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Our meticulous examination revealed the clinicopathological impacts of copy number alterations at various chromosomal loci.
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The C3(1) SV40 Tag mouse model is being used for a wide variety of studies, ranging from evaluating effects of interventional and preventive therapies [ 17- 30], to understanding molecular and genetic alterations occurring at various stages of disease progression [ 31- 36].
Specifically for cystatin C, alterations were described at various levels of protein synthesis.
Although gene alterations were detected at various sites on chromosomes in both AIS (Types A or B) and early-invasive adenocarcinoma (Types D and E), the total number observed was significantly higher in Type D or E than in Type A or B (P < 0.01; data not shown).
Conversely, when co-electroporated with shRNA at a 0.5 1 ratio, S404D rSynIII significantly rescued the delay in radial migration caused by SynIII KD at E21. CDK5 is a downstream effector in the Sema3A pathway, and alterations in this pathway at various levels all cause a phenotype similar to SynIII KD in the cortex (Polleux et al., 2000; Behar et al., 1996).
In contrast, the increased levels of aneuploidy (irreversible genetic alterations) displayed in blood lymphocytes at various stages of disease are not eliminated following transplantation.
The development and progression of cervical carcinoma is dependent on both genetic and epigenetic events, including alterations in the cell cycle machinery at various checkpoints.
Both CTCs and ctDNA provide snapshots of genomic alterations in primary tumors and metastases at various stages during the course of disease.
miRNA processing can be regulated at various steps, and any alteration in processing either increases or decreases the level of miRNAs [ 113].
Therefore, common defects associated with NTAP AtCTF7∆B include a delay and alterations in both megasporogenesis and megagametogenesis with embryo sacs arresting at various stages of development.
However, due to the difficulties in obtaining serial tumor biopsies from patients at various stages of therapy, the identification of molecular alterations that occur as tumors become resistant to therapy has been a vexing problem.
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