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Cyclin‐dependent kinase 9 (CDK9), a catalytic subunit of the positive transcription elongation factor b (P‐TEFb) complex, is a global transcriptional elongation factor associated with cell proliferation. CDK9 activity is regulated by certain histone acetyltransferases, such as p300, GCN5 and P/CAF. However, the impact of males absent on the first (MOF) (also known as KAT8 or MYST1) on CDK9 activity has not been reported. Therefore, the present study aimed to elucidate the regulatory role of MOF on CDK9. We present evidence from systematic biochemical assays and molecular biology approaches arguing that MOF interacts with and acetylates CDK9 at the lysine 35 (i.e. K35) site, and that this acetyl‐group can be removed by histone deacetylase HDAC1. Notably, MOF‐mediated acetylation of CDK9 at K35 promotes the formation of the P‐TEFb complex through stabilizing CDK9 protein and enhancing its association with cyclin T1, which further increases RNA polymerase II serine 2 residues levels and global transcription. Our study reveals for the first time that MOF promotes global transcription by acetylating CDK9, providing a new strategy for exploring the comprehensive mechanism of the MOF–CDK9 axis in cellular processes. [ABSTRACT FROM AUTHOR]

Introduction. Rosacea is a common chronic inflammatory skin disease of the central facial skin with unknown origin, significantly impacting quality of patient's life and causing various psychosocial problems. Erythematotelangiectatic rosacea (ETR) is characterized by paroxysmal flushing that occurs repeatedly and is easily resistant to therapeutic drugs. While microinjection of type A botulinum toxin (BTX) can treat ETR, there is no consensus on the injection dose, and strong evidence to verify its efficacy and safety is lacking. This randomized, double‐blind, split‐face clinical study aimed to investigate the efficacy, safety, and optimal dose of two different single‐point injection doses (0.5 U and 1 U) of BTX in the treatment of rosacea. Methods. Twenty‐six patients with ETR were randomly assigned to receive different single‐point injections of BTX (0.5 U and 1 U, respectively) every 1 cm on one half of the face. The Clinical Erythema Score (CEA), VISIA red area absolute value, Global Aesthetic Improvement Scale Score (GAIS), and recurrence at 12‐week follow‐up were evaluated at baseline, 2,4, 8, and 12 weeks after injection. Additionally, the Dermatological Quality of Life Index (DLQI) questionnaire survey and adverse reactions were also recorded. Results. All twenty‐six patients completed the follow‐up visits and were included in the analysis. Compared to the 0.5 UBTX‐treated side, the CEA score showed significantly improvement in erythema and flushing at 2, 4, and 8 weeks after injection on the 1 U BTX‐treated side (P < 0.05). The mean absolute value of the red area of VISIA was ‐19.12 ± 51.91 on 1 U BTX‐treated side and 2.5 ± 42.08, on 0.5 UBTX‐treated side at 4 weeks after treatment, showing significant improvement on the 1 U side (P < 0.05). GAIS and DLQI were also significantly improved from Week 4 to Week 12 and Week 2 to Week 12, respectively (P < 0.05). There was no recurrence of symptoms with either 0.5 U or 1 U injection by 12 weeks. Apart from one patient who experienced facial tightness and three patients who had temporary aggravation of erythema, all of which resolved without treatment, 22 patients did not report any side effects except for injection pain during the procedure. Conclusions. BTX‐A can significantly improves symptoms and quality of life in patients with refractory rosacea with few side effects. A single‐point injection of 1 U was more effective. This trial is registered with NCT06282679. [ABSTRACT FROM AUTHOR]

