PUVA照射与青黛丸口服对银屑病患者血c—AMP,cGMP,SOD及LPO含…

研究ＰＵＶＡ及青黛丸口服治疗寻常型银屑病对患者血清中ＳＯＤ活力、ＬＰＯ水平、ｃＡＭＰ及ｃＧＭＰ含量的影响。方法：寻常型银屑病患者７４例，随机分成ＰＵＶＡ照射组及青黛丸服用组，按常规行治疗方案，采用微量指血超经物歧化酶快速地测定红细胞内ＳＯＤ活力，荧光分光光度法测定血清脂质过氧经物值、放射免疫分析法测定血浆ｃＡＭＰ及ｃＧＭＰ量。结果：治疗前患者ＳＯＤ和皆低于对照组（Ｐ〈０．０１），ＬＰＯ水平晚明显差     

光量子血疗法治疗寻常型银屑病

我们用光量子血疗法即激光紫外光量子血氧疗法（ｌａｓｅｒｑｕａｎｔｕｍｉｒｒａｄｉａｔｉｏｎｏｎｂｌｏｏｄ，简称ＬＱＢ疗法）治疗４０例寻常型银屑病（ＰＶ）患者，随意选择１５例ＰＶ患者测定治疗前后血浆过氧化脂质（ＬＰＯ）及红细胞超氧化物歧化酶（ＳＯＤ）活...     

银屑病患者血液抗氧化能力的测定

银屑病患者血液抗氧化能力的测定蔡茂庆，李君蒂银屑病是一种慢性炎症性皮肤病，迄今病因不明，我们对２５例寻常型银屑病患者进行了血液超氧化物歧化酶（ＳＯＤ）、脂质过氧化物（ＬＰＯ）和还原型谷胱甘肽（ＧＳＨ）水平的测定，并以３３例正常人作对照，以探讨血液抗氧...     

豚鼠和小鼠光变态反应性接触性皮炎模型的建立及比较

目的 比较两种运动作为光变态反应性接触性皮炎（ＰＡＣＤ）模型各自的优势，以选择其在临床工作中发现潜在的光敏性物质。方法 以６－甲基香豆素（６－ＭＣ）为光敏剂分别制作豚鼠和小鼠ＵＶＡ的ＰＡＣＤ模型，并以外涂６－ＭＣ经ＵＶＢ照射组作为对照。结果 成功的建立了两种运动外涂６－ＭＣ并经ＵＶＡ照射的ＰＡＣＤ模型。结论 两种动物ＰＡＣＤ模型各占优势，可以根据实际情况选择所需要的模型。     

寻常性银屑病外周血免疫调节T细胞变化的研究

寻常性银屑病外周血免疫调节Ｔ细胞变化的研究曹克诚，曹煦，李忆芝天津医科大学第二医院（邮政编码３００２１１）我们应用ＭｃＡｂ技术，对寻常性银屑病（ＰＳＶ）患者系统地动态研究了从进行期到退行期外周血和细胞百分率变化，现报告如下。资料与方法一、研究对象随机...     

银屑病患者LPO MDA SOD GSH-Px及TNF水平测定

鉴于自由基、脂质过氧化反应与银屑病的关系已引起人们的普遍关注［１～４］，我们对该病患者进行了过氧化脂质（ＬＰＯ）、丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ Ｐｘ）及肿瘤坏死因子（ＴＮＦ）水平的联合检测，旨在了解银屑病患者...     

