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Effect of Clostridium Butyricum Against Microglia-Mediated Neuroinflammation in Alzheimer's Disease Via Regulating gut Microbiota and Metabolites Butyrate.

Recent evidences demonstrated that abnormal gut microbiota (GM) might be involved in the pathogenesis of Alzheimer's disease (AD). However, the role of probiotics in preventing AD by regulating GM-gut-brain axis remain unclear. Here, we investigated the anti-neuroinflammatory effect and its mechanism of probiotic Clostridium butyricum (CB) against AD by regulating GM-gut-brain axis.

2464 related Products with: Effect of Clostridium Butyricum Against Microglia-Mediated Neuroinflammation in Alzheimer's Disease Via Regulating gut Microbiota and Metabolites Butyrate.

Beta Amyloid (1 40) ELISA Beta Amyloid (42) ELISA K Beta Amyloid (40) ELISA K Beta Amyloid (1 40) ELISA Multiple diseases of live Breast disease spectrum t Renal disease spectrum ti Male genitourinary system Skin disease tissue array Kidney disease spectrum ( Colon disease spectrum (c Anti-HBcAg (HBcAb) test s

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Updates in Hepatitis E virus (HEV) field; lessons learned from human liver chimeric mice.

Hepatitis E virus (HEV) is the most common cause of viral hepatitis globally, and it is an emerging pathogen in developed countries. In vivo studies of HEV have long been hindered due to the lack of an efficient small animal model. Recently, human liver chimeric mice were described as an elegant model to study chronic HEV infection. HEV infection was established in mice with humanized liver that were challenged with stool preparations containing HEV genotype (gt)1 and/or gt3. An increase in viral load and the level of HEV Ag in mouse samples were markers of active infection. Plasma-derived HEV preparations were less infectious. The kinetics of HEV ORF2 Ag during HEV infection and its impact on HEV diagnosis were described in this model. In addition, the nature of HEV particles and HEV ORF2 Ag were characterized. Moreover, humanized mice were used to study the impact of HEV infection on the hepatic innate transcriptome and evaluation of anti-HEV therapies. This review highlights recent advances in the HEV field gathered from well-established experimental mouse models, with an emphasis on this model as a tool for elucidating the course of HEV infection, the study of the HEV life cycle, the interaction of the virus with the host, and the evaluation of new anti-HEV therapies.

2076 related Products with: Updates in Hepatitis E virus (HEV) field; lessons learned from human liver chimeric mice.

Human anti hepatitis A vi Human E Antigen of Hepati Human Anti-Core Antigen o Human Anti-E Antigen of H Human Epstein-Barr Virus ELISA Human , Interleukin Beta Amyloid (1 40) ELISA Goat Anti-Human EGR2, (in Human Liver Sinusoidal Mi Goat Anti-Human EPHB2 DRT Human Internal Mammary Ar ELISA Human , Interleukin

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Chemokines and their receptors promoting the recruitment of myeloid-derived suppressor cells into the tumor.

Myeloid-derived suppressor cells (MDSCs) expand in tumor-bearing host. They suppress anti-tumor immune response and promote tumor growth. Chemokines play a vital role in recruiting MDSCs into tumor tissue. They can also induce the generation of MDSCs in the bone marrow, maintain their suppressive activity, and promote their proliferation and differentiation. Here, we review CCL2/CCL12-CCR2, CCL3/4/5-CCR5, CCL15-CCR1, CX3CL1/CCL26-CX3CR1, CXCL5/2/1-CXCR2, CXCL8-CXCR1/2, CCL21-CCR7, CXCL13-CXCR5 signaling pathways, their role in MDSCs recruitment to tumor tissue, and their correlation with tumor development, metastasis and prognosis. Targeting chemokines and their receptors may serve as a promising strategy in immunotherapy, especially combined with other strategies such as chemotherapy, cyclin-dependent kinase or immune checkpoints inhibitors.

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Multiple organ cancer tis Tissue array of ovarian g Pfu DNA Polymerase protei Multiple organ tumor tiss CSL Gradient Thermal Cycl Rat monoclonal anti mouse Single Strand DNA Ligase, FDA Standard Frozen Tissu Recombinant Human PKC the Normal rat multiple organ BACTERIOLOGY BACTEROIDES Recombinant Thermostable

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Discovery of novel 1,2,3-triazole oseltamivir derivatives as potent influenza neuraminidase inhibitors targeting the 430-cavity.

A novel series of 1,2,3-triazole oseltamivir derivatives, which could simultaneously occupy the classical NA catalytic site and the newly reported 430-cavity, were designed, synthesized, and evaluated for their anti-influenza activities. The results demonstrated that four compounds (6g, 6l, 6y and 8c) showed robust anti-influenza potencies against H5N1, H5N2 and H5N6 strains in both enzymatic assay and cellular assay. Especially, 6l was proved to possess the most potent and broad-spectrum anti-influenza activity, with IC values of 0.12 μM, 0.049 μM and 0.16 μM and EC values of 2.45 μM, 0.43 μM and 2.8 μM against H5N1, H5N2 and H5N6 strains, respectively, which were slightly weaker than oseltamivir carboxylate. In addition, in the embryonated egg model, 6l achieved the similar protective effect against H9N2 strain with oseltamivir carboxylate in the tested concentrations. Preliminary structure-activity relationships (SARs), molecular modeling, and calculated physicochemical properties of selected compounds were also discussed.

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DiscoveryPak™ EGFR Tyro Cell Meter™ NIR Mitocho DiscoveryPak™ Stem Cell DiscoveryPak™ Hedgehog Screen Quest™ Membrane Cell Meter™ Mitochondri Mouse Anti-Influenza B Vi EnzyChrom™ Neuraminidas Cell Meter™ JC 10 Mitoc Peptoid Ligand Assay Deve Screen Quest™ Membrane DiscoveryPak™ HDAC Inhi

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HPV33+ HNSCC is associated with poor prognosis and has unique genomic and immunologic landscapes.

To determine the influence of high-risk HPV genotype on outcomes in HNSCC patients.

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Bovine Androstenedione,AS Androgen Receptor , Mouse Androgen Receptor (5α)-2'H-Androst-2-eno[3 Rabbit Anti-Human Androge (3β)-Androsta-5,16-diene Rabbit Anti-Rat Androgen (5α)-Androstane-3,11,17- Androgen Receptor (Ab-650 Androstane 3a,17b diol Gl ∆1-Androstene-3β,17β- (5α,16β)-N-Acetyl-16-ac

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Bioactive indanes: Development and validation of an LC-MS/MS bioanalytical method for the determination of PH46A, a new potential anti-inflammatory agent, in dog and rat plasma and its application to a pharmacokinetic study in dog.

A new chemical entity, which is a chiral indane dimer, PH46A, has been developed by our research group. As a clinical candidate. PH46A has recently completed Phase I clinical studies in man. Previously, during its pre-clinical development, in in vivo pre-clinical studies PH46A showed potent anti-inflammatory properties, which can be targeted at a range of diseases, including inflammatory bowel disease (IBD). To support the pre-clinical development of this drug candidate, we developed a LCMS/MS method for determining PH46 (the acid form of PH46A salt) in both dog and rat plasma using Compound 1 as internal standard (IS). Those species were selected for safety pharmacology and toxicology, as well as pharmacokinetics studies. The method was validated over the range 10-10000 ng/mL for both matrices and the linearity, accuracy, precision and specificity over this range were demonstrated to be acceptable. No significant matrix effects or carryover were observed for both PH46 and IS and recovery was consistent. PH46 was found to be stable in both dog and rat plasma under the test conditions, such as at room temperature for >24 h, through 3 freeze/thaw cycles, and at -20 °C for >1 month. PH46 and IS in dog and rat plasma extracts were also found to be stable in the autosampler against fresh standard extracts on re-injection after 143.5 h and 243.5 h, respectively at 4 °C. 10- and 100-fold dilutions with control matrix were found not to affect the performance of the assay. This method was successfully applied to a pharmacokinetic study in the dog. With the exception of one dog, 003 M, oral administration of PH46A in gelatine capsules was well tolerated at a dose level of 100 mg/kg. The highest C was observed in animal 003 M. The rapid absorption and high plasma concentration observed for animal 003 M compared to the data for animals 001 M and 002 M may account for the sickness observed in this animal; however, the reasons for this have not been investigated.

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FDA Standard Frozen Tissu FDA Standard Frozen Tissu Mouse Anti-Insulin-Like G FDA Standard Frozen Tissu FDA Standard Frozen Tissu Mesothelioma tissue array Rabbit Anti-Rat Androgen Goat Anti-Human Androgen Oral squamous cell cancer Rabbit Anti-IAA (Indole-3 Mouse Anti Salmonella typ Anti beta3 AR Human, Poly

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Volumetric Absorptive Microsampling (VAMS) technology for IGF-1 quantification by automated chemiluminescent immunoassay in dried blood.

For medical diagnostics and anti-doping analyses, insulin-like growth factor 1 (IGF-1) can be measured in serum using automated chemiluminescent immunoassays. The aim of this study was to assess the feasibility of using dried blood instead of serum to measure IGF-1 concentrations with an automated IGF-1 immunoassay and to evaluate if IGF-1 concentrations from dried capillary blood and serum were comparable. Blood samples (venous blood and capillary blood obtained from the arm skin using a device from Seventh Sense Biosystem) were collected with 20 μL Volumetric Absorptive Micro samplers (VAMS) (Mitra®, Neoteryx). These samplers offer the possibility of collecting a fixed volume of blood without perturbation by hematocrit. Starting from dried blood, an aqueous desorption in 0.9% NaCl was efficient to release IGF-1. The solution was directly analyzed on the automated IGF-1 immunoassay. IGF-1 concentrations after extraction from VAMS were lower than in serum (due to the dilution performed for the elution of IGF-1) but measurable for serum concentrations over 50 ng/mL. In addition, IGF-1 on VAMS was stable for at least one month at room temperature. Following adjustment for dilution, serum and dried blood IGF-1 concentrations were of the same order. However lower concentrations were obtained from the capillary blood in particular for high serum concentrations. In conclusion, a micro volume of dried capillary blood could be used to quantify IGF-1 with an automated chemiluminescent immunoassay. However, more data are needed to establish specific IGF-1 reference concentrations using dried capillary blood instead of serum.

