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Comparison of two kits of anti-infliximab antibodies plasmatic measurement.

Infliximab (IFX) is a chimeric monoclonal antibody which has proven its efficacy in the treatment of inflammatory diseases. However, its efficacy can be limited by the development of anti-IFX antibodies (ATI) resulting in a therapeutic failure of IFX. ATI plasmatic monitoring is then indicated to optimize IFX treatment. The aim of this study was to validate an ELISA (enzyme linked immuno sorbent assay) method of ATI plasmatic monitoring.

1463 related Products with: Comparison of two kits of anti-infliximab antibodies plasmatic measurement.

Sheep Anti-Human ALB Anti Rat monoclonal anti mouse Rabbit Anti-Human G6PD An Mouse Anti-Influenza A Vi Rabbit Anti-Human PEN2 (N Mouse Anti-Myelin Basic P Guinea pig Anti-Human Pro Rabbit Anti-T. gondii Tro Sheep Anti-Bovine ALB [+H Rabbit Anti-Human BACE2 A Rat monoclonal anti mouse Sheep Anti-Human Hemoglob

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Effect of M2 Macrophages on Injury and Apoptosis of Renal Tubular Epithelial Cells Induced by Calcium Oxalate Crystals.

M2 macrophages have important roles in diseases such as tumours, cardiovascular diseases and renal diseases. This study aimed to determine the effects and protective mechanism of M2 macrophages against oxidative stress injury and apoptosis induced by calcium oxalate crystals (CaOx) in renal tubular epithelial cells (HK-2) under coculture conditions.

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Mouse Anti-Human Fibrobla Ofloxacin CAS Number [824 Rabbit Anti-Human Apoptos Mouse Anti-Human Fibrobla anti CD7 All T cells Reco (5α)-Androst-2-en-17-one GFP Expressing Human Glom Goat Anti-Human Androgen Annexin V PE Apoptosis De Calcium trifluoromethanes Recombinant Human PEDF [f Rabbit Anti-Renalase Poly

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Development of ligand-coated beads to measure macrophage antimicrobial activities.

After macrophage recognizes and phagocytoses the microorganism, their phagosome undergoes maturation process, which creates a hostile environment for the bacterium. The lumen is acidified and proteolysis occurs to kill and degrade pathogen for further antigen presentation. It is important to understand the association between the macrophage intracellular activities and the outcome of infection. Different methods have been developed to measure the phagosome dynamics of macrophages but there are still limitations.

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Analysis Tool for Custom Analysis Tool for Custom Peptoid Ligand Assay Deve Homogenizer for 24 sample Rabbit Anti-Azurocidin Ca Analysis Tool for AAH-CYT Adar's Divinyl Sulfone (D Bilirubin, Direct & Total Adar's Anti Mouse Beads Hsp90 total Monoclonals A Angiogenesis (Human) Quan Sheep Anti-S. aureus Exfo

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Quantitative Modulation of PpIX Fluorescence and Improved Glioma Visualization.

5-Aminolevulinic acid (5-ALA) induced fluorescence to augment surgical resection for high grade glioma has become a standard of care. Protoporphyrin IX (PpIX) visibility is however subject to the variability of the single tumor expression and to the interobserver interpretation. We therefore hypothesized that in different glioma cell lines with variable 5-ALA induced fluorescence, the signal can be pharmacologically increased. We therefore analyzed in three different GBM cell lines, with different expression of epidermal growth factor receptor (EGFR), the variability of 5-ALA induced PpIX fluorescence after the pharmacological blockade at different steps of PpIX breakdown and influencing the outbound transport of PpIX. Using flow cytometry, fluorescence microplate reader, and confocal microscopy the PpIX fluorescence was analyzed after exposure to tin protoporphyrin IX (SnPP), deferoxamine (DFO), and genistein. We furthermore constructed a microscope (Qp9-microscope) being able to measure quantitatively the concentration of PpIX. These values were compared with the extraction of PpIX in tumor biopsy taken during the GBM surgery. Although all three cell lines showed an increase to 5-ALA induced fluorescence their baseline activity was different. Treatment with either SnPP, DFO and genistein was able to increase 5-ALA induced fluorescence. Qp9-microscopy of tumor sample produced a color coded PpIX concentration map which was overlaid on the tumor image. The PpIX extraction from tumor sample analyzed using the plate reader gave lower values of the concentration, as compared to the expected values of the Qp9-microscope, however still in the same decimal range of μg/mL. This may be due to homogenization of the values during extraction and cell disaggregation. In conclusion pharmacological augmentation in GBM cell lines of PpIX signal is possible. A quantitative PpIX map for surgery is feasible and may help refine surgical excision. Further correlations of tumor tissue samples and Qp9-microscopy is needed, prior to develop an intraoperative surgical adjunct to the already existing 5-ALA induced surgery.

