Skin Research and Technology最新文献

Objective: This study aimed to assess differences in various scalp parameters between patients with androgenetic alopecia (AGA) and healthy volunteers using 22 MHz ultrasound.

Methods: Thirty patients with AGA (AGA group) and 30 healthy volunteers (control group) who visited the Department of Dermatology at the Second Affiliated Hospital of Soochow University from September 2021 to June 2022 were randomly selected. The patients with AGA met the diagnostic criteria outlined in the Chinese Guidelines for the Diagnosis and Treatment of Androgenetic Alopecia. The severity of alopecia was assessed for males between grades 2 and 4 on the Norwood-Hamilton scale, and for females between stages 2 and 3 on the Ludwig scale. No artificial interventions were conducted at the vertex, and all examination conditions remained consistent. Ultrasound examinations at 22 MHz were performed on the scalp at the vertex in both the AGA and control groups. Seven parameters were measured, namely, epidermis + dermis thickness, entire scalp thickness, subcutaneous tissue thickness, average follicle width, average follicle length, follicle count, and the presence of color flow signals in the subcutaneous tissue. The differences in these parameters were then compared.

Results: The AGA group showed reduced thickness of the entire scalp and subcutaneous tissue, narrower average follicle width, shorter average follicle length, lower hair follicle count, and fewer instances of color flow signals in the subcutaneous tissue at the vertex area (p < 0.05).

Conclusion: High-frequency (22 MHz) ultrasonography can be employed to visualize the entrance echo, dermis, subcutaneous tissue, and hair follicles of the scalp, thereby providing imaging for the clinical assessment of hair loss.

Background: Dermatomyositis (DM) is a kind of dermatologically associated autoimmune disease that is notably associated with an increased risk of concurrent malignancies, although the underlying mechanisms remain to be fully elucidated. The purpose of this investigation was to examine the immunological parallels between DM and nasopharyngeal carcinoma (NPC), with the aim of identifying pivotal biomarkers that could facilitate a deeper understanding and enhance the predictive capabilities of NPC in DM patients.

Method: Data for DM and NPC were sourced from the Gene Expression Omnibus (GEO) database. Immune infiltration was analyzed using the "cibersort" R package, differentially expressed genes (DEGs) were identified with the "limma" package, and functional pathways were investigated through Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses. Characteristic genes were determined by Utilizing Protein-Protein Interaction (PPI) and Least Absolute Shrinkage and Selection Operator (LASSO), and their features were validated using the GSE53819 dataset.

Results: In comparison to normal samples, significant infiltration of macrophage M1 was observed in both DM and NPC. The analysis revealed 77 DEGs in DM and 1051 DEGs in NPC, with 22 genes found to be co-DEGs. Following PPI and LASSO analysis, six distinctive genes were retained. Notably, CCL8, IFIH1, CXCL10, and CXCL11 exhibited optimal diagnostic efficacy for NPC and displayed significant correlation with macrophage M1 infiltration within the carcinoma.

Conclusion: Four characteristic genes, CCL8, IFIH1, CXCL10, and CXCL11 are risk factors for both DM and NPC. They exhibit a robust correlation with the incidence of NPC and offer a commendable diagnostic efficacy. Furthermore, they may serve as prospective predictive biomarkers for the emergence of NPC in DM.

Background: Alopecia areata is an autoimmune hair loss disorder with an incompletely understood etiology. Although trace elements, serum metabolites, and inflammatory factors are implicated in the disease, the potential causal relationships between these factors and alopecia areata require further investigation.

Methods: This study employed Mendelian randomization (MR), utilizing data from genome-wide association studies, to explore the causal relationships between 15 trace elements, 1400 serum metabolites, and 91 inflammatory factors and alopecia areata. The analysis was conducted using the inverse variance weighted (IVW) method complemented by various sensitivity analyses, including Cochran's Q test, MR-Egger regression intercept test, MR-PRESSO global test, and leave-one-out analysis, to assess the robustness of the results.

