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In tumour cells, but not in normal cells, the S phase block has been shown to be followed by apoptosis.
Genome-wide statistics were calculated on the total number of phase blocks and the N50 of individual phase block sizes in the pseudohap outputs produced in the Supernova 10x assembly.
For cells requiring a phase block the cells were incubated with 50 μM Nocodazole for 20 h at 37 °C per 5% CO2, counted and checked for viability using a Vi-Cell counter (Beckman Coulter, Inc., USA).
Although the full genome representation is contained in the two resulting pseudohap outputs, it is phased only locally within a phase block (see Fig. 1 in the Supernova paper for an Illustration16).
Haplotype phasing is still limited to the distance of individual phase blocks within scaffolds, these lengths are primarily determined based on the lengths spanning a heterozygous element such as a SNP and structural variants, so phase block lengths will differ between species as well as individuals.
During the second phase, predictive modeling, the previously sensed information is stored in the database, and based upon the past history, future status about the channels is predicted and forwarded to the decision phase block.
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Three-phase block diagram of pedimentation of an upland in a desert.
Cells were synchronized using a double thymidine block (early S-phase block).
The dishes were transferred to a microscope humidified stage incubator containing 5% CO2 at 37°C, 4 hours after release from the early S-phase block.
We depleted PIASγ from HeLa cells before a double thymidine synchrony and then collected the cells that became arrested in mitosis after release from the S-phase block.
FACS analysis confirmed that lovastatin (column 2) synchronized cells in G1 (82%), that a thymidine treatment (column 3) induced an S-phase block (61%) and that nocodazol (column 4) lead to an arrest in G2/M (72%) compared to asynchronous cells (column 1).
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