Explore the vast range of titles available.

A significant disparity was observed between AV individuals and healthy individuals in various biochemical parameters such as total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and TG (p ≤ 0.05). Clinical and laboratory characteristics of both patients and controls Variables Acne patients N = 70 Healthy controls N = 70 P-Value Age (mean ± SD) 25.62 ± 1.7 26.53 ± 2.6 0.130 Male (N/%) 30 (42.8%) 34 (48.5%) 0.721 Female (N/%) 40 (57.2%) 36 (51.5%) 0.124 BMI (N/%) - Underweight < 18.5 8 (11.4%) 18 (25.7%) 0.0001* - Normal 18.5–24.9 36 (51.4%) 42 (60.0%) 0.132 - Obese 30-34.9 26 (37.2%) 10 (14.3%) 0.0001* - Extremely obese 35< --- --- --- Waist Circumference (N/%) - ≥ 102 cm in men 28 (93.3%) 9 (26.47%) 0.02 - ≥ 88 cm in women 37 (92.5%) 5 (13.88%) 0.01 Blood Pressure (N/%) - ≥ 130 mmHg Systolic BP (mmHg) 43 (61.42) 5 (7.14) 0.03 - ≥ 85 mmHg Diastolic BP (mmHg) 57 (81.42) 8 (11.4) 0.01 Duration of disease (years) - < 5 19 (27.14%) NA NA - ≥ 5 51 (72.85%) NA NA Acne vulgaris severity - Mild 25 (35.7%) NA NA - Moderate 19 (27.1%) NA NA - Severe 26 (37.2%) NA NA Fasting glucose mmoL/L 93.25 ± 1.7 90.15 ± 2.1 0.510 Fasting insulin mlu/L 15.4 ± 7.5 11.78 ± 5.6 0.0005** Insulin resistance (HOMA-IR) 92.5 ± 7.2 52.6 ± 5.2 0.0001* TG mg/dL (mean ± SD) 164.2 ± 22.5 57.4 ± 21.4 0.01** TC mg/dL (mean ± SD) 225.4 ± 22.1 172.2 ± 20.2 0.02** LDL mg/dL (mean ± SD) 128.1 ± 10.2 84.2 ± 11.5 0.03** HDL mg/dL (mean ± SD) 59.1 ± 3.1 41.4 ± 1.2 0.045** Estradiol pg/ml (mean ± SD) 86.2 ± 11.2 29.1 ± 12.1 0.02** Free testosterone ng/dl (mean ± SD) 16.8 ± 11.2 2.3 ± 11.3 0.01** Total testosterone ng/dl (mean ± SD) 388.2 ± 22.2 234.2 ± 11.2 0.02** Metabolic syndrome (N/%) - Fulfilling criteria 58 (82.8%) 3 (4.2%) 0.02 - Not Fulfilling criteria 12 (17.2%) 67 (95.8%) 0.01 N: number, %: percentage, SD: standard deviation, **: mild significant differences P ≤ 0.05, BMI: Body mass index, TG: triglycerides, TC: total cholesterol, LDL: low-density lipoprotein, HDL: high-density lipoprotein and NA: not applied AV group demonstrated significantly higher levels of fasting insulin and IR (p ≤ 0.05).

Background MicroRNAs (miRNAs) are small RNA molecules that play a regulatory role in various biological processes by acting as intracellular mediators. They hold great potential as therapeutic agents for targeting human disease pathways; however, there is still much to be uncovered about their mechanism of gene regulation. Alopecia areata (AA) is a commonly occurring inflammatory condition characterized by the infiltration of T cells that specifically target the anagen‐stage hair follicle. The limited understanding of its precise cellular mechanism may be the reason behind the scarcity of effective treatments for AA. Aim The significance and function of hsa‐miR‐193a‐5p as a genetic marker for AA and its potential influence on the advancement of the disease. Subjects and methods A case‐control study comprised 77 individuals diagnosed with AA who were matched with 75 healthy controls. In order to measure the expression of miR‐200c‐3p in both groups, the real‐time PCR technique was utilized. The prediction of suitable genes for hsa‐miR‐193a‐5p, as well as the identification of pathways and gene‐gene interactions, were carried out using bioinformatic tools. Results The levels of hsa‐miR‐193a‐5p expression were notably elevated in AA patients in comparison to healthy controls. Our prediction suggests that the involvement of hsa‐miR‐193a‐5p in the development of AA is significant due to its influence on the inositol phosphorylation pathway and the Phosphatidylinositol signaling system, achieved through its direct impact on the IPPK gene. Conclusion For the first time, our study demonstrates the significant over‐expression of a new miRNA, hsa‐miR‐193a‐5p, in the blood of AA patients compared to controls, and highlights its impact on the IPPK gene and the inositol phosphorylation and Phosphatidylinositol signaling pathways, suggesting a potential therapeutic role for hsa‐miR‐193a‐5p in AA.

Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact. Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.

Background Artificial Intelligence (AI) is transforming healthcare by enhancing diagnostics, treatment personalization, and operational efficiency. In aesthetic medicine—a field blending medical expertise with artistic judgment—AI is increasingly being used to improve precision, optimize treatment outcomes, and personalize patient care. However, its integration presents both opportunities and ethical challenges, necessitating a critical evaluation of its role in this evolving field. Objective This study examines AI's applications in aesthetic medicine, focusing on its role in facial analysis, robotic‐assisted procedures, predictive patient outcome modeling, and personalized treatment planning. Additionally, it explores ethical concerns, algorithmic biases, data privacy issues, and regulatory challenges affecting AI adoption in aesthetic practices. Methods A comprehensive review of AI‐driven technologies in aesthetic medicine was conducted, analyzing literature on machine learning (ML), deep learning, and computer vision applications. Case studies on AI‐assisted facial symmetry analysis, robotic hair transplantation, and predictive analytics in patient care were examined to evaluate AI's effectiveness and limitations. Results AI enhances aesthetic procedures by improving diagnostic accuracy, offering virtual simulations of treatment outcomes, and enabling hyper‐personalized treatment plans based on patient data. AI‐driven chatbots and virtual assistants streamline patient interactions, while robotic systems assist in precision‐based tasks such as laser treatments and hair restoration. However, challenges such as biased training data, lack of transparency in AI decision‐making, and inconsistencies in regulatory approvals hinder widespread adoption. The integration of AI in aesthetic medicine presents a paradigm shift from traditional approaches to data‐driven, personalized interventions. However, ethical concerns such as data privacy, informed consent, and algorithmic fairness must be addressed. Overreliance on AI may diminish the human‐centric approach essential in aesthetic procedures, where patient expectations and subjective perceptions of beauty play a crucial role. Collaboration between technologists, clinicians, and policymakers is necessary to develop standardized AI guidelines that ensure fairness, safety, and efficacy. Conclusion AI has the potential to revolutionize aesthetic medicine by improving precision, efficiency, and patient satisfaction. However, its successful implementation requires balancing technological advancements with ethical considerations and regulatory frameworks. Future research should focus on integrating AI with emerging technologies such as augmented reality (AR) and genomic‐based personalization to enhance aesthetic outcomes while maintaining transparency and patient trust.

Depigmentation of specific areas of the skin is a persistent and long-lasting dermatologic disorder known as vitiligo, stemming from the impairment and disruption of melanocytes both structurally and functionally, leading to the loss of pigmentation in those regions. Our objective was to identify the pivotal genes and upstream regulators, transcription factors (TFs), microRNAs (miRNAs), and pathways implicated in the pathogenesis of vitiligo. An integrated analysis was conducted using microarray datasets on vitiligo obtained from the Gene Expression Omnibus (GEO) database. The functional annotation and potential pathways of differentially expressed genes (DEGs) were additionally investigated through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Various bioinformatics approaches were utilized, making use of publicly accessible databases to identify appropriate TFs and miRNAs. Our investigation identified TYR, MLANA, TYRP1, PMEL, OCA2, SLC45A2, GPR143, DCT, TRPM1, and EDNRB as the most appropriate genes associated with vitiligo. Our suggestion is that the identified biological processes include developmental pigmentation (GO:0048066) and pigment metabolic processes (GO:0042440) as the most suitable biological processes. In contrast, the KEGG pathways that showed significance in our analysis are Tyrosine metabolism (Path: hsa00350) and Melanogenesis (Path: hsa04916). We hypothesized the involvement of ten TFs and 73 miRNAs in the regulation of genes related to vitiligo. TYR, MLANA, TYRP1, PMEL, OCA2, SLC45A2, GPR143, DCT, TRPM1, and EDNRB are the top ten genes that are pivotal in the progression and exhibition of vitiligo. The biological, cellular, molecular, and KEGG pathways of those genes has an imperative role in the pathogenesis of vitiligo. TFs and miRNAs that interact with this gene are listed, shedding light on the regulatory mechanisms governing the expression of these key genes in vitiligo.

