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Protective anti-E3 mouse mAbs have also been described [ 117].
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A series of anti-E1 and anti-E2 mouse and humanized mAbs have been described recently.
Human anti-influenza MAbs have been successfully prepared and tested in mice for use against H5N1 infection [33] but for mouse-derived MAbs, the additional step of "humanizing" mouse-derived MAbs to reduce hypersensitivity [32] for parenterally delivered preparations also increases cost and lead time to product availability.
Since 1997, eight MAbs have been licensed for human therapeutic use; three of these are mouse-human chimerics and five are humanized murine MAbs (4).
Towards this goal and to recapitulate patient polyclonal responses, a panel of six new mouse monoclonal antibodies (MAbs) has been generated against AAV8 and AAV9 capsids, two vectors being developed for therapeutic application.
Notch4 was not expressed during osteoclastogenesis and anti-mouse Notch4 mAb had no effect on osteoclast differentiation.
In keeping with the increased bacterial burden, mice treated with anti-IL-17 mabs had ∼3-fold more IFNγ in their lungs than the control groups, but this difference was not statistically significant.
While engagement of the inhibitory Fcγ-receptor (FcγR) IIB is an absolute requirement for in vivo antitumor activity of agonistic mouse anti-CD40 monoclonal antibodies (mAbs), a similar requirement for human mAbs has been disputed.
Our data indicate that blockade of B7-H1 did not have a significant effect on disease onset, but enhanced the chronic course of TMEV-IDD during the autoimmune phase of disease (Figure 8), although mice treated with anti-B7-H1 mAb have similar TMEV viral loads in the brains at day 7 post-infection compared to isotype controls (Figure 9).
The treatment with the mouse anti-HM1.24 mAb has resulted in a decrease of the serum levels of M-proteins and the size of the tumors and has resulted in not only a prolonged survival of the mice but also a cure in some of them.
Anti-mouse Dll4 blocking mAb had no effect on osteoclast differentiation, consistent with no expression of Dll4 during osteoclastogenesis.
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