A biocompatible Ni(II) complex as an amyloid sensor for human PrP fibrillar aggregates.

KRS-1, a biocompatible nickel(II) complex, is introduced as a potent fluorescent probe for PrP fibrillar aggregates. KRS-1 shows a 15-fold enhancement in PL intensity and detects all stages of PrP aggregation. Fluorescence microscopy confirms its efficacy in identifying PrP fibrillar aggregates in HT-22 cells.

High Glucose-Induced Transcriptomic Changes in Human Trabecular Meshwork Cells.

Glaucoma is a leading cause of irreversible blindness, often associated with elevated intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction. Diabetes mellitus (DM) is recognized as a significant risk factor for glaucoma; however, the molecular mechanisms through which hyperglycemia affects TM function remain unclear. This study investigated the impact of high glucose on gene expression in human TM (HTM) cells to uncover pathways that contribute to TM dysfunction and glaucoma pathogenesis under diabetic conditions.

Epigenetic Disordering Drives Stemness, Senescence Escape and Tumor Heterogeneity.

Tumor heterogeneity is the substrate for tumor evolution and the linchpin of treatment resistance. Cancer cell heterogeneity is largely attributed to distinct genetic changes within each cell population. However, the widespread epigenome repatterning that characterizes most cancers is also highly heterogenous within tumors and could generate cells with diverse identities and malignant features.

Genetics of intracerebral hemorrhage.

Spontaneous intracerebral hemorrhage(ICH) represents a life-threatening form of stroke, marked by its impact on survival and quality of life. ICH can be categorized from monogenic disorders linked to causal germline variants in ICH-related genes to complex sporadic cases, highlighting the interaction among lifestyle factors, environmental influences, and genetic components in determining risk. Among sporadic ICH, the influence of these factors varies across ICH subtypes, evidenced by heritability rates of up to 73% for lobar ICH versus 34% for non-lobar ICH.

ICAM-1 K469E gene polymorphism, genotype-phenotype correlation, and retinopathy in Type 2 diabetes mellitus patients.

Context: The role of genetic factors in the development of diabetic retinopathy is evident from the fact that only 50% of patients with the non-proliferative type of diabetic retinopathy progress to proliferative diabetic retinopathy. Though the K469E polymorphism of the ICAM-1 (Intercellular Adhesion Molecule-1) gene is known to increase the risk of developing Diabetic Retinopathy (DR) among Type 2 diabetic patients, its role in the development of severe DR has not been extensively studied.

Aim: Hence, we aimed to determine the risk due to association of K469E polymorphism of ICAM-1 gene and sight threatening diabetic retinopathy.