BACKGROUND There is a significant dearth of clinical biochemistry researches to evaluate facility of exploitation of folate targeted radioactive gold-labeled anti-cancer drugs against various cancer cell lines. OBJECTIVE The aim of this paper was to develop a gold-based compound with an efficient therapeutic potential against the breast cancer. To this end, the synthesis of the 198Au/PAMAM-MPEG-FA composite was considered here.  https://www.selleckchem.com/products/sd-208.html  METHODS The radioactive gold (198Au) nanoparticles were encapsulated into Folic acid (FA)-targeted Polyamidoamine dendrimer (PAMAM) modified with Maleimide-Polyethylene glycol Succinimidyl Carboxymethyl ester (MPEG). After that, anticancer assessments of the prepared 198Au/PAMAM-MPEG-FA hybrid mater against breast cancer were investigated. Further studies were also devised to compare the anticancer capabilities of the 198Au/PAMAM-MPEG-FA composite with the synthesized P-MPEG, 197Au/P-MPEG, 197Au/P-MPEG-FA, 197Au/P-FA and 198Au/P-MPEG-FA conjugates. The prepared drugs were characterizedreast cancer, although further experimental and clinical investigations are required. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Nucleotide binding domain Leucine rich Repeat Protein 3 (NLRP3) plays a regulatory role in the immune and inflammatory responses, and has been implicated in Colorectal Cancer (CRC) progression and metastasis. However, the underlying molecular mechanisms have not been fully elucidated. METHODS In this study, we analyzed the expression levels of NLRP3 in human CRC tissues, and performed functional assays in CRC cell lines and a subcutaneous tumor model to elucidate its role in the development and progression of CRC. RESULTS In this study, we found that NLRP3 was significantly upregulated in human CRC tissues and was associated with tumor size and invasion, lymph node metastasis, venous invasion, neural invasion and TNM staging. Furthermore, knockdown of NLRP3 in CRC cells inhibited their migration and growth in vitro and in vivo, and reversed Epithelial-Mesenchymal Transition (EMT) in vitro. CONCLUSION Our findings indicate that NLRP3 likely regulates CRC metastasis by activating the EMT program, and is a potential therapeutic target. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.The liver is a vital organ for life and the only internal organ that is capable of natural regeneration. Although the liver has high regeneration capacity, excessive hepatocyte death can lead to liver failure. Various factors can lead to liver damage including drug abuse, some natural products, alcohol, hepatitis and autoimmunity. Some models for studying liver injury are APAP-based model, Fas ligand (FasL), D-galactosamine/endotoxin (Gal/ET), Concanavalin A, and carbon tetrachloride, based models. The regeneration of the liver can be carried out using umbilical cord blood stem cells, which have various advantages over other stem cell types used in liver transplantation. UCB-derived stem cells lack tumorigenicity, have karyotype stability and high immunomodulatory, low risk of graft versus host disease (GVHD), low risk of transmitting somatic mutations or viral infections, low immunogenicity. They are readily available and their collection is safe and painless. This review is focussed on recent development and modern trends for the use of umbilical cord stem cells for the regeneration of liver fibrosis. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.INTRODUCTION Cardiovascular, together with renal disease, claims a significant proportion of morbidity and mortality in association with type 2 diabetes mellitus (T2DM) and obesity. To improve on the long-term renal and cardiovascular outcome, there is the incorporation of bariatric surgery (BS), which seems to be a pivotal intervention. Areas explored Cohort studies and randomized controlled trial (RCT) research of BS among patients with T2DM, are investigated by screening, then information on renal effects and cardiovascular outcome gathered. Metabolic surgery (MS) and BS reduce both mortality and the risk of cardiovascular disorder, chronic kidney diseases and albuminuria. MS refers to a surgical approach whose primary intent is the control of metabolic alterations/hyperglycemia in contrast to BS which is a mere weight-reduction therapy. Patients suffering from poor glycaemic control and other macro and micro-vascular diseases will benefit from a surgical approach. The approach implicates hypertension glomerular remission, gut microbiota shift, reduced renal inflammation and fewer instances of chronic cardiac remodelling. CONCLUSION MS is beneficial where the main aim is to attain a significant and long-lasting weight loss results. The RCTs have depicted the superiority which surgical mechanisms hold over medically based therapy, for enhancing glycaemic control, and achieving remission of diabetes. This type of surgery improves life quality, reduces incidences of other obesity and diabetes relating diseases like microvascular illness, sleep apnea, fatal disorder, and fatty liver disease. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Infection with Shiga toxin-producing Escherichia coli (STEC) may cause hemorrhagic colitis, hemolytic uremic syndrome (HUS) and encephalopathy. The mortality rate derived from HUS adds up to 5% of the cases, and up to 40% when the central nervous system (CNS) is involved. In addition to the well-known deleterious effect of Stx, the gram-negative STEC releases lipopolysaccharides (LPS) and may induce a variety of inflammatory responses when released in the gut. Common clinical signs of severe CNS injury include sensorimotor, cognitive, emotional and/or autonomic alterations. In the last few years, a number of drugs have been experimentally employed to establish the pathogenesis of, prevent or treat CNS injury by STEC. The strategies in these approaches focus on 1) inhibition of Stx production and release by STEC, 2) inhibition of Stx bloodstream transport , 3) inhibition of Stx entry into the CNS parenchyma , 4) blockade of deleterious Stx action in neural cells, and 5) inhibition of immune system activation and CNS inflammation.