Results: MR analysis indicated a negative correlation between copper levels and the risk of developing alopecia areata (odds ratio = 0.86, 95% confidence interval: 0.75-0.99, p = 0.041). Additionally, causal relationships were identified between 15 serum metabolites and 6 inflammatory factors and the risk of alopecia areata (IVW, all p values < 0.05).

Conclusion: This study provides genetic evidence of the relationships between trace elements, serum metabolites, and alopecia areata, underscoring the potential value of targeted therapeutic strategies and preventive measures. Future research should expand to diverse populations and further explore the specific roles of these biomarkers in the disease mechanism.

Background: An increasing number of studies have focused on the association between Human papillomavirus (HPV) infection and systemic lupus erythematosus (SLE). However, current evidence is largely based on retrospective studies, which are susceptible to confounding factors and cannot establish causation.

Methods: A bidirectional two-sample Mendelian randomization (MR) design was used to evaluate the causal relationship between HPV and SLE. Mononucleoside polymers (SNPS) with strong evidence for genome-wide association studies (GWAS) were selected from the HPV exposure dataset and used as an instrumental variable (IV) for this study. For the MR Analysis results, the MR-Egger intercept P test, MR-Presso global test, CochranQ test and leave-one test were used for sensitivity analysis.

Results: Based on the evidence of MR Analysis, this study finally determined that there was no causal association between HPV16 and HPV18 and SLE.

Conclusions: Possible regulation of HPV infection is not significantly associated with regulation of SLE. These findings provide new insights into the underlying mechanisms of HPV and SLE and need to be validated by further studies.

Background: Dermal fillers have emerged as a popular non-surgical solution for facial rejuvenation and enhancement. Apart from botulinum toxin injections, they are the most common non-surgical procedure performed in the US. Line-field optical coherence tomography (LC-OCT; deepLive system Damae Medical, France) represents one of the most recent developments in non-invasive skin imaging technologies.

Materials and methods: We performed LC-OCT image acquisition on six patients that were treated with hyaluronic acid (HA) dermal fillers in various locations on the face. The images were acquired before the application of the fillers (T0), immediately after (T1), and at a 6- to 8-week (T2) follow-up visit.

Results: At T0, we were able to appreciate a normal-appearing epidermis, dermoepithelial junction, and dermis. At T1, the intradermal filler deposits appeared as homogeneously hyporeflective areas, clearly discernible from surrounding vessels and other structures. At T2, the deposits were distinguishable as hyporeflective areas, although they were diminished in size compared to T1. On enface view, collagen fibers had increased thickness and were more homogeneously organized and hyperreflective.

Conclusions: We established the usefulness of LC-OCT in the non-invasive evaluation of dermal HA fillers to visualize both short-term and medium-term effects. LC-OCT may be a valuable tool in evaluating the precise location of filler placement and follow-up of resulting in vivo changes.

Background: Psoriasis is a chronic inflammatory skin disease that can cause systemic inflammation in various organs. Rutin has been suggested to fight psoriasis, but the signaling pathways by which it works need to be explored.

Materials and methods: HaCaT cells co-stimulated with interleukin (IL)-17, IL-22, tumor necrosis factor-alpha (TNF-α), IL-1α, and oncostatin M (M5) were used as an in vitro cell model of psoriasis. The proliferation and viability of HaCaT cells were determined by 5-ethynyl-2'-deoxyuridine and cell counting assays. Relative mRNA levels of IL-6, TNF-α, chemokines (CXCL1 and CXCL2), and anti-microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase-quantitative PCR. Release of IL-6 and TNF-α from HaCaT cells was measured by enzyme-linked immunosorbent assay. Keratin1, Keratin5, p-JAK2, and p-STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.

