Only in Titles

           Search results for: Anti_STAT1 alpha Poly   

paperclip

#29671072   // Save this To Up

Reversion of Multidrug Resistance by Co-Encapsulation of Doxorubicin and Metformin in Poly(lactide-co-glycolide)-d-α-tocopheryl Polyethylene Glycol 1000 Succinate Nanoparticles.

P-glycoprotein (P-gp) mediated multidrug resistance (MDR) has been recognized as the main obstacle against successful cancer treatment. To address this problem, co-encapsulated doxorubicin (DOX) and metformin (Met) in a biodegradable polymer composed of poly(lactide-co-glycolide) (PLGA) and D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS) was prepared. We reported in our previous study that Met inhibits P-gp in DOX resistant breast cancer (MCF-7/DOX) cells. TPGS is a bioactive compound which has also been shown to inhibit P-gp, further to its pharmaceutical advantages.

2805 related Products with: Reversion of Multidrug Resistance by Co-Encapsulation of Doxorubicin and Metformin in Poly(lactide-co-glycolide)-d-α-tocopheryl Polyethylene Glycol 1000 Succinate Nanoparticles.

BCIP INT Solution Rabbit Anti-Human Androge 12mm Flange Cap Low Densi 12mm Hollow Plug Cap Asso 12mm Two Position Cap Low Recombinant HIV-1 pol Int Recombinant HIV-1 p31 Int BYL-719 Mechanisms: PI3K- MM-1000, Overhead stirrer Rabbit Anti-IAA (Indole-3 Rabbit Anti-Integrin alph Rabbit Anti-TNIP2 ABIN2 T

Related Pathways

paperclip

#29670349   // Save this To Up

Fabrication of a triptolide-loaded and poly-γ-glutamic acid-based amphiphilic nanoparticle for the treatment of rheumatoid arthritis.

Triptolide (TP) exhibits immunosuppressive, cartilage-protective and anti-inflammatory effects in rheumatoid arthritis. However, the toxicity of TP limits its widespread use. To decrease the toxic effects, we developed a novel nano-drug carrier system containing TP using poly-γ-glutamic acid-grafted di-tert-butyl L-aspartate hydrochloride (PAT). PAT had an average diameter of 79±18 nm, a narrow polydispersity index (0.18), a strong zeta potential (-32 mV) and a high drug encapsulation efficiency (EE=48.6%) and loading capacity (EE=19.2%), and exhibited controlled release (=29 h). The MTT assay and flow cytometry results indicated that PAT could decrease toxicity and apoptosis induced by free TP on RAW264.7 cells. PAT decreased lipopolysaccharides/interferon γ-induced cytokines expression of macrophage (<0.05). In vivo, PAT accumulated at inflammatory joints, improved the survival rate and had fewer side effects on tumor necrosis factor α transgenic mice, compared to TP. The blood biochemical indexes revealed that PAT did not cause much damage to the kidney (urea nitrogen and creatinine) and liver (alanine aminotransferase and aspartate aminotransferase). In addition, PAT reduced inflammatory synovial tissue area (<0.05), cartilage loss (<0.05), tartrate-resistant acid phosphatase-positive osteoclast area (<0.05) and bone erosion (<0.05) in both knee and ankle joints, and showed similar beneficial effect as free TP. In summary, our newly formed nanoparticle, PAT, can reduce the toxicity and guarantee the efficacy of TP, which represents an effective drug candidate for RA with low adverse side effect.

2612 related Products with: Fabrication of a triptolide-loaded and poly-γ-glutamic acid-based amphiphilic nanoparticle for the treatment of rheumatoid arthritis.

Amplite™ Fluorimetric G Acetyl L Glutamic Acid N-Acetyl-D-glutamic Acid N-Acetyl-L-glutamic Acid (5Z)-7-[(5-Acetyloxy-2-fo (5Z)-7-[(5-Acetyloxy-2-fo N-L-Alanyl-L-glutamic Aci N-L-Alanyl-L-glutamic Aci N-(4-Aminobenzoyl)-L-glut N-(4-Aminobenzoyl-d4)-L-g Androst-4-ene-3,17-dion-1 3-Formylindol-1-yl-acetic

Related Pathways

paperclip

#29666865   // Save this To Up

Preparation of lactic acid- and glucose-responsive poly(ε-caprolactone)-b-poly(ethylene oxide) block copolymer micelles using phenylboronic ester as a sensitive block linkage.

