Noise-induced hearing loss (NIHL) is a significant occupational health issue, characterized by permanent damage to the cochlea due to prolonged exposure to high-intensity noise. Circulating microRNAs (c-miRNAs) have emerged as promising non-invasive indicators of inner ear pathology and potential modulators of cellular stress responses. Nevertheless, their specific roles in NIHL remain inadequately characterized. This study evaluated miRNA expression in the peripheral blood of individuals with bilateral NIHL (n = 12) and matched healthy controls (n = 6) using GeneChip^® miRNA 4.0 arrays. The Transcriptome Analysis Console software was used for differential expression analysis, and bioinformatic predictions of gene targets and pathway enrichment were performed using TargetScan (version 8.0) and the Enrichr tool. Among the 72 differentially expressed miRNAs (FDR < 0.05), hsa-miR-486-2, hsa-miR-664b-3p, hsa-miR-4485, hsa-miR-501, and hsa-miR-663b were notably upregulated, while hsa-miR-6723, hsa-miR-194-2, hsa-miR-668-5p, hsa-miR-4722-3p, and hsa-miR-4716 showed significant downregulation. Enrichment analyses indicated involvement in apoptosis regulation, mitochondrial stability, and cell cycle control. Principal component analysis (PCA) and clustering methods revealed clear molecular distinctions between the patient and control groups. The observed alterations in c-miRNA profiles highlight their relevance to NIHL-related cellular stress and degeneration. These findings support their utility as candidate biomarkers for diagnosis and prognosis, warranting further validation in functional and longitudinal studies.

Alzheimer’s disease (AD) and major depressive disorder (MDD) are prevalent central nervous system (CNS) disorders that share overlapping symptoms but differ in underlying molecular mechanisms. Distinguishing these mechanisms is essential for developing targeted diagnostic and therapeutic strategies. In this study, we integrated multi-tissue transcriptomic datasets from brain and peripheral samples to identify differentially expressed microRNAs (miRNAs) in AD and MDD. Functional enrichment analyses (KEGG, GO) revealed that dysregulated miRNAs in AD were associated with MAPK, PI3K–Akt, Ras, and PD-1/PD-L1 signaling, pathways linked to synaptic plasticity, neuroinflammation, and immune regulation. In contrast, MDD-associated miRNAs showed enrichment in Hippo signaling and ubiquitin-mediated proteolysis, implicating altered neurogenesis and protein homeostasis. Network analysis highlighted key disease- and tissue-specific miRNAs, notably hsa-miR-1202 and hsa-miR-24-3p, with potential roles in neuronal survival and molecular network regulation. These findings suggest that miRNAs may serve as non-invasive biomarkers for diagnosis, prognosis, and treatment monitoring in both disorders. While therapeutic targeting of miRNAs offers promise, challenges such as blood–brain barrier penetration and tissue-specific delivery remain. This integrative approach provides a translational framework for advancing miRNA-based strategies in CNS disease research.

The objectives of this study comprise the identification of key miRNAs and their target genes associated with severe tolerance in individuals exposed to aluminum and welding fumes, and the elucidation of the underlying regulatory mechanisms. In this study, the levels of seven miRNAs (hsa-miR-19a-3p, hsa-miR-130b-3p, hsa-miR-25-3p, hsa-miR-363-3p, hsa-miR-92a-3p, hsa-miR-24-3p, and hsa-miR-19b-3p) were analyzed using both hsa-miR-16-5p and RNU6 (U6 snRNA) as reference miRNAs to validate normalization reliability. The qRT-PCR method was used on blood serum samples from 16 workers who were exposed to aluminum, 16 workers who were exposed to welding fumes, and 16 healthy controls who were not exposed to aluminum or welding fumes. We determined heavy metal levels from serum samples of workers exposed to aluminum and welding fumes and control groups using the ICP-OES method. The expression levels of hsa-miR-19a-3p and hsa-miR-19b-3p in aluminum-exposed and control groups were found to be statistically significant (p < 0.05). When workers exposed to welding fumes were compared with the those in the control groups, the expression levels of hsa-miR-19a-3p, hsa-miR-130b-3p, hsa-miR-92a-3p, and hsa-miR-24-3p were observed to be statistically significant (p < 0.05). This study shows that the identification of miRNAs and target genes in different biological functions and pathways plays an important role in understanding the molecular mechanisms of responses to heavy metal toxicity. We share the view that the study will make a significant contribution to the literature in that seven candidate miRNAs can be used as possible biomarkers for exposure to aluminum and welding fumes in humans.

