mice given an adoptive transfer of syngeneic spleen cells immediately after UVR exposure. Fluorescein-labeled spleen cells used for adoptive transfer were observed within the epidermis of splenectomized mice 1 and 3 days after UVR exposure. Indirect immunofluorescent staining employing phycoerythrin-labeled reagents revealed that the fluorescein-labeled splenic EC expressed Ia, MAC-1, CLA, and Fc-receptor molecules. These results indicate that a portion of the ATPase/Ia+ EC that recovery after UVR exposure originate from the spleen. These cells may be distinct from LC, but appear to restore APC function to the skin following LC depletion by UVR exposure.

Adenosine Triphosphatases↗