The present study describes the synthesis, self-assembly and responsiveness to glucose and lactic acid of biocompatible and biodegradable block copolymer micelles using phenylboronic ester as the linkage between hydrophobic poly(ε-caprolactone) (PCL) and hydrophilic poly(ethylene oxide) (PEO). The PCL block with pendant phenylboronic acid (PCLBA) was synthesized by combining ε-caprolactone (ε-CL) ring-opening polymerisation (ROP), using 4-hydroxymethyl(phenylboronic) acid pinacolate as the initiator, and pinacol deprotection. The glucose-terminated PEO (PEOGlc) was prepared by 1,3-dipolar, Cu(i)-catalysed, alkyne-azide cycloaddition of α-methoxy-ω-propargyl poly(ethylene oxide) and 1-azido-1-deoxy-d-glucopyranose. All new compounds were evaluated by 1H NMR spectroscopy and by SEC analysis. PCLBA and PEOGlc blocks were linked in NaOH acetone solution, which was indirectly confirmed by Alizarin Red S fluorescence and directly by 1H NMR spectroscopy. Dialysis against Milli-Q water induced the self-assembly of PCLBA-b-PEOGlc nanoparticles, which were characterised by static (SLS) and dynamic (DLS) light scattering and by cryogenic transmission electron microscopy (cryo-TEM). Furthermore, the microscopic properties of the charged interface between the hydrophobic PCLBA core and the hydrophilic PEOGlc shell were examined by electrophoretic light scattering (zeta potential) and by fluorescence spectroscopy using the fluorescent probe 5-(N-dodecanoyl)aminofluorescein (DAF) as a pH indicator. Subsequently, the nanoparticles were transferred to a phosphate buffer saline (PBS) solution supplemented with different concentrations of glucose to simulate the physiological conditions in blood or lactic acid to simulate acidic cytosolic or endosomal conditions in tumour cells. Adding a surplus of glucose or lactic acid, which competitively binds to PBA, removes the stabilising hydrophilic PEOGlc blocks, thereby triggering marked nanoparticle aggregation. However, the rate of aggregation induced by lactic acid is considerably faster than that induced by glucose, as confirmed by light scattering. Thus, this novel block copolymer may contribute to the field of selective, lactic acid- and/or glucose-responsive drug delivery vehicle design under both pathological and physiological conditions.

2777 related Products with: Preparation of lactic acid- and glucose-responsive poly(ε-caprolactone)-b-poly(ethylene oxide) block copolymer micelles using phenylboronic ester as a sensitive block linkage.

ASC Blocking Peptide 50 u ASAH2 Blocking Peptide AS160 TBC1 Blocking Pepti (S)-4-Aminobenzyl Ethylen rac (Aminomethyl)ethylene N-Benzyloxycarbonyl-L-asp EnzyChrom™ D-Lactate As EnzyChrom™ D-Lactate As MarkerGeneTM Live Dead As Green FAM Poly Caspases A Green FAM Poly Caspases A Red Sulforhodamine Poly C

Related Pathways

paperclip

#29666242   // Save this To Up

Characterization and engineering of a plastic-degrading aromatic polyesterase.

