Disease pathogenesis in amyotrophic lateral sclerosis (ALS) involves a number of interconnected mechanisms all resulting in the rapid deterioration of motor neurons.
Multifactorial diseases such as type 2 diabetes mellitus (T2DM), are driven by a complex network of interconnected mechanisms that translate to a diverse range of complications at the physiological level.
This argues for the generalisable nature of these interconnected mechanisms, and implicates a hierarchy of immune modulators, known to promote the establishment of an immunosuppressive microenvironment [ 2], in the process of IFNγ-driven adaptive immune resistance.
The regulation of sphingolipid metabolism is complex, incompletely understood, and involves a network of multiple interconnected mechanisms [6, 61].
Therefore, it is crucial to study disease in light of the full complexity of the underlying network of interconnected mechanisms contributing to pathology [ 1].
Delineating the relative contribution of these interconnected mechanisms to disease onset is a major challenge.
Upon the grounds of the phenotype that characterizes the unique animal model developed so far to investigate in vivo about the nature of the signaling involved in the regulation of spermatid-Sertoli cell junctions [ 27], here we propose two interconnected mechanisms that could unravel the question of the regulation of a highly dynamic and essential junction like the aES is.
The existence of two separate, although interconnected, mechanisms underlying the what- and why- of understanding was confirmed by a behavioral study in humans.
Current salivary gland tissue engineering approaches are limited in that they either lack sufficient physical cues and surface area needed to facilitate epithelial cell differentiation, or they fail to provide a mechanism for assembling an interconnected branched network of cells.
Thus, transient suppression of the maternal immune response is necessary for fetal survival, and it is likely that several interconnected mechanisms have evolved to prevent rejection of the fetus.
