Search results for: ELISA Human , TGF-beta2
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Soluble form of LR11 is highly increased in the vitreous fluids of patients with idiopathic epiretinal membrane.LR11 (also called SorLA or SORL1) is a migration regulator of adherent cells with the immature proliferative phenotype. The present study investigated the clinical and pathological involvement of the soluble form of LR11 (sLR11) in the idiopathic epiretinal membrane (iERM).
2732 related Products with: Soluble form of LR11 is highly increased in the vitreous fluids of patients with idiopathic epiretinal membrane.Nuclear Membrane Receptor Angiogenesis (Human) Anti Angiogenesis (Human) Anti Angiogenesis (Mouse) Anti Apoptosis (Human) Antibod Atherosclerosis (Human) A Atherosclerosis (Mouse) A Chemokine (Human) Antibod Cytokine (Human) Antibody Cytokine (Human) Antibody Cytokine (Human) Antibody Cytokine (Human) Antibody
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The relationship between anti-vascular endothelial growth factor and fibrosis in proliferative retinopathy: clinical and laboratory evidence.To investigate the progression of epiretinal membranes after intravitreal bevacizumab (IVB) injection therapy in patients with proliferative membranes and evaluate the changes in fibrosis-related cytokines in retinal pigment epithelial cells and glial cells after treatment with bevacizumab.
2543 related Products with: The relationship between anti-vascular endothelial growth factor and fibrosis in proliferative retinopathy: clinical and laboratory evidence.Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Mouse Vascular Endothelia Goat Anti-Human Fibroblas Mouse Anti-Insulin-Like G Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse
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Prognostic significance of in situ and plasma levels of transforming growth factor β1, -2 and -3 in cutaneous melanoma.Melanoma is an aggressive type of cutaneous malignancy. Transforming growth factor (TGF)‑β has been demonstrated to be an important mediator of tumor progression. However, to the best of our knowledge, the systemic roles of plasma TGF‑β and TGF‑β in situ have not been investigated in Han Chinese melanoma patients. The results of the present study demonstrated that the in situ and plasma levels of TGF‑β1, TGF‑β2 and TGF‑β3 protein and messenger RNA were significantly elevated in tumor tissues compared with those of normal tissues. The survival rates of the patients which were triple‑positive (TGF‑β1+, TGF‑β2+ and TGF‑β3+) were found to be markedly decreased compared to those which were single‑ (TGF‑β1+, TGF‑β2+ or TGF‑β3+) or double‑positive (TGF‑β1+, TGF‑β2+; TGF‑β2+, TGF‑β3+; or TGF‑β1+, TGF‑β3+). These results may therefore contribute to the use of TGF‑β as a prognostic biomarker, and to the development of novel therapies for melanoma treatment.
1876 related Products with: Prognostic significance of in situ and plasma levels of transforming growth factor β1, -2 and -3 in cutaneous melanoma.Human Insulin-like Growth IGF-1R Signaling Phospho- Goat Anti-Human Fibroblas Insulin promoter factor 1 Human Transforming Growth Human Insulin-like Growth Human Interleukin-33 IL-3 Human Interleukin-32 alph Mouse Insulin-like Growth Mouse Interleukin IL-31 I Rat Insulin-like Growth F LY-2090314 Mechanisms: GS
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Circulating serum markers and QRS scar score in Chagas cardiomyopathy.Approximately 8 million people have Trypanosoma cruzi infection, and nearly 30% will manifest Chagas cardiomyopathy (CC). Identification of reliable early indicators of CC risk would enable prioritization of treatment to those with the highest probability of future disease. Serum markers and electrocardiogram (EKG) changes were measured in 68 T. cruzi-infected individuals in various stages of cardiac disease and 17 individuals without T. cruzi infection or cardiac disease. T. cruzi-infected individuals were assigned to stage A (normal EKG/chest x-ray [CXR]), B (abnormal EKG/normal CXR), or C (abnormal EKG/cardiac structural changes). Ten serum markers were measured using enzyme-linked immunosorbent assay (ELISA)/Luminex, and QRS scores were calculated. Higher concentrations of transforming growth factor-β1 (TGFβ1), and TGFβ2 were associated with stage B compared with stage A. Matrix Metalloproteinase 2 (MMP2), Tissue Inhibitors of MMP 1, QRS score, and Brain Natriuretic Protein rose progressively with increasing CC severity. Elevated levels of several markers of cardiac damage and inflammation are seen in early CC and warrant additional evaluation in longitudinal studies.