Poly(ethylene terephthalate) (PET) is one of the most abundantly produced synthetic polymers and is accumulating in the environment at a staggering rate as discarded packaging and textiles. The properties that make PET so useful also endow it with an alarming resistance to biodegradation, likely lasting centuries in the environment. Our collective reliance on PET and other plastics means that this buildup will continue unless solutions are found. Recently, a newly discovered bacterium, 201-F6, was shown to exhibit the rare ability to grow on PET as a major carbon and energy source. Central to its PET biodegradation capability is a secreted PETase (PET-digesting enzyme). Here, we present a 0.92 Å resolution X-ray crystal structure of PETase, which reveals features common to both cutinases and lipases. PETase retains the ancestral α/β-hydrolase fold but exhibits a more open active-site cleft than homologous cutinases. By narrowing the binding cleft via mutation of two active-site residues to conserved amino acids in cutinases, we surprisingly observe improved PET degradation, suggesting that PETase is not fully optimized for crystalline PET degradation, despite presumably evolving in a PET-rich environment. Additionally, we show that PETase degrades another semiaromatic polyester, polyethylene-2,5-furandicarboxylate (PEF), which is an emerging, bioderived PET replacement with improved barrier properties. In contrast, PETase does not degrade aliphatic polyesters, suggesting that it is generally an aromatic polyesterase. These findings suggest that additional protein engineering to increase PETase performance is realistic and highlight the need for further developments of structure/activity relationships for biodegradation of synthetic polyesters.

1573 related Products with: Characterization and engineering of a plastic-degrading aromatic polyesterase.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst- 5α-N-Acetyl-2'H-androst- 3-O-Acetyl 5,14-Androstad

Related Pathways

paperclip

#29665972   // Save this To Up

Intranasal delivery of influenza antigen by nanoparticles, but not NKT-cell adjuvant differentially induces the expression of B-cell activation factors in mice and swine.

Intranasal vaccination of pigs with poly lactic-co-glycolic acid and polyanhydride nanoparticles delivered inactivated influenza virus provides cross-reactive T-cell response, but not antibody response, resulting in incomplete protection and no reduction in nasal virus shedding. Expression of BAFF and Th2 transcription factor GATA-3 were downregulated in lungs of pigs vaccinated with influenza nanovaccine, but in mice it upregulated the expression of BAFF and cytokine TGFβ in cervical lymph nodes. However, the intranasal iNKT cell adjuvant, α-Galctosylceramide upregulates the expression of BAFF in pig lungs. In conclusion, expression of BAFF is differentially regulated by intranasal nanovaccine and α-Galctosylceramide in pig respiratory tract.

1485 related Products with: Intranasal delivery of influenza antigen by nanoparticles, but not NKT-cell adjuvant differentially induces the expression of B-cell activation factors in mice and swine.

Anti C Reactive Protein A anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl CELLKINES Natural Human I CELLKINES INTERLEUKIN 2 ( CELLKINES INTERLEUKIN 2 ( Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Macrophage Colony Stimula

Related Pathways

paperclip

#29664171   // Save this To Up

Capsaicin Reduces PLGA-Induced Fibrosis by Promoting M2 Macrophages and Suppressing Overall Inflammatory Response.

Capsaicin reduced poly(lactic-co-glycolic) acid (PLGA)-induced fibrosis by promoting IL-10 secretion and suppressing alpha-smooth muscle actin (α-SMA) expression. The lifetime and efficacy of tissue engineering scaffolds are determined by the foreign body response. In this study, we investigated the in vitro and in vivo effects of capsaicin to reduce biomaterial-induced fibrosis. RAW 264.7 cells cultured on PLGA films with capsaicin responded with significant (p<0.05) upregulation in M2 markers arginase-1 and IL-10 and downregulation of M1 markers iNOS and IL-12, demonstrating the potential of capsaicin to reduce PLGA-induced inflammation. Subsequent animal studies were conducted where PLGA and capsaicin-embedded PLGA discs were implanted in C57BL/6 mice for 2 and 14 days. Explanted capsaicin-embedded PLGA implants had 40% less collagen than PLGA-only implants. Capsaicin caused a 35% increase in IL-10 which played a key role in suppressing fibrosis. Macrophage phenotype markers in peritoneal cells and adherent cells were unaffected by capsaicin; however, capsaicin suppressed the myofibroblast marker α-SMA in adherent cells by day 14. Overall, our results revealed that capsaicin reduced biomaterial-induced fibrosis and demonstrates that capsaicin has the potential to extend the lifetime of a tissue engineering scaffold when used in long-term drug release applications from hydrophobic biomaterials. This article is protected by copyright. All rights reserved.

