Millipore Sigma Vibrant Logo
 

ZA,MILLI


32 Results Búsqueda avanzada  
Mostrar
Productos (0)
Documentos (13)
Páginas (19)

Acote sus resultados Utilice los filtros siguientes para refinar su búsqueda

Tipo de documento

  • (13)
¿No encuentra lo que está buscando?
Póngase en contacto con
el Servicio de Atención
al Cliente

 
¿Necesita ayuda para encontrar un documento?

  • Optimisation of ICP-MS collision/reaction cell conditions for the determination of elements likely to be interfered (V, Cr, Fe, Co, Ni, As and Se) in foodstuffs. 21962690

    A strategy for the accurate determination in foodstuffs of seven elements liable to be interfered with (V, Cr, Fe, Co, Ni, As and Se), was successfully applied. Firstly, to reduce spectroscopic interferences, four influential factors (hexapole and quadrupole bias, helium and hydrogen flows) of the collision/reaction cell device were optimised through the experimental design methodology. Secondly, non-spectroscopic interferences, which may severely disturb the analysis of matrices containing large amounts of non-target elements, were significantly reduced by a limited decrease in the flow rate of the optimum initial nebuliser rather than with a specific time-consuming dilution. Finally, the optimised multi-element method was subjected to a full validation that demonstrated its acceptable analytical performance.
    Tipo de documento:
    Referencia
    Referencia del producto:
    03-115
    Nombre del producto:
    RIPAb+ Musashi 2 - RIP Validated Antibody and Primer Set, rabbit monoclonal

  • Heparin reduces neuroinflammation and transsynaptic neuronal apoptosis in a model of subarachnoid hemorrhage. 22707992

    Subarachnoid hemorrhage (SAH) can lead to disabling motor, cognitive, and neuropsychological abnormalities. Part of the secondary injury to cerebral tissues associated with SAH is attributable to the neuroinflammatory response induced by blood. Heparin is a pleiotropic compound that reduces inflammatory responses in conditions outside the central nervous system. Using a model of SAH devoid of global insult, we evaluated the effect of delayed intravenous (IV) infusion of heparin, at a dose that does not produce therapeutic anticoagulation, on neuroinflammation, myelin preservation, and apoptosis. Adult male rats underwent bilateral stereotactic injections of autologous blood (50 μL) into the subarachnoid space of the entorhinal cortex. The rats were implanted with mini-osmotic pumps that delivered either vehicle or unfractionated heparin (10 U/kg/h IV) beginning 12 h after SAH. No mechanical or hemorrhagic injury was observed in the hippocampus. In vehicle controls assessed at 48 h, SAH was associated with robust neuroinflammation in the adjacent cortex [neutrophils, activated phagocytic microglia, nuclear factor-kappa B, tumor necrosis factor-alpha, and interleukin-1beta] and neurodegeneration (Fluoro-Jade C staining and loss of NeuN). In the hippocampus, a muted neuroinflammatory response was indicated by Iba1-positive, ED1-negative microglia exhibiting an activated morphology. The perforant pathway showed Fluoro-Jade C staining and demyelination, and granule cells of the dentate gyrus had pyknotic nuclei, labeled with Fluoro-Jade C and showed upregulation of cleaved caspase-3, consistent with transsynaptic apoptosis. Administration of heparin significantly reduced neuroinflammation, demyelination, and transsynaptic apoptosis. We conclude that delayed IV infusion of low-dose unfractionated heparin may attenuate adverse neuroinflammatory effects of SAH.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB1435
    Nombre del producto:
    Anti-Macrophages/Monocytes Antibody, clone ED-1

  • Glut1 deficiency (G1D): epilepsy and metabolic dysfunction in a mouse model of the most common human phenotype. 22683290

    Brain glucose supplies most of the carbon required for acetyl-coenzyme A (acetyl-CoA) generation (an important step for myelin synthesis) and for neurotransmitter production via further metabolism of acetyl-CoA in the tricarboxylic acid (TCA) cycle. However, it is not known whether reduced brain glucose transporter type I (GLUT-1) activity, the hallmark of the GLUT-1 deficiency (G1D) syndrome, leads to acetyl-CoA, TCA or neurotransmitter depletion. This question is relevant because, in its most common form in man, G1D is associated with cerebral hypomyelination (manifested as microcephaly) and epilepsy, suggestive of acetyl-CoA depletion and neurotransmitter dysfunction, respectively. Yet, brain metabolism in G1D remains underexplored both theoretically and experimentally, partly because computational models of limited brain glucose transport are subordinate to metabolic assumptions and partly because current hemizygous G1D mouse models manifest a mild phenotype not easily amenable to investigation. In contrast, adult antisense G1D mice replicate the human phenotype of spontaneous epilepsy associated with robust thalamocortical electrical oscillations. Additionally, and in consonance with human metabolic imaging observations, thalamus and cerebral cortex display the lowest GLUT-1 expression and glucose uptake in the mutant mouse. This depletion of brain glucose is associated with diminished plasma fatty acids and elevated ketone body levels, and with decreased brain acetyl-CoA and fatty acid contents, consistent with brain ketone body consumption and with stimulation of brain beta-oxidation and/or diminished cerebral lipid synthesis. In contrast with other epilepsies, astrocyte glutamine synthetase expression, cerebral TCA cycle intermediates, amino acid and amine neurotransmitter contents are also intact in G1D. The data suggest that the TCA cycle is preserved in G1D because reduced glycolysis and acetyl-CoA formation can be balanced by enhanced ketone body utilization. These results are incompatible with global cerebral energy failure or with neurotransmitter depletion as responsible for epilepsy in G1D and point to an unknown mechanism by which glycolysis critically regulates cortical excitability.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB302
    Nombre del producto:
    Anti-Glutamine Synthetase Antibody, clone GS-6

