Search results for: C57BL6 Mouse Whole Blood 25 ml
#28687713 2017/07/08 Save this To Up
TLR9 is up-regulated in human and murine NASH: pivotal role in inflammatory recruitment and cell survival.Background and aims: TLR9 deletion protects against steatohepatitis due to choline-amino acid depletion and high-fat diet. We measured TLR9 in human non-alcoholic steatohepatitis (NASH) livers, and tested whether TLR9 mediates inflammatory recruitment in three murine models of non-alcoholic fatty liver disease (NAFLD). Methods: We assayed TLR mRNA in liver biopsies from bariatric surgery patients. Wild-type (Wt), appetite-dysregulated Alms1 mutant (foz/foz), Tlr9(-/-), and Tlr9(-/-)foz/foz C57BL6/J mice and bone marrow (BM) chimeras were fed 0.2% cholesterol, high-fat, high sucrose (atherogenic[Ath]) diet or chow, and NAFLD activity score (NAS)/NASH pathology, macrophage/neutrophil infiltration, cytokines/chemokines, and cell death markers measured in livers. Results: Hepatic TLR9 and TLR4 mRNA were increased in human NASH but not simple steatosis, and in Ath-fed foz/foz mice with metabolic syndrome-related NASH. Ath-fed Tlr9(-/-) mice showed simple steatosis and less Th1 cytokines than Wt. Tlr9(-/-)foz/foz mice were obese and diabetic, but necroinflammatory changes were less severe than Tlr9(+/+).foz/foz mice. TLR9-expressing myeloid cells were critical for Th1 cytokine production in BM chimeras. BM macrophages from Tlr9(-/-) mice showed M2 polarization, were resistant to M1 activation by necrotic hepatocytes/other pro-inflammatory triggers, and provoked less neutrophil chemotaxis than Wt Livers from Ath-fed Tlr9(-/-) mice appeared to exhibit more markers of necroptosis [receptor interacting protein kinase (RIP)-1, RIP-3, and mixed lineage kinase domain-like protein (MLKL)] than Wt, and ∼25% showed portal foci of mononuclear cells unrelated to NASH pathology.
1156 related Products with: TLR9 is up-regulated in human and murine NASH: pivotal role in inflammatory recruitment and cell survival.Rabbit Anti-Cell death in Rabbit Anti-Cell death in Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon CELLKINES Natural Human I Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Gro g Macrophage In Goat Anti-Human Laforin (
#28682508 2017/07/06 Save this To Up
Bone marrow endothelial progenitor cells activate hepatic stellate cells and aggravate carbon tetrachloride induced liver fibrosis in mice via paracrine factors.Bone marrow derived endothelial progenitor cells (BM-EPCs) are increased in chronic liver disease (CLD). Their role in hepatic fibrosis and regeneration remains an area of intense studies. We investigated the migration and secretory functions of BM-EPCs in fibrotic mice liver.
1781 related Products with: Bone marrow endothelial progenitor cells activate hepatic stellate cells and aggravate carbon tetrachloride induced liver fibrosis in mice via paracrine factors.anti Transferrin receptor Human Liver Sinusoidal Mi GFP Expressing Human Live RFP Expressing Human Live Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Anti C Reactive Protein A anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl
#28319461 2017/03/20 Save this To Up
Monocytes/Macrophages Mobilization Orchestrate Neovascularization after Localized Colorectal Irradiation.In patients undergoing radiotherapy for cancer, radiation dose to healthy tissue can occur, causing microvascular damage. Monocytes that have been shown to promote tissue revascularization comprise the subsets: CD11b(+)Ly6G(-)7/4(hi)/monocytes(hi) and CD11b(+)Ly6G(-)7/4(lo)/monocytes(lo). We hypothesized that monocytes were implicated in postirradiation blood vessel formation. C57Bl6 mice underwent localized colorectal irradiation and were sacrificed at different times after exposure. Bone marrow, spleen, blood and colon were collected. Fourteen days postirradiation, colons expressed proangiogenic actors and adhesion molecules. Monocytes(hi), which were the main subset of infiltrating monocytes, mobilized to the blood from spleen and bone marrow, peaking at day 14 postirradiation, and were associated with lymphocyte Th1 polarization. At day 28 postirradiation, angiographic score and capillary density increased by ∼1.8-fold, and then returned to nonirradiated levels at day 60. Clodronate-mediated depletion of circulating monocytes prior to irradiation resulted in a ∼1.4-fold decrease in angiographic score and capillary density compared to the nontreated control. Histological analysis of the colon in clodronate-treated mice revealed a massive decrease of macrophage and lymphocyte infiltration as well as reduced collagen deposition in crypt area at day 21. However, late depletion of monocytes from day 25 postirradiation had no effect on fibrotic process. These findings demonstrate a central role for monocyte/macrophage activation in the orchestration of a neovascularization mechanism after localized colorectal irradiation.
