Search results for: Human Neuroglobin(NGB)ELISA Kit
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Human Erythroblasts with c-Kit Activating Mutations Have Reduced Cell Culture Costs and Remain Capable of Terminal Maturation.A major barrier to the in vitro production of red blood cells for transfusion therapy is the cost of culture components, with cytokines making up greater than half of the culture costs. Cell culture cytokines also represent a major expense for in vitro studies of human erythropoiesis. HUDEP2 cells are an E6/E7 immortalized erythroblast line used for the in vitro study of human erythropoiesis. In contrast to other cell lines used to study human erythropoiesis, such as K562 cells, HUDEP2 cells are capable of terminal maturation, including hemoglobin accumulation and chromatin condensation. As such, HUDEP2 cells represent a valuable resource for studies not amenable to primary cell cultures, however reliance on the cytokines stem cell factor (SCF) and erythropoietin (EPO) make HUDEP2 cultures very expensive to maintain. To decrease culture costs, we used CRISPR/Cas9 genome editing to introduce a constitutively activating mutation into the stem cell factor receptor gene KIT, with the goal of generating human erythroblasts capable of SCF-independent expansion. Three independent HUDEP2 lines with unique KIT receptor genotypes were generated and characterized. All three lines were capable of robust expansion in absence of SCF, decreasing culture costs by approximately half. Importantly, these lines remained capable of terminal maturation. Together, these data suggest that introduction of c-Kit activating mutations into human erythroblasts may help reduce the cost of erythroblast culture making the in vitro study of erythropoiesis, and the eventual in vitro production of RBCs, more economically feasible.
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BDNF Val66Met genetic variation and its plasma level in patients with morbid obesity: A case-control study.Obesity is a major public health concern worldwide. Genetic, behavioral, and environmental factors contribute to the multifactorial etiology of obesity. Evidence suggests an association between human Brain-Derived Neurotrophic Factor (BDNF) Val66Met single nucleotide polymorphism (SNP) and obesity. Reduced plasma BDNF levels have also been reported in patients with eating disorders and obesity. We aimed to evaluate the BDNF Val66Met (rs6265) SNP and also plasma BDNF levels in morbidly obese patients compared with healthy normal controls in southern Iran. One hundred morbidly obese patients and one hundred eight healthy normal controls were enrolled. Blood-derived DNA samples were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and confirmed by DNA sequencing. Plasma BDNF levels were evaluated using a commercially available sandwich enzyme-linked immunosorbent assay (ELISA) kit for human BDNF. Data analysis was performed by SPSS software, version 18.0. Genotype distribution was not significantly different between obese patients and controls. However, plasma BDNF levels were significantly lower in obese patients compared with controls. Interestingly, a significant association was found between BDNF Val66Met SNP and plasma BDNF levels. No relationship was observed between BDNF Val66Met SNP and all assessed demographic and clinical characteristics of obese patients. It seems that plasma BDNF levels were associated with both obesity and BDNF Val66Met SNP. However, this association was not found between BDNF Val66Met SNP and obesity. Further studies with larger sample sizes are needed for more detailed assessment of this genetic variation as a potential biomarker for obesity.
1929 related Products with: BDNF Val66Met genetic variation and its plasma level in patients with morbid obesity: A case-control study.Incu Tissue(square vessel Incu Tissue(square vessel Cell Cycle Control Phosph Obesity (Human) Antibody Obesity (Human) Antibody Breast cancer tissue arra Breast cancer tissue arra Colon carcinoma tissue ar Colon carcinoma tissue ar Multiple colon cancer tis Colon adenocarcinoma tiss Bovine Androstenedione,AS
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Pro-apoptotic and anti-inflammatory effects of araloside A on human rheumatoid arthritis fibroblast-like synoviocytes.Rheumatoid arthritis fibroblast-like synoviocytes play an essential role in the occurrence and progression of rheumatoid arthritis. As the main pharmacologically active components of Aralia taibaiensis, total saponins, particularly triterpenoid saponins, have been shown to possess multiple pharmacological activities including relieving rheumatism. However, the effect of araloside A, a triterpenoid saponin extracted from the root bark of Aralia taibaiensis, on rheumatoid arthritis remains unknown. Cell counting kit-8 assay was employed to determine cell viability. Flow cytometry analysis, caspase-3/7 activity assay and Western blot analysis of cytochrome c and B-cell lymphoma 2 were conducted to evaluate cell apoptosis. Inflammation was assessed by detecting the production of inflammatory cytokines including interleukin-6 and interleukin-8, as well as inflammatory mediators including nitric oxide and prostaglandin E. The changes of the nuclear factor kappa B pathway were examined by Western blot. Results showed that araloside A concentration-dependently inhibited the proliferation of MH7A cells. Meanwhile, araloside A dose-dependently augmented the apoptotic rate and caspase-3/7 activity, increased cytochrome c level and decreased B-cell lymphoma 2 level in MH7A cells. Araloside A concentration-dependently curbed the production of interleukin-6, interleukin-8, prostaglandin E and nitric oxide in MH7A cells. In addition, we found that araloside A inhibited the nuclear factor kappa B pathway and inhibition of the nuclear factor kappa B pathway by BAY11-7082 and PDTC showed a similar role to araloside A in MH7A cells. Taken together, araloside A exerted pro-apoptotic and anti-inflammatory effects in rheumatoid arthritis fibroblast-like synoviocytes via inhibition of the nuclear factor kappa B pathway.
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Coupling Langmuir with Michaelis-Menten-A practical alternative to estimate Se content in rice?Selenium plays an important, but vastly neglected role in human nutrition with a narrow gap between dietary deficiency and toxicity. For a potential biofortification of food with Se, as well as for toxicity-risk assessment in sites contaminated by Se, modelling of local and global Se cycling is essential. As bioavailability of Se for rice plants depends on the speciation of Se and the resulting interactions with mineral surfaces as well as the interaction with Se uptake mechanisms in plants, resulting plant Se content is complex to model. Unfortunately, simple experimental models to estimate Se uptake into plants from substrates have been lacking. Therefore, a mass balance of Se transfer between lithosphere (represented by kaolinite), hydrosphere (represented by a controlled nutrient solution), and biosphere (represented by rice plants) has been established. In a controlled, closed, lab-scale system, rice plants were grown hydroponically in nutrient solution supplemented with 0-10 000 μg L-1 Se of either selenate or selenite. Furthermore, in a series of batch experiments, adsorption and desorption were studied for selenate and selenite in competition with each of the major nutrient oxy-anions, nitrate, sulfate and phosphate. In a third step, the hydroponical plants experiments were coupled with sorption experiments to study synergy effects. These data were used to develop a mass balance fitting model of Se uptake and partitioning. Adsorption was well-described by Langmuir isotherms, despite competing anions, however, a certain percentage of Se always remained bio-unavailable to the plant. Uptake of selenate or selenite by transporters into the rice plant was fitted with the non-time differentiated Michaelis-Menten equation. Subsequent sequestration of Se to the shoot was better described using a substrate-inhibited variation of the Michaelis-Menten equation. These fitted parameters were then integrated into a mass balance model of Se transfer.
