ABSTRACT Given the pivotal role of galactose‐deficient IgA1 (Gd‐IgA1) in the pathogenesis of IgA Vasculitis Nephritis (IgAV‐N), telitacicept, a dual inhibitor targeting both B lymphocyte stimulator (BLyS) and a proliferation‐inducing ligand (APRIL), represents a promising biologic therapeutic alternative offering safer and more effective options. To our knowledge, this is the first case report describing the feasibility of telitacicept combined with glucocorticoids as initial therapy for pediatric IgAV‐N. A 14‐year‐old male presented with a history of purpura, gross hematuria, nephrotic‐range proteinuria (proteinuria 4100.39 mg/24 h), and impaired renal function (serum creatinine 156.52 μmol/L). Renal biopsy confirmed a diagnosis of moderate IgAV‐N (ISKDC IIIa). The patient also had a concurrent pulmonary infection. To avoid the risk of infection exacerbation and reproductive toxicity associated with conventional immunosuppressive agents, initial therapy was administered as telitacicept combined with glucocorticoids (methylprednisolone). After 3 months, methylprednisolone had been rapidly tapered, renal function normalized, proteinuria stabilized below 500 mg/24 h, and hematuria had resolved. During 1 year of follow‐up, no disease recurrence or deterioration was noted, and no serious infectious events occurred. This case provides preliminary clinical evidence for expanding the indications for telitacicept and optimizing treatment strategies for moderate IgAV‐N.

INTRODUCTION:The efficacy and safety of finerenone in patients with idiopathic membranous nephropathy (IMN) remain unclear, especially given the need for additional supportive therapeutic options. METHODS:This prospective-retrospective, multicentre, observational real-world study evaluated the efficacy and safety of finerenone in IMN patients with proteinuria ≥1 g/24 h. The primary outcome was the percentage change in proteinuria from baseline to 6 months with finerenone treatment. Secondary outcomes included the stratified reduction in proteinuria, and changes in estimated glomerular filtration rate (eGFR), serum albumin (ALB), and total cholesterol (TCHO). Safety assessment focused on serum potassium. Data were primarily analysed using linear mixed-effects models. RESULTS:Among 112 IMN patients treated with finerenone, 79 were ultimately analysed. All of them received tolerated doses of ACEIs or ARBs, and 53.2% (42/79) were treated with immunosuppressive therapy. The median baseline proteinuria was 3,212.5 mg/24 h (IQR 1,977.0-7,113.6). After 6 months of finerenone treatment, the geometric mean reduction in proteinuria was -58.5% (95% CI: -67.7 to -46.6; p < 0.001). The reduction was significantly greater in patients receiving immunosuppressive therapy than supportive treatment (-67.1% vs. -45.3%, p = 0.023). eGFR showed an initial decline but subsequently stabilized (-1.3 mL/min/1.73 m2, p = 0.226). Significant improvements were observed in ALB (4.6 g/L, p < 0.001) and TCHO (-0.8 mmol/L, p = 0.003). Although hyperkalaemia (>5 mmol/L) occurring in 5.1% of participants (4/79), no cases exceeded 5.5 mmol/L. CONCLUSION:In combination with ACEIs or ARBs, finerenone appeared to reduce proteinuria in IMN patients with or without immunosuppressive therapy. Serum potassium did not exceed 5.5 mmol/L in any cases.

