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Biomedical subjects

P D Forbes

Publications and source records attributed to P D Forbes.

At least 37 records · Page 2Linked to original sources
PubMed1984

An animal model to determine sunscreen protectiveness against both vascular injury and epidermal cell damage.

Sunscreen preparations can reduce the erythemogenic ( sunburning ) effects of solar ultraviolet radiation (UVR). Less is known about the ability of sunscreens to protect against other forms of UVR-induced damage. This study was designed to yield data on epidermal cell damage at UVR doses sufficient to provoke vascular changes (edema and erythema) in hairless mice, and to determine the comparative effectiveness of a commercial sunscreen in protecting against these two criteria of injury. The sunscreen (Piz Buin 12 Sun Protection Cream) was used at full concentration and at three serial dilutions. The dorsa of 144 hairless mice were treated with one of six sunscreen or vehicle preparations and subsequently irradiated with one of six exposures to an appropriately filtered xenon arc solar simulator. Vascular responses were determined by observing the animals for alterations in the gross appearance of the treated and irradiated sites (edema and erythema). Epidermal cell damage was assessed by determining the sunburn cell ( SBC ) indices in the epidermis removed 24 hours after irradiation. Both the vascular responses and SBC indices indicated that the sunscreen provided concentration-dependent protection against radiation damage. Furthermore, SBC indices provided a relatively continuous variable for quantification of sunscreen effectiveness.

Animals↗
PubMed1984

Different biologic effectiveness of blacklight fluorescent lamps available for therapy with psoralens plus ultraviolet A.

In 1976 we reported a change in spectral distribution of "blacklight" fluorescent lamps. It was not possible to determine the spectral composition of these lamps by any codes or packaging materials. Phototherapy booths utilizing standard BL-HO lamps will accept lamps of at least two spectral distributions; both types are commercially available. This study was conducted to determine the biologic efficacy of these two lamp types that we refer to as BL-O and BL-N. The BL-O spectrum had a peak emission at approximately 350 nm with 98% of the energy between 320 and 400 nm. The BL-N spectrum had its peak emission at 365 nm with a range from 340 to 400 nm. The BL-O spectrum was at least 2.5 to 4 times as effective as BL-N in causing minimally perceptible phototoxicity in albino hairless mice given oral doses of 8 mg/kg of 8-methoxypsoralen. Food and Drug Administration (FDA)-approved specifications imply that the BL-O spectrum is to be used for psoralens and ultraviolet A (PUVA) phototherapy. If lamps with the BL-N spectrum are replaced by lamps with the BL-O spectrum, the metered dose must be reduced to no more than one-fourth of the previous dose or the patient may suffer serious phototoxic reactions.

Animals↗
PubMed1983

Interactions of ultraviolet radiation, 12-O-tetradecanoyl-phorbol-13-acetate and retinoic acid in the skin of hairless mice.

Epidermal changes (mitosis, DNA synthesis, hyperplasia and acanthosis) were used to assay the effects of three different treatments on the dorsal skin of hairless mice: ultraviolet radiation (UVR), all-trans retinoic acid (RA) and/or 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Mice receiving 20 exposures to fluorescent sunlamps in 4 wk (200 Robertson-Berger counts, or about one erythema dose daily, 5 days/wk) and subsequent topical application of methanol (3 applications/wk, beginning 3 wk after the end of UVR treatment) still displayed hyperproliferative cellular activity at least 17 wk after the final UV irradiation. Alone, either RA or TPA (0.001% in methanol, applied topically 3 times/wk) had similar hyperproliferative effects on the epidermis initially, but the skin appeared to adapt to continued treatment with TPA after 14 wk while RA-treated skin remained hyperproliferative. To study the effects of each reagent on UVR-exposed skin, an initiation-promotion protocol was used: repeated applications of the test compound were started 3 wk after the end of 4 wk of UVR exposures. By this method, treatment with either TPA or RA resulted in additional epidermal activity initially. However, although TPA-treated epidermis returned to the control level of activity by wk 21, no significant adaptation to RA treatment was seen.

Animals↗
PubMed1982

Erythema and skin blood content.

We have studied the inflammatory response produced by painting pigs and hairless mice with anthracene and subsequently exposing the skin to fluorescent blacklight lamps. Erythema and oedema appeared in pig skin shortly after the onset of irradiation; oedema but no erythema was evident in mouse skin. The response in both animals became increasingly severe as long as irradiation continued, and began to resolve when irradiation ceased. Hyperaemia (increased tissue blood content) was quantified by the increased in 51Cr-RBC content (c.p.m./wet weight) of the skin. Erythema (appearance of redness) was assessed by the use of an 'erythema grading scale' consisting of red gelatin filters of increased red saturation sandwiched between clear acrylic sheets. Mouse skin responded with a nine-fold hyperaemia compared with unirradiated skin, although no erythema was produced. In contrast, pig skin responded with intense erythema with no corresponding increase in hypaeremia. It is apparent that a stimulus which produced hyperaemia will not necessarily produced erythema, and erythema can develop without hyperaemia.

