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Our finding that HBP rapidly induced histological changes consistent with acute lung injury supports the hypothesis that HBP induces increased capillary leak in the lung in vivo and supports a causal relationship between HBP and ARDS.
Our investigations indicated that HBP with higher molecular weight was obtained in relatively lower concentration.
The statement expresses the hope that HBP will unite the neuroscience, medical, and computing communities.
Results obtained from DMA tests showed that HBP has good compatibility with the epoxy resin.
Therefore, we used a murine model to test the hypothesis that HBP causes acute lung injury (ALI) in vivo.
However, given the controversy and the international interest, the commission wanted at least a summary to be published, says the source, who adds that HBP agreed to this.
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The study showed that HBP and LLDPE are immiscible, and HBP has a tendency to migrate to the surface, subsequently, it seems to form a lubricating layer between the metal surfaces and the bulk material.
This has led to the view that HBP/SLBP is localised to both the nucleus and cytoplasm during S phase.
It has been proposed that HBP/SLBP binds SLIP1 that in turn binds the 5′ cap-binding protein, eIF4E and hence circularises the mRNA.
It has been reported that HBP/SLBP localises predominantly to the nucleus at the beginning and end of S phase [ 13].
In conclusion, our findings indicate that HBP/SLBP activity is not only controlled by cell-cycle regulated expression but also by alternative splicing of HBP/SLBP mRNA.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com