Background: Long noncoding RNAs (lncRNAs) play pivotal roles in various malignant tumors. Epidermal growth factor receptor (EGFR) signaling is associated with the pathogenesis of cutaneous squamous cell carcinoma (cSCC). This study aimed to explore the role of LINC00520 in the development of cSCC via EGFR and phosphoinositide 3-kinase-protein kinase B (PI3K/Akt) signaling pathways. Methods: A microarray analysis was applied to screen differentially expressed lncRNAs in cSCC samples. The A431 cSCC cell line was transfected and assigned different groups. The expression patterns of LINC00520, EGFR, and intermediates in the PI3K/Akt pathway were characterized using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting analysis. Cell proliferation, migration, and invasion were detected using the MTT assay, scratch test, and Transwell assay, respectively. Cell-based experiments and a tumorigenicity assay were conducted to assess the effect of LINC00520 on cSCC progression. This study was ended in September 2017. Comparisons between two groups were analyzed with t -test and comparisons among multiple groups were analyzed using one-way analysis of variance. The nonparametric Wilcoxon rank sum test was used to analyze skewed data. The enumerated data were analyzed using the chi-square test or Fisher exact test. Results: Data from chip GSE66359 revealed depletion of LINC00520 in cSCC. Cells transfected with LINC00520 vector and LINC00520 vector + si-EGFR showed elevated LINC00520 level but decreased levels of the EGFR, PI3K, AKT, VEGF, MMP-2 and MMP-9 mRNAs and proteins, and inhibition of the growth, migration and adhesion of cSCC cells, while the si-LINC00520 group showed opposite trends (all P < 0.05). Compared with the LINC00520 vector group, the LINC00520 vector + si- EGFR group showed decreased levels of the EGFR, PI3K, AKT, VEGF, MMP-2 and MMP-9 mRNAs and proteins, and inhibition of the growth, migration and adhesion of cSCC cells, while the LINC00520 vector + EGFR vector group showed opposite results (all P < 0.05). Conclusion: Based on our results, LINC00520-targeted EGFR inhibition might result in the inactivation of the PI3K/Akt pathway, thus inhibiting cSCC development.

Background:Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening diseases with high mortality rates. This study was designed to analyze the pathogenic factors, clinical manifestations, complications, treatment, and prognosis of SJS/TEN and to explore the differences between surviving and deceased patients.Methods:SJS/TEN patients admitted to Beijing Friendship Hospital from January 2006 to December 2015 were included in the study. Patients’ data were retrospectively analyzed. Comparative studies were performed on the survival group and the deceased group, and Fisher's exact probability test was used for statistical analysis.Results:Among the 88 patients included, 40 (45.5%) were male with a mean age of 45 ± 18 years. Forty-eight (54.5%) had SJS, 34 (38.6%) had SJS/TEN, and 6 (6.8%) had TEN. Fifty-three (60.2%) cases were caused by medications, mainly antibiotics (n = 24) followed by traditional Chinese medicines (n = 7). Forty-two cases (47.7%) developed visceral damage. Eighty-two patients improved or recovered and were discharged from hospital, and six patients died. Comparative studies on the survival group and the deceased group showed that the presence of malignant tumor (χ2 = 27.969, P < 0.001), connective tissue diseases (χ2 = 9.187, P = 0.002), previous abnormal liver/kidney functions (χ2 = 6.006, P = 0.014), heart rate >100 times/min (χ2 = 6.347, P = 0.012), detached skin area >20% (χ2 = 5.594, P = 0.018), concurrent mucosal involvement at the mouth, eyes, and external genitals (χ2 = 4.945, P = 0.026), subsequent accompanying liver/kidney damage (χ2 = 11.839, P = 0.001, and χ2 = 36.302, P < 0.001, respectively), and SCORTEN score >2 (χ2 = 37.148, P < 0.001) increased the risk of death.Conclusions:SJS/TEN is mainly caused by medications, and nearly half of patients develop visceral damage. Multiple factors increase the mortality risk.

Intense pulsed light (IPL) is effective for the treatment of lentigines, telangiectasia, and generalized erythema, but is less effective in the removal of skin wrinkles. Fractional laser is effective on skin wrinkles and textural irregularities, but can induce postinflammatory hyperpigmentation (PIH), especially in Asians. This study evaluated the safety and efficacy of ablative fractional laser (AFL) in combination with IPL in the treatment of photoaging skin in Asians.This study included 28 Chinese women with Fitzpatrick skin type III and IV. The side of the face to be treated with IPL alone (3 times) or AFL in combination with IPL (2 IPL treatments and 1 AFL treatment) was randomly selected. Skin conditions including hydration, transepidermal water loss, elasticity, spots, ultraviolet spots, brown spots, wrinkle, texture, pore size and red areas, as well as adverse effects were evaluated before the treatment and at 30 days after the treatment.Compared with IPL treatment alone, AFL in combination with IPL significantly increased elasticity, decreased pore size, reduced skin wrinkles, and improved skin texture (P = .004, P = .039, P = .015, and P = .035, respectively). Both treatment protocols produced similar effects in relation to the improvement of photoaging-induced pigmentation. The combined therapy did not impair epidermal barrier function. No postoperative infection, hypopigmentation, or scarring occurred after IPL and AFL treatments. PIH occurred at 1 month after AFL treatment and disappeared at 30 days after completion of the combined therapy.AFL in combination with IPL is safe and effective for photoaging skin in Asians.