Background Insulin resistance (IR) is a condition where cells become resistant to insulin, causing impaired glucose uptake and increased blood glucose levels. Interleukin‐12 (IL‐12), a cytokine, regulates the immune system. High levels of IL‐12 can lead to chronic inflammation, exacerbate resistance to insulin, and contribute to type 2 diabetes. Also, link IR to acne vulgaris (AV), as it reduces tissue sensitivity to insulin, causing increased insulin levels and sebum production, which can contribute to acne development. Aim To explore the role of IL‐12 gene expression on IR in AV patients and to study the role of IL‐12 gene in the development of AV. Subjects and Methods A case–control study was performed on 68 AV patients and 68 healthy controls. The biochemical analysis included fasting glucose, fasting insulin, (HOMA‐IR), and serum IL‐12 level. IL‐12 gene expression was performed by quantitative real‐time PCR for both two groups. In addition, folding change was calculated by using the standard 2–(∆∆Ct) method. Result IL‐12 level, IL‐12 folding change, fasting insulin, and IR were all increased in acne patients. A highly significant linear correlation was found between IL‐12 folding change and both IL‐12 levels and IR. There is a substantial positive significant simple linear association between IL‐12 level and IL‐12 folding change, as well as IR and IL‐12 folding change, in moderate and severe acne. Conclusion IL‐12 gene has an important role in IR and the development of acne in AV patients.

Background and Aims The pathophysiology of drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is complex and poorly understood. Genetic predispositions play a significant role. We aimed to explore the genetic factors and molecular mechanisms driving DRESS, focusing on gene expression, transcription factors (TFs), microRNAs (miRNAs), and chemical interactions. Methods We utilized RNA‐seq data from the GSE160369 data set in the gene expression omnibus (GEO) database to identify differentially expressed genes (DEGs) related to DRESS. The analysis was conducted using GEO2R for identifying upregulated and downregulated genes. Protein–protein interaction (PPI) networks were constructed using STRING and further analyzed with Cytoscape and CytoHubba. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to identify biological pathways. miRNAs and TFs were predicted using bioinformatics tools like TargetScan, miRDB, and ChEA3, while chemical interactions with key genes were explored using CTDbase. Results A total of 336 DEGs were identified, including 239 upregulated and 97 downregulated genes. The PPI network highlighted TNF, IL2, and CD40 as central genes involved in immune‐related pathways. Functional enrichment analyses revealed significant pathways related to immune activation, such as leukocyte‐mediated immunity. We predicted 15 miRNAs, including hsa‐miR‐1296‐5p, and identified 10 TFs, such as MTF1 and NFKB2, which regulate the expression of key genes. Chemical interaction analysis revealed decitabine and tetradecanoylphorbol acetate as prominent agents modulating gene expression. Conclusion miRNAs, TFs, and chemical modulators, which play a key role in the development of DRESS syndrome. Knowledge of the molecular underpinnings of DRESS, imperative for therapeutic targets.

Background Alopecia areata (AA) is an autoimmune condition characterized by sudden and unpredictable hair loss, with a lifetime incidence of 2%. AA can be divided into three categories: patchy alopecia, alopecia totalis, and alopecia universalis. It can affect a person's psychological health and overall quality of life. Elevated C‐reactive protein (CRP) levels in the liver may indicate an inflammatory response in autoimmune diseases. Vitamin D, essential for immune system control and skin health, may be related to AA. Hair follicles contain vitamin D receptors, which control immunological responses in the skin. However, no study has found a relationship between CRP and vitamin D in AA patients in our region. Subjects and Methods An analytical cross‐sectional study with a case‐control design research investigation of 82 AA patients and 81 healthy controls was carried out. Both groups’ medical histories were taken. Biochemical analysis was done for both groups as well as the serum vitamin D levels, and CRP. Genetic analysis for CDX2 rs11568820 variant detected by PCR (T‐ARMS‐PCR) method and vitamin D receptor (VDR) gene expression measured by real‐time PCR analysis for both patients and healthy subjects. Results CRP levels are higher in AA patients, AA patients with G/G genotypes exhibited higher concentrations of CRP when compared to those with A/A and A/G genotypes while patients with A/A genotypes have higher levels of Serum vitamin D as compared to the A/G and G/G genotypes. G allele was more abundant in AA patients. VDR gene expression was lower in AA compared to control and lower in ophiasis compared to localized and multiple patchy AA. An important inverse linear correlation was observed between vitamin D and CRP levels in ophiasis AA. Conclusion CRP concentrations were found to be elevated in AA patients. The considerable accuracy of CRP in the diagnosis of AA is substantiated by a statistically significant al. A noteworthy inverse linear association was observed between serum vitamin D and CRP concentrations in ophiasis AA.

Background and aims Psoriasis is a chronic, non‐contagious autoimmune condition marked by dry, itchy,erythematous and scaly plaques. From modest, localized plaques to total body coverage, the severity of psoriasis varies. Plaque, guttate, inverted, pustular, and erythrodermic psoriasis are the five primary kinds. About 90% of cases are of plaque psoriasis, commonly known as psoriasis vulgaris. Study aims to determine the impact of an rs2228570 (FokI) variant and an rs11568820 (CDX2) variant on serum vitamin D levels (SVD) in patients with psoriasis, and the correlation between the two variants and disease severity. Methods A case‐control study consisting of 95 psoriasis vulgaris patients and 84 healthy controls. The clinical investigation, molecular genetics analysis, and biochemical analysis were done for both groups. Results SVD levels were significantly decreased in psoriasis patients group. FokI genotypes analysis, we found no significant variance between groups. CDX2 G/G genotype is more prevalent in patients than controls. Moderate psoriasis vulgaris patients with CDX2 G/G genotypes have higher SVD levels than CDX2 G/A, and CDX2 A/A p = 0.003. Conclusion The study found a difference in vitamin D levels between patients and healthy subjects, as well as a difference in vitamin D levels with different FoKI and CDX2 genotypes.

Background The Shiga toxin-producing Escherichia coli (STEC) represented a great risk to public health. In this study, 60 STEC strains recovered from broiler and duck fecal samples, cow’s milk, cattle beef, human urine, and ear discharge were screened for 12 virulence genes, phenotypic and genotypic antimicrobial resistance, and multiple-locus variable-number tandem-repeat analysis (MLVA). Results The majority of strains harbored Shiga toxin 1 ( stx 1 ) and stx 1d , stx 2 and stx 2e , and ehx A genes, while a minority harbored stx 2c subtype and eae A. We identified 10 stx gene combinations; most of strains 31/60 (51.7%) exhibited four copies of stx genes, namely the stx 1 , stx 1d , stx 2 , and stx 2e , and the strains exhibited a high range of multiple antimicrobial resistance indices. The resistance genes bla CTX-M-1 and bla TEM were detected. For the oxytetracycline resistance genes, most of strains contained tet A, tet B, tet E, and tet G while the tet C was present at low frequency. MLVA genotyping resolved 26 unique genotypes; genotype 21 was highly prevalent. The six highly discriminatory loci DI = 0.9138 are suitable for the preliminary genotyping of STEC from animals and humans. Conclusions The STEC isolated from animals are virulent, resistant to antimicrobials, and genetically diverse, thus demands greater attention for the potential risk to human.