紫外线诱导皮肤过敏的损伤类型和机理

本文介绍了紫外线诱导皮肤损伤的四种类型：日晒红斑、日晒黑化、肤光老化及皮肤光敏反应，对各自的引发机理做了简要概述。并对目前市场上在化妆品中使用的天然植物抗光敏添加剂进行了介绍，以期对今后抗敏添加剂的研究和开发提供参考。     

紫外线固化涂料用光敏引发剂的进展

光敏引发剂的引发反应机理大致分为四类:分解反应、氢提取反应、离子反应和三缔合体能量转移反应机理。叙述主要光敏引发剂,如芳基重氮盐、芳基碘、苯乙酮及其衍生物、芳香酮化合物和噻唑酮的特性。     

紫外线对皮肤的光辐射损伤与防护研究

研究了阳光紫外线对皮肤造成的各种光辐损伤，探讨了如何采取积极有效的防护措施，各类防晒剂的应用状况，以及防晒化妆品的发展趋势，并对此进行了详细的论述。     

防止头发褪色和头皮损伤的新型紫外线过滤剂

介绍了禾大公司新开发出的一种防止头发褪色和头皮损伤的新型紫外线过滤剂Chromaveil,并介绍了该产品在香波、护发素以及头发免洗产品中的应用。Chromaveil具有广泛的紫外线吸收光谱,吸收范围为250nm-350nm,峰值为310nm,在波长为310nm时的消光系数为38．47L／（g·cm）。由于Chromaveil的正电荷作用,在冲洗产品中能很好地沉积在头发表面。经测试证明,Chromaveil具有很好的护色效果,可对头发表面的色氨酸、抗张力强度和表皮完整性提供很好的紫外线保护作用。     

柚皮苷对紫外线诱导小鼠皮肤屏障损伤的保护作用及机制研究

研究了柚皮苷对紫外线诱导昆明小鼠皮肤屏障损伤的保护作用。将25只SPF级昆明小鼠随机分为5组:空白对照组,模型组(UV照射组),阳性对照组(28.39 mmol/L维生素C),低、高剂量柚皮苷涂抹组(0.35和3.5 mmol/L柚皮苷)。除空白对照组,其他4组小鼠模拟日光紫外线(UVA+UVB)照射,建立小鼠光损伤皮肤模型,每次UV照射前,提前2 h分别涂抹相同剂量(100μL/只)的药物。通过测试小鼠皮肤经表皮失水(TEWL)、HE染色、胶原纤维染色(Masson染色),以及小鼠皮肤组织中的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活力,丙二醛(MDA)的含量,活性氧(ROS)清除能力来探究柚皮苷对皮肤光损伤的作用途径;免疫组化染色(IHC染色)检测丝聚合蛋白(FLG)、内披蛋白(IVL)、水通道蛋白3 (AQP3)以评价柚皮苷对紫外线损伤皮肤的屏障相关功能。与模型组相比,柚皮苷涂抹组小鼠皮肤抑制皮肤表皮厚度增加,给药组胶原量增加;低、高剂量柚皮苷涂抹组可以显著减少光损伤小鼠皮肤中水分的流失(p0.05);柚皮苷显著提高小鼠皮肤组织中SOD、CAT的活力(p0.05),显著降低MDA的含量(p0.05)及清除ROS的含量;IHC染色研究表明柚皮苷涂抹组皮肤中FLG、IVL、AQP3蛋白表达量增加(p0.05)。     

紫外线的防护

对紫外线防护的深入研究进行了综述。描述了有关专业术语，紫外线吸收和屏蔽剂的性能、应用范围、安全性问题、在法规上的禁忌和配方使用，展望了防晒剂未来的发展趋势。     

陶瓷基复合材料损伤失效机理和模型研究进展

随着科学技术的进步,复合材料在航空领域得到了广泛的发展。陶瓷基复合材料因其具有高比强度、高比模量、耐高温和耐腐蚀的特性被广泛应用于航空发动机的热端部件。然而,制备过程中产生的初始损伤和残余以及复杂的失效模式,给建立陶瓷基复合材料的损伤本构模型、研究陶瓷基复合材料的损伤失效机理带来了巨大的困难。本文对陶瓷基复合材料损伤失效机理的研究进展进行综述。首先,介绍了陶瓷基复合材料的发展历史细观建模研究现状;然后,综述了陶瓷基复合材料损伤失效机理的研究现状;最后,对陶瓷基复合材料损伤失效机理研究的发展趋势进行了展望。     

