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stroke

Neuronal Chemokine-Like-Factor 1 (CKLF1) Up-Regulation Promotes M1 Polarization of Microglia in Rat Brain after Stroke

[Acta Pharmacologica Sinica] Researchers showed that CKLF1 was significantly up-regulated in cultured rat cortical neurons subjected to oxygen-glucose deprivation/reoxygenation (ODG/R) injury, but not in cultured rat microglia, astrocytes and oligodendrocytes.

A Neurovascular-Unit-on-a-Chip for the Evaluation of the Restorative Potential of Stem Cell Therapies for Ischaemic Stroke

[Nature Biomedical Engineering] Researchers used the model to track the infiltration of a number of candidate stem cells and to characterize the expression levels of genes associated with post-stroke pathologies.

Athersys Partner HEALIOS K.K. Completes Enrollment in the TREASURE Study of MultiStem Treatment for Ischemic Stroke

[Athersys, Inc.] Athersys, Inc. announced that its partner, HEALIOS K.K., has completed enrollment in its TREASURE study in Japan, evaluating MultiStem® cell therapy treatment in patients who have suffered an ischemic stroke.

Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells in Ischaemic Stroke (AMASCIS-02): A Phase IIb, Multicenter, Double-Blind, Placebo-Controlled Clinical Trial Protocol

[Bmj Open] Investigators developed a Phase IIb, multicentre, randomized, double-blind, placebo-controlled clinical trial protocol to evaluate the safety and efficacy of intravenous administration of allogeneic adipose tissue-derived MSCs in patients with acute ischaemic stroke, concurrently with conventional stroke treatment.

The Voltage-Gated K+ Channel Kv1.3 Modulates Platelet Motility and α2β1 Integrin-Dependent Adhesion to Collagen

[Platelets] Scientists showed that Kv1.3-deficient platelets displayed enhanced ADP-evoked platelet aggregation and secretion, and an increased surface expression of platelet integrin αIIb.

Senescent Cells Suppress Innate Smooth Muscle Cell Repair Functions in Atherosclerosis

[Nature Aging] The authors found that senescent cells inhibited vascular smooth muscle cells (VSMCs) promigratory phenotype switching in the first interfiber space of the arterial wall directly beneath the atherosclerotic plaque, thereby limiting lesion entry of medial VSMCs for fibrous cap assembly or reinforcement.

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