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However, POH-N would be a useful tool for translational studies using small animals.
Concurrent studies using small and large animal models are ongoing.
However, these systems are not yet thoroughly developed, are still scarce and are also very expensive when developed for studies using small rodents.
Inhibition studies using small chromogenic substrates demonstrated that the activity of mutant tPA-LMWP could be significantly inhibited by heparin binding.
Recent progress in whole organ engineering based on decellularization/recellularization techniques has enabled pre-clinical in vivo studies using small animal models; however, these in vivo studies have been limited to short-term assessments.
As it approaches its third decade, imaging genetics is confronted by many challenges, including the proliferation of studies using small sample sizes and diverse designs, limited replication, problems with harmonization of neural phenotypes for meta-analysis, unclear mechanisms, and evidence that effect sizes may be more modest than originally posited, with increasing evidence of polygenicity.
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For studies using small-animal models of these brain disorders, CBF assessment meaningfully enhances the understanding of pathology in model animals and facilitates evaluation of drug efficacy.
As compared with several studies using smaller scale gene array, this array completely covers the entire human genome with over 47,000 transcripts.
To date, studies using small-scale gene sets have hinted at relationships between the AIS and 2R-WGD [ 2, 10, 22] and between the AIS and NS [ 22- 25].
While the studies using small-molecule inhibitors and genetic modulators provide the proof of concept for the potential therapeutic application of Stat3-inhibitory drugs, no small-molecule Stat3-inhibitory agent has thus far advanced to the clinic.
A number of knockdown studies using small-interfering RNA have shown that loss of HDAC1 leads to reduced proliferation, cell cycle arrest, and induction of apoptosis in a variety of human tumour cell lines (Glaser et al, 2003; Senese et al, 2007; Thangaraju et al, 2009), indicating that HDAC1 is essential for tumour cell survival.
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