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  • Calcium hydroxide regulates bone sialoprotein gene transcription in human osteoblast-like Saos2 cells. 21467818

    Bone sialoprotein (BSP) is a mineralized tissue-specific protein expressed in differentiated osteoblasts that appears to function in the initial mineralization of bone. Calcium hydroxide (Ca(OH)(2)) is a basic salt that has been widely used for a variety of applications in dentistry, due to its antimicrobial effects and its capability of inducing hard tissue formation. However, details of the mechanism involved in the mineralization induced by Ca(OH)(2) are still unclear. In the present study, Ca(OH)(2) (0.4 mM) was found to increase the levels of BSP and Runx2 mRNA at 3 h in human osteoblast-like Saos2 cells. Transient transfection assays were performed using chimeric constructs of the human BSP gene promoter linked to a luciferase reporter gene. Treatment of Saos2 cells with Ca(OH)(2) (0.4 mM) increased the luciferase activities of the constructs between -60LUC and -927LUC at 12 h. Gel shift analysis showed that Ca(OH)(2) (0.4 mM) increased the binding of nuclear protein to CRE1, CRE2 and FRE. Antibodies against CREB1, c-Fos, c-Jun, JunD, Fra2 and P300 disrupted the formation of the CRE1- and CRE2-protein complexes, and antibodies against Dlx5, Msx2, Runx2 and Smad1 disrupted the formation of the FRE-protein complex. These findings demonstrate that Ca(OH)(2) stimulates BSP transcription by targeting the CRE1, CRE2 and FRE elements in the human BSP gene promoter.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    AB5728

  • Aluminum hydroxide adjuvants activate caspase-1 and induce IL-1beta and IL-18 release. 17404311

    Aluminum hydroxide (Alum) is the only adjuvant approved for routine use in humans, although the basis for its adjuvanticity remains poorly understood. In this study, we show that Alum activates caspase-1 and induce secretion of mature IL-1beta and IL-18. Human PBMC or dendritic cells stimulated with pure TLR4 and TLR2 agonists released only traces of IL-1beta or IL-18, despite the fact that the IL-1beta mRNA was readily induced by both TLR agonists. In contrast, cells costimulated with TLR agonists plus Alum released large amount of IL-1beta and IL-18. Alum-induced IL-1beta and IL-18 production was not due to enhancement of TLR signaling but rather reflected caspase-1 activation and in mouse dendritic cells occurred in a MyD88-independent fashion. Secretion of other proinflammatory cytokines such as IL-8 was not affected by Alum treatments. However, TLR-induced production of IL-10 was increased and that of IFN-gamma-inducible protein decreased by Alum cotreatment. Considering the immunostimulatory activities of these cytokines and the ability of IL-1beta to act as adjuvant, our results suggest a mechanism for the adjuvanticity of Alum.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    06-503
    Produktbezeichnung:
    Anti-Caspase 1 Antibody

  • Fracture resistance and histological findings of immature teeth treated with mineral trioxide aggregate. 18410392

    The objective of the present study was to test the hypothesis that the fracture strength of calcium hydroxide and mineral trioxide aggregate (MTA)-filled immature teeth decreased over time. Immature mandibular incisors from sheep were extracted and the pulps were extirpated using an apical approach with a barbed broach, and the teeth were divided into three experimental groups. Group 1: untreated teeth. Group 2: the root canals were filled with calcium hydroxide paste. Group 3: the root canals were filled with MTA. All specimens were kept in saline with 1% antibiotics at 4 degrees C for certain periods of time: 2 weeks, 2 months, and 1 year. Then they were tested for fracture strength in an Instron testing machine. The results were subjected to statistical analysis by the Tukey-Kramer tests. A P-value (0.05) was considered statistically significant. One tooth from each group was selected randomly for a histological study, examining matrix metalloproteinases (MMP2 and MMP14) and tissue inhibitor of metalloproteinase (TIMP). The results showed the mean fracture strengths decreased over time for all the three groups. Although the untreated teeth showed the highest value (45.5 MPa) at 2 weeks, the fracture strengths decreased significantly after 2 months (P 0.05). On the other hand, the teeth treated with calcium hydroxide or MTA decreased, but not significantly over time (P 0.05). For the MTA-treated teeth, the fracture strengths were not found significantly different from the untreated or calcium hydroxide-treated teeth at 2 weeks or 2 months (P 0.05). However, the strength was significantly higher in the MTA group compared with the other two groups after 1 year (P 0.05). Immunofluorescence images revealed expression of collagen type 1, MMP-2 and MMP-14 in both untreated and endodontically treated teeth. However, TIMP-2 was only observed in the MTA-treated teeth. In conclusion, the teeth with root treatment with MTA showed the highest fracture resistance at 1 year (P 0.05). An explanation could be that MTA induced the expression of TIMP-2 in the dentin matrix and thereby possibly prevented destruction of the collagen matrix.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    MAB3310
    Produktbezeichnung:
    Anti-TIMP-2 Antibody, clone 67-4H11

  • Proteomic analyses of corneal tissue subjected to alkali exposure. 20861482

    To determine whether exposure to alkaline chemicals results in predictable changes in corneal protein profile. To determine whether protein profile changes are indicative of severity and duration of alkali exposure.Enucleated bovine and porcine (n = 59 each) eyes were used for exposure to sodium, ammonium, and calcium hydroxide, respectively. Eyes were subjected to fluorescein staining, 5-bromo-2'-deoxy-uridine (BrdU) labeling. Excised cornea was subjected to protein extraction, spectrophotometric determination of protein amount, dynamic light scattering and SDS-PAGE profiling, mass spectrometric protein identification, and iTRAQ-labeled quantification. Select identified proteins were subjected to Western blot and immunohistochemical analyses.Alkali exposure resulted in lower protein extractability from corneal tissue. Elevated aggregate formation was found with strong alkali exposure (sodium hydroxidegreater than ammonium, calcium hydroxide), even with a short duration of exposure compared with controls. The protein yield after exposure varied as a function of postexposure time. Protein profiles changed because of alkali exposure. Concentration and strength of the alkali affected the profile change significantly. Mass spectrometry identified 15 proteins from different bands with relative quantification. Plexin D1 was identified for the first time in the cornea at a protein level that was further confirmed by Western blot and immunohistochemical analyses.Exposure to alkaline chemicals results in predictable and reproducible changes in corneal protein profile. Stronger alkali, longer durations, or both, of exposure resulted in lower yields and significant protein profile changes compared with controls.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    MAB374
    Produktbezeichnung:
    Anti-Glyceraldehyde-3-Phosphate Dehydrogenase Antibody, clone 6C5