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It has already been speculated that inflammatory reactions are less expressed in peri-implant tissues in contact with zirconia than titanium surfaces.
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It was speculated that inflammatory cytokines, such as tumor necrosis factor (TNF) or interleukin 1 (IL-1), stimulate these CD11b+ cells to produce VEGF-C because TNF and IL-1 increase VEGF-C expression in human lung fibroblasts and human umbilical vein endothelial cells in vitro [ 18, 19].
It has been speculated that this pulmonary inflammatory syndrome is secondary to the extrapleural dissemination of the talc particles.
Moreover, it has been speculated that the anti-inflammatory properties of α-MSH may also affect melanoma progression.
It has been speculated that certain anti-inflammatory actions of macrolides were involved in such clinically beneficial effects.
It has been speculated that the upregulation of the inflammatory response may predispose MEFV carriers to certain types of inflammatory conditions.
It has been speculated that both fibrosis and the anti-inflammatory response restrict the arrival of new macrophages that are able to phagocytose the apoptotic bodies [46], thus allowing them to accumulate and favoring the mineralization process.
It has been speculated that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during and after surgery could not only modify the tumor microenvironment in which micrometastasis are present but also reduce migration and invasion of circulating malignant cells; therefore, the administration of these drugs in the perioperative period might have a significant impact on cancer recurrence 11– 11.
In addition, it has been speculated that since mut.hIL-10 only has immunosuppressive and anti-inflammatory characteristics, it might be a superior cytokine for therapy of inflammatory diseases, as it would be less antigenic than vIL-10.
Since IL-32 expression is regulated by inflammatory cytokines in human peripheral lymphocyte cells, it has been speculated that it may play a role in inflammatory/autoimmune diseases [5].
It has been speculated that accumulation of ICs involving GPI may activate the alternative complement pathway to cause inflammatory arthritis [ 16].
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