6 Matching Annotations
  1. Dec 2021
    1. Genomic DNA (250 ng) is digested by NspI and amplified using a ligation-mediated PCR with adapters covalently linked to the restriction fragments. In the next step PCR products are purified using magnetic beads, fragmented using DNase I, labeling with biotin and hybridized overnight (16–18 h) to a 49-format array. After incubation samples are washed and stained with streptavidin using a GeneChip Fluidics Station 450. Finally, arrays are scanned by GeneChip Scanner 3000, using the GeneChip Command Console Software (Thermo Fisher Scientific), to generate the CEL files that includes the intensity probe signals.

      MSc Microarray practical procedure source

  2. Nov 2021
    1. d gDNA to wells marked 1 through 6 in the plate diagram.2. Thaw Nsp I Buffer and 100X BSA at room temperature. Vortex and spin down, then place on ice.3. Leave Nsp I enzyme at –20°C until ready to use.4. Add 5 μL of the Genomic DNA, supplied in the kit as positive control, to the well marked “+”.5. Add 5 μL of Low EDTA TE as negative control to the well marked “–”.6. Prepare the Digestion Master Mix

      Digestion

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  3. Sep 2018
    1. Whilespatial biases may contribute to these findings,asnodes belonging to the same module tend to be anatomically colocalized [7,8],they cannot explain these effects entirely [94,95].

      Very nice review. Please note the reference [94] (Pantazatos et al.) is misplaced because they did not argue that spatial biases cannot entirely explain the putative links between CGE and functional segregation. Instead, they argued there was insufficient evidence in the original Richiardi et al. study linking elevated CGE with resting state functional networks, and that spatial biases may in fact entirely account for their findings. To describe the debate/exchange more accurately, I would suggest replacing the below sentence

      “While spatial biases may contribute to these findings, as nodes belonging to the same module tend to be anatomically colocalized [7,8], they cannot explain these effects entirely [94,95].”

      with the below paragraph:

      “Spatial biases may contribute to these findings, as nodes belonging to the same module tend to be anatomically colocalized [7,8]. Pantazatos et al. argued that these findings are entirely explained by spatial biases [94]. They showed that elevated CGE, as defined in the original Richiardi et al. study, falls monotonically as longer distance edges are removed. Moreover, they showed that 1,000 sets of randomly spaced modules all have significantly high CGE when using the same null distribution defined in the original Richiardi et al. analyses. Therefore, elevated CGE is not specifically related to functional segregation as defined by resting state functional networks, which is in direct contradiction to the main conclusion of the original Richiardi et al. study. Since randomly placed modules do not align (spatially) with any distributed pattern of functional segregation, the finding of elevated CGE may instead be attributed entirely to anatomical colocalization of the nodes within each module. In their rebuttal to [94], Richiardi et al. argue spatial biases cannot explain their findings entirely [95]. However, the authors do not offer an explanation for significantly high CGE observed for randomly spaced sets of modules, other than to note that nodes tend to be closer on average compared to when modules are defined by resting state fMRI. Future work is required to dissociate the effects of spatially proximity on relationships between CGE and spatially distributed functional networks.”

  4. Nov 2017
  5. Oct 2017
  6. Jul 2017
    1. global dye-bias equalization step to control for the different average intensities in the red and green channels. This procedure scales the background-corrected intensities, dividing by the average intensity of the positive control probes in the same channel, red or green, and multiplying by the average intensity of all positive controls in a reference array.