  • Neuroprotection by ulinastatin in experimental autoimmune encephalomyelitis. 21667278

    Ulinastatin has previously been used as a drug for patients with acute inflammatory disorders. The goal of the present study was to investigate the protective effects of ulinastatin on myelin sheaths and oligodendrocytes in experimental autoimmune encephalomyelitis (EAE), and to explore the possible underlying mechanism. Mice were divided into an ulinastatin treatment group, a normal saline treatment group, and a normal control group. EAE was induced in the mice with and without ulinastatin treatment. Demyelination was evaluated, as was the number of oligodendrocytes. The ulinastatin treatment group had a significantly lower clinical score, demyelinating score, and large numbers of oligodendrocytes compared with the group without ulinastatin treatment. Furthermore, ulinastatin treatment increased the expression of nerve growth factor and brain-derived neurotrophic factor, and protected against oligodendrocyte apoptosis. Thus, ulinastatin is shown to have a protective effect against EAE.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB326
    Nombre del producto:
    Anti-CNPase Antibody, clone 11-5B

  • Rat brain gamma-secretase activity is highly influenced by detergents. 17536783

    Gamma-secretase is important for the development of Alzheimer's disease, since it is a crucial enzyme for the generation of the pathogenic amyloid beta-peptide (Abeta). Most data on gamma-secretase is derived from studies in cell lines overexpressing gamma-secretase components or amyloid precursor protein (APP), and since gamma-secretase is a transmembrane protein complex, detergents have been frequently used to facilitate the studies. However, no extensive comparison of the influence of different detergents at different concentrations on gamma-secretase activity in preparations from brain has been made. Here, we establish the optimal conditions for gamma-secretase activity in rat brain, using an activity assay detecting endogenous production of the APP intracellular domain, which is generated when gamma-secretase cleaves the APP C-terminal fragments. We performed a subcellular fractionation and noted the highest gamma-secretase activity in the 100000g pellet and that the optimal pH was around 7. We found that gamma-secretase was active for at least 16 h at 37 degrees C and that the endogenous substrate levels were sufficient for activity measurements. The highest activity was obtained in 0.4% CHAPSO, which is slightly below the critical micelle concentration (0.5%) for this detergent, but the complex was not solubilized efficiently at this concentration. On the other hand, 1% CHAPSO solubilized a substantial amount of the gamma-secretase components, but the activity was low. The activity was fully restored by diluting the sample to 0.4% CHAPSO. Therefore, using 1% CHAPSO for solubilization and subsequently diluting the sample to 0.4% is an appropriate procedure for obtaining a soluble, highly active gamma-secretase from rat brain.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB5232

  • Extensive degradation of myelin basic protein isoforms by calpain following traumatic brain injury. 16893416

    Axonal injury is one of the key features of traumatic brain injury (TBI), yet little is known about the integrity of the myelin sheath. We report that the 21.5 and 18.5-kDa myelin basic protein (MBP) isoforms degrade into N-terminal fragments (of 10 and 8 kDa) in the ipsilateral hippocampus and cortex between 2 h and 3 days after controlled cortical impact (in a rat model of TBI), but exhibit no degradation contralaterally. Using N-terminal microsequencing and mass spectrometry, we identified a novel in vivo MBP cleavage site between Phe114 and Lys115. A MBP C-terminal fragment-specific antibody was then raised and shown to specifically detect MBP fragments in affected brain regions following TBI. In vitro naive brain lysate and purified MBP digestion showed that MBP is sensitive to calpain, producing the characteristic MBP fragments observed in TBI. We hypothesize that TBI-mediated axonal injury causes secondary structural damage to the adjacent myelin membrane, instigating MBP degradation. This could initiate myelin sheath instability and demyelination, which might further promote axonal vulnerability.
    Tipo de documento:
    Referencia
    Referencia del producto:
    CC119

  • Vaccination stimulates retinal ganglion cell regeneration in the adult optic nerve. 12609484

