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Among inflammation-related genes, factors of the complement system showed up-regulation with aging.
The factors of the complement system, which are activated in cascade and normally adhere to the surface of the plates, can be detected by using antibodies.
Another consideration for initiation of TPE was the possibility of aHUS which is associated with alterations in regulatory factors of the complement system [ 4].
Although components of complement appear less critical our study only used C1q−/− mice, and to rule out other factors of the complement system further studies are required.
Local immune responses to cerebral Aβ aggregates are a pathological hallmark of Alzheimer's disease involving activation of cellular components of the brain's innate immunity, such as microglia and astrocytes, and release of various immune molecules and inflammatory mediators, including cytokines, acute phase proteins and factors of the complement cascade, among others [ 4– 7].
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The complement factor B, an element of the complement system which bridges the innate and adaptive immunity with a critical importance for the generation of a potent humoral response [30] was also inhibited throughout the infection in iWT frogs (−1.63 fold, day 7 and −3.33 fold, day 42; Table S1, Figure 2A).
The involvement of the initial factors of the classical complement pathway in sepsis, antibodies, and complement C1q has been reviewed elsewhere [ 25].
Components C4 and C1q were both decreased in expression in the ASL group, and both are major factors of the classical complement pathway [ 69] involved in the binding of immunoglobulin molecules to pathogens during an adaptive immune response.
Adipose tissue also produces all the factors of the alternative pathway for the complement activation [ 27], and human adipocytes express the genes that code the proteins activating the complement system [ 28].
The complement factors of the CP that we examined here did not show any direct correlation with platelet levels; however, factor H did show strong correlation, supporting our conclusion that the lack of AP regulation is one of the mechanisms contributing to complement activation and disease severity.
In biopsies where only C3d was found indicating the existence of possible amplification loops that only augments C3, but not C4 deposition under the influence of certain risk factors, the complement cascade is initiated through the classic, alternative, and lectin pathways.
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