Acute kidney injury (AKI) is a common clinical syndrome characterized by abnormal renal function and structure. Microcirculatory perfusion disorders and inflammatory responses are critical pathophysiologies of AKI. Recently, ultrasound molecular imaging has been considered a valuable tool for preclinical and clinical diagnostics that can sensitively target histological structures of interest, particularly in evaluating renal microcirculation. The purpose of this study was to explore a lipid microbubble (MBE-selectin) that targets E-selectin molecules expressed on the activated endothelium and to perform ultrasound molecular imaging for the kidney in cisplatin-induced AKI in rats. Using freeze-drying methods, three formular nontargeted microbubbles (NMBs-1, NMBs-2, NMBs-3) were prepared, and three corresponding MBE-selectin suspensions (MBE-selectin-1, MBE-selectin-2, MBE-selectin-3) were constructed via maleimide-thiol conjugation chemistry. The results revealed that the physicochemical characteristics of three NMBs and MBE-selectin suspensions were usable for intravenous injection as ultrasound contrast agents (UCAs), and the anti-E-selectin antibody successfully conjugated to the lipid shell surface of the bubbles in three MBE-selectin suspensions, which could bind specifically to E-selectin molecules expressed on human umbilical vein endothelial cells (HUVECs) treated with tumor necrosis factor-alpha (TNF-α). During ultrasound imaging for the kidney in the cisplatin-induced AKI model, the time-to-peak (TTP) and area under the curve (AUC) of the MBE-selectin-2 suspension significantly increased, but the wash-in rate (WIR) and wash-out rate (WOR) significantly decreased compared with those of the NMBs-2 suspension or the control group. The normalized differential targeted enhancement (NdTE) of the MBE-selectin-2 suspension was significantly greater than that of the NMBs-2 suspension in the model group, as was the residual-to-saturation ratio (RSR) at 8 min. In conclusion, we successfully prepared a novel MBE-selectin suspension carrying an anti-E-selectin antibody that can be used for intravenous injection and can enhance ultrasound imaging of the kidney as a UCA, particularly in a cisplatin-induced AKI model. Ultrasound molecular imaging of the MBE-selectin suspension may be helpful for evaluating renal microcirculation or injury in AKI diseases.

Background: Although it has been established that activating adenosine monophosphateactivated protein kinase (AMPK) inhibits cell proliferation in several cells, it is unknown whether AMPK is involved in inhibiting biliary fibroblast growth. Objective: The objective of this study is to specifically investigate the influence of AMPK isoforms on proliferation. Methods: To further address its underlying molecular mechanisms, primary cultured rat biliary fibroblasts were transfected with sequence-specific AMPK1 or AMPK2 siRNA. Results: Our findings show that knocking down AMPK2 greatly increased the proliferation of primary cultured biliary fibroblasts, accompanied by the activation of mTOR, an increase in S-phase kinaseassociated protein 2 (Skp2) expression, and a decrease in p27 protein levels. AMPK2 inhibition-triggered Skp2 overexpression and concomitant p27 decrease, as well as biliary fibroblast proliferation, were reversed by rapamycin inhibition or previous silencing of Skp2 production by targeted small interfering RNA (siRNA) transfection. Conclusion: We concluded that AMPK2 regulates the mTOR/Skp2/p27 signaling pathway and causes endogenous suppression of primary cultured biliary fibroblast growth. The reduction of biliary fibroblast proliferation by AMPK2 could be a potential method in treating benign biliary stricture (BBS).

Flowering promoting factor (FPF) genes play a substantial regulatory role in the process of flowering. In the present study, four MiFPF genes, namely, MiFPF1, MiFPF2, MiFPF3a, and MiFPF3b, were obtained from mango (Mangifera indica L.). Tissue expression analysis showed that MiFPFs were expressed in all mango tissues. Specifically, MiFPF1 and MiFPF2 were highly expressed in leaves, while MiFPF3a and MiFPF3b were highly expressed in flowers and buds. The four MiFPF proteins localize to the nucleus. Overexpression of MiFPFs in transgenic Arabidopsis resulted in early flowering and upregulated the expression of APETAL1 (AP1), FLOWERING LOCUS D (FD) and FLOWERING LOCUS T (FT). MiFPF genes increased the root growth of transgenic Arabidopsis plants under gibberellin treatment. BiFC assays showed that MiFPFs can interact with several DELLA proteins. Taken together, our results demonstrate that the MiFPF gene was involved not only in promoting flowering but also in increasing root growth under gibberellin (GA3) treatment.

End-stage renal disease（ESRD） patients undergoing outpatient hemodialysis（HD） and home peritoneal dialysis（PD） are high risk population of severe and critical types caused by SARS-CoV-2 infection. In order to improve the quality of diagnosis and treatment in dialysis patients with SARS-CoV-2 infection, we wrote this recommendation for primary care clinicians. During the epidemic period of SARS-CoV-2 infection, all patients should be instructed to strengthen self-management. Once the SARS-CoV-2 infection was found in dialysis patients, early stratified management should be carried out within 72 hours after the first positive nucleic acid or antigen test results, which includes early antiviral therapy, early recognition, and transferring severe patients from community or primary hospital to a referral hospital promptly. Guidance for dietary and sports rehabilitation after SARS-CoV-2 infection should also be started as soon as possible.