Animals↗
PubMed1982

Immune responses in nonhaired mice.

Ten stocks and strains of genetically nonhaired mice were evaluated for the ability to respond to two mitogens (concanavalin A and lipopolysaccharide) and to two antigens (sheep erythrocytes and pneumococcal polysaccharide, type III). The number of T and B lymphocytes in the thymus, spleen and pooled lymph nodes of individual animals were determined using immunofluorescent techniques; the values for each group of animals were found to be comparable. The antibody-forming ability was evaluated by determining the number of plaque-forming cells in the spleen after immunization with either antigen. All strains of mice responded to both antigens and the responses are discussed. All groups of mice responded to the mitogens tested.

Animals↗
PubMed1982

Modification of photocarcinogenesis by chemical agents.

The evidence is long standing and compelling that chemical agents can modify the carcinogenic effects of light. Various types of chemical-light interaction are discussed, and events in chemical photocarcinogenesis, chemically enhanced photocarcinogenesis, and promotion of photocarcinogenesis are described. Specific examples of each type of process are given, and the importance of interaction of various wavelengths of UV radiation for these processes is stressed.

Animals↗
PubMed1982

Simulated stratospheric ozone depletion and increased ultraviolet radiation: effects on photocarcinogenesis in hairless mice.

Solar ultraviolet radiation at the surface of the earth is a recognized cause of skin cancer. Postulated anthropogenic reductions in the thickness of the ozone layer would lead to an increased amount of ultraviolet radiation and hence would be expected to increase the risk of skin carcinogenesis. This study uses hairless (Skh:HR) mice as an animal model to study this increased risk. The mice were exposed 5 days/week to graded doses of ultraviolet radiation from a xenon arc lamp attenuated by five different thicknesses of Schott glass filters (WG320) to simulate various ozone layer thicknesses. A Robertson-Berger sunburning ultraviolet meter was used as one of the forms of dosimetry. The results of the various exposure treatments are expressed as the percentage of animal with tumors (incidence) versus time after commencing irradiation and as cumulative tumor yield (average number of tumors per survivor) versus time. With any given filter, the time to 50% incidence is inversely related to daily dose in Robertson-Berger meter units. The time to 50% incidence for comparable Robertson-Berger meter doses through different filter thicknesses increases with increasing thickness. These results indicate that the effective dose for skin cancer induction may be estimated from the Robertson-Berger meter dose but that the Robertson-Berger meter response spectrum underestimates the photocarcinogenic effectiveness of the shorter wavelengths. The cumulative tumor yield data are also consistent with these conclusions. Alternate weighting of the source spectra with the acute-response action spectrum for mouse skin edema gave a better correlation between unit dose and time to a tumor response, independent of the source spectral distribution. This suggests that the mouse skin edema action spectrum, indistinguishable from a human skin erythema action spectrum for lambda greater than 295 nm, is similar in shape to the mouse skin photocarcinogenesis action spectrum for lambda greater than 295 nm.

Animals↗
PubMed1981

Photocarcinogenesis: an overview.

This paper reviews factors that have been reported to influence photocarcinogenesis in laboratory animals. Such factors include the sensitivity of the test animals, the amount of the ultraviolet radiation (UVR) delivered, the mode of its delivery, and interactions of other radiations or of chemicals in the process of carcinogenesis. New data are presented in these areas: reduction in the size of each unit dose (and thus an increase in dosing frequency) increases the carcinogenic effectiveness of a given lifetime dose; certain inbred strains of albino hairless mice exhibit heritable differences in their susceptibility; several chemicals are known to enhance photocarcinogenesis, but they appear to have so little in common, either structurally or functionally, that they offer limited guidance about which other compounds may be effective in this way. Prevention of long-term UVR effects on skin is a desirable goal; development of personal UVR dosimeters will aid in defining the quantitative nature of the problem; improved sunscreens should provide the means to achieve significant reduction in the incidence of UVR-induced human skin cancer.

Animals↗
PubMed1980

Quantitation of phototoxic hyperemia and permeability to protein: II. Inhibition by histamine (H1 and H2) receptor antagonists in mouse skin.