Results: Rutin treatment undercut M5-urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL-6, TNF-α, CXCL1, CXCL2, S100A7, and S100A8 was partially reversed after Rutin treatment. In addition, M5 stimulation induced downregulation of Keratin1 and Keratin5 proteins as well as upregulation of p-JAK2 and p-STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5-promoted aberrant differentiation and impaired M5-mediated activation of the JAK2/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.

Conclusion: Rutin treatment blocked the JAK2/STAT3 signaling, thus attenuating psoriasis-related inflammation and anomalous differentiation in keratinocytes.

Objective: Oxidative stress is strongly associated with atopic dermatitis (AD), and increased antioxidant intake could potentially reduce the risk of or alleviate its symptoms. However, the argument is disputed. Therefore, we conducted a Mendelian randomization (MR) analysis to explore the causal relationship between dietary antioxidant vitamin intake and AD.

Methods: We applied MR analysis to examine the causative association between dietary antioxidant vitamin intake (vitamin C, vitamin E, carotene, and retinol) and AD. The genome-wide association study (GWAS) summary data for antioxidant vitamins intake and AD were obtained from the IEU OpenGWAS database and the UK biobank. Our study consisted of two major parts, MR analysis to detect the causal relationship between exposure and outcome, and sensitivity analysis as supplemental evidence to verify the robustness of the results.

Result: The results revealed a suggestive causal relationship between vitamin E intake and AD (p = 0.038, OR 95% CI = 0.745-0.992). However, there was no causal relationship between the other three vitamins (vitamin C, carotene, and retinol) and AD (p = 0.507, OR 95% CI = 0.826-1.099) (p = 0.890, OR 95% CI = 0.864-1.184) (p = 0.492, OR 95% CI = 0.893-1.264). None of the single nucleotide polymorphisms (SNPs) were detected as heterogeneous and pleiotropy in the sensitivity analysis (p > 0.05).

Conclusion: The analysis suggested that dietary intake of vitamin E may potentially lower the risk of AD. Conversely, intake of vitamin C, retinol, and carotene is not causally related to AD. Although vitamin E intake could be protective against AD, intake of dietary antioxidant vitamins to prevent or treat AD is not necessary.

Background: Pressure ulcer (PU) is known to be associated with abnormalities of micronutrient status. However, to date, it is not clear whether a causal relationship exists between circulating levels of micronutrients and their supplementations and PU.

Methods: A two-sample Mendelian randomization (MR) study was conducted using summary statistics from Genome-Wide Association Studies (GWAS). Genetic instrumental variables (IVs) for 13 micronutrients were identified from a GWAS of 67 582 participants, IVs for supplement zinc were acquired from 18 826 cases and 44 255 880 controls, and IVs for PU were obtained from 663 PUs and 207 482 controls. The MR analysis was conducted using the MR base platform. The main analysis method was inverse variance weighted (IVW) analysis, supplemented by MR Egger, Weighted median, Weighted mode, and Simple mode analyses. Heterogeneity was assessed using Cochran's Q statistic for MR-IVW and Rucker's Q statistic for MR-Egger. Pleiotropy was determined by the MR-Egger regression. Sensitivity analysis was conducted using the leave-one-out method, and publication bias was evaluated using funnel plots.

Results: Genetically predicted lower circulating zinc levels were found to be causally linked to the development of PU (OR = 0.758, 95%CI 0.583-0.987, P = 0.040). However, there was no significant evidence of a causal relationship between supplemental zinc intake and PU development (P > 0.05). Additionally, no causal association was observed between the other circulating micronutrients and the occurrence of PU. Furthermore, there was no indication of horizontal pleiotropy or heterogeneity among genetic variants (P > 0.05), and the robustness of the findings was confirmed through leave-one-out tests and funnel plots.

Conclusions: Our findings indicate a potential causal association between circulating zinc levels and decreased risk of PU. However, zinc supplementation did not demonstrate a significant reduction in the risk of PU. Further research is warranted to elucidate the underlying mechanisms through which zinc influences the pathogenesis of PU and evaluate the efficacy of zinc supplementation in the prevention and management of PU.