Acne vulgaris is a common skin disorder with a complicated etiology. Papules, lesions, comedones, blackheads, and other skin lesions are common physical manifestations of Acne vulgaris, but the individual who has it also regularly has psychological repercussions. Natural oils are being utilized more and more to treat skin conditions since they have fewer negative effects and are expected to provide benefits. Using network pharmacology, this study aims to ascertain if neem oil has any anti-acne benefits and, if so, to speculate on probable mechanisms of action for such effects. The neem leaves (Azadirachta indica) were collected, verified, authenticated, and assigned a voucher number. After steam distillation was used to extract the neem oil, the phytochemical components of the oil were examined using gas chromatography–mass spectrometry (GC-MS). The components of the oil were computationally examined for drug-likeness using Lipinski’s criteria. The Pharm Mapper service was used to anticipate the targets. Prior to pathway and protein–protein interaction investigations, molecular docking was performed to predict binding affinity. Neem oil was discovered to be a potential target for STAT1, CSK, CRABP2, and SYK genes in the treatment of Acne vulgaris. In conclusion, it was discovered that the neem oil components with PubChem IDs: ID_610088 (2-(1-adamantyl)-N-methylacetamide), ID_600826 (N-benzyl-2-(2-methyl-5-phenyl-3H-1,3,4-thiadiazol-2-yl)acetamide), and ID_16451547 (N-(3-methoxyphenyl)-2-(1-phenyltetrazol-5-yl)sulfanylpropanamide) have strong affinities for these drug targets and may thus be used as therapeutic agents in the treatment of acne.

Introduction: Type 2 Diabetes Mellitus (T2DM), dyslipidemia, and periodontitis are interconnected conditions that exacerbate systemic inflammation and metabolic dysregulation. Understanding the molecular and clinical profiles of these comorbidities is crucial for developing targeted interventions. This study investigates the molecular and clinical profiles of individuals with T2DM, dyslipidemia, and periodontitis to identify key markers and pathways underlying disease severity and progression.Methods: Peripheral blood mononuclear cells (PBMCs) were analyzed from five patient groups: T2DM poorly controlled with dyslipidemia and periodontitis (T2DMpoorly-DLP-H), T2DM well-controlled with dyslipidemia and periodontitis (T2DMwell-DLP-H), dyslipidemia and periodontitis (DL-P), periodontitis alone (P), and healthy controls (H). Correlations between molecular and clinical markers were assessed.Results: The T2DMpoorly-DLP-H group exhibited the most extensive molecular dysregulation, including unique upregulation of Plasminogen Activator, Tissue Type (PLAT) and consistent overexpression of Vanin-1 (VNN1), a key regulator of oxidative stress. HbA1c and fasting plasma glucose were highest in this group (HbA1c >12%, glucose >300 mg/dL), correlating strongly (R² = 0.88, p < 0.001). In contrast, the T2DMwell-DLP-H group demonstrated reduced gene dysregulation and improved glycemic control (HbA1c ~6.5%). Sex-specific differences were observed, with females exhibiting higher glycemic markers (p = 0.014) and males showing elevated lipid levels (p = 0.021).Discussion: This study identifies Vanin-1 (VNN1) as a potential biomarker for systemic inflammation and highlights the role of Plasminogen Activator, Tissue Type (PLAT) in vascular dysfunction, emphasizing the critical importance of glycemic control in mitigating molecular and clinical dysregulation. These findings underscore the need for personalized, sex-specific strategies to manage these comorbidities effectively.