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(7’-Benzyloxy-indolymet Indole 5 carboxaldehyde ( Indole 7 carboxaldehyde ( PGE2 Chemiluminescent Imm Indole 6 carboxaldehyde ( Indole 4 carboxaldehyde ( Recombinant HIV-1 pol Int Swine Whole Blood 100ml N Rabbit Anti-NOS-2 iNOS Po PLX-4720 Mechanisms: B-Ra Anti beta3 AR Human, Poly interleukin 17 receptor C

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Nicotine attenuates concanavalin A-induced liver injury in mice by regulating the α7-nicotinic acetylcholine receptor in Kupffer cells.

Nicotine, a potent parasympathomimetic alkaloid, manifests anti-inflammatory properties by activating nicotinic acetylcholine receptors (nAChRs). In this study, we evaluated the effects of nicotine on concanavalin A (ConA)-induced autoimmune hepatitis. Nicotine (0.5 and 1 mg/kg) was intraperitoneally administered to BALB/c mice and mice were intravenously injected with ConA (15 mg/kg) to induce hepatitis. The results showed that nicotine treatment ameliorated pathological lesions in livers and significantly suppressed the expression of pro-inflammatory cytokines in the livers. Such effects were mediated by inhibiting the nuclear factor-kappa B (NF-κB) signaling in livers. Interestingly, nicotine inhibited the ConA-induced inflammatory response in primary cultured Kupffer cells (KCs) but did not alter the proliferation of splenocytes. The protective effects of nicotine against ConA-induced hepatitis were abolished in KC-depleted mice, indicating the requirement of KCs in this process. Additionally, the expression of α7-nAChR on KCs was dramatically increased by nicotine treatment, and the protective effects of nicotine on ConA-induced liver injury were significantly suppressed by treatment with methyllycaconitine (MLA), a specific α7-nAChR antagonist. Consistently, in primary cultured KCs, the activation of NF-κB signaling was also regulated by nicotine treatment. This study suggests that nicotine increases α7-nAChR-mediated cholinergic activity in KCs resulting in decrease of ConA-induced autoimmune hepatitis through inhibiting NF-κB signaling.

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Interleukins Recombinant Mouse Anti-Human Interleu DiscoveryPak™ Receptor Rabbit Anti-Insulin Recep Goat Anti- Dopamine recep Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Liver late stage tumor ti Rabbit Anti-Insulin Recep Goat Anti-Human Serotonin Rabbit Anti-Insulin Recep

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RM, a novel resveratrol derivative, attenuates inflammatory responses induced by lipopolysaccharide via selectively increasing the Tollip protein in macrophages: A partial mechanism with therapeutic potential in an inflammatory setting.

Although the novel resveratrol derivative RM has therapeutic potential for the treatment of inflammatory bowel disease, little is currently known regarding the manner whereby RM regulates excessive inflammatory responses. In this study, we initially investigated the molecular mechanisms underlying the anti-inflammatory effects induced by RM in Toll-like receptor (TLR)-activated macrophages. Upon stimulation with lipopolysaccharide, we found that RM-treated activated macrophages down-regulated the increase in pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-12p70), nitric oxide (NO) production, and activating interleukin-1 receptor-associated kinase 1 (IRAK-1) phosphorylation, mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways. Interestingly, the TLR negative regulator Toll-interacting protein (Tollip) was selectively enhanced during RM stimulation in time- and dose-dependent manners. In response to knockdown of Tollip expression by RNA interference, RM-treated activated macrophages showed augmented expression of inflammatory mediators (pro-inflammatory cytokines, NO, inducible nitric oxidase, and cyclooxygenase-2, and surface molecules) and restored the expression of MAPK and NF-κB signals inhibited by RM treatment. Taken together, our findings indicate that RM has therapeutic potential for treating TLR-induced inflammatory diseases via the promotion of Tollip expression.

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FDA Standard Frozen Tissu FDA Standard Frozen Tissu Human Macrophage Inflamma FDA Standard Frozen Tissu Mouse Macrophage Inflamma Human Macrophage Inflamma Rat Macrophage Inflammato FDA Standard Frozen Tissu Mouse Macrophage Inflamma Multiple organ tumor tiss Rabbit Anti-Human Toll In FDA Standard Frozen Tissu

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Melatonin alleviates oxidative stress in sleep deprived mice: Involvement of small intestinal mucosa injury.

Previous research demonstrated that sleep deprivation (SD) resulted in intestinal homeostasis disorder in colon. The present study was further performed to clarify the role of melatonin in SD-induced small intestinal (SI) mucosal injury.

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Small intestine disease ( Non small cell lung carci Rabbit Anti-intestinal FA Rabbit Anti-intestinal FA Monoclonal Anti Alkaline Tissue array of gastritis Non-small cell lung cance Alkaline Phospatase (ALP) High density non small ce 8 Isoprostane oxidative s Rabbit Anti-intestinal FA Trefoil factor 3 (Intesti

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