Sterile filtered goat se Sterile filtered goat se Sterile filtered mouse s Sterile filtered rat ser Goat Anti-Human LIMP2 SCA PSA test card, serum , Ca Troponin I test card, ser Myoglobin test card, seru Breast cancer tissue arra Breast disease spectrum t Bovine Androstenedione,AS Human interleukin 2(IL-2)
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A mutation protective against Alzheimer's disease renders amyloid β precursor protein incapable of mediating neurotoxicity.Expression of a familial Alzheimer's disease (AD)-linked mutant of amyloid β precursor protein (APP) or the binding of transforming growth factor β2 to wild-type (wt)-APP causes neuronal death by activating an intracellular death signal (a APP-mediated intracellular death signal) in the absence of the involvement of amyloid β (Aβ) toxicity in vitro. These neuronal death models may therefore be regarded as Aβ-independent neuronal death models related to AD. A recent study has shown that the A673T mutation in the APP isoform APP770 , corresponding to the A598T mutation in the most prevalent neuronal APP isoform APP695 (an AD-protective mutant of APP), is linked to a reduction in the incidence rate of AD. Consistent with this, cells expressing the AD-protective mutant of APP produce less Aβ than cells expressing wt-APP. In this study, transforming growth factor β2 caused death in cultured neuronal cells expressing wt-APP, but not in those expressing the AD-protective mutant of APP. This result suggests that the AD-protective mutation of APP reduces the incidence rate of AD by attenuating the APP-mediated intracellular death signal. In addition, a mutation that causes hereditary cerebral hemorrhage with amyloidosis-Dutch type also attenuated the APP-mediated intracellular death signal. The A598T mutation of amyloid precursor protein APP is linked to a reduction in the incidence rate of Alzheimer's disease (AD). This study shows that TGFβ2 causes death in neuronal cells expressing wild-type APP, but not in those expressing the AD-protective mutant of APP, suggesting that the AD-protective mutation of APP reduces the incidence rate of AD by attenuating the APP-mediated intracellular death signal.
1505 related Products with: A mutation protective against Alzheimer's disease renders amyloid β precursor protein incapable of mediating neurotoxicity.amyloid beta precursor pr Beta Amyloid (42) ELISA K Beta Amyloid (1 40) ELISA Beta Amyloid (40) ELISA K Beta Amyloid (1 40) ELISA Anti-BACE-1 (Memapsin-2, to BACE-1 (Memapsin-2, B Anti-BACE-1 (Memapsin-2, Human Amyloid Beta Precur Breast cancer membrane pr G protein-coupled recepto ubiquinol-cytochrome c re
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HOXA10 promotes cell invasion and MMP-3 expression via TGFβ2-mediated activation of the p38 MAPK pathway in pancreatic cancer cells.HOXA10 is closely related to tumor progression in many human cancers. However, the role of HOXA10 in pancreatic cancer remains unclear. The aim of this study was to determine the involvement of HOXA10 in pancreatic cancer cell invasion and migration.
2108 related Products with: HOXA10 promotes cell invasion and MMP-3 expression via TGFβ2-mediated activation of the p38 MAPK pathway in pancreatic cancer cells.Glucagon ELISA KIT, Rat G Cultrex96 Well 3D BME Cel anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl DNA (cytosine 5) methyltr Macrophage Colony Stimula Macrophage Colony Stimula GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Leptin ELISA Kit, Rat Lep Cultrex 24 Well BME Cell
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Periostin promotes the generation of fibrous membranes in proliferative vitreoretinopathy.Proliferative vitreoretinopathy (PVR) is a severe, vision-threatening disorder characterized by the fibrous membrane formation that leads to tractional retinal detachment. There has been no effective therapeutic approach other than vitreoretinal surgery. In this study, DNA microarray analysis of the fibrous membranes revealed significant up-regulation of periostin. We also found increased periostin expression in the vitreous and retinal pigment epithelial (RPE) cells from fibrous membranes of PVR patients. In vitro, periostin increased proliferation, adhesion, migration, and collagen production in RPE cells through integrin αV-mediated FAK and AKT phosphorylation. Periostin blockade suppressed migration and adhesion induced by TGFβ2 and PVR vitreous. In vivo, periostin inhibition had the inhibitory effect on progression of experimental PVR in rabbit eyes without affecting the viability of retinal cells. These results identified periostin as a pivotal molecule for fibrous membrane formation as well as a promising therapeutic target for PVR.
