PURPOSE:To report the case of uveal effusion syndrome (UES) in a 35-year-old woman with psoriasis vulgaris, emphasizing scleral pathology and systemic inflammatory contributions mediated by proteomic alterations. METHODS:Medical history, clinical findings and treatment were reviewed, along with histopathological and proteomic analysis. RESULTS:A 35-year-old woman presented with retinal and choroidal detachments in the left eye and scleral thickening (3 mm vs. normal 1 mm). Concurrently, her psoriasis symptoms worsened. Histology revealed collagen disorganization and extracellular matrix remodeling in the sclera, accompanied by elevated inflammatory factors (e.g. MCP-4, RANTES, Fractalkine). Treatment included partial sclerotomy, leading to resolution of detachments and improved visual acuity. CONCLUSION:Systemic inflammation associated with psoriasis may contribute to UES pathogenesis. Dermatologists should refer psoriasis patients for ophthalmologic examinations, while ophthalmologists should be aware of underlying health conditions when treating UES.

A 20-year-old male presented with a 6-year history of facial rashes, which were getting worse.He had been diagnosed with aplastic anemia for more than 8 years, and his condition was deteriorating.He needed to control the facial rashes and get his hematopoietic stem cell transplantation as soon as possible. Dermatological examination showed there were multiple pimples, papules and pustules on the head, chest and back, of which the most severe skin rash was on the face, with a large number of cysts and atrophic scars.Blood routine examination showed a typical manifestation of tertiary depression, and bone puncture results showed extremely low bone marrow hyperplasia.He was diagnosed as severe acne with severe aplastic anemia.His treatment regimen was ALA-PDT treatment once a week, combined with oral clarithromycin and topical fusidic acid.After 4 times of photodynamic therapy, the active acne resolved completely, and hematopoietic stem cell transplantation was successfully performed in the cabin.The acne didn’t recur in a 6-month follow up.

Background: Photodynamic therapy (PDT) with 5-aminolevulinic acid (ALA) is a reliable treatment for actinic keratosis (AK), but its effect needs to be enhanced in thick lesions. Plum-blossom needle is a traditional Chinese cost-effective instrument for enhancing the transdermal delivery of ALA. However, whether it could improve the efficacy of AK treatment has not yet been investigated.Objective: To compare the efficacy and safety of plum-blossom needle-assisted PDT in facial AK in the Chinese population.Methods: In this multicenter, prospective study, a total of 142 patients with AKs (grades I-III) were randomized into the plum-blossom needle-assisted PDT group (P-PDT) and control PDT group (C-PDT). In the P-PDT group, each AK lesion was tapped vertically by a plum-blossom needle before the application of 10% ALA cream. In the C-PDT group, each lesion was only wiped with regular saline before ALA cream incubation. Then, 3 hours later, all the lesions were irradiated with light-emitting diode (LED) at a wavelength of 630 nm. PDT was performed once every 2 weeks until all lesion patients achieved complete remission or completed six sessions. The efficacy (lesion response) and safety (pain scale and adverse events) in both groups were evaluated before each treatment and at every follow-up visit at 3-month intervals until 12 months.Results: In the P-PDT and C-PDT groups, the clearance rates for all AK lesions after the first treatment were 57.9% and 48.0%, respectively (P < 0.05). For grade I AK lesions, the clearance rates were 56.5% and 50.4%, respectively (P = 0.34). For grade II AK lesions, the clearance rates were 58.0% and 48.9%, respectively (P = 0.1). For grade III AK lesions, the clearance rates were 59.0% and 44.2%, respectively (P < 0.05). Moreover, grade III AK lesions in the P-PDT group required fewer treatment sessions (P < 0.05). There was no significant difference in the pain score between the two groups (P = 0.752). Conclusion: Plum-blossom needle tapping may enhance the efficacy of ALA-PDT by facilitating ALA delivery in the treatment of AK.

