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A role for T cells in the response to PTH was first suggested by Hory et al [24], who reported that transplantation of human parathyroid gland fragments from patients with primary and secondary hyperparathyroidism into nude mice fails to stimulate OC formation and bone resorption.
Intranasal HY peptide administration, which induces tolerance to syngeneic male grafts in WT mice, fails to induce tolerance in C1qa−/− or C3−/− mice.
Alternatively, hypercholesterolemia in atherosclerosis-prone mice fails to robustly trigger this primary response in marked contrast to the vigorous reaction after immunization or bacterial infection.
This can be attributed to the fact that the SCV in macrophages derived from tlr4 −/−/tlr2 −/−/tlr9 −/− mice fails to acidify.
In contrast, adoptive transfer of AMs from OVA-sensitized mice fails to restore homeostasis compared to transfer of naive AMs 19.
Even more striking, upon withdrawal of the HFD the adipose tissue in these mice fails to properly contract, leading to severe necrosis of the adipose tissue [ 77].
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Solvent-only-treated mice failed to develop elevated TEWL values above the physiological threshold (A).
CCR2/CCR6 deficient mice fail to recruit Ly6C+ monocytes and are thus protected from CCL4-induced hepatic fibrosis [251,252].
These mice failed to suckle and died a day or so after birth.
We found that E-cadherin conditional knockout mice failed to survive, dying within the first 24 hours of birth.
When compared to platelets from wild-type littermates, platelets from α2-null mice failed to adhere to type I collagen under either static or shear-stress conditions.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com