Photodynamic therapy (PDT) is a noninvasive therapeutic strategy that utilizes the synergistic interaction among a photosensitizer, light of a specific wavelength, and tissue oxygen to generate cytotoxic reactive oxygen species (ROS), thereby selectively destroying pathological tissues. Against the backdrop of increasingly severe global antibiotic resistance, PDT has demonstrated significant potential in the treatment of infectious skin diseases, owing to its unique multitarget mechanism of action and low propensity for inducing resistance. This review systematically elucidates the core antimicrobial mechanisms of PDT, summarizes its clinical advances in bacterial, fungal, and viral skin infections, and specifically discusses treatment strategies for special populations (such as children and pregnant women) and refractory cases. Finally, the article analyzes the current challenges in the clinical translation of PDT, including the lack of standardized treatment parameters and limited PS delivery efficiency, and offers perspectives on future directions, encompassing the development of novel PSs, the application of nanotechnology, and personalized treatment.

Photobiomodulation therapy (PBMT) is a safe and effective option for multiple skin diseases. To promote standardized clinical use, this expert consensus was developed by 35 dermatology experts through 2 rounds of Delphi surveys and addressed 19 clinical questions with a consensus degree of over 80.0%. This consensus summarizes current evidence on PBMT’s mechanisms of action, indications, contraindications, treatment parameters, and adverse event management. Although encouraging outcomes have been observed regarding acne vulgaris, photoaging, alopecia, and other dermatologic conditions, considerable variability in treatment protocols and the scarcity of high-quality, large-scale clinical trials continue to limit broader clinical adoption. This consensus provides evidence-based and practical guidance to support the safe and effective incorporation of PBMT into dermatologic practice in China.

Compound betamethasone combined with 595 nm pulsed dye laser (PDL) is widely used in the clinical management of hypertrophic scars. However, the mechanisms underlying this enhanced effect remain poorly understood. This study evaluated its therapeutic efficacy and investigated whether induction of autophagy in myofibroblasts is associated with scar improvement. A rabbit ear hypertrophic scar model was established and divided into control, compound betamethasone injection (BI), PDL, and combined (BI + PDL) groups. Scar morphology and histological changes were assessed. Autophagy was evaluated using transmission electron microscopy (TEM) and immunohistochemical detection of LC3B and p62. In vitro, hypertrophic scar–derived myofibroblasts were treated with betamethasone dipropionate (BD), PDL, or their combination (BD + PDL). Cell viability, collagen expression, and autophagic activity were analyzed using CCK-8 assays, Western blotting, MDC staining, immunofluorescence, and TEM. Chloroquine was used to assess autophagic flux. The combined BI + PDL treatment produced the most pronounced improvement in scar architecture, with reduced collagen deposition, decreased microvessel density, and increased number of apoptotic cells. Autophagy levels were significantly elevated in the combination group both in vivo and in vitro. In cultured myofibroblasts, BD + PDL markedly inhibited cell viability and reduced type I and type III collagen expression. This effect was accompanied by increased autophagosome formation, an elevated LC3II/LC3I ratio, and decreased p62 expression. Importantly, inhibition of autophagic flux with chloroquine attenuated the collagen-suppressive effect of the combined treatment. Compound betamethasone combined with 595 nm PDL significantly improves hypertrophic scars, an effect associated with enhanced autophagic activity in myofibroblasts which may partly mediate collagen degradation.

Trichosporon asahii is a significant pathogen of invasive fungal infections, exhibiting low susceptibility to multiple first-line antifungal drugs, which poses severe challenges in clinical treatment. This study discovered for the first time that ferrous sulfate (FeSO₄) has a potent inhibitory effect against this fungus by inducing a ferroptosis-like cell death. This process ischaracterized by non-apoptotic cell death, iron ion dependence, reactive oxygen species (ROS) burst, lipid peroxide accumulation, and damage to key membrane systems including the loss of mitochondrial membrane potential. This process can be partially reversed by the ferroptosis-specific inhibitor Ferrostatin-1, and provided a modest improvement in fungal survival. Transcriptomic analysis further revealed that FeSO₄ treatment causes significant alterations in the expression of genes related to redox processes, glutathione metabolism, and the proteasome pathway. This study, for the first time, elucidates a ferroptosis-like death pathway in Trichosporon asahii triggered by exogenous Fe2+, which depends on iron accumulation and lipid peroxidation, thereby revealing a novel, ferroptosis-based mechanism with potential for future antifungal development.

