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Choose fixed kits that allow you to explore entire pathways or processes. Or design your own kits by choosing single plex MAPmates™, following the provided guidelines.
The following MAPmates™ should not be plexed together:
-MAPmates™ that require a different assay buffer
-Phospho-specific and total MAPmate™ pairs, e.g. total GSK3β and GSK3β (Ser 9)
-PanTyr and site-specific MAPmates™, e.g. Phospho-EGF Receptor and phospho-STAT1 (Tyr701)
-More than 1 phospho-MAPmate™ for a single target (Akt, STAT3)
-GAPDH and β-Tubulin cannot be plexed with kits or MAPmates™ containing panTyr
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
Space Saver Option Customers purchasing multiple kits may choose to save storage space by eliminating the kit packaging and receiving their multiplex assay components in plastic bags for more compact storage.
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Based on knowledge from traditional herbal medicine, Ferula assa-foetida (asafoetida) has several therapeutic applications but there is less knowledge about its effect on neurons.In order to evaluate neuronal differentiation, neuronal like cells were stained against neuronal specific markers β-Tubulin III and MAP2. After establishment of neuronal differentiation in cultured cells, aqueous extract of gum-resin of asafoetida were applied on culture medium of neurons with different concentrations then survival rate of neurons were evaluated by cell counting and methyl tetrazolium bromide (MTT) tests.The results showed that asafoetida gum resin particularly with 0.01 and 1 µg/ml concentrations could improve survival rate of neurons, while10 µgr/ml treated group was toxic.RESULTS of this study indicated that gum resin of asafoetida in low doses has neuroprotective effect on neurons and improves survival rate of them, however in higher concentrations it is toxic for neurons.
Based on knowledge from traditional herbal medicine, Ferula assa-foetida (asafoetida) has several therapeutic applications but there is less knowledge about its effect on neurons.In order to evaluate neuronal differentiation, neuronal like cells were stained against neuronal specific markers β-Tubulin III and MAP2. After establishment of neuronal differentiation in cultured cells, aqueous extract of gum-resin of asafoetida were applied on culture medium of neurons with different concentrations then survival rate of neurons were evaluated by cell counting and methyl tetrazolium bromide (MTT) tests.The results showed that asafoetida gum resin particularly with 0.01 and 1 µg/ml concentrations could improve survival rate of neurons, while10 µgr/ml treated group was toxic.RESULTS of this study indicated that gum resin of asafoetida in low doses has neuroprotective effect on neurons and improves survival rate of them, however in higher concentrations it is toxic for neurons.
Competent vehicles are highly sought after as a means to transplant cells for tissue regeneration. In this study, novel hydrogel-based microspherical cell carriers are designed and developed with an FDA-approved natural polysaccharide, gellan gum. The bulk fabrication of these microspheres is performed via a water-in-oil (W/O) emulsion process followed by a series of redox (oxidation-reduction) crosslinking treatments; this enables the microspherical dimensions to be precisely manipulated in terms of injectability, and simultaneously ensures the structural stability. To acquire adhesion affinity with anchorage-dependent cells (ADCs), a covalent coating of gelatin is further applied on the microspherical surfaces. The final product is constructed as a variety of gelatin-grafted-gellan microspherical cell carriers, abbreviated as TriG microcarriers. The cell-loading tests are conducted, respectively, with human dermal fibroblasts (HDFs) and human fetal osteoblasts (hFOBs). Morphological observation from optical microscopy and field emission scanning electron microscopy indicates that the HDFs spread well and populate rapidly on surfaces of TriG microcarriers. Immunofluorescent staining reveals the activation of focal adhesion and subsequent organization of F-actin from the attached cell surfaces, which suggests the TriG microspherical substrate is favorable to ADC adhesion and therefore capable of promoting HDF proliferation to achieve confluence by turning over three times within 10 days. The hFOBs are also cultivated on the TriG carriers, where ideal viability and clear potentials for osteogenesis are demonstrated by fluorescent Live/Dead screening and specific histobiochemical indications. All these findings suggest that the TriG microcarriers are suitable to provide open platforms for therapeutic ADC proliferation and differentiation.