A variety of evidence suggest that 5-Aminolevulinic acid-based photodynamic therapy (ALA-PDT) is clinically effective in management of acne vulgaris. Several clinical guidelines for acne recommend PDT as an alternative treatment modality for severe acne. However, there is a lack of detailed clinical guideline for PDT in acne treatment. To propose up-to-date, evidence-based and practical recommendations on application of ALA-PDT for acne vulgaris, dermatologists and PDT experts from the Photodynamic Therapy Research Center of the CMA and Photodynamic Therapy Rehabilitation Training Center of CARD achieved consensus and guidelines based on careful evaluation of published literature, expert opinions and experience. ALA-PDT plays a therapeutic role in all four major pathogenesis of acne, and is suitable for moderate to severe acne and scar-prone acne, especially for patients who cannot tolerate or refused systemic antibiotics and isotretinoin. The efficacy and adverse re-actions of ALA-PDT are closely related to therapeutic parameters including ALA concentration, incubation time, light source and dosage. Proper pretreatment helps to improve transdermal absorption of ALA and enhances its efficacy. We reviewed and proposed recommended protocols for four PDT procedures including conventional PDT (C-PDT), modified painless PDT (M-PDT), intense pulsed light PDT (IPL-PDT) and daylight PDT (DL-PDT). M-PDT with lower ALA concentration (3-5%), shorter incubation time (30 mins), and lower dose but prolonged illumination (630nm, 40-60 mW/cm2, 150 J/cm2) can improve lesions of moderate to severe acne vulgaris effectively with minimal pain and easier manipulation, and thus was recommended by Chinese dermatologists. Lastly, management of adverse reactions were addressed.

Papular elastorrhexis (PE) is a rare disorder of dermal elastic fibers, which presents as firm, hypopigmented papules, commonly distributed on the trunk and extremities. The facial area is rarely involved. We report the case of a 47-year-old woman with multiple asymptomatic, soft, skin-colored facial papules whose histopathological features are compatible with PE. Facial PE may be a variant of PE, and special staining in showing changes in both elastic and collagen fibers may be of great value in diagnosis.

Peng, Fen; Yang, Xiaojing; Li, Wenhai; Huang, Jingyi; Chen, Zhou; Zhang, JianzhongEditor(s): Guo, Lishao Author Information