掌跖顽固性皮肤病的PUVA水浴光化学治疗

ＰＵＶＡ水浴疗法已被证实可以避免一些由口服 8-甲氧补骨脂素 (8-ＭＯＰ)疗法所致的不良反应。为了观察ＰＵＶＡ水浴疗法对慢性掌跖皮肤病的疗效 ,选择 3 0例 (男 1 2例 ,女 1 8例 ,平均年龄 40 3岁 )掌跖皮肤病患者进行研究 ,其中斑块型或脓疱型银屑病 1 0例、特应性湿疹6例、出汗不良性湿疹 1 2例和角化过度性皮炎2例。这些患者过去 8周未曾系统使用维Ａ酸或糖皮质类固醇 ,并在 4周内未外用抗银屑病或抗炎药物。治疗时用每升含 1 0ｍｇ 8-ＭＯＰ的 3 7℃温水浸泡手或脚 2 0分钟 ,随后照射ＵＶＡ。ＵＶＡ照射剂量从 0 3Ｊ/ｃｍ2 开始 ,…     

银屑病患者血液中抗氧化能力的检测

我们对银屑病患者进行了脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）、还原型谷胱甘肽（ＧＳＨ）和谷胱甘肽过氧化酶（ＧＳＨ－Ｐｘ）水平的测定，并以正常人作对照，现报道如下。一、病例和方法１．研究对象：寻常型银屑病（进行期）患者３０例，男１２例，女１８...     

系统性红斑狼疮病人活性氧基与自身抗体变化的观察

对比观察６０例ＳＬＥ病人血浆脂质过氧化物（ＬＰＯ）、红细胞超氧化物歧化酶（ＳＯＤ）及过氧化氢酶（ＣＡＴ）含量与ＡＮＡ、ｄｓ－ＤＮＡ、Ｓｍ和Ｕ１ＲＮＰ自身抗体的变化。活动期病人活性氧基（ＯＲ）水平增高，以致ＳＯＤ及ＣＡＴ活性下降，ＬＰＯ含量增高；非活动期ＳＯＤ及ＣＡＴ活性相对增高，ＬＰＯ含量降低，提示体内ＯＲ水平下降。抗ｄｓ－ＤＮＡ抗体滴度与红细胞ＳＯＤ、ＣＡＴ、血浆ＬＰＯ含量及疾病的严重程度密切相关。内源性ＯＲ的增加可导致Ｔ抑制细胞功能下降，Ｂ淋巴细胞异常增殖，以致体内产生多种自身抗体，诱发免疫炎症反应     

氧化苦参碱诱导角质形成细胞凋亡研究

目的 探讨苦参治疗银屑病的机制。方法 采用流式细胞仪测定亚二倍体细胞含量、ＤＮＡ片段化分析和ＡｎｎｅｘＶ（膜联蛋白Ｖ）凋亡检测法，观察氧化苦参碱９ＯＭＴ）对角质形成细胞凋亡的影响。结果 ＯＭＴ使角质形成细胞的亚二倍体细胞、ＤＮＡ片段化率及磷脂酰丝氨酸（ＰＳ）膜外化细胞含量明显升高（Ｐ〈０．０１），首次发现一定浓度的ＯＭＴ可诱导角质形成细胞凋亡。结论 ＯＭＴ诱发角质形成细胞凋亡，这可能是苦参治疗银屑病的主要机制之一。     

Quantitative analysis of the proliferation of epidermal cells using a human skin organ culture system and the effect of DbcAMP using markers of proliferation (BrdU, Ki-67, PCNA)

Abstract The process of re-epithelialization of a wound in the epidermis comprises the following steps: proliferation of epidermal basal cells, migration of epidermal cells to the wound surface, and cell differentiation. In the present study, we evaluated the proliferation of epidermal basal cells, an important process in wound healing, in the wound margin using a human skin organ culture system and immunohistochemical labeling with bromodeoxyuridine (BrdU), Ki-67, and proliferating cell nuclear antigen (PCNA), as markers of cell proliferation. Dibutyryl cyclic adenosine monophosphate (DbcAMP) is a derivative of cAMP and has been shown to modulate human keratinocyte proliferation. The proliferation of keratinocytes was promoted by DbcAMP and particularly strong effects in terms of BrdU labeling index, Ki-67-positive ratio, and PCNA-positive ratio, were seen at 10^–5 M. The skin organ culture system presented here uses adult preputial skin and is a simple technique that uses easily available materials. In addition to identifying S phase cells using BrdU as an index of cell proliferation, the immunohistochemical method for evaluating the expression of Ki-67 and PCNA is very simple. Accordingly, the method described here seems to be useful for evaluating cell dynamics in wound healing. Received: 6 June 2000 / Revised: 21 July 2000 / Accepted: 23 November 2000     