The objectives of the study include identifying key miRNAs and their target genes associated with severe tolerance in individuals exposed to aluminum and welding fumes and providing a molecular basis for the demonstration of the underlying regulatory mechanisms. In this study, the levels of seven miRNAs (hsa-miR-19a-3p, hsa-miR-130b-3p, hsa-miR-25-3p, hsa-miR-363-3p, hsa-miR-92a-3p, hsa-miR-24-3p, and hsa-miR-19b-3p) were compared to a reference miRNA (hsa-miR-16-5p). The qRT-PCR method was used on blood serum samples from 16 workers who were exposed to aluminum, 16 workers who were exposed to welding fumes, and 16 healthy controls who were not exposed to aluminum or welding fumes. We determined heavy metal levels from serum samples of workers exposed to aluminum and welding fumes and control groups using the ICP-OES method. The expression levels of hsa-miR-19a-3p and hsa-miR-19b-3p in aluminum-exposed and control groups were found to be statistically significant (p < 0.05). When workers exposed to welding fumes were compared with the those in the control groups, the expression levels of hsa-miR-19a-3p, hsa-miR-130b-3p, hsa-miR-92a-3p, and hsa-miR-24-3p were observed to be statistically significant (p < 0.05). This study shows that the identification of miRNAs and target genes in different biological functions and pathways plays an important role in understanding the molecular mechanisms of responses to heavy metal toxicity. We share the view that the study will make a significant contribution to the literature in that seven candidate miRNAs can be used as possible biomarkers for exposure to aluminum and welding fumes in humans.

