ABSTRACT
Hexagonal boron nitride nanosheets (BNNSs) possess remarkable potential for various applications due to their unprecedented properties. However, the scalable production of BNNSs with both expansive surface and high solubility continues to present a significant challenge. Herein, we propose an innovative and efficient two-step method for manufacturing hydroxyl-functionalized BNNSs (OH-BNNSs). Initially, hydroxyl groups are covalently attached to bulk hexagonal boron nitride (h-BN) surfaces through H2O2 treatment. Then, the hydroxyl-functionalized h-BN undergoes exfoliation on account of a sudden increase in interlayer gas pressure generated by the vigorous decomposition of H2O2 in alkali solutions, resulting in the creation of OH-BNNSs. This approach produces relatively large flakes with an average dimension of 1.65 µm and a high yield of 45.2%. The resultant OH-BNNSs exhibit remarkable stability and dispersibility in a range of solvents. Their integration into thermoplastic polyurethane (TPU) significantly enhances both thermal conductivity and stability, attributed to the excellent compatibility with the resin matrix. This study represents a significant advancement in the functionalization and exfoliation of h-BN, opening new avenues for its promising applications in polymer composites.
ABSTRACT
AIMS: Prolyl hydroxylase domain 2 (PHD2), encoded by the Egln1 gene, serves as a pivotal regulator of the hypoxia-inducible factor (HIF) pathway and acts as a cellular oxygen sensor. Somatic inactivation of Phd2 in mice results in polycythemia and congestive heart failure. However, due to the embryonic lethality of Phd2 deficiency, its role in development remains elusive. Here, we investigated the function of two egln1 paralogous genes, egln1a and egln1b, in zebrafish. MAIN METHODS: The egln1 null zebrafish were generated using the CRISPR/Cas9 system. Quantitative real-time PCR assays and Western blot analysis were employed to detect the effect of egln1 deficiency on the hypoxia signaling pathway. The hypoxia response of egln1 mutant zebrafish were assessed by analyzing heart rate, gill agitation frequency, and blood flow velocity. Subsequently, o-dianisidine staining and in situ hybridization were used to investigate the role of egln1 in zebrafish hematopoietic function. KEY FINDINGS: Our data show that the loss of egln1a or egln1b individually has no visible effects on growth rate. However, the egln1a; egln1b double mutant displayed significant growth retardation and elevated mortality at around 2.5 months old. Both egln1a-null and egln1b-null zebrafish embryo exhibited enhanced tolerance to hypoxia, systemic hypoxic response that include hif pathway activation, increased cardiac activity, and polycythemia. SIGNIFICANCE: Our research introduces zebrafish egln1 mutants as the first congenital embryonic viable systemic vertebrate animal model for PHD2, providing novel insights into hypoxic signaling and the progression of PHD2- associated disease.