To the Editor: Epidemiological studies have confirmed that fine particulate matter (PM2.5) is related to skin hyperpigmentation, but experimental evidence is lacking.[1] Here, we used normal human epidermal keratinocytes (NHEKs), melanocytes (NHEMs), and reconstructed human epidermis models (MelaKutis®) to investigate the impact of PM2.5 on skin melanogenesis. MelaKutis® is a 3D skin model with a stratified structure, which is composed of human keratinocytes and melanocytes. Its structure and metabolic features are highly similar to those of the natural human skin. Moreover, external factors can stimulate the melanocytes located in the basal layer to produce melanin, resulting in hyperpigmentation. In our study, to simulate the effect of PM2.5 on human skin, we utilized PM2.5 collected in Beijing, China. Zhang et al[2] previously analyzed the components of PM2.5 (collected in Beijing) and revealed that benzo[a]pyrene (BAP) was one of the most abundant and toxic components of PM2.5. Thus, we chose BAP as positive control. PM2.5 samples were collected continuously for 24 h in haze days from November 2018 to March 2019. An HY-1000 intelligent large-flow TSP sampler (optional PM2.5 cutter, Qingdao Hengyuan Technology Development Co., Ltd.) was employed for quartz filter sampling at an average flow rate set at 1000 L/min. Then, the samples were immersed in 75% ethanol, followed by ultrasonically shaking for 60 min in a water bath for particle elution. Sterile water was used to prepare a high concentration stock solution, which was then stored at −20°C. BAP was purchased from Sigma-Aldrich Chemical (St. Louis, MO, USA). NHEKs, NHEMs, and MelaKutis® were manufactured by Biocell Biotechnology (Dongguan, Guangdong, China). The other chemicals were of reagent grade. PM2.5 and BAP were diluted to different concentrations using certain cell culture media (KC2500, Medium 254 or M-TA medium). The effects of PM2.5 on the viability of NHEKs and NHEMs were determined by MTT assay. NHEKs were cultured in KC2500 (Guangdong Biocell Biotechnology), and NHEMs in Medium 254 (Gibco, Grand Island, NY, USA). Cells were incubated with various concentrations of PM2.5 (3.13, 6.25, 12.50, 25.00, 50.00, 100.00, 200.00, and 400.00 μg/mL) or BAP (0.50, 1.00, 2.50, 3.50, 5.00, 10.00, 20.00, and 50.00 μmol/L) at 37 °C in 5% CO2 for 24 h. Then, we treated the cells with MTT dye for another 4 h in dark and recorded the absorbance (optical density) at 490 nm using a Spectrophotometer (BioTek, Winooski, VT, USA). To observe the effects of PM2.5 and BAP on cell morphology, NHEKs were treated with different concentrations of PM2.5 (3.13, 6.25, 12.50, 25.00, and 50.00 μg/mL) or BAP (1.00, 2.50, 3.50, 5.00, and 10.00 μmol/L). Next, 24 h later, the cell morphology was observed at 200× magnifications under an inverted microscope (Olympus Corporation, Tokyo, Japan). All the cell experiments above contain three repeat groups (n = 3). MelaKutis® were maintained in M-TA medium (Biocell Biotechnology, China) at 37 °C in 5% CO2, according to the manufacturer's instructions. Further, we added 10 μL of different concentrations of PM2.5 (7.50 and 12.50 μg/mL) or BAP (3.00 and 5.00 μmol/L) to each model on the surface and changed the medium. Further, 24 h later (we defined this as Day 1), before repeating the drug administration as on Day 0, we wiped the sample residue gently using sterilized cotton swab. On Days 2 to 6, the procedures of Day 0 and Day 1 were repeated. On Day 7, all models were collected and subjected to appearance observation, apparent brightness (L ∗value), melanin content, melanin distribution, and tissue morphology (Hematoxylin-Eosin staining [H&E]) analysis. We divided the six experimental groups (each group contained six repeat models, n = 6) randomly into group A and group B, each of which contained 6 × 3 = 18 models (each group had three repeat models, n = 3). Group A: MelaKutis® images were subjected to appearance observation, and then harvested the models for immunohistochemistry and histology examinations. After paraffin embedding, 5 to 8-μm thick tissue blocks were sectioned, which were stained with Fontana-Masson and H&E staining to observe their melanin distribution and tissue morphology. Pictures of the slides were taken under an upright microscope (Olympus Corporation, Japan, 400×). Group B: The L∗ value was measured by a Colorimeter (DSM II, Denmark). Then, we transferred the models into 1.5-mL centrifuge tubes, followed by centrifugation (2000 r/min for 10 min). Next, we discarded the medium, washed the pellets with 1 mL of 1× phosphate buffered solution, and centrifuged again (3000 r/min for 5 min). Further, we dissolved the sediments in 1 mL of 1 mol/L NaOH containing 10%Dimethyl sulfoxide at 80 °C for 40 min. The melanin content in each sample was determined by measuring the absorbance at 405 nm. Each specimen was read three times. SPSS 24.0 was used for statistical analysis, and one-way analysis of variance was applied to analyze the results. P < 0.05 was considered to indicate a statistically significant difference. Based on the cell viability of the PM2.5-treated/BAP-treated NHEKs and the cell viability curves we drew [Supplementary Figure 1, https://links.lww.com/CM9/A873], we found that the lower concentrations of PM2.5 (≤12.50 μg/mL) or BAP (≤5.00 μmol/L) did not cause a significant decrease in cell viability or cell morphology change. The change of cell viability of NHEMs was similar to that of NHEKs. Therefore, we defined PM2.5 = 12.50 μg/mL/BAP = 5.00 μmol/L as the maximum safe concentrations (Cmax) of NHEKs and NHEMs. We selected PM2.5 (7.50 and 12.50 μg/mL) and BAP (3.00 and 5.00 μmol/L) for subsequent studies. Continuous stimulation on MelaKutis® with PM2.5/BAP for 7 days caused no obvious abnormality in the tissue morphology. Compared with the control groups, the 12.50 μg/mL PM2.5-treated MelaKutis® and 5.00 μmol/L BAP-treated MelaKutis® became darker, and melanin particles increased mainly in the lower parts of the sections. Furthermore, fissures were observed in the 5.00-μmol/L-BAP group [Figure 1]. The L∗ values of MelaKutis® treated by both 12.50 μg/mL PM2.5 and 5.00 μmol/L BAP decreased (P = 0.000, P = 0.000), whereas the changes in the 7.50 μg/mL PM2.5 and 3.00 μmol/L BAP groups were not statistically significant (P = 1.000, P = 1.000). Meanwhile, the melanin contents of both the 12.50 μg/mL PM2.5 and 5.00 μmol/L BAP groups increased (P = 0.001, P = 0.047), but the changes in the 7.50 μg/mL PM2.5 group and 3.00 μmol/L BAP group were not statistically significant (P = 0.948, P = 1.000) [Supplementary