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The development of these changes in capillary supply is fairly well understood [ 3].
Muscle retraction is not essential for the development of these changes.
The development of these changes during an exponential rise in plasma and brain leucine levels suggests a causative relationship and provides further evidence for competition at the blood brain barrier between leucine and other essential large neutral amino acids.
46, 47 The absence of any absolute cortical thickness changes observed in this cohort may be due to any changes being so subtle as to escape detection, yet the development of these changes is reflected in the organization of the cortical thickness network.
This study reinforces the concept that changes in systolic and diastolic functions are common in septic shock and severe septic patients, and that the development of these changes (as an adaptation mechanism) seems to correlate inversely with the acute mortality rate during ICU stay [ 2, 4].
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The development of these degenerative changes is often accompanied by restriction of segmental mobility [ 1].
The development of these pathological changes is strongly related to hyperglycemia.
The development of these morphological changes is most likely due to defective biliary phospholipid secretion resulting in an increased concentration of free non-micellar bile acid [92].
In the last decade, numerous studies have investigated the molecular triggers and biological key elements associated to the development of these clinical changes, but the complete picture of this process is still incomplete [ 20- 22].
This suggests that the initial traumatic dislocation and difficulty in reduction may be more important than the number of dislocation episodes before stabilization in the development of these histopathologic changes.
Experimental studies have provided evidence that activation of microglia, the macrophages of the CNS, as well as the cerebral vasculature, plays a key role in the development of these behavioural changes, by inducing pro-inflammatory mediators, such as IL-1β, TNF-α and PGE2 in the CNS.
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CEO of Professional Science Editing for Scientists @ prosciediting.com