Search results for: Mouse Anti-Influenza-B
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Design, synthesis, and neuroprotective effects of dual-brain targeting naproxen prodrug.A new dual-targeting naproxen prodrug conjugated with glucose and ascorbic acid for central nervous system (CNS) drug delivery was designed and synthesized in order to effectively deliver naproxen to the brain. Naproxen could be released from the prepared prodrugs when incubated with various buffers, mouse plasma, and brain homogenate. Also, the prodrug showed superior neuroprotective effect in vivo over naproxen. Our results suggest that chemical modification of therapeutics with warheads of glucose and ascorbic acid represents a promising and efficient strategy for the development of brain targeting prodrugs by utilizing the endogenous transportation mechanism of the warheads.
1354 related Products with: Design, synthesis, and neuroprotective effects of dual-brain targeting naproxen prodrug.Human Brain Derived Neuro Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Human Brain derived neuro Androgen Receptor (Ab 650 Cell Meter™ Cell Viabil Recombinant Human pro-Bra AE 6220 Dual Slab Chamber AE 6220 Dual Slab Chamber Beta Amyloid (42) ELISA K
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The Immunogenicity and Anti-Tumor Efficacy of a Rationally Designed EGFR Vaccine.The abnormally activated EGFR promotes tumor growth, invasion and metastasis. Current therapeutics targeting EGFR have markedly improved the clinical outcome, but they are limited in use due to transient efficacy, frequent administration, high cost and significant toxicity.
2856 related Products with: The Immunogenicity and Anti-Tumor Efficacy of a Rationally Designed EGFR Vaccine.Rabbit Anti-Human Androge Rabbit Anti-Human Androge Rabbit anti EGFR (Ab-1070 Rabbit anti EGFR (Ab-1092 Rabbit anti PKC theta (Ab Rabbit anti EGFR (Ab-678) Rabbit anti EGFR (Ab-693) Rabbit anti EGFR (Ab-1172 Rabbit anti EGFR (Ab-1197 Rabbit anti EGFR (Ab-869) Rabbit anti EGFR (Ab-1110 Rabbit anti PKC theta (Ab
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Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress.Increased endoplasmic reticulum (ER) stress contributes to development of cardiorenal syndrome (CRS), and Silent Information Regulator 1 (SIRT1), a class III histone deacetylase, may have protective effects on heart and renal disease, by reducing ER stress. We aimed to determine if SIRT1 alleviates CRS through ER stress reduction.
2776 related Products with: Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress.stress-associated endopla Anti beta3 AR Human, Poly anti H inh human blood an CAL-101 Mechanisms: PI3K- IPI-145 (INK-1197) Mechan Signal transduction antib AKT Phospho-Specific Arra AMPK Signaling Phospho-Sp Cancer Apoptosis Phospho- Chromatin Transcription P CREB Phospho-Specific Arr Cytoskeleton II Phospho-S
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Modulation of Hepatic Gene Expression Profiles by Vitamins B1, B2 and niacin Supplementation in Mice Exposed to Acute Hypoxia.This study was aimed to observe the effects of vitamins B1, B2 and niacin supplementation on hepatic gene expression profiles in mice exposed to acute hypoxia. Thirty mice were randomly divided into normal, acute hypoxia, and acute hypoxia plus vitamins B1, B2 and niacin supplementation groups and fed corresponding diets for two weeks and then exposed to a simulated altitude of 6000 meters for 8 hours. Hepatic gene expression profiles were analyzed using a microarray technique. Several biochemical markers were also assayed. The results showed that a total of 2476 genes were expressed differentially after acute hypoxia exposure (1508 up-regulated genes and 968 down-regulated genes). Compared to the acute hypoxia group, there were 1382 genes differentially expressed (626 up reregulated genes and 756 down regulated genes) in the acute hypoxia plus vitamins B1, B2 and niacin supplementation group. Pathway analysis indicated that carbohydrate, lipid and amino acid metabolism, as well as electron transfer chain, were improved to some extent after vitamins B1, B2 and niacin supplementation. Supportive results were obtained from biochemical assays. Our findings suggest that the supplementation of vitamins B1, B2 and niacin is beneficial in improving nutritional metabolism partly via gene expression under acute hypoxia condition.
2145 related Products with: Modulation of Hepatic Gene Expression Profiles by Vitamins B1, B2 and niacin Supplementation in Mice Exposed to Acute Hypoxia.DNA (cytosine 5) methyltr Human Epstein-Barr Virus Mouse Epstein-Barr Virus Rat TGF-beta-inducible ea Rat TGF-beta-inducible ea Recombinant Human Interfe Native Influenza HA (A To Native Influenza HA (A To Native Influenza HA (A To Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri Thromboxane B2 Blocking P
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IL-7 suppresses macrophage autophagy and promotes liver pathology in Schistosoma japonicum-infected mice.In schistosomiasis japonica and mansoni, parasite eggs trapped in host liver elicit severe liver granulomatous inflammation that subsequently leads to periportal fibrosis, portal hypertension, haemorrhage or even death. Macrophages are critical for granuloma formation and the development of liver fibrosis during schistosomiasis. However, whether the aberrant regulation of macrophage autophagy has an effect on the development of liver immunopathology in schistosomiasis remains to be elucidated. In this study, we showed that Schistosoma japonicum (S. japonicum) egg antigen (SEA)-triggered macrophage autophagy limited the development of pathology in host liver. However, engagement of IL-7 receptor (IL-7R/CD127) on macrophages by S. japonicum infection-induced IL-7 significantly suppressed SEA-triggered macrophage autophagy, which led to an enhanced liver pathology. In addition, anti-IL-7 neutralizing antibody or anti-CD127 blocking antibody treatment increased macrophage autophagy and suppressed liver pathology. Finally, we demonstrated that IL-7 protects macrophage against SEA-induced autophagy through activation of AMP-activated protein kinase (AMPK). Our study reveals a novel role for IL-7 in macrophage autophagy and identifies AMPK as a novel downstream mediator of IL-7-IL-7R signalling and suggests that manipulation of macrophage autophagy by targeting IL-7-IL-7R signalling may have the potential to lead to improved treatment options for liver pathogenesis in schistosomiasis.
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Enhancing amplification of late-outgrowth endothelial cells by bilobalide.Transfusion of autologous late-outgrowth endothelial cells (OECs) is a promising treatment for restenosis after revascularization. Preparing cells by in vitro amplification is a key step to implement the therapy. This study aimed to demonstrate that bilobalide, a terpenoid, enhances the OEC amplification. Human-, rabbit- and rat OECs and a mouse femoral artery injury model were used. Expanding OECs used endothelial growth medium-2 as the standard culture medium while exploring the mechanisms used endothelial basal medium-2. Proliferation assay used MTT method and BrdU method. Migration assay used the modified Boyden chamber. Intracellular nitric oxide, superoxide anion, hydroxyl radical/peroxynitrite and HOwere quantified with DAF-FM DA, dihydroethidium, hydroxyphenyl fluorescein and a HOassay kit, respectively. Activated ERK1/2 and eNOS were tested with the Western blot. Bilobalide concentration-dependently enhanced OEC number increase in vitro. Transfusion of bilobalide-based human OECs into femoral injured athymia nude mouse reduced the intimal hyperplasia. Bilobalide promoted OEC proliferation and migration and increased the intracellular nitric oxide level. L-NAME, a NOS inhibitor, inhibits but not abolishes OEC proliferation, migration and ERK1/2 activation. Bilobalide concentration-dependently enhanced the eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in activated OECs. Bilobalide alleviates the increase in hydroxyl radical/peroxynitrite, superoxide anion and HOin proliferating OECs. In conclusion, nitric oxide plays a partial role in OEC proliferation and migration; bilobalide increases OEC nitric oxide production and decreases nitric oxide depletion, promoting the OEC number increase; Bilobalide-based OECs are active in vivo. The findings may simplify the preparation of OECs, facilitating the implementation of the autologous-OECs-transfusion therapy.
