Patients undergoing surgery frequently develop neuropsychological disturbances, including cognitive decline or memory impairment, and routine clinical procedures such as mechanical ventilation (MV) may affect acute-phase brain outcome.
Given the association of the androgen receptor with the production of a critical mediator of vascular tone suggests that endogenous testosterone levels and subsequently, androgen receptor expression, may affect the acute dilation responses to exogenous androgen administration.
However, CKD patients may have associated underlying chronic neuropathic pain that could affect acute pain response or management.
Therefore not only the positive end-expiratory pressure, but also the tidal volume, the inspired oxygen fraction, repeated tracheal suctioning as well as sedation and paralysis may affect recruitment of acute respiratory distress syndrome lungs that are particularly prone to alveolar instability.
This result suggests that independent factors may affect interictal WPH or acute CA. The sensitization of different neuronal populations may induce migraine associated with interictal WPH or acute CA. All prominent symptoms of migraine are known to result from activation of the thalamus and/or cortex [62 68] and they are associated with acute CA but not interictal WPH.
Recent experimental data suggest that manipulating the mitochondrial fission and fusion proteins in the heart may affect the susceptibility to acute IRI, providing novel therapeutic targets for cardioprotection.
The fact that chemotherapy, a nondosimetric patient factor, may affect the risk of acute diarrhea toxicity is an issue of special concern.
These results suggest that acute stress may affect ingestive behavior by increasing satiation and to some extent by enhancing grooming, and this may be due to stimulation of the hypothalamic POMC neurons.
The mechanisms by which acute inflammation may affect the risk of vascular events are uncertain but may include endothelial dysfunction.
Several factors may affect cell survival in the acute phase of cerebral infarction, including limited blood supply, hypoxia, trophic factor deficiency, oxidative stress, inflammatory response, and others [ 169].