1370 related Products with: Capsaicin Reduces PLGA-Induced Fibrosis by Promoting M2 Macrophages and Suppressing Overall Inflammatory Response.

CAR,CAR,Constitutive acti Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon FSH antibody, Monoclonal FSH antibody, Monoclonal Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma

Related Pathways

paperclip

#29661104   // Save this To Up

Effect of micro-roughening of poly(ether ether ketone) on bone marrow derived stem cell and macrophage responses, and osseointegration.

Poly(ether ether ketone) (PEEK) has emerged as a candidate to replace metal implants because of its satisfactory mechanical properties, radiolucency, and lack of metal allergy. However, PEEK lacks osseointegration ability limiting its clinical applications. To overcome this problem, we prepared PEEK with a micro-rough surface using the sandblast method to modulate its osseointegration property; the sandblast method is simple, cost-effective, and is already applied to clinical metal implants. The surface roughness of the sandblasted PEEK was about 2.3 μm, whereas that of mirror-polished PEEK was 0.06 μm. Rat bone marrow-derived mesenchymal stem cells (RMSCs) showed higher proliferation, osteocalcin (OC) expression and bone-like nodule formation on micro-roughened PEEK compared with those cultured on mirror-polished PEEK, suggesting that micro-roughening facilitated RMSCs proliferation and differentiation. The micro-roughened surface slightly mitigated secretion of inflammatory C-C motif chemokine 2 (CCL-2) from lipopolysaccharide (LPS)-stimulated macrophages, but not of tumor necrosis factor α (TNFα) and interleukin-6 (IL-6). Finally, to compare osseointegration, specimens were implanted in rat femur bone marrow cavities, and then the pull-out force was measured. The pull-out force of micro-roughened PEEK was about four times higher than that of the mirror-polished PEEK. These results showed that micro-roughening of PEEK using the sandblast method was able to improve osseointegration, partly through elevating proliferation and differentiation of RMSCs.

2053 related Products with: Effect of micro-roughening of poly(ether ether ketone) on bone marrow derived stem cell and macrophage responses, and osseointegration.

Macrophage Colony Stimula Macrophage Colony Stimula CELLKINES MACROPHAGE COLO CELLKINES MACROPHAGE COLO CELLKINES PLATELET DERIVE CELLKINES PLATELET DERIVE Human Stem Cell Factor SC Human Stromal Cell-Derive Human Stromal Cell-Derive Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge

Related Pathways

paperclip

#29659906   // Save this To Up

Increased Chromogranin A-positive Hormone Negative Cells in Chronic Pancreatitis.

Chronic pancreatitis (CP) is characterized by inflammation, fibrosis and a loss of pancreatic acinar cells which can result in exocrine and eventually endocrine deficiency. Pancreatitis has been reported to induce formation of new endocrine cells (neogenesis) in mice. Our recent data has implicated Chromogranin A-positive hormone negative (CPHN) cells as potential evidence of neogenesis in humans.

2886 related Products with: Increased Chromogranin A-positive Hormone Negative Cells in Chronic Pancreatitis.

GLP 1 ELISA Kit, Rat Gluc Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor ( Macrophage Colony Stimula Macrophage Colony Stimula GLP 2 ELISA Kit, Rat Prog Anti 3 DG imidazolone Mon

Related Pathways

paperclip

#29659531   // Save this To Up

Gold Nanoparticles Grafted with PLL--PNIPAM: Interplay on Thermal/pH Dual-Response and Optical Properties.

