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In this study, we present for the first time clear evidence that under physiological conditions GBE improved metabolic energy pathways by increasing the coupling state of mitochondria.
Taken together, respiratory analyses showed that GBE enhanced metabolic pathways by increasing the coupling state of OXPHOS promoting finally a rise of ATP synthesis in both cell types but with the strongest effects on APP cells.
Therefore, to study the molecular mechanism of human sperm chemotaxis towards P, we combined different strategies which involve: the suppression of chemotaxis with specific inhibitors of signaling molecules, the determination of intracellular level of second messengers, and the activation of the chemotactic signaling pathways by increasing the cyclic nucleotide intracellular level.
p66shc has been suggested to mediate mitochondrial cell death pathways by increasing lipid peroxidation-induced apoptosis.
Moreover, we assessed how the novel anti-tumour agent, Dp44mT, may target these integrated pathways by increasing NDRG1 expression.
All of these agents have been described to act, among other pathways, by increasing endogenous Cer [ 44- 48].
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Relative hypocortisolism may explain pain in certain subgroups by enhancing both central and peripheral sensitization of pain pathways by increased pro-inflammatory activity [ 42, 43].
Cells can compensate for some of the dysfunction in ATP production through two alternative pathways: by increased glyocolysis and the use of adenlyate kinase pathway of ATP formation [5].
ALS-causing SOD1 mutations apparently alter this pathway by increasing exposure of buried epitopes in misfolded species populated at endpoint.
Li-ESWT activated protein kinase RNA-like ER kinase (PERK) pathway by increasing the phosphorylation levels of PERK and eukaryotic initiation factor 2a (eIF2α) and by increasing activating transcription factor 4 (ATF4).
Moreover, compound 81 induced lung cancer cells death by inhibiting NF-κB signaling pathway, and activated the JNK-mitochondrial apathwayc pathway by increasing reactive oxygen species (ROS) generation resulting in apoptosis.
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