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It drives the progression of neuroimaging research due to the recognition of the clinical benefits of multimodal data [96], and the better access to hybrid devices, such as PET/MRI [97].
Though other cell types certainly make important contributions, we focus here on the "pas de deux" (steps of two), or perhaps more appropriate to IPF pathogenesis, the "folie à deux" (madness of two) of epithelial cells and fibroblasts that drives the progression of pulmonary fibrosis.
A prevailing view in the established model of influenza infection is that dysregulated inflammatory response in the lungs drives the progression towards a more severe disease [4], [5], [6], [12].
But, in fact, recent studies have revealed that alcohol induces immune activation, which drives the progression of ALD.
There is strong epidemiological evidence that previous exposure to hyperglycemia drives the progression of diabetic complications through a mechanism called "metabolic memory".
Therefore, there is a constant cycle of evolution between the cells and their newly synthesized ECM, forming a positive feedback loop, which drives the progression of OA.
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There has been significant interest in the development of autologous therapies because they contain growth factors and cytokines which could inhibit numerous inflammatory signaling pathways which may drive the progression of OA (Filardo et al. 2013).
This bundling appears to be an irreversible step in the degradation process, as the stress concentrations drive the progression of damage, forming larger bundles and cracks that eventually form lesions.
In this context, infections, which suddenly trigger exacerbations of the otherwise mild lupus disease, may drive the progression of neuroinflammation and neurodegeneration via different mechanisms involving a network of effector molecules and cells.
Although the key inciting events that drive the progression from autoantibodies to clinical disease remain to be clarified, new light has been shed on the factors contributing to disease susceptibility and the role of genetic factors in determining Sjögren's syndrome (SS) disease phenotypes.
These findings indicate that a complete loss of betaglycan results in uncoupling of the reciprocal inductive signalling pathways that operate between the metanephric mesenchyme and ureteric epithelium to drive the progression of branching morphogenesis and nephrogenesis.
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