Search results for: Human BDNF ELISA ELISA
#29513745 // Save this To Up
Nicotinic acetylcholine receptor (CHRN) expression and function in cultured human adult fungiform (HBO) taste cells.In rodents, CHRNs are involved in bitter taste transduction of nicotine and ethanol. Currently, it is not clear if CHRNs are expressed in human taste cells and if they play a role in transducing the bitter taste of nicotine and ethanol or in the synthesis and release of neurohumoral peptides. Accordingly, we investigated the expression and functional role of CHRNs in HBO cells. Using molecular techniques, we demonstrate that a subset of HBO cells express CHRNs that also co-express TRPM5, T1R3 or T2R38. Exposing HBO cells to nicotine or ethanol acutely or to nicotine chronically induced a differential increase in the expression of CHRN mRNA and protein in a dose- and time-dependent manner. Acutely exposing HBO cells to a mixture containing nicotine plus ethanol induced a smaller increase in CHRN mRNAs relative to nicotine or ethanol treatment alone. A subset of HBO cells responded to nicotine, acetylcholine and ATP with a transient increase in [Ca2+]i. Nicotine effects on [Ca2+]i were mecamylamine sensitive. Brain-derived neurotrophic factor (BDNF) protein was detected in HBO cells using ELISA. Acute nicotine exposure decreased BDNF in HBO cells and increased BDNF release in the medium. CHRNs were also detected in HEK293 cells by RT-PCR. Unlike HBO cells, CHRNs were localized in most of HEK293 cells and majority of HEK293 cells responded to nicotine and ethanol stimulation with a transient increase in [Ca2+]i. BDNF levels in HEK293 cells were significantly higher than in HBO cells but the nicotine induced release of BDNF in the media was a fraction of the BDNF cellular content. We conclude that CHRNs are expressed in TRPM5 positive HBO cells. CHRN mRNA expression is modulated by exposure to nicotine and ethanol in a dose- and time-dependent manner. Nicotine induces the synthesis and release of BDNF in HBO cells.
1410 related Products with: Nicotinic acetylcholine receptor (CHRN) expression and function in cultured human adult fungiform (HBO) taste cells.Interferon-a Receptor Typ Mouse Anti-Human Interleu Rabbit Anti-Human Androge Rabbit Anti-Human Androge Macrophage Colony Stimula Macrophage Colony Stimula interleukin 17 receptor C interferon-alpha receptor Human integrin aVb3, affi anti Transferrin receptor Human Small Intestine Mic Human Large Intestine Mic
#29502978 // Save this To Up
Combined Transplantation of Mesenchymal Stem Cells and Endothelial Progenitor Cells Restores Cavernous Nerve Injury-Related Erectile Dysfunction.Whether combined transplantation of mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) is more effective than transplantation of a single cell type in the restoration of erectile function is unknown.
2079 related Products with: Combined Transplantation of Mesenchymal Stem Cells and Endothelial Progenitor Cells Restores Cavernous Nerve Injury-Related Erectile Dysfunction.Rat Mesenchymal Stem Cell Macrophage Colony Stimula Macrophage Colony Stimula Rat Mesenchymal Cells Human Umbilical Vein Endo GFP Expressing Human Umbi Mitochondria GFP Tag Huma Plasma Membrane GFP Tag H RFP Expressing Human Umbi Human Brain Microvascular GFP Expressing Human Brai Human Dermal Lymphatic Mi
#29366645 // Save this To Up
Serum nerve growth factor beta, brain- and glial-derived neurotrophic factor levels and psychopathology in unmedicated patients with schizophrenia.There is accumulating evidence that neurotrophic factors may be involved in the pathophysiology of patients with schizophrenia. This study aimed to explore the relationship between serum nerve growth factor beta (NGF-beta), brain-derived neurotrophic factor (BDNF), and glial-derived neurotrophic factor (GDNF) levels and psychopathology in unmedicated patients with schizophrenia.
