INTRODUCTION:Bixie Shenshi Decoction (BSSD), a traditional Chinese herbal formula, has long been used to treat inflammatory skin conditions. This study aimed to investigate the therapeutic effects of BSSD on psoriasis-like mouse models and elucidate its underlying mechanisms. METHODS:We evaluated inflammatory factors and signaling pathways via Western blot and RT-qPCR in mouse models. HPLC-MS was used to analyze BSSD components, while network pharmacology combined with database mining predicted its target pathways. RESULTS:BSSD treatment improved psoriatic skin lesions, reduced epidermal hyperproliferation, and reduced levels of pro-inflammatory cytokines in skin tissue and plasma. Additionally, BSSD decreased phosphorylation of STAT3 and Akt in mouse skin lesions. Network pharmacology analysis revealed that BSSD's targets were primarily enriched in the Th17 signaling pathway and metabolic pathways, with IL-6, TNF, ESR1, CASP3, TP53, and MMP9 identified as core targets. Molecular docking predicted the binding interactions between these targets and BSSD compounds. DISCUSSION:BSSD's multi-target mechanism aligns with psoriasis pathogenesis. By integrating multicomponent, multi-target modulation, BSSD offers a complementary approach to single-target therapies, which are limited by a narrow focus on individual disease drivers. CONCLUSION:BSSD exerts therapeutic effects against psoriasis by targeting key biological factors and inhibiting the activation of the JAK/STAT3 and PI3K/Akt pathways.

Cutaneous squamous cell carcinoma (cSCC) is a malignant skin cancer which is derived from epidermal keratinocytes, and long-term exposure to ultraviolet rays is its main risk factor. Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2) is a crucial gene for the formation and stability of collagen intermolecular cross-links, being vital in the development of cancer. Nevertheless, the interaction between cSCC and PLOD2 has not been elucidated. Here, we found PLOD2 upregulated in human cSCC. Its knockdown in cSCC cells suppressed proliferation, migration, invasion, and angiogenesis while inducing apoptosis and cell cycle arrest; overexpression promoted these malignant phenotypes. In mouse xenografts, PLOD2 knockdown inhibited tumor growth and collagen deposition. Furthermore, in a DMBA/TPA-induced carcinogenesis model, topical PLOD2 inhibition by minoxidil suppressed tumor development as well. Mechanistically, our studies revealed that PLOD2 acts as a key downstream effector of STAT3 to activate ERK and AKT signaling evidenced by rescue experiments. As a result, our study not only establishes the STAT3/PLOD2/ERK-AKT axis as a key driver of cSCC but also identifies the clinically approved drug minoxidil as a potent PLOD2 inhibitor, demonstrating immediate promise as a repurposed therapeutic agent.

Cutaneous squamous cell carcinoma (cSCC) is one of the most common skin cancers. Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2), a pivotal enzyme in one‑carbon metabolism, is upregulated in several cancers, yet its role and mechanisms in cSCC remain unclear. Here, we show that MTHFD2 is significantly overexpressed in cSCC tissues and cell lines. MTHFD2 enhanced cSCC cell proliferation, migration, and invasion while suppressing apoptosis in vitro, and promoted tumor growth in vivo. Mechanistically, MTHFD2 promotes cSCC progression by sustaining glycolytic metabolism and redox homeostasis, while also exerting a non-metabolic function through interaction with fatty acid synthase (FASN), which in turn modulates the PI3K-AKT signaling pathway. Importantly, pharmacological inhibition of MTHFD2 effectively suppressed cSCC cell proliferation in vitro and tumor growth in vivo, highlighting MTHFD2 as a promising therapeutic target.

Objective To evaluate the informational quality and user engagement of acne-related videos on Bilibili and TikTok, and examine associations with uploader characteristics, disease-related topics, presentation formats, and factors linked to high-quality content. Methods A cross-sectional analysis was conducted on 272 videos (122 from Bilibili, 150 from TikTok) retrieved in May 2025. Video characteristics, uploader types, disease-related topics, and presentation formats were recorded. Quality was assessed using the Journal of the American Medical Association benchmark criteria (JAMA), modified DISCERN instrument (mDISCERN), Global Quality Scale (GQS), and Video Information and Quality Index (VIQI). Engagement metrics (likes, comments, collections, shares) were analyzed. Correlation and predictive modeling were applied to examine associations between quality and engagement. Results Bilibili videos were longer (median 409 s vs 51 s; P < 0.001) and scored higher on VIQI (12.05 ± 2.94 vs 10.90 ± 1.97; P = 0.002). TikTok videos were more often uploaded by verified (68.10% vs 33.33%) and professional accounts (65.52% vs 25.64%), achieved higher JAMA (1.28 ± 0.45 vs 0.92 ± 0.98; P < 0.001) and mDISCERN scores (2.10 ± 0.52 vs 2.02 ± 0.93; P = 0.009), and demonstrated higher daily engagement. High-quality content was primarily produced by verified and professional uploaders, particularly in anatomy/physiology topics and doctor monologues. Official media, epidemiology, and television programs/documentaries achieved the greatest engagement. VIQI and GQS were strongly correlated (ρ = 0.755). VIQI (area under the curve [AUC] 0.922) and collections (AUC 0.901) were the strongest discriminators of high-quality content. Conclusions Acne-related videos on Bilibili and TikTok were generally of suboptimal quality. Bilibili favored coherence and accuracy, while TikTok favored transparency and engagement. Quality assessments outperformed engagement metrics in identifying high-quality content. These findings highlight the need to improve credentialing and promote engaging, evidence-based formats to enhance the reliability and impact of dermatologic information on short-video platforms.

Psoriasis is a common, chronic, inflammatory skin disease that affects many patients and exerts a heavy physical and mental burden. Wogonin (WG), derived from the root extract of Scutellaria Baicalensis, has shown therapeutic effects in a variety of inflammatory diseases. However, its specific effects and mechanisms in psoriasis treatment remain poorly understood. This study aimed to investigate the therapeutic effects and underlying mechanisms of WG in psoriasis. In this study, we first identified potential therapeutic targets of WG for psoriasis by intersecting the corresponding targets of psoriasis and WG, then performed Protein-Protein Interaction (PPI) network analysis and enrichment analyses. Next, we employed Cytoscape to identify potential key targets and performed molecular docking to predict possible targets. M5-induced HaCaT cells and imiquimod (IMQ)-mouse models were used to explore the effects and mechanisms. Bioinformatic analyses indicated that WG may exert anti-inflammatory effects through inhibiting PI3K/AKT pathway activation and oxidative stress. In vitro results showed that WG suppressed the increase of pro-inflammatory cytokine expression levels, reactive oxygen species (ROS) level, phosphorylation of Akt and p65, and several key target mRNA expression levels induced by M5 stimulation. Oral administration of WG remarkably alleviated psoriatic like lesions in IMQ-induced mice, inhibited inflammatory cytokines and Ki-67 expression level in mouse skin lesions. Our results indicate that WG exhibits significant anti-inflammatory effects in psoriasis by suppressing reactive oxygen species (ROS) production and inhibiting the AKT/NF-κB signaling pathway. These results highlight WG’s potential as a promising therapeutic agent for psoriasis treatment.

Psoriasis, a globally prevalent immune-mediated dermatosis, requires novel therapeutic strategies that address its multifactorial pathogenesis, involving oxidative stress, cell-free DNA (cfDNA)-driven inflammation, and keratinocyte hyperproliferation. Here, we presented a pH-responsive two-dimensional (2D) MXene nano-scavenger integrating Ti3C2Tx-mediated antioxidant activity, polyethylenimine (PEI)- facilitated cfDNA scavenging, and 2,3-dimethylmaleic anhydride (DMMA)-induced charge reversal for targeted ATIC inhibitor delivery. Comprehensive material characterization confirmed pH-dependent charge reversal and sustained drug release. In vitro, the MXene-based platform (MPDA) exhibited superior reactive oxygen species (ROS) scavenging (superior to Trolox at the same concentration) and cfDNA adsorption (3-fold higher than pure MXene), while in vivo administration in imiquimod-induced psoriatic mice markedly alleviated disease severity (PASI score reduction of approximately 50%), reduced epidermal thickness (37% decrease compared to the IMQ group), and suppressed inflammatory cytokines-significantly outperforming monotherapies. Transcriptomic analysis further revealed that MPDA cooperatively inhibited multiple inflammatory pathways, including the TNF and IL-17 signaling, thereby effectively disrupting the self-perpetuating inflammatory cycle of psoriasis. This work establishes a promising paradigm for combinatorial nanotherapy in psoriasis treatment.

BACKGROUND:Atopic dermatitis (AD) is a chronic inflammatory skin disorder involving complex interactions among multiple cell types. The cellular heterogeneity and intercellular communication networks driving AD pathogenesis remain to be fully elucidated. METHODS:Single-cell RNA sequencing datasets were employed to identify cell types in lesional skin of AD patients and analyze the transcriptomic characteristics of keratinocytes, T cells, and macrophages. Cell clusters were identified based on marker gene expression, and intercellular communication networks were analyzed to investigate cell-cell interactions. The findings were validated using in vitro cell models (HaCaT, HEK, primary keratinocytes, and THP-1 cells) and an MC903-induced AD mouse model, with MIF expression assessed by qPCR and Luminex. Immunofluorescence staining was used to evaluate the distribution and aggregation of macrophages. Functional studies were conducted using MIF098 to inhibit MIF signaling. RESULTS:scRNA-seq revealed significant cellular remodeling in AD lesions, with marked enrichment of keratinocytes, T cells, and macrophages. The proportion of Th2 cells was increased in AD lesion tissues, and an MRC1+ macrophage subset (Cluster3-Mac) was specifically enriched in AD lesions. Intercellular communication analysis demonstrated that proliferative keratinocytes may interact with Cluster3-Macrophages via the MIF-CD74/CD44 signaling axis, with proliferative keratinocytes acting as senders and macrophages as receivers. Furthermore, MRC1+ macrophages may engage with Th2 cells through PTPRC. Consistent with these findings, MIF expression was significantly upregulated in the serum of AD patients, in IL-13-treated HaCaT and HEK cells, and in the epithelial tissues of AD model mice. In the MC903-induced AD mouse model, lesional skin showed epidermal thickening, inflammatory infiltration, and accumulation of M2-polarized macrophages (F4/80+CD206+). Functional validation using MIF098 showed that inhibition of MIF downregulated its expression in primary keratinocytes and reduced the ability of THP-1 cells to secrete CCL17, CCL22, and IL-10. CONCLUSION:Our findings identify a critical role for the MIF signaling axis in mediating crosstalk between proliferative keratinocytes and M2-polarized macrophages, thereby promoting Th2-driven inflammation in AD. Targeting MIF may represent a potential therapeutic strategy for AD.

Cutaneous squamous cell carcinoma (cSCC) is a common malignant skin neoplasm for which current therapeutic options for advanced and metastatic cases remain limited and are associated with considerable toxicity. Plasma-activated solution (PAS)—prepared by exposing media such as culture medium, water, or phosphate-buffered saline (PBS) to cold atmospheric plasma (CAP)—has emerged as a novel antitumor strategy. In recent years, PAS has garnered increasing attention owing to its advantages over direct CAP application, including ease of storage and clinical administration. In the present study, we investigated the therapeutic potential of PAS in cSCC. In this study, we established an in vitro skin cancer model treated with PAS, as well as an in vivo xenograft tumor model. In vivo experiments demonstrated that PAS significantly suppressed xenograft tumor growth, as evidenced by reductions in both tumor volume and weight, along with a decreased number of Ki-67-positive proliferating cells, without inducing body weight loss or organ damage in treated mice. These antitumor effects were associated with upregulation of the pro-apoptotic protein Bax, downregulation of the anti-apoptotic protein Bcl-2, and suppression of Matrix metalloproteinase-9 (MMP9) expression. In vitro assays revealed that PAS elevated intracellular reactive oxygen species (ROS) levels and induced mitochondrial dysfunction, while modulating the expression of apoptosis-related proteins (Bax/Bcl-2) and the migration-associated molecule MMP9. These effects were consistently validated in two squamous cell carcinoma cell lines, HSC-1 and SCL-1. The activation of the NF-κB signaling pathway and subsequent upregulation of pro-inflammatory cytokine expression were also detected in PAS-treated cells. PAS treatment led to tumor cell apoptosis in a time-dependent manner, rather than inducing significant cell cycle arrest. Collectively, PAS exhibits potent antitumor activity without appreciable systemic toxicity. Our findings provide a promising therapeutic approach for cSCC and suggest PAS as a potential strategy for the treatment of other solid tumors.

Psoriasis is a chronic inflammatory skin disease characterized by keratinocytes(KCs) hyperproliferation and persistent inflammation. Current biologics are limited by high relapse rates and long-term safety concerns, prompting the search for multi-target natural small molecules. A murine psoriasis model was induced by 6-day continuous topical imiquimod (IMQ) application; cellular models were established by stimulating keratinocyte lines with tumor necrosis factor-alpha (TNF-α)/interleukin-17A (IL-17A). Network pharmacology and molecular docking were employed to predict targets, and small interfering RNA targeting Nrf2(siNrf2) was used for mechanistic validation. Neferine administration significantly attenuated epidermal hyperplasia, splenomegaly and cutaneous inflammation in vivo. In KCs, Neferine dose-dependently suppressed inflammatory cytokines and pathway proteins, elevated oxidative stress levels, decreased mitochondrial membrane potential (ΔΨm) and promoted apoptosis. Neferine bound Keap1, reduced its level, enhanced Nrf2 nuclear translocation and up-regulated HO-1/NQO1. siNrf2 abolished Nef-mediated inhibition of NF-κB/ERK phosphorylation, cytokine down-regulation and ΔΨm loss. Neferine ameliorates psoriasis by inducing oxidative stress-driven apoptosis in hyper-proliferative keratinocytes and by activating Keap1-Nrf2-mediated anti-inflammatory signaling to block the IL-23/IL-17 axis, offering a promising small-molecule strategy for psoriasis management.

Psoriasis is a type of chronic inflammatory skin disease, with a rising incidence and high recurrence rate over the past decades. The crosstalk between the epidermis and the dermis is crucial in psoriasis. Here, we found that procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2), also known as lysyl hydroxylase 2 (LH2), may be a key component linking epidermal and dermal dysfunctions during the development of psoriasis. Upregulation of PLOD2 was closely related to collagen and fibrosis, indicating that fibroblasts played an essential role in the progression. PLOD2 expression was increased in psoriatic lesions in both patients and an imiquimod-induced mouse model, as well as in M5-induced HaCaT/HFF-1 coculture cells. When PLOD2 was inhibited, inflammatory responses were reduced both in vitro and in vivo, whereas overexpression of PLOD2 had the opposite effect. In this study, we demonstrated that PLOD2 could be transcriptionally activated by STAT3, leading to increased collagen I and cytokines/chemokines in the extracellular matrix, which promotes the proliferation of both fibroblasts and keratinocytes. Mechanistically, cytokines may facilitate the release of heparin-binding EGF-like growth factor (HB-EGF) by fibroblasts, which then leads to the phosphorylation of EGFR and stimulates STAT3 activation in keratinocytes, further inducing the upregulation of PLOD2. Ultimately, through this positive feedback loop, dermatitis symptoms aggravated, and psoriasis developed. Treatment with the PLOD2 inhibitor (compound 12) significantly ameliorated imiquimod-induced psoriatic symptoms by inactivating STAT3 and reducing cytokine levels. In summary, we have demonstrated that PLOD2 plays a crucial role in the pathogenesis of psoriasis and may serve as a therapeutic target in clinical settings.

Adaptive resistance to MAPK inhibitors remains a major clinical obstacle in BRAF-mutant melanoma, driven by reversible transcriptional and epigenetic reprogramming. Previous studies have implicated loss of SRY-box transcription factor 10 (SOX10) and concurrent activation of TGF-β signaling in this process, but the molecular link between them has remained unresolved. Here, we identify a SOX10-miR-106a/363-TGFBR2 regulatory axis that governs adaptive resistance. SOX10 directly activates transcription of the miR-106a/363 cluster through a distal cis-regulatory element. In turn, the miR-106a/363 cluster members miR-106a-5p and miR-20b-5p suppress TGFBR2 post-transcriptionally, while miR-363-3p indirectly reduces TGFBR2 expression by targeting SOX4, a transcriptional activator of TGFBR2. This dual-layered repression restrains TGF-β signaling and maintains drug sensitivity. Loss of SOX10 diminishes miR-106a/363 expression, derepresses TGFBR2, and promotes a mesenchymal-like, drug-tolerant state. Restoring miR-106a/363 expression partially re-sensitizes melanomas to RAF inhibitors in vivo. These findings reveal a previously unrecognized regulatory circuit linking SOX10 to TGF-β signaling and highlight the miR-106a/363 cluster as a potential therapeutic target to overcome adaptive resistance in melanoma.