Acne Vulgaris is a chronic inflammatory skin disorder driven by a combination of microbial colonization, immune dysregulation, and disruption of the epidermal barrier. Although isotretinoin remains the most effective treatment, the molecular mechanisms underlying its anti-inflammatory effects are incompletely understood. This study integrates transcriptomic meta-analysis and computational drug screening to identify novel therapeutic targets and candidate compounds for acne management. Three publicly available GEO datasets (GSE6475, GSE10433, GSE11792) were analyzed to identify differentially expressed genes (DEGs) associated with isotretinoin response. Among these, Spectrin beta, non-erythrocytic 1 (SPTBN1) and Signal-induced proliferation-associated 1-like protein 1 (SIPA1L1) emerged as consistently regulated genes with known roles in cytoskeletal organization and immune signaling, respectively. To assess the druggability of these targets, molecular docking was conducted using gentamicin and natural compounds derived from Cymbopogon winterianus, including citronellol, citral, citronellal, and geraniol. Gentamicin demonstrated the strongest binding affinity to SIPA1L1 (−8.6 kcal/mol) and SPTBN1 (−5.9 kcal/mol), forming multiple hydrogen bonds and hydrophobic contacts. Subsequent 100 ns molecular dynamics (MD) simulations confirmed the stability of the gentamicin–protein complexes, as evidenced by favorable RMSD, RMSF, and energy profiles. Interaction energy decomposition revealed strong contributions from electrostatic and van der Waals forces. These findings highlight the potential of gentamicin, and possibly structurally related natural compounds, as modulators of host inflammatory pathways implicated in acne. The study further underscores the utility of integrating transcriptomics, molecular docking, and MD simulation for early-phase therapeutic discovery targeting inflammation and barrier dysfunction in dermatological diseases.

RNA sequencing (RNA-seq) is widely used to define disease-associated transcriptional programs, but consistent, end-to-end workflows are required to ensure reproducible comparisons across experimental groups and to facilitate biologically interpretable outputs. Here, a complete RNA-seq analysis protocol is presented for evaluating brain transcriptomic changes in experimental cerebral malaria (ECM) and following artesunate treatment using the public dataset GSE162535. The workflow analyzes three groups-control brain (CB), ECM brain (MB), and artesunate-treated ECM brain (AB)-starting from an HTSeq-count matrix. After importing and formatting raw counts, the protocol constructs a DESeq2 dataset with CB as the reference level, filters low-count genes, and performs quality control using library-size visualization, principal component analysis, and sample distance clustering. Differential expression is then calculated for three primary contrasts (MB vs CB, AB vs MB, AB vs CB), with log2 fold-change shrinkage applied for stable effect-size estimation. The protocol exports full and significant differential-expression tables, generates volcano plots and MA plots, and produces heatmaps of the most variable genes and top-ranked differentially expressed genes per contrast. To support mechanistic interpretation, the workflow includes targeted immune marker extraction (e.g., cytokines, chemokines, microglial activation markers, BBB/endothelial genes) and conducts Gene Ontology and KEGG enrichment analyses for significantly up- and downregulated gene sets. This protocol provides a reproducible template for characterizing ECM-associated neuroinflammatory transcriptional programs and for quantifying artesunate-associated modulation of these signatures.

Exportin-1, the ubiquitous nuclear protein transporter, is widely confirmed as an active chemotherapeutic target in non-small cell lung cancer condition while Juglans mandshurica is a well-studied anticancer plant in some lung cancer cell lines. We intend to find novel exportin-1 inhibitor from Juglans mandshurica with better potential tolerability and pharmaco-dynamo-kinetic properties than the current selective inhibitors of nuclear export in non-small cell lung cancer treatment. Osiris property explorer DataWarrior, Glide standard precision docking, quantum mechanics polarized ligand docking, MMGBSA binding free energy calculations, Jaguar density functional theory analysis, and the online web-based SwissADME were employed respectively in this study to filter the retrieved compounds based on tolerability, toxicity, and Lipinsky’s rule of five violation potential, determine their druggability, establish relative stability of the lead compound in water solvation model, and evaluates druglikeness, lead-likeness, as well as synthetic accessibility of the lead compound. This study reveals eriodictyol as having higher binding free energy (-40 kcal/mol) than that of standard (-39.56 kcal/mol) in exportin-1 active site, better synthetic accessibility score (3.15 versus 3.29), high GI absorption, non-blood brain barrier permeant, lacks Brenk and PAINS alert, obeying Lipinski’s, Ghose’s, Veber’s, Egan’s, and Muegge’s rule of druglikeness and lead-likeness as well as non-cytotoxic to HepG2 cells. We therefore found eriodictyol as a lead-like, non-toxic exportin-1 inhibitor with good predictive stability and pharmacokinetic potential and thus provided data for further validation of eriodictyol as a candidate exportin-1 inhibitor in both preclinical and clinical studies involving lung cancer therapy.