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Clinically, both of these groups of mice developed marked inflammation as characterized by increased swelling and decreased mobility of the affected leg and were euthanized on post-operative day 5. Thus, inocula of 5×103 or 5×104 CFUs of S. aureus induced markedly high bioluminescent signals and produced clinical signs of infection that was consistent with an acute purulent joint infection.
Finally, LS- G6pc−/− mice developed marked vascular and sinusoidal amyloidosis.
One of the 10 Tet2 gt/gt mice developed marked splenomegaly (>300 mg).
Two weeks after TAC, Het mice developed marked impairment of left ventricular ejection fraction (p < 0.05), while wild-type (WT) TAC mice did not.
Evidence has emerged that TLR4 defective mice do not develop LV dysfunction after LPS stimulation whereas wild type mice developed marked defects in LV contraction and relaxation [ 25].
We next analyzed Tet2 gt/gt mice older than 60 weeks and found that five in seven mice developed marked splenomegaly, multiple swollen lymph nodes and multiple nodules in the liver and lungs (median age, 67 weeks old).
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When challenged with doxorubicin (Adriamycin), these mice develop marked albuminuria, glomerulosclerosis, mitochondrial injury, and impaired autophagy of damaged mitochondria.
Infected mice develop marked lung pathology, with necrotic granulomas more closely resembling human lesions that harbor latent bacilli ("Kramnik mouse model").
However, when placed on an HFD, FGF1 knockout mice develop marked fibrosis in adipose tissue, structurally restricting adipose tissue expansion and resulting in a severe diabetic phenotype.
Db RAS mice, however, developed marked albuminuria (at least 6-fold higher than db sham mice) that persisted throughout the observation period.
The liver of mice exposed acutely to (PhTe 2 developed marked steatosis and changes consistent with cellular necrosis such as nuclear pyknosis and dense eosinophilic bodies unaccompanied by inflammation.
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