The aim of the study is to reach objective results about the ergonomic risks of nurses’ working postures not only by using questionnaires but also by using Rapid Entire Body Assessment (REBA) and Rapid Upper Limb Assessment (RULA) methods, which are risk assessment methods used in engineering fields. This study is a cross-sectional study. First of all, 383 nurses were evaluated with a survey. 91.4% of the nurses were women and 6.5% were men. Average age (female: 38.20; male: 31.5), average weight (female: 65.60 kg; male: 81.50 kg), average height (female: 162.7 cm; male: 176.80 cm) and average body mass index (female: 24.80; male: 26) were calculated. In the hospital, which we grouped into in the hospital, which we divided into eight workstations, the REBA and RULA scores of the three nurses working at each workstation were calculated and the average REBA and RULA scores of the workstations were determined. The percentage of those who experienced musculoskeletal pain in the last 1 year at each workstation and the mean REBA–RULA scores were as follows; ward (92%; 6.92–5.69), operating room (98%; 10–7), emergency department (100%; 6.08–5.33), outpatient clinic (75%; 5.5–5.16), intensive care (94%; 6.21–5.57), administrative affairs (94%; 5–5), laboratory (95%; 5.80–5.2) and interventional procedure (92%; 6.4–5.4). In these stations, the highest scores were seen in the operating room. In the questionnaire, 92.46% of the nurses reported having complaints in at least one part of the musculoskeletal system in the last year. The hospital weighted mean score was REBA 6.86 and RULA 5.71. When REBA and RULA measurements were evaluated, it was determined that the risk in the departments where the nurses worked was generally at the medium risk level. REBA and RULA scores indicate that ergonomic changes and adjustments should be made. For this determination, the risks of working postures should be determined with quantitative methods.

Dementia is mostly caused by neurodegenerative diseases like Alzheimer’s disease (AD). AD is the most common form of dementia. It is caused by both genetic and environmental factors. Due to neuronal death in a number of brain regions, including the hippocampus, entorhinal areas, temporal lobe, and cingulate cortex, AD causes memory loss and gradual cognitive impairment. The condition’s two main pathogenic components are intracellular neurofibrillary tangles created by clusters of hyperphosphorylated tau protein and amyloid plaques made up of extracellular amyloid (Aβ) peptide aggregates. In contrast to the APOE- ε4 allele, which was found to have a significant impact on late-onset AD, presenilin 1, presenilin 2, amyloid precursor protein were genetic risk factors that were causal for early-onset AD. Misfolded proteins accumulate within the neuron, causing prolonged cellular stress in AD, a progressive neurodegenerative disease. Neurofibrillary tangles and senile plaques are two of the neuropathological hallmarks of Alzheimer’s disease that lead to the destruction of synapses and the death of neurons. AD is mostly caused by the death of nerves, particularly cholinergic nerves. In the absence of these cholinergic neurons, acetylcholine levels fall. This review discusses key genes involved in the pathogenesis and pathophysiology of AD, as well as the disease’s molecular mechanisms.

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.

Background: Thromboangiitis obliterans (TAO) causes vascular insufficiency due to chronic inflammation and abrupt thrombosis of the medium and small arteries of the extremities. In our study, we aimed to determine biomarkers for the diagnosis of TAO by evaluating 15 male TAO patients with Shinoya diagnostic criteria and 5 healthy controls who did not have TAO-related symptoms in their family histories. Methods: The Clariom D Affymetrix platform was used to conduct microarray analysis on total RNA extracted from whole blood. A total of 477 genes (FC ≤ 5 or >5) common to the fifteen patient and five control samples were selected using comparative microarray analysis; among them, 79 genes were upregulated and 398 genes were downregulated. Results: According to FC ≤ 10 or >10, in the same TAO patient and control group, 13 genes out of 28 were upregulated, whereas 15 genes were downregulated. The 11 key genes identified according to their mean log2FC values were PLP2, RPL27A, CCL4, FMNL1, EGR1, EIF4A1, RPL9, LAMP2, RNF149, EIF4G2, and DGKZ. The genes were ranked according to their relative expression as follows: FMNL1 > RNF149 > RPL27A > EIF4G2 > EIF4A1 > LAMP2 > EGR1 > PLP2 > DGKZ > RPL9 > CCL4. Using protein–protein interaction network analysis, RPL9, RPL27A, and RPL32 were found to be closely related to EIF4G2 and EIF4A1. The Reactome pathway found pathways linked to 28 genes. These pathways included the immune system, cellular responses to stress, cytokine signaling in the immune system, and signaling by ROBO receptors. Conclusions: By figuring out the protein expression levels of the genes that have been found to explain how TAO disease works at the molecular level, it will be possible to figure out how well these chosen transcripts can diagnose and predict the disease.

Identification of Target Genes Associated with Vitamin C Treatment in Renal Cell Carcinoma

Early detection of breast cancer (BC) remains a challenge despite advances in screening, leading to poor prognosis in late-stage disease. Circulating microRNAs (miRNAs) have emerged as promising non-invasive biomarkers for early diagnosis. The study aimed to evaluate the diagnostic utility of serum miR-197-3p, miR-1236, and miR-1271 levels in distinguishing BC patients from healthy individuals. Serum samples from 92 BC patients and 31 healthy controls were analyzed. Total RNA was extracted, and miRNA expression levels were quantified using quantitative real-time PCR (qRT-PCR). Expression differences were assessed using the ΔCt method. Receiver Operating Characteristic (ROC) curve analysis evaluated diagnostic performance. Serum miR-197-3p levels were significantly upregulated (fold change = 8.939, p = 0.0048), while miR-1236 was downregulated (fold change = 0.112, p = 0.0029) in BC patients. miR-1271 showed no significant association. miR-1236 demonstrated superior diagnostic performance (AUC = 0.731, sensitivity = 80.7%, specificity = 51.3%) compared to miR-197-3p (AUC = 0.667, sensitivity = 67.0%, specificity = 45.6%). The combination of miR-197-3p and miR-1236 improved diagnostic accuracy (AUC = 0.842, CI: 0.764–0.936). Serum miR-197-3p and miR-1236 hold promise as complementary biomarkers for early BC detection. Larger multicenter studies are warranted to validate their clinical utility.