Scope of clinical photodermatology.
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Dermatology↗
Biomedical subjects
H C Wulf
Publications and source records attributed to H C Wulf.
Pretreatment with long-wave ultraviolet light inhibits ultraviolet-induced skin tumor development in hairless mice.
The carcinogenic effects of long-wave ultraviolet radiation (UV-A) (320 to 400 nm) irradiation followed by exposure to broad-spectrum ultraviolet (UV) irradiation were studied in 200 lightly pigmented, hairless, hr/hr C3H/Tif mice. No skin tumors were observed in the group irradiated with UV-A for four weeks (total dose, 4050 kJ/m2, observed for 57 weeks). Ultraviolet exposure induced skin tumors in a dose-dependent manner. In a group exposed to UV irradiation for 13 weeks, 35% of the mice had developed tumors after 57 weeks. Twenty-six weeks of exposure resulted in 88% of the animals being affected. In contrast it was found that treatment with UV-A irradiation (four weeks, total dose up to 4200 kJ/m2) preceding exposure to UV irradiation (13 or 26 weeks) resulted in a significantly delayed tumor development. Exposure with UV-A induced no visible changes of the skin, and subsequent microscopic examination revealed no measurable changes in epidermal thickness or melanin content. Our results suggest that, depending on the exposure schedule, UV-A in addition to previously reported carcinogenic properties also may act as an antitumor agent.
Animals↗
Normal sister chromatid exchange in lymphocytes from patients with multiple epidermal cancer?
Exposure to toxins in the environment and due to personal habits, e.g., tobacco smoking, may increase the rate of spontaneous sister chromatid exchange (SCE). The SCE in lymphocytes from a group of 31 patients with multiple epidermal cancer, who in the past had been exposed to various skin carcinogens, as a whole exceeded that of a control group--matched by sex, age, and smoking habits--but the difference was not statistically significant (p = 0.08). The individual SCE in these patients was also statistically independent of the nature of the carcinogenic exposure. We were unable to detect correlations between the SCE and UVC-radiation induced DNA synthesis, UVC-radiation tolerance, or rate of X-ray damage repair. This suggests that the molecular mechanisms involved in SCE induction and in repair of radiation damage are basically independent.
Adult↗
The nevoid basal cell carcinoma syndrome: sensitivity to ultraviolet and x-ray irradiation.
Demographic studies in patients with skin cancer have demonstrated the importance of exposure to ultraviolet and x-ray irradiation. This paper describes in vitro studies in peripheral lymphocytes from three patients with the nevoid basal cell carcinoma syndrome. Particular stress was placed on the following factors: (1) the distribution of the lymphocyte subsets, (2) the frequency of spontaneous sister chromatid exchange, (3) the effect of ultraviolet C (UVC) (254 nm) on deoxyribonucleic acid (DNA) synthesis, (4) the effect of UVC on the phytohemagglutinin-stimulated lymphocyte proliferation, and (5) the capacity to repair x-ray-induced DNA damage. Our data indicate that the distribution of the peripheral lymphocytes was normal, while the frequency of spontaneous sister chromatid exchange was high. The capacity of the lymphocytes to repair x-ray-induced DNA damage was low in all three patients. In two patients the UVC-induced DNA synthesis was reduced, while an increased UVC-induced inhibition of lymphocyte proliferation was observed. These cellular responses in vitro to ultraviolet and x-ray irradiation correspond to the clinical features of the nevoid basal cell carcinoma syndrome. A clearly defective in vitro cellular response to x-ray irradiation, reflecting the clinically evident x-ray sensitivity in the nevoid basal cell carcinoma syndrome, has not been reported previously.
Adult↗
Dose response and time course for induction of T6- DR+ human epidermal antigen-presenting cells by in vivo ultraviolet A, B, and C irradiation.
In vivo ultraviolet (UV) exposure of human skin abrogates the antigen-presenting function of T6+ DR+ Langerhans cells and induces the appearance of antigen-presenting T6- DR+ epidermal melanophages. UV-exposed epidermal cells containing T6- DR+ epidermal antigen-presenting cells, in contrast to unexposed epidermal cells containing T6+ DR+ Langerhans cells, potently activate autoreactive regulatory T cells in the absence of exogenous antigens. Autoreactive T cells may be important for regulation of other immune responses such as those which occur in photosensitive lupus erythematosus and in immune surveillance of UV-induced skin cancers. It is therefore imperative to determine the factors that govern their appearance in the skin. It was found that UVB and UVC, but not UVA, induced a dose-dependent appearance of T6- DR+ epidermal melanophages. The optimal time of appearance was 2 or 3 days after UVB and UVC exposure. In contrast, UVA was a poor inducer of T6- DR+ cells at all doses and all time points tested. Although UVA was a poor inducer of T6- DR+ epidermal cells, UVA radiation resulted in depletion of T6+ DR+ Langerhans cells from the epidermis, as did UVB and UVC radiation. This differential effect of UV wave bands on the immunocompetent cells in human skin may be related to the greater potential of UVB exposure to induce skin cancers and to exacerbate systemic lupus erythematosus.
