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We have shown that biallelic loss of Nf2 is rate-limiting for meningioma development with mice developing a range of meningioma subtypes histologically similar to WHO grade I human meningiomas.
In a murine lymphoma model, the addition of a CpG ODN to antitumor mAb therapy (with an anti-idiotype Ab) reduced the percentage of mice developing a tumor by 70% (Wooldridge et al., 1997).
The selective expression of 4-1BB only on CD8+ T cells in mice developing a massive, non-protective IFN-γ response opens novel strategies for intervention in tuberculosis pathology and vaccination through T-cell co-stimulatory-based molecular targeting.
The first involves transplantation of primary cells from CML patients, resulting in a general low engraftment and only few mice developing a myeloproliferative disorder associated with increased levels of myeloid cells in the bone marrow (BM) and spleen.
Despite all the immunised mice developing a strong humoral response we did not observe consistent tumour protection when the mice were vaccinated with MUC1-pep-STn or MUC1-prot-STn.
There is strong evidence for a role of DNase I in SLE with DNase activity low in SLE patients and SLE-prone mice, and Dnase1-/ mice developing a spontaneous lupus-like phenotype.
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Subsequently, these mice develop a lymphoproliferative syndrome that culminates with the development of lymphomas displaying features typical of human DLBCL.
Within five months, 13 of the 30 mice developed a blood disease that mimicked human chronic myelogenous leukemia.
The normal mice developed a fatty liver and became resistant to insulin.
Nf1 heterozygous (Nf1+/-) mice develop a robust neointima that mimics human disease.
Madsen, K. L. et al. Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora.
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