OBJECTIVE:The objective of this study was to explore the molecular mechanism underlying the occurrence of benign bile duct stricture and the target of low-dose paclitaxel in the prevention of benign bile duct stricture.METHODS:Under the stimulation of transforming growth factor beta 1, the expression of collagen type I and connective tissue growth factor were detected on isolated primary fibroblasts. The phosphorylation levels of JNK and Smad2L were detected using Western blot. The effect of low-dose paclitaxel on the transforming growth factor beta 1-induced inhibition of type I collagen and connective tissue growth factor expression and JNK and Smad2L phosphorylation was also observed.RESULTS:Transforming growth factor beta 1 induced the secretion of type I collagen and connective tissue growth factor as well as JNK phosphorylation in biliary fibroblasts. The JNK inhibitor or siRNA-Smad2 inhibited the transforming growth factor beta 1-induced secretion of type I collagen and connective tissue growth factor. Low-dose paclitaxel inhibited the expression of type I collagen induced by transforming growth factor beta 1 and may inhibit the secretion of collagen in biliary fibroblasts.CONCLUSION:The activation of JNK/Smad2L induced by transforming growth factor beta 1 is involved in the occurrence of benign bile duct stricture that is mediated by the overexpression of type I collagen and connective tissue growth factor, and low-dose paclitaxel may inhibit the phosphorylation of JNK/Smad2L.

目的 揭示纤溶酶原激活物抑制因子1(plasminogen activator inhibitor 1,PAI-1)在腹膜透析患者中的表达及其功能.方法 选择100例腹膜透析患者作为研究对象,透析7个月后,根据腹膜平衡试验结果将患者分为高转运组和低转运组.透析1个月时和7个月时,使用酶联免疫吸附测定试剂盒检测所有患者透析液中PAI-1、基质金属蛋白酶-2(matrix metalloproteinase 2,MMP-2)和血管内皮生长因子(vascular endothelial growth factor,VEGF)水平.对C57/BL6小鼠连续28 d腹腔注射3 mL含4.25％葡萄糖的腹膜透析液来建立腹膜纤维化(peritoneal fibrosis,PF)小鼠模型.将小鼠按随机数字表法分为3组(n=12):对照组、PF+si-NC组和PF+si-PAI-1组.PF+si-NC组和PF+si-PAI-1组小鼠分别腹腔注射300μL阴性对照siRNA(si-NC)或靶向PAI-1的siRNA(si-PAI-1).通过蛋白质印迹法检测PAI-1、MMP-2、VEGF、磷酸化血管内皮细胞生长因子受体2(phosphorylated vas-cular endothelial growth factor 2,pVEGFR2)和磷酸化细胞外调节蛋白激酶(phosphorylated extracellu-lar regulated protein kinases,pErk)的蛋白表达.通过免疫组织化学染色检测巨噬细胞表面标志物(macrophage surface markers,CD68)、VEGF和血小板-内皮细胞黏附分子(platelet endothelial cell ad-hesion molecule-1,PECAM-1/CD31)的阳性表达.结果 与透析1个月时相比,透析7个月后患者透析液中PAI-1、MMP-2和VEGF的水平均显著升高(P<0.05).与低转运组相比,高转运组患者透析液中PAI-1、MMP-2和VEGF的水平均显著升高(P<0.05).PAI-1、MMP-2和VEGF联合诊断高转运的曲线下面积(area under curve,AUC)、敏感性和特异性依次为0.909、82.61和92.45.与PE+si-NC组比较,PE+si-PAI-1组的间质细胞外基质(extracellular matrix,ECM)沉积和炎症细胞浸润明显减轻.与PE+si-NC组比较,PE+si-PAI-1组腹膜组织的CD68、VEGF和CD31阳性率降低(P<0.05).与PE+si-NC组比较,PE+si-PAI-1组腹膜组织的PAI-1、MMP-2、VEGF、pVEGFR2和pErk的蛋白表达水平降低(P<0.05).结论 本研究显示PAI-1、MMP-2和VEGF的联合诊断对腹膜溶质转运速率具有较高的诊断价值.下调PAI-1可能通过抑制MMP-2/VEGF/细胞外调节蛋白激酶1/2信号通路来抑制血管生成,从而抑制腹膜纤维化.

