Immunogenic Modulations Induced by Prospective Anti-Malarial Herbal Extracts in Murine Model

Keeping in view the ever increasing problem of drug resistance and affordability of the antimalarial drugs by the poor mass, herbal medicines can become an important and alternative sustainable strategy for malaria treatment. Aqueous extracts of three Himalayan herbs― _Equisetum ravense_, _Artemisia vulgaris_ and _Centella asiatica_, with reported antimalarial property were screened for clinical efficacy against a local strain of _Plasmodium vivax_ antigen in murine model. _E. arvense_ extract was consistent in boosting phagocytic activity, nitric oxide generation, acid phosphatase and alkaline phosphatase activities in the peritoneal macrophages. The effectiveness of the rest herbals was discrete. A need for further detailed investigation to evaluate the clinical efficacy of these herbals seems essential

RAGE signaling contributes to neuroinflammation in infantile neuronal ceroid lipofuscinosis

AbstractPalmitoyl-protein thioesterase-1 (PPT1) deficiency causes infantile neuronal ceroid lipofuscinosis (INCL), a devastating childhood neurodegenerative storage disorder. We previously reported that neuronal apoptosis in INCL is mediated by endoplasmic reticulum-stress. ER-stress disrupts Ca2+-homeostasis and stimulates the expression of Ca2+-binding proteins. We report here that in the PPT1-deficient human and mouse brain the levels of S100B, a Ca2+-binding protein, and its receptor, RAGE (receptor for advanced glycation end-products) are elevated. We further demonstrate that activation of RAGE signaling in astroglial cells mediates pro-inflammatory cytokine production, which is inhibited by SiRNA-mediated suppression of RAGE expression. We propose that RAGE signaling contributes to neuroinflammation in INCL

An exploratory study on marketing strategies of selected home appliances at kolkata metropolitan

A study focuses on two aspects first, how existing marketing strategy provides a push the customer for selecting particular home appliances and the second one how demand on customers are motivated though using that marketing strategy. Because marketing strategies are just the ingredients which help to attract the consumer towards the product. So we conclude that our study focuses on two aspects first, how existing marketing strategy proves a push the customer for selecting particular home appliances and the second one how demand on customers are motivated though using that marketing strategy. In both cases, we found that there must be a strong correlation between the marketing strategies which prove a push or poke (shock- knock at the customer’s choice) while selecting a particular home appliance

Ccn2a is an injury-induced matricellular factor that promotes cardiac regeneration in zebrafish

The ability of zebrafish to heal their heart after injury makes them an attractive model for investigating the mechanisms governing the regenerative process. In this study, we show that the gene cellular communication network factor 2a (ccn2a), previously known as ctgfa, is induced in endocardial cells in the injured tissue and regulates CM proliferation and repopulation of the damaged tissue. We find that, whereas in wild-type animals, CMs track along the newly formed blood vessels that revascularize the injured tissue, in ccn2a mutants CM proliferation and repopulation are disrupted, despite apparently unaffected revascularization. In addition, we find that ccn2a overexpression enhances CM proliferation and improves the resolution of transient collagen deposition. Through loss- and gain-of-function as well as pharmacological approaches, we provide evidence that Ccn2a is necessary for and promotes heart regeneration by enhancing the expression of pro-regenerative extracellular matrix genes, and by inhibiting the chemokine receptor gene cxcr3.1 through a mechanism involving Tgfβ/pSmad3 signaling. Thus, Ccn2a positively modulates the innate regenerative response of the adult zebrafish heart

Palmitoyl protein thioesterase-1 deficiency impairs synaptic vesicle recycling at nerve terminals, contributing to neuropathology in humans and mice

Neuronal ceroid lipofuscinoses represent the most common childhood neurodegenerative storage disorders. Infantile neuronal ceroid lipofuscinosis (INCL) is caused by palmitoyl protein thioesterase-1 (PPT1) deficiency. Although INCL patients show signs of abnormal neurotransmission, manifested by myoclonus and seizures, the molecular mechanisms by which PPT1 deficiency causes this abnormality remain obscure. Neurotransmission relies on repeated cycles of exo- and endocytosis of the synaptic vesicles (SVs), in which several palmitoylated proteins play critical roles. These proteins facilitate membrane fusion, which is required for neurotransmitter exocytosis, recycling of the fused SV membrane components, and regeneration of fresh vesicles. However, palmitoylated proteins require depalmitoylation for recycling. Using postmortem brain tissues from an INCL patient and tissue from the PPT1-knockout (PPT1-KO) mice that mimic INCL, we report here that PPT1 deficiency caused persistent membrane anchorage of the palmitoylated SV proteins, which hindered the recycling of the vesicle components that normally fuse with the presynaptic plasma membrane during SV exocytosis. Thus, the regeneration of fresh SVs, essential for maintaining the SV pool size at the synapses, was impaired, leading to a progressive loss of readily releasable SVs and abnormal neurotransmission. This abnormality may contribute to INCL neuropathology