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Local effects of UV radiation on immunization with contact sensitizers. I. Down-regulation of contact hypersensitivity by application of TNCB to UV-irradiated skin. 紫外线辐射对接触致敏剂免疫的局部影响。1 .紫外光照射皮肤应用TNCB下调接触性超敏反应。
Pub Date : 1988-06-01
P D Cruz, J Nixon-Fulton, R E Tigelaar, P R Bergstresser

Exposure of mouse skin to UV radiation in doses comparable to those commonly received by humans has been shown to diminish the capacity of irradiated skin to mediate the induction of contact hypersensitivity to dinitrofluorobenzene (DNFB). In other studies, contact sensitization reactions to the structurally related hapten, trinitrochlorobenzene (TNCB), have been used to test the immunogenic properties of haptenated subpopulations of epidermal cells. To extend the applicability of TNCB to experiments that examine UVB modulation of immunization by epidermal cells, we examined the sensitivity of TNCB-induced contact hypersensitivity to low doses of UVB radiation. Abdominal skin of C3H mice was exposed to daily doses of 660 J/m2 broad-band UV radiation for 4 successive days. Immediately following the final exposure, 7% TNCB was applied to irradiated or non-irradiated skin of designated mice. After 5 days, mice were ear-challenged with 2% TNCB, and incremental ear-swelling responses were measured. Mice sensitized with TNCB through irradiated skin exhibited significantly diminished responses compared with UVB-treated mice sensitized through non-irradiated skin. We also found that mice initially sensitized with TNCB through irradiated skin but subsequently painted with oxazolone on normal skin developed full responses to ear-challenge with oxazolone. In contrast, mice sensitized initially with TNCB through irradiated skin failed to fully immunize even after TNCB was repainted on normal skin at a later date. We conclude that low-dose UVB radiation interrupts the induction of contact hypersensitivity to TNCB, leading to hapten-specific nonresponsiveness rather than hypersensitivity, and that this capacity to prevent successful immunization with TNCB is limited to the site of irradiation.(ABSTRACT TRUNCATED AT 250 WORDS)

将小鼠皮肤暴露在与人类通常接受的剂量相当的紫外线辐射下,已证明会降低受照射皮肤介导对二硝基氟苯(DNFB)接触性超敏反应的能力。在其他研究中,对结构相关的半抗原三硝基氯苯(TNCB)的接触致敏反应已被用于测试表皮细胞半抗原亚群的免疫原性。为了将TNCB的适用性扩展到检测中波辐射对表皮细胞免疫调节的实验中,我们检测了TNCB诱导的接触超敏反应对低剂量中波辐射的敏感性。将C3H小鼠腹部皮肤连续4天暴露于660 J/m2的宽带紫外线辐射下。在最后一次暴露后,将7% TNCB立即应用于指定小鼠的辐照或未辐照皮肤。5天后,用2%的TNCB刺激小鼠耳,并测量耳肿胀反应。与未照射皮肤致敏的uvb处理小鼠相比,通过照射皮肤致敏的TNCB小鼠的反应明显减弱。我们还发现,最初通过辐照皮肤致敏TNCB的小鼠,随后在正常皮肤上涂上恶唑酮,对恶唑酮的耳朵攻击产生完全反应。相比之下,最初通过辐照皮肤致敏的小鼠即使在稍后将TNCB重新涂在正常皮肤上也未能完全免疫。我们得出结论,低剂量UVB辐射阻断了对TNCB接触性超敏反应的诱导,导致半抗原特异性无反应而不是超敏反应,并且这种阻止TNCB成功免疫的能力仅限于照射部位。(摘要删节250字)
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引用次数: 0
Corneocyte changes after acute UV irradiation and chronic solar exposure. 急性紫外线照射和慢性太阳照射后角膜细胞的变化。
Pub Date : 1988-06-01
P Corcuff, J L Leveque