OBJECTIVE: The aim of this study was to investigate whether rosiglitazone-activated peroxisome proliferator-activated receptor gamma can inhibit the occurrence of benign biliary stricture and further elucidate the relevant molecular signaling mechanism. METHODS: The primary cultured rat biliary fibroblasts following experiments were performed using within the fifth generation cells, which were separated from the bile ducts of Sprague-Dawley rats. The primary cultured rat biliary fibroblasts were co-cultured with 10 ng/mL transforming growth factor-beta 1 for stimulating collagen formation. Competent cells were transfected with siRNA that specifically target Smad3 or connective tissue growth factor to inhibit the expression of the corresponding proteins. The cells were incubated with 10 mu mol/L rosiglitazone to activate peroxisome proliferator-activated receptor gamma. The cells were incubated with 10 mu mol/L GW9662 in the pretreatment session to inactivate peroxisome proliferator-activated receptor gamma. ELISA was used to determine the levels of connective tissue growth factor and type I collagen in the cell supernatant. Western blotting was used to detect the levels of intracellular p-Smad3/t-Smad3. RESULTS: Rosiglitazone-activated peroxisome proliferator-activated receptor gamma inhibited the secretion of type I collagen induced by transforming growth factor-beta 1. Peroxisome proliferator-activated receptor gamma inhibitor GW9662 could significantly reverse the rosiglitazone-triggered inhibition of transforming growth factor-beta 1-induced type I collagen secretion by suppressing peroxisome proliferator-activated receptor gamma activation (p<0.01). Furthermore, we also found that the activation of peroxisome proliferator-activated receptor gamma was accompanied by the inhibition of transforming growth factor-beta 1-induced Smad3 phosphorylation (p<0.01), increased connective tissue growth factor expression (p<0.01), and production of type I collagen (p<0.01), all of which effects elicited by rosiglitazone could be reversed by peroxisome proliferator-activated receptor gamma inhibitor GW9662. CONCLUSION: Peroxisome proliferator-activated receptor gamma activated by rosiglitazone inhibits the transforming growth factor-beta1-induced phosphorylation of Smad3 and the increased connective tissue growth factor expression as well as inhibits the secretion of type I collagen in biliary fibroblasts.

目的：对多元化教学模式应用于肝胆外科临床带教的价值进行探析。方法：随机将我院2019年1月到2022年1月之间的 肝胆外科实习生20例分为两组，对照组采用常规教学模式，观察组采用多元化教学模式，对比效果。结果：对照组 实习生考核评分低于观察组（P<0.05）。对照组实习生对带教工作满意度低于观察组（P<0.05）。结论：在肝胆外科 临床带教中，应用多元化教学模式能够显著改善实习生的实习成绩，促进带教质量和带教满意度的提升，具有探究 和参考价值。

目的 探讨分析肾内科临床教学中应用临床路径式教学法的价值.方法 选取2018年4月—2019年4月于医院肾内科实习的60名医学生作为研究对象,根据不同的教学方式分为对照组与实验组,两组各30人,对照组予以肾内科传统教学方式,实验组予以临床路径式教学方式,比较两组教学方式的应用价值.结果 实验组学生在自学能力、处事能力、学习能力以及思维能力各方面均高于对照组学生,差异具有统计学意义(P<0.05);实验组学生的病例书写、病例分析以及理论成绩和操作成绩均高于对照组学生,差异具有统计学意义(P<0.05);实验组学生对教学质量的满意度高于对照组(96.67％vs.80.00％)差异具有统计学意义(P<0.05).结论 肾内科临床教学方式中,应用临床路径式教学方式比传统教学方式更能提高实习医学生的自学能力、处事能力、学习能力以及思维能力等各方面,从而有效提高其学习成绩与对教学质量的满意度,具有较高的应用价值.