Table 1, https://links.lww.com/CM9/A873].Figure 1: Sections showing the melanin distribution. The number of melanin particles of PM2.5-/BAP-treated MelaKutis® increased, mainly in the lower part of the slices. Fissures were observed in the 5.00 μmol/L-BAP group. (BC: blank control, SC: solvent control, and SC:BC + 0.01% DMSO, n = 3). BAP: Benzo[a]pyrene; DMSO: Dimethyl sulfoxide; PM2.5: Particulate matter 2.5.In our study, we found that lower concentrations of PM2.5 (≤12.50 μg/mL) did not cause a significant decrease in the cell viability or a change in the cell morphology of keratinocytes/melanocytes, whereas higher doses led to cell death and cell deformation in a dose-dependent manner. Since this was a qualitative experiment, the selection criteria for PM2.5/BAP concentrations were not so strict. However, at selected concentrations that were too close to Cmax, the results were not considered representative. Thus, we chose 7.50 μg/mL of PM2.5 and 3.00 μmol/L of BAP for the subsequent experiments, whose cytotoxicity was negligible. Our results showed that 12.50 μg/mL PM2.5 induced hyperpigmentation in the reconstructed human epidermis model, suggesting that low concentrations of PM2.5 may lead to skin hyperpigmentation. Since no significant change in the cell numbers of the keratinocytes or melanocytes was observed in the cell or MelaKutis® experiments, we speculated that PM2.5 induced hyperpigmentation mainly by increasing the melanin synthesis. Clear corneum, the strongest barrier against environmental stressors, including PM, was observed. Therefore, little possibility exists for PM2.5 to enter the epidermis and directly contact with melanocytes to cause melanogenesis. We preferred to explain our results using the scheme PM2.5 → keratinocyte → melanocyte → increased melanin production. The epidermal-melanin unit was composed of keratinocytes and melanocytes, which is essential to melanogenesis. This unit responded rapidly to a variety of external stimuli through paracrine and autocrine pathways leading to melanin production.[3–5] A large number of studies have been conducted on the impact of environmental PM on keratinocytes, including polycyclic aromatic hydrocarbons (PAHs) and PM2.5. The existing evidence includes the activation of the aryl hydrocarbon receptor (AhR) signaling pathway, oxidative stress, and the induction of inflammatory cascade.[1,5] As an external sensor, AhR is expressed in all skin cell types and has been found to induce the expression of several target genes after binding to its ligands (such as PAHs). One of the target genes, cytochrome P450 family enzyme, metabolized PAHs, and the formed metabolites induced reactive oxygen species (ROS) production.[5] PM2.5 also triggered the production of ROS by keratinocytes through various pathways, which promoted higher melanin production by melanocytes.[1,5,6] Moreover, PM exposure induced keratinocytes to produce a series of inflammatory factors, such as melanocyte stimulating hormone (α-MSH), Interleukin (IL)-1α, IL-1β, IL-6, IL-8, Matrix Metalloproteinase (MMP)-1, MMP-2, MMP-9, and Tumor necrosis factor-α,[5,6] which are considered to be at least partly related to ROS.[5] α-MSH was established as one of the main paracrine cytokines secreted by keratinocytes that contributed to melanogenesis.[6] IL-1 promoted the secretion of endothelin-1 in keratinocytes, enhancing the migration and differentiation of melanocytes.[3,4] We speculate that PM2.5 could directly act on melanocytes in people with damaged skin barrier, inducing melanin production. Some metals (such as Fe) in PM2.5[1] could combine with sulfhydryl groups in epidermal cells and enhance the activity of tyrosinase.[3] In addition to melanocytes and keratinocytes, the interactions between other cells in the human skin should also be considered.[1,3] We also found that the increased melanin was mainly distributed in the lower part of the slices, which was consistent with the metabolism of melanin.[3] MelaKutis® successfully simulated the process of melanogenesis: the melanosomes were converted into melanocytes, and then they were transmitted to the surrounding keratinocytes by endocytosis/exocytosis. In the process of epidermal replacement, the melanosomes moved up with keratinocytes and were gradually digested and absorbed.[3,4] In our investigation, the function of melanocytes was promoted by external stimuli, leading to an increased ability for synthesis and transportation of melanosomes.[3] Our experimental duration was only seven days, whereas the turnover time was 28 days. This may explain why melanin was distributed mainly in the lower part of the slices. Furthermore, we found fissures in the 5.00 μmol/L-BAP group, which might have been related to the inflammatory response and the increased dendritic degree of the melanocytes. An earlier study confirmed that PM damaged the skin barrier by adjusting or even destroying the tight junction of the epithelial cells.[5] As mentioned above, PM2.5 stimulated the keratinocytes to produce a variety of inflammatory factors. Some of these cytokines further promoted the secretion of cytokines and adhesion molecules such as IL-8 and IL-1 by epithelial cells, fibroblasts, and endothelial cells.[7] All these cell types can induce skin inflammation, cause barrier disruption, and increase the damage of PM2.5 to the skin. Interestingly, a previous investigation established that the acantholysis of pemphigus vulgaris (PV) was strongly associated with MMPs, especially MMP-9.[8] The presence of PV was similar to that of the 5.00 μmol/L-BAP group. As MMPs showed wide proteolytic activities and overlapping specificities, and PM2.5 upregulated the levels of MMP-1, MMP-2, and MMP-9 in cultured keratinocytes,[5] we speculated that MMPs were associated with the fissures in the sections. In summary, we propose that low concentrations of PM2.5 may cause skin hyperpigmentation. To the best of our knowledge, this is the first study to investigate the effect of PM2.5 on melanogenesis, in which a 3D epidermis model has been applied. Further in vitro and in vivo studies are warranted to clarify the mechanism involved. Acknowledgements The authors thank Prof. Hong-Wei Zhang in the Toxicology Laboratory of the Environmental and Health-related Product Safety Institute of the Chinese Center for Disease Control and Prevention for her kindly help in collecting PM2.5 samples. The authors also thank Wendy Song for her help in our English expression. Funding This study was supported by the National Natural Science Foundation of China (No. 2101000271).

