Methods: For the optimisation and validation protocol, β-cells were plated onto 35 mm plastic petri dishes and maintained in RPMI-1640 media supplemented with 10 mM glucose, 10% FCS and 25 mM of N-2-hydroxyethylpiperazine-N-ethanesulfonic acid (HEPES). The treatment effects of 10 mM glucose and 30 μM fluoxetine on KATP channels NPo of β-cells were assessed via cell-attached patch-clamp recordings. For hippocampus cell experiments, hippocampi were harvested from day 17 of maternal Lister-hooded rat foetus, and then transferred to a Ca2+ and Mg2+-free HEPES-buffered Hank's salt solution (HHSS). The dissociated cells were cultured and plated onto a 25 mm round cover glasses coated with poly-d-lysine (0.1 mg/mL) in a petri dish. The KATP channels NPo of hippocampus cells when perfused with 1 mM and 10 mM of KA were determined.
Results: NPo of β-cells showed significant decreasing patterns (P < 0.001) when treated with 10 mM glucose 0.048 (0.027) as well as 30 μM fluoxetine 0.190 (0.141) as compared to basal counterpart. In hippocampus cell experiment, a significant increase (P < 0.001) in mean NPo 2.148 (0.175) of neurons when applied with 1 mM of KA as compared to basal was observed.
Conclusion: The two concentrations of KA used in the study exerted contrasting effects toward the mean of NPo. It is hypothesised that KA at lower concentration (1 mM) opens more KATP channels, leading to hyperpolarisation of the neurons, which may prevent neuronal hyper excitability. No effect was shown in 10 mM KA treatment, suggesting that only lower than 10 mM KA produced significant changes in KATP channels. This implies further validation of KA concentration to be used in the future.
RECENT FINDINGS: Climate change is responsible for extreme weather conditions (shifts in rainfall, floods, droughts, and forest fires) and global warming. These consequences affect basic human needs of water and food, causing changes in population dynamics and pose significant threats to digestive health, including common esophageal disorders like GERD, EoE, and esophageal cancers. The changing patterns of esophageal diseases with climate change are likely mediated through risk factors, including nutrition, pollutants, microplastics, and the microbiota-gut-brain axis. The healthcare process itself, including GI endoscopy practices commonly employed in diagnosing and therapeutics of esophageal diseases, may, in turn, contribute to climate change through plastic wastage and greenhouse gas emissions, thus creating the climate change lifecycle. Breaking the cycle would involve changes at the individual level, community level, and national policy level. Prevention is key, with individuals identifying and remediating risk factors and reducing carbon footprints. The ABC (Advocacy, Broadcast, and Collaborate) activities would help enhance awareness at the community level. Higher-level programs such as the Bracing Resilience Against Climate Effects (BRACE) would lead to broader and larger-scale adoption of public health adaptation strategies at the national level. The impact of climate change on esophageal disorders is likely real, mediated by several risk factors, and creates a climate change lifecycle that may only break if changes are made at individual, community, and national levels.