Introduction: The use rate of electronic cigarettes (e-cigarettes) among adolescents is continuously rising globally, posing new challenges to public health and negatively impacting adolescent health. This study employs bibliometric methods to systematically present the current state and evolving trends in global research on adolescent e-cigarette use. Methods: This study uses CiteSpace to conduct a bibliometric analysis of articles related to adolescent e-cigarette use from the Web of Science (WoS) Core Collection database. Firstly, performance analysis and collaboration network analysis were utilized to clarify the basic publication status, main knowledge producers, and knowledge collaboration networks in adolescent e-cigarette use research. Secondly, a co-citation network analysis was performed to visually analyze the disciplinary characteristics and 'hot topics' in this field. Finally, keyword burst detection and clustering techniques were employed to further explain the development trends and frontiers of research on adolescent e-cigarette use. Results: A total of 2063 research articles and review articles were included in this study. Research on adolescent e-cigarette use has significantly increased from 2002 to 2024. The United States, the United Kingdom and Canada are the main contributors, with their institutions and researchers playing key roles in the international collaborative network. Current research increasingly adopts interdisciplinary approaches. Keyword co-occurrence and burst identified current research 'hotspots' including vaping, substance use, public policy, prevention, advertising, and cessation. Co-citation cluster analysis revealed promising research areas such as attractiveness, environment and health, accessibility and smoking behavior, and mental health. Conclusions: Through data mining and visualization techniques, this study provides a comprehensive bibliometric analysis of published work on e-cigarettes and adolescence. The results of this work offer references for researchers in future investigations. [ABSTRACT FROM AUTHOR]

High-cholesterol diet (HCD) and fine particulate matter (PM2.5) are related to stroke. However, little is known about the combined effects of stroke, especially for females. This study investigated the brain injuries in Apolipoprotein E−/− (ApoE−/−) female mice exposed to HCD plus PM2.5 for 6 months. The protein levels of the genes related to stroke and the blood–brain barrier (BBB) in different groups of mice were measured. The molecular regulation mechanisms were explored. The results showed that HCD and PM2.5 co-exposure altered brain–body weight ratio, behavior, brain pathology, and inflammatory markers in mice relative to exposure to HCD or PM2.5 alone. Co-exposure significantly changed the expressions of HIF-1α and the key genes in its signaling pathway in the brains of mice compared to the single exposure. It suggests that the HIF-1α pathway exerts an important regulatory role in brain injury and behavioral abnormality in female mice after 6-month exposure to HCD plus PM2.5, which are potential mechanisms for HCD and PM2.5-triggering stroke in female individuals. [ABSTRACT FROM AUTHOR]

This document is a corrigendum for an article titled "Effect of Chloroquine on Type 2 Inflammatory Response in MC903-Induced Atopic Dermatitis Mice." The authors have identified errors in the Y-axis labels and figures of the original article. The corrections have been made to accurately represent the data, but they do not significantly impact the overall findings and conclusions of the paper. The authors apologize for any confusion caused by these errors. [Extracted from the article]

The atmosphere's fine particulate matter (PM2.5) can enter the liver through the circulatory system, leading to hepatic inflammation and fibrosis. As a non-flavonoid polyphenolic compound, resveratrol (RES) has anti-oxidant, anti-inflammatory and hepatoprotective effects, but the molecular mechanisms of liver fibrosis induced by PM2.5 exposure are still limited. In this study, we established an in vitro cell model to investigate the intervention effect of RES with different concentrations (5 and 20 μmol/mL) on mouse hepatic stellate cells (mHSCs) injury induced by PM2.5 (100 μg/mL). We determined the cell viability in mHSCs after treatment with PM2.5 or/and RES for 24 h. We investigated the intracellular oxidative stress by detecting the changes in reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) levels. We also measured the protein expressions of fibrosis-related genes (α-SMA, Collagen I and Collagen III) and key genes (SIRT1, NF-κB, NLRP3, Cleaved-Caspase1, IL-1β) in the NLRP3 pathway in mHSCs exposed to PM2.5 with or without RES. The results showed that (1) PM2.5 has cytotoxic effects on mHSCs, whereas RES (5 μmol/L and 20 μmol/L) inhibited PM2.5-induced cytotoxicity and LDH leakage; (2) RES effectively reduces ROS and MDA production caused by PM2.5 while concurrently enhancing SOD levels, thereby improving cellular anti-oxidant capacity; (3) the expression of α-SMA, Collagen I and Collagen III were notably downregulated in the PM2.5 plus RES treatment group compared to the PM2.5-exposed group; (4) RES significantly increased SIRT1 expression and decreased the expression of NF-κB, NLRP3, Cleaved-Caspase1 and IL-1β in mHSCs exposure to PM2.5 compared to the PM2.5 group. These results demonstrate that RES can up-regulate SIRT1 and mitigate PM2.5-induced fibrosis by suppressing oxidative stress in mHSCs and the SIRT1/NF–κB/NLRP3 pathway activated by PM2.5. [ABSTRACT FROM AUTHOR]