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- 저자 : Mingcheng Huang (검색결과 2 건)
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Zhihua Zheng,Jiasi Chen,Keping Wu,Yan Lei,Mingcheng Huang,Lokyu Cheng,Hui Guan,Jiawen Lin,Ming Zhong,Xiaohua Wang 대한내분비학회 2023 Endocrinology and metabolism Vol.38 No.2
Background: Ferroptosis, which is caused by an iron-dependent accumulation of lipid hydroperoxides, is a type of cell death linked todiabetic 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 glucosein 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 (CPT1A), 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, suppressing 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 lipiddeposition, 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.
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Ming Cheng,Qian Zhang,Mengjing Wang,Bihong Huang,Ye Tao,Chunyan Fan,Hongying Wang,Minmin Zhang 대한이비인후과학회 2023 Clinical and Experimental Otorhinolaryngology Vol.16 No.3
Objectives. We aimed to develop a new calculation model for calcium requirements in dialysis patients following parathy-roidectomy. Methods. A total of 98 patients with secondary hyperparathyroidism receiving parathyroidectomy from January 2014 toJanuary 2022 were enrolled in this study. Among these patients, 78 were randomly selected for construction of thecalcium requirement calculation model, and the remaining 20 patients were selected for model validation. The calci-um requirement model estimated the total calcium supplementation for 1 week after surgery using variables withsignificant relationships in the derivation group by stepwise multiple linear regression analysis. Bias, precision, andaccuracy were measured in the validation group to determine the performance of the model. Results. The model was as follows: calcium requirement for 1 week after surgery =33.798–8.929×immediate postoperativecalcium+0.190×C-reactive protein–0.125×age+0.002×preoperative intact parathyroid hormone+0.003×preopera-tive alkaline phosphatase (R2 =0.8). The model was successfully validated. Conclusion. We generated a novel model to guide calcium supplementation. This model can assist in stabilizing the serumcalcium levels of patients during the early postoperative period. Furthermore, it contributes to the individualized andprecise treatment of hypocalcemia in patients following parathyroidectomy.
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