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Cell Meter™ Caspase 3 7 Cytokine (Mouse) Quantita Androgen Receptor (Phosph Cell Meter™ Live Cell C Cell Meter™ Annexin V B IL (Mouse) Quantitative A Anti-Androgen Receptor pr Cell Meter™ Live Cell C Cell Meter™ Fluorimetri Brain glioma tissue array Androgen Receptor Amplite™ Fluorimetric G

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Monoamine oxidase A inhibition by toxic concentrations of metaxalone.

Serotonin toxicity is a reported complication associated with both therapeutic use and overdose of metaxalone while on therapeutic doses of serotonergic drugs such as serotonin reuptake inhibitors. Monoamine oxidase A (MAO-A) inhibition by metaxalone has been proposed as the etiology of this toxicity. Metaxalone concentrations reported with cases of serotonin toxicity range from 31 to 61 mcg/ml (140-276 µM). We investigated the effect of metaxalone on MAO-A activity using an model. Metaxalone at concentrations ranging from 1.56 to 400 µM were incubated with a proprietary MAO substrate and recombinant human MAO-A for 1 h. After that, an esterase and luciferase were added and luminescence measured. Clorgyline, a known MAO-A inhibitor, was used as a positive control. Luminescence was measured using a Biotek Synergy HT microplate reader. Metaxalone demonstrated significant dose-related inhibition of MAO-A activity. Four-parameter logistic regression analysis demonstrated a strong dose-response relationship at increasing concentrations. Our model shows that at toxic concentrations similar to those reported in case reports metaxalone shows significant MAO-A inhibition. Clinicians should be aware of this mechanism and understand the potentially lethal interactions metaxalone can have when prescribed with other serotonergic drugs and consider this as a potential cause of serotonin toxicity, especially in overdose scenarios.

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Amplite™ Fluorimetric M Goat Anti-Human Monoamine EnzyChrom™ Monoamine Ox EpiQuik Histone Methyltra Anti-Bilirubin Oxidase An Rabbit Anti-Glucose Oxida Rabbit Anti-Toxic Shock S EpiQuik Histone Methyltra Anti-Ascorbate Oxidase An Anti-D-Amino Acid Oxidase cytochrome c oxidase subu Mouse Anti-Lipoprotein Li

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[Alteration of oxidative stress and expression of antioxidases in diaphragm of severely burned rats].