2849 related Products with: Serum nerve growth factor beta, brain- and glial-derived neurotrophic factor levels and psychopathology in unmedicated patients with schizophrenia.Human Brain Derived Neuro Human Glial Derived Neuro Human Nerve Growth Factor Mouse Nerve Growth Factor Dog Brain-derived neurotr ELISA Kit for Brain Deriv Brain derived Neurotrophi Anti-Human Brain-Derived Anti Human Brain Derived Monoclonal Anti-Brain-der Monoclonal Anti Brain der Brain Derived Neurotrophi
#29108879 // Save this To Up
Remyelination modulators in multiple sclerosis patients.Multiple Sclerosis (MS) is a complex autoimmune neuro-inflammatory disorder characterized by persistent MS plaques in the central nervous system. Resolution of MS plaques is dependent on the remyelination competence of surviving oligodendrocytes and surrounding environment. Here, we assessed myelination modulators in a 100 MS patients against 77 healthy controls. Plasma fractions were used for the assessment of insulin growth factor binding protein1 (IGFBP1), brain-derived neurotrophic factor (BDNF), and lipocalin2 (LCN2) using a Luminex multiplex assay, whereas neurofilament light chain (NF-L) was assessed with an enzyme-linked immunosorbent assay. Circulating levels of IGFBP1, LCN2 and NF-L were significantly higher in MS patients (p<0.01). Whereas BDNF levels were significantly lower in MS patients (p=0.014). MS Female patients had significantly higher levels of IGFBP1 compared to male MS patients (p=0.006). MS patients treated with fingolimod had higher LCN2 levels compared to those on natalizumab (r=0.25, p=0.03). Higher NF-L levels associated with clinically isolated syndrome's (CIS) conversion into MS (p=0.002). We conclude that low BDNF and high LCN2 and NF-L levels are associated with MS pathogenesis, and high IGFBP1level is a biomarker for female MS only, suggesting different MS progression pathways between the sexes. LCN2 is a candidate predictor of response to natalizumab treatment, and NF-L is a candidate predictor of CIS conversion into MS.
AEE-788 Mechanisms: Multi Inflammation (Human) Quan Inflammation (Human) Quan Inflammation (Human) Quan Inflammation (Mouse) Quan Inflammation (Rat) Quanti Multiple organs tumor and Multiple organ cancer tis Multiple organ cancer and Multiple organ tumor and High density (188 cases 2 High density (188 cases 2
#29084332 // Save this To Up
Assessment of Neurotrophins and Inflammatory Mediators in Vitreous of Patients With Diabetic Retinopathy.To assess vitreous levels of inflammatory cytokines and neurotrophins (NTs) in diabetic retinopathy (DR) and elucidate their potential roles.
1212 related Products with: Assessment of Neurotrophins and Inflammatory Mediators in Vitreous of Patients With Diabetic Retinopathy.Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Gro g Macrophage In Mouse Macrophage Inflamma Mouse Macrophage Inflamma Mouse Macrophage Inflamma Mouse Macrophage Inflamma Rat Macrophage Inflammato Ofloxacin CAS Number [824
#29069228 // Save this To Up
Different levels of brain-derived neurotrophic factor and cortisol in healthy heavy smokers.Studies suggest that brain-derived neurotrophic factor (BDNF) and the hypothalamic-pituitary-adrenal (HPA) axis modulate dopaminergic activity in response to nicotine and that the concentrations of BDNF and cortisol seem to be dependent on the amount and duration of smoking. Therefore, we investigated BDNF and cortisol levels in smokers ranked by daily cigarette consumption. Twenty-seven adult males (13 non-smokers and 14 smokers) participated in the study. The smokers were divided in two groups: light (n=7) and heavy smokers (n=7). Anthropometric parameters and age were paired between the groups, and plasma BDNF and salivary cortisol levels were measured. Saliva samples were collected on awakening, 30 min after awakening, at 10:00 and 12:00 am, 5:00 and 10:00 pm. Additionally, cotinine serum levels were measured in smokers. Heavy smokers had higher mean values of BDNF compared to the control group (P=0.01), whereas no difference was observed in light smokers. Moreover, heavy smokers presented lower cortisol levels in the last collection (10:00 pm) than the control group (P=0.02) and presented statically higher values of cotinine than the light smokers (P=0.002). In conclusion, changes in BDNF and cortisol levels (10:00 pm) appear to be dependent on heavy cigarette smoking and can be involved in activation and in the relationship between the mesolimbic system and the HPA axis.
2049 related Products with: Different levels of brain-derived neurotrophic factor and cortisol in healthy heavy smokers.Human Brain Derived Neuro Dog Brain-derived neurotr ELISA Kit for Brain Deriv Brain derived Neurotrophi Anti-Human Brain-Derived Anti Human Brain Derived Monoclonal Anti-Brain-der Monoclonal Anti Brain der Brain Derived Neurotrophi Brain Derived Neurotrophi Human Glial Derived Neuro Macrophage Colony Stimula
#29023633 // Save this To Up
BDNF and BMI effects on brain structures of bipolar offspring: results from the global mood and brain science initiative.To compare brain-derived neurotrophic factor (BDNF) levels between offspring of individuals with bipolar disorders (BD) and healthy controls (HCs) and investigate the effects of BDNF levels and body mass index (BMI) on brain structures.