The effects of UV irradiation on the human stratum corneum (SC) were studied under both artificial and natural conditions. Artificial UV exposure was performed with a solar simulator. Single doses of radiation from 1 to 3 MED were delivered on the backs of volunteers and the measurements were recorded for a period of one month. Corneocytes were harvested from the skin surface by using a "turbine-machine". Their count and projected area were measured by image analysis. The evolution of corneocyte counts showed 3 steps: 1) a background level of desquamation until the 8th day; 2) a sharp increase from day 9 to day 11; and 3) a plateau until the 20th day. No evolution of the corneocyte size occurred at 1 MED, but a decrease was recorded at day 20 for 2 MED and earlier for 3 MED. Natural sun exposure was investigated in 2 different experiments: on a population living in a sunny coastline and on professional racing cyclists. In these natural conditions, the response of the SC to UV led to an increase in corneocyte count associated with a decreased size. Even though natural environment involves both weather and sun influences, results showed similar SC responses. In case of acute irradiation, the skin recovers its initial state one month later, but in the natural environment, it maintains altered features as long as the UV irradiation occurs.

在人工和自然条件下研究了紫外线照射对人角质层的影响。用太阳模拟器进行人工紫外线照射。在志愿者背上接受1至3个毫微当量的单剂量辐射,并记录一个月的测量结果。使用“涡轮机器”从皮肤表面获取角质层细胞。通过图像分析测量它们的数量和投影面积。角膜细胞计数的演变分为3个步骤:1)至第8天达到脱屑的背景水平;2)从第9天到第11天急剧增加;3)平稳期直到第20天。在1个MED时,角膜细胞大小没有发生变化,但在第20天,2个MED和3个MED时,角膜细胞大小减少。在2个不同的实验中研究了自然阳光照射:生活在阳光明媚的海岸线上的人群和职业赛车手。在这些自然条件下,SC对紫外线的反应导致角质层细胞计数的增加,同时细胞大小减小。即使自然环境包括天气和太阳的影响,结果显示相似的SC反应。在急性照射的情况下,皮肤在一个月后恢复到初始状态,但在自然环境中,只要紫外线照射发生,皮肤就保持改变的特征。
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引用次数: 0
Concentration of trimethylpsoralen in blood and skin after oral administration. 口服三甲基补骨脂素后血液及皮肤的浓度变化。
Pub Date : 1988-06-01
A M Ros, G Wennersten, I Wallin, H Ehrsson

Trimethylpsoralen (TMP) concentrations were determined in blood and skin of 21 patients given oral TMP therapy and were compared to data obtained from 5 patients treated with TMP baths. The quantitative determination was performed by gas chromatography with selected ion monitoring. Concentrations of up to 5.6 ng/ml were detected in whole blood from orally TMP treated patients, with about the same concentrations in patients given TMP baths. Whole skin biopsies from patients ingesting TMP showed concentrations in 14 patients that ranged from 30 to 1250 ng/g skin, median value 85 ng/g. Large interindividual variations were observed. Stripped skin from 5 patients after TMP baths showed a somewhat higher median value of 160 ng/g and their entire skin had fairly high concentrations, with a median value of 390 ng/g, probably mostly bound to stratum corneum. Different concentrations in different parts of the skin may explain the difference in phototoxic capacity when the drug is given locally.

测定了21例口服TMP治疗患者血液和皮肤中的三甲基补骨脂素(TMP)浓度,并与5例用TMP浴治疗患者的数据进行了比较。采用选定离子监测气相色谱法进行定量测定。在口服TMP治疗患者的全血中检测到的浓度高达5.6 ng/ml,在服用TMP浴的患者中检测到的浓度大致相同。对摄入TMP的患者进行的全皮肤活检显示,14例患者的皮肤浓度在30至1250 ng/g之间,中位数为85 ng/g。观察到很大的个体间差异。5例患者经TMP浴后剥去的皮肤中值略高,为160 ng/g,其整个皮肤中浓度相当高,中值为390 ng/g,可能主要与角质层结合。皮肤不同部位的不同浓度可以解释局部给药时光毒性能力的差异。
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引用次数: 0
Delayed sensorineural deafness and skin carcinogenesis in a Japanese xeroderma pigmentosum group D patient. 迟发性感音神经性耳聋与皮肤癌变一例日本色素性干皮病D组患者。
Pub Date : 1988-04-01
A Mamada, S Kondo, A Kawada, Y Satoh, Y Fujiwara

