Life

Glycosylation plays a critical role in maintaining cardiac structure and function, yet its modulation during aging and hypertrophic cardiomyopathy (HCM) in feline hearts remains uncharacterized. This study provides a systematic analysis of lectin-binding patterns in feline myocardium across different age groups and disease states. Post-mortem feline hearts (n = 64), classified by age (newborn to senior) and diagnostic status (healthy vs. HCM-affected), were evaluated using tissue microarrays stained with five plant-derived lectins— Concanavalin A (ConA), Wheat Germ Agglutinin (WGA), RCA (Ricinus communis Agglutinin I), Tomato (Lycopersicon esculentum Agglutinin), and Griffonia (Bandeiraea) simplicifolia Lectin I (BS)—alongside Draq5 nuclear counterstaining. Lectin histochemistry revealed distinct, region-specific glycosylation patterns, with notable remodelling in both aged and HCM-affected hearts. These glycan alterations reflect underlying molecular and structural changes associated with cardiac aging and pathology. Although lectin histochemistry has been used to examine cardiac glycosylation in species such as mice, rats, zebrafish, and humans, comparable data for felines have been lacking, even if domestic cat represents a spontaneous model for human HCM. This study provides the first essential step in characterizing the feline cardiac glycosylation. The observed shifts in lectin-binding profiles reveal specific remodelling associated with aging and HCM in cats. These results provide a foundation for future studies assessing the utility of glycan motifs as potential post-mortem markers of disease progression in felines.

Alterations of pancreatic islet cell phenotypes are well established in diabetic conditions and considered to be one of the possible causes of insulin deficiency. However, there is limited information about alterations of islet cell phenotypes in opposite metabolic conditions such as hypoglycemia in infants with congenital hyperinsulinism (CHI). Surgical biopsies of the pancreas from six infants with diffuse CHI and five infants with focal CHI were examined using double immunofluorescence with antibodies against insulin, glucagon and the key transcriptional factor responsible for β-cell differentiation and maturation—PDX1. The phenotypes of cells within the pancreatic islets in diffuse CHI and within the focus in focal CHI were compared to those in unaltered pancreatic islets located outside the focus. In diffuse CHI, the proportion of bi-hormonal insulin+/glucagon+ cells was increased. Additionally, an increase in the proportion of insulin+ cells lacking PDX1 was observed in diffuse CHI and within the focus. It can be assumed that alterations of the phenotype of β-cells may occur under hypoglycemic conditions, but the role of islet cell plasticity in infants with CHI remains to be established.

Aggressive behavior is a complex and multifactorial trait influenced by several genes and shaped by societal and cultural constraints. To trace adaptation signals and identify potential new genes related to aggressive behavior, we explored variations in nine genes previously linked to aggressive behavior, as well as their 74 interacting genes retrieved from the STRING database. We identified 15 SNPs under positive selection in four genes (SEC24B, NCOA2, CTNNA1, and ALDH3A2), with selection consistently confirmed by both iHS and xp-EHH analyses. Among these, 15 SNPs showed high pairwise F_ST values and pronounced allele frequency differences between populations, suggesting their potential role in the local adaptation of the studied populations. The functional importance of these SNPs was confirmed by ten acting as eQTLs and five located in transcription factor binding sequences. The observed selection signatures may reflect adaptation in diverse biological processes, including protein trafficking and signal transduction, cell proliferation and differentiation, endocrine regulation, and lipid and aldehyde detoxification. Although these processes are not directly linked to aggression, they may have downstream effects on neurodevelopmental and hormonal regulation that could indirectly influence behavioral phenotypes. Experimental validation is required to confirm these signals and to clarify their functional and biological significance.