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Vincent, K.A. et al. Angiogenesis is induced in a rabbit model of hindlimb ischemia by naked DNA encoding an HIF-1α/VP16 hybrid transcription factor.
The optimally designed eECMs will then be coinjected with iPSC-EC for treatment of peripheral arterial disease in a mouse model of hindlimb ischemia (Sponsor: NIH).
To determine if mMSCs grown in hypoxia+bFGF retained the therapeutic ability to improve neovascularization, and thus perfusion, in a murine model of hindlimb ischemia, we used a similar model.
(C) To test if late passage murine MSCs can promote and rescue neovascularization in a murine model of hindlimb ischemia, mMSCs (p11) were encapsulated in alginate and delivered to the ischemic hind limb (IL) by subcutaneous implantation.
In in vivo, SHP-1 mRNA, SHP-1 protein levels and VEGF were increased in a rat model of hindlimb ischemia.
Labeled and non-labeled GFP-ADSCs were injected into a mouse model of hindlimb ischemia, and 3T magnetic resonance imaging (MRI) was acquired.
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Many experimental models of hindlimb ischemia are characterized by spontaneous and rapid normalization of resting muscle blood flow (BF) rates which complicates the long-term evaluation of angiogenic therapies to reverse limb ischemia.
VPC have the capacity of tube formation in vitro and improve blood flow in murine models of hindlimb ischemia [19].
We therefore developed a rat model of chronic hindlimb ischemia and compared the effects of chronic ischemia with those of acute ischemia on hindlimb skeletal muscle.
We hypothesized that a model of chronic hindlimb ischemia would develop more collateral arteries, more blood flow, and less necrosis and inflammation than would acute hindlimb ischemia.
We evaluated the efficacy of a new model of rabbit hindlimb ischemia created through a percutaneous approach using embolization with calibrated particles.
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