To explore the occurrence of oxidative stress and antioxidases expression in diaphragm of severely burned rats, so that the mechanism of respiratory muscle atrophy and dysfunction post-burn injury will be further clarified. Eighty male Wistar rats (aged 7 to 8 weeks) were divided into sham injury group and burn injury group according to the random number table, with 40 rats in each group. Rats in burn injury group were inflicted with 50% total body surface area full-thickness scald (hereinafter referred to as burn) on the back and abdomen by immersing into 80 ℃ water for 15 s and 8 s respectively. Immediately after injury, 40 mL/kg normal saline was injected through abdomen for resuscitation, and the wounds were treated with iodine. Except for immersing into 37 ℃ warm water and no resuscitation, the other treatments of rats in sham injury group were the same as those of burn injury group. Whole diaphragms of 8 rats per time point per group were collected after anesthesia at post injury hour (PIH) 2 and on post injury day (PID) 1, 3, 7, and 14, and muscle mass was determined. The protein carbonyl content was determined by microplate reader. The protein expressions of catalase, superoxide dismutase 2 (SOD2), and glutathione peroxidase 1 were determined by Western blotting. Data were processed with analysis of variance of factorial design, test, and Bonferroni correction. (1) There were no statistically significant differences in the diaphragm mass of rats between the 2 groups at PIH 2 and on PID 1 (=0.453, 0.755, >0.05). The diaphragm mass of rats in burn injury group started to decrease from PID 3, which was significantly lower than that of sham injury group (=3.321, <0.01). The diaphragm mass of rats in burn injury group started to increase from PID 7 to PID 14, which was significantly lower than that of sham injury group (=4.622, 4.380, <0.01). (2) Protein carbonyl content in diaphragm of rats in burn injury group at PIH 2, and on PID 1, 3, 7, and 14 [(2.7±0.3), (2.5±0.5), (2.4±0.4), (2.5±0.4), (3.2±0.6) pg/mL] was significantly higher than that of sham injury group respectively [(1.2±0.4), (1.6±0.3), (1.5±0.7), (1.7±0.3), (1.8±0.4) pg/mL, =5.994, 3.263, 3.666, 3.158, 5.763, <0.05 or <0.01]. (3) Protein expressions of catalase in diaphragm of rats in burn injury group on PID 1 and 3 were close to those of sham injury group (=0.339, 0.324, >0.05). There were no statistically significant differences in protein expressions of SOD2 in diaphragm of rats between the 2 groups at PIH 2 and on PID 1, 3, 7, and 14 (=1.446, 1.385, 0.757, 1.561, 0.531, >0.05). There were no statistically significant differences in protein expressions of glutathione peroxidase 1 in diaphragm of rats in the 2 groups at PIH 2 and on PID 1, 3, and 7 (=0.200, 0.729, 0.385, 1.559, >0.05). Continuous oxidative stress and relatively insufficient expression of antioxidases in diaphragm induced by burn injury could be a contributor to diaphragm atrophy.

1319 related Products with: [Alteration of oxidative stress and expression of antioxidases in diaphragm of severely burned rats].

Ofloxacin CAS Number [824 OXI TEK (Oxidative Stress 8 Isoprostane oxidative s Anti beta3 AR Human, Poly pCAMBIA0105.1R Vector, (G Transcription factors: O DNA (cytosine 5) methyltr Goat Anti-Human PXR NR1I2 Goat Anti-Human, Rat NRAS Rabbit Anti-Integrin alph IGF1R & MDM2 Protein Prot Recombinant Mouse Interle

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Protein binding kinetics quantification via coupled plasmonic-photonic resonance nanosensors in generic microplate reader.

Almost no analytical assays, either colorimetric or fluorescence assays, for generic microplate readers is capable of dynamic measurements of protein-protein binding or the quantification of kinetic association and dissociation constants of protein interactions. On the other hand, protein binding kinetics quantification can be uniquely done on special expensive surface plasmon resonance (SPR) sensing equipment. Here we report the integration of coupled plasmonic-photonic resonance nanosensors in standard 96-well plate format and by using which, for the very first time, the demonstration of label-free dynamic SPR-like protein binding measurement and kinetics quantification in a generic microplate reader. Our low-cost label-free nanosensor plate enables very sensitive detection of immobilized protein interactions based on the transmission optical density (OD) value changes at specific wavelengths measured in a generic microplate reader. The relative end-point OD value changes show a good linear response with protein concentrations (from 0.05 to 50 μg/ml). And the protein quantification in serum results are consistent with the concurrent hospital lab tests. Most importantly, the kinetic association and dissociation constants of protein interactions in our sensor plate wells are determined by time-lapse dynamic OD value measurement in the generic microplate reader. Enabled by our unique nanosensor plate, SPR-like measurement of protein binding kinetics is now available using generic microplate reader ubiquitous in many chemistry and biomedical research labs.

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Rat monoclonal anti mouse ELISA Microplate Reader ( Rat monoclonal anti mouse Rat intestinal fatty acid Rat monoclonal anti mouse Rat monoclonal anti mouse Goat Anti-Human Vitamin D Cell Meter™ Cell Viabil Rat monoclonal anti mouse Prolactin-Inducible Prote G Protein Coupled Recepto Proteinase Inhibitor 9 (P

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Rapid and selective detection of Fe (III) by using a smartphone-based device as a portable detector and hydroxyl functionalized metal-organic frameworks as the fluorescence probe.