Cutaneous squamous cell carcinoma (cSCC) is a common skin malignancy characterized by aggressive growth and metabolic reprogramming. Alpha-enolase (ENO1), a key glycolytic enzyme that is frequently over-expressed in cancer, has not been thoroughly investigated in cSCC, particularly with regard to how it coordinates glycolysis and oxidative phosphorylation (OXPHOS). ENO1 expression was interrogated in Gene Expression Omnibus datasets and validated in cSCC patient specimens. ENO1 was silenced in cSCC cell lines, and the resulting effects on cell viability, migration, invasion, apoptosis, and reactive oxygen species (ROS) levels were quantified. The impact of ENO1 knockdown on tumour growth was assessed in a xenograft model. Metabolic flux was analysed with Seahorse XFe96 extracellular-flux assays. ENO1 was significantly elevated in cSCC relative to normal skin and correlated positively with proliferative and invasive markers, but negatively with apoptosis markers. ENO1 silencing curtailed cell viability, migration, and invasion, while inducing apoptosis. Additionally, tumour growth was significantly impaired in vivo. Seahorse analysis showed that ENO1 knockdown suppressed glycolysis and redirected metabolic flux toward OXPHOS. Consistent with this shift, intracellular ROS increased and partially suppressed cell viability by modulating the ROS-sensitive Akt/mTOR pathway. In conclusion, ENO1 knockdown compromises tumorigenicity and promotes OXPHOS. Combining ENO1 inhibition with oxidative-stress-enhancing treatments, such as chemotherapy or radiotherapy, may further enhance efficacy.

Mitochondrial malfunction is traditionally viewed as a major factor in tumor growth and malignancy, while recent studies have introduced conflicting views suggesting the necessity of functional mitochondria for tumor growth. Despite these differing perspectives, the specific role of mitochondria in cutaneous squamous cell carcinoma (cSCC) remains poorly understood. In this study, we observed increased mitochondrial abundance and function during the development of cSCC. We also identified retinoic acid receptor response 1 (RARRES1), which is dramatically decreased in human cSCC samples, as a key regulator of mitochondrial homeostasis. Mechanistically, RARRES1 can translocate into mitochondria and facilitate the degradation of TFAM by binding to LONP1, thereby regulating mitochondrial biogenesis. While RARRES1 suppression unleashed TFAM to promote mitochondrial biogenesis, leading to the progression of cSCC. Targeting RARRES1-LONP1/TFAM axis shows significant potential for inhibiting cSCC development. This study reveals a unique network for regulating mitochondrial homeostasis and emphasizes the crucial role of mitochondria in cSCC development, positioning the RARRES1-LONP1/TFAM axis as promising therapeutic target for future clinical applications.

Atopic dermatitis (AD) is a common inflammatory skin disorder, and oxidative stress plays a central role in its pathogenesis. Nanoceria, owing to its redox-regulating properties, hold promise as a treatment option for AD. Porous ceria nanorods (PN-CeO2) were synthesized to scavenge reactive oxygen species (ROS). PN-CeO2 was characterized by transmission electron microscopy, nitrogen adsorption/desorption tests, energy dispersive spectroscopy, X-ray diffraction, and X-ray photoelectron spectroscopy. Cytotoxicity was assessed using light microscopy and a Cell Counting Kit-8 assay. ROS-scavenging activity was evaluated in keratinocytes and macrophages using flow cytometry. Inflammatory cytokine regulation was analyzed using RT-qPCR and ELISA. An indirect co-culture system was used to examine the effects of PN-CeO2 on keratinocyte-macrophage interactions. Finally, we tested the therapeutic potential of PN-CeO2 in DNFB and MC903 induced AD mouse model. In vitro, PN-CeO2 decreased ROS and modulated cytokine expression in TNFα-stimulated keratinocytes, LPS-stimulated M1 macrophages, and IL4-stimulated M2 macrophages. Cytokine expression in HaCaT cells was also affected by the conditioned medium from M1 type macrophages incubated with PN-CeO2. PN-CeO2 demonstrated a dose-dependent antioxidative effect, outperforming vitamin C to some extent. In vivo, it alleviated skin lesions; reduced mast cell infiltration; and decreased scratching behavior, serum IgE levels, and spleen indices. Mechanistically, PN-CeO2 decreased the tissue ROS levels and activated Nrf2. It also exhibited excellent biocompatibility. Our findings demonstrated that PN-CeO2 effectively reduced ROS and inflammatory cytokines, offering a promising antioxidative approach for AD treatment.