    We examined whether vaccination of adult rats with spinal cord homogenate (SCH) can promote regeneration of retinal ganglion cells (RGCs) after microcrush lesion of the optic nerve. Injured animals vaccinated with SCH showed axon growth into the optic nerve and such regeneration was not observed in animals vaccinated with liver homogenate (LH). Regeneration was not a consequence of neuroprotection since our vaccine did not protect RGCs from axotomy-induced cell death. Sera of vaccinated animals were tested for antibodies against myelin-associated glycoprotein, NogoA, Nogo-66 receptor, or chondroitin sulphate proteoglycans (CSPG), but no significant levels were detected. Antibodies to myelin basic protein were present in the serum of some SCH-vaccinated animals. In culture, serum from SCH-vaccinated animals promoted RGC growth on myelin but not on CSPG. Our results show that the effect of the pro-regenerative vaccine is mediated by antibodies to SCH. However, we were not able to detect a significant immune reaction to growth inhibitory proteins, suggesting alternative mechanisms for the success of vaccination to promote regeneration.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB1567
    Nombre del producto:
    Anti-Myelin Associated Glycoprotein Antibody, clone 513

  • Growth-associated gene and protein expression in the region of axonal sprouting in the aged brain after stroke. 16782355

    Aged individuals exhibit reduced functional recovery after stroke. We examined the expression profile in aged animals of a recently identified group of growth-associated genes that underlies post-stroke axonal sprouting in the young adult. Basal levels of most growth-promoting genes are higher in aged cortex compared with young adult, and are further induced after stroke. Compared with the young adult, these genes are induced at later time points after stroke. For growth-inhibitory molecules, myelin-associated glycoprotein and ephrin A5 are uniquely induced in the aged brain; chondroitin sulfate proteoglycans and oligodendrocyte myelin glycoprotein are induced at earlier time points; and Nogo-A, semaphorin IIIa and NG2 decline in aged vs. young adult after stroke. The aged brain does not simply have a reduction in growth-associated molecules after stroke, but a completely unique molecular profile of post-stroke axonal sprouting.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB347
    Nombre del producto:
    Anti-Growth Associated Protein 43 Antibody, clone 9-1E12

  • Schwann cells are removed from the spinal cord after effecting recovery from paraplegia. 11124999

    Remyelination of the CNS is necessary to restore neural function in a number of demyelinating conditions. Schwann cells, the myelinating cells of the periphery, are candidates for this purpose because they have more robust regenerative properties than their central homologs, the oligodendrocytes. Although the ability of Schwann cells to remyelinate the CNS has been demonstrated, their capacity to enter the adult spinal cord in large numbers and effect functional recovery remains uncertain. We used cholera toxin B-subunit conjugated to saporin to demyelinate the rat lumbar spinal cord, remove macroglia, and produce paraplegia. After the removal of oligodendrocyte and astrocyte debris by invading macrophages, there was a spontaneous entry of Schwann cells into the spinal cord, along with axonal remyelination and concomitant functional recovery from paraplegia occurring within 75 d. The Schwann cells appeared to enter the dorsal funiculi via the dorsal root entry zone and the lateral funiculi via rootlets that had become adherent to the lateral spinal cord after the inflammation. In the following weeks, Schwann cell myelin surrounding central axons was progressively replaced by oligodendrocyte myelin without lapse in motor function. Our results show that endogenous Schwann cells can reverse a severe neurological deficit caused by CNS demyelination and enable later oligodendrocyte remyelination.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB1580
    Nombre del producto:
    Anti-Oligodendrocytes Antibody, clone NS-1

  • Matrix metalloproteinase-9 controls proliferation of NG2+ progenitor cells immediately after spinal cord injury. 21756907

    We have demonstrated that overcoming matrix metalloproteinase (MMP)-mediated suppression of glial proliferation stimulates axonal regeneration in the peripheral nervous system. The regenerative capacity of the adult CNS in response to injury and demyelination depends on the ability of multipotent glial NG2+ progenitor cells to proliferate and mature, mainly into oligodendrocytes. Herein, we have established the important role of MMPs, specifically MMP-9, in regulation of NG2+ cell proliferation in injured spinal cord. Targeting transiently induced MMP-9 using acute MMP-9/2 inhibitor (SB-3CT) therapy for two days after T9-10 spinal cord dorsal hemisection produced a significant increase in mitosis (assessed by bromodeoxyuridine incorporation) of NG2+ cells but not GFAP+astrocytes and Iba-1+ microglia and/or macrophages. Acute MMP-9/2 blockade reduced the shedding of the NG2 proteoglycan and of the NR1 subunit of the N-methyl D-aspartate (NMDA) receptor, whose decline is believed to accompany NG2+ cell maturation into OLs. Increase in post-mitotic oligodendrocytes during remyelination and improved myelin neuropathology in the hemisected spinal cord were accompanied by locomotion and somatosensory recovery after acute MMP-9/2 inhibition. Collectively, these data establish a novel role for MMPs in regulation of NG2+ cell proliferation in the damaged CNS, and a long-term benefit of acute MMP-9 block after SCI.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo