Sentence examples for mediators of cerebral from inspiring English sources

Free radicals have gained wide acceptance as mediators of cerebral ischemic injury.

There is a growing recognition that the classical morphological division of cerebral astrocytes – key cellular mediators of cerebral edema formation – into white matter (fibrous) and grey matter (protoplasmic) subtypes [ 12] is developmentally [ 13– 15], molecularly [ 16– 19], and physiologically [ 20– 22] justifiable.

The elevated level of inflammation biomarkers such as CRP and UA, which triggers secretion of pro-inflammatory cytokines [ 40], mediators for incidence of cerebral malaria pathology, observed in mice treated with khat extract followed by PbA infection strengthen the relative risk of khat users to severe malaria pathologies.

Similarly, a recent study of P. berghei ANKA implicated C5a as an early mediator of experimental cerebral malaria [53].

Proinflammatory cytokines, such as interleukin (IL -1β, IL -1βnd tissue necrosis fandor (tissue, have beenecrosisated as important mediators ofactorry following cerebral ischemia [ 13] and conTNF -αe TNF -αhavenesis, exacerbeenng braimplicateddasage followimportantmediatorsfusiof (injurynjury [ 14].

We suggest that hypertensive pregnancy disorders and menopause activate vascular components, i.e., vascular endothelium and blood elements, including platelets and leukocytes, to release cell-membrane derived microvesicles that are potential mediators of changes in cerebral blood flow, and may ultimately affect cognition in women as they age.

Hence, during brain injury and inflammation, HMGB-1 might be secreted from reactive astrocytes as a potential mediator in the regulation of cerebral remodeling and recovery, involving the preconditioned favorable effects to subsequent injurious challenge.

As described above, we demonstrate significant upregulation of pituitary expression of TNF and IL-6 mRNA following CLP, indicating that the pituitary might be an additional source of cerebral proinflammatory mediators.

IFN-γ, TNF-α and their downstream effector molecule NOS2 are considered the mediators of resistance against ocular and cerebral toxoplasmosis [15], [16], [17], [18], [19], [20].

Activation of the stress activated MAP kinase JNK and of its target substrate c-Jun are important mediators of neuronal stress response after cerebral ischemia and central nerve fiber tract transection [27].

Prostaglandins (PGs) as the major inflammatory mediators in the brain participate in the pathophysiological processes of cerebral ischemia injury.