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To date, the main cause of AD remains unclear, but it is considered that the β-amyloid and tau protein aggregation, reduced acetylcholine (ACh), and glutamatergic deficit are regarded as principal pathogenesis of AD [ 3].
Although best-practice procedures of catheter insertion and catheter care to prevent bacterial colonization have been proven effective in CRBSI prevention, the principal pathogenesis of CRBSI is related to the catheter material itself promoting colonization with microorganisms and the formation of biofilm.
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Surface delivery of AMPARs plays a principal role in pathogenesis of neuropsychiatric disorders; interestingly, palmitoylation regulates AMPARs trafficking.
Bacterial LPS is the principal component in the pathogenesis of endotoxic shock, and evokes an acute phase response, resulting in excessive production of pro-inflammatory cytokines.
Inflammatory cytokines such as TNFα and IL-6 trigger apoptosis in tubular epithelial cells, probably playing a role in tissue damage, and TNFα and IL-1 are the principal culprits in the pathogenesis of cardiac dysfunction during sepsis [ 137, 143- 146].
Although beta-amyloid (Aβ) has been regarded as the principal toxic factor in the pathogenesis of Alzheimer's disease (AD), it plays important physiological roles in phenomena such as neuron survival, synaptic plasticity, and memory formation.
In particular, tumor necrosis factor-α (henceforth referred to as TNF, in agreement with Clark [7]) is a principal cytokine involved in the pathogenesis of muscular dystrophy and other disease states such as cachexia [8] [10].
Fibroblast-like synoviocytes (FLS) are among the principal effector cells in the pathogenesis of rheumatoid arthritis (RA).
The fibroblast-like synoviocytes (FLS) that comprise the synovial lining, a thin membrane in direct contact with cartilage and bone, are one of the principal cells responsible for the pathogenesis of RA.
In this article, the principal role of NRs in the pathogenesis of various cholestatic disorders and how they may serve as drug targets in the management of cholestatic patients are discusssed.
The macrophage is one of the principal cell types that contribute to the pathogenesis of RA, since macrophage depletion suppresses the chronic phase of SCW-induced arthritis [ 21].
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