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In vitro effects of sEng and TGF-β on human umbilical vein endothelial cells and trophoblasts.

The aim of this study was to evaluate the in vitro effects of sEng and TGF-β on human umbilical vein endothelial cells (HUVECs) and trophoblasts.

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Human Umbilical Vein Endo GFP Expressing Human Umbi Mitochondria GFP Tag Huma Plasma Membrane GFP Tag H RFP Expressing Human Umbi Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Human Saphenous Vein Endo GFP Expressing Human Saph RFP Expressing Human Saph

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Investigating Effect of Rapamycin and Metformin on Angiogenesis in Hepatocellular Carcinoma Cell Line.

Human hepatocellular carcinoma is one of the most common causes of death in the world. Metformin and rapamycin may decrease the expression of VEGF protein and subsequently angiogenesis. The purpose of this study was to evaluate the effect of these two drugs on expression of VEGF protein and the cell proliferation in the hepatocellular carcinoma cell line (ATCC HB-8065). HepG2 was cultured in RPMI-1640 medium at 37°C for 48h as a pre-culture and then treated by different concentrations of metformin (0, 5, 10 and 20 mM) and rapamycin (0, 5, 10 and 20 nM) at different times (12, 24 and 48 h). Cell viability was assessed by the MTT assay. Total RNA was extracted by the Trizol reagent and VEGF gene expression was analyzed by quantitative real-time PCR and was calculated by 2 method. The VEGF protein level was determined by Elisa assay. Finally, Apoptosis index was calculated by DAPI staining. Metformin and rapamycin significantly decrease cancer cells viability (p<0.05). Rapamycin but not metformin decreases VEGF gene expression in HepG2 cells. Metformin and rapamycin significantly induce cell apoptosis in hepatocellular carcinoma (HCC) cells. Metformin and rapamycin have an anti-tumor effect on HCC. According to our data rapamycin might have an anti-angiogenesis effect via inhibition of VEGF expression. Our results provide an insight into future clinical strategies to improve chemotherapy outcomes in HCC.

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MiR-193a-3p functions as a tumour suppressor in human aldosterone-producing adrenocortical adenoma by down-regulating CYP11B2.

The mechanism of aldosterone-producing adrenocortical adenoma (APA) pathogenesis and the role of microRNAs (miRNAs) in APA pathogenesis have not been completely clarified. We examined the expression and function of miR-140-3p, miR-193a-3p and miR-22-3p, which have binding sites in CYP11B2. Expression of miRNAs and CYP11B2 mRNA was measured by quantitative reverse transcription PCR (qRT-PCR). Cell proliferation was monitored by colorimetric analysis, and cell apoptosis and cell cycle progression were analysed by flow cytometry. ELISA was carried out to detect aldosterone levels in cell culture supernatants. Luciferase reporter assays, qRT-PCR and Western blotting were performed to identify CYP11B2 as a target of miR-193a-3p. Of the three miRNAs examined, miR-193a-3p exhibited a significant decrease and CYP11B2 mRNA exhibited a significant increase in expression in APA compared with adjacent normal adrenal gland tissue. Transfection of miR-193a-3p mimic into the human adrenocortical cell line H295R showed that elevated miR-193a-3p expression inhibits proliferation and aldosterone secretion, induces G1-phase arrest and promotes apoptosis in H295R cells. Furthermore, in luciferase reporter assays, overexpression of miR-193a-3p in H295R cells significantly reduced the luciferase activity of the wild-type CYP11B2 3'-UTR construct, which could be reversed by mutation of the miR-193a-3p-binding site. Moreover, miR-193a-3p overexpression downregulated CYP11B2 mRNA and protein expression. Finally, overexpression of CYP11B2 diminished the effects of miR-193a-3p on H295R cells. Taken together, our results suggest that CYP11B2 levels may be modulated by miR-193a-3p in APA, which could explain, at least partially, why downregulation of miR-193a-3p during APA formation may promote cell growth and suppress apoptosis.

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Goat Anti-Human AS160 TBC Goat Anti-Human ASF1A HSP Goat Anti-Human, Mouse As Goat Anti-Human ASRGL1 AL Goat Anti-Human, Mouse, R Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon anti CD16 monoclonal anti Human Macrophage Inflamma Human Macrophage Inflamma Human Interleukin-32 alph Human Interleukin-1-alpha

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MicroRNA-155 inversely correlates with esophageal cancer progression through regulating tumor-associated macrophage FGF2 expression.

Esophageal cancer (EC) is one of the most common malignancies with high incidence and mortality. Tumor-associated macrophages (TAMs) in the tumor microenvironment have been linked to the accelerated tumor progression. MicroRNAs (miR) are 19-25 nucleotide-long, noncoding RNA molecules, functioning as modulators of gene expression, and mediate a variety of biological functions, including tumor growth. In the present study, the effects and molecular mechanism of miR-155 in TAMs isolated from EC were explored. The expression of miR-155 and fibroblast growth factor-2 (FGF2) in EC tissues and cell lines were analyzed using reverse transcription-quantitative PCR (qRT-PCR) and western blot assays. TAMs were also transfected with the described constructs. Following, the culture medium from TAMs was collected for further analysis. The released FGF2, and inflammatory cytokines were quantified using ELISA. The cell viability, migrated and invaded levels were calculated through Cell Counting kit-8 (CCK8), and transwell analysis. Moreover, human umbilical vein endothelial cells (HUVEC) vasculature formation was determined using matrigel angiogenesis analysis. The results indicated that miR-155 expression was decreased in EC tissues and cell lines, while FGF2 expression was increased in comparison to those in the normal control group. Moreover, miR-155 mimics transfection up-regulated tumor necrosis factor α (TNF-α), interleukin (IL)-12 and inducible nitric oxide synthase (iNOS), while down-regulated IL-10, Arginase-1 (Arg-1) and IL-22 levels in the culture medium from TAMs. And enhancing miR-155 expression in TAMs suppressed the cell viability, migration and invasion of ECA109 cells and reduced the angiogenesis. Nevertheless, over-expressing FGF2 abolished the role of miR-155 in cancer cell survival, migration, invasion as well as angiogenesis. Our findings indicated that miR-155-regulated FGF2 expression from TAMs suppressed EC cell proliferation, migration, invasion and inhibited vasculature formation. Thus, miR-155-modulated FGF2 might be a potential therapeutic target to prevent EC progression.

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Esophageal cancer progres Esophageal disease spectr Cancer Apoptosis Phospho- Adrenal gland disease spe Multiple esophageal cance Rectum disease spectrum ( Kidney disease spectrum ( Bladder disease spectrum Bladder disease spectrum Bone disease spectrum (bo Bone and cartilage diseas Breast disease spectrum (

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Initial Response of Human Bone Marrow-Derived Stem Cells after Contact with Ultrahigh-Molecular-Weight Polyethylene (UHMWPE) Material: An Study on Cell Viability and Interleukin-6 Expression.

Ultrahigh-molecular-weight polyethylene (UHMWPE) is a thermoplastic polymer useful in biomaterial applications, especially in orthopedic field. Yet, little is known concerning its initial effect on human bone marrow stem cells (hBMSCs) after implantation.

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Astra Blue 6GLL, Stain fo Anti C Reactive Protein A Macrophage Colony Stimula Macrophage Colony Stimula glial cells missing homol thymic dendritic cell-der Anti RAGE (Receptor for A anti CD7 All T cells Reco anti CD38 Hematopoietic p anti CD45 RA B cells, T c anti Transferrin receptor Human Cord Blood CD34+ Ce

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Inflammatory Response of Pulmonary Artery Smooth Muscle Cells Exposed to Oxidative and Biophysical Stress.

Pulmonary hypertension in the neonate requires treatment with oxygen and positive pressure ventilation, both known to induce lung injury. The direct response of pulmonary artery smooth muscle cells, the most abundant cells in the artery wall, to the stress of positive pressure and hyperoxia has not been previously studied. Pulmonary artery smooth muscle cells were cultured in temperature- and pressure-controlled air-tight chambers under conditions of positive pressure or hyperoxia for 24 h. Control cells were cultured in room air under atmospheric pressure. After the exposure period, culture medium was collected and samples were analyzed by ELISA, Human Cytokine 25-Plex Panel using a Luminex 200 analyzer and Western blot. Secretion of various inflammatory mediators, specifically IL-6, IL-8, IL-2R, MIP-1β, MCP-1, IP-10, IL-7, IL-1RA, and IFN-α, was higher in the positive pressure and hyperoxia groups compared with control. The level of cyclin D1 was decreased in the hyperoxia and positive pressure group compared with control. Levels of fibronectin and α-smooth muscle actin were not different among the groups. Pulmonary artery smooth muscle cells directly produce multiple inflammatory mediators in response to oxidative and biophysical stress in vitro, which may be part of a cascade that leads to the vascular and perivascular changes in pulmonary hypertension.

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Actin, Alpha-Smooth Musc Actin, Alpha-Smooth Musc Actin, Alpha-Smooth Musc OXI TEK (Oxidative Stress Alpha Smooth Muscle Actin Anti beta3 AR Human, Poly T-2 Toxin Mycotoxins ELIS 8 Isoprostane oxidative s Mouse Anti-SM Myosin (Smo Human Aortic Artery Endot GFP Expressing Human Aort Human Coronary Artery End

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Lectin microarray and mass spectrometric analysis of hepatitis C proteins reveals N-linked glycosylation.

