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Interaction-dominant dynamics do not assume specific component deficiencies to underlie developmental dyslexia, but rather a much more general reduction of system interactions (and hence, coordination) among multiple task-specific processes.
In particular, deficiencies of the alternative pathway and terminal component deficiencies seem to have a large effect on susceptibility to, as well as severity of, meningococcal disease, emphasising the importance of the complement-dependent defence against this particular pathogen.
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The strongest mean intra-disorder correlation observed was for the genes causing Complement Component Deficiency, Ehlers-Danlos Syndrome and myopathy which all have mean intra-disorder correlation of over 0.26, which are highly significant and also are consistent with high expression in perhaps a restricted tissue or cell type.
This is in contrast to the known association of early complement component deficiency with lupus.
Anyone who has terminal complement component deficiency (an immune system disorder).
Other complement-component deficiencies associated with an increased susceptibility to meningococcal disease are deficiencies in properdin and factor D, both components of the alternative pathway.
The distribution of the different allotypes was no different in individuals with late-complement-component deficiency (LCCD) from that in the general population, but again the severity of disease was positively correlated with the FcγRIIa-R/R131 allotype [ 17].
IL = interleukin; LBP = lipopolysaccharide-binding protein; LCCD = late-complement-component deficiency; LPS = lipopolysaccharide; MBL = mannose-binding lectin; PAI-1 = plasminogen-activator-inhibitor-1; TLR = Toll-like receptor; TNF = tumour necrosis factor.
In a condition known as complement component 7 deficiency, human patients are more susceptible to recurrent infections, particularly to bacterial diseases such as caused by meningococcal infection [ 47].
However, we must note that the RBL based self-referenced setups have to deal with some loss of the low-frequency components, which deficiency generates a diffraction-fringe-like noise on the reconstruction.
Looking more specifically into different light reaction components, SA-deficiency strongly affected the virus-induced expression profiles of PSI and PSII-related genes.
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