Environmental-friendly synthesis of Au-Ag alloy nanoparticles using Anethum graveolens leaf extract and their application to Surface Enhanced Raman Scattering (SERS)

We report an Environmental-friendly method for the synthesis of Au-Ag alloy nanoparticles (ANPs) by using Anethum graveolens fresh leaf extract as a reducing and stabilizing agent. The precursor solutions of Au (HAuCl4: 3H2O), Ag (AgNO3) and leaf extract were mixed by varying molar ratios and heated with continuous stirring at 70℃ for an hour leads a formation of Au-Ag ANPs with different atomic compositions. The periodic observation of colour changes indicated the formation of Au-Ag ANPs and got confirmed by the measurement of UV-Vis spectroscopy. The synthesized Au-Ag ANPs were characterized for morphological and elemental composition using Transmission Electron Microscopy (TEM) in conventional and scanning TEM (STEM) mode. The TEM image analysis shows that the synthesized Au-Ag ANPs were found to be in spherical shape with a broad size distribution with a mean size of 23 ± 18 nm. The energy dispersive X-ray (EDX) spectrometry in the STEM mode confirms the formation of Au-Ag ANPs . To show that these biosynthesized Au-Ag ANPs can be used as SERS (Surface Enhanced Raman Scattering) substrates, we carried out SERS studies using Crystal Violet (CV) and Rhodamine 6G (R6G) as test molecules by using 514.5 nm laser excitation wavelength. The detection level achieved was 50µM of CV and R6G, which would lead to exploring biosensing applications

Trigger versus Substrate: Multi-Dimensional Modulation of QT-Prolongation Associated Arrhythmic Dynamics by a hERG Channel Activator

Background: Prolongation of the QT interval of the electrocardiogram (ECG), underlain by prolongation of the action potential duration (APD) at the cellular level, is linked to increased vulnerability to cardiac arrhythmia. Pharmacological management of arrhythmia associated with QT prolongation is typically achieved through attempting to restore APD to control ranges, reversing the enhanced vulnerability to Ca²⁺-dependent afterdepolarisations (arrhythmia triggers) and increased transmural dispersion of repolarisation (arrhythmia substrate) associated with APD prolongation. However, such pharmacological modulation has been demonstrated to have limited effectiveness. Understanding the integrative functional impact of pharmacological modulation requires simultaneous investigation of both the trigger and substrate. Methods: We implemented a multi-scale (cell and tissue) in silico approach using a model of the human ventricular action potential, integrated with a model of stochastic 3D spatiotemporal Ca²⁺ dynamics, and parameter modification to mimic prolonged QT conditions. We used these models to examine the efficacy of the hERG activator MC-II-157c in restoring APD to control ranges, examined its effects on arrhythmia triggers and substrates, and the interaction of these arrhythmia triggers and substrates. Results: QT prolongation conditions promoted the development of spontaneous release events underlying afterdepolarisations during rapid pacing. MC-II-157c applied to prolonged QT conditions shortened the APD, inhibited the development of afterdepolarisations and reduced the probability of afterdepolarisations manifesting as triggered activity in single cells. In tissue, QT prolongation resulted in an increased transmural dispersion of repolarisation, which manifested as an increased vulnerable window for uni-directional conduction block. In some cases, MC-II-157c further increased the vulnerable window through its effects on INa. The combination of stochastic release event modulation and transmural dispersion of repolarisation modulation by MC-II-157c resulted in an integrative behavior wherein the arrhythmia trigger is reduced but the arrhythmia substrate is increased, leading to variable and non-linear overall vulnerability to arrhythmia. Conclusion: The relative balance of reduced trigger and increased substrate underlies a multi-dimensional role of MC-II-157c in modulation of cardiac arrhythmia vulnerability associated with prolonged QT interval