Malaria is one of the major public health problems caused by parasites belonging to plasmodium genus in the tropical and subtropical countries. Advancement of nanotechnology is opening up a window of huge opportunities for better treatment of malaria. Different nano drug delivery systems such as liposomes, solid lipid nanoparticles, dendrimer, nano-emulsion and polymeric nanoparticles are widely investigated for treating malaria. In this review, the recent advances in nanomedicine for antimalarial drug delivery are summarised.

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Neural development is a multi-factorial process, one that is governed by several interconnected factors. Fate of neural progenitor cells is determined by an intricate interplay between developmental genes, promoters, transcription factors, and epigenetic modifiers that act as transcription activators or silencers. Gradients of signalling molecules such as - SONIC HEDGEHOG, Retinoic Acid, BMP4, WNT and NOGGIN are generated during development and differentiat on, these bind to their cognate receptors leading to activation or repression of specific genes necessary for differentiation. Silencing of nonlineage sp cific genes is a key factor in maintaining the identity of a cell during subsequent proliferation and maturation post gastrulation. Gene silencing or repression of genes can be carried out by nucleotide modifications (cytosine methylation), histone modifications (acetylation, methylation, phosphorylation and ubiquitylation) and/or heterochromatization. Histone modifiers such as Polycomb Group proteins (PcGs), Histone Acetyltransferases (HAT), Histone Deacetylases (HDAC) regulate gene expression in early development as well as play an important role in adult organism. Polycomb Group proteins (PcGs) bring aboutgene repression by catalysing histone modifications such as di- and trimethylation on histone H3 (H3K27me2 and H3K27me3) and mono-ubiquitylation of histone H2A (H2AK119Ub) at the promoters of specific genes. In this review, we would discuss the activity of Polycomb group (PcG) proteins in neurogenesis, their role in histone modification and silencing of key development genes to bring about precise development and differentiation.

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Neural plasticity refers to the brain’s ability to make new cellular connections. Drugs that can induce neural plasticity are of basic as well as clinical interest. Lithium, a drug already in use, has been demonstrated to be neuroprotective and is likely to find wider use. The spectrum of diseases that can be potentially treated with lithium suggests that there could be a common cellular mechanism, such as neural plasticity, in operation. We review effects of lithium on major cellular processes that comprise neuroplasticity – alterations, in vitro and in vivo, in neurites, axons and synapse formation. Lithium is known to support extension of cytoplasmic outgrowths. Lithium alters patterns of axonal modifications including their extensions or retractions and sprouting of new branches. However, there are few studies directly demonstrating lithium action of synapse formation. The molecular basis of lithium action is complex with various pathways involved in cross talk. Of these multiple pathways, we have focused on lithium induced inhibition of glycogen synthase kinase-3β, block of inositol phosphate pathway and up regulation of neurotrophins as there are direct evidences of involvement of these in lithium induced neuroplasticity. This review provides a bird’s eye view of studies that could provide insight into special aspect of lithium action, induction of plasticity, which have implication for treating a wide variety of neurological conditions

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Cancer research is primarily dependent on rodent models. There has been a huge advancement in anticancer drug discovery in the last two decades, which is mainly due to improved animal models and introduction of non-invasive imaging technologies. Non-invasive imaging technology plays an important role in cancer and other biomedical research areas including neurology, cardiology, nanotechnology and stem cell biology. The intricate pathways in cancer initiation, progression and metastasis can be visualized and the processes can be analyzed quantitatively using these techniques. Robust preclinical data is the backbone of anticancer drug discovery, which can be obtained precisely using imaging technology. This review is focused on the dedicated preclinical imaging modalities such as Positron Emission Tomography (PET), Single Photon Emission Computed Tomography (SPECT), X-ray Computed Tomography (CT), Magnetic Resonance Imaging (MRI), Optical imaging and Cerenkov imaging. This paper discusses their present roles in basic and translational research towards evaluation of suitability of target molecules for further clinical trials.The unique features of the imaging modalities enable them to provide information necessary for understanding structural, functional and molecular processes involved in various stages of cancer development thus bridging the gap between bench and bedside.

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Klotho, the anti-aging gene, has various roles, one of them being a tumor suppressor. Dysregulation of insulin/insulin growth factor-1 (IGF-1), Wnt and fibroblast growth factor (FGF) signalling is major contributor to cancer. The tumor suppressor effects of Klotho have been attributed to its ability to modulate these pathways. In cancer cells, Klotho gene is silenced primarily through promoter hypermethylation. The ectopic expression or the restoration of Klotho directly corresponds to reduction in cancer. This implies its role in cancer therapeutics. In this article, the role of Klotho in oral and gastrointestinal cancers has been reviewed.

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