Background:Facial skin aging drives demand for minimally invasive rejuvenation. The technique of injecting skin boosters into the dermis through mesotherapy is increasingly used to improve signs of skin aging. This study evaluates the efficacy and safety of a novel sodium hyaluronate-based composite solution (containing sodium hyaluronate, glycine, proline, leucine, and lysine) for facial rejuvenation. Methods:Participants aged 18 to 65 years with facial skin concerns (dryness, dullness, enlarged pores, reduced elasticity, or fine wrinkles) were randomized in a 2:1 ratio into a treatment group or a control group. The treatment group received 3 monthly intradermal injections, whereas the control group received no intervention. The primary endpoint was the efficacy rate 1 month after the final treatment using the Global Aesthetic Improvement Scale. Secondary endpoints included efficacy rates at different time points and changes in skin hydration and elasticity. Safety was monitored throughout. Results:Of 456 enrolled participants, 439 completed the study (287 treatment, 152 control; 92.94% women). One month posttreatment, the treatment group showed a 97.56% efficacy rate, significantly higher than the control group's 3.95% (P < 0.001). Significant improvements in skin hydration and elasticity were observed in the treatment group (P < 0.05) and sustained for up to 3 months. The adverse event incidence was only 1.67%, and all of them were mild to moderate, with no serious events reported. Conclusions:The skin booster (a novel sodium hyaluronate composite solution) delivered via mesotherapy is effective for improving signs of skin aging. With a favorable safety profile, it offers a validated therapeutic option for facial rejuvenation.

Background:While growing evidence suggests the intricate relationship between immune cells and the pathogenesis of acne, the causative implications underlying these associations remain poorly characterized. This study aimed to elucidate the causal links between various immune cell phenotypes and the development of acne using Mendelian randomization (MR) analysis. Methods:Leveraging data of 731 immune cell traits and acne from genome-wide association studies, we conducted a bidirectional MR analysis. Rigorous instrumental variables selection was followed by causal inference using five complementary methods, including MR-Egger, weighted median, simple mode, inverse variance weighted (IVW), and weighted mode methods. Heterogeneity and pleiotropy were evaluated using Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis. Results:Genetically predicted alterations in 26 immune cell phenotypes demonstrated causal associations with acne risk. Notably, 18 immune cell types exhibited protective effects, such as CD25 on IgD+ (IVW: OR 0.922, 95% CI 0.868-0.979; p = 0.008), naive-mature B cell %lymphocytes (IVW: OR 0.824, 95% CI 0.698-0.972; p = 0.022), and CD19 on sw mem (IVW: OR 0.841, 95% CI 0.752-0.940; p = 0.002). Conversely, 8 immune cell types conferred increased risk, such as IgD+ CD38dim AC (IVW: OR 1.054, 95% CI 1.002-1.108; p = 0.043), CD25 on unsw mem (IVW: OR 1.058, 95% CI 1.005-1.114; p = 0.030), and CD28+ DN (CD4-CD8-) %DN (IVW: OR 1.117, 95% CI 1.019-1.225; p = 0.019). The absence of significant heterogeneity or horizontal pleiotropy (p > 0.05) strengthens the credibility to the observed associations. Conclusion:In conclusion, this research provides compelling genetic evidence for causal immunomodulatory influences on acne development, thus laying the groundwork for future investigational efforts aimed at uncovering targeted therapeutic strategies in acne management.