紫外线伤害皮肤的机理与防护

论述了由于人们对臭氧层的破坏导致紫外线对人体皮肤的伤害以及防晒化妆品的防晒机理,人们应该如何科学选用防晒化妆品,同时介绍了防晒化妆品的相关规定。     

抗过敏牙膏的抗过敏机理与牙本质过敏症治疗机理的对比探讨

通过对牙本质过敏现象度产生原因的研究，对口腔医学方面治疗牙本质过敏的方法和机理以及抗过敏牙膏的抗过敏机理进行了对比分析，从而得出抗过敏牙膏的抗过敏机理与口腔医学方面对牙本质过敏症的治疗机理基本一致的结论。     

UV Radiation and the Skin

UV radiation (UV) is classified as a “complete carcinogen” because it is both a mutagen and a non-specific damaging agent and has properties of both a tumor initiator and a tumor promoter. In environmental abundance, UV is the most important modifiable risk factor for skin cancer and many other environmentally-influenced skin disorders. However, UV also benefits human health by mediating natural synthesis of vitamin D and endorphins in the skin, therefore UV has complex and mixed effects on human health. Nonetheless, excessive exposure to UV carries profound health risks, including atrophy, pigmentary changes, wrinkling and malignancy. UV is epidemiologically and molecularly linked to the three most common types of skin cancer, basal cell carcinoma, squamous cell carcinoma and malignant melanoma, which together affect more than a million Americans annually. Genetic factors also influence risk of UV-mediated skin disease. Polymorphisms of the melanocortin 1 receptor (MC1R) gene, in particular, correlate with fairness of skin, UV sensitivity, and enhanced cancer risk. We are interested in developing UV-protective approaches based on a detailed understanding of molecular events that occur after UV exposure, focusing particularly on epidermal melanization and the role of the MC1R in genome maintenance.     

IL-33 and IL-37: A Possible Axis in Skin and Allergic Diseases

Interleukin (IL)-37 and IL-33 are among the latest cytokines identified, playing a role in several inflammatory conditions, spanning from systemic conditions to tumors to localized diseases. As newly discovered interleukins, their role is still scarcely understood, but their potential role as therapeutic targets or disease activity markers suggests the need to reorganize the current data for a better interpretation. The aim of this review is to collect and organize data produced by several studies to create a complete picture. The research was conducted on the PubMed database, and the resulting articles were sorted by title, abstract, English language, and content. Several studies have been assessed, mostly related to atopic dermatitis and immunologic pathways. Collective data demonstrates a pro-inflammatory role of IL-33 and an anti-inflammatory one for IL-37, possibly related to each other in an IL-33/IL-37 axis. Although further studies are needed to assess the safety and plausibility of targeting these two interleukins for patients affected by skin conditions, the early results indicate that both IL-33 and IL-37 represent markers of disease activity.     

Intermittent Hypoxia on the Attenuation of Induced Nasal Allergy and Allergic Asthma by MAPK Signaling Pathway Downregulation in a Mice Animal Model

Intermittent hypoxia (IH) has been an issue of considerable research in recent years and triggers a bewildering array of both detrimental and beneficial effects in several physiological systems. However, the mechanisms leading to the effect are not yet clear. Consequently, we investigated the effects of IH on allergen-induced allergic asthma via the mitogen-activated protein kinase (MAPK) signaling pathway. Forty BALB/c mice were dived into four groups. We evaluated the influence of IH on the cell signaling system of the airway during the allergen-induced challenge in an animal model, especially through the MAPK (mitogen-activated protein kinase) pathway. The protein concentrations of p-ERK/ERK, p-JNK/JNK, p-p38/p38, and pMEK/MEK were significantly reduced in the allergen-induced+IH group, compared to the allergen-induced group (p-value < 0.05 as considered statistically significant). The number of eosinophils, neutrophils, macrophages, and lymphocytes in the bronchoalveolar lavage fluid and Dp (Dermatophagoides pteronyssinus)-specific IgG2a and interleukins 4, 5, 13, and 17 were significantly reduced in the Dp+IH group, compared to the Dp group. These findings suggest that the MAPK pathway might be associated with the beneficial effect of IH on the attenuation of allergic response in an allergen-induced mouse model.     

