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Therefore, the present study demonstrates that LPS can induce sp-a gene expression in human type II epithelial A549 cells through TLR2-mediated sequential activation of MyD88 MEK4 JNK1 AP-1.
The purpose of this study was to compare the effect of a single 48-hour exposure to betamethasone or dexamethasone in the NCI-H441 cell line and in human type II pneumocytes.
Increased levels of circulating glucagon are a common feature in human type 2 diabetes [22].
P. falciparum malaria parasites (3D7 and FCB strains MR4/ATCC, Manassas,VA) were cultured in human type O+ erythrocytes as previously described [35].
These include the microbial proteins Efb from Staphylococcus aureus [30] and Sfb1 Streptococcus pyogenes [31] and a segment in human type I collagen which induces Fn fibrillogenesis [32].
Asexual blood stage parasites were cultured in human type O negative blood and RPMI 1640 (supplemented with 5.96 g l−1 HEPES, 2 gL−1 sodium bicarbonate, 50 mg l−1 hypoxanthine, 3.96 g l−1 glucose and 10% blood type AB serum) and incubated at 37°C in 3% CO2/1% O2/96% N2 according to established protocols [28].
These results demonstrate that, despite a two- to three-fold reduction in both SMN levels and snRNP assembly activity, snRNP biogenesis is not affected in human type I SMA fibroblasts because fibroblasts contain an excess capacity for Sm core formation relative to their actual requirement for snRNP synthesis in vivo.
The involvement and therapeutic potential of IL-1β in the treatment of type 2 diabetes was recently demonstrated by treatment with the IL-1β receptor antagonist Anakinra, which resulted in improved beta cell secretory function and glycaemia control in human type 2 diabetic patients [11].
What is the exact involvement of the innate immune systems in human type 1 diabetes?
Whether proinsulin is the primary autoantigen in human type 1 diabetes remains to be established.
We investigated if proapoptotic molecules are also upregulated in human type 2 diabetes.
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