We used lectin microarray and mass spectrometric analysis to identify the N-linked glycosylation patterns of hepatitis C virus (HCV) particles. HCV J6/JFH-1 chimeric cell culture (HCVcc) in the culture supernatant was concentrated and purified by ultrafiltration and sucrose gradient ultracentrifugation. Twelve fractions were collected from the top and analyzed for viral infectivity and HCV RNA content after sucrose gradient separation. HCV RNA and proteins were separated by ultracentrifugation in a continuous 10% to 60% sucrose gradient to purify viral particles based on their sedimentation velocities. HCVcc particles were found mainly in fractions 6 to 8, as determined by quantitative polymerase chain reaction (qPCR) analysis for HCV RNA and ELISA of the HCV core protein. The N-glycans on HCV proteins were analyzed by lectin microarray and mass spectrometry. We identified that 32 of 37 lectins displayed the positive binding signals and 16 types of N-glycoforms of which the major HCV glycoforms were high mannose-type N-linked oligosaccharides, hybrid N-glycans, and fucosylated N-glycans. Our study provided new detailed information regarding the majority of the glycan-protein profile, complementing to previous findings of glycan-HCV protein interactions.

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MarkerGeneTM Hydrophobic Hepatitis B Core Antigen Hepatitis B Core Antigen Hepatitis B Core Antigen Hepatitis B Core Antigen HbcAg - Hepatitis B Viru HbcAg - Hepatitis B Viru HbcAg - Hepatitis B Viru Fontana-Masson Stain Kit Fontana-Masson Stain Kit Hepatitis C Virus antibod Proteins: Mouse CD40 Lig

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The microRNA-1908 up-regulation in the peripheral blood cells impairs amyloid clearance by targeting ApoE.

To give a new insight into the mechanism of ApoE dysregulation and microRNA-1908 in Alzheimer's disease (AD).

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Acute Hypoxia Induces Enkephalin Production and Release in an Adrenergic Cell Line Model of Neonatal Chromaffin Cell Responses to Hypoxic Stress.

 Prior to maturation of the human sympathetic nervous system, the neonatal adrenal medulla senses and responds to hypoxia. In addition to catecholamine release, the adrenal medulla synthesizes and stores opioid peptides, notably enkephalin (ENK). However, it is not known whether acute hypoxia evokes adrenal ENK production and release, as seen in the central nervous system (CNS). We hypothesize that acute hypoxia stimulates synthesis and release of ENK in chromaffin cells.

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Generation and characterization of a novel recombinant scFv antibody specific for Campylobacter jejuni.

Campylobacter jejuni is a leading cause of foodborne illness worldwide, mainly due to consumption and handling of contaminated raw chicken. Rapid detection methods for C. jejuni are vital for monitoring contamination levels in chicken products and reducing human Campylobacteriosis cases. The 'gold standard' culture-based method of Campylobacter detection takes 3-5 days and is too slow to permit effective intervention. Immuno-based methods are faster, but usually necessitate use of animals or hybridoma technology to produce antibodies; making them difficult and expensive to produce. Here, we report the generation and characterization of recombinant single-chain variable fragment (scFv) antibodies specific for C. jejuni cells, and evaluation of one scFv antibody for an immunomagnetic separation-quantitative PCR (IMS-qPCR) method to rapidly, sensitively, and specifically detect low numbers of C. jejuni. An scFv antibody phage-display library was constructed using spleen mRNA derived from a rabbit immunized with gamma-irradiated C. jejuni cells. This library was screened by surface biopanning against C. jejuni whole cells. Enriched clones were analyzed by enzyme-linked immunosorbent assay (ELISA). Two scFv antibodies that strongly and specifically recognized C. jejuni cell were expressed in Escherichia coli. Western blot analysis showed that one antibody, scFv80, was expressed as a soluble protein and retained its specific and strong binding to C. jejuni cells. This recombinant monoclonal scFv antibody was purified and used to covalently coat paramagnetic beads to be used for IMS-qPCR. The IMS-qPCR method was able to specifically and sensitively detect C. jejuni in mixed cultures within 3 h.

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MOUSE ANTI BOVINE ROTAVIR Campylobacter jejuni anti MOUSE ANTI BORRELIA BURGD RABBIT ANTI GSK3 BETA (pS MOUSE ANTI CANINE DISTEMP MOUSE ANTI HUMAN CD15, Pr MOUSE ANTI HUMAN CD19 RPE MOUSE ANTI HUMAN CD15, Pr MOUSE ANTI APAAP COMPLEX, Bone Morphogenetic Protei Growth Differentiation Fa Androgen Receptor (Phosph

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