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Low Serum Interleukin-10 Is an Independent Predictive Factor for the Risk of Second Event in Clinically Isolated Syndromes.

To evaluated the prognostic ability of several serum cytokines in clinically isolated syndrome (CIS) patients regarding second events and conversion to multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD). We enrolled 69 CIS patients whose serum samples were collected during the acute phase of the first onset before immunotherapy. Fifteen other non-inflammatory neurological disorder (OND) patients were also included. The serum levels of interleukin (IL)-2, IL-4, IL-6, IL-10, IL-13, IL-17A, IL-21, IL-23, interferon-γ (IFN-γ), and transforming growth factor beta 1 (TGF-β1) were measured using the human cytokine multiplex assay or ELISA. Patients were seen every 3-6 months. Unscheduled visits occur in case of exacerbations. Clinical measures of disease progression were recorded. Twenty CIS cases had second events during follow-up at a mean time of 15.3 ± 9.9 months. Serum IL-10 levels were significantly lower in CIS patients who relapsed compared to patients who did not. Low serum IL-10 levels were associated with higher risk and shorter times to second events. In clinical correlations, a significantly higher CSF white blood cells count, number of T2 lesions, and gadolinium-enhancing (Gd+) lesions in baseline MRI were found in the low serum IL-10 level group. Of the 20 relapsed cases, seven converted to MS, and eight converted to NMOSD. No significant differences were found in any cytokine levels between these patients at first onset. These findings support using serum IL-10 as a biomarker associated with the risk of relapse and the time to second events in patients with CIS. However, serum cytokine levels can not differentiate between the conversion from CIS to MS or NMOSD.

2926 related Products with: Low Serum Interleukin-10 Is an Independent Predictive Factor for the Risk of Second Event in Clinically Isolated Syndromes.

interleukin 17 receptor C Rabbit Anti-APIP Apaf1 In Rabbit Anti-G protein alp Rabbit Anti-APIP Apaf1 In Rabbit Anti-Phospho-INPPL Rabbit Anti-G protein alp Rabbit Anti-CD11b Integri Rabbit Anti-Insulin Recep Rabbit Anti-Integrin β2 Mouse Anti-Insulin(1G11) Rabbit Anti-intestinal FA Rabbit Anti-Integrin β2

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Generation of non-standard macrocyclic peptides specifically binding TSC-22 homologous gene-1.

Transforming growth factor-β 1 (TGFβ1)-stimulated clone 22 (TSC22) family includes proteins containing a leucine zipper domain and a TSC-box that are highly conserved during evolution. Currently, limited data are available on the function of this protein family, especially of TSC-22 homologous gene-1 (THG-1)/TSC22 domain family member 4 (TSC22D4). Similar to other family members, THG-1 functions depending on its interaction with the partner proteins and it is suggested to mediate a broad range of biological processes. THG-1-specific binding molecules will be instrumental for elucidating its functions. Therefore, the Random non-standard Peptide Integrated Discovery (RaPID) system was modified using commercially available materials and used for selecting macrocyclic peptides (MCPs) that bind to THG-1. Several MCPs were identified to bind THG-1. Fluorescein- and biotin-tagged MCPs were synthesized and employed as THG-1 detection probes. Notably, a fluorescein-tagged MCP specifically detected THG-1-expressing cells. Biotin-tagged MCPs can be successfully used for Enzyme-Linked Protein Sorbent Assay (ELISA) like assay of THG-1 protein and affinity-precipitation of purified THG-1 and endogenous THG-1 in esophageal squamous cell carcinoma cell lysates. The modified RaPID system rapidly and successfully identified THG-1-binding MCPs in vitro and the synthesized THG-1 binding MCPs are useful alternatives acting for antibodies.

2835 related Products with: Generation of non-standard macrocyclic peptides specifically binding TSC-22 homologous gene-1.

