English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic cytokine and preclinically proven neuroprotectant. A potential reason for the clinical failure of G-CSF may be that relevant G-CSF effects such as the mobilization of mononuclear hematopoietic stem/progenitor cells from the bone marrow may take too long in humans (up to 9 days) to counter initial stroke consequences. Systemic transplantation of bone marrow mononuclear cells (BMMNCs) is feasible within a relatively short time after stroke onset and may provide an external resource of aforementioned stem/progenitor cells, thereby “bridging the gap” until G-CSF comes to full effect. Male spontaneously hypertensive rats (SHR) were randomly assigned into four groups after permanent middle cerebral artery occlusion (MCAO). Groups 1–3 received IP G-CSF treatment (50 μg/kg) for 5 days starting 1 h after stroke onset. Groups 2 and 3 also received 1.5 × 107/kg BMMNCs IV at 6 or 48 h following stroke, respectively. Group 4 received placebo treatment. Functional deficits (adhesive removal test), infarct volume, and edema (T2 TSE MRI) were repeatedly assessed for 1 month. Peripheral leukocyte counts and BMMNC biodistribution were analyzed by flow cytometry during the first week after stroke. G-CSF monotreatment reduced functional deficits (p < 0.05) and partially reversed poststroke immune depression [overall leuko-/monocyte as well as B-, natural killer (NK), and T-cell counts; p < 0.01] and as expected increased peripheral leukocyte counts massively (p < 0.01). G-CSF did not affect infarct volume or edema. BMMNC cotransplantation at 6 h did not further improve functional deficits (p > 0.05 each). Surprisingly, BMMNC transplantation at 48 h abolished G-CSF effects. Early biodistribution studies (at 52 h after stroke onset) revealed splenic accumulation of granulocytes and BMMNCs as well as a granulocyte overload in the peripheral circulation and the brain (p < 0.05). Splenic accumulation of transplanted BMMNCs may have impaired peripheral granulocyte clearance. Subsequently, increased granulocyte numbers in the circulation and the poststroke brain prompted a proinflammatory bias of the innate immune system’s response to stroke, ultimately abolishing G-CSF effects. These surprising findings indicate that systemic effects of experimental stroke therapies need to be carefully considered when assessing the therapeutic potential of such novel approaches

Abstracts for the 22nd Annual Meeting of the American Society for Neural Therapy and Repair