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We observed a nearly 40% increased rate of cell death as judged by increased annexin V labelling 48 h following transfection of either RAW macrophage and BV-2 microglial cells with Tmem176b overexpression vectors as compared with cells transfected with GFP-only overexpression vectors.
Tumour cells' uncontrolled growth typically is reflected in an increased rate of cell division and in the failure of tumour cells to die.
When regeneration does occur, some specialized cells usually lose their specialized characteristics and enter a period of an increased rate of cell division; subsequently, the new cells respecialize into the tissues of the original body part.
The combination of these pathways may be the reason for the increased rate of cell inhibition even at lower concentration.
The increased rate of cell death was confirmed by monitoring activation and increased expression of Bax (Figures 5C and 5D).
The different growing behavior in glutathione depleted cells (with DEM) was not due to an increased rate of cell death (figure 6C).
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Beyond a link to proliferation, high telomerase activity reflects a deregulation of cell cycle associated with an increased rate of cells entering S phase and a higher degree of malignancy[ 13].
However, under hypoxic conditions, loss of K-ras significantly increased rates of cell death from 22% to 57% when compared with control siRNA treatment (Fig. 4C, middle and right panel).
Increased rates of cell death accompanied by protein degradation could explain the modest decrease in activity after 24 hr, as anoxic growth appeared to cease at this time.
Human and murine tumor cells exposed to hCG demonstrated increased viability as well as increased rates of cell proliferation (Fig. 1a and b).
Khandan Keyomarsi (University of Texas MD Anderson Cancer Center, Houston, Texas, USA) emphasized that breast cancer reflects deregulation of cell cycle control and not simply increased rates of cell growth (abstract MS1-2 [ 1]).
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