Diabetic wound therapy faces significant challenges due to the complexity of the wound microenvironment, especially dysregulated immune cell responses and persistent pro-inflammatory sate. Targeting immune cells to reverse pathological wound conditions has increasingly become a promising strategy to promote diabetic wound healing. It has been reported that prolonged memory to acute inflammation sensitizes epidermal stem cells (EpSCs) to tissue damage. The increasing importance of interactions between immune cells and tissue stem cells has raised interest in the potential of EpSCs to induce inflammatory adaptations in diabetic wounds, and meanwhile, the inflammation memory patterns also provide new insight in EpSCs for tissue repair. Here, bioinspired cell-derived mimetic nanovesicles (MNVs) were obtained from inflammation memory-activated EpSCs. LPS treatment could trigger acute inflammation response and activate inflammation memory. MNVs derived from LPS-pretreated EpSCs (LEM) can effectively promote diabetic wound healing by manipulating crucial neutrophil regulatory mechanisms. The in vitro and in vivo studies demonstrated that LEM could stimulate neutrophil mitochondrial metabolic reprogramming, overcome phenotypic switching deficiency of neutrophils, and skew neutrophils toward N2 anti-inflammatory phenotype via regulating miR-193a-5p/TLR4/ JNK/P38 MAPK pathways in diabetic models. Our findings highlighted the great potential of inflammation memory in EpSCs, and also provided an alternative for diabetic wound treatment.

Background:Café-au-lait macules (CALMs) are common skin manifestations, and their number and distribution may indicate potential genetic disorders, such as Neurofibromatosis Type 1 (NF1). This study aimed to investigate the clinical characteristics of multiple CALMs and their significance in the early screening of genetic disorders. Methods:This retrospective study included 98 patients diagnosed between May 2021 and May 2024 in two hospitals. Patients were divided into three groups based on the number of CALMs and whether other skin manifestations were present: Group 1 (≥ 6 CALMs with other skin manifestations), Group 2 (≥ 6 CALMs without other skin manifestations), and Group 3 (< 6 CALMs without other skin manifestations). Detailed clinical evaluations and imaging examinations were conducted to record the number, size, distribution of CALMs, and associated symptoms. Multivariate logistic regression analysis was performed to explore the relationship between CALMs and other systemic symptoms. Results:Group 1 patients showed significantly higher incidences of neurological symptoms (eg, neurofibromas 54%, P < 0.001) and skeletal system symptoms (eg, bone deformities 38%, P = 0.001) compared to Groups 2 and 3. Imaging examinations revealed an abnormality rate of 90% in Group 1 (P < 0.001). Logistic regression analysis indicated that the number of CALMs (≥ 10) was significantly associated with neurological (OR = 7.664, P = 0.001) and skeletal system symptoms (OR = 4.623, P = 0.014). The distribution of CALMs on the face and neck also showed a certain influence on symptoms. Conclusion:The number and distribution of CALMs are significant in the early screening of genetic diseases, particularly in identifying patients with potential neurological and skeletal system abnormalities.

Cell pyroptosis serves as a critical regulatory mechanism by which host cells respond to fungal infections. However, whether pyroptosis contributes to alterations in fungal pathogenicity during microevolution remains unclear. In this study, we investigated the role of pyroptosis in the pathogenicity of Trichosporon asahii (T. asahii) intraspecies variation, as well as the underlying mechanisms. An in vitro model was established by co-culturing a strain (Ori 2.2174) and a intraspecies variation (Evo 1403.3) of T. asahii with mouse macrophages, while an in vivo model was developed by inoculating immunosuppressed ICR mice with these strains. Survival analysis was performed to assess mortality differences between groups. In vitro experiments revealed that the macrophages infected with Evo 1403.3 exhibited significantly lower lysis rates, pyroptosis levels, and inflammatory cytokine production compared to those infected with Ori 2.2174. Similarly, mice inoculated with Evo 1403.3 showed significantly higher survival rates and reduced fungal burden and lesion areas in organ tissues compared to those infected with Ori 2.2174. Furthermore, pyroptosis mediated by the NLRP3/Caspase-1/GSDMD signaling axis was observed in macrophages infected with both strains, with the extent of pyroptosis positively correlating with strain pathogenicity. Collectively, these findings indicate that cell pyroptosis mediated through the NLRP3/Caspase-1/GSDMD pathway plays a pivotal role in regulating the pathogenicity of T. asahii intraspecies variation.