İş Sağlığı ve Güvenliği Tarihçesi-İlkeleri Hakan DEMİRHİNDİ İş Sağlığı ve Güvenliği Mevzuatı Zeki OKUR Çalışanların Yasal Hak ve Sorumlulukları Zeki OKUR Çalışma Ortamının Fiziksel Risk Etkenleri Halim İŞSEVER Gözde ÖZTAN Tuğçe İŞSEVER Çalışma Ortamının Kimyasal Risk Etkenleri Emel YILDIZ Mesut BAŞIBÜYÜK Çalışma Ortamının Biyolojik Risk Etkenleri Ertan KARA Çalışma Ortamının Psiko-Sosyal Risk Etkenleri Ferdi TANIR Çalışma Ortamının Ergonomik Risk Etkenleri Rengin GÜZEL Aylin SARIYILDIZ Çalışma Ortamının Toz Etkenleri Abdulkadir ÜRÜNVEREN İşyerinde Risk Yönetimi ve Değerlendirmesi Ali KOKANGÜL Çalışma Ortamı Gözetimi Emel Ceyhun SABIR Çalışanların Sağlık Gözetimi Mehmet Tibet ATLI İşyeri Sağlık ve Güvenlik Birimi Hizmetleri Rahime KAÇMAZ İş Sağlığı ve Güvenliği Profesyonelleri İlkay YAVUZ Sevinç ZENGİN İş Sağlığı ve Güvenliği Kurulu Ferdi TANIR Çalışma Yaşamında Özel Risk Grupları Mehmet Tibet ATLI İş Hijyeni Halim İŞSEVER Tuğçe İŞSEVER Gözde ÖZTAN İş Kazaları ve Korunma Ahmet Mahmut KILIÇ Meslek Hastalıkları ve İşle İlgili Hastalıklar Ferruh Niyazi AYOĞLU Bilgehan AÇIKGÖZ Meslekler Kanserler Ferruh Niyazi AYOĞLU Bilgehan AÇIKGÖZ Acil Durum Planı, Tahliye ve Kurtarma Özen KILIÇ Yangın Güvenliği ve Patlamadan Korunma Cemal KOZACI Kemal ÜÇÜNCÜ Elektrikle İlgili Tehlikeler, Riskler ve Önlemler Ahmet TEKE İş Ekipmanlarının Güvenli Kullanımı Ali BAYAT Kişisel Koruyucu Donanım Kullanımı Ali BAYAT Sağlık ve Güvenlik İşaretleri Fatih ZENGİN Elle Kaldırma ve Taşımada Çalışan Sağlığı ve Güvenliği Özen KILIÇ Ekranlı Araçlarla Çalışmada Çalışan Sağlığı ve Güvenliği Özen KILIÇ İlk Yardım Azade SARI Zeynep KEKEÇ Tütün Ürünlerinin Zararları ve Pasif Etkilenme Nureddin ÖZDENER Yüksekte Çalışmalarda Çalışan Güvenliği Serkan AYDINLI Laboratuvarlarda Güvenli Çalışma İlkeleri Emel YILDIZ İş Makinelerinde Çalışan Güvenliği Abdulkadir YAŞAR Radyasyonlu Ortamda Sağlık ve Güvenlik Ahmet YILMAZ Havalandırma - İklimlendirmede Sağlık ve Güvenlik Engin PINAR Basınçlı Kaplarla Çalışmalarda Sağlık ve Güvenlik Serdar GÜLTEK Nuri Egemen YILMAZ Kaynak İşlerinde Sağlık ve Güvenlik Özen KILIÇ Kapalı Alan Çalışmalarında Sağlık ve Güvenlik Özen KILIÇ İş Sağlığı ve Güvenliği Yönetim Sistemleri Mesut BAŞIBÜYÜK İş Sağlığı ve Güvenliği Epidemiyolojisi Burak METE İşyerinde Sağlığın Geliştirilmesi Zühtü ŞAHİN İş Sağlığı ve Güvenliği Kültürü Ersin NAZLICAN İşyerinde Sağlık Eğitimi ve Sağlık Okuryazarlığı Burak METE İş Sağlığı ve Güvenliği Hizmetlerinin Denetimi Semiha DOSTLAR Mesleki Solunum Sistemi Hastalıkları Oya BAYDAR TOPRAK Mesleki Kalp Damar Sistemi Hastalıkları Çağlar Emre ÇAĞLIYAN Murat Türkeün ILGINEL Mesleki Sinir Sistemi Hastalıkları Ahmet Turan EVLİCE Zeynep ŞANLI Mesleki Üro-Genital Sistem Hastalıkları İbrahim Atilla ARIDOĞAN Nebil AKDOĞAN Mesleki Deri Hastalıkları Dilek DAŞGIN Bilge F. KARAMAN

Dementia with Lewy bodies (DLB) shares substantial clinical and molecular features with Alzheimer’s disease (AD) and Parkinson’s disease dementia (PDD), complicating the identification of disease-specific molecular alterations. This study aimed to characterize transcriptomic differences among these disorders and to integrate expression findings with published Lewy body dementia (LBD) genetic evidence. Gene-level expression profiles from 42 postmortem prefrontal cortex samples in GSE150696, including controls, AD, DLB, and PDD, were analyzed using age- and sex-adjusted empirical-Bayes models with false discovery rate (FDR) correction, followed by sensitivity analyses, post hoc exploratory candidate selection, and integration with an external LBD multi-omics gene-prioritization dataset. No gene reached FDR < 0.05 in the DLB-versus-AD comparison. In contrast, SLC19A2, VAMP1, and COX5B were lower in DLB than in PDD and were FDR-supported in the primary age- and sex-adjusted model, although their statistical significance was partly model-dependent. A post hoc cross-disease analysis identified 60 exploratory candidates, of which SYT11 was the only gene overlapping with the published LBD-prioritized gene set. The overall 60-gene set was not significantly enriched for LBD-associated genes. These findings did not demonstrate broad robust disease–disease differences and are consistent with substantial molecular overlap, while remaining compatible with limited statistical power. A limited number of transcriptomic candidates, including the exploratory SYT11 overlap, warrant independent validation.