美白剂的发展现状及其黑色素抑制机理的研究进展

鉴于黑色素抑制剂在美白型化妆品中的不断开发、应用,使得对近年来的黑色素抑制剂的发展状况作一综述显向尤为必要;在黑色素形成机理研究的基础上,从亚细胞结构层次上对黑色素的抑制机理作一综述,最后,为黑色素抑制剂在化妆品等领域的研究、开发提出未来发展思路。     

Biological Mechanisms Underlying the Ultraviolet Radiation-Induced Formation of Skin Wrinkling and Sagging I: Reduced Skin Elasticity,Highly Associated with Enhanced Dermal Elastase Activity,Triggers Wrinkling and Sagging

The repetitive exposure of skin to ultraviolet B (UVB) preferentially elicits wrinkling while ultraviolet A (UVA) predominantly elicits sagging. In chronically UVB or UVA-exposed rat skin there is a similar tortuous deformation of elastic fibers together with decreased skin elasticity, whose magnitudes are greater in UVB-exposed skin than in UVA-exposed skin. Comparison of skin elasticity with the activity of matrix metalloproteinases (MMPs) in the dermis of ovariectomized rats after UVB or UVA irradiation demonstrates that skin elasticity is more significantly decreased in ovariectomized rats than in sham-operated rats, which is accompanied by a reciprocal increase in elastase activity but not in the activities of collagenases I or IV. Clinical studies using animal skin and human facial skin demonstrated that topical treatment with a specific inhibitor or an inhibitory extract of skin fibroblast-derived elastase distinctly attenuates UVB and sunlight-induced formation of wrinkling. Our results strongly indicated that the upregulated activity of skin fibroblast-derived elastase plays a pivotal role in wrinkling and/or sagging of the skin via the impairment of elastic fiber configuration and the subsequent loss of skin elasticity.     

Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging

Skin disorders showing abnormal pigmentation are often difficult to manage because of their uncertain etiology or pathogenesis. Abnormal pigmentation is a common symptom accompanying aging skin. The association between skin aging and skin pigmentation abnormalities can be attributed to certain inherited disorders characterized by premature aging and abnormal pigmentation in the skin and some therapeutic modalities effective for both. Several molecular mechanisms, including oxidative stress, mitochondrial DNA mutations, DNA damage, telomere shortening, hormonal changes, and autophagy impairment, have been identified as involved in skin aging. Although each of these skin aging-related mechanisms are interconnected, this review examined the role of each mechanism in skin hyperpigmentation or hypopigmentation to propose the possible association between skin aging and pigmentation abnormalities.     

Evaluating Whether Radiofrequency Irradiation Attenuated UV-B-Induced Skin Pigmentation by Increasing Melanosomal Autophagy and Decreasing Melanin Synthesis

Autophagy is involved in the degradation of melanosomes and the determination of skin color. TLR4 and tumor necrosis factor (TNF) signaling upregulates NF-kB expression, which is involved in the upregulation of mTOR. The activation of mTOR by UV-B exposure results in decreased autophagy, whereas radiofrequency (RF) irradiation decreases TLR4 and TNF receptor (TNFR) expression. We evaluated whether RF decreased skin pigmentation by restoring autophagy by decreasing the expression of TLR4 or TNFR/NF-κB/mTOR in the UV-B-irradiated animal model. UV-B radiation induced the expressions of TNFR, TLR, and NF-κB in the skin, which were all decreased by RF irradiation. RF irradiation also decreased phosphorylated mTOR expression and upregulated autophagy initiation factors such as FIP200, ULK1, ULK2, ATG13, and ATG101 in the UV-B-irradiated skin. Beclin 1 expression and the expression ratio of LC3-I to LC3-II were increased by UV-B/RF irradiation. Furthermore, melanin-containing autophagosomes increased with RF irradiation. Fontana-Masson staining showed that the amount of melanin deposition in the skin was decreased by RF irradiation. This study showed that RF irradiation decreased skin pigmentation by restoring melanosomal autophagy, and that the possible signal pathways which modulate autophagy could be TLR4, TNFR, NF-κB, and mTOR.     

对表面活性剂在煤炭上应用及其作用原理的探讨

介绍了表面活性剂在煤炭开采、洗选加工、煤炭贮、装、运和煤炭燃烧等过程中的应用情况, 并对其作用的原理进行探讨。