Background: Silver nanomaterials have been widely proven to have antifungal effects against Trichosporon asahii. However, the antifungal mechanism of silver nanomaterials with different morphologies still needs to be explored. Methods: Herein, the antifungal effect of silver nanomaterials against fungus was comparative investigated via silver nanowires and silver nanoparticles with a similar size (30 nm). Results: The optimal antifungal concentration of silver nanowires is 6.24 mu g/mt, meanwhile the antifungal concentration of silver nanoparticles is 100 mu g/mt. The silver nanowires are significantly superior to the silver nanoparticles. SEM and TEM results indicated that both silver nanoparticles and silver nanowires showed significant morphological changes in the mycelium of the strain, compared with the control. The lower MFC value of silver nanowires indicates good sterilization effect and suitability for eradication treatment, which is slower than that of silver nanoparticles. Moreover, we also investigated the toxicological effects of silver nanoparticles and silver nanowires. Conclusion: We comparative studied and transcriptomic analyzed the antifungal mechanism of Ag nanoparticles and nanowires against Trichosporon asahii. The antifungal effects of silver nanowires were better than the silver nanoparticles, especially in the metabolic processes and oxidative phosphorylation. RNA sequencing results indicated that 15 key targets were selected for experimental verification to interpret the potential antifungal mechanism of Ag nanomaterials against fungus. This work proves that silver nanomaterials with different morphologies have potential applications in fungus therapy such as T. asahii.

Background:Neutrophils rapidly accumulate in large numbers at sites of tissue damage, exhibiting not only their well-known bactericidal capabilities but also playing crucial roles in angiogenesis and tissue repair. While exosomes derived from human umbilical cord mesenchymal stem cells (HucMSC-Exo) have emerged as a promising therapeutic tool, their exact mechanisms of action remain partly elusive. We hypothesize that HucMSC-Exo treatment may modulate neutrophil phenotypes, thereby significantly influencing wound healing outcomes.Methods:HucMSC-Exo were isolated via ultracentrifugation and subsequently administered through subcutaneous injection into full-thickness cutaneous wounds in mice. To determine the impact of host neutrophils on the healing effects of HucMSC-Exo in skin injuries, strategies including neutrophil depletion and adoptive transfer were employed. Flow cytometry was used to evaluate the proportion of N2 subtype neutrophils in both normal and diabetic wounds, and the effect of HucMSC-Exo on this proportion was assessed. Furthermore, the mitochondrial metabolic reprogramming driven by HucMSC-Exo during N2 polarization was investigated through JC1 staining, ATP quantification, fatty acid uptake assays, and assessment of FAO-related genes (Cpt1b, Acadm, and Acadl).Results:Depleting host neutrophils strikingly dampened prohealing effect of HucMSC-Exo on skin injury, while adoptive transfer of bone marrow neutrophils rescued this process. During normal healing process, some neutrophils expressed N2 markers, in contrast, diabetic wounds exhibited a reduced expression of N2 markers. After treatment with HucMSC-Exo, most neutrophils increased the phosphorylation of STAT6, leading to mitochondrial metabolic reprogramming and thus acquired an N2 phenotype. These N2 neutrophils, polarized by HucMSC-Exo, boosted the release of proangiogenic factors, particularly BV8, a myeloid cell-derived proangiogenic factor, and induced angiogenesis thereby favoring tissue restoration.Conclusion:This research uniquely demonstrates the identification of N2 neutrophils in skin injury and shows that HucMSC-Exo could skew neutrophils toward N2 phenotype, enhancing our insight into how cells react to HucMSC-Exo.

Background:Solar lentigines (SLs), serving as a prevalent characteristic of skin photoaging, present as cutaneous aberrant pigmentation. However, the underlying pathogenesis remains unclear and there is a dearth of reliable diagnostic biomarkers.Objective:The aim of this study was to identify diagnostic biomarkers for SLs and reveal its immunological features.Methods:In this study, gene expression profiling datasets (GSE192564 and GSE192565) of SLs were obtained from the GEO database. The GSE192564 was used as the training group for screening of differentially expressed genes (DEGs) and subsequent depth analysis. Gene set enrichment analysis (GSEA) was employed to explore the biological states associated with SLs. The weighted gene co-expression network analysis (WGCNA) was employed to identify the significant modules and hub genes. Then, the feature genes were further screened by the overlapping of hub genes and up-regulated differential genes. Subsequently, an artificial neural network was constructed for identifying SLs samples. The GSE192565 was used as the test group for validation of feature genes expression level and the model's classification performance. Furthermore, we conducted immune cell infiltration analysis to reveal the immune infiltration landscape of SLs.Results:The 9 feature genes were identified as diagnostic biomarkers for SLs in this study. And an artificial neural network based on diagnostic biomarkers was successfully constructed for identification of SLs. GSEA highlighted potential role of immune system in pathogenesis of SLs. SLs samples had a higher proportion of several immune cells, including activated CD8 T cell, dendritic cell, myeloid-derived suppressor cell and so on. And diagnostic biomarkers exhibited a strong relationship with the infiltration of most immune cells.Conclusion:Our study identified diagnostic biomarkers for SLs and explored its immunological features, enhancing the comprehension of its pathogenesis.