2011 related Products with: Monocytes/Macrophages Mobilization Orchestrate Neovascularization after Localized Colorectal Irradiation.Rat Anti-Mouse Macrophage Rat Anti-Mouse Macrophage anti CD16 NK cells, monoc Signal Transduction Anti Signal Transduction Anti Colorectal cancer tissue Colorectal carcinoma and Colorectal (colon and rec Colorectal (colon and rec Mouse Anti-Human Macropha Mouse Anti-Human Macropha Mouse Anti-Human Macropha
#27931520 2016/12/09 Save this To Up
Translational potential of long-term decreases in mitochondrial lipids in a mouse model of Gulf War Illness.Gulf War Illness (GWI) affects 25% of veterans from the 1990-1991 Gulf War (GW) and is accompanied by damage to the brain regions involved in memory processing. After twenty-five years, the chronic pathobiology of GWI is still unexplained. To address this problem, we examined the long-term consequences of GW exposures in an established GWI mouse model to identify biological processes that are relevant to the chronic symptoms of GWI. Three-month old male C57BL6 mice were exposed for 10days to GW agents (pyridostigmine bromide and permethrin). Barnes Maze testing conducted at 15- and 16-months post-exposure revealed learning and memory impairment. Immunohistochemical analyses showed astroglia and microglia activation in the hippocampi of exposed mice. Proteomic studies identified perturbation of mitochondria function and metabolomics data showed decreases in the Krebs cycle compounds, lactate, β-hydroxybutyrate and glycerol-3 phosphate in the brains of exposed mice. Lipidomics data showed decreases in fatty acids, acylcarnitines and phospholipids, including cardiolipins in the brains of exposed mice. Pilot biomarker studies showed that plasma from exposed mice and veterans with GWI had increases in odd-chain, and decreases in long-chain, acylcarnitines compared to their respective controls. Very long-chain acylcarnitines were decreased in veterans with GWI compared to controls. These studies suggest that mitochondrial lipid disturbances might be associated with GWI and that further investigation is required to determine its role in the pathophysiology of this illness. Targeting mitochondrial function may provide effective therapies for GWI, and that lipid abnormalities could serve as biomarkers of GWI.
2150 related Products with: Translational potential of long-term decreases in mitochondrial lipids in a mouse model of Gulf War Illness.Goat Anti-Mouse APOBEC1, Goat Anti- Fibrillin 2 (m Goat Anti-Human, Mouse GC Goat Anti-Human, Mouse In Goat Anti-Rat IRAK3 (mous Goat Anti-Mouse ATG16L1, Goat Anti-Rat AVPR1B (mou Interleukin-34 IL34 (N-t Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon HIV1 integrase antibody, Goat Anti-Mouse SAR1, (in
#27547968 2016/08/23 Save this To Up
Maternal Fat Feeding Augments Offspring Nephron Endowment in Mice.Increasing consumption of a high fat 'Western' diet has led to a growing number of pregnancies complicated by maternal obesity. Maternal overnutrition and obesity have health implications for offspring, yet little is known about their effects on offspring kidney development and renal function. Female C57Bl6 mice were fed a high fat diet (HFD, 21% fat) or matched normal fat diet (NFD, 6% fat) for 6 weeks prior to pregnancy and throughout gestation and lactation. HFD dams were overweight and glucose intolerant prior to mating but not in late gestation. Offspring of NFD and HFD dams had similar body weights at embryonic day (E)15.5, E18.5 and at postnatal day (PN)21. HFD offspring had normal ureteric tree development and nephron number at E15.5. However, using unbiased stereology, kidneys of HFD offspring were found to have 20-25% more nephrons than offspring of NFD dams at E18.5 and PN21. Offspring of HFD dams with body weight and glucose profiles similar to NFD dams prior to pregnancy also had an elevated nephron endowment. At 9 months of age, adult offspring of HFD dams displayed mild fasting hyperglycaemia but similar body weights to NFD offspring. Renal function and morphology, measured by transcutaneous clearance of FITC-sinistrin and stereology respectively, were normal. This study demonstrates that maternal fat feeding augments offspring nephron endowment with no long-term consequences for offspring renal health. Future studies assessing the effects of a chronic stressor on adult mice with augmented nephron number are warranted, as are studies investigating the molecular mechanisms that result in high nephron endowment.