目的 探究纤溶酶原激活物抑制因子1(PAI-1)在腹膜透析患者中的表达及其功能.方法 通过免疫组化和Wes-tern blot检测30例腹膜透析患者和30例终末期肾病患者腹膜组织中PAI-1的表达水平.将人腹膜间皮细胞(HPMCs)分为3组:正常对照组、TGF-β1+si-NC组和TGF-β1+si-PAI-1组.TGF-β1+si-NC组和TGF-β1+si-PAI-1组细胞用10 ng/ml TGF-β1培养24 h,并分别转染靶向PAI-1的siRNA(si-PAI-1)和阴性对照(si-NC).通过Western blot检测腹膜间皮细胞中PAI-1、p-STAT3、STAT3、p-Smad3、Smad3、CollagenⅠ、E-cadherin、α-SMA、EGFR、p-EGFR和Acetylα-tubulin的蛋白表达.对C57/BL6小鼠连续28 d腹腔注射3 ml含4.25％葡萄糖的腹膜透析液来建立腹膜纤维化(PF)模型.将小鼠随机分为3组,每组12只:正常对照组、PF+si-NC组和PF+si-PAI-1组.PF+si-NC组和PF+si-PAI-1组小鼠分别腹腔注射300μl si-NC或si-PAI-1(0.1 mg/kg).通过免疫组织化学染色检测小鼠腹膜组织中PAI-1、CollagenⅠ和 α-SMA的阳性表达.结果 与终末期肾病组比较,腹膜透析组患者腹膜组织中的PAI-1表达水平显著升高(P<0.05).与正常对照组比较,TGF-β1+si-NC组腹膜间皮细胞中PAI-1、CollagenⅠ、α-SMA、p-Smad3、p-EGFR和p-STAT3蛋白相对表达量显著升高(P<0.05),E-cadherin、Acetylα-tubulin显著降低(P<0.05).与TGF-β1+si-NC组比较,TGF-β1+si-PAI-1组腹膜间皮细胞中PAI-1、CollagenⅠ、α-SMA、p-Smad3、p-EGFR和p-STAT3蛋白相对表达量显著降低(P<0.05),E-cadherin、Acetylα-tubulin显著升高(P<0.05).与正常对照组比较,PE+si-NC组腹膜组织中E-cadherin阳性率显著降低,α-SMA显著增加(P<0.05).与PE+si-NC组比较,PE+si-PAI-1组腹膜组织中E-cadherin阳性率显著增加,α-SMA显著降低(P<0.05).结论 本研究证明了下调PAI-1可抑制腹膜纤维化的发展,推测这种抗纤维化机制可能与TGF-β1/Smad3和EGFR/STAT3信号通路的失活有关.

Background Peritoneal fibrosis (PF) can reduce the efficiency of peritoneal dialysis and eventually lead to ultrafiltration failure. Epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) is the start of PF. Macrophages are involved in the process. This study was to investigate the effect of macrophage polarization on EMT of PMCs. Methods Monocyte-macrophage cells (THP-1) were treated to induce macrophage subsets (M1, M2a, M2c). The inducing was assessed by detecting protein and mRNA expression of cytokines using ELISA and RT-PCR. Subsequently, PMCs were co-cultured with M1, M2a and M2c, respectively, in Transwell chambers for 48 h and then expressions of E-cadherin and alpha-SMA were determined in PMCs. The PMCs that were not co-cultured with macrophages served as control PMCs. One-way ANOVA and SNK-q test were used to conduct statistics and P Results Detection of the cytokines, including IL-6, IL-10, IL-12, TGF-beta 1, CCL17 and CXCL13, verified that the inducting of macrophage subtypes was successful. Compared to control, E-cadherin protein expression was significantly decreased and alpha-SMA protein expression increased in M1-treated PMCs (P < .05); M2a-treated PMCs had an increased gene expression of alpha-SMA (P < .05); E-cadherin protein and gene expression were decreased and alpha-SMA protein and gene expression increased significantly in M2c-treated PMCs (P P < .01). Conclusions EMT of PMCs is enhanced by M2c macrophage polarization; meanwhile, M1 and M2a polarization may have the effect to some extent, but not as definite as M2c.

