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Obligate autotrophic and acidophilic characteristics of iron oxidizing bacteria were exploited in order to prevent or attenuate the generation of acid mine drainage.
They attenuate the generation and release of inflammatory cytokines i.e., interleukin [IL-1, IL-3, IL-6, tumor necrosis factor [TNF-a]) [ 38].
One study reported that high levels of TNF downregulate Foxp3 expression [ 69], whereas a second proposed that TNF may attenuate the generation of adaptive or inducible Tregs in vitro and in vivo [ 70].
Lp(a) competes with plasminogen in binding to fibrin and plasminogen receptors on the surfaces of monocytes and vascular endothelial cells, which may attenuate the generation of plasmin, and reduces fibrinolytic activity in blood circulation [ 11, 12].
While an increase in the levels of enzymes related to energy synthesis (e.g. succinate dehydrogenase and cytochrome c oxidase) increases oxidative capacity, higher levels of ANT and UCP3 might constitute an antioxidant defense mechanism to attenuate the generation of reactive oxygen species and oxidative stress.
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Moreover, SalB attenuated the generation of oxidative stress via suppression of NADPH oxidase 2 and 4, which might probably contribute to the inhibition of PARP-1.
Pretreatment with Pb acetate (500 nm–10 μm) attenuated the generation of NO in a concentration-dependent manner up to 90%, and suppressed iNOS protein expression, as well as interfered with the homeostatic functions of calcium in the cytokine-induced NO signal transduction pathway.
Development of knee inflammation evoked significant spinal release of IL-6, and spinal application of sgp130 attenuated the generation of spinal hyperexcitability during development of inflammation.
Although the generation rates of sAPPβ and Aβ in APP A673T cells were attenuated, the generation rate of C99 in these cells was comparable to that observed in APP WT cells (Fig. 2b and c).
Occlusion of PI3P by FYVE domain protein also attenuated the generation of small vesicles active in LC3 lipidation, consistent with the requirement for PI3P production on the donor membrane to generate the vesicles active in the lipidation of LC3.
Importantly, spinal application of either etanercept or an antibody to TNFR1 during the development of joint inflammation significantly attenuated the generation of inflammation-evoked spinal hyperexcitability, which is characterized by widespread pain sensitization beyond the inflamed joint.
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