Standard Pipet Tips200ul Corticosterone rat mouse TUCAN CARD8 Blocking Pept Wnt-6 Blocking Peptide;Ap HDAC-7 Blocking Peptide;A Anti-actin binding protei 5(6) TAMRA, SE [5 (and 6) Rabbit Anti-IEX1 Differen Standard grade heat shoc AM-2201 C24H22FNO CAS: 33 F box and leucine rich re 2 Chloro 5 nitro 6 picoli

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What is the impact of intravitreal injection of conbercept on neovascular glaucoma patients: a prospective, interventional case series study.

The aim of the present study was to evaluate the efficacy and safety of intravitreal conbercept combined with trabeculectomy and panretinal photocoagulation for neovascular glaucoma (NVG).

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Rabbit Anti-CSNK1D Casein Normal rat multiple organ anti-Casein Kinase II α Multiple organ tumor tiss Oncocytoma tissue array, FDA Standard Frozen Tissu Normal rat multiple organ anti-Casein kinase II β Rabbit Anti-CSNK1D Casein Multiple organ cancer tis anti-Casein Kinase II α Tissue array of ovarian g

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BioRoot RCS Extracts Modulate the Early Mechanisms of Periodontal Inflammation and Regeneration.

The balance between periapical tissue inflammation and regeneration after the removal of necrotic/infected tissues is pivotal in determining the success of endodontic treatment. This study was designed to investigate the effect of silicate-based root canal sealer BioRoot RCS (BRCS; Septodont, Saint-Maur-des-Fossés, France) on modulating the inflammatory mechanisms and early steps of regeneration initiated by human periodontal ligament (PDL) fibroblasts.

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AZD-3514 Mechanisms: Andr Mouse Anti-Human CD34 Tar Monoclonal Anti-Adenoviru BEZ-235 Mechanisms: PI3K LDK-378 Mechanisms: ALK i FDA Standard Frozen Tissu Androgen Receptor Pp-242 Mechanisms: mTORC1 GSK-2636771 Mechanisms: P Multiple organ cancer tis 5α-N-Acetyl-2'H-androst- OSI-906 Mechanisms: IGF-1

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NF-κB-mediated inflammatory damage is differentially affected in SH-SY5Y and C6 cells treated with 27-hydroxycholesterol.

Previous studies have demonstrated that 27-hydroxycholesterol (27-OHC), a cholesterol metabolite, was involved in the inflammatory process of Alzheimer's disease (AD). The present study aimed to investigate the 27-OHC-induced inflammatory damage to neurons and astrocytes and the underlying mechanism(s) accounting for this damage. Human neuroblastoma cells (SH-SY5Y cells) and rat glioma cells (C6 cells) were treated with vehicle or 27-OHC (5, 10, or 20 μM) for 24 hr. The levels of secreted interleukin-1β (IL-1β), interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), and inducible nitric oxide synthase (iNOS) were determined by using an enzyme-linked immunosorbent assay (ELISA). Immunofluorescence staining was used to determine the cellular expression of toll-like receptor 4 (TLR4) and transforming growth factor-β (TGF-β). The mRNA and protein expression levels of nuclear factor-κB p65 (NF-κB p65), nuclear factor-κB p50 (NF-κB p50) and cyclooxygenase-2 (COX-2) in both SH-SY5Y and C6 cells were also detected by real-time PCR and Western blot, respectively. The results of this study showed that 27-OHC treatment increased secretion of TNF-α and iNOS and decreased secretion of IL-10, upregulated expression of TGF-β, NF-κB p65 and p50, and downregulated expression of COX-2 in SH-SY5Y cells. In C6 cells, treatment with 27-OHC resulted in decreased secretion of IL-1β, IL-10, TNF-α, and iNOS, and increased expression of TLR4 and TGF-β. These results suggest that 27-OHC may cause inflammatory damage to neurons by activating the TGF-β/NF-κB signaling pathway and to astrocytes by activating the TLR4/TGF-β signaling, which results in the subsequent release of inflammatory cytokines.

