ABSTRACT Background Androgenetic alopecia (AGA) is a common disorder that negatively affects quality of life. Platelet‐rich plasma (PRP) has shown efficacy in hair regeneration. Ozone treatment amplifies the biological effects of PRP, thereby strengthening its role in follicular regeneration. Objective To evaluate the efficacy and safety of oxygen‐enriched PRP combined with 5% minoxidil compared with minoxidil monotherapy in AGA. Methods In this retrospective comparative study, treatment of 72 patients was reviewed. Patients were categorized according to the treatment they had received: oxygen‐enriched PRP combined with minoxidil or minoxidil monotherapy. The combination group received 5 PRP injection sessions at two‐week intervals with daily topical minoxidil, while the control group used minoxidil alone. Efficacy was assessed by dermoscopic parameters and satisfaction scores; adverse events were recorded. Results The combination group showed significantly greater improvements in hair density, hair diameter, and follicular density compared with monotherapy ( p < 0.05). No significant differences were observed in terminal hair ratio or mean number of hairs per follicular unit ( p > 0.05). Patient and physician reported satisfaction scores were higher in the combination group. Adverse events were mild and transient, with no serious complications. Conclusion Oxygen‐enriched PRP combined with minoxidil is more effective than minoxidil alone for improving hair growth parameters and patient satisfaction. These findings support ozone‐treated PRP as a promising therapy for AGA.

BackgroundThe efficacy of dupilumab in atopic dermatitis (AD) has been widely validated; however, systematic investigations into treatment adherence are lacking.ObjectiveTo analyze clinical factors influencing dupilumab adherence in patients with moderate-to-severe AD and develop a multidimensional adherence prediction model to support precision management of biologic therapies.MethodsUsing a single-center prospective cohort, a three-stage modeling approach was applied: (1) univariable Cox proportional hazards regression to identify potential predictors; (2) XGBoost modeling with SHAP method for feature importance ranking and dimensionality reduction; (3) multivariable Cox proportional hazards model for final prediction.ResultsUnivariable analysis indicated that treatment discontinuation was significantly associated with age, sex, combination therapy, baseline disease activity, and treatment response. Machine learning identified EASI/NRS and EASI-75/SLS-75 as key predictors of baseline disease activity and treatment response, respectively. The multivariable model confirmed independent predictive value for age, baseline EASI/NRS scores, and achievement of EASI-75/SLS-75.ConclusionThis study identified key determinants of dupilumab adherence and developed a predictive adherence model that offers personalized risk visualization via nomograms, providing an evidence-based tool for the precision management of AD biologic therapies.

OBJECTIVES:Patients with moderate-to-severe atopic dermatitis (AD) often experience intense pruritus and extensive skin lesions, which markedly impair quality of life. Current treatment options, including biologics and small-molecule agents, may provide limited efficacy and are associated with adverse effects. For patients who respond inadequately to dupilumab, particularly those with insufficient control of pruritus, more effective therapeutic strategies are needed. This study aims to evaluate the efficacy, safety, and clinical value of combining dupilumab with Janus kinase inhibitors (JAKis) in the treatment of refractory AD. METHODS:This retrospective study assessed the efficacy and safety of combination therapy with dupilumab and JAKis in 7 patients with refractory moderate-to-severe AD. Patients received either abrocitinib (100 mg/d) or upadacitinib (15 mg/d) in combination with dupilumab. Disease severity before and after combination therapy was evaluated using the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD), Patient-Oriented Eczema Measure (POEM), Dermatology Life Quality Index (DLQI), Itch Numerical Rating Scale (Itch-NRS), and Sleep Disorder Numerical Rating Scale (Sleep-NRS). Adverse events were also recorded. RESULTS:After 4 weeks of combination therapy, patients with AD who had shown an inadequate response to dupilumab monotherapy exhibited marked improvement in skin lesions. Significant reductions were observed in EASI, SCORAD, POEM, DLQI, Itch-NRS, and Sleep-NRS scores (all P<0.05). All patients achieved an EASI50 (defined as ≥50% reduction in EASI score from baseline) criteria. No serious adverse events were reported, except for one case of mild acne. CONCLUSIONS:In patients with AD who show an inadequate response to continued dupilumab treatment, the addition of JAKis can significantly enhance therapeutic efficacy and is generally well tolerated. This combination regimen may represent a promising treatment option for refractory AD.

Background:Acanthosis nigricans (AN) is a recognized cutaneous marker of insulin resistance and metabolic syndrome. Despite its clinical significance and associations with various comorbidities, a comprehensive, quantitative overview of the research landscape is lacking. Objective:This study aimed to conduct a bibliometric analysis to map the global research output, identify key themes and trends, and elucidate the comorbidity network and potential therapeutic strategies for AN. Methods:We performed a bibliometric analysis using publications retrieved from the Web of Science Core Collection (until May 13, 2024). Data from 2098 publications were analyzed using VOSviewer for co-authorship and keyword co-occurrence networks, CiteSpace for temporal trend and burst detection, and the R package bibliometrix for thematic mapping and publication metrics. Results:Analysis revealed that original articles constituted 85.7% of the literature. Research output has accelerated markedly since 2010. Four core research clusters were identified: obesity/metabolic, hormonal, genetic, and malignancy-related. Key comorbidities with strong bibliometric linkages included psoriasis, hidradenitis suppurativa (HS), and acne, centered on shared mechanisms of insulin resistance and inflammation. The analysis highlighted emerging therapeutic directions, particularly the potential of GLP-1 receptor agonists (eg, semaglutide) due to their dual metabolic and anti-inflammatory (eg, TNF-α, IL-17 inhibition) effects, and the complex role of biologics targeting Th1/Th17 pathways. Conclusion:This first bibliometric study of AN delineates its evolving research architecture, confirming its position at the intersection of dermatology, endocrinology, and immunology. The findings underscore shared pathophysiological pathways with several inflammatory skin diseases and point to novel, mechanism-based therapeutic strategies. Future research should prioritize clinical trials to validate these targeted interventions.

BACKGROUND:Port-wine stain (PWS) is a disfiguring vascular anomaly characterized by persistent cutaneous erythema and progressive tissue hyperplasia. Although pulsed dye laser (PDL) is the first-line treatment and alleviates certain clinical manifestations, incomplete lesion clearance and high recurrence rates persist in some patients, posing significant therapeutic challenges. OBJECTIVE:To evaluate the efficacy and safety of sequential therapy with a 755 nm picosecond laser (PSL) combined with 595 nm PDL versus 595 nm PDL alone in treating PWS. METHODS:Thirty-four patients with PWS were enrolled. Lesions were randomly divided into paired subregions (PDL and PDL + PSL) using a subregional control design. Efficacy was assessed through objective and subjective measures: standardized clinical and dermoscopic images were used to quantify visual scores and clearance rates; reflectance confocal microscopy (RCM) quantitatively analyzed changes in vascular density and diameter; patient satisfaction and adverse reactions were also evaluated. RESULTS:The PSL + PDL group showed significantly greater improvement in visual assessment scores, lesion area clearance, vascular density, vascular diameter, and patient satisfaction compared to the PDL group (all p < 0.05). While no statistically significant difference was observed in adverse event incidence rates between the two treatment modalities (p > 0.05), both regimens exhibited favorable safety profiles. CONCLUSION:The PSL + PDL regimen shows significantly superior efficacy over PDL alone, thus presenting a promising and advanced therapeutic alternative for PWS treatment.

Dysfunction of the skin barrier is a central pathological feature in dermatology, driving the need for innovative repair strategies. Mesenchymal stem cell-derived exosomes (MSC-exos) represent a promising cell-free therapeutic paradigm, leveraging their innate cargo to modulate regeneration and immune responses. This review systematically examines the multifaceted role of MSC-exos in restoring skin barrier integrity. We delineate their molecular mechanisms in repairing physical, immunological, and microbial barrier components, supported by evidence from preclinical disease models. The influence of MSC source and preconditioning on exosome efficacy is analyzed, alongside emerging bioengineering approaches. Crucially, we identify and discuss the key translational challenges—including standardization, scalable manufacturing, and regulatory pathways—that must be addressed to advance these nanotherapeutics toward clinical application. This synthesis provides a critical framework for future research aimed at harnessing MSC-exos for targeted barrier repair.