患者女，24岁，因面部皮疹伴疼痛半月就诊。患者10年前诊断再生障碍性贫血，口服环孢素、中药等无明显好转。5个月前因准备接受造血干细胞移植开始口服司坦唑醇片2 mg每日3次。服药4个月后，患者面部、躯干出现绿豆大小红色疙瘩，伴明显疼痛，当地医院予外用药治疗（具体不详）无效，并出现化脓、破溃及疼痛加重。患者再生障碍性贫血症状持续恶化，需尽快接受造血干细胞移植术，因术前需要清除皮肤感染灶，遂就诊。患者既往月经前面部偶尔出现单发的类似皮疹，外用夫西地酸乳膏等治疗，皮疹可消退。平素月经规律。

Objective:To establish a safe, effective, simple, and more economically feasible method to obtain platelet-rich plasma (PRP).Methods:Whole blood was collected from 24 patients with atrophic acne scars on the face. For the preparation of PRP, a slight modification of Choukroun＇s method was used. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of platelet derived growth factor-β(PDGF-β), transforming growth factor-β1 (TGF-β1), epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), isulin-like growth factor-1 (IGF-1) in normal plasma and PRP.Results:The average concentration of PDGF-β in PRP was (755.61±418.31) ng/L, which was higher than [(479.93±279.18) ng/L] in normal plasma ( t=3.479, P<0.01). The average concentration of TGF-β1 in PRP was (2267.00±1223.68), which was higher than [(1535.50±910.91) ng/L] in normal plasma ( t=7.082, P<0.01). The average concentration of EGF in PRP was (30.70±12.39) ng/L, which was higher than [(20.77±10.31) ng/L] in normal plasma ( t=6.899, P<0.01). The average concentration of VEGF in PRP was (25.42±17.69) ng/L, which was higher than [(12.01±7.77) ng/L] in normal plasma ( t=5.230, P<0.01). The average concentration of bFGF was (17.85±7.17) ng/L, which was higher than [(10.90±4.73) ng/L] in normal plasma ( t=6.050, P<0.01). The average concentration of IGF-1 was (201.22±36.80) ng/ml, which was higher than [(174.90±33.80) ng/ml] in normal plasma ( t=3.760, P<0.01). Conclusions:Compared to normal plasma, modified PRP contains higher levels of growth factors. The modified method is a reliable option for liquid PRP, especially applicable for invasive cosmetic laser surgery to promote wound repair.