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Effects of Sleep Deprivation (SD) on Rats via ERK1/2 Signaling Pathway.BACKGROUND Sleep deprivation (SD) is common in humans, and sleep loss has a significant influence on health and produces related diseases. Orexin-A has been demonstrated to play a role in physiological processes, including feeding, sleep/wake cycle, and energy metabolism. The aim of this study was to investigate the effect of SD on rats and to define the underlying mechanism. MATERIAL AND METHODS We constructed an SD rat model. The Morris water maze test was used to assess rat learning and memory. Imaging of hippocampus and hippocampal tissue in rats were captured by magnetic resonance imaging or electron microscopy. We used the CCK-8 kit to assess cell viability. The level of protein was measured using Western blot analysis, and qRT-PCR was used to evaluate mRNA level. RESULTS SD rats had poorer learning and memory and had damage to the hippocampus. SD resulted in shrinkage of hippocampal volume and encephalocele size. SD increased the expression of Orexin-A, OX1R, OX2R, and PARP-1, and decreased the expression of ERK1/2 and p-ERK1/2. Orexin-A (0-10 μM) improved neuron viability, whereas orexin-A (10-100 μM) attenuated neuron viability. SB334867 treatment reduced the viability of neurons treated with orexin-A. NU1025 treatment increased cell viability, especially in neurons treated with orexin-A. SB334867 treatment decreased the p-ERK1/2 levels in neurons treated with orexin-A. NU1025 increased the expression of p-ERK1/2 in neurons treated with orexin-A. CONCLUSIONS SD decreases learning and memory through damage to the hippocampus. Higher concentrations of orexin-A had a major negative effect on hippocampal neurons via OX1R and PARP-1 through inhibition of the ERK1/2 signaling pathway.
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LncRNA PVT1 knockdown affects proliferation and apoptosis of uveal melanoma cells by inhibiting EZH2.To detect the expression of long non-coding ribonucleic acid (lncRNA) plasmacytoma variant translocation gene 1 (PVT1) in uveal melanoma (UM) tissues, and to investigate its influence on the proliferation and apoptosis of UM cells as well as its mechanism.
2754 related Products with: LncRNA PVT1 knockdown affects proliferation and apoptosis of uveal melanoma cells by inhibiting EZH2.Epidermal Growth Factor ( Epidermal Growth Factor ( EZH2 KMT6 Control Peptid EZH2 KMT6 antibody Isoty Melanoma; Clone HMB45 Melanoma; Clone HMB45 Melanoma; Clone HMB45 Fontana-Masson Stain Kit Fontana-Masson Stain Kit EZH2 Anti C Reactive Protein A anti HSV (II) gB IgG1 (mo
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Is Atrial Natriuretic Peptide (ANP) and Natriuretic Peptide Receptor-A (NPR-A) Expression in Human Placenta and Decidua Normal?BACKGROUND Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates blood pressure and the salt-water balance in the blood. It acts through natriuretic peptide receptors (NPR), and the major biologically active ANP receptor is natriuretic peptide receptor-A (NPR-A). Aberrant forms of ANP and its receptors have been reported in patients with preeclampsia. However, whether aberrant forms of ANP or NPR-A are present in preeclamptic placenta, and what their role is in preeclampsia pathogenesis, has not yet been elucidated clearly. The aim of this study was to assess the expression of ANP and NPR-A in the placenta and decidua and its role in preeclampsia development. MATERIAL AND METHODS The expression of ANP and NPR-A in the first-trimester villous and decidua, full-term placenta, and preeclamptic placenta was determined using immunohistochemistry and Western blot analysis. The HTR8/SVneo cell line was used to investigate the role of NPR-A in proliferation, apoptosis, and invasion using Cell Counting Kit-8 analysis, flow cytometry analysis, and a Transwell invasion assay, respectively. RESULTS ANP and NPR-A were localized in the syncytiotrophoblasts, cytotrophoblasts, and trophoblast columns of human first-trimester villous trophoblast cells of decidua, and in the glandular epithelium and extravillous trophoblast cells of decidua. ANP-positive and NPR-A-positive cells in the decidual stroma were clustered around and infiltrated into the vascular wall of the spiral artery undergoing remodeling. NPR-A expression was significantly reduced in preeclamptic placentas, and NPR-A knockdown significantly impaired the invasion ability of HTR8/SVneo cells, although it had no effect on cell proliferation and apoptosis. CONCLUSIONS ANP and NPR-A are involved in human placental development. Decreased levels of NPR-A may contribute to the development of preeclampsia.
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Oncogenic kinase inhibition limits Batf3-dependent dendritic cell development and antitumor immunity.Gastrointestinal stromal tumor (GIST) is driven by an activating mutation in the proto-oncogene. Using a mouse model of GIST and human specimens, we show that intratumoral murine CD103CD11b dendritic cells (DCs) and human CD141 DCs are associated with CD8 T cell infiltration and differentiation. In mice, the antitumor effect of the Kit inhibitor imatinib is partially mediated by CD103CD11b DCs, and effector CD8 T cells initially proliferate. However, in both mice and humans, chronic imatinib therapy decreases intratumoral DCs and effector CD8 T cells. The mechanism in our mouse model depends on Kit inhibition, which reduces intratumoral GM-CSF, leading to the accumulation of Batf3-lineage DC progenitors. GM-CSF is produced by γδ T cells via macrophage IL-1β. Stimulants that expand and mature DCs during imatinib treatment improve antitumor immunity. Our findings identify the importance of tumor cell oncogene activity in modulating the Batf3-dependent DC lineage and reveal therapeutic limitations for combined checkpoint blockade and tyrosine kinase inhibition.
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Reduction of β-ODAP and IP contents in Lathyrus sativus L. seed by high hydrostatic pressure.Grass pea (Lathyrus sativus L.) seeds contain an endogenous neurotoxic non-proteinogenic amino acid, β-N-oxalyl-l-α,β-diaminopropionic acid (β-ODAP), a major limiting factor-for their human consumption. Furthermore, phytate (IP), a well-known antinutrient is present in concentration capable of hindering bioavailability of iron (Fe), zinc (Zn), calcium (Ca), phosphorus (P) and other micronutrients from the seeds. Due to the reported capability of high hydrostatic pressure (HHP) to reduce the content of certain antinutritional/toxic agents in seeds and grains, the impact of HHP on the reduction of β-ODAP and IP were investigated. The contents of β-ODAP of accessions from different regions in Ethiopia were found to be in the range of 51.94 to 806.52 mg/100 g. Accession (GF- Alemu, AK) exhibiting the highest β-ODAP content was selected for HHP treatment in soaked and batter forms using Central Composite Face Centered Design of experiments. The best HHP conditions in respect to β-ODAP reduction were also applied to the accession (GP-240038) with the lowest β-ODAP-content, a genetically improved variety (Wassie) and a variety from Germany (GR). The HHP treatment at 600 MPa for 25 min of seeds soaked for 6 h and 12 h exhibited the maximum reduction of β-ODAP (232.11 mg/100 g) and IP (21.11 mg/100 g) respectively. The combined incremental effect of pressure and soaking time resulted in a more significant (p ≤ .001) reduction in both compounds than the interaction of pressure with holding time (p ≤ .05). A reduction of β-ODAP from 36.00 to 71.22% by soaked-HHP treatment was observed. β-ODAP reductions were always higher for soaked compared to batter grass pea seeds. IP contents after HHP treatment ranged from 33.65 mg/100 g to nill. It can be concluded that pressure, soaking and holding time as well as the grass pea seed accession/variety had great impact on molecular structure changes, enhancement of enzyme activity and reduction in β-ODAP and IP content.
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Human β-defensin-3 participates in intra-amniotic host defense in women with labor at term, spontaneous preterm labor and intact membranes, and preterm prelabor rupture of membranes.Human β-defensin-3 (HBD-3) has a broad spectrum of antimicrobial activity, and activity and, therefore, plays a central role in host defense mechanisms against infection. Herein, we determined whether HBD-3 was a physiological constituent of amniotic fluid during midtrimester and at term and whether the concentration of this defensin was increased in amniotic fluid of women with spontaneous preterm labor and intact membranes and those with preterm prelabor rupture of membranes (pPROM) with intra-amniotic inflammation or intra-amniotic infection.
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