This work focused on exploring the bioenergy potential of biomass produced on salt-affected soils by growing two types of grasses, namely Parthenium hysterophorus (carrot grass) and Pennesetum benthiumo (mott grass), without using fertilizers or pesticides. The whole plant biomass of both grasses was pyrolyzed at three heating rates (10, 30, and 50 °C min⁻¹) in a joined Thermogravimetry–Differential Scanning Calorimetry (TGA–DSC) analyzer under an inert (nitrogen) environment. The pyrolysis of both grasses was shown to occur in a three-stage process, while most of the thermal transformation occurred at the temperature range of 240–400 °C. The pyrolytic behavior was assessed by estimating the kinetic parameters, using the isoconversional models of Kissenger–Akahira–Sunose and Ozawa–Flynn–Wall. The average values of the activation energy of carrot and mott grasses were shown to be 267 kJ mol⁻¹ (R² ≥ 0.98) and 188 kJ mol⁻¹ (R² ≥ 0.98), indicating the suitability of both grasses for co-pyrolysis. Whereas, the difference in the values of enthalpy change and the activation energy was shown to be <~5 kJ mol⁻¹ at each fractional point, which indicated that the product formation was being favored. Moreover, the high heating values of carrot grass (18.25 MJ kg⁻¹) and mott grass (18.63 MJ kg⁻¹) have shown a remarkable bioenergy potential and suitability of co-pyrolysis for both grasses. This study will lead to establishing an energy-efficient and cost-effective process for the thermal transformation of biomass to bioenergy.

Alzheimer's disease (AD) is a chronic neurodegenerative disorder that is marked by cognitive dysfunctions and the existence of neuropathological hallmarks such as amyloid plaques, and neurofibrillary tangles. It has been observed that a persistent immune response in the brain has appeared as another neuropathological hallmark in AD. The sustained activation of the microglia, the brain’s resident macrophages, and other immune cells has been shown to aggravate both tau and amyloid pathology and may consider as a connection in the AD pathogenesis. However, the basic mechanisms that link immune responses in the pathogenesis of AD are unclear until now since the process of neuroinflammation can have either a harmful or favorable effect on AD, according to the phase of the disease. Numerous researches recommend that nutritional fruits, as well as vegetables, possess neurodefensive properties against the detrimental effects of neuroinflammation and aging. Moreover, these effects are controlled by diverse phytochemical compounds that are found in plants and demonstrate anti-inflammatory, neuroprotective, as well as other beneficial actions. In this review, we focus on the link of neuroinflammation in AD as well as highlight the probable mechanisms of alkaloidal phytochemicals to combat the neuroinflammatory aspect of AD.

Egg yolk peptides were successfully prepared from egg yolk protein by-products after lecithin extraction. Defatted egg yolk protein was hydrolyzed with pepsin and pancreatin and purified by gel filtration to produce egg yolk gel filtration fraction (EYGF-33) with antiproliferative activity. The highlight of this study was that the peptide EYGF-33 (1.0 mg/ml) significantly inhibits cell viability of colon cancer cells (Caco-2) with no inhibitory effects on the viability of human colon epithelial normal cells (HCEC) after 48 h. Reduced cell viability can be explained by cell cycle arrest in the S-phase in which DNA replication normally takes place. EYGF-33 significantly enhanced the production of superoxide anions in the mitochondria of Caco-2 cells; this could activate a mitochondrial apoptotic pathway leading to typical Poly Adenosine diphosphate-ribose polymerase (PARP) cleavage as observed in the Western blot result. The induction of apoptotic cell death by EYGF-33 was supported by the externalization of phosphatidylserine (PS). However, further elucidation of the mechanism of EYGF-33-mediated apoptosis would provide further support for its use as a potential therapeutic and chemopreventive agent.