2725 related Products with: Periostin promotes the generation of fibrous membranes in proliferative vitreoretinopathy.Angiogenesis (Human) Anti Angiogenesis (Human) Anti Angiogenesis (Mouse) Anti Apoptosis (Human) Antibod Atherosclerosis (Human) A Atherosclerosis (Mouse) A Chemokine (Human) Antibod Cytokine (Human) Antibody Cytokine (Human) Antibody Cytokine (Human) Antibody Cytokine (Human) Antibody Cytokine (Human) Antibody
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CCN2 plays a key role in extracellular matrix gene expression in severe hypertrophic cardiomyopathy and heart failure.Hypertrophic cardiomyopathy (HCM) is the most common inherited primary myocardial disorder. HCM is characterized by interstitial fibrosis and excessive accumulation of extracellular matrix (ECM) proteins. Fibrosis in HCM has been associated with impaired cardiac function and heart failure, and has been considered a key substrate for ventricular arrhythmias and sudden death. The molecular triggers underpinning ECM production are not well established. We have previously developed a double-mutant mouse model of HCM that recapitulates the phenotype seen in humans with multiple mutations, including earlier onset of the disease, progression to a dilated phenotype, severe heart failure and premature mortality. The present study investigated the expression of ECM-encoding genes in severe HCM and heart failure. Significant upregulation of structural Fn1, regulatory Mmp14, Timp1, Serpin3A, SerpinE1, SerpineE2, Tgfβ1, and Tgfβ2; and matricellular Ccn2, Postn, Spp1, Thbs1, Thbs4, and Tnc was evident from the early, pre-phenotype stage. Non-myocytes expressed ECM genes at higher levels than cardiomyocytes in normal and diseased hearts. Synchronous increase of secreted CCN2 and TIMP1 plasma levels and decrease of MMP3 levels were observed in end-stage disease. CCN2 protein expression was increased from early disease in double-mutant hearts and played an important role in ECM responses. It was a powerful modulator of ECM regulatory (Timp1 and SerpinE1) and matricellular protein-encoding (Spp1, Thbs1, Thbs4 and Tnc) gene expression in cardiomyocytes when added exogenously in vitro. Modulation of CCN2 (CTGF, connective tissue growth factor) and associated early ECM changes may represent a new therapeutic target in the treatment and prevention of heart failure in HCM.
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Endothelium-dependent epithelial-mesenchymal transition of tumor cells: exclusive roles of transforming growth factor β1 and β2.Induction of epithelial-mesenchymal transition (EMT) is essential for the metastasis of tumor cells and maintaining their stemness. This study aimed to examine whether endothelial cells, which are most closely located to tumor cells in vivo, play a role in inducing EMT in tumor cells or not.
2730 related Products with: Endothelium-dependent epithelial-mesenchymal transition of tumor cells: exclusive roles of transforming growth factor β1 and β2.Epidermal Growth Factor ( Epidermal Growth Factor ( Human Transforming Growth Human Transforming Growth Rat transforming growth f ELISA Kit for Tumor Necr Epidermal Growth Factor ( Epidermal Growth Factor ( Fibroblast Growth Factor Fibroblast Growth Factor Fibroblast Growth Factor Fibroblast Growth Factor
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Immune response and survival of refractory cancer patients who received TGF-β2 antisense/GM-CSF gene modified autologous tumor cell (TAG) vaccine.TAG vaccine is a novel 'triad vaccine' that involves transfection of autologous tumor with a dual plasmid, TGFβ2 antisense gene and GM-CSF gene. Patients with advanced cancer who failed standard therapy were treated. IFN-γ ELISPOT analysis (Enzyme-Linked Immunospot Assay for Interferon Gamma) using TAG autologous vaccine target cells was performed prior to vaccination and at week 12 after the third vaccination. The purpose of this assessment was to correlate the IFN-γ ELISPOT immune response with long-term survival of advanced cancer patients who received TAG vaccination. Twenty-three of 28 patients received ≥ 3 TAG vaccinations (two patients withdrew consent and three had disease progression prior to the third vaccination). Eleven patients demonstrated a positive ELISPOT response (>10 spots and ≥ 2 × baseline) at week 12 and 12 patients did not (P=0.002). Median survival from time of treatment between ELISPOT-positive and -negative groups was significantly different (550 vs 159 days, P=0.036), as was median survival from the time of procurement (627 vs 257 days, respectively, P=0.043). In conclusion, the IFN-γ ELISPOT assay may provide an effective measure of immune response following treatment with 'triad vaccines', but additional patient numbers and/or other immune modulatory parameters are necessary for future testing.
2788 related Products with: Immune response and survival of refractory cancer patients who received TGF-β2 antisense/GM-CSF gene modified autologous tumor cell (TAG) vaccine.Rat TGF-beta-inducible ea Rat TGF-beta-inducible ea CELLKINES MACROPHAGE COLO CELLKINES MACROPHAGE COLO Mouse Anti-Human GM-CSF C Mouse Anti-Human GM-CSF C Macrophage Colony Stimula Macrophage Colony Stimula PEPTONE PASTE (BACTERIOLO Recombinant Human GM-CSF Recombinant Human GM-CSF Recombinant Human GM-CSF
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