Arch Med Sci
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Hemolysis due to ineffective erythropoiesis is a serious problem β-thalassemia major (β-TM) patients. The role of complement system in the etiopathogenesis of hemolysis observed in β-TM were released. Hemolysis induced by activation of complement system is prevented by complement regulatory proteins. Decay accelerating factor (CD55), membrane inhibitor of reactive lysis (CD59), and complement reception 1 (CR1, CD35) are among these proteins. The absence of these proteins thus accounts for the increased susceptibility of erythrocytes to complement lysis. Splenomegaly and hypersplenism are common complications among thalassemia major patients necessitating splenectomy. ⋯ Increased erythrocyte destruction and iron deposition in organs due to deficiency of these regulatory proteins may be the underlying mechanism of organ damage developing in β-TM patients.
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Fibroblast growth factor-19 (FGF-19) and its co-receptor, beta-klotho, regulate bile acid synthesis in the liver as an enterohepatic feedback mechanism. In this study, our aim was to investigate the circulating FGF-19 and β-klotho levels in intrahepatic cholestasis of pregnancy (ICP) cases. ⋯ The serum FGF-19 and β-klotho concentrations did not differ between the pregnancies with ICP and the healthy controls. However, in some cases, abnormalities in the FGF-19, β-klotho, and FGFR4 signaling system may play roles in the pathogenesis of ICP.
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Childhood-onset schizophrenia with obsessive-compulsive symptoms (COSO) and without obsessive-compulsive symptoms (COS) share considerable overlap in clinical features and genetic risk factors. However, the extent of brain functional abnormalities in COSO and COS is poorly understood. ⋯ Our findings increase the understanding of the pathophysiology of schizophrenia and may provide imaging evidence for early diagnosis of COSO or COS.
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Oxidative stress is currently proposed as a risk factor associated with the development and progression of osteoporosis. Here, the effect of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glycoside (THSG) on oxidative damage was investigated in an osteoblast-like MC3T3-E1 cell model. ⋯ THSG could significantly attenuate oxidative damage induced by H2O2 via the Nrf2/NF-κB signaling pathway, providing new insights for treatments of osteoporosis induced by oxidative injury.
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Exercise training is a coadjuvant therapy in preventive cardiology, and it delays cardiac dysfunction and exercise intolerance in heart failure (HF). However, the mechanisms underlying muscle function improvement and cardioprotection are poorly understood. In this study, we tested whether exercise training would counteract skeletal muscle atrophy via activation of the BDNF pathway in myocardial infarction (MI)-induced HF mice. ⋯ Taken together, our data provide evidence for exercise training may counteract HF-induced muscle atrophy through induced activation of BDNF pathway.