Photodynamic Therapy with 5-aminolevulinic acid (ALA-PDT) has been widely applied in the treatment of skin diseases in China. To further standardize, guide, and promote the clinical applications of ALA-PDT in dermatology, the Chinese Society of Dermatology, Chinese Association of Rehabilitation Dermatology, Photomedicine Therapeutic Equipment Group of Committee on Skin Disease, and Cosmetic Dermatology of China Association of Medical Equipment invited relevant experts engaged in ALA-PDT to revise and update the first edition of "Clinical application of 5-aminolevulinic acid-based photodynamic therapy: an expert consensus statement" and establish a more current edition, to provide an updated reference for Chinese dermatologists in clinical practice. In the guideline, the expert group reached consensus opinions on ALA-PDT with regard to mechanisms of action, therapeutic protocol, clinical applications, adverse reactions and countermeasures, precautions, care, and evaluation of efficacy.

患者男,6岁,躯干散在扁平丘疹2个月余,无自觉症状.皮肤科情况:胸腹部可见4个散在、黄豆至蚕豆大边界清楚的卵圆形淡白色丘疹,表面光滑,质韧,触诊无落空感及囊性感.病变部位真皮弹力纤维染色示:弹力纤维减少及显著碎片化,胶原纤维局灶性轻度不规则增粗及均质化.诊断:丘疹性弹力纤维溶解.该患者发病年龄较小,应注意与弹力纤维溶解相关的系统性先天性疾病进行鉴别.

Objective. In order to investigate the effects of PM2.5 on proliferation, cell cycle, apoptosis, and potential mechanism of human keratinocyte cell line HaCaT. Methods. HaCaT cells were treated with different concentrations of PM2.5 suspension for 24 hours. Cell viability was detected by the CCK-8 method. Cell cycle distribution and apoptosis were detected by flow cytometry. Microarray analyses were used to find out the microarray gene expression profiling; data processing included gene enrichment and pathway analysis. Western blot was conducted to validate the key pathways and regulators in the microarray analysis. Results. The cell activity decreased, and the cell cycle was significantly inhibited with the increase in PM2.5 concentration. Also, by conducting the gene expression microarray assay, we identified 541 upregulated genes and 935 downregulated genes in PM2.5-treated HaCaT cells. Real-time qPCR and western blot confirmed that PM2.5 treatment could induce the expression of ABCA1 while inhibiting that of END1 and CLDN1. Conclusion. Our results showed that PM2.5 could potentially regulate cell apoptosis and cell cycle arrest via ABCA1-, END1-, ID1-, and CLDN1-mediated pathways in human HaCaT cells, which laid a good foundation for follow-up drug intervention and drug development against skin damage caused by PM2.5 exposure.

Objective To investigate sun protection behavior among middle-aged and elderly women in Beijing.Methods The central (Xuanwumen district) and peripheral areas (Yanqing district) of Beijing city were selected for investigation from May to June in 2016.By random sampling and field investigation,interviewees completed questionnaires with the help of dermatologists.Results A total of 400 females aged 40-90 years were investigated,including 190 in the Xuanwumen district and 210 in the Yanqing district.Among all the subjects,the average duration of outdoor activities was 2 hours.Moreover,117 (29.2％) of the 400 interviewees had the active sun exposure habit,including 38 (18.1％) in the Yanqing district and 79 (41.6％) in the Xuanwumen district,and the proportion of subjects with the active sun exposure habit significantly differed between the two districts (x2 =26.582,P ＜ 0.001).In addition,67 (16.8％) interviewees had a sunburn history,and 130 (32.5％) were used to applying sunscreen.The proportion of sunscreen users was significantly higher in moderately or highly educated women (103 [45.2％]) than in lowly educated women (28/172 [16.3％],P ＜ 0.001).The proportion of sunscreen users in women with skin type Ⅲ (41.2％ [70/170]) was significantly higher than that in those with skin type Ⅳ (26.5％ [61/230],P =0.002).The scores for facial skin aging and dorsal hand skin aging were both significantly lower in sunscreen users than in non-users (Z =18.536,10.731,P =0.002,0.026,respectively).Conclusion The active sun exposure habit in the middle-aged and elderly women differs between the central and peripheral areas of Beijing,and the use of sunscreen is associated with education level.

Ambient particulate matter 2.5 (PM2.5) is one of the main components of air pollutants, which can absorb many polycyclic aromatic hydrocarbons and metals. The effect of PM2.5 on human skin and its biological significance in skin homeostasis remain incompletely understood. Previous studies demonstrated that PM2.5 can activate aryl hydrocarbon receptor (AhR), generate reactive oxygen species, and induce skin inflammation. These processes may be involved in melanocyte homeostasis and melanogenesis. We hypothesize that AhR signaling may be responsible for PM2.5-related hyperpigmentation.

>患者男, 58岁, 2018年2月2日因躯干、四肢红色斑块3个月就诊。患者3个月前无明显诱因左胸出现乒乓球大小红色斑块, 边界清楚。近1个月皮疹逐渐扩大增多, 臀部、左大腿屈侧亦出现皮疹, 伴局部感觉迟钝, 无明显痛痒。曾外用铍药师软膏, 皮疹未好转。诉左肩周围疼痛, 无发热、腹泻, 否认毛发脱落。患者自发病以来, 精神食欲可, 体重稍有下降, 大小便正常。既往史无特殊。个人及家族史:久居于福建,

Atopic dermatitis (AD) is an inflammatory skin disease The study was conducted in accordance with the characterized by chronic recurrent dermatitis with proDeclaration of Helsinki and all the study participants found pruritus. Most patients have personal and/or family history of atopic diseases. Allergy to air allergens and food allergens was regarded as an important feature of AD. There have been few studies for contact sensitization in patients with AD. The question remains if patch testing to a greater extent should be used as a screening tool in AD patients, to exclude hidden allergies possibly maintaining or aggravating their skin symptoms. In this study, we compared patch test results between patients with AD and non-AD patients including patients with facial dermatitis, eczema, psoriasis, pruritus and urticaria, and including some healthy population.

A 24-year-old female came to our clinic because of painful lesions on her face and trunk. She has been suffered from refractory aplastic anemia for 10 years. She presented pustules, nodules and inflammatory sinus tract with pus on her face and trunk 5 months after took Stanozolol. What’s worse is that her aplastic anemia continued to deteriorate, so she needed autologous stem cell transplantation. We used topical photodynamic therapy mediated with 5-aminolevulinic acid for her severe inflammatory acne. After five sessions, all of the inflammatory acne had been cleared to satisfy the needs of transplantation.

Skin lipids, compose of sebocyte-, keratinocyte-, and microbe- derived lipids, dramatically influence skin status by different mechanisms. (I) Physical chemistry function: They are "mortar" to establish the physico-chemical barrier function of skin; (II) Biochemistry function: They function as signals in the complex signaling network originating at the epidermal level; (III) Microecology function: Sebocyte- and keratinocyte-derived lipids vary the composition of microbial skin flora, and microorganisms metabolize them to produce lipids as signal starting signaling transduction. Importantly, further research needs lipidiomics, more powerful analytical ability and high-throughput manner, to identify skin lipid components into individual species. The validation of lipid structure and function to research the process that lipid species involved in. Additional, the integration of lipidomics data with other omics strategies can develop the power to study the mechanism of skin lipids influencing skin status.

