Background: Structural abnormalities in the brain of patients with atopic dermatitis (AD) have been reported; however, the cause has not been determined yet. Herein, we used Mendelian randomization (MR) to reveal the causal effect of AD on brain structure. Methods: This study utilized summary statistics from genome‐wide association studies (GWASs) to investigate a collection of cerebral structural measures, encompassing cortical thickness (CT), cortical surface area (CA), and subcortical volumes in T1 images. A comprehensive GWAS meta‐analysis identified a total of 20 independent single nucleotide polymorphisms linked to AD, surpassing the genome‐wide significance threshold ( p < 5 × 10⁻⁸). MR estimates were aggregated through the application of the inverse variance weighted method. Additional complementary analyses (i.e., MR‐Egger and weighted median approaches) were conducted to further assess the robustness of the obtained results. Sensitivity analysis and multivariate MR (MVMR) while adjusting for brain structural changes risk factors (i.e., depression and anxiety) were performed to assess the reliability and stability of observed causality. Results: Genetically determined AD exhibited a causal link with reduced caudate volumes (IVW‐MR: β = ‐0.186, p = 0.001, p ‐corrected = 0.009). Furthermore, we identified potential causal associations between AD and reduced CT in the cingulate region (posterior cingulate, IVW‐MR: β = ‐0.065, p = 0.018, p ‐corrected = 0.551; isthmus cingulate, IVW‐MR: β = ‐0.086, p = 0.003, p ‐corrected = 0.188), as well as abnormal cortical surface area (CA) in the supramarginal (IVW‐MR: β = ‐0.047, p = 0.044, p ‐corrected = 0.714) and isthmus cingulate (IVW‐MR: β = 0.053, p = 0.018, p ‐corrected = 0.714). Additional supplementary analyses yielded consistent outcomes. There was no evidence of horizontal pleiotropy. MVMR analysis showed that the causal effects of AD on abnormal brain structure remained significant while adjusting for depression and anxiety. Conclusion: This MR study provided suggestive evidence that decreased caudate nucleus, posterior cingulate cortex, isthmus cingulate cortex and supramarginal gyrus are suggestively associated with higher AD risk. Future investigation into the brain regions is recommended, which helps to clarify the underlying mechanisms and point to new therapies against AD.

Invasive fungal infections are a leading cause of mortality and morbidity in patients with severely impaired host defenses, while treatment options remain limited. Fatty acid synthase (FASN), the key enzyme regulating de novo biosynthesis of fatty acids, is crucial for the lethal infection of fungi; however, its pathogenic mechanism is still far from clear. Here, we identified the α subunit of FASN as a potential immunotherapeutic target against systemic Candida albicans infection. The avirulence of the encoded gene (FAS2) -deleted mutant in a mouse model of systemic candidiasis is not due to its fitness defects, because sufficient exogenous fatty acids in serum can overcome FASN inhibition. However, the FAS2-deleted mutant displays increased circulating innate immune responses and enhances activated neutrophil fungicidal activity through the unmasking of immunogenic cell wall epitopes via the Rho-1 dependent Mkc1-MAPK signaling pathway, which facilitates fungal clearance, reduces renal tissue damage and inflammatory cell infiltration, ultimately lowers fungal pathogenicity. Priming with the FAS2-deleted mutant provided significant protection against subsequent lethal infection with wild-type C. albicans in mice as early as one week, and it was well-tolerated with limited toxicity. Our findings indicate that the FASN-α subunit plays key roles in the regulation of neutrophil-associated antifungal immunity and could be a potential target for immunotherapeutic intervention.

