In Chronic Kidney Disease, vascular calcification (VC) is highly prevalent even at early stages and is gradually enhanced, along with disease progression to End-Stage Renal Disease (ESRD). The calcification pattern in uremia includes all types of mineralization and contributes to the heavy cardiovascular (CV) burden that is common in these patients. Ectopic mineralization is the result of the imbalance between inhibitors and promoters of vascular calcification, with the latter overwhelming the former. The most powerful, natural inhibitor of calcification is Matrix Gla Protein (MGP), a small vitamin K dependent protein, secreted by chondrocytes and vascular smooth muscle cells. In uremia, MGP was reported as the only molecule able to reverse VC by "sweeping" calcium and hydroxyapatite crystals away from the arterial wall. check details To become biologically active, this protein needs to undergo carboxylation and phosphorylation, reactions highly dependent on vitamin K status. The inactive form of MGP reflects deficiency of vitamin K and has been associated with CV events and mortality in ESRD patients. During the past decade, vitamin K status has emerged as a novel risk factor for vascular calcification and CV disease in various populations, including dialysis patients. This review presents the evidence regarding the association between vitamin K and CV disease in ESRD patients, which are prone to atherosclerosis and atheromatosis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Normal pregnancy is associated with increased insulin resistance as a metabolic adaptation to the nutritional demands of the placenta and fetus, and this is amplified in obese mothers. Insulin resistance is normally compensated for by an adaptive increase in pancreatic β-cell mass together with enhanced glucose-stimulated insulin release. Placentally-derived hormones and growth factors are central to the altered pancreatic morphology and function. A failure of β-cells to undergo adaptive change after first trimester has been linked with gestational diabetes. In the pregnant mouse an increase in β-cell replication contributes to a 2-3-fold increase in mass peaking in late gestation, depending on proliferation of existing β-cells, the differentiation of resident progenitor β-cells, or islet cell trans-differentiation. Using mouse models and human studies placenta- and islet of Langerhans-derived molecules have been identified that are likely to contribute to the metabolic adaptations to pregnancy and whose physiology is altered in the obese, glucose intolerant mother. Maternal obesity during pregnancy can create a pro-inflammatory environment that can disrupt the response of the β-cells to the endocrine signals of pregnancy and limit the adaptive changes in β-cell mass and function, resulting in an increased risk of gestational diabetes. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Inflammatory Bowel Disease (IBD) is an umbrella term used to describe disorders that involves Crohn's disease (CD) ulcerative colitis (UC) and pouchitis. The disease occurrence is more prevalent in working group population which not only hampers the well being of an individual but also have negative economical impact on society. The current drug regime used therapy is very costly owing to chronic nature of the disease leading to several side effects. The condition gets more aggravated due to lower concentration of drug at desired site. Therefore, in present scenario, a therapy is needed which can maximize efficacy, adherence and quality of life, minimize toxicity and doses, helpful in maintaining and stimulating physical growth of mucosa with minimum disease complications. In this aspect, nanotechnology intervention is one of promising field as it can act as carrier to reduce toxicity, doses and frequency which in turn help in faster recovery. Moreover, nanomedicine and nanodiagnostic techniques will further open a new window for treatment in understanding pathogenesis along with better diagnosis which is poorly understood till now. Therefore present review is more focused toward recent advancement in IBD by application of nanotechnology. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Nature offered mankind the first golden era of discovery of novel antimicrobials based on the ability of eukaryotes or micro-organisms to produce such compounds. The microbial world proved to be a huge reservoir of such antimicrobial compounds which play important functional roles in every environment. However, most of those organisms are still uncultivable in the classical way and therefore the use of extended culture or DNA based methods (metagenomics) to discover novel compounds promises usefulness. In the past decades, the advances in next generation sequencing and bioinformatics revealed the enormous diversity of the microbial worlds and the functional repertoire available for studies. Thus, data-mining becomes of particular interest in the context of the increased need for new antibiotics due to antimicrobial resistance and the rush in antimicrobial discovery. In this review, we will present an overview of the environmental sources to discover new natural compounds from the microbiome, the culture-based and culture independent (metagenomic) approaches that have been developed to identify new antimicrobials, the input of those methods in the field and their limitations. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.AIMS The purpose of this study was to investigate the influences of apigenin on proliferation, differentiation and function of renal fibroblast after TGF-β1 stimulation and to uncover the underlying mechanisms. BACKGROUND Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. OBJECTIVE Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. METHOD Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 µM) followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed.