An evaluative technique for drought impact on variation in agricultural LULC using remote sensing and machine learning.

Drought events threaten freshwater reservoirs and agricultural productivity, particularly in semi-arid regions characterized by erratic rainfall. This study evaluates a novel technique for assessing the impact of drought on LULC variations in the context of climate change from 2018 to 2022. Various data sources were harnessed, encompassing Sentinel-2 satellite imagery for LULC classification, climate data from the CHIRPS and AgERA5 databases, geomorphological data from JAXA's ALOS satellite, and a drought indicator (Vegetation Health Index (VHI)) derived from MODIS data. Two classifier models, namely gradient tree boost (GTB) and random forest (RF), were trained and assessed for LULC classification, with performance evaluated by overall accuracy (OA) and kappa coefficient (K). Notably, the GTB model exhibited superior performance, with OA > 90% and a K > 0.9. Over the period from 2018 to 2022, Fez experienced LULC changes of 19.92% expansion in built-up areas, a 34.86% increase in bare land, a 17.86% reduction in water bodies, and a 37.30% decrease in agricultural land. Positive correlations of 0.81 and 0.89 were observed between changes in agricultural LULC, rainfall, and VHI. Furthermore, mild drought conditions were identified in the years 2020 and 2022. This study emphasizes the importance of AI and remote sensing techniques in assessing drought and environmental changes, with potential applications for improving existing drought monitoring systems.

Beneficial Role of Vitexin in Parkinson's Disease.

Today, Parkinson's disease (PD) is the foremost neurological disorder all across the globe. In the quest for a novel therapeutic agent for PD with a multimodal mechanism of action and relatively better safety profile, natural flavonoids are now receiving greater attention as a potential source of neuroprotection. Vitexin have been shown to exhibit diverse biological benefits in various disease conditions, including PD. It exerts its anti-oxidative property in PD patients by either directly scavenging reactive oxygen species (ROS) or by upregulating the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhancing the activities of antioxidant enzymes. Also, vitexin activates the ERK1/1 and phosphatidyl inositol-3 kinase/Akt (PI3K/Akt) pro-survival signalling pathway, which upregulates the release of anti-apoptotic proteins and downregulates the expression of pro-apoptotic proteins. It could be antagonistic to protein misfolding and aggregation. Studies have shown that it can also act as an inhibitor of monoamine oxidase B (MAO-B) enzyme, thereby increasing striatal dopamine levels, and hence, restoring the behavioural deficit in experimental PD models. Such promising pharmacological potential of vitexin could be a game-changer in devising novel therapeutic strategies against PD. This review discusses the chemistry, properties, sources, bioavailability and safety profile of vitexin. The possible molecular mechanisms underlying the neuroprotective action of vitexin in the pathogenesis of PD alongside its therapeutic potential is also discussed.

MPTP-induced mouse model of Parkinson's disease: A promising direction of therapeutic strategies.

Among the popular animal models of Parkinson's disease (PD) commonly used in research are those that employ neurotoxins, especially 1-methyl- 4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). This neurotoxin exerts it neurotoxicity by causing a barrage of insults, such as oxidative stress, mitochondrial apoptosis, inflammation, excitotoxicity, and formation of inclusion bodies acting singly and in concert, ultimately leading to dopaminergic neuronal damage in the substantia nigra pars compacta and striatum. The selective neurotoxicity induced by MPTP in the nigrostriatal dopaminergic neurons of the mouse brain has led to new perspectives on PD. For decades, the MPTP-induced mouse model of PD has been the gold standard in PD research even though it does not fully recapitulate PD symptomatology, but it does have the advantages of simplicity, practicability, affordability, and fewer ethical considerations and greater clinical correlation than those of other toxin models of PD. The model has rejuvenated PD research and opened new frontiers in the quest for more novel therapeutic and adjuvant agents for PD. Hence, this review summarizes the role of MPTP in producing Parkinson-like symptoms in mice and the experimental role of the MPTP-induced mouse model. We discussed recent developments of more promising PD therapeutics to enrich our existing knowledge about this neurotoxin using this model.