Glycation is the result of covalent bonding of a free amino group of biological macromolecules with a reducing sugar, which results in the formation of a Schiff base that undergoes rearrangement, dehydration and cyclization to form a more stable Amadori product. The final products of nonenzymatic glycation of biomacromolecules like DNA, proteins and lipids are known as advanced glycation end products (AGEs). AGEs may be generated rapidly or over long times stimulated by distinct triggering mechanisms, thereby accounting for their roles in multiple settings and disease states. Both Schiff base and Amadori glycation products generate free radicals resulting in decline of antioxidant defense mechanisms and can damage cellular organelles and enzymes. This critical review primarily focuses on the mechanistic insight of glycation and the most probable route for the formation of glycation products and their therapeutic interventions. Furthermore, the prevention of glycation reaction using therapeutic drugs such as metformin, pyridoxamine and aminoguanidine (AG) are discussed with special emphasis on the novel concept of the bioconjugation of these drugs like, AG with gold nanoparticles (GNPs). At or above 10 mM concentration, AG is found to be toxic and therefore has serious health concerns, and the study warrants doing this novel bioconjugation of AG with GNPs. This approach might increase the efficacy of the AG at a reduced concentration with low or no toxicity. Using the concept of synthesis of GNPs with abovementioned drugs, it is assumed that toxicity of various drugs which are used at high doses can be minimized more effectively.

The objective of this research was to determine the effect of zinc oxide nanoparticles (ZnONPs) and/or salicylic acid (SA) under arsenic (As) stress on rice (Oryza sativa). ZnONPs are analyzed for various techniques viz., X-ray diffraction (XRD), Fourier-transform infrared spectroscopy (FTIR), transmission electron microscopy (TEM), and scanning electron microscopy (SEM). All of these tests established that ZnONPs are pure with no internal defects, and can be potentially used in plant applications. Hence, we further investigated for better understanding of the underlying mechanisms and the extent of ZnONPs and SA induced oxidative stress damages. More restricted plant growth, gas exchange indices, significant reduction in the SPAD index and maximum quantum yield (Fv/Fm) and brutal decline in protein content were noticed in As-applied plants. In contrast, foliar fertigation of ZnONPs and/or SA to As-stressed rice plants lessens the oxidative stress, as exposed by subordinate levels of reactive oxygen species (ROS) synthesis. Improved enzymatic activities of catalase (CAT), peroxidase (POX), and superoxide dismutase (SOD), proline and total soluble protein contents under ZnONPs and SA treatment plays an excellent role in the regulation of various transcriptional pathways participated in oxidative stress tolerance. Higher content of nitrogen (N; 13%), phosphorus (P; 10%), potassium (K; 13%), zinc (Zn; 68%), manganese (Mn; 14%), and iron (Fe; 19) in ZnONPs and SA treated plants under As-stress, thus hampered growth and photosynthetic efficiency of rice plants. Our findings suggest that toxicity of As was conquering by the application of ZnONPs and SA in rice plants.

Vascular dementia (VaD) is the second most common form of dementia after Alzheimer’s disease (AD); where Alzheimer’s accounts for 60–70% of cases of dementia and VaD accounts for 20% of all dementia cases. VaD is defined as a reduced or lack of blood flow to the brain that causes dementia. VaD is also known occasionally as vascular contributions to cognitive impairment and dementia (VCID) or multi-infarct dementia (MID). VCID is the condition arising from stroke and other vascular brain injuries that cause significant changes to memory, thinking, and behavior, and VaD is the most severe stage while MID is produced by the synergistic effects caused by multiple mini strokes in the brain irrespective of specific location or volume. There are also subtle differences in the presentation of VaD in males and females, but they are often overlooked. Since 1672 when the first case of VaD was reported until now, sex and gender differences have had little to no research done when it comes to the umbrella term of dementia in general. This review summarizes the fundamentals of VaD followed by a focus on the differences between sex and gender when an individual is diagnosed. In addition, we provide critical evidence concerning sex and gender differences with a few of the main risk factors of VaD including pre-existing health conditions and family history, gene variants, aging, hormone fluctuations, and environmental risk factors. Additionally, the pharmaceutical treatments and possible mitigation of risk factors is explored.