2530 related Products with: BDNF and BMI effects on brain structures of bipolar offspring: results from the global mood and brain science initiative.Human Brain Derived Neuro Human Brain derived neuro Dog Brain-derived neurotr ELISA Kit for Brain Deriv Brain derived Neurotrophi Anti-Human Brain-Derived Anti Human Brain Derived Brain Derived Neurotrophi Brain Derived Neurotrophi Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge
#28951710 // Save this To Up
Brain-derived neurotrophic factor is increased in serum levels of patients with symptomatic dermographism.Symptomatic dermographism (SD) is the most common form of physical urticaria. However, the role of neuroimmune mechanisms in SD is unclear.
1559 related Products with: Brain-derived neurotrophic factor is increased in serum levels of patients with symptomatic dermographism.Human Brain Derived Neuro Dog Brain-derived neurotr ELISA Kit for Brain Deriv Brain derived Neurotrophi Anti-Human Brain-Derived Anti Human Brain Derived Monoclonal Anti-Brain-der Monoclonal Anti Brain der Brain Derived Neurotrophi Brain Derived Neurotrophi Human Glial Derived Neuro Human Brain derived neuro
#28939187 // Save this To Up
The ameliorative effects and underlying mechanisms of dopamine D1-like receptor agonist SKF38393 on Aβ-induced cognitive impairment.Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by extracellular amyloid plaques and intracellular neurofibrillary tangles. It is the most common form of human cognitive decline and dementia. In this study, we aim to systematically investigate the ameliorative effects of dopamine D1-like receptor agonist SKF38393 on cognitive dysfunction and explore its underlying mechanisms. The Aβwas injected intracerebroventricularly to establish cognitive disorder model. Then, a series of behavior tests were used. In order to further study the mechanisms, some relevant protein was assessed by ELISA method and Western blot. The results in behavior tests revealed that SKF38393 significantly ameliorated all the test indexes compared with the model mice. Then SKF38393 increased phosphorylation of cAMP response element binding protein (CREB) and expression of Bcl-2 in Western blot analyses. Furthermore, in ELISA assay, SKF38393 significantly increased the brain-derived neurotrophic factor (BDNF) levels and reduced the β-site APP cleaving enzyme1 (BACE1) and Aβlevels in hippocampus and cortex of mice. However, compared with SKF38393-H, all these results were significantly reversed by the dopamine D1 receptor antagonist SCH23390. These results indicated that SKF38393 could ameliorate Aβ-induced cognitive dysfunction in mice, which may be related to D1 receptor activation. It leads to the phosphorylation of CREB, which promote the expression of BDNF, Bcl-2 and decrease the expression of Aβof mice. Our findings suggest that dopamine D1-like receptor may be a potential target for the treatment of AD and its agonists may become a novel drug in the future.
1911 related Products with: The ameliorative effects and underlying mechanisms of dopamine D1-like receptor agonist SKF38393 on Aβ-induced cognitive impairment.AZD-3514 Mechanisms: Andr Goat Anti- Dopamine recep Rabbit Anti-Dopamine D1 R Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge TGR5 Receptor Agonist Androgen Receptor (Ab 650 Screen Quest™ Dopamine Rabbit Anti-Human Androge Goat Anti-Human Androgen
#28831019 // Save this To Up
Multiplex quantitative assays indicate a need for reevaluating reported small-molecule TrkB agonists.Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase B (TrkB), have emerged as key regulators of brain plasticity and represent disease-modifying targets for several brain disorders, including Alzheimer's disease and major depressive disorder. Because of poor pharmacokinetic properties of BDNF, the interest in small-molecule TrkB agonists and modulators is high. Several compounds have been reported to act as TrkB agonists, and their increasing use in various nervous system disorder models creates the perception that these are reliable probes. To examine key pharmacological parameters of these compounds in detail, we have developed and optimized a series of complementary quantitative assays that measure TrkB receptor activation, TrkB-dependent downstream signaling, and gene expression in different cellular contexts. Although BDNF and other neurotrophic factors elicited robust and dose-dependent receptor activation and downstream signaling, we were unable to reproduce these activities using the reported small-molecule TrkB agonists. Our findings indicate that experimental results obtained with these compounds must be carefully interpreted and highlight the challenge of developing reliable pharmacological activators of this key molecular target.
1430 related Products with: Multiplex quantitative assays indicate a need for reevaluating reported small-molecule TrkB agonists.Obesity (Human) Quantitat Obesity (Human) Quantitat Angiogenesis (Human) Quan Angiogenesis (Human) Quan Angiogenesis (Human) Quan Chemokine (Human) Quantit Cytokine (Human) Quantita Cytokine (Human) Quantita Cytokine (Human) Quantita Cytokine (Human) Quantita Cytokine (Human) Quantita Growth Factor (Human) Qua
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia