Waste-driven single crystalline sulphur-doped GQDs are synthesized via a green hydrothermal route with the highest quantum yield and excellent biocompatibility for bioimaging.
Uncontrolled seizure or epilepsy is intricately related with an increase risk of pharmacoresistant epilepsy. The failure to achieve seizure control with the first or second drug trial of an anticonvulsant medication given at the appropriate daily dosage is termed as pharmacoresistance, despite the fact that these drugs possess different modes of action. It is one of the devastating neurological disorders act as major culprit of mortality in developed as well as developing countries with towering prevalence. Indeed, the presence of several anti-epileptic drug including carbamazepine, phenytoin, valproate, gabapentin etc. But no promising therapeutic remedies available to manage pharmacoresistance in the present clinical scenario. Hence, utility of alternative strategies in management of resistance epilepsy is increased which further possible by continuing developing of promising therapeutic interventions to manage this insidious condition adequately. Strategies include add on therapy with adenosine, verapamil etc or ketogenic diet, vagus nerve stimulation, focal cooling or standard drugs in combinations have shown some promising results. In this review we will shed light on the current pharmacological and non pharmacological mediator with their potential pleiotropic action on pharmacoresistant epilepsy.
Reactive oxygen species (ROS) are an inevitable by-product of cellular metabolism. ROS generation can be associated with the interaction of ionizing radiation with biological molecules, and devoted enzymes in phagocytic cells (NADPH oxidase and myeloperoxidase) or may be the result of an imbalance between radical generating and scavenging systems. Typically ROS have been consider as Pandora's box, they have several innovative physiological roles in the body. ROS serve as signalling messengers for the activation of transcription factors from cytokine-receptor interactions. This facilitates the evolution and membrane fusion of spermatozoon and oocyte during fertilization. NADPH oxidase enzyme and nitric oxide (NO) function as potent vasodilators and immunity boosters. ROS have been suggested as prevalent regulators of several nuclear factors, including erythroid 2-related factor 2 (Nrf2), nuclear factor kappa-B (NFkB) cells, mitogen-activated protein kinase (MAPK) and p53, which are further associated with several signalling cascades. Under physiological conditions the amount of ROS generated in the body can be counterbalanced by natural antioxidants in the body. However, aberrant augmented levels of ROS predominantly lead to various defined disorders comprising myocardial infarction, autoimmune diseases, atherosclerosis, Alzheimer's and Parkinson's diseases and emphysema.Ordinarily, it is observed that the physiological roles of ROS are insubstantial compared with their pathological action. But there is a need to clearly define the line between pathological and physiological functions of ROS. Of particular worth is to reveal the beneficial responsibilities of ROS in different cellular pathways and metabolic functions, over its injurious consequences.
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Neurodegeneration is a complex neurological phenomenon characterized by disturbed coherence in neuronal efflux. Progressive neuronal loss and brain damage due to various age-related pathological hallmarks perturb the behavioral
balance and quality of life. Sirtuins have been widely investigated for their neuroprotective role, with SIRT1 being the most
contemplated member of the family. SIRT1 exhibits significant capabilities to enhance neurogenesis and cellular lifespan by
regulating various pathways, which makes it an exciting therapeutic target to inhibit neurodegenerative disease progression.
SIRT1 mediated neuronal fortification involves modulation of molecular co-factors and biochemical pathways responsible
for the induction and sustenance of pro-inflammatory and pro-oxidative environment in the cellular milieu. In this review,
we present the major role played by SIRT1 in maintaining cellular strength through the regulation of genomic stability, neuronal growth, energy metabolism, oxidative stress, inhibiting mechanisms and anti-inflammatory responses. The therapeutic
significance of SIRT1 has been put into perspective through a comprehensive discussion about its ameliorating potential
against neurodegenerative stimuli in a variety of diseases that characteristically impair cognition, memory and motor coordination. This review enhances the acquaintance concerned with the neuroprotective potential of SIRT1 and thus promotes
the development of novel SIRT1 regulating therapeutic agents and strategies.
Current study synthesized and investigated the effect of low-dose copper nanoparticles (CuNPs) against diabetes mellitus and -induced experimental micro- (nephropathy) and macro-vascular (cardio and endothelium) complications.
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