BACKGROUND: Metalloproteinase-9 (MMP-9) is a type IV collagenase found at elevated levels in chronic wounds. As wounds heal, MMP-9 diminishes. In this study, we investigated whether MMP-9 directly contributes to chronic wound pathogenesis. METHODS: Recombinant proMMP-9 was prepared using immortalized keratinocytes transduced by a lentivirus. ProMMP-9 was purified from cell culture media and activated using 4-aminophenylmercuric acetate. Active MMP-9 was then suspended in xanthan gum to a concentration paralleling that found in human chronic wounds. Two parallel 6-mm punch biopsies were made on the backs of C57BL mice. Wounds were treated daily with MMP-9 or vehicle. Wound areas were measured and tissues examined by densitometry, real-time RT-PCR, histology, and immunohistochemistry at days 7, 10, and 12. RESULTS: Exogenous MMP-9, at the level found within chronic wounds, delayed wound healing in this animal model. By 7 days, wounds in the MMP-9-injected group were 12% larger than control wounds (P = .008). By day 12, wounds in the MMP-9-injected group were 25% larger than those of the control group (P = .03). Histologic examination shows that high levels of active MMP-9-impaired epithelial migrating tongues (P = .0008). Moreover, consistent with elevated MMP-9, the collagen IV in the leading edge of the epithelial tongue was diminished. CONCLUSION: MMP-9 appears to directly delay wound healing. Our data suggests that this may occur through interference with re-epithelialization. We propose that MMP-9 interferes with the basement membrane protein structure, which in turn impedes keratinocyte migration, attachment, and the reestablishment of the epidermis.
Background. Our previous study has demonstrated that nobiletin could reverse the behavioral alterations in stressed mice. However, the relation of its antidepressant-like action with neurotrophic molecular expression remains unknown. This study aimed to explore the antidepressant-like mechanism of nobiletin related to the neurotrophic system in rats exposed to chronic unpredictable mild stress (CUMS). Methods. Depressive-like anhedonia (assessed by sucrose preference) and serum corticosterone secretion were evaluated in the CUMS, followed by brain-derived neurotrophic factor (BDNF), its tropomyosin-related kinase receptor B (TrkB), and the downstream target synapsin I expressions in the hippocampus. Results. Anhedonia, which occurred within week 2, was rapidly ameliorated by nobiletin. While fluoxetine needed additional 2 weeks to improve the anhedonia. In addition, nobiletin administration for 5 weeks significantly ameliorated CUMS-induced increase in serum corticosterone levels. Furthermore, we also found that CUMS-induced deficits of hippocampal BDNF, TrkB, and synapsin I were ameliorated by nobiletin. Conclusions. Taken together, these findings suggest that nobiletin produces rapidly acting antidepressant-like responses in the CUMS and imply that BDNF-TrkB pathway may play an important role in the antidepressant-like effect of nobiletin.
The relationship between running, glial cell activation and pro-inflammatory cytokines was studied in the context of neuroprotection against ischemic stroke induced by middle cerebral artery occlusion (MCAO). This was investigated in four groups of rats, namely, (1) nonrunner, (2) runner after 12 weeks of treadmill running, (3) nonrunner with MCAO and (4) runner with MCAO. The horizontal diagonal band of Broca (HDB) in the septum was scrutinized for qualitative cum quantitative changes in the microglia and astrocytes. Reverse transcription-polymerase chain reaction and immunoblot work were carried out in the forebrain homogenate to determine, respectively, the gene and protein expression of several pro-inflammatory cytokines. Our results indicated that the runner exhibited less immunoreactivity and reduced numbers of glial cells within the HDB compared with the nonrunner. Interestingly, the mRNA and protein levels of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and interferon-gamma, were significantly downregulated in the runner. Our data also suggest albeit with some inconsistency that the runner/MCAO rats had benefited from running. These observations suggest that running can result in changes to the microenvironment, in which the microglia and astrocytes exist in a state of quiescence concomitant with a reduced expression of pro-inflammatory cytokines, that may lead to beneficial effects seen in ischemic stroke induced by MCAO.