Atopic dermatitis (AD) is characterized by epidermal barrier dysfunction and immune dysregulation. Notably, metabolic disorders such as obesity can influence AD susceptibility; however, the specific molecular drivers underlying this association, particularly those involving dysregulated RNA metabolism, remain incompletely understood. Our study demonstrates that obesity-associated upregulation of the N6-methyladenosine demethylase FTO (fat mass and obesity-associated) in lesional epidermis, specifically in keratinocytes, drives AD pathology. Integrated transcriptomic and epitranscriptomic sequencing analyses identified SOCS6 (suppressor of cytokine signaling 6) as a key FTO target. Mechanistically, FTO selectively binds and demethylates N6-methyladenosine modifications within the coding sequence of SOCS6 mRNA, reducing SOCS6 mRNA stability and protein expression. This site-specific epigenetic silencing activates inflammatory programs in keratinocytes. We further identified IL-1β, S100A8, and S100A9 as major downstream effectors of this FTO/SOCS6-N6-methyladenosine axis, promoting keratinocyte apoptosis, barrier impairment, and inflammation. Critically, topical FTO knockdown in vivo ameliorated AD-like pathology and restored SOCS6 expression, confirming FTO's causative role. Collectively, we elucidate the FTO/SOCS6-N6-methyladenosine epigenetic axis as a fundamental obesity-AD link, highlighting its components as promising therapeutic targets for precision AD management.

Circadian rhythm, an inherent 24-hour periodic rhythm in organisms, is regulated by circadian clock genes. As a key component of the transcription-translation feedback loop, the core circadian gene period (PER) 1, not only maintains circadian rhythm homeostasis but also plays a significant role in the pathophysiological processes of various human diseases. This review summarizes the biological characteristics and regulatory mechanisms of PER1, as well as its roles and molecular mechanisms in cardiovascular diseases, nervous system diseases, metabolic disorders, immune-related diseases, and tumors. In cardiovascular diseases, PER1 helps regulate blood pressure, renal function, and vascular inflammation. In the nervous system, it influences ischemic brain injury, sleep homeostasis, and neurodegenerative diseases. In metabolic disorders, PER1 modulates endocrine function, glucose-lipid metabolism, and energy balance. In immune-related diseases, it regulates immune cell functions and inflammatory signaling. In tumors, PER1 has tumor-suppressive effects, with low expression correlating to poor prognosis. This review highlights the critical role of PER1 as a core circadian gene in maintaining physiological homeostasis and regulating disease progression, providing a comprehensive perspective for understanding its complex functions in physiological and pathological processes, offering new insights for developing precision therapies targeting PER1 and its associated signaling pathways.

The research aimed to explore the application effectiveness, advantages, and disadvantages of Team-Based Learning (TBL) in undergraduate cosmetic dermatology education and to analyze directions for pedagogical improvement using interpretable machine learning (IML). A total of 154 undergraduate clinical medicine students from Xiangya School of Medicine, Central South University were included as study subjects. Using the cosmetic dermatology chapter (two teaching units) from the Dermatology and Venereology course, a comparative design was implemented between traditional Lecture-Based Learning (LBL) and interest-oriented TBL. Teaching feedback was collected through questionnaires, and IML and correlation analysis were applied to identify key nodes for pedagogical optimization. Surveys showed that 83.8

BACKGROUND:The pathogenesis of atopic dermatitis (AD) involves a complex immune regulatory network between dendritic cells (DCs) and keratinocytes (KCs). Recent studies have found that N6-methyladenosine (m6A) RNA modification modulates immune regulation and skin barrier homeostasis, but it is unclear whether it participates in AD through the DCs-KCs interaction crosstalk. This study aimed to investigate whether m6A modification contributes to the pathological features of atopic dermatitis by regulating ALOX15 expression in dendritic cells. METHODS:We integrated bioinformatics analysis with clinical sample validation to examine ALOX15 expression in AD skin lesions. Methylated RNA immunoprecipitation-qPCR (MeRIP-qPCR) was performed to quantify changes in the m6A methylation of ALOX15. Three co-culture systems using primary mouse bone marrow-derived DCs (BMDCs), DC 2.4 cells, and primary mouse KCs were established to investigate how ALOX15 mediates DC activation and influences the biological behavior of KCs. RESULTS:ALOX15 expression was significantly upregulated in DCs from AD lesions. Mechanistically, WTAP-mediated m6A modification enhanced ALOX15 expression, prompting DCs activation and inflammatory factor secretion. Co-culture experiments demonstrated that ALOX15-overexpressing DCs secreted elevated levels of inflammatory factors and arachidonic acid metabolites (LTB4, 12-HETE, and 15-HETE), leading to abnormal KCs' differentiation, proliferation disorders, and lipid metabolism disorders, which are characteristic phenotypic changes of AD. CONCLUSIONS:Our findings underscore the critical role of the WTAP-m6A-ALOX15 axis in regulating DCs-KCs interactions in AD, providing new theoretical foundations and potential intervention targets for future interventions.

Traditional teaching in undergraduate dermatology and venereology often prioritizes theoretical knowledge over clinical competency development. To address this limitation, we implemented a hybrid instructional model that combines scenario-based simulation with lecture-based learning (Sim + LBL). This prospective cohort study included two consecutive undergraduate cohorts from Xiangya School of Medicine, Central South University. The 2018 cohort (n = 164) received traditional LBL, while the 2019 cohort (n = 182) was taught using Sim + LBL in the dermatology and venereology course. Both groups completed the same sexually transmitted diseases (STDs) module. Academic performance was assessed through a post-class test and an anonymous questionnaire. An eXtreme Gradient Boosting (XGBoost) model with SHapley Additive exPlanations (SHAP) was used to identify factors associated with test performance, and mediation analysis was applied to investigate the mechanisms through which the teaching model produced its effects. The Sim + LBL group achieved higher post-class scores than those in the LBL group (median difference = + 6.0, 95

OBJECTIVES:Verrucous epidermal nevus (VEN), seborrheic keratosis (SK), verruca plana (VP), verruca vulgaris (VV), and nevus sebaceous (NS) are common verrucous proliferative skin diseases with similar clinical appearances, often posing diagnostic challenges. Dermoscopy and reflectance confocal microscopy (RCM) can aid in their differentiation, yet their specific features under these tools have not been systematically described. This study aims to summarize and analyze the dermoscopic and RCM features of VEN, SK, VP, VV, and NS. METHODS:A total of 121 patients with histopathologically confirmed verrucous proliferative skin diseases were enrolled. Dermoscopy and RCM imaging was used to observe and analyze the microscopic features of these conditions. RESULTS:Under dermoscopy, the 5 diseases displayed distinct characteristics: VEN typically showed gyriform structures; SK was characterized by gyriform structures, comedo-like openings, and milia-like cysts; VP and VV featured dotted vessels and frogspawn-like structures; NS presented as brownish-yellow globules. RCM revealed shared features such as hyperkeratosis and acanthosis across all 5 diseases. Specific features included gyriform structures and elongated rete ridges in VEN; pseudocysts and gyriform structures in SK; evenly distributed ring-like structures in VP; vacuolated cells and papillomatous proliferation in VV; and frogspawn-like structures in NS. CONCLUSIONS:These 5 verrucous proliferative skin conditions exhibit distinguishable features under both dermoscopy and RCM. The combination of these 2 noninvasive imaging modalities holds significant clinical value for the differential diagnosis of verrucous proliferative skin diseases.

