Objective To study the changes in number and function of peripheral blood T helper cell 17(Th17) in acute urticaria patients .Methods The percentages of Th17 in peripheral blood from 50 acute urticaria patients and 50 healthy persons were ana‐lyzed by immunofluorescence staining and bicolor flow cytometry (FCM ) in vitro .Retinoic acid‐related orphan nuclear receptor γt (RORγt) mRNA from the same research objects were detected by quantitative realtime PCR (qPCR) method .Peripheral blood transforming growth factor‐β(TGF‐β) ,interleukin(IL)‐6 ,IL‐17A and IL‐17F were tested by enzyme linked immunosorbent assay (ELISA) from the same research objects .Results The quantity of percentages of Th17(t= 36 .634 1 ,P< 0 .05) and levels of RORγt mRNA(t=23 .840 1 ,P<0 .05) in urticaria patients were higher than those in healthy persons obviously .Meanwhile ,the levels of TGF‐β(t=15 .521 1 ,P<0 .05) ,IL‐6(t=7 .247 3 ,P<0 .05) ,IL‐17A(t=15 .415 3 ,P<0 .05) and IL‐17F(t=13 .032 1 , P<0 .05) in urticaria patients were higher than those in healthy persons significantly .Conclusion Dysfunction of Th17 in periph‐eral blood may involve in the immunopathogenesis of acute urticaria .

Ischemic stroke has become the leading cause of mortality and disability among adults in China.After ce-rebral ischemia,various pathological and physiological pathways,including the increase in oxygen free radicals,inflam-matory response,calcium overload,and energy metabolism disorders,can disrupt cellular homeostasis,cause mitochon-drial dysfunction,and finally lead to cell apoptosis.By generating new functional mitochondria to replace damaged ones and restoring mitochondrial function,mitochondrial biogenesis(MB)is the primary mechanism for maintaining mitochon-drial homeostasis and plays a crucial role in mitochondrial quality control.In recent years,with the in-depth research on the mechanisms of ischemic stroke injury,MB has emerged as a potential therapeutic target.This article reviews the re-search advances in the role and mechanisms of MB in cerebral ischemic injury,in order to provide a theoretical reference for neuroprotective treatment in ischemic stroke.