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Clinical Analysis of Esophageal Stricture in Patients Treated with Intralesional Triamcinolone Injection after Endoscopic Submucosal Dissection for Superficial Esophageal Cancer.Endoscopic submucosal dissection (ESD) has been widely used in the resection of superficial esophageal cancers. Since its use has been extended to cases involving large esophageal tumors occupying nearly the whole or the whole circumference of the lumen, the occurrence of esophageal stricture has increased. Although endoscopic injection of triamcinolone (TA) is widely used for the prevention of postoperative stricture, a significant number of patients still develop stricture after TA injection therapy.
There is about (9473) Related Products to Clinical Analysis of Esophageal Stricture in Patients Treated with Intralesional Triamcinolone Injection after Endoscopic Submucosal Dissection for Superficial Esophageal Cancer.Esophageal disease spectr Esophageal cancer tissue Esophageal cancer tissue Esophageal cancer test ti Esophageal cancer test ti Esophageal squamous cell Middle advanced stage eso Esophageal adenocarcinoma Metastatic esophageal can Esophageal cancer progres Multiple esophageal cance Esophageal cancer tissue
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Can faecal calprotectin predict relapse in inflammatory bowel disease: a mini review.Crohn's disease and ulcerative colitis are chronic inflammatory disorders affecting the gastrointestinal tract. Faecal calprotectin is a protein complex of the S-100 family of calcium-binding proteins present in inflammatory cells that can be measured in stool samples, which act as a biomarker for bowel inflammation. Elevated faecal calprotectin has been shown to reflect the presence of ongoing mucosal inflammation, which improves with mucosal healing. The aim of this review was to evaluate the available evidence on the ability of faecal calprotectin to predict a relapse in inflammatory bowel disease. Multiple retrospective studies have shown that patients who relapse have significantly higher levels of calprotectin in their stool compared with non-relapsers, especially in ulcerative colitis. Elevated faecal calprotectin postoperatively in Crohn's disease was also shown to be indicative of a relapse. However, the association of a raised faecal calprotectin and relapse is not universal and may be explained by the different patterns of mucosal inflammatory activity that exist. In conclusion, we put forward our hypothesis that changes such as a rise in faecal calprotectin levels may be more predictive of a relapse than absolute values.
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Deficit of IgG2 in HIV-positive pregnant women is responsible of inadequate IgG2 levels in their HIV-uninfected children in Malawi.Transplacental passage of IgGs is impaired in HIV + pregnant women, possibly determining an inadequate immunological protection in their children. We aimed to determine the impact of maternal immunological IgG profile and immunoactivation status on the efficiency of transplacental passage of IgG subclasses in HIV + mothers.
There is about (8514) Related Products to Deficit of IgG2 in HIV-positive pregnant women is responsible of inadequate IgG2 levels in their HIV-uninfected children in Malawi.Mouse Anti-IgG2 Antibodie Sheep Anti-IgG2 [+HRP] An Mouse Anti-Human IgG2 (Fa Mouse Anti-Human IgG2 F(a Goat antiGuinea Pig IgG2 Mouse Anti-IgG2 Antibodie Sheep Anti-IgG2 Antibodie Mouse Anti-Human IgG2 Ant Mouse Anti-Human IgG2 (Fa Native Human IgG2, kappa Mouse Anti-Human IgG2 Ant anti CD45 RA IgG2 monoclo
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Effect of tumor necrosis factor-α-induced protein 8 on the immune response of CD4+ T lymphocytes in mice following acute insult.Tumor necrosis factor-α-induced protein 8 (TNFAIP8), which was the first identified member of the TNFAIP8 family, shares considerable sequence homology with other members of the TNFAIP8 family. It is expressed in various normal human tissues, with relatively higher levels detected in lymphoid tissues and the placenta. The present study aimed to examine the effect of TNFAIP8 on cell‑mediated immunity of cluster of differentiation (CD)4+ T lymphocytes in a cecal ligation and puncture (CLP) murine model. A total of 100 male mice were randomly divided into four groups as follows: The sham injury group (n=30), the CLP group (n=30), the CLP with lentivirus‑RNA‑TNFAIP8 group (n=20) and the CLP with negative control group (n=20), and they were sacrificed 24 h following CLP. Splenic CD4+ T cells were isolated using MACS microbeads. T cell proliferation was analyzed using the MTT assay, and cytokine levels were determined with ELISA kits. Upregulation of TNFAIP8 by lentivirus‑RNA‑TNFAIP8 infection was demonstrated to promote CD4+ T lymphocyte proliferative activity following CLP, and the increase in TNFAIP8 expression in vivo affected splenic CD4+ T lymphocyte polarization following CLP‑induced sepsis. In conclusion, TNFAIP8 expression following CLP may be associated with the pathogenesis of immune dysfunction in splenic T lymphocytes in mice.
There is about (9575) Related Products to Effect of tumor necrosis factor-α-induced protein 8 on the immune response of CD4+ T lymphocytes in mice following acute insult.ELISA p55,p60,Pig,Sus scr TNFRSF1B - Goat polyclona Human, Complement C1q tum Rat Tumor Necrosis Factor Human Tumor necrosis fact Tumor necrosis factor (TN Mouse Tumor Necrosis Fact Human Tumor Necrosis Fact ELISA Kit for Tumor Necr Human Tumor Necrosis Fact Mouse Tumor Necrosis Fact ELISA Kit for Tumor Necro
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ATRA improves endothelial dysfunction in atherosclerotic rabbits by decreasing CAV‑1 expression and enhancing eNOS activity.The aim of the present study was to explore the protective effects and possible mechanisms of all‑trans‑retinoic acid (ATRA) against atherosclerosis (AS). Rabbits were randomly allocated for standard or high‑fat diet with or without ATRA. After 12 weeks, the aortic rings of the rabbits were removed. Endothelium‑dependent relaxation (EDR) induced by acetylcholine and non‑endothelium‑dependent relaxation induced by sodium nitroprusside in the thoracic aorta were evaluated. NO level and eNOS activity were measured according to the protocol of NO and eNOS ELISA kits. The permeability and morphology of the arterial walls were identified by immunofluorescence and H&E staining respectively. The expression of caveolin‑1 (CAV‑1) and occludin was analyzed using western blotting and immunohistochemistry. The EDR function was significantly reduced in the AS rabbits compared with the normal group, however it was elevated following treatment with ATRA. The eNOS activity and NO level were reduced in the AS group, however were notably increased following oral administration of ATRA. There was an enhancement of endothelial permeability in the AS group compared with the normal group, which decreased following ATRA treatment. Western blot analysis and immunohistochemical analysis identified an increase in occludin expression after treatment with ATRA, in contrast to CAV‑1 expression under the same conditions. ATRA is able to ameliorate high‑fat‑induced AS in rabbits, which is mediated through the activation of eNOS and downregulating CAV‑1 expression.
There is about (17335) Related Products to ATRA improves endothelial dysfunction in atherosclerotic rabbits by decreasing CAV‑1 expression and enhancing eNOS activity.MarkerGeneTM beta Glucuro SOD Activity Activity Ass HAT Activity Activity Ass DAB (Post) Enhancing Sol eNOS Antibody eNOS Peptide DAB (Post) Enhancing Sol eNOS Polyclonal Ab 100 ug eNOS Blocking Peptide FluoroQuest™ Fluorescen eNOS (Ab 495) Antibody Ho eNOS (Ab 1177) Antibody H
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Inhibition of Autophagy Attenuated Ethylene Glycol Induced Crystals Deposition and Renal Injury in a Rat Model of Nephrolithiasis.Nephrolithiasis is a common and frequently occurring disease, its exact pathogenesis is remains unclear. Emerging data suggest that autophagy plays a vital role in the pathophysiological processes of kidney diseases. Therefore, this study was designed to investigate the potential role of autophagy in the formation of calcium oxalate (CaOx) kidney stones in rat model.
There is about (19838) Related Products to Inhibition of Autophagy Attenuated Ethylene Glycol Induced Crystals Deposition and Renal Injury in a Rat Model of Nephrolithiasis.Ethylene glycol CAS: [107 Tri(ethylene glycol) di p High density renal cancer TRIS Pre set crystals Rea Cell Meter™ Autophagy A Human Kidney injury molec NC1 fragment of mouse ren Renal carcinoma and norma Renal disease spectrum ti Kidney disease spectrum ( 1-Aminooctaethylene Glyco 1-Aminohexaethylene Glyco
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DNMT3L interacts with transcription factors to target DNMT3L/DNMT3B to specific DNA sequences: role of the DNMT3L/DNMT3B/p65-NFκB complex in the (de-)methylation of TRAF1.DNMT3L i.e. DNA (cytosine-5)-methyltransferase 3-like protein, is devoid of cytosine methyltransferase activity, despite clear homology to DNMT3A and DNMT3B, due to the mutation of key catalytic residues. However, DNMT3L participates in de novo methylation reactions through its direct interaction with DNMT3A and DNMT3B. In the present study, we investigated if DNMT3L interacts also directly with transcription factors (TFs). Using TF arrays, we identified 73 TFs that interacted with DNMT3L, 13 of which (ASH2L, ATF1, ATF3, BLZF1, CDX2, CERM, E2F3, E2F4, GCNF, GTF2I, GTF3C5, NFkB-p65 and RXRα) interacted only with DNMT3L, but not with DNMT3A/B. By focusing on the interaction with NFkB-p65, we demonstrate that DNMT3L forms a complex with DNMT3B and NFkB-p65 and that this complex is required for the control of DNA methylation at the TRAF1 promoter in the T98G glioma cell line. In addition, our experiments describe the DNA methylation at TRAF1 as being dynamic with a demethylation phase involving TET3. Thus, our data suggests that DNMT3L can address DNMT3A/B to specific sites by directly interacting with TFs that do not directly interact with DNMT3A/B. In summary, our data provide a new avenue for the direction of site-specific de novo DNA methylation catalyzed by DNMT3A/B.
There is about (15289) Related Products to DNMT3L interacts with transcription factors to target DNMT3L/DNMT3B to specific DNA sequences: role of the DNMT3L/DNMT3B/p65-NFκB complex in the (de-)methylation of TRAF1.DNMT3L Polyclonal Antibod DNMT3B Polyclonal Antibod Chromatin Transcription P Transcription factors: N Transcription Factors: N Transcription Factors: T Transcription factors: O MOUSE ANTI APAAP COMPLEX, Rat AntiORC6 (origin reco Rat AntiORC1 (origin reco Rat AntiORC2 (origin reco Rat AntiORC3 (origin reco
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Elevation of adenylate energy charge by angiopoietin-like 4 enhances epithelial-mesenchymal transition by inducing 14-3-3γ expression.Metastatic cancer cells acquire energy-intensive processes including increased invasiveness and chemoresistance. However, how the energy demand is met and the molecular drivers that coordinate an increase in cellular metabolic activity to drive epithelial-mesenchymal transition (EMT), the first step of metastasis, remain unclear. Using different in vitro and in vivo EMT models with clinical patient's samples, we showed that EMT is an energy-demanding process fueled by glucose metabolism-derived adenosine triphosphate (ATP). We identified angiopoietin-like 4 (ANGPTL4) as a key player that coordinates an increase in cellular energy flux crucial for EMT via an ANGPTL4/14-3-3γ signaling axis. This augmented cellular metabolic activity enhanced metastasis. ANGPTL4 knockdown suppresses an adenylate energy charge elevation, delaying EMT. Using an in vivo dual-inducible EMT model, we found that ANGPTL4 deficiency reduces cancer metastasis to the lung and liver. Unbiased kinase inhibitor screens and Ingenuity Pathway Analysis revealed that ANGPTL4 regulates the expression of 14-3-3γ adaptor protein via the phosphatidylinositol-3-kinase/AKT and mitogen-activated protein kinase signaling pathways that culminate to activation of transcription factors, CREB, cFOS and STAT3. Using a different mode of action, as compared with protein kinases, the ANGPTL4/14-3-3γ signaling axis consolidated cellular bioenergetics and stabilized critical EMT proteins to coordinate energy demand and enhanced EMT competency and metastasis, through interaction with specific phosphorylation signals on target proteins.
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RNA sequencing uncovers the key microRNAs potentially contributing to sudden sensorineural hearing loss.This study aimed to identify miRNAs that may contribute to the pathogenesis of sudden sensorineural hearing loss (SSNHL) by RNA-seq (RNA-sequencing).RNA was extracted from SSNHL patients and healthy volunteers, respectively. Sequencing was performed on HiSeq4000 platform. After filtering, clean reads were mapped to the human reference genome hg19. Differential expression analysis of miRNAs between the SSNHL samples and the normal samples was performed using DEseq to identify differentially expressed microRNAs (DEMs). The target genes of the DEMs were predicted using the online tool miRWalk, which were then mapped to DAVID (https://david.ncifcrf.gov/) for functional annotation based on GO database and for pathway enrichment analysis based on KEGG. Finally, a miRNA-target-protein-protein interaction (PPIs) network was constructed using the DEMs and their target genes with interaction.Differential expression analysis reveals 24 DEMs between the SSNHL group and control group. A total of 1083 target genes were predicted. GO functional annotation analysis reveals that the target genes in the top 10 terms are mainly related to the development of salivary glands, neurotransmission, dendritic development, and other processes. KEGG pathway enrichment analysis reveals that the target genes were functionally enriched in pathways arachidonic acid metabolism, complement and coagulation cascades, linoleic acid metabolism, and MAPK signaling pathway. In the miRNA-target-PPI network, hsa-miR-34a/548n/15a/143/23a/210/1255a/18b/ /1180/99b had the most target genes; genes YWHAG, GSK3B, CDC42, NR3C1, LCK, UNC119, SIN3A, and NFKB2, interact with most other genes among all the predicted target genes.Hsa-miR-34a/15a/23a/210/18b/548n/143 is likely to have a role in the pathogenesis of SSNHL.
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De Novo Mutations in YWHAG Cause Early-Onset Epilepsy.Massively parallel sequencing has revealed many de novo mutations in the etiology of developmental and epileptic encephalopathies (EEs), highlighting their genetic heterogeneity. Additional candidate genes have been prioritized in silico by their co-expression in the brain. Here, we evaluate rare coding variability in 20 candidates nominated with the use of a reference gene set of 51 established EE-associated genes. Variants within the 20 candidate genes were extracted from exome-sequencing data of 42 subjects with EE and no previous genetic diagnosis. We identified 7 rare non-synonymous variants in 7 of 20 genes and performed Sanger sequence validation in affected probands and parental samples. De novo variants were found only in SLC1A2 (aka EAAT2 or GLT1) (c.244G>A [p.Gly82Arg]) and YWHAG (aka 14-3-3γ) (c.394C>T [p.Arg132Cys]), highlighting the potential cause of EE in 5% (2/42) of subjects. Seven additional subjects with de novo variants in SLC1A2 (n = 1) and YWHAG (n = 6) were subsequently identified through online tools. We identified a highly significant enrichment of de novo variants in YWHAG, establishing their role in early-onset epilepsy, and we provide additional support for the prior assignment of SLC1A2. Hence, in silico modeling of brain co-expression is an efficient method for nominating EE-associated genes to further elucidate the disorder's etiology and genotype-phenotype correlations.
Recombinant Human YWHAG [ Rabbit Anti-YWHAG Antibod Recombinant Human YWHAG P Recombinant Human YWHAG P Recombinant Human YWHAG P Recombinant Human YWHAG [ Recombinant Human YWHAG [ Mouse Anti-HSV-6 Human Ea Mouse Anti-EBV Early Nucl Anti CMV Immediately earl Mouse Anti-EBV Early Anti Mouse Anti-EBV Early Anti
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