A 65-year-old patient with xeroderma pigmentosum (XP), XP77TO, was assigned to complementation Group D by the cell-fusion study and comprised the fifth Group D case in Japan. The patient had mild solar sensitivity by age 7, dyspigmentation by 10 years, and he still currently has moderate symptoms. The skin phototest by 290, 300 and 305 nm monochromatic ultraviolet (UV) light revealed a delayed peak of erythema 48 h post-irradiation and lowered minimal erythemal doses. The XP77TO skin fibroblasts, as well as a reference Group D strain, exhibited the same 7-fold higher sensitivity to the lethal effect of 254 nm UV as did normal cells. Unscheduled DNA synthesis (UDS) induced in XP77TO cells by 254 nm UV (10 J/m2) was 42% of normal, falling into the Group D range of 25-50% UDS. In spite of such a similar cellular phenotype, XP77TO developed squamous cell carcinomas at 44 and 65 years of age and audiometric sensorineural deafness in a delayed fashion at advanced age.

一名65岁的色素性干皮病(XP)患者XP77TO,通过细胞融合研究被分配到补体D组,这是日本的第五例D组病例。患者7岁时出现轻度日光敏感,10岁时出现色素沉着,目前仍有中度症状。290、300和305 nm单色紫外(UV)光测试显示,照射后48 h红斑峰值延迟,最小红斑剂量降低。XP77TO皮肤成纤维细胞,以及参考D组菌株,对254 nm紫外线致死效应的敏感性比正常细胞高7倍。254 nm UV (10 J/m2)诱导XP77TO细胞的非预定DNA合成(Unscheduled DNA synthesis, UDS)为正常细胞的42%,D组为25-50%。尽管如此相似的细胞表型,XP77TO在44岁和65岁时发展为鳞状细胞癌,并在老年时以延迟的方式发展为听力感音神经性耳聋。
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引用次数: 0
Immediate pigment-darkening reaction. 立即变色反应。
Pub Date : 1988-04-01
H Beitner

The immediate pigment-darkening reaction (IPD) is a gray-brown discoloration of the skin induced mainly by long-wave ultraviolet (UVA) radiation. The threshold value of IPD can be used as an important parameter in a series of light tests. The principle mechanism of the reaction is a photo-oxidative process causing darkening of preformed melanin and the production of free radicals. It has also been suggested that the reaction involves micromorphological changes in the melanocytes and a changed distribution pattern of melanosomes in the keratinocytes. This concept has recently been questioned by independent investigators. The physiological function of IPD still remains largely unknown. No photoprotective effect of the reaction has been observed. It has been suggested that IPD might have been of value during human evolution.

直接色素变黑反应(IPD)是一种主要由长波紫外线(UVA)辐射引起的皮肤灰褐色变色。IPD的阈值可以作为一系列光测试的重要参数。该反应的主要机制是引起预形成黑色素变暗和自由基产生的光氧化过程。也有人认为,该反应涉及黑素细胞的微形态学改变和角化细胞中黑素小体分布模式的改变。这一概念最近受到独立调查人员的质疑。IPD的生理功能在很大程度上仍然未知。未观察到该反应的光保护作用。有人认为,IPD可能在人类进化过程中有价值。
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引用次数: 0
Solar urticaria with delayed onset: a case report. 迟发性日光性荨麻疹1例报告。
Pub Date : 1988-04-01
G Monfrecola, P Nappa, D Pini
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引用次数: 0
Change in epidermal transmission due to UV-induced hyperplasia in hairless mice: a first approximation of the action spectrum. 紫外线诱导的无毛小鼠增生引起的表皮透射变化:作用谱的初步近似。
Pub Date : 1988-04-01
H J Sterenborg, J C van der Leun

