Cinnamaldehyde inhibits Enterococcus faecalis biofilm formation and promotes clearance of its colonization by modulation of phagocytes in vitro.

The nosocomial pathogen, Enterococcus faecalis plays a crucial role in the pathogenesis of variety of infections including endocarditis, urinary tract, and recurrent root canal infections. Primary virulence factors of E. faecalis such as biofilm formation, gelatinase production and suppression of host innate immune response can severely harm host tissue.

DDX3-mediated miR-34 expression inhibits autophagy and HBV replication in hepatic cells.

HBV entry to the host cells and its successful infection depends on its ability to modulate the host restriction factors. DEAD box RNA helicase, DDX3, is shown to inhibit HBV replication. However, the exact mechanism of inhibition still remains unclear.

Hepatitis B Virus X Protein Inhibits the Expression of Barrier To Autointegration factor1 via Upregulating miR-203 Expression in Hepatic Cells.

Hepatitis B virus (HBV) infection targets host restriction factors that inhibit its replication and survival. Previous studies have shown that barriers to autointegration factor1 (BANF1) inhibited the replication of herpes simplex virus and vaccinia virus by binding to phosphate backbone of dsDNA. To date, no reports are available for the interplay between BANF1 and HBV.

Biocidal activity of Ba-doped CeO NPs against and bacterial strains.

Mishandling of antibiotics often leads to the development of multiple drug resistance (MDR) among microbes, resulting in the failure of infection treatments and putting human health at great risk. As a response, unique nanomaterials with superior bioactivity must be developed to combat bacterial infections. Herein, CeO-based nanomaterials (NMs) were synthesized by employing cerium(iii) nitrate and selective alkaline ions.

Cloning of human ene in . required the removal of an intragenic Pribnow-Schaller Box before it's Insertion into genomic safe harbor AAVS1 site using CRISPR-Cas9.

Genomic safe harbors are sites in the genome which are safe for gene insertion such that the inserted gene will function properly, and the disruption of the genomic location doesn't cause any foreseeable risk to the host. The AAVS1 site is the genetic location which is disrupted upon integration of adeno associated virus (AAV) and is considered a 'safe-harbor' in human genome because about one-third of humans are infected with AAV and so far there is no apodictic evidence that AAV is pathogenic or disruption of AAVS1 causes any disease in man.  Therefore, we chose to target the AAVS1 site for the insertion of , a bile acid transporter which is defective in progressive familial intra hepatic cholestasis type-2 (PFIC-2), a lethal disease of children where cytotoxic bile salts accumulate inside hepatocytes killing them and eventually the patient.

Glibenclamide, ATP and metformin increases the expression of human bile salt export pump ABCB11.

Bile salt export pump (BSEP/ABCB11) is important in the maintenance of the enterohepatic circulation of bile acids and drugs. Drugs such as rifampicin and glibenclamide inhibit BSEP. Progressive familial intrahepatic cholestasis type-2, a lethal pediatric disease, some forms of intrahepatic cholestasis of pregnancy, and drug-induced cholestasis are associated with BSEP dysfunction.

Biocidal (bacterial and cancer cells) activities of chitosan/CuO nanomaterial, synthesized via a green process.

Biopolymer-based nanomaterials have been developed as antimicrobial and anticancer agents due to their advanced physical, chemical and biomedical characteristics. Herein, chitosan-copper oxide nanomaterial was, successfully synthesized by a green method. In this process, copper salt was nucleated with Psidium guajava leaves extract in order to form the nanomaterial in the chitosan network.

Inhibitory potential of EGCG on Streptococcus mutans biofilm: A new approach to prevent Cariogenesis.

Dental caries is a common cause for tooth loss and Streptococcus mutans is identified as the etiologic pathogen. This study evaluates the inhibitory potential of Epigallocatechin gallate (EGCG) on S.mutans glucansucrase enzyme and its biofilm.

TGF-β induces liver fibrosis via miRNA-181a-mediated down regulation of augmenter of liver regeneration in hepatic stellate cells.

Objective: To study the role of miRNA-181a and augmenter of liver regeneration in TGF-β-induced fibrosis in hepatic stellate cells.

Methods: LX2 cells were treated with 20 ng/ml TGF-β for 24 h. miRNA-181a, ALR plasmid and empty vectors were transfected using siPORT NeoFx reagent.

Anticancer potential of NF-κB targeting apoptotic molecule "flavipin" isolated from endophytic Chaetomium globosum.

Background: Anticancer compounds from natural sources have drawn attention due to their structural diversity and relatively lesser side effects. Endophytic fungi are one such natural resource from, which plethoras of anticancerous compounds have been isolated.

Purpose: The objective of the study was to isolate and characterize the bioactive metabolite from Chaetomium globosum that exhibits astonishing antiproliferative activity against cancerous cell lines.

Augmenter of liver regeneration: A key protein in liver regeneration and pathophysiology.

Liver is constantly exposed to pathogens, viruses, chemicals, and toxins, and several of them cause injury, leading to the loss of liver mass and sometimes resulting in cirrhosis and cancer. Under physiological conditions, liver can regenerate if the loss of cells is less than the proliferation of hepatocytes. If the loss is more than the proliferation, the radical treatment available is liver transplantation.

Triiodothyronine stimulates VEGF expression and secretion via steroids and HIF-1α in murine Leydig cells.

Unlabelled: Leydig cells are the principal steroidogenic cells of the testis. Leydig cells also secrete a number of growth factors including vascular endothelial growth factor (VEGF) which has been shown to regulate both testicular steroidogenesis and spermatogenesis. The thyroid hormone, T is known to stimulate steroidogenesis in Leydig cells.

