Humans ; Hypersensitivity

Humans ; Penicillins ; adverse effects ; immunology ; therapeutic use ; Skin Tests ; classification ; methods ; standards

Asthma ; prevention & control ; Child ; Humans ; Hypersensitivity ; prevention & control

Animals ; Apoptosis ; genetics ; immunology ; Apoptosis Regulatory Proteins ; genetics ; Autoimmune Lymphoproliferative Syndrome ; genetics ; immunology ; physiopathology ; Humans ; Mutation ; T-Lymphocytes ; immunology

Calcineurin ; metabolism ; Cardiovascular System ; growth & development ; metabolism ; Humans ; NFATC Transcription Factors ; metabolism ; Signal Transduction

Cephalosporins ; adverse effects ; therapeutic use ; Humans ; Infant, Newborn ; Penicillins ; adverse effects ; therapeutic use ; Skin Tests

Animals ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Central Nervous System ; drug effects ; growth & development ; Female ; Organophosphorus Compounds ; toxicity ; Pesticides ; toxicity ; Pregnancy ; Rats

Anti-Inflammatory Agents ; therapeutic use ; Biomarkers ; analysis ; Child ; Child, Preschool ; China ; Diagnostic Imaging ; methods ; Evidence-Based Medicine ; Female ; Glucocorticoids ; administration & dosage ; Humans ; Immunosuppressive Agents ; therapeutic use ; Male ; Practice Guidelines as Topic ; Purpura, Schoenlein-Henoch ; diagnosis ; etiology ; therapy

Objective To explore the role of endothelial nitric oxide synthase(eNOS) in the regulatory effects of erythropoie‐tin (EPO) on mitochondiral biogenesis in cardiomyocytes exposed to chronic hypoxia .Methods H9c2 cardiomyocytes were cultured in the environment of hypoxia for 1 week(94% N2 ,5% O2 ) ,establishing the chronic hypoxic cardiomyocyte model .All the cells were divided into 3 groups :HC(chronic hypoxic control) ,HE[treated with chronic hypoxia and 20 U/mL recombinant human EPO (rhEPO) ]and HR(cells transfected with eNOS shRNA plasmid and treated with 20 U/mL rhEPO and chronic hypoxia) .Fluores‐cent probe was used to detect the changes of mitochondial number .Mitochondial DNA (mtDNA) relative express level was assayed by RT‐PCR .The expression and phosphorylation of eNOS protein were analyzed with Western blot .Results rhEPO significantly increased the phosphorylation of eNOS and elavated the mitochondialt number and mtDNA (P< 0 .05) .shRNA interference on eNOS significantly blocked all the above changes induced by rhEPO (P<0 .05) .Conclusion Phosphory lation of eNOS is the im‐portant signalling pathway for the enhanced mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia by EPO .