Leptin ELISA Kit, Rat Lep Rat intestinal fatty acid DiscoveryPak™ Stem Cell Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Fatty acid free heat sho Fatty acid free heat sho Fatty acid free heat sho Fatty acid free heat sho Sterile filtered goat se Sterile filtered goat se Sterile filtered mouse s
#27450968 2016/09/26 Save this To Up
Effect of oral administration of AZD8309, a CXCR2 antagonist, on the severity of experimental pancreatitis.Acute pancreatitis is a common gastrointestinal disorder burdened with a high mortality. Two pathophysiological events during experimental pancreatitis are thought to determine the clinical course: premature digestive protease activation and tissue infiltration by inflammatory cells. We have investigated the effect of AZD8309, a potent and orally bioavailable antagonist of the chemokine receptor CXCR2, which has been proposed to regulate the transmigration of neutrophils.
2644 related Products with: Effect of oral administration of AZD8309, a CXCR2 antagonist, on the severity of experimental pancreatitis.Ofloxacin CAS Number [824 Hh Signaling Pathway Anta MIF Antagonist, ISO 1 PPARγ Antagonist, G3335 PPARγ Antagonist, G3335; PPARγ Antagonist, G3335 PPARγ Antagonist, G3335; TCP-1 theta antibody Sour Recombinant Chicken GH An Recombinant Chicken GH An Recombinant Chicken GH An Recombinant Sheep GH Anta
#26823282 2016/05/04 Save this To Up
Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O2- dismutation on renal autoregulation in the time and frequency domains.Renal blood flow autoregulation was investigated in anesthetized C57Bl6 mice using time- and frequency-domain analyses. Autoregulation was reestablished by 15 s in two stages after a 25-mmHg step increase in renal perfusion pressure (RPP). The renal vascular resistance (RVR) response did not include a contribution from the macula densa tubuloglomerular feedback mechanism. Inhibition of nitric oxide (NO) synthase [N(G)-nitro-l-arginine methyl ester (l-NAME)] reduced the time for complete autoregulation to 2 s and induced 0.25-Hz oscillations in RVR. Quenching of superoxide (SOD mimetic tempol) during l-NAME normalized the speed and strength of stage 1 of the RVR increase and abolished oscillations. The slope of stage 2 was unaffected by l-NAME or tempol. These effects of l-NAME and tempol were evaluated in the frequency domain during random fluctuations in RPP. NO synthase inhibition amplified the resonance peak in admittance gain at 0.25 Hz and markedly increased the gain slope at the upper myogenic frequency range (0.06-0.25 Hz, identified as stage 1), with reversal by tempol. The slope of admittance gain in the lower half of the myogenic frequency range (equated with stage 2) was not affected by l-NAME or tempol. Our data show that the myogenic mechanism alone can achieve complete renal blood flow autoregulation in the mouse kidney following a step increase in RPP. They suggest also that the principal inhibitory action of NO is quenching of superoxide, which otherwise potentiates dynamic components of the myogenic constriction in vivo. This primarily involves the first stage of a two-stage myogenic response.
2661 related Products with: Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O2- dismutation on renal autoregulation in the time and frequency domains.Thermal Shaker with cooli CAR,Car,Constitutive andr FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Normal mouse multiple org Normal rat multiple organ Normal rat multiple organ Normal rat multiple organ
#26202300 2015/11/02 Save this To Up
HMGB1 binds to activated platelets via the receptor for advanced glycation end products and is present in platelet rich human coronary artery thrombi.High mobility group box 1 (HMGB1) acts as both a nuclear protein that regulates gene expression, as well as a pro-inflammatory alarmin that is released from necrotic or activated cells. Recently, HMGB1-expression in human atherosclerotic plaques was identified. Therapeutic blockade of HMGB1 reduced the development of diet-induced atherosclerosis in ApoE knockout mice. Thus, we hypothesised an interaction between HMGB1 and activated platelets. Binding of recombinant HMGB1 to platelets was assessed by flow cytometry. HMGB1 bound to thrombin-activated human platelets (MFI 2.49 vs 25.01, p=0.0079). Blood from wild-type, TLR4 and RAGE knockout mice was used to determine potential HMGB1 receptors on platelets. HMGB1 bound to platelets from wild type C57Bl6 (MFI 2.64 vs 20.3, p< 0.05), and TLR4-/- mice (MFI 2.11 vs 25.65, p< 0.05) but failed to show binding to platelets from RAGE-/- mice (p > 0.05). RAGE expression on human platelets was detected by RT-PCR with mRNA extracted from highly purified platelets and confirmed by Western blot and immunofluorescence microscopy. Platelet activation increased RAGE surface expression (MFI 4.85 vs 6.74, p< 0.05). Expression of HMGB1 in human coronary artery thrombi was demonstrated by immunohistochemistry and revealed high expression levels. Platelets bind HMGB1 upon thrombin-induced activation. Platelet specific expression of RAGE could be detected at the mRNA and protein level and is involved in the binding of HMGB1. Furthermore, platelet activation up-regulates platelet surface expression of RAGE. HMGB1 is highly expressed in platelet-rich human coronary artery thrombi pointing towards a central role for HMGB1 in atherothrombosis, thereby suggesting the possibility of platelet targeted anti-inflammatory therapies for atherothrombosis.
2309 related Products with: HMGB1 binds to activated platelets via the receptor for advanced glycation end products and is present in platelet rich human coronary artery thrombi.Anti RAGE (Receptor for A Anti 3 DG imidazolone Mon Rat monoclonal anti mouse interleukin 17 receptor C Anti AGE 3 Monoclonal Ant anti Transferrin receptor Human Coronary Artery End GFP Expressing Human Coro Human Internal Mammary Ar GFP Expressing Human Inte Human Anti-Advanced Glyco Anti AGO2 Human, Monoclon
#25978344 2015/06/13 Save this To Up
Increased adipose tissue secretion of Fetuin-A, lipopolysaccharide-binding protein and high-mobility group box protein 1 in metabolic syndrome.Adipose Tissue (AT) dysregulation contributes to the pro-inflammatory state and insulin resistance of Metabolic Syndrome (MetS). We examined AT secretion of the hepatokine, Fetuin-A, LBP, sCD14 and HMGB-1, and toll-like receptor 2 and 4 protein levels in MetS and controls.
1066 related Products with: Increased adipose tissue secretion of Fetuin-A, lipopolysaccharide-binding protein and high-mobility group box protein 1 in metabolic syndrome.Human High Mobility Group HMG2 (High mobility group Rabbit Anti-Rat Androgen Goat Anti-Human Vitamin D Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Taq SSB (Single Stranded Taq SSB (Single Stranded S100 alpha - Rabbit polyc
#25848815 2015/04/08 Save this To Up
Inhibition of HMGCoA reductase by simvastatin protects mice from injurious mechanical ventilation.Mortality from severe acute respiratory distress syndrome exceeds 40% and there is no available pharmacologic treatment. Mechanical ventilation contributes to lung dysfunction and mortality by causing ventilator-induced lung injury. We explored the utility of simvastatin in a mouse model of severe ventilator-induced lung injury.
2116 related Products with: Inhibition of HMGCoA reductase by simvastatin protects mice from injurious mechanical ventilation.Anti C Reactive Protein A Simvastatin Simvastatin; Appearance W Simvastatin Simvastatin; Appearance W ubiquinol-cytochrome c re ubiquinol-cytochrome c re L-xylulose reductase anti Directed In Vivo Angiogen HMG-CoA Reductase Antibod Aldose Reductase Aldose Reductase Aldose R
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