: Background: Atopic dermatitis (AD) is a chronic inflammatory skin condition influenced by lipid metabolism. Apolipoprotein B (ApoB), a crucial component of lipid transport, may be linked to AD risk, but this relationship has not been extensively studied in large cohorts.Objectives: To investigate the association between ApoB and the risk of developing AD using data from a large, prospective cohort in the UK Biobank (UKB).Methods: The study analyzed 454,974 participants from the UKB, with ApoB measured via blood biochemistry and nuclear magnetic resonance (NMR) spectroscopy. Cox proportional hazard models were used to evaluate the relationship between ApoB and AD risk, adjusting for demographic, lifestyle, and clinical covariates. Restricted cubic spline (RCS) analysis was employed to assess potential nonlinear relationships. Sensitivity analyses included adjusting for lipid-lowering medication use, comparing apolipoprotein A (ApoA) levels, and repeating analyses with NMR-measured ApoB.Results: Higher ApoB levels were significantly associated with a reduced risk of AD (hazard ratio for continuous ApoB: 0.74, 95% confidence interval: 0.64-0.86, P < 0.001). RCS analysis confirmed a linear inverse relationship between ApoB and AD risk (P for overall <0.001; P for nonlinear: 0.803). Sensitivity analyses reinforced these findings, showing consistent results across different measures and adjustments, with no significant association found between ApoA levels and AD.Conclusions: This study establishes a significant inverse association between ApoB levels and AD risk, underscoring the role of lipid metabolism in AD pathogenesis in the UKB population. ApoB might be a potential biomarker or therapeutic target for AD prevention, meriting further investigation.

RNA N6-methylation (m6A) modification is common in eukaryotic mRNA and has been linked to various physiological disorders, including UVB-induced photoaging. To identify biological differences among photoaging. Three pairs of normal and photoaged skin tissues were collected for m6A RNA sequencing assay. Transcriptome profiles showed differential m6A methylation modifications in 1365 mRNAs in photoaging skin tissues. Pathway analysis revealed the involvement of cellular stress response and regulation of cell cycle G2/M phase transition in m6A-mRNAs. Further experiments validated the differential expression of m6A methyltransferases (METTL3 and METTL14) and hypermethylation modification in mRNAs (CENPE, PPM1B and TPM1). In vitro studies demonstrated that increased METTL3 and METTL14 levels promoted m6A methylation of CENPE, PPM1B and TPM1 in UVB-induced photoaging cells, and further experiments on mice showed that downregulation of METTL3 and METTL14 reduced m6A modifications in CENPE, PPM1B and TPM1, leading to the delayed appearance of photoaging phenotypes, suggesting that these genes could serve as potential therapeutic targets for treating photoaging. Our study characterized key transcriptome changes in photoaging and identified the role of METTL3 and METTL14 in mediating m6A modification, resulting in the upregulation of CENPE, PPM1B and TPM1 expression, which may be crucial in UVB-induced photoaging.

Background: Ozone can enhance the expression of some growth factors (GFs) in platelet rich plasma (PRP), recent study showed oxygen-rich PRP (ozonized PRP) have better therapeutic effects on bone and joint diseases. PRP injection has been widely used in the treatment of facial rejuvenation, but the efficacy of sufficient oxygen-rich PRP in facial rejuvenation has not been studied. Objective: Firstly, we examined whether ozone treatment can increase the concentration of GFs of PRP in vitro. And then a variety of subjective and objective detection methods were used to evaluate the effect of sufficient(10-12 mL each time for the injection of face and neck) oxygen-rich (ozonized PRP) PRP injection in facial rejuvenation by follow-up for 6 months. At last, we investigated the satisfaction, side effects and pain score of the treatment through a questionnaire survey. Methods: The concentration of main GFs in PRP treated with different dose of ozone in vitro was measured by ELISA. Clinical picture, the collagen thickness of dermis by reflectance confocal microscope(RCM), skin conditions (including spots, ultraviolet (UV) spots, brown spots, red area, pores, wrinkles, texture and porphyrin) by VISIA were collected before treatment and each month follow-up visit after treatment until 6-month follow-up period was finished. Patients' satisfaction, side effects and pain score were collected at the end of follow-up period. Results: PRP treated by high-dose ozone (57 mg/mL, ozone/PRP volume ratio:1/1) in vitro showed a significant increase in endothelial growth factor (EGF) and transforming growth factor-b (TGF-b) compared to baseline(P < 0.05). Collagen thickness of forehead, cheek and neck improved significantly compare to the baseline until to the 6 months after treatment. Spots, UV spots, brown spots, red area and texture improved significantly compare to the baseline(P < 0.05). All of participants reported improvement and have a median pain score of 4.19. No serious adverse events were observed. Conclusions: Ozone treatment can increase the concentration of GFs such as EGF and TGF-b in PRP in vitro. Sufficient oxygen-rich PRP injection may be an effective and promising method to treat facial rejuvenation. (c) 2024, The Japanese Society for Regenerative Medicine. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/ 4.0/).

One of the most common and significant symptoms for skin disorders is pruritus. Additionally, it serves as a significant catalyst for the exacerbation or reoccurrence of skin diseases. Pruritus seriously affects patients' physical and mental health, and even the quality of life. It brings a heavy burden to the patients, the families, even the whole society. The pathogenesis and regulation mechanisms for pruritus are complicated and have not yet been elucidated. Previous clinical studies have shown that itch worsens at night in scabies, chronic pruritus, atopic dermatitis, and psoriasis, suggesting that skin pruritus may change with circadian rhythm. Cortisol, melatonin, core temperature, cytokines, and prostaglandins are the main regulatory factors of the circadian rhythm of pruritus. Recent studies have shown that some CLOCK genes, such as BMAL1, CLOCK, PER, and CRY, play an important role in the regulation of the circadian rhythm of pruritus by regulating the Janus tyrosine kinase (JAK)-signal transducer and activator of transcription (STAT) and nuclear factor kappa-B (NF-κB) signaling pathways. However, the mechanisms for circadian clock genes in regulation of circadian rhythm of pruritus have not been fully elucidated. Further studies on the mechanism of circadian clock genes in the regulation of circadian rhythm of pruritus will lay a foundation for elucidating the regulatory mechanisms for pruritus, and also provide new ideas for the control of pruritus and the alleviation of skin diseases.

BACKGROUND:Abnormal biological behaviour of keratinocytes (KCs) is a critical pathophysiological manifestation of psoriasis. Ferroptosis is programmed cell death induced by the accumulation of lipid reactive oxygen species (ROS) in the presence of increased intracellular iron ions or inhibition of GPX4. OBJECTIVES:The purpose of this study was to investigate the effects of ferroptosis on the biological behaviour of Keratinocytes (KCs) in psoriasis vulgaris and its possible regulatory mechanisms in clinical samples, cells, and mouse models. METHODS:We first examined the differences in the expression of GPX4 and 4-HNE between psoriasis and normal human lesions. And detected KRT6, FLG, and inflammatory cytokines after inducing ferroptosis in animal and cell models by RT-qPCR, Western blot, immunohistochemistry, and flow cytometry. RESULTS:We found that GPX4 was decreased and that the oxidation product 4-hydroxy-2-nonenal (HNE) was increased in the skin lesions of patients with psoriasis vulgaris. The expression level of GPX4 correlates with the severity of skin lesions. Moreover, inducing ferroptosis promoted the expression of FLG and reduced the expression of KRT6 and inflammatory cytokines in vitro, and alleviated the phenotype of skin lesions in vivo. LIMITATIONS:Our study has limitations, notably small sample size. Larger clinical trials are necessary to investigate the association between ferroptosis and disease progression further. More research is necessary to explore how the ferroptosis inducer RSL3 regulates the abnormal biological behaviour of KCs at both cellular and animal levels and establish ferroptosis inhibitors as controls. CONCLUSIONS:This study confirms the existence of ferroptosis in psoriatic lesions, which may be inversely correlated with disease severity. The ferroptosis inducer RSL3 ameliorated psoriatic symptoms by improving the abnormal biological behaviour of KCs.

N6-methyladenosine (m6A) is the most abundant dynamic and reversible internal chemical modification of RNA in eukaryotic cells and is essential in multiple pathophysiological processes. However, it has not been reported in atopic dermatitis (AD). We used Arraystar m6A-mRNA epitranscriptomic microarray to screen for differentially expressed genes and their m6A levels and m6A-related enzymes in patients with AD. We confirmed that were significantly upregulated in keratinocytes in public data and epidermal lesions of patients with AD. In vitro cell experiments confirmed that WTAP influenced the expression of the 2 candidate differentially expressed genes and promoted primary human epidermal keratinocyte proliferation while inhibiting human epidermal keratinocyte differentiation. Furthermore, we showed that WTAP, S100A9, and SERPINB3 expression correlated with AD severity. Our findings revealed that WTAP-mediated m6A modification promoted the expression of S100A9 and SERPINB3 to aggravate human epidermal keratinocyte proliferation and dysdifferentiation contributing to the pathophysiological development of AD.