背景 不同剥脱性激光治疗萎缩性痤疮瘢痕的疗效及其影响因素临床资料有限.目的 探讨不同剥脱性激光治疗面部萎缩性痤疮瘢痕的临床疗效和影响因素.方法 回顾性分析 2014年 7月-2022年 8月在解放军医学院第七医学中心皮肤科激光中心采用剥脱性激光治疗面部萎缩性痤疮瘢痕患者的临床资料,包括二氧化碳点阵激光(Deep模式,能量密度12.5～22.5 mJ,光斑密度 5%～10%)、铒像素激光(能量 800～1400 mJ,能量密度 3～6 J/cm2)及等离子体射频(滚动式功率60～70 W,3～4遍/次),间隔 1～12个月治疗 2次.对患者治疗前后照片采用痤疮瘢痕评估量表(Echelle d'Evaluation Clinique des Cicatrices d'acne,ECCA)评分以评估疗效,并根据ECCA评分下降率,分为有效组和无效组,分析影响治疗疗效的影响因素.结果 共纳入 61例患者,治疗前 ECCA评分为(110.16±30.54)分,2次治疗后为(85.98±25.03)分(P＜0.001),临床有效率为 31.15%.Logistic回归提示治疗前ECCA评分是治疗效果的独立影响因素(OR=0.297,95%CI:0.090～0.976,P=0.046),而年龄对治疗效果无显著影响.结论 剥脱性激光治疗面部萎缩性痤疮瘢痕有较好疗效,治疗前ECCA评分是治疗效果的独立影响因素.

敏感性皮肤是一种与皮肤神经系统异常相关的综合征，认知已由先前的单一皮肤屏障受损逐步发展至与基因、皮肤神经系统改变有关的神经源性炎症；这种神经源性炎症可能是系统性神经高反应性的皮肤表现。近年来关于敏感性皮肤的研究日益增多，其中神经相关发病因素是研究热点之一。从病因与发病机制、诊断、治疗方面概述敏感性皮肤的近期研究进展，旨在为相关研究提供信息。

Melanosomes can more effectively absorb energy from a 532 nm laser, destroying the melanosomes. We used a PSNYL pulse width of 240– 400 ps and QSNYL pulse width of 5– 20 ns, both of which are significantly lower than the heat relaxation time (50– 250 ns) of melanosomes and can effectively destroy the melanin particles in the epidermis. In this study, although there was a statistical difference of the lesion clearance rate between QSNYL treatment groups and PSNYL treatment groups, the two groups showed similar visual efficacy. However, shortening the pulse width has a positive effect; for example, for the treatment of nevus of Ota, a shorter pulse width can improve the efficacy of a single treatment significantly, reducing the number of treatments. 5

BackgroundTrichosporon asahii is an opportunistic pathogenic yeast-like fungus. Phospholipase B1 (PLB1) is an important virulence factor of pathogenic fungi such as Candida albicans and Cryptococcus neoformans, and there are few studies on the role of PLB1 in the pathogenicity of T. asahii. ObjectivesTo investigate the role of PLB1 in the pathogenicity of T. asahii. MethodsA strain with low secretion of PLB1 (4848) was screened, a PLB1 overexpression strain (PLB1(OX)) was constructed, and the differences in histopathology, fungal load of organ, survival time of mice, the levels of IL-6, IL-10, TNF-alpha, and GM-GSF in the serum and organs caused by the two strains were compared. ResultsHistopathology showed that spores and hyphae were observed in both groups, and PLB1(OX) led to more fungal invasion. The fungal loads in the kidney, lung, spleen and liver in the PLB1(OX)group were significantly higher than those in the 4848 group, and the survival time of mice was significantly lower than that in the 4848 group. The levels of TNF-alpha in the serum, liver, spleen, lung and kidney of the PLB1(OX) group were lower than those of the 4848 group, while the level of IL-10 in the serum was higher than that of the 4848 group. ConclusionsThese results suggest that PLB1 can enhance the invasive function of T. asahii and affect the secretion of TNF-alpha and IL-10 which may affect the host antifungal immune response, providing evidence that PLB1 plays a role in the pathogenic infection of T. asahii.