Adult↗
UVB and UVC, but not UVA, potently induce the appearance of T6- DR+ antigen-presenting cells in human epidermis.
Non-Langerhans cell, antigen-presenting T6- DR+ epidermal cells (EC) appear 3 days following broad band ultraviolet radiation exposure of human skin and are responsible for the increased antigen presentation capacity of EC seen 3 days after UV exposure. To determine the UV wavelengths that induce T6- DR+ EC, volar forearm skin of 10 human volunteers was irradiated in vivo with 4 minimal erythema doses (MED) each of pure UVA (mean 482 J cm-2), UVB (mean 0.390 J cm-2), and UVC (mean 0.397 J cm-2). The purity of the light sources was as follows: UVB, 98% of the emission was in the UVB range; UVC, 97% of the irradiance was in the UVC range; UVA, 100% of the energy had wavelengths longer than 340 nm. Three days after UV irradiation with 4 MED of each wavelength band, suction blister-derived EC suspensions were prepared from the UV-exposed and unirradiated sites. Percentages of T6+ DR+ Langerhans cells (LC) and T6- DR+ EC were quantitated. Relative to control EC, which contained 2.4 +/- 0.3% T6+ DR+ LC, the mean percentage (+/- SEM) of T6+ DR+ LC contained within UV-exposed EC was significantly decreased as follows: UVB, 0.5 +/- 0.2%; UVC, 0.9 +/- 0.1%; UVA, 0.5 +/- 0.2% (n = 10). T6- DR+ EC, absent in control EC, were induced both by UVB, 5.2 +/- 1.7% and UVC; 1.5 +/- 0.4%. Despite the use of more than 1200 times greater doses in J cm-2 of UVA than UVB and UVC, UVA was a poor inducer of T6- DR+ EC (0.5 +/- 0.2%) and in about half of these individuals, T6- DR+ EC were undetectable. The UV wavelengths for induction of T6- DR+ EC lies predominantly within the UVB band, but also to a lesser extent within the UVC band. These wavelengths appear to be analogous to both the wavelengths for generation of increased host susceptibility to UV-induced murine tumors and to the wavelengths for UV-induced systemic suppression of contact hypersensitivity. However, our data indicate that UV wavelengths for decreasing the number of T6+ DR+ LC in humans differs from the wavelengths for induction of systemic suppression of contact hypersensitivity in mice. Taken together, these data suggest that the appearance of T6- DR+ EC, but not the disappearance of T6+ DR+ LC, following UV exposure may be related to the induction of such antigen-specific suppressor T cells.
Antigen-Presenting Cells↗
Extremely high sister chromatid exchange baseline levels in normal, healthy individuals.
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Chromosome Aberrations↗
Mustard gas: clinical, toxicological, and mutagenic aspects based on modern experience.
Based on a study of the literature and our own experience treating fisherman poisoned by mustard gas, this article outlines the clinical effects, and toxicological and mutagenic properties of the agent. Mustards are very persistent chemical agents that easily penetrate clothing. Mustard gas usually causes clinical symptoms after the liquid penetrates the skin or the vapor is inhaled. Skin lesions are similar to first- or second-degree burns and usually heal spontaneously in 4 to 6 weeks. Eye symptoms are photophobia and reduced vision. Following inhalation of the agent, pulmonary edema and long-term dyspnea may be seen. As mustard gas is an alkylating substance, it is conceivable that the risk of developing cancer may be increased, as observed in people who were involved with the production of mustard gas and in animals exposed to the gas. Also, transient significantly increased sister chromatid exchange rates have been found in fishermen exposed to mustard gas. Patients exposed to mustard gas must be treated immediately after exposure. Treatment should consist of cleaning of the exposed skin and clothes with an antigas powder and water and soap. The skin lesions should be treated as burns. Eye lesions and respiratory problems should be treated symptomatically.
Eye Diseases↗
Effects of 254 nm UV irradiation of human lymphocytes in vitro studied on chromosomes, cell cycle phase distribution and cell surface antigens.
Isolated human peripheral blood lymphocytes were exposed to 254 nm UV light and stimulated with PHA. Chromosome analysis revealed significant increases in sister chromatid exchanges (SCE's) and micronuclei, and also in gross chromosomal aberrations, but not in breaks and gaps on the chromatid level. By means of flow cytometry it was shown that UV exposure perturbed the cell cycle in that the S and G2/M fraction decreased when UV was given before stimulation with PHA. Labelling the cells with fluorescein-conjugated antibodies did not reveal any changes in the relative frequencies of lymphocyte subsets after exposure, but an overall diminished ability to bind antibody was observed.
Antibodies, Monoclonal↗
Comparison of a fluorescent monoclonal antibody assay and a tissue culture assay for routine detection of infections caused by Chlamydia trachomatis.
The applicability of a commercial direct immunofluorescent monoclonal antibody assay for detection of Chlamydia trachomatis elementary bodies was studied on endocervical smears from 506 women attending a venereal disease clinic. The aim of this prospective examination was to simulate a daily routine. The results were compared to those of a well-functioning tissue culture assay. The overall positivity was 22.7%. Based on a positivity criterion of greater than or equal to 1 elementary body in the fluorescent antibody assay, the two assays agreed in 84.8% of the cases. In 50 specimens the antibody assay was positive and the culture assay negative, whereas in 23 the culture assay was positive and the antibody assay negative. The positive predictive value was 63.8%. Most of the discrepancies were found in specimens containing few elementary bodies or inclusions. Based on a criterion of greater than or equal to 10 elementary bodies, the positive predictive value was 70.9%, but the sensitivity fell to 67.5%.
Antibodies, Monoclonal↗
Very low sister-chromatid exchange rate in Seventh-Day Adventists.
42 Seventh-Day Adventists (SDAs) and 42 controls matched for sex, age and occupation had their sister-chromatid exchange (SCE) examined in peripheral blood lymphocytes. This was done to examine if the SCE frequency was lower in this group of people, who are known to have a decreased cancer risk compared to the general population. The average SCE/cell in 30 cells from each person was 5.54 +/- 0.07 (mean +/- standard error of the mean) for the SDAs and 8.00 +/- 0.15 for the controls, the difference being statistically significant (p less than 0.00001). No difference in SCE frequency was found between SDAs eating only an ovo-lacto-vegetarian diet and those eating some fish or meat. The mitotic index (MI) was significantly higher and the replication index (RI) was significantly lower in SDAs than in controls. No correlation was found between gamma (a statistical transformation of SCEs/cell) and MI or RI within the groups of SDAs or controls. In the pooled data there was a negative correlation of gamma and MI and a positive correlation of gamma and RI. Of the interpersonal variation in gamma 8% and 14% could be explained by MI and RI. The finding of a lower SCE frequency in a group of SDAs who have a low risk of cancer might indirectly indicate a relation between SCE and cancer and encourages further studies of SCE and diet.
Adolescent↗
Sister chromatid exchange (SCE) in Greenlandic Eskimos. Dose-response relationship between SCE and seal diet, smoking, and blood cadmium and mercury concentrations.
The mutagenicity of the chromosomes of the peripheral lymphocytes of 147 Greenlandic Eskimos living in the district of Angmagssalik, Greenland, and in Denmark, was evaluated by means of the sister chromatid exchange (SCE) test. Thirty cells from each person were examined. The purpose of the investigation was to determine if there was any relationship between mutagenic activity and diet, and hence the elements selenium, cadmium, mercury and lead. The probands were divided into three groups according to their intake of seal meat or industrially prepared food: group 1, those eating seal at least six times per week; group 2, two to five times per week; and group 3 once each week or not at all. The statistical analysis was performed by means of multiple linear regression analyses, with diet, living district, sex, age, tobacco smoking, and blood lead and mercury concentrations as variables. Forty-eight percent of the variation in SCE could be explained by differences in diet, living district, age, and tobacco consumption. Groups 1 and 2 had a 1.7 and 0.65 times higher SCE/cell, respectively, than group 3. For every additional 10 years of age of the probands, the SCE/cell increased by 0.4, and for every 10 g of tobacco smoked per day the SCE/cell was 0.7 higher compared to non-smokers. When priority was given to blood Hg concentration in the calculation, 16.3% of the total variation in SCE/cell could be explained. An increase in the blood Hg concentration of 10 micrograms l-1 corresponded to an increase of 0.3 SCE/cell. In 92 individuals blood Se and Cd concentrations were also analysed. The variables, tobacco smoking, diet, living district and Cd explained 53% of the total variation in SCE. Giving priority to the blood Hg and Cd concentrations, explained 21.4% of the total variation in SCE/cell. An increase of 10 micrograms l-1 in blood Cd and Hg corresponded to an increase in SCE/cell of 0.7 and 0.2, respectively. No influence on the SCE/cell could be attributed to the blood Pb and Se concentrations. Evaluated by the SCE test, seal diet, smoking, living district and blood Hg and Cd concentrations all contribute to mutagenicity in Greenlandic Eskimos, with seal diet as the most important of the factors examined.
