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The first is a defect in chondrocyte apoptosis, as seen in mice with defective tumor necrosis factor receptors (Gerstenfeld et al. 2001).
OPC migration in vivo was disrupted in mice with defective vascular architecture but was normal in mice lacking pericytes.
Surprisingly, the mice with defective hemostasis have greater angiogenesis during the healing process.
Controls and mice with defective Fas-ligand marrow both rejected the graft after about 40 days.
The researchers measured gene activity in four different strains of mice with defective rod cells.
Further, blocking G-CSF but not IL-1R signaling in vivo rescues this neutrophilia, suggesting that a G-CSF-dependent, IL-1β-independent pathway plays a role in promoting neutrophil production in mice with defective clearance of apoptotic cells.
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They demonstrated that disruption of Smad4 in CNS ECs led to a mouse with defective pericyte coverage, intracranial hemorrhage and BBB breakdown.
We do not support such possibility, since we are not aware of any report indicating that mouse strains with defective selection defects in the thymus are prone to tumorigenesis in the T cell compartment.
Most importantly, however, in vivo studies with Jo2 and various mice strains with defective expression of one or more Fc γRs revealed a crucial role of the inhibitory Fc γRII receptor in Jo2-induced hepatotoxicity, the deadly hallmark of systemic CD95 activation.
In this case, the defective gene dominates the normal version, so the mice with one defective copy should have white feet and tails, just like their parents, but the mice with two normal genes should have brown feet.
When mice with one defective gene are fed their normal chow, they remain sleek.
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