Here, a label-free fluorescent sensor was developed for detection Fe (III) by utilizing the quenching effect of Fe (III) on the fluorescence of the hydroxyl functionalized metal-organic framework MIL-53(Fe)-(OH), which was synthesized by using a one-step solvothermal method. The specific binding interaction between Fe (III) and hydroxyl facilitated the absorption of free Fe (III) to MIL-53(Fe)-(OH) which leads to rapid fluorescent intensity quenching effect. The potential quenching mechanism was proved to be the photo-induced electron transfer (PET) from electron-rich ligands of MIL-53(Fe)-(OH) to the half-filled 3d orbitals of free Fe (III) in the sample solution. For in-field applications, the fluorescence signal was detected rapidly by using a homemade 3D-printed, portable, and low-cost smartphone sensor. A commercial 365 nm UV LED light was adopted as the excitation light source, while the camera in a smartphone was utilized as the optical detector. The fluorescent signals obtained by using the smartphone sensor were in a good agreement with those obtained from a commercial microplate reader. Under the optimal assay conditions, the linear detection range of Fe (III) was 5.0-200 μM, and the limit of detection is 1.7 μM. This result is compatible with the commercial microplate reader. The developed method was successfully adopted to detect Fe (III) in human serum and environmental water samples with acceptable recovery values of 90-108.5%. The portable, low-cost, fast-response, user-friendly and sensitive fluorescent protocol based on a self-quenching fluorescent nanoprobe can be conducted at home or anywhere else without sophisticated instruments, showing a great application potential in clinical diagnosis, on-site environmental monitoring and healthcare at home.

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MarkerGeneTM Fluorescent Cell Meter™ Cell Viabil Cell Meter™ Caspase 3 7 Cell Meter™ Caspase 9 A Annexin V PE Apoptosis De Cell Meter™ Annexin V B MitoCapture Apoptosis Det Amplite™ Fluorimetric G Cell Meter™ Live Cell C Amplite™ Fluorimetric X Amplite™ Fluorimetric G Screen Quest™ Membrane

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Resveratrol attenuates endothelial oxidative injury by inducing autophagy via the activation of transcription factor EB.

Endothelial oxidative injury is a key event in the pathogenesis of atherosclerosis (AS). Resveratrol (RSV) attenuates the oxidative injury in human umbilical vein endothelial cells (HUVECs). Autophagy is critical for the RSV-induced protective effects. However, the exact underlying mechanisms haven't been completely elucidated. Thus, we aimed to explore the role of autophagy of the anti-oxidation of RSV and the underlying mechanism in palmitic acid (PA)-stimulated HUVECs.

1133 related Products with: Resveratrol attenuates endothelial oxidative injury by inducing autophagy via the activation of transcription factor EB.

Transcription factors: O Activating Transcription Rat Vascular Endothelial Mouse Vascular Endothelia Anti Apoptosis Inducing F Apoptosis Inducing Factor Human Endocrine Gland Vas Human Vascular Endothelia Transcription factor E3 a Activating Transcription HSF EMSA Kit: Heat shock Activating Transcription

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Genomic Analysis of a New Estrogen-Degrading Bacterial Strain, sp. DSSKY-A-001.

In this study, we isolated a new estrogen-degrading bacterium from a soil sample collected near a pharmaceutical factory in Beijing, China. Morphological observations, physiological and biochemical analyses, and sequence analysis showed that the strain was in the genus , and it was named DSSKY-A-001. The estrogen degradation rate and growth density of strain DSSKY-A-001 were determined by high-performance liquid chromatography and a growth assay using a microplate reader, respectively. The estrogen degradation rate was 76% on the third day and 90% on the sixth day of culture. Three kinds of estrogen metabolism intermediates were detected by high-performance liquid chromatography and mass spectrometry, and the estrogen metabolic pathway and possible estrogen-degrading enzymes were predicted. RT-PCR was used to verify whether the three putative enzymes, catechol 1,2-dioxygenase, dioxygenase, and 7-hydroxysteroid dehydrogenase, were expressed in the strain. The results of the validation were consistent with the predictions that these three enzymes were present and expressed in DSSKY-A-001. To further understand the estrogen-degrading activity of the strain at the genetic level, we sequenced the genome and performed a functional gene annotation. Through this gene sequence analysis, we identified genes predicted to encode the previously detected enzymes, catechol 1,2-dioxygenase, dioxygenase, and 7-hydroxysteroid dehydrogenase, as well as six other enzymes that may be involved in estrogen degradation. Therefore, a total of nine enzymes related to estrogen degradation were found.

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