A new esterase gene est906 was identified from paper mill wastewater sediments via a function-based metagenomic approach. The gene encoded a protein of 331 amino acids, that shared 86% homology with known esterases. Based on the results of multiple sequence alignment and phylogenetic analysis, it was confirmed that Est906 contained a characteristic hexapeptide motif (G-F-S-M-G-G), which classified it as a lipolytic enzyme family V protein. Est906 displayed the highest hydrolysis activity to p-nitrophenyl caproate (C6), and its optimal temperature and pH were 54 degrees C and 93, respectively. Additionally, this enzyme had good stability under strong alkaline conditions (pH 10.0-11.0) in addition to moderate heat resistance and good tolerance against several metal ions and organic solvents. Furthermore, a specific nucleic acid aptamer (Apt1) bound to Est906 was obtained after five rounds of magnetic bead SELEX screening. Apt1 displayed high specific recognition and capture ability to Est906. In conclusion, this study not only identified a new esterase of family V with potential industrial application by metagenomic technology but also provided a new method to purify recombinant esterases via nucleic acid aptamers, which will facilitate the isolation and purification of target proteins in the future. (C) 2020 Elsevier B.V. All rights reserved.

OBJECTIVE To clarify the molecular signaling mechanism underlying the inhibitory effect of metformin on transforming growth factor-β1 (TGF-β1)-stimulated collagen I production in rat biliary fibroblasts. METHODS Primary biliary fibroblasts were isolated under aseptic condition from 50 Sprague-Dawley rats (half male and half female), and microscopic observation identified no obvious difference in the morphology or viability of the cells from rats with different sexes or body weight. The cells were treated with TGF-β1 (10 ng/mL), Smad3 siRNA+TGF-β1, CTGF siRNA+TGF-β1, metformin (10 mmol/L)+ TGF-β1, or Compound C (10 μmol/L)+metformin+TGF-β1. The expressions of CTGF and collagen I in the treated cells were determined using ELISA kit or Western blotting; the phorsphorylated and total Smad3 and AMPK expressions were detected using immunoblotting. RESULTS TGF-β1 time- and dose-dependently induced collagen I production in rat biliary fibroblasts. The activated AMPK by metformin dose-dependently inhibited TGF-β1-induced collagen I production. Pre-incubation of cells with the AMPK inhibitor Compound C restored the inhibitory effect of AMPK on TGF-β1-induced collagen I secretion (P < 0.01). Activation of AMPK by metformin significantly reduced TGF-β1-induced collagen I production by suppressing Smad3-driven CTGF expression (P < 0.01), and the application of Compound C reversed such changes in the fibroblasts (P < 0.01). CONCLUSIONS Metformin inhibits TGF-β1-stimulated collagen I production by activating AMPK and inhibiting Smad3- driven CTGF expression in rat biliary fibroblasts.

目的 将两种不同的教学方法 在肾内科临床教学中,对学生考核成绩的影响作为探究方向,分析改善措施.方法 为得到有效结果 ,本次截选肾内科实习的100名实习生,所选实习时间在2017年3月～2019年4月中,分为两组,两组实习生的区分方式为应用于教学方式,对照组以常规临床带教作为教学方式,观察组实习生选择的方式为分阶段目标教学.为确定教学效果差异,对比两组实习生考核成绩数据,探究教学方式的不同,对实习生带来的不同结果 .结果 对比分析整理后发现,两组实习生接受不同带教方式后,在实习生考核成绩上观察组高于对照组,而且观察组与对照组相比差异较大,从统计学角度上来看,具有实际对比价值.结论 对于实习生来说,以分阶段目标教学为主的教学方式,能够有效提高实习生的考核成绩以及肾内科的教学质量,对带教工作教学方式扩展有推进作用.

[目的]探讨慢性肾炎患者尿N-乙酰-β-D-葡萄糖苷酶(NAG)、β2-微球蛋白(β2-MG)水平及临床意义.[方法]比较慢性肾炎患者和同期体检的健康成年人(对照组)尿NAG、β2-MG、血炎症因子超敏C反应蛋白(hs-CRP)、肿瘤坏死因子-α(TNF-α)、肾功能指标血肌酐(SCr)、尿素氮(BUN)和营养指标白蛋白(ALB)、血红蛋白(HGB)、红细胞计数(RBC)的差异,并分析慢性肾炎患者尿NAG、β2-MG与相关指标的相关性.[结果]慢性肾炎组患者的NAG、β2-MG水平高于对照组(P＜0.01);慢性肾炎组患者的hs-CRP、TNF-α和SCr、BUN水平高于时照组(P＜0.01),RBC、HGB和ALB水平均低于对照组(P＜0.01);慢性肾炎患者NAG、β2-MG与hs-CRP、TNF-a、SCr、BUN呈正相关,与RBC、HGB和ALB呈负相关.[结论]慢性肾炎患者NAG、β2-MG水平较高,且与炎症因子、肾功能等指标相关.

