Nanozymes capable of generating reactive oxygen species have recently emerged as promising treatments for wounds infected with drug‐resistant bacteria, possessing a reduced possibility of inducing resistance. However, the therapeutic effect is limited by a shortage of endogenous oxy‐substrates and undesirable off‐target biotoxicity. Herein, a ferrocenyl coordination polymer (FeCP) nanozyme, featuring pH switchable peroxidase (POD)‐ and catalase (CAT)‐like activity is incorporated with indocyanine green (ICG) and calcium peroxide (CaO2) to fabricate an H2O2/O2 self‐supplying system (FeCP/ICG@CaO2) for precise treatment of bacterial infections. At the wound site, CaO2 reacts with water to generate H2O2 and O2. Acting as a POD mimic under an acidic bacterial microenvironment, FeCP catalyzes H2O2 into hydroxyl radicals to prevent infection. However, FeCP switches to CAT‐like activity in neutral tissue, decomposing H2O2 into H2O and O2 to prevent oxidative damage and facilitate wound healing. Additionally, FeCP/ICG@CaO2 shows photothermal therapy capability, as ICG can emit heat under near‐infrared laser irradiation. This heat assists FeCP in fully exerting its enzyme‐like activity. Thus, this system achieves an antibacterial efficiency of 99.8% in vitro for drug‐resistant bacteria, and effectively overcomes the main limitations of nanozyme‐based treatment assays, resulting in satisfactory therapeutic effects in repairing normal and special skin tumor wounds infected with drug‐resistant bacteria.

Objective: To describe and explore the clinical characteristics and associated factors of growth in children after kidney transplantation (KT). Method: Retrospective study was performed on the clinical data of 111 children who underwent allogeneic KT and met the inclusion criteria (provided by Guangzhou Women and Children’s Medical Center and the Sun Yat-sen University First Affiliated Hospital). Catch-up growth was defined as present if the increment of height standard deviation score (∆Ht-SDS) was ≥0.5 per year. Described the clinical characteristics and compared possible associated factors between children with catch-up growth and no catch-up growth groups. Result: The median age at KT was 9(6,12) years, and 54.1% (60/111) are females. Mean height-SDS before KT was -2.14±1.29, 55.9% (62/111) showed growth retardation. Catch-up growth within the first years post-KT was present in 47.7% (53/111) recipients, the mean ∆Ht-SDS was 0.53±0.71. The Ht-SDS before KT was positively associated with last follow-up Ht-SDS (R=0.78, P<0.001). The baseline Ht-SDS, transplantation age, serum creatinine, and GC dose were significantly lower in the chase group (all P≤0.05), multivariate logistic regression analysis indicated that lower baseline Ht-SDS and serum creatinine were the protect factors for catch-up growth on the 1st year of post-transplantation (OR=0.62, 0.97, respectively, P<0.05). The last follow-up Ht-SDS affected by baseline Ht-SDS and ∆Ht-SDS. HtSDS was no statistical difference among different age groups (patient age at KT: <6years,6-9 years,9-12years,>12years), but ∆Ht-SDS showed significant difference between groups (0.74±0.80, 0.82±0.73, 0.28±0.67, 0.32±0.47, respectively, P<0.05). Younger Children showed significant catch-up rate after KT(<9years:68%,>9years:31%), however the ∆Ht-SDS was decrease in the second year (P<0.05). Conclusion: Growth assessment and management should be performed in any pediatric KT recipients. Even in younger children with more catch-up potential, ∆Ht-SDS decreased significantly at second year, growth continues to be suboptimal after KT. Given that baseline ∆Ht-SDS is a significantly associated factor, it is important for children with severe growth retardation need early identification and plan interventions in terms of growth improvement. We expected the children recipients achieved the ideal target height of post-transplantation.

