Pharmacogenomics and personalised medicine are emerging as important tools in individualised drug therapy. Many of the genes which encode drug metabolising enzymes, transporters and receptors are polymorphic. Individuals with polymorphic genes are likely to experience therapeutic failure or drug toxicity. This is clinically important for drugs with low safety margin such as oral anticoagulants, anti-epileptics and anticancer drugs. Prior genetic testing may help to predict responders and non-responders to the above mentioned drugs, besides avoiding drug toxicity. CIDRF is planning to introduce CYP2C9, CYP2C19 and CYP2D6 genetic testing shortly, which shall help to integrate pharmacogenomics with clinical practice.

Recent understandings in the genetic basis of diseases emphasize the need for potential therapeutic strategies. Latest molecular techniques such as RNA interference, gene therapy and gene editing that can modify nucleic acids within disease affected tissues can have great potential for treating genetic disorders. In this context, the present review summarizes the tools available for human gene editing and advances in research with reference to CRISPR/Cas9 based human genome editing. This review also discusses various ethical concerns associated with human gene editing.

microRNAs, small non-coding RNAs, have recently emerged as powerful regulators in a variety of cellular processes especially important roles in disease and tissue remodeling. Apart from involvement in a variety of biological processes, microRNAs were early recognized for their potential use as biomarkers in disease diagnostics and prognosis. Currently, there are number of microRNAs helping clinicians to determine the origins of cancer in disseminated tumors. The development of microRNA therapeutics has proved more challenging mainly due to delivery issues. This review focuses on the potential role of as clinical diagnostic and prognostic biomarkers. In addition, it highlights the microRNA profiling techniques, thereby leading to the advance opportunities to safely pursue microRNA as therapeutic modalities.

Successful completion of the Human Genome Project gave the hope for development of novel therapeutics, diagnostics for the welfare of humankind. Individual genetic studies and genome wide association studies revealed the genetic risk factors for various diseases which can be used in predetermination. This eventually led to the growth of pharmacogenomics that confers individual drug dosage adjustment preventing from adverse effects. However, it addresses only the hitches raised by the underlying genetic sequence but not external factors that influences the genotypic and phenotypic expression. Epigenetic research deals with these factors and studies the modifications caused along with their phenotype. These modifications are reversible which can be used as target for therapeutics, thus improving the treatment strategies of various diseases. In this review, we attempt to discuss the use of epigenetic modifications as drug targets and their mechanism of action.

Understanding the nature of memory storage is one of the holy grails of modern neuroscience. It has long been recognized that memory storage would involve structural changes in the brain. The development of fluorescence labeling and in vivo imaging techniques have shed unprecedented light on how sub-cellular structures in the brain are modified in an experience dependent manner. Here, I review some of the recent findings on the nature of memory traces in the mammalian brain.

Music therapy is a rapidly gaining acceptance in clinical setting due to its emerging supportive evidence and harmless nature of the therapy. Understanding the effects of sounds (both musical sounds and “noise”) on neonatal development, physiology, and behaviour has made it possible to apply music for therapeutic purposes in neonates. Music therapy has showed positive effects on heart rates, blood pressure, respiratory rates, oxygen saturation, stress-reduction, pain-control, hospital stay, etc. in neonates admitted in NICUs in different studies. In NICUs, masking of ambient noise is also an important effect. Music therapy positively influences neonatal feeding behaviour and weight gain. Recorded instrumental music and vocal music (including mother's voice) is used more commonly, however, live music therapy by qualified music therapists seems to be more promising due to obvious reasons. Mothers’ singing seems to be a convenient, acceptable and cost-effective option. Music therapy to mothers also benefits neonates. This article aims to discuss applications of music therapy in neonatology. Limitations, unanswered questions, and need for further research in Indian settings are also discussed.

If you thought vegetables only grew in soil on land, you\'re mistaken. Simple to cook and easy to serve in your favourite dishes, sea vegetables are plentiful, full of flavour and have a gamut of health benefits. Nutritionists and chefs around the world consider sea vegetables as pearls of the vegetable family as they add depth to cooking repertoire. Sea vegetables are neither plant nor animals but classified in a group known as ‘algae’ popularly “Seaweeds”. They commonly grow on coral reefs or in rocky landscapes and can be found in the sea. This article provides an overview of edible seaweeds.

Natural herbs have been widely used in orthopedic clinical practice in India, China and other countries since ancient times. The increase of aging population and the prevalence of osteoporosis, demands new therapeutic agents and nutritional supplements for the promotion of bone health. The Indian diet includes rich medicinal herbs. This review intends to highlight scienti.c information on naturally-occurring herbs like onion, garlic, clover, walnut, beans etc., consumed regularly in Indian diet which has been documented to possess osteoprotective properties. Focus has been put on literature available in the last ten years on Indian medicinal plants used for bone metabolic disorders like osteoporosis.

Glioblastoma multiforme (GBM) are one of the most refractory brain tumors characterized by aggressive invasive growth and resistance to therapy. These tumors are highly heterogeneous at the molecular and histological levels. Specific hallmarks like necrosis and microvascular proliferation distinguish GBM from lower-grade gliomas. GBMs are one of the most hypoxic as well as angiogenic tumors. GBMs consist of specific niches within the tumor microenvironment that regulates metabolic needs, tumor survival and invasion, as well as cancer stem cell (CSC) maintenance. This review features the distinct GBM niches, the functional status of the vasculature, and discusses the prospects of therapeutically targeting GBM niche constituents.

