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The patent-pending process involves growing rat heart tissue on a scaffold of collagen, a fibrous protein.
This study was designed to examine the effect of ethanol on rat heart tissue with an experimental model mimicking human binge drinking.
In biological media, MTX cIBR had short half lives in rat plasma (44 min) and homogenized rat heart tissue (38 min).
At sub-lethal dose of mercury chloride (1.30 mg/kg body weight 45 days daily) administered in rat, heart tissue shows an elevated level of lipid peroxidation (LPO) content and simultaneously decreased level of cardiac marker enzymes.
Moreover, selective NET binding in in vitro autoradiography was observed in human brain and rat heart tissue samples.
Fig. 7 a NET-autoradiography and b immunohistochemistry of [11C]Me@HAPTHI on 10 μm slices of human cortex, thalamus, hypothalamus, cerebellum and nucleus caudatus as well as rat heart tissue and blocking with 100 nM FMeNER-D2, 1 μM FMeNER-D2, 100 nM Me@HAPTHI and 1 μM Me@HAPTHI.
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To overcome these limitations, in this study, we developed a supercritical carbon dioxide and ethanol co-solvent (scCO2-EtOH) decellularization method, which is a detergent-free system that prevents ECM structure disruption and retains various angiogenic proteins in the heart dECM, and tested on rat heart tissues.
Rat heart tissues were examined histopathologically for terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) immunoreactivity to detect the presence of DNA fragmentation.
We observed a significant increase in the production of VEGF, pNOS3 and NOS2 and decrease in the production of MMP9 in rat heart tissues treated with stem cells overexpressing VEGF and PDGF genes.
For quantitative analyses, the normalized spot volumes of the 2-D gels from EAM rat heart tissues were compared with those of age-matched control rat heart tissues.
Consistent with this feature, EAM rat heart tissues did have similar levels of total and activated AKT1 compared to the control rat heart tissues.
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