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Desmoplastic trichilemmoma (DT) of the scalp is a rare disease. In this report, we describe a 67-year-old man who had a small papule lesion around the hairline of the left scalp for more than 40 years. The lesion had rapidly grown to become a solitary, round, 15-mm neoplasm within 6 months. Histopathological examination showed that the mass was composed of a peripheral layer of columnar cells with nuclear palisading resembling the outer root sheath; the mass was surrounded by a thickened glassy basement membrane. The stroma in the center of the mass displayed solid, hyaline degeneration and an eosinophilic pattern, streaked with epithelial cords or islands. Immunohistochemical evaluation showed diastase-resistant, periodic acid–Schiff-positive desmoplastic stroma at the center, and Ber-EP4-negative tumor cells (CD34-positive focally and Bcl-2-positive at the periphery). The tumor was completely resected, and no recurrence occurred during the follow-up period. In this report, we also summarize immunohistochemical features from previous reports of DT, facilitating differential diagnosis of DT from some invasive skin tumors.

BackgroundIncreasing numbers of studies demonstrated that picosecond lasers (Picos) were effective and safe for melasma. However, A limited number of randomized controlled trials (RCTs) regarding Picos contribute to a modest level of evidence. Topical hydroquinone (HQ) remains to be the first-line therapy.ObjectiveTo compare the efficacy and safety of non-fractional picosecond Nd:YAG laser (PSNYL), non-fractional picosecond alexandrite laser (PSAL), and 2% HQ cream in the treatment of melasma.MethodSixty melasma patients with Fitzpatrick skin types (FST) III-IV were randomly assigned to the PSNY, PSAL, and HQ groups at a 1:1:1 ratio. Patients in PSNYL and PSAL groups received 3 laser sessions at 4-week intervals. The 2% HQ cream was applied twice daily for 12 weeks in patients of the HQ group. The primary outcome, the melasma area and severity index (MASI) score, was evaluated at weeks 0, 4, 8, 12, 16, 20, and 24. The patient assessment score by quartile rating scale was rated at weeks 12, 16, 20, and 24.ResultsFifty-nine (98.3%) subjects were included in the analysis. Each group showed significant change from baseline in MASI scores from week 4 to week 24. The MASI score in the PSNYL group showed the greatest reduction compared to the PSAL group (p = 0.016) and HQ group (p = 0.018). The PSAL group demonstrated comparable MASI improvement as the HQ group (p = 0.998). The PSNYL group had the highest patient assessment score, followed by the PSAL group and then the HQ group, although only the differences between PSNYL and HQ groups at weeks 12 and 16 were significant. Four patients (6.8%) experienced recurrence. Other unanticipated events were transient and subsided after 1 week to 6 months.ConclusionThe efficacy of non-fractional PSNYL was superior to that of non-fractional PSAL, which was not inferior to 2% HQ, thus non-fractional Picos providing an alternative for melasma patients with FSTs III-IV. The safety profiles of PSNYL, PSAL, and 2% HQ cream were similar.Clinical Trial Registrationhttps://www.chictr.org.cn/showprojen.aspx?proj=130994, ChiCTR2100050089.

Psoriasis is a chronic skin disorder associated with multiple sequelae, such as psoriatic arthritis and cardiovascular diseases. Increasing evidence has shown that γδ T cells, as sources of IL-17A, play critical roles in psoriatic inflammations. However, there still lack effective ways to manipulate these pathogenic γδ T cells, which are less well studied than αβ T cells. The present study aims to characterize the phenotype of γδ T cells and evaluate the impact of D-mannose (a C-2 epimer of glucose) on γδ T cell-mediated psoriasis. We found that skin-draining LN γδ T cells underwent robust proliferation and acquired an IL-17-producing phenotype during psoriasis. The transcriptomic profiles of these psoriatic γδ T cells had elevated glycolytic signatures. Importantly, D-mannose treatment suppressed the γδ T cell reaction and successfully alleviated the local and systematic inflammation induced by imiquimod. The decreased AKT/mTOR/HIF-1α signaling and glycolytic ability may contribute to the suppression of γδ T cells achieved by D-mannose. Our study increased understanding of γδ T cells in psoriasis and promoted D-mannose utilization as a potential clinical application for autoimmune diseases driven by γδ T cells.