The role of Mn oxide in the abiotic formation of humic substances has been well demonstrated. However, information on the effect of crystal structure and surface-chemical characteristics of Mn oxide on this process is limited. In the present study, hexagonal and triclinic birnessites, synthesized in acidic and alkali media, were used to study the influence of the crystal-structure properties of birnessites on the oxidative polymerization of hydroquinone and to elucidate the catalytic mechanism of birnessites in the abiotic formation of humic-like polymers in hydroquinone-birnessite systems. The intermediate and final products formed in solution and solid-residue phases were identified by UV/Visible spectroscopy, atomic absorption spectrometry, Fourier-transform infrared spectroscopy, X-ray diffraction, solid-phase microextraction-gaschromatography-mas ss pectrometry, ion chromatography, and ultrafiltration. The degree of oxidative polymerization of hydroquinone wasenhanced with increase in the interlayer hydrated H⁺, the average oxidation state (AOS), and the specific surface area of birnessites. The nature of the functional groups of the humic-like polymers formed was, however, almost identical when hydroquinone was catalyzed by hexagonal and triclinic birnessites with similar AOS of Mn. The results indicated that crystal structure and surface-chemistry characteristics have significant influence on the oxidative activity of birnessites and the degree of polymerization of hydroquinone, but have little effect on the abiotic formation mechanism of humic-like polymers. The proposed oxidative polymerization pathway for hydroquinone isthat, asit approachesthe birnessite, it formsp recursor surface complexes. Asa strong oxidant, birnessite accepts an electron from hydroquinone, which is oxidized to 1,4-benzoquinone. The coupling, cleavage, polymerization, and decarboxylation reactionsaccompany the generation of 1,4-benzoquinone, lead to the release of CO₂ and carboxylic acid fragments, the generation of rhodochrosite, and the ultimate formation of humic-like polymers. These findings are of fundamental significance in understanding the catalytic role of birnessite and the mechanism for the abiotic formation of humic substances in nature.

To refine the biological and prognostic significance of DNMT3A mutations in acute myeloid leukemia (AML), we assessed the impact of DNMT3A variant allele frequency (VAF) and its comutations in this study. Using targeted next‐generation sequencing, we analyzed 171 adult patients with de novo cytogenetically normal AML for DNMT3A mutations and associated comutations. DNMT3A^mut was detected in 35 patients. DNMT3A^mut patients were divided into DNMT3A^High and DNMT3A^Low using a cut‐off VAF value of 42%. We observed that DNMT3A^High patients at diagnosis had increasing white blood cell (WBC) counts (p < 0.001) and a higher lactate dehydrogenase (LDH) level (p = 0.027), and were associated with lower complete remission (CR) rate (p = 0.015) and shorter overall survival (OS) (p = 0.032) than DNMT3A^Low patients. We classified two different comutated genetypes, including DNMT3A^mutNPM1^mutFLT3‐ITD^mut and DNMT3A^mutIDH1/IDH2^mut. Patients with DNMT3A^mutNPM1^mutFLT3‐ITD^mut showed worse OS (p = 0.026) and relapse‐free survival (RFS) (p = 0.003) than those with DNMT3A^mutIDH1/IDH2^mut, and showed a shorter OS (p = 0.027) than those with DNMT3A^wtNPM1^mutFLT3‐ITD^mut. We also observed that patients with DNMT3A^mutIDH1/IDH2^mut had higher platelet counts (p = 0.009) and a lower BM blast percentage (p = 0.040) than those with DNMT3A^wtIDH1/IDH2^mut. In multivariate analyses, DNMT3A^High was independently associated with a lower CR rate (OR = 5.883; p = 0.004) and shorter OS (HR = 3.768; p < 0.001). DNMT3A^mutNPM1^mutFLT3‐ITD^mut independently affected worse OS (HR = 6.030; p < 0.001) and RFS (HR = 8.939; p < 0.001). Our findings might be potentially useful for predicting clinical outcomes.

We analyzed 156 adult patients with primary cytogenetically normal AML for ASXL1 mutations and co-mutations using targeted next-generation sequencing with a panel of 34 genes associated with myeloid neoplasms. ASXL1^mut were identified in 15(10%) patients, more frequent at an older age (≥60years) (p = .014), and had significant associations with co-mutations in TET2, KIT, CBL and SRSF2, whereas inversely correlated to NPM1 and CEBPA mutations. ASXL1^mut clustered in ELN2017 intermediate-risk group (p = .028). In the context of intermediate-risk, ASXL1^mut had a worse overall survival(OS) (p = .038) and Relapse-free survival(RFS) (p = .016) than ASXL1^wt. When coexisting DNMT3A or TET2 mutations, ASXL1^mut/DNMT3A^mut genetype revealed a superior OS than ASXL1^mut/DNMT3A^wt (p = .027), and ASXL1^mut/TET2^mut confered a worse RFS than ASXL1^mut/TET2^wt (p = .031). No significant prognosis impact of VAF (a cutoff value of 30%) and clone ranks of ASXL1^mut were observed in this corhort. Our study provided a new understanding of characteristics of ASXL1^mut AML.

Platelet-derived growth factor receptor beta (PDGFR beta) plays a crucial role in murine haematopoiesis. Baicalein (BAI), a naturally occurring flavonoid, can alleviate disease damage through anti-oxidative, anti-apoptotic, and anti-inflammatory mechanisms. However, whether BAI attenuates oxidative damage in murine haematopoietic cells by PDGFR beta remains unexplored. In this study, we utilized a tert-butyl hydroperoxide (TBHP)-induced BaF3 cell injury model and an ionising radiation (IR)-induced mice injury model to investigate the impact of the presence or absence of PDGFR beta on the pharmacological effects of BAI. In addition, the BAI-PDGFR beta interaction was characterized by molecular docking and dynamics simulations. The results show that a specific concentration of BAI led to increased cell viability, reduced reactive oxygen species (ROS) content, upregulated nuclear factor erythroid 2-related factor 2 (NRF2) expression, and its downstream target genes heme oxygenase 1 (HO-1) and NAD(P)H Quinone Dehydrogenase 1 (NQO1), and activated protein kinase B (AKT) pathway in cells expressing PDGFR beta plasmid and experiencing damage. Similarly, BAI elevated lineage- Sca1+cKIT+ (LSK) cell proportion, promoted haematopoietic restoration, enhanced NRF2-mediated antioxidant response in PDGFR beta+/+ mice. However, despite BAI usage, PDGFR beta knockout mice (PDGFR beta-/- ) showed lower LSK proportion and less antioxidant capacity than the total body irradiation (TBI) group. Furthermore, we demonstrated an interaction between BAI and PDGFR beta at the molecular level. Collectively, our results indicate that BAI attenuates oxidative stress injury and helps promote haematopoietic cell recovery through regulation of PDGFR beta.