was 74 [95% CI [67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82] for plasmepsin 2 and 42 [37][38][39][40][41][42][43][44][45][46] for plasmepsin 3-1) than with MDR1 inhibition for plasmepsin 2 and 29 [24][25][26][27][28][29][30][31][32][33][34] for plasmepsin 3-1; appendix pp 2, 4).In the previous studies, crt mutations associated with piperaquine resistance arose on a genetic background of amplified plasmepsin genes. 1,2 Together with our data, this finding suggests that although initial selection of plasmepsin and mdr1 copy number variations does not cause a resistant phenotype in itself, it generates a favourable P falciparum genetic background for crt mutations to arise.Altogether, our results recapitulate in vitro a complementary mechanism between plasmepsins, mdr1, and crt involved in piperaquine resistance, supporting the molecular epidemiological data in southeast Asia 1,2 and furthering understanding of how piperaquine drug resistance evolves.

BackgroundBackground: Alzheimer’s disease (AD) is the most common form of old age dementia. The formation of amyloid plaques (Aβ), neurofibrillary tangles and loss of basal forebrain cholinergic neurons are the hallmark events in the pathology of AD.Literature ReviewCholinergic system is one of the most important neurotransmitter system involved in learning and memory which preferentially degenerates in the initial stages of AD. Activation of cholinergic receptors (muscarinic and nicotinic) activates multiple pathways which result in post translational modifications (PTMs) in multiple proteins which bring changes in nervous system. Cholinergic receptors-mediated PTMs “in-part” substantially affect the biosynthesis, proteolysis, degradation and expression of many proteins and in particular, amyloid precursor protein (APP). APP is subjected to several PTMs (proteolytic processing, glycosylation, sulfation, and phosphorylation) during its course of processing, resulting in Aβ deposition, leading to AD. Aβ also alters the PTMs of tau which is a microtubule associated protein. Therefore, post-translationally modified tau and Aβ collectively aggravate the neuronal loss that leads to cholinergic hypofunction.ConclusionDespite the accumulating evidences, the interaction between cholinergic neurotransmission and the physiological significance of PTM events remain speculative and still needs further exploration. This review focuses on the role of cholinergic system and discusses the significance of PTMs in pathological progression of AD and highlights some important future directions.

The study revealed that BP improves memory and chavicine is a lead compound producing pharmacological effects of BP.

No abstract

With the onset of coronavirus disease in December 2019, the normal routine and lifestyle of the humans has adversely affected all over the world. This change in lifestyle not only increased the level of stress and anxiety, but also badly modified the eating habits during the lockdown period. This increased the rate of binge eating disorder in people who were already immune-compromised. This rapid communication aims to develop awareness among people to stay calm during this pandemic and eat healthy.