Stimulatory effects of dibutyryl cyclic adenosine monophosphate on cytokine production by keratinocytes and fibroblasts

BACKGROUND: Clinical studies have shown that ointment containing dibutyryl cyclic adenosine monophosphate (DBcAMP) promotes wound healing. OBJECTIVES: We aimed to elucidate the mechanisms of the beneficial effect of DBcAMP in wound healing. METHODS: An investigation was made of the effects of DBcAMP on in vitro cytokine release from cultured keratinocytes and fibroblasts derived from normal human skin. RESULTS: DBcAMP stimulated keratinocyte proliferation through increased interleukin (IL)-6 production by fibroblasts, and transiently enhanced production of transforming growth factor (TGF)-beta1 by fibroblasts at an early stage of incubation. DBcAMP also stimulated fibroblast proliferation, resulting in further increases in IL-6 and TGF-beta1. CONCLUSIONS: We conclude that this series of stimulative actions on cytokine secretion, together with the facilitation of cell proliferation, contribute to the effects of DBcAMP on the healing of skin ulcers.     

Ginsenoside F1 attenuates hyperpigmentation in B16F10 melanoma cells by inducing dendrite retraction and activating Rho signalling

Ginsenoside F1 (GF1) is a metabolite produced by hydrolysis of the ginsenoside Re and Rg1 in Panax ginseng. According to various studies, high amounts of ginseng components are absorbed in the metabolized form, which are key constituents responsible for the biological effects of P. ginseng. Recently, GF1 was reported to have beneficial effects on skin. However, there has not been a sound understanding of its antimelanogenic effect and underlying molecular mechanisms. In this study, GF1 reduced α‐melanocyte‐stimulating hormone‐induced melanin secretion in B16F10 cell culture media by 60%. However, it did not suppress intracellular melanin levels, tyrosinase activity and expression. Immunofluorescence assay showed that GF1 had no effect on melanosome transport, but significantly induced dendrite retraction. Pull‐down assay demonstrated that GF1 primarily modulates the Rho family GTPases resulting in dendrite retraction. Collectively, these data suggest that GF1 could act as a potent skin‐whitening agent.     

Favorable response to apremilast in a patient with refractory psoriasis verrucosa

A 67‐year‐old man, who had been diagnosed with psoriasis 30 years prior, visited our hospital with a complaint of verrucous nodules in the lower legs, which had developed 15 years previously. We diagnosed him as having psoriasis verrucosa of the legs and plaque psoriasis of the torso. Because the lesions were resistant to topical glucocorticoids and vitamin D₃, a verrucous lesion in the right leg was treated with surgical ablation, which resulted in the development of generalized pustular psoriasis. After pustular lesions were cleared by systemic glucocorticoids and methotrexate, we treated him with etretinate and cyclosporin, but the verrucous lesions accompanied by chronic bacterial infection persisted over time. One year ago, treatment with recently‐approved apremilast was started. It immediately attenuated the plaques and erythropapular lesions of the trunk. Surprisingly, the verrucous nodules of both legs showed reduction in size in 2 months.     

Cyclic AMP as a negative regulator of DNA synthesis in FRSK cells, a fetal rat epidermal cell line

In FRSK cells, a cell line derived from fetal rat epidermal cells, cyclic AMP-elevating agents forskolin (10 microM) and cholera toxin (10 ng/ml) increased cellular cyclic AMP content and suppressed [3H] thymidine incorporation. These effects of forskolin were enhanced by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0.1 mM). Dibutyryl cyclic AMP (1 mM), an analog of cyclic AMP, decreased not only basal but also both tumor promoter 12-O-tetradecanoylphorbol-13-acetate- and epidermal growth factor-stimulated [3H] thymidine incorporation. From these results, we suggest that cyclic AMP may be a negative regulatory factor of DNA synthesis in FRSK cells.     