Journal of the European Academy of Dermatology and VenereologyVolume 32, Issue 7 p. e288-e289 Letter to the Editor Patch testing in facial dermatitis using Chinese Baseline Series (60 allergens) and Cosmetic Series (58 allergens) F. Peng, F. Peng Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorZ. Mu, Z. Mu Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorC. He, C. He Beijing Key Laboratory of Plant Resources Research and Development, Beijing Technology and Business University, Beijing, 100012 ChinaSearch for more papers by this authorC. Xue, C. Xue Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorW. Li, W. Li Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorQ. Wang, Q. Wang Beijing Key Laboratory of Plant Resources Research and Development, Beijing Technology and Business University, Beijing, 100012 ChinaSearch for more papers by this authorZ. Chen, Corresponding Author Z. Chen chenzhou54@sohu.com Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaCorrespondene: Z. Chen. E-mail: chenzhou54@sohu.comSearch for more papers by this authorJ. Zhang, J. Zhang Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this author F. Peng, F. Peng Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorZ. Mu, Z. Mu Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorC. He, C. He Beijing Key Laboratory of Plant Resources Research and Development, Beijing Technology and Business University, Beijing, 100012 ChinaSearch for more papers by this authorC. Xue, C. Xue Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorW. Li, W. Li Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this authorQ. Wang, Q. Wang Beijing Key Laboratory of Plant Resources Research and Development, Beijing Technology and Business University, Beijing, 100012 ChinaSearch for more papers by this authorZ. Chen, Corresponding Author Z. Chen chenzhou54@sohu.com Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaCorrespondene: Z. Chen. E-mail: chenzhou54@sohu.comSearch for more papers by this authorJ. Zhang, J. Zhang Dermatology, Peking University People's Hospital, Xizhimennan Avenue, Xicheng District, Beijing, 100044 ChinaSearch for more papers by this author First published: 29 January 2018 https://doi.org/10.1111/jdv.14822Citations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume32, Issue7July 2018Pages e288-e289 RelatedInformation

Objective To evaluate effects of fine particulate matter PM2.5 in ambient air on the proliferation,cell cycle and apoptosis of a human keratinocyte cell line HaCaT.Methods PM2.5 in hazefog episodes during the heating season was collected in Beijing from 2015 to 2016,and processed into PM2.5 suspensions.HaCaT cells were divided into several groups to be treated with culture medium alone (control group),PM2.5 suspensions at different concentrations of 100-400 mg/L (experiment groups,50-800 mg/L for observation of cellular morphology and analysis of cell proliferation) for 24 hours,or cell culture medium without cells or PM2.5 suspensions (blank group).Cellular morphological changes were observed under an inverted microscope.Cell counting kit-8 (CCK-8) assay was performed to determine cell survival rate,flow cytometry to determine the cell cycle distribution and detect cell apoptosis,and Western blot analysis to determine the protein expression of cyclin A2 and cyclin-dependent kinase1 (CDK1).Results Along with the increase of PM2.5 concentration,HaCaT cells lost their normal shape gradually,and the number of viable cells gradually decreased.Compared with the control group (100％ ± 4.95％),the 50-mg/L PM2.5 group showed no changes in cell survival rates (P ＞ 0.05),while the 100-,200-,400-and 800-mg/L PM2.5 group showed significantly lower survival rates (91.77％ ± 2.04％,80.01％ ± 1.57％,57.80％ ± 1.56％,21.98％ ± 0.86％,respectively,all P ＜ 0.05).Flow cytometry revealed that the 100-,200-and 400-mg/L PM2.5 groups showed gradually increased proportion of cells at S phase,but gradually decreased proportion of cells at G2/M phase compared with the control group (all P ＜ 0.05).As Western blot analysis showed,the protein expression of cyclin A2 and CDK1 significantly decreased in the 100-,200-and 400-mg/L PM2.5 groups compared with the control group,which was lowest in the 200-mg/L PM2.5 group(all P ＜ 0.05).In addition,the 100-,200-and 400-mg/L PM2.5 groups showed significantly higher total apoptosis rates (9.98％ ± 0.21％,12.56％ ± 0.74％,16.74％ ± 1.48％,respectively) compared with the control group (6.24％ ± 0.17％,all P ＜ 0.05).Conclusion PM2.5 can inhibit cell proliferation and promote apoptosis of HaCaT cells,likely by downregulating the expression of cyclin A2 and CDK1 and arresting HaCaT cells at S phase.