It was speculated that abnormal fermentation was due to the change of the characteristics of strain which led to the following results: (1) glutamate production ability decreased and (2) fermentation environment changed after glucose was fed and the strain failed to adapt to the change, resulting in intracellular abnormal metabolism and stoppage of glutamate synthesis.
Thus, it can be speculated that abnormal regulation of VEGF might be involved in the process of cognitive impairment in AD [ 8, 9].
It could thus be speculated that abnormal segregation of chromosomes during mitosis in tumor cells results, at least in part, from persistent activation of Pak1 in these cells.
It is speculated that abnormal regulation of VEGF might be involved in the process of cognitive impairment in AD through activation of deposition of neurotoxic agent such as the beta amyloid plaque [ 8, 40].
It has been speculated that excessive or abnormal forces within the MTPJ, provoked by severe overextension of the joint in combination with hindlimb rotation in particular, will heavily load the plantar supporting structures, especially the PSBs and the ISL [ 2].
It has been speculated that dysfunction of autophagy may result in abnormal mitochondrial function and oxidative or nitrative stress.
It has been speculated that the pathophysiology of Olmsted syndrome might not be explained solely by abnormal TRPV3 function in keratinocytes, but might also involve immune dysfunction arising in other cells, such as cutaneous Langerhans cells.
It may be speculated that an abnormal ReHo may be a clue to disrupted local functionality and may provide insight into the pathophysiology of brain disorder [ 35].
Although residual amounts of abnormally spliced Pink1 transcript would exist in all these Pink1 mutant mouse lines and it could be speculated that residual amounts of PINK1 protein with abnormal 3' sequences are relevant, it is highly probable that mouse phenotypes would result from the engineered deficiency rather than from sequence abnormalities of residual PINK1.
From the results shown here, it is speculated that AIEC could take advantage of the abnormal expression of Gp96 in patients with CD to invade the ileal mucosa.
