Ni Zeng

Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit. Accurate and objective assessment of inflammatory activity remains a challenge in clinical practice. Dermoscopy, as a noninvasive imaging technique, enables visualization of vascular and color changes associated with inflammation. In this cross-sectional study, 40 patients with mild-to-moderate acne vulgaris were enrolled, and 80 dermoscopic images were obtained. Background color, vascular morphology, vascular distribution, and perifollicular yellow halo were analyzed and compared between severity grades (mild vs. moderate) and among lesion types (comedonal, papular, pustular). In the mild group, a light-red background predominated (41.7%), whereas red and dark-red backgrounds were more common in the moderate group (both 38.6%), with a significant difference (χ² = 10.13, P = 0.006). Vascular morphology suggested a trend toward transition from dotted to branched forms with increasing inflammation, although this did not reach statistical significance (P > 0.05). By lesion type, comedonal lesions mainly displayed light-red backgrounds with dotted vessels, while papular and pustular lesions exhibited red-to-dark-red backgrounds with branched or atypical vessels (P < 0.05). Progressive deepening of background color and transformation of vascular morphology on dermoscopy are associated with increasing inflammatory activity in acne vulgaris. Quantitative evaluation of these dermoscopic parameters may contribute to preliminary objective severity grading and therapeutic monitoring. Dermoscopy may represent a potentially valuable, noninvasive imaging modality for assessing inflammatory activity in acne.

Background: Melasma is a prevalent, cosmetically, and psychologically distressing pigmentary disorder. Combination therapies offer promising management strategies. Photobiomodulation therapy (PBMT) modulates melanogenesis and vascular components noninvasively. Cord blood–derived platelet‐rich plasma (CB‐PRP), rich in growth factors and anti‐inflammatory molecules, may enhance melanin suppression and skin repair. Picosecond lasers effectively target pigment particles and melanocytes. Methods: In this prospective, randomized, split‐face study, 28 female melasma patients were enrolled (26 completed). All participants received whole‐face PBMT bilaterally. One randomly assigned facial side received adjunctive CB‐PRP injections; the contralateral side received adjunctive picosecond laser treatment. Outcomes were assessed using the modified Melasma Area and Severity Index (mMASI), VISIA‐CR analysis, and patient satisfaction at baseline, 2 weeks, 3 months, and 6 months post‐treatment. Statistical analysis was performed using generalized linear mixed models (GLMMs) with the Bonferroni correction. Results: Both sides showed significant mMASI reductions post‐treatment, with the PBMT + CB‐PRP side decreasing by 38.3% and the PBMT + picosecond laser side by 38.0% at 6 months (both p < 0.001 for within‐group changes). No significant between‐group differences in mMASI were observed at any time point (Bonferroni‐corrected p > 0.05 for all comparisons). GLMM analysis confirmed a significant time main effect (Wald χ ² = 154.800, p < 0.001) with no significant group × time interaction ( p = 0.943). For VISIA‐CR parameters, both sides showed significant improvements in pores ( p < 0.001 for time effect), with no significant between‐group differences for any of the eight measured parameters at any follow‐up time point (all Bonferroni‐corrected p > 0.05). The PBMT + CB‐PRP side showed significant within‐group improvements in spots and brown spots ( p < 0.05), whereas the PBMT + picosecond laser side did not; however, direct between‐group comparisons for these parameters did not reach statistical significance. Patient satisfaction rates were 88.5% (PBMT + CB‐PRP side) and 80.8% (PBMT + picosecond laser side). No serious adverse events occurred in either group. Conclusion: PBMT combined with either CB‐PRP or picosecond laser significantly improved melasma, with comparable efficacy in reducing mMASI scores through 6 months post‐treatment. PBMT + CB‐PRP side showed higher satisfaction rate. Both combination regimens were well tolerated with no serious adverse effects, and PBMT + CB‐PRP represents a potential nonlaser alternative for melasma treatment.