枣环磷酸腺苷提取液抗缺氧作用实验研究

目的观察枣环磷酸腺苷提取液对人体的抗缺氧作用的有效性,为其应用提供数据支持。方法采用双盲对照的研究方法,选取120名武警战士为实验对象,随机分为高剂量组（CAMP浓度为15mg／100g）、低剂量组（CAMP浓度为7．5mg／100g）和对照组（糖浆）,连续服用实验样品40d,分别于干预前和末次干预后,利用3公里跑造成机体缺氧环境测定血氧饱和度;同时抽血5mL,测定血乳酸和血红蛋白含量。结果连续服用40d后,与空白对照组相比,高、低剂量组血乳酸含量较空白对照组明显降低,P〈0．01;高剂量组血红蛋向含量低于对照组,有统计学意义,P〈0．05;高剂量组血氧饱和度与空白对照组相比升高,P〈0．01。结论枣环磷酸腺苷提取液具有较为明显的抗缺氧作用。能降低运动缺氧条件下血乳酸、血红蛋白含量,提高缺氧条件下的血氧饱和度。     

Severe cyclical thrombocytopenia in a patient with a large lymphatic–venous malformation: A potential association?

The case is reported of an infant who had a large vascular malformation involving his left arm and axilla. It was initially believed to be purely lymphatic in composition but some venous elements were identified subsequently, at operation. The lesion was unusual in that there was a total absence of skin over one area of it at birth, that it underwent spontaneous shrinkage in the early weeks of life, and that a circumferential scarring developed which led to severe functional disability of the limb. At 12 months of age the patient developed a profound cyclic thrombocytopenia that spontaneously resolved after 1 year. The cause of the platelet cycling is unresolved but might have been secondary to intermittent production by the malformation of a cytokine which was destructive against the platelets.     

Contact allergy to petrolatums. (III). Allergenicity prediction and pharmacopoeial requirements

Several pharmacopoeias set limits on the polycyclic aromatic hydrocarbon content in petrolatum. UV absorbance measurement of aromatic extracts of petrolatum sample has been shown to be a more reliable method than direct UV absorbance measurement as prescribed by several pharmacopoeias for the determination of that content, but the presence of allergenic polycyclic aromatic hydrocarbons does not always correlate with lower UV absorbance. Biological tests are ultimately the only certain method of detecting biologically active compounds. Polycyclic aromatic hydrocarbons can also be irritant and carcinogenic. Therefore, University uniform and very stringent limits should be set restricting their presence in pharmaceutical grade petrolatum.     

Effects of in vitro PUVA treatment on adenylate cyclase responses of epidermis

We investigated the effect of 8-methoxypsoralen (8-MOP) plus long wave ultraviolet irradiation (PUVA) on the pig skin epidermal cyclic AMP (cAMP) system. Following PUVA treatment in vitro, pig skin squares were incubated in RPMI 1640 medium, and the cAMP accumulation by various adenylate cyclase stimulators was determined. A significant increase of the beta-adrenergic adenylate cyclase response was observed as early as 6-h following PUVA treatment; the maximal effect was reached at 24-h and lasted at least for 72-h. This augmentation effect of PUVA treatment was potentiated by increasing the 8-MOP concentration (0.5–160 μg/ml) and UVA irradiation dose (0.05–1.4 J/cm²). At higher irradiation doses (2.1–2.8 J/cm²), the beta-adrenergic augmentation effect was less marked. There were no significant differences in the adenosine-and histamine-adenylate cyclase response up to 1.4 J/cm² irradiation; however, the latter was decreased at a higher irradiation dose (2.8 J/cm²). Although UVA irradiation alone had no effect on the beta-adrenergic response, 8-MOP treatment alone increased this receptor response at higher concentrations; this effect was much weaker than that induced by PUVA treatment. Cyclic AMP phosphodiesterase activities were not affected by PUVA treatment. These results indicate that epidermal adenylate cyclase response is affected by in vitro PUVA treatment.