Psoriasis is an immune-mediated inflammatory skin disease with a complex etiology involving environmental and genetic factors. Psoriasis patients often require long-term treatment. Shanyaotianua decoction (STT), a typical traditional Chinese medicine prescription, positively affects psoriasis, although its molecular targets remain unknown. To elucidate its molecular mechanisms, a combination of network pharmacology, bioinformatics analysis, and drug similarity comparisons were employed. Participants were separated into 3 groups: non-lesional (NL), lesions after medication (LM), and psoriasis lesion groups (LS). Based on the Gene Ontology/kyoto encyclopedia of genes and genomes enrichment analyses, the key targets were mainly enriched for biological processes (immuno-inflammatory responses, leukocyte differentiation, lipid metabolic disorders, and viral infection) with the relevant pathways (Janus kinase/signal transducers and activators of transcription and adipocytokine signaling and T-helper 17 cell differentiation), thus identifying the possible action mechanism of STT against psoriasis. Target prediction for 18 STT compounds that matched the screening criteria was performed. Then, the STT compounds were intersected with the differentially expressed genes of the psoriatic process, and 5 proteins were potential targets for STT. Based on the open-source toolkit RDKit and DrugBank database, and through molecular docking and drug similarity comparisons, spinasterol, diosgenin, and 24-Methylcholest-5-enyl-3belta-O-glucopyranoside_qt may be potential drugs for psoriasis.

Chromoblastomycosis(CBM), particularly caused by Fonsecaea monophora, presents significant clinical challenges due to its difficulty in treatment and high recurrence rates, with no established gold standard for therapy. This case report highlights a successful treatment approach that addresses this challenging disease. We report a 65-year-old female patient with a one-year history of a skin lesion on the dorsum of her right hand, diagnosed with CBM through histopathological and mycological examinations. The patient was treated with oral itraconazole at a dosage of 200 mg daily, in conjunction with photodynamic therapy using 5-aminolevulinic acid photodynamic therapy (ALA-PDT), administered biweekly. After one month of ALA-PDT treatment, the patient showed marked improvement. Continued oral itraconazole for three months resulted in complete clinical resolution, with no recurrence observed during a one-year follow-up. The combination of ALA-PDT and antifungal treatment demonstrates an effective strategy for managing skin CBM caused by Fonsecaea monophora.

Talaromyces marneffei (TM) infection is a rare but potentially fatal deep fungal disease that typically affects immunocompromised individuals in endemic regions. However, an increasing number of cases have been reported in HIV-negative, immunocompetent patients without classical risk factors. We report the case of a 15-year-old girl residing in urban southern China who presented with chronic cutaneous plaques and cervical lymphadenopathy, initially misdiagnosed as tuberculous lymphadenitis. Despite one year of anti-tuberculosis therapy, her condition worsened and liver dysfunction developed. Subsequent skin biopsy, fungal culture, and metagenomic next-generation sequencing (mNGS) confirmed localized cutaneous TM infection. The patient responded well to oral itraconazole, and lesions resolved after four months of treatment, with no recurrence during an 18-month follow-up. This case highlights the importance of considering deep fungal infections in the differential diagnosis of chronic granulomatous skin lesions, even in immunocompetent hosts, and emphasizes the diagnostic utility of mNGS in atypical presentations.

Background Thyroid dysfunction have been demonstrated to be associated with vitiligo through observational studies. However, the causal relationship between thyroid disorders and vitiligo remains uncertain. In this study, we utilized Mendelian Randomization (MR) to assess the potential contribution of thyroid dysfunction to the development of vitiligo.Methods Genome-wide association study (GWAS) summary data for vitiligo, hypothyroidism, and hyperthyroidism were sourced from the IEU GWAS database, while free thyroxine (FT4) and thyrotropin (TSH) GWAS summary data were extracted from the ThyroidOmics Consortium. The two-sample Mendelian randomization (MR) analyses using inverse variance weighting (IVW), MR-Egger, and weighted median methods was employed to estimate the causal relationships between thyroid functions, as measured by the diagnosis of hypothyroidism, hyperthyroidism, and blood levels of FT4 and TSH. Sensitivity analyses, including Cochran's Q test, MR-Egger regression, and the leave-one-out test, were conducted to evaluate the robustness of our findings. Additionally, we performed the MR-pleiotropy test to examine potential pleiotropic effects.Results Our results demonstrated that hypothyroidism was significantly associated with an increased risk of vitiligo (OR = 1.005, 95% CI: 1.002–1.007; p < 0.001). However, no significant relationship was observed between hyperthyroidism, FT4, TSH, and vitiligo. Sensitivity analyses did not show significant horizontal pleiotropy or heterogeneity in the study.Conclusions Our study revealed that individuals with hypothyroidism exhibit a higher susceptibility to developing vitiligo. This finding carries significant implications for the prediction, prevention, and treatment of vitiligo.