Lung cancer remains the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) representing the majority of cases. Molecular profiling of NSCLC has identified multiple genomic alterations, including BRAFV600E mutation, which occurs in 1-5% of patients, predominantly in adenocarcinomas. Detection of this mutation is clinically relevant due to the availability of targeted therapies. Immunohistochemistry using the VE1 antibody offers a rapid and practical screening method, although interpretation criteria and methodological variability remain challenging.

A laboratory toolbox for detecting and quantifying DNA breaks in animal cells and tissues includes various methods that employ biochemical tests, DNA sequencing, or imaging approaches. Various methods based on microscopy were developed to detect DNA breaks in fixed and live cells, including the nick translation assay, TUNEL, STRIDE, and detection methods based on imaging of histone modifications (γH2A.X), recruitment of repair factors (XRCC1, PCNA, 53BP1, Rad51) or poly-ADP-ribosylation. This review discusses the advantages and limitations of various microscopy-based methods for the detection and quantification of single- and double-strand DNA breaks.

. The adrenal glands are central regulators of endocrine homeostasis and stress adaptation. Despite decades of research, the molecular mechanisms governing adrenal zonation and cortical renewal remain incompletely understood.

Bronchopulmonary dysplasia (BPD) is a common chronic respiratory disease in premature infants. Hyperoxia is the main pathogenic factor of BPD. Nintedanib is a small-molecule tyrosine kinase inhibitor that has been confirmed to affect several cellular processes in different diseases. The aim of this study was to explore the function of nintedanib in the treatment of BPD.

Age-related degenerative changes in intervertebral discs (IVDs) can lead to lower back pain, and even paralysis. This topic is therefore garnering growing attention in an increasingly ageing society. The oxidative stress-induced degenerative process is a major contributor to apoptosis in nucleus pulposus cells. However, the regulatory mechanism of NAD-dependent protein deacetylase Sirtuin-1 (SIRT1) on apoptosis in oxidative stress-induced rat nucleus pulposus cells remains unclear.

Sepsis, a life-threatening condition caused by a host response that goes out of control, leads to severe organ dysfunction. MicroRNA 939 (miRNA-939) plays a pivotal role in this process by post-transcriptionally regulating the mRNA expression of key enzymes in the NO/cGMP pathway. This pathway is crucial in the development of refractory hypotension and organ failure in sepsis. The aim of the study was to explore the effects of miRNA-939 on a caecum ligation puncture (CLP) rat model of sepsis in kidneys and lungs in order to elucidate its role in modulating the NO/cGMP pathway and related organ protection mechanisms.

Osteoporosis is a bone disease characterised by low bone mass, deterioration of bone tissue, and disruption of bone microarchitecture. MicroRNAs have been found to play an important role in osteoporosis. MicroRNA (miR)-494 is inhibited during bone angiogenesis, and its overexpression reduces osteogenic differentiation gene expression. Sirtuin 1 (Sirt1) is a histone deacetylase with multiple cellular activities including increasing bone mass and delaying the onset of osteoporosis. MiR-494-3p has been predicted in computer-assisted bioinformatics analysis to target the 3'UTR of Sirt1 mRNA. The aim of the present study was to assess the effect of miR-494-3p on ovariectomy (OVX)-induced osteoporosis in rats and the relevant mechanisms.

Increasing evidence shows that Hox transcript antisense RNA (HOTAIR) plays a vital role in liver cancer initiation and progression by affecting the proliferation, invasion, migration, and apoptosis of liver cancer cells. However, the underlying mechanism of how HOTAIR exerts its functions in liver cancer cells remains unclear. Previous studies have shown that HOTAIR affects the invasion and migration of liver cancer cells by regulating the expression of E-cadherin. Snail2, a transcription factor involved in epithelial-mesenchymal transition, directly binds to the E-boxes of the E-cadherin promoter to repress its transcription. The aim of the study was to examine the correlation between HOTAIR and Snail2 in the HOTAIR/Snail2/E-cadherin signal pathway and explore the role of HOTAIR in the proliferation, invasion, migration, and apoptosis of liver cancer cells.

Hepatocellular carcinoma (HCC) is the sixth most common type of cancer and the second leading cause of cancer death worldwide [19]. Opioid growth factor (OGF) has been shown to exhibit antitumour potential, binding to OGF receptor (OGFr). Naltrexone (NTX), an OGFr antagonist, is considered as a potential anti-cancer agent. However, the specific mechanism of how OGFr acts on HCC cells is yet to be elucidated.

This study investigated the therapeutic mechanisms of electroacupuncture (EA) in chronic unpredictable stress (CUS)-induced depression rat model. Since SIRT1 plays in oligodendrocyte differentiation and neuroprotection, we hypothesize that it may mediate the effect of electroacupuncture (EA) on myelin regeneration in depression.

Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy, encompassing distinct histological variants and a wide spectrum of clinical behaviors. Advances in molecular diagnostics have identified key genetic alterations - particularly BRAFV600E, RAS mutations, RET/PTC fusions, and TERT promoter mutations - that are strongly linked to tumor aggressiveness and prognosis. This study aimed to determine the prevalence of these alterations and evaluate their clinicopathological significance in a Saudi Arabian patient cohort.

Papillary thyroid carcinoma (PTC) constitutes the predominant subtype among thyroid malignancies. Despite its generally favorable prognosis, certain aggressive subtypes, along with recurrent and metastatic manifestations, substantially affect patient survival outcomes. Recent advancementsin the diagnostic and therapeutic strategies for PTC have ushered in a new era, characterized by the integration of molecular mechanisms and imaging-based evaluations. This review offers an integrated perspective of the clinicopathological features, molecular genetic characteristics, epigenetic regulation, and the contribution of the immune microenvironment to the aggressiveness of PTC. Primary inve stigation targets include BRAF/RAS/RET-related molecular mechanisms and the functional significance of non-coding RNAs [especially long non-coding RNAs (lncRNAs) and microRNAs (miRNAs)] in molecular regulation. Additionally, the impact of clinical factors such as age, sex, obesity, and comorbidity with Hashimoto's thyroiditis on the aggressiveness of PTC is thoroughly examined. Furthermore, this review systematically synthesizes the clinical advances in the early detection and risk assessment of aggressive PTC by emerging imaging modalities such as conventional ultrasound, interventional ultrasound, ultrasound elastography, contrast-enhanced ultrasound, and artificial intelligence-assisted analysis. Looking ahead, multidisciplinary collaborations integrating pathology, genomics, and imaging are anticipated to enhance the precise evaluation of PTC aggressiveness and facilitate the development of individualized treatment strategies. This review serves as a comprehensive reference for mechanistic exploration and clinical translation in the study of PTC aggressiveness, and provides guidance for the progression of precision medicine and management models for PTC patients.

Diabetic retinopathy involves retinal pigment epithelium (RPE) dysfunction. Tectochrysin is a natural flavonoid and antioxidant. However, its effects on retinal pigment epithelial cells remain unveiled. In this study, the investigation undertook the question of whether tectochrysin could protect human adult RPE cells ARPE-19 from high-glucose (HG) damage. Also the potential regulatory mechanism was explored.

This study aimed to provide a comprehensive histopathological and immunohistochemical analysis of Meibomian adenomas and adenocarcinomas.

O-GlcNAcylation is a post-translational modification in which a single N-Acetyl-D-Glucosamine (GlcNAc) molecule is added to Ser or Thr residues of proteins. The O-N-acetylglucosaminyl transferase (OGT) enzyme is responsible for adding GlcNAc to the target proteins and N-acetyl-β-D-glucosaminidase (OGA) that removes the GlcNAc residue. O-GlcNAcylation has been described in the pathophysiology of several diseases; however, little has been studied in dental tissue. The aim of the present work is to characterise the product of O-GlcNAcylation and its enzymes at the tissue level in the dental pulp, as well as its expression in dental pulp stem cells (DPSCs) both in situ and in vitro. This enables the recognition of the behaviour of O-GlcNAcylation in pulp tissue without pathology.

Oxidative damage-induced retinal pigment epithelial (RPE) cell apoptosis and optic nerve inflammation and demyelination are closely related to the pathogenesis of optic neuritis (ON). STAT1 has been found to be activated in the retina and optic nerve of ON rats. This study aimed to determine whether STAT1 depletion exerts neuroprotective effects against ON in both cellular and animal models.

Pyroptosis is closely related to many chronic diseases including atherosclerosis, but the potential pathomechanisms are still unclear. This study was aimed at exploring how lncRNAs may contribute to pyroptosis and the potential mechanisms.

The aberrant activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signalling pathway is involved in spinal cord injury (SCI) progression. Electroacupuncture (EA) stimulation is effective in alleviating SCI, but the mechanism is poorly understood.

Transient global ischaemia in rodents causes selective loss of hippocampal CA1neurons, but the potential involvement of endocytic pathways has not been fully explored. The aim of this study was to investigate the changes in early endosomes in the CA1 subfield after ischaemia and reperfusion.

This study was aimed at exploring the effect of four units of polyethylene glycol (PEG4)-modified Ser-Val-Val-Tyr-Gly-Leu-Arg (SVVYGLR) peptide (SV peptide) on the proliferative potential and migrative capability of human gingival fibroblasts (HGFs) and the activation of adhesion-related proteins.