Elevated serum levels of free fatty acids (FFAs) are correlated with the deterioration of renal function in patients with chronic kidney disease (CKD). However, it was still unclear whether there would be and what were the effects of elevated FFAs on mesangial cells. A cell line of rat mesangial cells (HBZY-1) was treated with different concentrations of linoleic acids (LA) (0.25, 0.5, 1.0 mmol/L). Non-treated cells served as controls. Intracellular lipid deposition, cell proliferation activity, cell cycle, and apoptosis of mesangial cells were respectively assessed by Oil Red O staining, MTT, and flow cytometry at 24, 48, and 72 hours after stimulation. One-way ANOVA was used to do statistical analysis and P<0.05 considered as significant. Compared with controls, the cells treated with 0.5 and 1.0 mmol/L LA were significantly decreased in cell proliferation activity, but increased in the count of intracellular lipid droplets, percentage of G0/G1 cell cycle arrest, and apoptotic rate (P<0.05 or P<0.01). Elevated concentrations of FFAs (>= 0.5 mmol/L LA) may bring adverse effects on mesangial cells, including inhibition of cell proliferation activity and induction of cell cycle arrest and apoptosis.

Macrophages in the kidney play different roles in renal interstitial fibrosis (RIF) depending on their phenotypes. M2 phenotype macrophages are believed to protect the kidney against RIF. Free fatty acid receptor GPR120 is expressed in macrophages, and its activation induces macrophage transition to M2 phenotype. In this study, the effects of GPR120 agonist-programmed macrophages on RIF were investigated. The peritoneal macrophages collected from rats were incubated with GPR120 agonist TUG891 in vitro for 24 h, and then they were transplanted autologously to the kidney with ureteral obstruction by intrarenal injection for 7 days on the same day following unilateral ureteral obstruction (UUO) operation. RIF was identified by Masson trichrome histological staining, and the expression of RIF-related proteins was analyzed by immunohistochemistry and western blot. It was observed that TUG891-programmed macrophages up-regulated the expression of CD206 and arginase-1 while the expression of interleukin-6 and tumor necrosis factor-α were down-regulated. RIF in rats was significantly increased following UUO, which was markedly alleviated by TUG891-programmed macrophages but not untreated macrophages. TUG891-programmed macrophages inhibited the abnormal expression of TGF-β1 and SMAD2. The abnormal expression of epithelial-mesenchymal transition (EMT)-related proteins including vimentin, α-SMA and β-catenin was also significantly decreased in rats with transplantation of TUG891-programmed macrophages as compared to UUO rats. This study suggests that autologous administration of peritoneal macrophages programmed in vitro by GPR120 agonist to kidney has a protective effect against RIF following UUO.

A new bacterial lipolytic enzyme Est903 was obtained from paper mill sludge via metagenomic approach. Est903 displayed moderate similarities to two lipolytic enzymes from Rhodopirellula islandica and contained a distinctive pentapeptide motif (GFSAG) that differed from those of all known fourteen families of bacterial lipolytic enzymes. Est903 was regarded as from a new bacterial lipolytic enzyme family through multiple sequence alignment and phylogenetic analysis. The recombinant Est903 showed the highest activity for rho-nitrophenol butyrate. The pH optimum and temperature optimum of the recombinant enzyme was 9.0 and 51 degrees C, respectively. Also, this enzyme displayed moderate thermostability, high activity under alkaline conditions, and good tolerance against several organic solvents. In addition, the compatibility test and washing performance analysis revealed that Est903 had good compatibility with commercial laundry detergent and high cleaning ability of oil stains. These good properties make Est903 a potential candidate in organic synthesis or detergent industry. (C) 2019 Published by Elsevier B.V.