Adult↗
Sister-chromatid exchange in childhood in relation to age and sex.
Small children have been found to have a lower SCE/cell than adults and in recent reports females have had higher SCEs/cell than males. We here describe the relationship between SCE/cell and age and sex in 46 girls and 39 boys with an age range of 1.4-19.2 years and 2.6-18.7 years, respectively. For the calculation a transformation y = (sum SCE)1/2 + (sum SCE + 1)1/2 was used. The best fit to our material was represented by the equation y = b0 + b1 X log age. A common slope (b1) could be used for the boys and girls. This slope was significantly different from zero (P less than 0.0005). The levels of the regression lines for the two sexes were different (P = 0.0006). The girls had a 0.55-0.7 higher SCE/cell than the boys, depending on age. The following equations were found: Girls: y = 22.49 + 6.53 X log age. Boys: y = 21.11 + 6.53 X log age. By this model 43% of the variation in y could be explained. As a consequence of the result it is absolutely essential, when planning studies of children, to use age-matched groups to decrease the variability of the test system.
Adolescent↗
Sister chromatid exchanges in lymphocytes of dentists and chairside assistants: no indication of a mutagenic effect of exposure to waste nitrous oxide.
Cytogenetic methods are used increasingly for monitoring occupational exposure to potential mutagenic agents. By one such method, the sister chromatid exchange (SCE) test, previous studies of hospital operating room personnel did not indicate any mutagenic effect from exposure to waste anesthetic gases. Dentists and their assistants are exposed to much higher levels of nitrous oxide than hospital personnel, and in studies of dentists it is possible to eliminate bias from concomitant exposure to halogenated anesthetics by including unexposed persons engaged in the same professional activities as the exposed persons. SCE was examined in lymphocytes of venous blood from 38 female dentists and 74 chairside assistants, all working in the Child Dental Service, and 30 male dentists, of whom 23 worked in private practice. From studies of the model y = bo + b1 X age + b2 X cig./day + b3 X hours of exposure to nitrous oxide/week, by multiple linear regression, there was no indication of any influence of exposure to nitrous oxide on SCE. It was concluded that, from the SCE test, there is no indication of a mutagenic effect from exposure to waste nitrous oxide, and that possible health hazards from such exposure would be induced by other effects of nitrous oxide.
Adolescent↗
Sister chromatid exchange frequency correlates with age, sex and cigarette smoking in a 5-year material of 553 healthy adults.
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Adult↗
Semi-automatic karyotyping facility--a clinical test.
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Autoanalysis↗
Eskimoes and Caucasians have the same SCE levels both in Greenland and in Denmark.
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Adolescent↗
Immunological studies in homosexual men with and without antibodies to human T-cell lymphotropic virus type III.
T-cell subsets were studied in 559 homosexual or bisexual men attending outpatient clinics for AIDS-screening in Copenhagen during the period July 1984 to April 1985. Of the 559 individuals studied, HTLV III antibodies were found in 161 (29%). Persistent generalised lymphadenopathy (PGL) defined as the presence of lymph nodes greater than 1 cm in diameter at two or more extrainguinal sites for at least three months were found in 91 patients, 72 (79%) of whom had HTLV III antibodies. The seropositive group had lower counts of T-helper/inducer cells (p less than 0.001), higher counts of T-suppressor/cytotoxic cells (p less than 0.001), lower T-helper/T-suppressor ratios (p less than 0.001) and higher levels of IgG (p less than 0.001), compared to the seronegative group. Compared to seropositive men without PGL, seropositive men with PGL had higher levels of IgA and IgG (p less than 0.05) and lower T-helper/T-suppressor ratios (p less than 0.05), the latter primarily caused by an elevated number of T-suppressor/cytotoxic cells. It is concluded that HTLV III infection is accompanied by a number of immunological abnormalities, including depletion of T-helper/inducer cells and B-lymphocyte activation. A subgroup of patients is characterised by having PGL and increased serum concentrations of IgA and IgG. The clinical and prognostic importance of PGL and B-cell activation is unknown. To study this more closely, prospective studies are needed.
Acquired Immunodeficiency Syndrome↗