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Although synaptic α-synuclein aggregation has been neither postulated nor demonstrated before, a synaptic dysfunction has been assumed in explaining neurodegeneration for decades.
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The decrease and dysfunction of endothelial progenitor cells (EPCs) has been assumed as an important cause/consequence of diabetes mellitus (DM) and its complications, in which the senescence of EPCs induced by hyperglycemia may play an immensurable role.
Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease.
Endothelial dysfunction has been demonstrated in adult subjects with diabetes.
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GLUT1 is the principal glucose transporter in the brain and it has generally been assumed that neuronal dysfunction arises from energy failure.
Most acquired cardiovascular diseases affect primarily the LV and it has been previously assumed that mechanisms of LV function/dysfunction can also be applied to the RV.
Johnson may have been an assumed alias.
Therefore it has to be assumed that androgenic hormonal abnormalities described in literature, only occur in more severe endocrinological disorders like the polycystic ovary syndrome (PCOS), in combination with hirsutism or by severe dysfunctions of the hypothalamic-hypophyseal-axis.
When cardiac arrest occurs in patients with chronic ischemic LV dysfunction, they are assumed to have a lower chance of successful cardiopulmonary resuscitation (CPR) and lower likelihood of ultimate survival.
Bertie assumes she has been betrayed.
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