Amaranthus hybridus waste solid biofuel: comparative and machine learning studies.

The diminishing supply of fossil fuels, their detrimental environmental effects, and the challenges associated with the disposal of agro-waste necessitated the development of renewable and sustainable alternative energy sources. This study aims at developing bio-briquettes from Amaranthus hybridus waste, with cassava starch as a binder; both are agricultural wastes. Before and following delignification, alkali-treated Amaranthus hybridus (TAHB) and untreated (UAHB) briquettes were evaluated in terms of combustion and physicochemical parameters. FTIR and SEM were utilized to monitor the morphological transformation and bond restructuring of TAHB and UAHB samples. EDXRF was used to assess the Potential Toxic Elements (PTEs) composition and environmental friendliness of both TAHB and UAHB. Furthermore, Adaptive Neuro-Fuzzy Inference System (ANFIS) and fuzzy c-means (FCM) clustering machine learning models were used to optimize the production process and predict the efficiency of bio-briquettes. After delignification, a lower lignin value of 11.47 ± 0.00% in TAHB compared to 12.31 ± 0.01% (UAHB) was recorded. Calorific values of 10.43 ± 0.25 MJ kg-1 (UAHB) and 12.53 ± 0.30 MJ kg-1 (TAHB) were recorded at p < 0.05. EDXRF results showed a difference of 0.016% in Pb concentration in both samples. SEM reveals morphological restructuring, while FTIR reveals a 4 cm-1 difference in the C-O stretch. The root mean square error (RMSE), mean absolute percentage error (MAPE), and mean absolute error (MAE) gave values of 0.0249, 2.104, and, 0.0249; (MAE, training) and 0.0223 (MAE, testing) respectively. This shows that the model's predictions match the reality, thereby suggesting a strong agreement between the predicted and experimental data. The finding of this study shows that delignification-disruption improved the solid biofuel's ability to burn cleanly and sustainably.

mGluR-dependent plasticity in rodent models of Alzheimer's disease.

Long-term potentiation (LTP) and depression (LTD) are currently the most comprehensive models of synaptic plasticity models to subserve learning and memory. In the CA1 region of the hippocampus LTP and LTD can be induced by the activation of either NMDA receptors or mGluR5 metabotropic glutamate receptors. Alterations in either form of synaptic plasticity, NMDAR-dependent or mGluR-dependent, are attractive candidates to contribute to learning deficits in conditions like Alzheimer's disease (AD) and aging. Research, however, has focused predominantly on NMDAR-dependent forms of LTP and LTD. Here we studied age-associated changes in mGluR-dependent LTP and LTD in the APP/PS1 mouse model of AD and in Octodon degu, a rodent model of aging that exhibits features of AD. At 2 months of age, APP/PS1 mouse exhibited robust mGluR-dependent LTP and LTD that was completely lost by the 8th month of age. The expression of mGluR protein in the hippocampus of APP/PS1 mice was not affected, consistent with previous findings indicating the uncoupling of the plasticity cascade from mGluR5 activation. In O. degu, the average mGluR-LTD magnitude is reduced by half by the 3 rd year of age. In aged O. degu individuals, the reduced mGluR-LTD correlated with reduced performance in a radial arm maze task. Altogether these findings support the idea that the preservation of mGluR-dependent synaptic plasticity is essential for the preservation of learning capacity during aging.

Comparative bioenergetic study of neuronal and muscle mitochondria during aging.

Mitochondrial respiratory chain defects have been associated with various diseases and with normal aging, particularly in tissues with high energy demands, including brain and skeletal muscle. Tissue-specific manifestation of mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction are hallmarks of mitochondrial diseases although the underlying mechanisms are largely unclear. Previously, we and others have established approaches for transferring mtDNA from muscle and synaptosomes of mice at various ages to cell cultures. In this study, we carried out a comprehensive bioenergetic analysis of cells bearing mitochondria derived from young, middle-aged, and old mouse skeletal muscles and synaptosomes. Significant age-associated alterations in oxidative phosphorylation and regulation during aging were observed in cybrids carrying mitochondria from both skeletal muscle and synaptosomes. Our results also revealed that loss of oxidative phosphorylation capacity may occur at various ages in muscle and brain. These findings indicate the existence of a tissue-specific regulatory mechanism for oxidative phosphorylation.