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Mouse Anti-Insulin(1D4:) Rabbit Anti-Insulin Polyc Rabbit Anti-Insulin Recep Rabbit Anti-IAA (Indole-3 Rabbit Anti-NOS-2 iNOS Po Rabbit Anti-IAA (Indole-3 Rabbit Anti-Insulin Recep Rabbit Anti-Cell death in Rabbit Anti-Cell death in Mouse Anti P.aeruginosa s Rabbit Anti-CD11b Integri Rabbit Anti-TNIP2 ABIN2 T

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[Relationship between expression of high-mobility group box-1 and inflammatory cytokines in patients with bone cancer pain].

To investigate the change and relationship between serum high-mobility group box-1(HMGB1) and related inflammatory cytokines level in patients suffer with bone metastatic pain. Collection of the bone cancer pain patients who received analgesic therapy the department of pain in The First Affiliated Hospital of Jiaxing University from November 2016 to August 2016. Serum concentration of HMGB1, the Receptor of Advanced Glycation Endproducts (RAGE), monocyte chemotactic protein-1(MCP-1), tumor necrosis factor -α (TNF-α), interleukin-1β (IL-1β), interleukin-10 (IL-10), interleukin-13 (IL-13), and transforming growth factor-β (TGF-β) levels were determined in 15 healthy individuals as healthy donor and 15 patients with bone metastatic pain by enzyme-linked immunosorbent (ELISA) . The healthy individuals and patients with bone metastatic pain were collected before treatment and on 7 d after the treatment. The serum concentration of HMGB1 and RAGE were significantly increased in tumorous group compared with healthy group[(8.8±2.3) vs (1.9±1.1) μg/L,(231±16) vs (46±20) ng/L); 7.10,12.44, both 0.05], then decreased after analgesic therapy [(4.77±1.36) μg/L, (129.80±29.32) ng/L, 7.10, 12.44, both 0.05]. The serum concentration of proinflammatory cytokines such as MCP-1, TNF-α, and IL-1β were significantly increased in tumorous group when compared with healthy group, and decreased after analgesic therapy (all 0.05). The expression of anti-inflammatory cytokines such as IL-10, IL-13, and TGF-β were significantly increased in tumorous group when compared with healthy group, and decreased after analgesic therapy (all 0.05).Compared with healthy group, the levels of MCP-1/IL-10, MCP-1/IL-13, MCP-1/TGF-β, TNF-α/IL-10, TNF-α/IL-13, TNF-α/TGF-β, IL-1β/IL-10, IL-1β/IL-13, IL-1β/TGF-β were significantly increased in tumorous group (all 0.05). HMGB1 may adjust the proinflammatory-anti-inflammatory system homeostasis to participate in the development of bone metastatic pain.

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Liver cancer (hepatocellu High density cervix cance Small intestine cancer, m High density (208 cores), Stomach cancer high densi High density ovarian canc High density ovarian canc High density breast cance HMG2 (High mobility group Colon cancer high density High density stomach canc High density (188 cases 2

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Indoxyl Sulfate-Induced Extracellular Vesicles Released from Endothelial Cells Stimulate Vascular Smooth Muscle Cell Proliferation by Inducing Transforming Growth Factor-Beta Production.

Vascular access stenosis predominantly occurs as a result of neointimal hyperplasia (NH) formation at the anastomosis. Moreover, in the presence of NH, transforming growth factor-beta (TGF-β) promotes vascular smooth muscle cell (VSMC) proliferation. Extracellular vesicles (EVs) released by endothelial cells are closely associated with vascular dysfunction. Here, we investigated the effects of EVs on TGF-β signaling and VSMC proliferation. Specifically, EVs were collected from the culture medium of indoxyl sulfate (IS)-treated human umbilical vein endothelial cells and used (2 × 106) to stimulate human aortic smooth muscle cells (SMCs) (1 × 106). Western blotting was performed to assess the levels of Akt, ERK1/2, p38 MAPK, and Smad3. BrdU proliferation assays, quantitative PCR, and ELISA assays were performed to evaluate SMC proliferation and TGF-β production. The IS-induced EVs stimulated the proliferation of aortic SMCs in a concentration-dependent manner. The EVs both contained TGF-β and promoted TGF-β production by SMCs by phosphorylating Akt, ERK1/2, p38 MAPK, and Smad3, which was significantly inhibited by an anti-TGF-β antibody. SMC proliferation was suppressed by both an anti-TGF-β antibody and inhibitors of the downstream factors. These results suggest that EVs are involved in the pathogenesis of vascular access stenosis by modulating TGF-β signaling in VSMCs under uremic conditions.