OBJECTIVE:To evaluate the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfections among human immunodeficiency virus (HIV)-infected men who have sex with men (MSM) initiating their first antiretroviral therapy (ART) in Northwestern China, and to examine the impact of coinfections on hepatotoxicity risk. METHODS:This retrospective cohort study analyzed MSM who were newly diagnosed with HIV and initiated ART in Northwestern China between January 1st, 2005, and June 30th, 2019. A total of 4,690 MSM aged ≥18 years were included and categorized into three groups based on HBV or HCV coinfection status: HIV monoinfection, HIV/HBV coinfection, and HIV/HCV coinfection. Hepatotoxicity was classified into grades 0 (normal) to 4 (life-threatening) according to the degree of elevation in liver enzymes (AST or ALT). Kaplan-Meier curves were used to evaluate the incidence of hepatotoxicity, mortality, and ART failure rates, while Cox proportional hazards models assessed the independent impact of coinfections on hepatotoxicity risk. RESULTS:Among 4,690 HIV-infected MSM, the prevalence of HIV/HBV and HIV/HCV coinfections was 5.18% and 2.17%, respectively. Coinfected individuals had significantly elevated hepatotoxicity risks. HIV/HBV coinfection substantially increased the risk of any-grade hepatotoxicity (Hazard Ratio [HR]: 1.190, 95% Confidence Interval [CI]: 1.029-1.375) and grade ≥3 hepatotoxicity (HR: 3.161, 95% CI: 2.095-4.769). HIV/HCV coinfection was also associated with a higher risk of any-grade hepatotoxicity (HR: 1.311, 95% CI: 1.050-1.636). Older age at ART initiation, a shorter diagnosis-to-treatment interval, and HBV/HCV coinfection were identified as risk factors, while higher CD4 + T lymphocyte counts and lower hemoglobin levels were protective factors. CONCLUSION:HIV/HBV and HIV/HCV coinfections significantly increased the risk of hepatotoxicity in HIV-infected MSM receiving ART. These findings underscore the importance of vigilant liver function monitoring in coinfected patients on ART, particularly in consideration of baseline factors such as age, time to treatment, CD4 + T-cell count, and hemoglobin level, to minimize interruptions and optimize outcomes.

BACKGROUND:Hair loss disorders, including non-cicatricial forms such as alopecia areata (AA) and androgenetic alopecia (AGA), as well as cicatricial forms, represent significant dermatological concerns influenced by various factors, including lipid metabolism. While observational studies and clinical trials have suggested a link between lipid levels and hair loss, the causal relationship remains unclear. METHODS:We conducted a comprehensive analysis of 983 lipid variables [including triglycerides (TG), fatty acids, cholesterol, cholesterol esters, phospholipids, and lipoproteins] and 4 hair loss disorders. Two-sample univariable Mendelian randomization (UVMR) and multivariable Mendelian randomization (MVMR) analyses were employed to investigate the causal effects of lipids on hair loss disorders. Sensitivity analyses were performed to ensure the robustness of our findings. RESULTS:The UVMR analysis identified 56 significant causal associations between lipid levels and hair loss disorders, with cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), TG, apolipoprotein A1, apolipoprotein B, and lipoprotein(a) emerging as key contributors. The MVMR analysis evaluated the independent effects of HDL-C, LDL-C, and TG on alopecia disorders, identifying significant associations only between HDL-C, TG, and AA. Sensitivity analyses confirmed the consistency and robustness of these results. CONCLUSION:This study provides strong evidence for potential causal associations between lipids and hair loss disorders, highlighting potential therapeutic targets and the importance of lipid management in affected patients.