Systemic infection caused by T. asahii has recently been recognized as an important cause of mortality in hospitalized COVID-19 patients. Invasive trichosporonosis remains a significant challenge for clinicians, due to the limited therapeutic options.

Objective:To evaluate the efficacy and safety of radiofrequency introduction of L-vitamin C in patients with melasma.Methods:From March to June 2019, 20 patients with melasma were admitted to the Department of Dermatology, the Seventh Medical Center of PLA General Hospital, including 19 females and 1 male, aged 30-60 years, with an average age of 43.5 years. All patients were treated with 22 percent of L-vitamin C once a week, a total of 8 times of treatment and followed up for 12 weeks. Each subject was assessed with standardized clinical photo, skin tests (VISIA skin image analyzer and CK multifunctional skin tester) and patient self-assessment. In addition, the adverse reactions were recorded.Results:Physician evaluation and patient self-evaluation showed that skin symptoms were improved obviously after treatment. 90% of the subjects thought that all of the skin moisture, pores, fine lines, glossiness, and color spots were improved after 12 weeks. The skin texture, ultraviolet stain and the brown spots which were detected with VISIA skin image analyzer were all improved after one week and one month. Difference was statistically significant ( P<0.05). Skin glossiness was significantly improved, skin moisture content increased and melanin decreased, which were detected with CK multifunctional skin tester. The differences were statistically significant ( P<0.05). But there was no significant change in transdermal water loss and red pigment index ( P>0.05). Conclusions:22% L-vitamin C can be used to treat melasma and improve photoaging safely without affecting skin barrier function.

Background and objectives: Both artesunate and fractional CO2 laser have been proved effective in the treatment of hypertrophic scars, yet little data are available for the efficacy of artesunate combined with fractional CO2 laser. In order to assess the pre-clinical significance and the underlying mechanism of this combined treatment profile, we attempted to observe the effectiveness of this therapy in rabbit models through determining the expression of BMP-7 and Fas. Materials and methods: Twenty-Four New Zealand white rabbits with established hypertrophic scar samples were randomly divided into control group and three treatment groups. Artesunate (20 mu l/cm(2)) was injected into the rat's scar of artesunate and combination groups, while fractional CO2 laser (Combo mode, deep energy:10 mJ, super energy: 50 mJ) was applied to rats in fractional CO2 laser and combination groups at week 4 after model establishment. All rabbits underwent a total of 3 sessions of treatment once every 2 weeks. Histological and immunohistochemistry study, Western blot assay, cell viability, ELISA and RT-QPCR were performed at week 10 to observe the aspects of hypertrophic scar sample changes and expression of BMP-7 and Fas in the scar tissues. Results: Compared with control group, hypertrophic scars and the collagen fibers were significantly inhibited after treatment, and higher inhibition was seen in the samples in combination group compared to that in artesunate and fractional CO2 laser groups (P < 0.01). Meanwhile, BMP-7 and Fas expressions were both notably increased in all treatment groups, and upregulation of the two proteins was dominant in combination group (P < 0.01). Conclusions: Artesunate combined with fractional CO2 laser is effective in hypertrophic scarring in this rabbit model. Our findings can serve as a potential alternative strategy to treatment of hypertrophic scar in clinical practice. (C) 2021 Published by Elsevier Ltd.

33岁男性患者,臀部皮肤丘疹3个月余.皮损组织病理检查示肿瘤边界清楚,真皮浅中层有较多角囊肿形成,免疫组化染色示CK15、p63阳性,AR、BerEp4、CK20阴性.诊断:皮肤毛发腺瘤.予手术切除,预后良好.