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Findings from previous studies consistently implicate alterations of critical regions in DMN in patients with SAD [12], [23].
These findings thus implicate alterations in Ca2+ homeostasis in the observed atrial arrhythmic properties.
Enhanced central amplification and reduced central inhibition of pain [ 3, 4] implicate alterations in the central neural response to pain.
Changes in adipose tissue function implicate alterations in differentiation genes, remodelling genes, and inflammatory complications [ 40, 41, 55, 56].
Several lines of evidence implicate alterations in both antiviral pathways and cytosolic sensors of nucleic acids in the initial phases of autoimmunity.
Recent genetic studies implicate alterations in SNAP-25 gene structure, expression, and/or function in contributing directly to neuropsychiatric and neurological disorders.
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The high incidence of amino acid changing mutations implicates alterations in aerobic respiration in ACC carcinogenesis.
Clinical and basic science studies have implicated alterations in the retinal pigment epithelium (RPE) layer as a locus of early change.
A multitude of studies have implicated alterations in the hypothalamo-pituitary-adrenal (HPA) axis in the vulnerability to develop stress-related disorders like major depression [1] [7].
The findings implicated alterations in many vital aspects of cell homeostasis.
Thus recent reports have similarly implicated alterations in SR calsequestrin in such pathology (Chopra et al. 2007).
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