UV-induced epidermal hyperplasia was investigated by measuring the optical transmission of the epidermis of hairless mice exposed daily to ultraviolet radiation. The effects of 2 different radiation sources were investigated: Philips TUV 40W, emitting mainly 254 nm radiation, and Philips TL01 40W, emitting radiation in a narrow band around 312 nm. With both lamps a number of groups of animals were used, each receiving a different daily dose. In the experiments with both types of lamps, hyperplasia appeared to be fully determined by the accumulated dose, irrespective of the daily dose administered. This implies reciprocity between the daily dose and the time elapsed since the first exposure. Moreover, the change of transmission with time and daily dose showed very characteristic behaviour. A simple mathematical model was used to describe these changes. In a previous study we used this model to describe the results of a similar experiment with Westinghouse FS40 sunlamps. The combined data from the present and the previous experiments were used to calculate a first approximation of the action spectrum for UV-induced hyperplasia. In addition, we calculated the dose-response relationship for UV-induced increase in tolerance against ultraviolet radiation for the 3 irradiation sources.

通过测量每日暴露于紫外线照射下的无毛小鼠表皮的光透射率,研究了紫外线诱导的表皮增生。研究了Philips TUV 40W和Philips TL01 40W两种不同辐射源的辐射效应,前者主要发射254 nm的辐射,而前者发射312 nm左右的窄带辐射。两种灯都使用了许多组动物,每组动物每天接受不同的剂量。在两种灯的实验中,增生似乎完全由累积剂量决定,而与给予的日剂量无关。这意味着日剂量与第一次照射后所经过的时间之间存在相互关系。此外,传播率随时间和日剂量的变化表现出非常典型的行为。一个简单的数学模型被用来描述这些变化。在之前的研究中,我们使用这个模型来描述西屋FS40太阳灯的类似实验结果。本实验和以往实验的综合数据用于计算紫外线诱导增生的作用谱的第一个近似。此外,我们计算了3种辐照源对紫外线诱导的抗紫外线耐受性增加的剂量-反应关系。
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引用次数: 0
Photosensitive reaction to phenelzine: a case report. 苯乙肼光敏反应1例报告。
Pub Date : 1988-04-01
J D Case, J W Yusk, J P Callen
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引用次数: 0
The (6-4) photoproduct and human skin cancer. (6-4)光产物与人类皮肤癌。
Pub Date : 1988-04-01
D L Mitchell, R S Nairn
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引用次数: 0
Wavelength dependence for DNA synthesis inhibition in hairless mouse epidermis. 无毛小鼠表皮DNA合成抑制的波长依赖性。
Pub Date : 1988-04-01
K Kaidbey

Exposure of mammalian skin to ultraviolet radiation (UVR) results in a transient inhibition of scheduled DNA synthesis. The wavelength dependence for this response was investigated in the epidermis of albino hairless mice. Groups of animals were exposed to narrow wavebands of UVR (HPBW 6.6 nm) from a monochromator in the 260-335 nm range. A dose-dependent inhibition of DNA synthesis was observed following exposure to all test wavebands except that centered at 335 nm. An action spectrum constructed from dose-response regression lines showed peak effectiveness at 290 nm. This spectrum bears a close resemblance to published action spectra for the induction of pyrimidine dimers in vivo, suggesting that DNA is the primary chromophore for both events. The DNA synthesis inhibition spectrum bears little resemblance to a published therapeutic action spectrum for the clearing of psoriasis.

哺乳动物皮肤暴露于紫外线辐射(UVR)会导致预定DNA合成的短暂抑制。在白化病无毛小鼠表皮中研究了这种反应的波长依赖性。各组动物暴露于260-335 nm范围内单色器的窄波段UVR (HPBW 6.6 nm)。暴露于除335 nm外的所有测试波段后,观察到DNA合成的剂量依赖性抑制。由剂量-反应回归线构建的作用谱在290 nm处达到有效峰。该光谱与已发表的在体内诱导嘧啶二聚体的作用光谱非常相似,表明DNA是这两个事件的主要发色团。DNA合成抑制谱与已发表的银屑病清除治疗作用谱几乎没有相似之处。
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引用次数: 0
期刊
Photo-dermatology
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