Objec ive: o inves iga e he effec s of differen dose of bisoprolol on neurohormonal ac ivi y,cy okines,cardiac func ion,cardiac dea h in chronic sys olic hear failure pa ien s Me hods: One hundred and wen y chronic hear failure pa ien s were randomly divided in o large dose group (average 8 5? 1 2 mg) and small dose group (average 3 5?1 2 mg) he changes of norepinephrine (NE) ,angio ensionⅡ (AngⅡ) ,aldos erone (Ald) ,endo helin (E ) ,in erleukin 6 BF (IL 6) , umour necrosis fac or ? ( NF ?) Q ,plasm rennin ac ivi y (PRA) ,cardiona rin (ANP) ,brain na riure ic pep ide (BNP) ,cardiac func ion,cardiac dea h were observed Resul s:Af er rea men , he hear ra e were decreased in wo groups, p

BACKGROUNDTo observe the protective effect of hepatitis E virus (HEV) ORF2 recombinant protein expressed in prokaryote cell cynomolgus macaques (cynos) against challenging with wild-type HEV.

METHODSCynos were immunized with HEV ORF2 recombinant protein and then challenged with wild-type HEV, the unimmunized cynos were used as control. Blood samples were collected and tested to see if there were dynamic changes of ALT and antibody to HEV before and after challenge with wild-type HEV.

RESULTSAll the five unimmunized cynos re-presented hepatitis 3 weeks after challenging with wild-type HEV. However, all the five immunized cynos showed no hepatitis and pathological changes.

CONCLUSIONSCynos can be efficiently protected by immunization with HEV ORF2 recombinant protein against wild-type HEV. This protein can be a promising candidate for HEV vaccine.

Animals ; Female ; Hepatitis Antibodies ; blood ; Hepatitis E ; immunology ; prevention & control ; Hepatitis E virus ; immunology ; Macaca mulatta ; Male ; Recombinant Proteins ; immunology ; Viral Proteins ; immunology

Background: Ferroptosis, which is caused by an iron-dependent accumulation of lipid hydroperoxides, is a type of cell death linked to diabetic kidney disease (DKD). Previous research has shown that fatty acid binding protein 4 (FABP4) is involved in the regulation of ferroptosis in diabetic retinopathy. The present study was constructed to explore the role of FABP4 in the regulation of ferroptosis in DKD. Methods: We first detected the expression of FABP4 and proteins related to ferroptosis in renal biopsies of patients with DKD. Then, we used a FABP4 inhibitor and small interfering RNA to investigate the role of FABP4 in ferroptosis induced by high glucose in human renal proximal tubular epithelial (HG-HK2) cells. Results: In kidney biopsies of DKD patients, the expression of FABP4 was elevated, whereas carnitine palmitoyltransferase-1A (CP-T1A), glutathione peroxidase 4, ferritin heavy chain, and ferritin light chain showed reduced expression. In HG-HK2 cells, the induction of ferroptosis was accompanied by an increase in FABP4. Inhibition of FABP4 in HG-HK2 cells changed the redox state, sup-pressing the production of reactive oxygen species, ferrous iron (Fe2+), and malondialdehyde, increasing superoxide dismutase, and reversing ferroptosis-associated mitochondrial damage. The inhibition of FABP4 also increased the expression of CPT1A, reversed lipid deposition, and restored impaired fatty acid β-oxidation. In addition, the inhibition of CPT1A could induce ferroptosis in HK2 cells. Conclusion Our results suggest that FABP4 mediates ferroptosis in HG-HK2 cells by inhibiting fatty acid β-oxidation.