Glioblastoma Multiforme (GBM) is an aggressive, lethal brain tumor. Cellular metabolism is the major process affected during tumorigenesis. It is recently revealed that oncogenic signaling pathways are unswervingly involved in metabolic reprogramming of tumors. In GBM, metabolic pathways are reprogrammed and the underlying mechanisms causing these changes are yet to be unraveled. Interestingly, the pentose phosphate pathway in GBM shows differential association with glycolysis. This review discusses about the key metabolic enzymes and their association with several pathways in GBM highlighting the potential therapeutic targets.

Cancer is a disease where there is aberrant cellular behaviour characterized by uncontrolled growth and cellular signalling. Cancer though is viewed as a homogeneous pathology, does not show uniformity at the cellular level - there is difference in the characteristics within cells of a tumour. A major caveat in understanding the biology of cancer is the paucity of information on the origin and perpetuation of cancers. Towards salvaging these two models of cancer genesis and progression have been proposed: ‘Stochastic’ and ‘Cancer stem cell’ theories. The stochastic model holds that all cells in a tumour are identical while the cancer stem cell theory supports the existence of a subset of cells called cancer stem cells in a tumour that are responsible for the origin and perpetuation of the disease. Cancer stem cells are implicated in various aspects of cancer including metastasis, recurrence and therapeutic resistance. Though cancer stem cells have been reported from many cancers methods to identify and characterize them still rely on animal transplantation models along with surface protein studies. However better techniques of characterization of these cells would play a positive role in elucidating these cells better. The characterization of cancer stem cells would play an important role in the research and clinical management of the disease.

Mannose-binding lectin (MBL) is an important arm of innate immunity and plays a vital role in the first line of host defense. Genetic variation in MBL2 have been shown to associate with many infectious diseases, autoimmune and inflammatory disorders such as malaria, leishmaniasis, leprosy, tuberculosis, filariasis, HIV, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). MBL has been shown to bind with glycoconjugates on the surface of mannose rich microbes and deficiency of MBL has been associated with susceptibility and modulating the severity in bacterial, fungal, protozoan and viral infections. Many different approaches are being used to define ‘MBL deficiency’. It is more relevant in young children in whom immune system fails to mount an effective response to carbohydrate antigens. MBL replacement therapy has been tried in the past for patients with MBL deficiency. Currently, production of recombinant MBL is underway and provides a hope for children with innate immune disorders.

Obesity is linked to a variety of metabolic disorders, such as insulin resistance and atherosclerosis. The increased incidence of obesity has led to rise in interest in the biology of white adipose tissue (WAT). The tissue is no longer considered as a passive fat storage tissue but is a key endocrine and signaling organ secreting a multiplicity of protein factors called adipokines. In obesity, there is an enhanced secretion of a number of adipokines underpinning the role of inflammation in white adipose tissue towards the development of obesity and associated diseases. There is a substantial evidence, particularly from animal studies, that hypoxia develops in adipose tissue as the tissue mass expands in obesity, and the reduction in PO2 is considered to underlie the inflammatory response. The cells present within the WAT respond to hypoxia, by inhibiting the differentiation of pre-adipocytes to adipocytes and instead being transformed into leptin-secreting cells. The dynamic change found in the adipose tissue can be referred to as “adipose tissue remodeling,” in which stromal cells change dramatically in number and type during the course of obesity. Among stromal cells, infiltration of macrophages in the adipose tissue precedes the development of insulin resistance in animal models, suggesting that they are responsible for obesity-related adipose tissue inflammation. Understanding the molecular mechanism underlying adipose tissue remodeling may lead to the identification of novel, therapeutic strategies to prevent obesity-induced adipose tissue inflammation.

Obesity is linked to a variety of metabolic disorders, such as insulin resistance and atherosclerosis. The increased incidence of obesity has led to rise in interest in the biology of white adipose tissue (WAT). The tissue is no longer considered as a passive fat storage tissue but is a key endocrine and signaling organ secreting a multiplicity of protein factors called adipokines. In obesity, there is an enhanced secretion of a number of adipokines underpinning the role of inflammation in white adipose tissue towards the development of obesity and associated diseases. There is a substantial evidence, particularly from animal studies, that hypoxia develops in adipose tissue as the tissue mass expands in obesity, and the reduction in PO2 is considered to underlie the inflammatory response. The cells present within the WAT respond to hypoxia, by inhibiting the differentiation of pre-adipocytes to adipocytes and instead being transformed into leptin-secreting cells. The dynamic change found in the adipose tissue can be referred to as “adipose tissue remodeling,” in which stromal cells change dramatically in number and type during the course of obesity. Among stromal cells, infiltration of macrophages in the adipose tissue precedes the development of insulin resistance in animal models, suggesting that they are responsible for obesity-related adipose tissue inflammation. Understanding the molecular mechanism underlying adipose tissue remodeling may lead to the identification of novel, therapeutic strategies to prevent obesity-induced adipose tissue inflammation.