Exposure of anthracene treated skin to long-wave ultraviolet radiation (UVA) will produce hyperemia, increased vascular permeability, burning and itching. This photosensitized inflammation was produced in the skin of hairless mice by the topical application of a 0.025% (w/v) solution of anthracene followed by exposure to UVA. The resultant hyperemia was quantified by the increase in 51Cr-erythrocyte content (cpm/wet weight) of skin. After 1000 sec (1.3 x 10(4)J/M2) of UVA, the blood content of the skin had increased nine-fold. Pyrilamine (H1 antagonist), administered orally, did not inhibit the hyperemia in response to anthracene-UVA, whereas cimetidine (H2 antagonist) increased the blood content of the skin. However, a combination of pyrilamine and cimetidine significantly inhibited the hyperemia, indicating that histamine may mediate the anthracene-UVA hyperemia via H1 and H2 receptors on dermal vessels. Since neither antagonist alone blocked the response, the mechanism of histamine action in this response may involve histamine receptors on other dermal components in addition to the blood vessels. In particular, the exacerbation of this photosensitized inflammation by cimetidine lends support to the concept of H2 receptors on mast cells which negatively modulate histamine release.

Animals↗
PubMed1979

Enhancement of experimental photocarcinogenesis by topical retinoic acid.

Topical application of retinoic acid (RA) solutions greatly enhanced the response of hairless mouse skin to a moderate dose of simulated sunlight. Tumors appeared much earlier, and in much greater numbers, in animals treated daily with 1 or 10 micrograms of RA in methanol immediately after 2 h exposure to a xenon arc filtered through 2 mm of Schott WG 320 glass (approximately equivalent in human erythema effectiveness to 5 min of mid-summer noon solar exposure in northern mid-latitudes), compared to mice treated with light and methanol only. The higher amount of RA, in combination with light, produced moderate epidermal hyperplasia and some scaling and transient erythema, but no gross ulceration or inflammation of skin. The lower amount of RA, though about equally effective in carcinogenesis, produced minimal epidermal hyperplasia compared to the ultraviolet radiation + methanol control.

Administration, Topical↗
PubMed1979

Aging, environmental influences, and photocarcinogenesis.

Repeated exposure of human skin to solar ultraviolet radiation (UVR) over a period of many years is responsible for the induction of most nonmelanoma skin cancers in man. The tumors are progressively more common in chronologically older people. Is this fact purely a function of adequate dose accumulation and development time, or is tumor expression influenced by "physiological age"? The answer to this question influences risk estimates of the results of atmosphere modification. Data from animal studies indicate that the tumor incidence is affected by dose-delivery factors and not just by the accumulated lifetime dose. In addition, young mice are more prone to tumor induction by a given UVR dose than are older animals. Because the quanlity and quantity of the stimulus (UVR) can be readily manipulated and accurately described, studies on photocarcinogenesis offer distinct possibilities for untangling some of the interactive variables in the aging process.

Aged↗
PubMed1978

Experimental ultraviolet photocarcinogenesis: wavelength interactions and time-dose relationships.

Tumors were induced in the skin of SKH hairless mice by exposure to fluorescent FS sun lamps or to a long-arc xenon solar simulator. Tumores developed about equally well with varying amounts of UV-A radiation (lambda greater than 320 nm) given simultaneously. In contrast, incremental changes in the UV-B region (lambda less than 320 nm) led to substantial increases in carcinogenic effectiveness. A tumor-"initiating" dose of UV-B (4-10 wk of daily FS lamp exposures) was rendered less effective by subsequent exposures of the mice to UV-A (6 hr/day, F-40 T12BL lamps). The mechanism for this effect is not known. Most tumors induced by a short course (10 wk) of FS lamp exposure grew slowly or regressed, whereas mice exposed for a longer period (30 wk) developed more tumors, and many of those that appeared early grew aggressively. Effects of daily dose fractionation were less clear, and the subject requires further study. These and other variables are being tested in a program designed to yield useful information on the effects of changing spectrum, dose, and dose delivery rates on sunlight-induced cancer.

Animals↗
PubMed1977

Diester waxes from skin lipids of the feet of biotin depleted and biotin supplemented turkey poults.

The neutral lipids of the skin from the feet of turkey poults fed a biotin supplemented or a biotin deficient diet consist mainly of triacyglycerols, and of mono- and diester waxes. Diester waxes from both groups were characterized as fatty acid esters of erythro-2,3-alkanediols. A comparison between fatty acid composition of the two groups, however, revealed the following significant differences. Biotin deficient birds showed a fairly high concentration of very long chain fatty acids (C36-C40) which were completely absent in biotin supplemented birds. Further, almost one-third of the fatty acids of diester waxes in biotin deficient birds were unsaturated while those from biotin supplemented birds were predominantly (96%) saturated.

Animals↗