Susan M. Parker

TL;DR: Data show for the first time that focal cerebral ischemia results in dynamic and widespread activation of inflammatory cytokines, chemokines, and CCR in the peripheral immune system.

TL;DR: New evidence is provided to support the contention that damage to the brain caused by cerebral ischemia provides a powerful negative signal to the peripheral immune system that ultimately induces a drastic state of immunosuppression caused by cell death as well as an increased presence of CD4+FoxP3+ regulatory T cells.

TL;DR: The data quantify the damaging effect of T and B lymphocytes on early, evolving ischemic brain injury, and further implicate interleukin-1β in brain and interferon-γ and MIP-2 in spleen as inflammatory factors produced by cells other than T andB cells.

TL;DR: It is demonstrated that mitochondrial localization of PANK2 is demonstrated and speculated on mechanisms of secondary iron accumulation in PKAN, and that this common variant may cause mitochondrial dysfunction and impart susceptibility to late‐onset neurodegenerative disorders with brain iron accumulation, including Parkinson's disease.

TL;DR: While estradiol suppresses cerebral sEH expression, and sEH suppression diminishes inflammation after MCAO, the findings suggest that the effect of estrogen on inflammation is complex, and only partially explained by sEH suppressing.