Narrowly distributed poly(l-lysine---isopropylacrylamide) (PLL--PNIPAM) was prepared through ring-opening polymerization of ε-benzyloxycarbonyl-l-lysine -carboxy-α-amino anhydride and atom transfer radical polymerization of NIPAM, followed with the removal of ε-benzyloxycarbonyl group. Then gold nanoparticles (AuNPs) grafted with PLL--PNIPAM (PNIPAM-PLL-AuNPs) were obtained by the reduction of chloroauric acid with sodium citrate in the presence of PLL--PNIPAM. PNIPAM-PLL-AuNPs and its precursors were thoroughly characterized by proton magnetic resonance spectroscope, Fourier transform infrared spectroscope, UV-vis spectroscope, transmission electron microscopy, dynamic light scattering, thermogravimetric analysis, and circular dichroism. The obtained PNIPAM-PLL-AuNPs exhibited high colloid stability even at strong alkaline (pH = 12) and acidic (pH = 2) conditions. The thermal and pH dual-responsive behaviors of the grafting PLL--PNIPAM chains was observed to be affected by AuNPs, while not for the secondary structure of PLL chains. Correspondingly, the surface plasmon resonance (SPR) of AuNPs was found to be sensitive to both pH value and temperature. A blue shift in the SPR happened both with increasing pH value and increasing temperature. The stimuli-response was reversible in heating-cooling cycles. The gold nanoparticles with both pH and temperature response may have potential applications in biomedical areas and biosensors.

1255 related Products with: Gold Nanoparticles Grafted with PLL--PNIPAM: Interplay on Thermal/pH Dual-Response and Optical Properties.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Hyaluronidase Rabbit Anti-PH-4 P4H-TM P Rabbit Anti-Phospho-LATS1 Rabbit Anti-Phospho-MAP2( Rabbit Anti-Phospho-MLK3( Rabbit Anti-Phospho-MYPT1 Rabbit Anti-Phospho-NDRG1 Rabbit Anti-Phospho-NDRG1 Rabbit Anti-Phospho-Rb (S Rabbit Anti-Phospho-Ricto

Related Pathways

paperclip

#29656957   // Save this To Up

Muramyl dipeptide potentiates a Bacillus anthracis poly-γ-d-glutamic acid capsule surrogate that induces maturation and activation of mouse dendritic cells.

Poly-γ-d-glutamic acid (PGA) of anthrax is an important pathogenic factor due to its anti-phagocytic activity. Additionally, PGA has the ability to activate mouse macrophages for the secretion of cytokines through Toll-like receptor (TLR) 2. Peptidoglycan (PGN), a major bacterial cell-wall component, induces inflammatory responses in the host. We assessed whether PGA can induce maturation and cytokine expression in immature mouse dendritic cells (DCs) in the existence of muramyl dipeptide (MDP), the minimum motif of PGN with immunostimulatory activity. Stimulation of immature DCs with PGA or MDP alone augmented expression of costimulatory molecules and MHC class II proteins, which are all cell surface markers indicative of maturation. The observed effects were further enhanced by costimulation of PGA and MDP. PGA alone was sufficient to induce expression of TNF-α, IL-6, MCP-1, and MIP1-α, whereas MDP alone did not under the same conditions. Treatment with MDP enhanced PGA-induced expression of the tested inflammatory mediators; however, the synergistic effect found for PGA and MDP was not observed in TLR2- or nucleotide-binding oligomerization domain (NOD) 2-knockout DCs. Additionally, MDP augmented PGA-induced MAP kinases and NF-κB activation, which is crucial for expression of cytokines. Furthermore, MAP kinase and NF-κB inhibitors attenuated MDP enhancement of PGA-induced cytokine production. In addition, co-culture of splenocytes and PGA/MDP-matured DCs induced higher expression of IL-2 and IFN-γ compared to that of splenocytes and PGA-matured DCs. Collectively, our results suggest that PGA and MDP cooperatively induce inflammatory responses in mouse DCs through TLR2 and NOD2 via MAP kinase and NF-κB pathways, subsequently leading to lymphocyte activation.

2261 related Products with: Muramyl dipeptide potentiates a Bacillus anthracis poly-γ-d-glutamic acid capsule surrogate that induces maturation and activation of mouse dendritic cells.

Bacillus anthracis (Anthr Bacillus anthracis (Anthr Bacillus anthracis (Anthr Bacillus anthracis (Anthr Bacillus anthracis (Anthr Mouse Anti-Human Dendriti Rat Anti-Mouse Dendritic Mouse Anti-Human Follicul Mouse Anti-Human Follicul Mouse Anti-Human Follicul Mouse Anti-Human Follicul Folic Acid antibody, Mono

Related Pathways