This self-controlled prospective study evaluated the efficacy and safety of 450 nm blue laser-mediated aminolevulinic acid photodynamic therapy (ALA-BL-PDT) in 28 patients with plaque psoriasis. Participants received four treatment sessions at two-week intervals. At two weeks post-treatment, 67.9

Acne vulgaris is a chronic inflammatory skin disease closely linked to the abnormal colonization and proliferation of Cutibacterium acnes (C. acnes). Photodynamic therapy (PDT) has emerged as an ideal treatment. However, it still faces challenges such as low reactive oxygen species (ROS) production rates with porphyrin-based photosensitizers and low activation efficiency of conventional red light. This study investigated the in vitro and in vivo bactericidal effects of sinoporphyrin sodium (DVDMS) combined with a novel 450 nm blue laser-mediated photodynamic therapy (BL-PDT) on C. acnes, and explored the potential mechanisms, focusing on energy metabolism. In our results, C. acnes showed a time-dependent uptake of DVDMS, and BL-PDT demonstrated an excellent bactericidal effect on C. acnes in vitro by inducing a large amount of ROS production. RNA sequencing and metabolomic analysis revealed that BL-PDT inhibited C. acnes carbon metabolism while initially enhancing respiration; however, both fermentation and respiration were suppressed after 2 h, and ATP declined time-dependently in this process. Ultimately, the combined effects of ROS-induced damage (from DVDMS and enhanced respiration) and ATP depletion led to bacterial death. Similarly, in vivo experiments confirmed the favorable therapeutic efficacy and safety of BL-PDT in a rat model of acne. In conclusion, DVDMS-based BL-PDT may be a safe and effective new treatment against acne. Thus, our results provide compelling evidence for using DVDMS and BL-PDT in acne treatment.

Objective:Sexually transmitted diseases (STDs) remain a significant public health challenge globally and in China. This study analyzes incidence trends of three nationally notifiable STDs to assess their disease burden. Methods:Based on national surveillance data (2006-2020) from the Chinese Center for Disease Control and Prevention, this study analyzed incidence trends of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), syphilis, and gonorrhea using joinpoint regression. Age-period-cohort modeling was subsequently employed to evaluate the independent effects of age, period, and birth cohort. Rate ratios (RRs) with 95% confidence intervals (CIs) were calculated to quantify these associations. Results:Between 2006 and 2020, China observed a significant increase in the incidence of HIV/AIDS and syphilis (p < 0.001). Although gonorrhea incidence declined overall (p < 0.05), a notable increase was observed among adolescents under 20 years of age (p < 0.05). The average annual reported incidence was highest for syphilis (28.41 per 100,000), followed by gonorrhea (8.65 per 100,000) and HIV/AIDS (2.78 per 100,000). Geographically, HIV/AIDS incidence was highest in southwestern China. Syphilis incidence was elevated in the southwestern, southern, and northwestern regions, while gonorrhea showed a distinct concentration in southern China. Age-effect analysis revealed a bimodal pattern for both HIV/AIDS and syphilis, with incidence peaks in the 20-39 and ≥60 age groups. In contrast, gonorrhea showed a single peak in the 20-39 age group. Period-effect analysis, using the 2011-2015 period as reference (RR = 1), indicated evolving disease risks in subsequent years: HIV/AIDS risk increased markedly in 2016-2020 (RR = 1.53, 95% CI: 1.41-1.65), syphilis risk increased modestly (RR = 1.14, 95% CI: 1.06-1.22), while gonorrhea risk initially declined in 2006-2010 (RR = 1.43, 95% CI: 1.34-1.54) before a slight rise in 2016-2020 (RR = 1.11, 95% CI: 1.03-1.19). Cohort analysis showed that HIV/AIDS risk was highest among individuals born in 2011-2015 (RR = 124.81, 95% CI: 36.82-423.08). The peak risk for syphilis occurred in the 2006-2010 birth cohort (RR = 5.08, 95% CI: 1.28-19.99), while gonorrhea risk was highest in the 1921-1925 birth cohort (RR = 15.46, 95% CI: 2.00-119.62). Conclusion:HIV/AIDS and syphilis present growing threats in China, disproportionately affecting young adults and older populations, with increasing burden in recent birth cohorts. Although gonorrhea shows overall decline, its rise in adolescents warrants attention. A tiered prevention strategy is recommended: enhanced screening and education for HIV/syphilis in high-risk groups and regions, alongside sustained gonorrhea surveillance in key populations.