Objective: We explored circadian clock-related genes (CCRG) to establish a risk model and identify associations with the tumor immune microenvironment in cutaneous melanoma (CM). Methods: Circadian clock genes were downloaded from Circadian Gene Database. To explore CM-related circadian clock genes, we combined multivariate cox regression associated with least absolute shrinkage and selection operator (LASSO) regression in the Cancer Genome Atlas (TCGA) and validated it in the GSE65904 dataset. Time-dependent receiver operating characteristic curve (ROC) and Kaplan-Meier analysis were calculated to determine a CCRG risk score model. In addition, the overall survival nomograms of clinicopathological factors and circadian clock-related gene signatures. Additionally, we evaluated the connection between circadian clock-related genes with immune checkpoint inhibitors and immune cell infiltration. Results: Two circadian clock-related signatures were established. The risk model included SEMA4D (p<0.001, HR: 0.709, 95% CI: 0.581 to 0.867) and SOD-2 (p=0.009, HR: 0.790, 95% CI: 0.663 to 0.944) in patients with TCGA melanoma. The risk model was based on two CCRGs enriched in base excision repair, glycosylphosphatidyl (GPI), and one carbon of the folate pathway. The overall survival was lower in the high-risk group. In addition, the circadian-clock signature may be able to evaluate the immunotherapy response. Conclusions: We developed and validated a circadian signature to characterize the clinical significance and tumor microenvironment of cutaneous melanoma, revealing that circadian rhythms may impact cutaneous melanoma.

Objective. Malignant melanoma (MM) is one of the most malignant types of skin cancer and its incidence and mortality rates are increasing worldwide. Aging is well recognized as a significant risk factor for cancer. However, few studies have analyzed in depth the association between aging-related genes (AGs) and malignant melanoma prognosis with tumor immune microenvironment. Methods. Here, we downloaded 471MM patients from The Cancer Genome Atlas (TCGA) with RNA sequence and clinicopathological data. 58 AGs from the TCGA dataset were examined using Cox regression and the LASSO assay. As a result, a gene signature for aging-related genes was created. The time-dependent ROC curve and KaplanMeier analysis were calculated to determine its predictive capability. Moreover, we created a nomogram for the clinicopathologic variables and the AGs gene signature to determine overall survival (OS). We also explored the association between three immune checkpoints, immune cell infiltration, and the aging-related gene signature. Results. We established an aging risk model to identify and predict the immune microenvironment in malignant melanoma. Then we developed and validated a prognosis risk model using three AGs (CSNK1E, C1QA, and SOD-2) in the GSE65904 dataset. The aging signature was positively associated with clinical and molecular characteristics and can be used as a prognostic factor for malignant melanoma. The low aging risk score was associated with a poor prognosis and indicated an immunosuppressive microenvironment. Conclusions. To summarize, we established and validated a model of aging risk based on three aging-related genes that acted as an independent prognostic predictor of overall survival. Besides, it also characterized the immune response in the malignant melanoma microenvironment and could provide a potential indicator of individualized immunotherapy in malignant melanoma.

Purpose: To identify potential risk factors for herpes zoster infection in type 2 diabetes mellitus in southeast Chinese population. Patients and Methods: We built a model involving 266 herpes zoster patients collecting data from January 2018 to December 2019. The least absolute shrinkage and selection operator (Lasso) predictive model was used to test herpes zoster virus risk using the patient data. Multivariate regression was conducted to decide which variable would be the strongest to decrease the Lasso penalty. The predictive model was tested using the C-index, a calibration plot, and decision curve study. External validity was verified by bootstrapping by counting probabilities. Results: In the prediction nomogram, the prediction variables included age, sex, weight, length of hospital stay, infection, and blood pressure. The C-index of 0.844 (0.798– 0.896) indicated substantial variability and thus the model was adjusted appropriately. A score of 0.825 was achieved somewhere in the above interval. Examination of the decision curve estimated that herpes zoster nomogram was useful when the intervention was determined at the 16 percent of the herpes zoster infection potential threshold. Conclusion: The herpes zoster nomogram combines age, weight, position of the rash, 2-hour plasma glucose, glycosuria, serum creatinine, length of the hospital stay, and hypertension. This calculator can be used to assess the individual herpes zoster risks in patients diagnosed with type 2 diabetes mellitus.

Objective: In this research, we studied the genes associated with ferroptosis to develop a prognostic model and find out an association with tumor immune microenvironment in skin cutaneous melanoma (SKCM) patients. Methods: To find SKCM-related ferroptosis genes, we used Cox regression and LASSO approach on 60 genes related to ferroptosis and SKCM-related RNA-seq. Following that, a ferroptosis-related gene signature was created. Time-dependent ROC curve and Kaplan–Meier analysis were calculated to determine its capability of prediction. Besides, several assessments were used to evaluate overall survival (OS), accompanied by the creation of a nomogram for the clinicopathologic factors and the ferroptosis-related gene signature we established. We also investigated the relationship between ferroptosis-related gene signature with three immune checkpoints and immune cell infiltration. Results: Our prognostic model included two genes (ALOX5, CHAC1). In both TCGA and GEO cohorts, OS was lower in high-risk category. Using our gene signature, we can reliably predict OS. Additionally, our gene signature can predict immune cell infiltration and SKCM immunotherapy response. Conclusion: Our gene signature has shown to be a reliable predictor of OS, reflect the immune microenvironment, and predict the effectiveness of immunotherapy for SKCM patients.

Adrenocortical carcinoma (ACC) is a rare malignancy with dismal prognosis. Hypoxia is one of characteristics of cancer leading to tumor progression. For ACC, however, no reliable prognostic signature on the basis of hypoxia genes has been built. Our study aimed to develop a hypoxia-associated gene signature in ACC. Data of ACC patients were obtained from TCGA and GEO databases. The genes included in hypoxia risk signature were identified using the Cox regression analysis as well as LASSO regression analysis. GSEA was applied to discover the enriched gene sets. To detect a possible connection between the gene signature and immune cells, the CIBERSORT technique was applied. In ACC, the hypoxia signature including three genes (CCNA2, COL5A1, and EFNA3) was built to predict prognosis and reflect the immune microenvironment. Patients with high-risk scores tended to have a poor prognosis. According to the multivariate regression analysis, the hypoxia signature could be served as an independent indicator in ACC patients. GSEA demonstrated that gene sets linked to cancer proliferation and cell cycle were differentially enriched in high-risk classes. Additionally, we found that PDL1 and CTLA4 expression were significantly lower in the high-risk group than in the low-risk group, and resting NK cells displayed a significant increase in the high-risk group. In summary, the hypoxia risk signature created in our study might predict prognosis and evaluate the tumor immune microenvironment for ACC.

Adrenocortical carcinoma (ACC) is a rare malignant tumor with poor prognosis. Ferroptosis, a new form of cell death, differs from other forms of cell death and plays a vital role in tumor progress. Our study aimed to establish a ferroptosis-related signature with prognostic value in ACC. RNA-seq data and corresponding clinical characteristics for ACC were downloaded from TCGA and GEO databases. Genes included in ferroptosis risk signature were assessed by univariable and multivariable Cox regression analysis as well as lasso regression analysis. The prognostic value of the ferroptosis risk signature was assessed using K-M and ROC curves. Furthermore, we performed GSEA to discover the enriched gene sets in high-risk group. Additionally, TIMER website was applied to detect a possible connection between the signature and immune cells infiltration. ssGSEA was performed to evaluate scores of immune cells and immune-related pathways in two groups. A ferroptosis signature comprised of six genes (SLC7A11, TP53, HELLS, ACSL4, PCBP2, and HMGB1) was constructed to predict prognosis and reflect the immune infiltration in ACC. Patients in high-risk group were inclined to have worse prognosis. The ferroptosis model performed well in predicting prognosis and could be served as an independent indicator in ACC. GSEA revealed that gene sets correlated with biological processes including cell cycle, DNA replication, base excision repair, and P53 signaling pathway were highly enriched in high-risk group. In addition, we discovered that the expressional levels of hub genes were linked to six immune cells’ infiltration in ACC tumor. ssGSEA revealed that contents of most immune cells significantly decreased in the high-risk group. In conclusion, the novel ferroptosis risk signature could be useful in predicting prognosis and reflecting immune infiltration in ACC. It also brings us new insights into the possible value of targeting ferroptosis during the therapy of ACC.