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Still going strong, but not aging well.
Our data revealed reduced p38 MAP kinase phosphorylation in aged and obese mice, while leptin effectively restored p38 phosphorylation in young ob/ob but not aging mice.
Furthermore, short-term leptin supplementation at physiological levels (0.5 and 1.0 nM) significantly attenuated or ablated intracellular Ca2+ abnormalities in young but not aging ob/ob mice.
Low levels of leptin reconciled contractile, intracellular Ca2+ and cell signaling defects as well as O2− production and p47phox upregulation in young but not aging ob/ob mice.
Leptin supplementation at physiological levels (0.5 and 1.0 nM) ablated obesity-induced O2− production and p47phox NADPH oxidase expression in young but not aging ob/ob mice.
Consistent with its responsiveness to mechanical function, O2− production and p47phox expression, physiological levels of leptin effectively restored leptin deficiency-induced changes in the phosphorylation of Akt, eNOS, JNK, IκB and p38 in young but not aging ob/ob mice.
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The protection was not associated with HAI titers or HA specific CD8+ T cells, since both adjuvants boosted the VLP-induced serum HAI titers and CD8+ responses in adult mice, but not aged mice.
The first sample is Core C which was saturated but not aged by crude oil before imbibition tests.
Our findings further suggest that this mechanism must be functional in skeletal muscle from young, but not aged, individuals.
Therefore, according to the literature, we assume age-specific susceptibility to infection, but not age-specific infectiousness.
Log10RDI correlated with fasting insulin (P =.001) and BMI Z score (P =.03) (adjusted r 2 = 0.12, F = 3.9, P =.005), but not age or other metabolic variables.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com