Abstract Methods A whole-exome sequencing end stage renal disease patient whose original renal disease is unknown. Swiss model predict the 3D structure of the protein. The related literature was searched by using search terms “NPHP” in PubMed CNKI and VIP database from January 2000 to January 2020. Results The whole exome by next-generation sequencing and found two unreported TTC21B mutation sites, c.497del (p.Lys166Serfs) and c.2323−3T > A. The c.497del (p.Lys166Serfs) variant, which is a frame shift mutation, suggested deletion of a single nucleotide. A at position 497 from the TTC21B gene CDS results in replacement of lysine by serine at codon 166 of the TTC21B protein, as well as premature translational stop at position 201. The c.2323−3T > A variant indicates that the antepenultimate base of intron upstream of nucleotide 2323 in the CDS region of TTC21B gene changes from T to A. The change in the three-dimensional structure of the protein caused by the mutations in TTC21B may affect the functions associated with the protein length shorten. Further, this study summarized 25 NPHP gene mutations and the phenotypes that have been reported. Conclusion This study reported two novel mutations in the TTC21B gene resulting in NPHP in a Chinese patient and expanded on the spectrum of known causative mutations of TTC21B gene.

IntroductionThis study aimed to analyze the clinical characteristics of nephropathy associated with WT1 gene mutations in Chinese children and explore the relationship between genotype and clinical phenotype.MethodsCases diagnosed at the Guangzhou Women and Children's Medical Center, were combined with those retrieved from PubMed and China National Knowledge Infrastructure (CNKI) databases from January 2015 to June 2022 and integrated into a study cohort; grouped according to gene mutation sites, clinical phenotype, and renal pathological types. The clinical characteristics between groups were compared, and the relationship between genotype and age of onset, clinical phenotype, and pathological type were retrospectively analyzed.ResultsThe center enrolled 15 confirmed children: seven cases of non-simple nephropathy, including Denys-Drash syndrome (DDS) and Frasier syndrome (FS); eight cases of isolated steroid-resistant nephrotic syndrome (ISRNS); and 13 cases (86.7%) that progressed to end-stage renal disease (ESRD). The initial hemoglobin and bicarbonate levels of patients with clinical non-simple nephropathy were significantly lower than those with simple nephropathy, whereas the serum creatinine levels were higher than those of patients with simple nephropathy. A total of 75 cases of nephropathy associated with WT1 mutations in the study cohort met the inclusion and exclusion criteria. The most common clinical manifestations of WT1 mutations in this cohort were DDS (29/75, 38.7%) and ISRNS (37/75, 49.3%). A renal biopsy was performed in 43 patients, and the common types of renal pathology were focal segmental glomerulosclerosis (23/43, 53.5%) and DMS (13/43, 30.2%). Within the cohort, there were 12 cases (16.0%) in the exon 8 mutation group, 32 (42.6%) in the exon 9 group, 19 (25.3%) in the intron 9 group, and 12 (16.0%) in other gene site mutation groups. Common sites of WT1 mutations in Chinese children were exons 9 and intron 9. Exon 8 mutations were uniquely correlated with the age of onset within three months [5/7; 71.4%; Adjusted standardized residual (AR) = 4.2]. The renal survival time in the exon 8 mutation group was the shortest (P = 0.003).DiscussionThe molecular and biological characteristics of WT1 mutation-related nephropathy determine the clinical type, pathological features, and renal survival time of the disease; and there was a strong correlation between the genotype and clinical phenotype.

Background: This study aimed to investigate the expression characteristics of ANGPTL8 in patients with primary nephrotic syndrome and its possible correlationwith hyperlipidemia and proteinuria.Methods: ANGPTL8 levels were determined using Enzyme‑linked immunosorbentassay in 133 subjects with PNS, and 60 subjects with healthy controls.Results: Subjects with primary nephrotic syndrome had higher levels of serum andurine ANGPTL8 than healthy controls subjects (P < 0.001). In primary nephroticsyndrome patients, serum ANGPTL8 was positively correlated with cholesterol (r =0.209, P < 0.05) and triglycerides (r = 0.412, P < 0.001), while no correlation with24hUTP. Urine ANGPTL8 was positively correlated with high density lipoprotein-cholesterol (r = 0.181, P < 0.05), while urine ANGPTL8 was significantly negativelycorrelated with creatinine (r = -0.323, P<0.001) and 24hUTP (r = -0.268, P = 0.002).Interestingly, urine ANGPTL8 concentrations were different between membranousnephropathy and mesangial proliferative glomerulonephritis pathological types.Conclusions: Serum and urine ANGPTL8 levels in primary nephrotic syndromepatients were correlated with blood lipid levels and proteinuria, respectively, suggestingthat ANGPTL8 may play a role in the development of primary nephrotic syndromehyperlipidemia and proteinuria.