Elevated blood glucose levels, known as glycemia, play a significant role in sudden cardiac arrest, often resulting in sudden cardiac death, particularly among those with diabetes. Understanding the internal mechanisms has been a challenge for healthcare professionals, leading many research groups to investigate the relationship between blood glucose levels and cardiac electrical activity. Our hypothesis suggests that glucose-sensing biophysics mechanisms in cardiac tissue could clarify this connection. To explore this, we adapted a single-compartment, computational model of the human atrial node's action potential. We incorporated glucose-sensing mechanisms with voltage-gated sodium ion channels using ordinary differential equations. Parameters for the model were based on existing experimental studies to mimic the impact of glucose levels on atrial node action potential firing. Simulations using voltage clamp and current clamp techniques showed that elevated glucose levels decreased sodium ion channel currents, leading to a reduction in the sinoatrial node action potential frequency. In summary, our mathematical model provides a cellular-level understanding of how high glucose levels can lead to bradycardia and sudden cardiac death.

Elevated blood glucose levels, known as glycemia, play a significant role in sudden cardiac arrest, often resulting in sudden cardiac death, particularly among those with diabetes. Understanding this link has been a challenge for healthcare professionals, leading many research groups to investigate the relationship between blood glucose levels and cardiac electrical activity. Our hypothesis suggests that glucose-sensing mechanisms in cardiac tissue could clarify this connection. To explore this, we adapted a single-compartment, in-silico model of the human atrial node's action potential. We incorporated glucose-sensing mechanisms with voltage-gated sodium ion channels using ordinary differential equations. Parameters for the model were based on existing experimental studies to mimic the impact of glucose levels on atrial node action potential firing. Simulations using voltage clamp and current clamp techniques showed that elevated glucose levels decreased sodium ion channel currents, leading to a reduction in the sinoatrial node action potential frequency. In summary, our model provides a cellular-level understanding of how high glucose levels can lead to bradycardia and sudden cardiac death.

The key objective of the experiment was to show the environmental based of copper nanoparticles which counters the growth of bacterial pathogens such as Pseudomonas aeruginosa, and Staphylococcus aureus. To begin with the experiments, root extract of Asparagus racemosus was used to synthesise Copper nanoparticles. To confirm the formation of Cu-NPs, it was subjected to characterization such as Ultra Violet analysis, X-ray Diffraction method, Fourier Transform Infrared Spectroscopy and Scanning electron microscope images. Later the antibacterial activity of Cu-NPs was studied by incorporating it into two bacterial pathogens (Pseudomonas aeruginosa and Staphylococcus aureus). The outcome displayed a satisfactory antibacterial activity against the bacterial pathogens by the biosynthesized copper nanoparticles. To boost up the enzyme inhibition property of the Cu NPs, Antioxidant and Antidiabetic assay were also performed. The biosynthesised Cu NPs displayed a satisfied result in Antifouling function. The result was used assessed with green algae bloom water.