Global microRNA expression profiling in the liver biopsies of hepatitis B virus-infected patients suggests specific microRNA signatures for viral persistence and hepatocellular injury.

Unlabelled: Hepatitis B virus (HBV) can manipulate the microRNA (miRNA) regulatory networks in infected cells to create a permissive environment for viral replication, cellular injury, disease onset, and its progression. The aim of the present study was to understand the miRNA networks and their target genes in the liver of hepatitis B patients involved in HBV replication, liver injury, and liver fibrosis. We investigated differentially expressed miRNAs by microarray in liver biopsy samples from different stages of HBV infection and liver disease (immune-tolerant [n = 8], acute viral hepatitis [n = 8], no fibrosis [n = 16], early [F1+F2, n = 19] or late [F3+F4, n = 14] fibrosis, and healthy controls [n = 7]).

Effect of Mg(2+), Ca(2+), Sr(2+) and Ba(2+) metal ions on the antifungal activity of ZnO nanoparticles tested against Candida albicans.

The antifungal ability of pure and alkaline metal ion (Mg(2+), Ca(2+), Sr(2+) and Ba(2+)) doped ZnO nanoparticles (NPs) prepared by the co-precipitation method was tested against the pathogenic yeast, Candida albicans (C. albicans), and the results showed that the Mg-doped ZnO NPs possessed greater effect than the other alkaline metal ion doped ZnO NPs. The impact of the concentration of Mg doped ZnO sample on the growth of C.

Hepatitis B virus induces cell proliferation via HBx-induced microRNA-21 in hepatocellular carcinoma by targeting programmed cell death protein4 (PDCD4) and phosphatase and tensin homologue (PTEN).

Hepatitis B viral infection-induced hepatocellular carcinoma is one of the major problems in the developing countries. One of the HBV proteins, HBx, modulates the host cell machinery via several mechanisms. In this study we hypothesized that HBV enhances cell proliferation via HBx-induced microRNA-21 in hepatocellular carcinoma.

Impact of alkaline metal ions Mg, Ca, Sr and Ba on the structural, optical, thermal and antibacterial properties of ZnO nanoparticles prepared by the co-precipitation method.

Pure ZnO and alkaline metal ion (Mg, Ca, Sr and Ba)-doped ZnO nanoparticles (NPs) were synthesized by the co-precipitation method. The synthesized nanoparticles retained the wurtzite hexagonal structure, which was confirmed by X-ray diffraction studies. The micro-strain properties were analyzed through Williamson-Hall analysis.

Lentivirus-mediated superoxide dismutase1 gene delivery protects against oxidative stress-induced liver injury in mice.

Background: The exposure of liver to hepatotoxins, and their subsequent metabolism, results in increased reactive oxygen species (ROS), one of the major culprits in causing both acute liver cell injury and chronic liver diseases. The aim of this present study is to investigate the protective effects of lentiviral vector-mediated copper-zinc superoxide dismutase (LV-SOD1) gene transfer against ROS-induced cytotoxicity in Hep G2 cells and liver injury in mice.

Methods: In vitro SOD1 efficacy was tested against two ROS-generating systems: hypoxanthine/xanthine oxidase (HX/XO) and hydroxyethyl radicals (HER), whereas in vivo SOD1 efficacy was evaluated in carbon tetrachloride (CCl4)-induced liver injury in C57BL/6 mice.

Macrophage conditioned medium induces the expression of C-reactive protein in human aortic endothelial cells: potential for paracrine/autocrine effects.

C-reactive protein (CRP) is a risk marker for cardiovascular events in apparently healthy persons. Cogent data show that, aside from the liver, CRP is produced in atherosclerotic lesions, kidney, neurons, and alveolar macrophages. Because several proatherogenic effects of CRP have been documented in endothelial cells, we examined human aortic endothelial cells (HAEC) for CRP production.

Effect of C-reactive protein on vascular cells: evidence for a proinflammatory, proatherogenic role.

Purpose Of Review: C-reactive protein (CRP) is the prototypic downstream marker of inflammation. High levels of CRP predict future cardiovascular risk in apparently healthy men and women. Recent evidence from different cell types suggests that CRP is not only a risk marker but may also be a participant in atherogenesis.

RRR-alpha-tocopherol decreases the expression of the major scavenger receptor, CD36, in human macrophages via inhibition of tyrosine kinase (Tyk2).

The class B scavenger receptor, CD36, binds to oxidized LDL (OxLDL), is present in atherosclerotic lesions, and is upregulated by OxLDL or AcLDL. Previously we have shown that RRR-alpha-tocopherol (AT) enrichment of human monocyte-derived macrophages inhibited OxLDL or AcLDL induced CD36 expression. The mechanism by which AT inhibited CD36 expression is not known.

C-reactive protein decreases prostacyclin release from human aortic endothelial cells.

Background: In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs).

Alpha-tocopherol decreases superoxide anion release in human monocytes under hyperglycemic conditions via inhibition of protein kinase C-alpha.

Diabetes is a major risk factor for premature atherosclerosis, and oxidative stress appears to be an important mechanism. Previously, we showed that diabetic monocytes produce increased superoxide anion (O(2)(-)), and alpha-tocopherol (AT) supplementation decreases this. The aim of this study was to elucidate the mechanism(s) of O(2)(-) release and inhibition by AT under hyperglycemic (HG) conditions in monocytes.

Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells.

Background: C-reactive protein (CRP), the prototypic marker of inflammation, has been shown to be an independent predictor of cardiovascular events. Endothelial nitric oxide synthase (eNOS) deficiency is a pivotal event in atherogenesis.

Methods And Results: We tested the effect of CRP on eNOS expression and bioactivity in cultured human aortic endothelial cells (HAECs).