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Epidermal Growth Factor ( Epidermal Growth Factor ( Mouse Vascular Endothelia Recombinant Human Vascula Rat Vascular Endothelial Human Endocrine Gland Vas Human Transforming Growth Human Transforming Growth Mouse Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Human Vascular Endothelia

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Inhibitory effect of TGF-β gene modified human amniotic mesenchymal stem cells on rejection after xenotransplantation of peripheral nerves.

To explore the inhibitory effect of transforming growth factor-beta (TGF-β) gene modified human amniotic mesenchymal stem cells on rejection after xenotransplantation of peripheral nerves.

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Rat Mesenchymal Stem Cell Macrophage Colony Stimula Macrophage Colony Stimula Stemez hN2 Human Neuron D GFP Expressing Human Glom Recombinant Human HGF [fr Mouse Anti-Human Fibrobla RFP Expressing Human Live Recombinant Human PEDF [f Rat Anti-Rat RT6.2 (Perip Human Saphenous Vein Endo Recombinant Human IL-4 [f

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Candesartan inhibits inflammation through an angiotensin II type 1 receptor independent way in human embryonic kidney epithelial cells.

Besides stimulating vasoconstriction, Angiotensin II is also well known in inducing reactive oxygen species and promoting inflammatory phenotype switch via its type 1 receptor. In clinic, Angiotensin II type 1 (AT1) receptor blocker like candesartan has been widely applied as an antihypertensive medication. We previous have demonstrated that a higher dose of candesartan plays a protective role after kidney injury. However, whether candesartan could exhibit anti-inflammatory effects remains unclear. Here, by stimulating isolated human embryonic kidney epithelial cells with tumor necrosis factor-α (TNF-α), we observed the anti-inflammation capacity of candesartan ex vivo. It was found that pre-treat with candesartan significantly suppressed transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) expression after incubation with TNF-α. Surprisingly, silence of angiotensin II type 1 receptor has little effects on reducing TGF-β or IL-6 products. Furthermore, candesartan inhibited TNF-α-induced oxidative stress in the primary cultured tubular epithelial cells. Overall, our data indicates that candesartan suppresses TNF-α-induced inflammatory cytokine production by inhibiting oxidative stress, rather than block AT1 receptor activity.

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interferon-alpha receptor Interferon-a Receptor Typ interleukin 17 receptor C Inflammation (Human) Anti Alpha-1A adrenergic recep Goat Anti-Human Nogo 66 r Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-Cell death in Goat Anti-Human EP4 prost Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep

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The Role of Relaxin-2 in Tissue Remodeling of Chronic Rhinosinusitis With Nasal Polyps.

Relaxin is a small peptide hormone that regulates extracellular matrix remodeling and reduces fibrosis in a number of organs. Little is known about its impact on chronic rhinosinusitis with nasal polyps (CRSwNP); thus, we aimed to determine the expression of human H2 relaxin (relaxin-2) and its role in tissue remodeling in CRSwNP.

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FDA Standard Frozen Tissu Multiple organ tumor tiss FDA Standard Frozen Tissu FDA Standard Frozen Tissu MultiGene Gradient therm Prostate cancer, hyperpla FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu ABT-263 Mechanisms: Bcl-2 Rabbit Anti-APIP Apaf1 In Innovative Grade™ Canin

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