2209 related Products with: Enhancing amplification of late-outgrowth endothelial cells by bilobalide.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 GFP Expressing Human Derm Human Glomerular Microvas GFP Expressing Human Glom RFP Expressing Human Glom
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Ginsenoside Rg3 stereoisomers differentially inhibit vascular smooth muscle cell proliferation and migration in diabetic atherosclerosis.Ginsenoside 20(R/S)-Rg3, as a natural peroxisome proliferator-activated receptor gamma (PPARγ) ligand, has been reported to exhibit differential biological effects. It is of great interest to understand the stereochemical selectivity of 20(R/S)-Rg3 and explore whether differential PPARγ activation by Rg3 stereoisomers, if it exists, could lead to differential physiological outcome and therapeutic effects in diabetic atherosclerosis. Here, we investigated the binding modes of 20(R/S)-Rg3 stereoisomers in the PPARγ ligand-binding domain (PPARγ-LBD) using molecular modelling and their effects on smooth muscle cell proliferation and migration induced by advanced glycation end products (AGEs). The results revealed that 20(S)-Rg3 exhibited stronger antiproliferative and antimigratory effects due to stronger PPARγ activation. To validate the in vitro results, we used a mice model with diabetic atherosclerosis and obtained that 20(S)-Rg3 markedly reduced the plaque size secondary to reducing the proliferation and migration of VSMCs, while the plaques were more stable due to improvements in other plaque compositions. The results shed light on the structural difference between Rg3 stereoisomers that can lead to significant differential physiological outcome, and the (S)-isomer seems to be the more potent isomer to be developed as a promising drug for diabetic atherosclerosis.
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Oligodendrocyte gene expression is reduced by and influences effects of chronic social stress in mice.Oligodendrocyte gene expression is down-regulated in stress-related neuropsychiatric disorders, including depression. In mice, chronic social stress (CSS) leads to depression-relevant changes in brain and emotional behavior, and the present study demonstrates the involvement of oligodendrocytes in this model. In C57BL/6 (BL/6) mice, RNA-sequencing was conducted with prefrontal cortex, amygdala and hippocampus from CSS and controls; a gene enrichment database for neurons, astrocytes and oligodendrocytes was used to identify cell origin of affected genes, and cell deconvolution was applied. To assess the potential causal contribution of reduced oligodendrocyte gene expression to CSS effects, mice heterozygous for the oligodendrocyte gene cyclic nucleotide phosphodiesterase (Cnp1) on a BL/6 background were studied; a 2 genotype (WT, Cnp1) x 2 environment (control, CSS) design was used to investigate effects on emotional behaviour and amygdala microglia. In BL/6 mice, in prefrontal cortex and amygdala tissue comprising gray and white matter, CSS down-regulated expression of multiple oligodendroycte genes encoding myelin and myelin-axon-integrity proteins, and cell deconvolution identified a lower proportion of oligodendrocytes in amygdala. Quantification of oligodendrocyte proteins in amygdala gray matter did not yield evidence for reduced translation, suggesting that CSS impacts primarily on white matter oligodendrocytes or the myelin transcriptome. In Cnp1 mice, social interaction was reduced by CSS in Cnp1mice specifically; using IBA1 expression, microglia activity was increased additively by Cnp1and CSS in amygdala gray and white matter. This study provides back-translational evidence that oligodendrocyte changes are relevant to the pathophysiology and potentially the treatment of stress-related neuropsychiatric disorders.
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Inflammatory cytokine-mediated induction of serine racemase in atopic dermatitis.Serine racemase (SR) is an enzyme that catalyses the synthesis of d-serine, an endogenous coagonist for N-methyl-D-aspartate (NMDA)-type glutamate receptor in the central nervous system. Our previous study demonstrated that SR was expressed in the epidermis of wild-type (WT) mice but not in SR knockout (KO) mice. In addition, SR immune-reactivity was only found in the granular and cornified layers of the epidermis in WT mice. These findings suggested that SR is involved in the differentiation of epidermal keratinocytes and the formation of the skin barrier. However, its role in skin barrier dysfunction such as atopic dermatitis (AD) remains elusive. AD is a chronic inflammatory disease of skin, and the clinical presentation of AD has been reported to be occasionally associated with psychological factors. Therefore, this study examined the content of d-serine in stratum corneum in AD patients and healthy controls using a tape-stripping method. Skin samples were collected from the cheek and upper arm skin of AD patient's lesion and healthy individuals. The d-serine content was significantly increased in the involved skin of AD in comparison with healthy individuals. An immunohistochemical analysis also revealed an increased SR expression in the epidermis of AD patients. Furthermore, the SR expression in cultured human keratinocytes was significantly increased by the stimulation with tumour necrosis factor -α or macrophage migration inhibitory factor. Taken together, these findings suggest that d-serine expressed particularly strongly in AD lesional skin and that the SR expression in the keratinocytes is linked to inflammatory cytokines.
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Tadalafil attenuates hypotonicity-induced Cainflux via TRPV2 and TRPV4 in primary rat bladder urothelial cell cultures.To investigate the localization of phosphodiesterase 5 (PDE5) and the molecular mechanism underlying the effect of the PDE5 inhibitor tadalafil in signal transduction in the bladder urothelium.
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