Publications by authors named "Xing Jun Li"

Its high coordination number and tendency to cluster make Th suitable for constructing metal-organic frameworks (MOFs) with novel topologies. In this work, two novel thorium-based heterometallic MOF isomers (IHEP-17 and IHEP-18) were assembled from a Th cluster, a multifunctional organic ligand [4-(1-pyrazol-4-yl)benzoic acid (HPyba)], and Cu/Ni cations via the one-pot solvothermal synthesis strategy. The framework features a 6,12-connected new topology net and contains two kinds of supramolecular cage structures, ThM and ThM, suitable for guest exchange.

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Background: gene amplification is related to risk stratification. Therefore it is important to identify accurately the level of the gene as early as possible in neuroblastoma (NB); however, for patients with bone marrow (BM) metastasis who need chemotherapy before surgery, timely detection of the gene is not possible due to the unavailability of primary tumors.

Methods: gene status was evaluated in 81 BM metastases of NB by interphase fluorescence in situ hybridization (FISH) analysis of BM cells.

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Drug resistance is a growing problem that necessitates new strategies to combat pathogens. Neutrophil phagocytosis and production of intracellular ROS, in particular, has been shown to cooperate with antibiotics in the killing of microbes. This study tested the hypothesis that p85α, the regulatory subunit of PI3K, regulates production of intracellular ROS.

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Macrophages are vital to innate immunity and express pattern recognition receptors and integrins for the rapid detection of invading pathogens. Stimulation of Dectin-1 and complement receptor 3 (CR3) activates Erk- and Akt-dependent production of reactive oxygen species (ROS). Shp2, a protein-tyrosine phosphatase encoded by Ptpn11, promotes activation of Ras-Erk and PI3K-Akt and is crucial for hematopoietic cell function; however, no studies have examined Shp2 function in particulate-stimulated ROS production.

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Although hyperactivation of the Ras-Erk signaling pathway is known to underlie the pathogenesis of juvenile myelomonocytic leukemia (JMML), a fatal childhood disease, the PI3K-Akt signaling pathway is also dysregulated in this disease. Using genetic models, we demonstrate that inactivation of phosphatidylinositol-3-kinase (PI3K) catalytic subunit p110δ, but not PI3K p110α, corrects gain-of-function (GOF) Shp2-induced granulocyte macrophage-colony-stimulating factor (GM-CSF) hypersensitivity, Akt and Erk hyperactivation, and skewed hematopoietic progenitor distribution. Likewise, potent p110δ-specific inhibitors curtail the proliferation of GOF Shp2-expressing hematopoietic cells and cooperate with mitogen-activated or extracellular signal-regulated protein kinase kinase (MEK) inhibition to reduce proliferation further and maximally block Erk and Akt activation.

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By employment of a tripodal phosphoric carboxylate ligand, tris(4-carboxylphenyl)phosphine oxide (H3TPO), two novel porous metal-organic frameworks, namely, [Zn4(μ3-OH)2(TPO)2(H2O)2] (1) and [Zn6(μ6-O)(TPO)2](NO3)4·3H2O (2), have been synthesized by solvothermal methods. Complexes 1 and 2 exhibit three-dimensional microporous frameworks with flu and pyr topologies and possess rare butterfly-shaped Zn4(μ3-OH)2(CO2)6 and octahedral Zn6(μ6-O)(CO2)6 secondary building units, respectively. Large cavities and one-dimensional channels are observed in these two frameworks.

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The woodland and farmland soil nearby lead-zinc mine has been polluted seriously due to the mining. Bamboo forest of Phyllostachys edulis has high economic value and is distributed widely in China. The Phyllostachys edulis forest nearby lead-zinc mine was selected, and the distribution characteristics of main heavy metal Cu, Zn, Pb and Cd in soil were studied.

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A series of novel two-dimensional (2D) lanthanide coordination polymers with 4-hydroxyquinoline-2-carboxylate (H(2)hqc) ligands, [Ln(Hhqc)(3)(H(2)O)](n)·3nH(2)O (Ln = Eu (1), Tb (2), Sm (3), Nd (4), and Gd (5)) and [Ln(Hhqc)(ox)(H(2)O)(2)](n) (Ln = Eu (6), Tb (7), Sm (8), Tm (9), Dy (10), Nd (11), Yb (12), and Gd (13); H(2)ox = oxalic acid), have been synthesized under hydrothermal conditions. Complexes 1-5 are isomorphous, which can be described as a two-dimensional (2D) hxl/Shubnikov network based on Ln(2)(CO(2))(4) paddle-wheel units, and the isomorphous complexes 6-13 feature a 2D decker layer architecture constructed by Ln-ox infinite chains cross-linked alternatively by bridging Hhqc(-) ligands. The room-temperature photoluminescence spectra of complexes Eu(III) (1 and 6), Tb(III) (2 and 7), and Sm(III) (3 and 8) exhibit strong characteristic emissions in the visible region, whereas Nd(III) (4 and 11) and Yb(III) (12) complexes display NIR luminescence upon irradiation at the ligand band.

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The protein tyrosine phosphatase, SHP2, is widely expressed; however, previous studies demonstrated that hematopoietic cell development more stringently requires Shp2 expression compared to other tissues. Furthermore, somatic gain-of-function SHP2 mutants are commonly found in human myeloid leukemias. Given that pharmacologic inhibitors to SHP2 phosphatase activity are currently in development as putative antileukemic agents, we conducted a series of experiments examining the necessity of SHP2 phosphatase activity for human hematopoiesis.

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Reactions of a tripodal ligand, N,N',N″-tris(3-pyridinyl)phosphoric triamide (TPPA), and a series of transition-metal ions result in the assembly of five discrete M(6)L(8) coordination cages [M(6)(TPPA)(8)(H(2)O)(12)](ClO(4))(12)·57H(2)O [M = Ni(2+) (1), Co(2+) (2), Zn(2+) (3), Cd(2+) (4)] and [Pd(6)(TPPA)(8)]Cl(12)·22H(2)O (5). X-ray structural analyses reveal that the cages have large internal cavities and flexible windows. The flexible ligand TPPA adopts the syn conformation in cages 1-4, but it transforms to the anti conformation in cage 5.

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The assembly of cytosolic subunits p47(phox), p67(phox), and p40(phox) with flavocytochrome b(558) at the membrane is required for activating the neutrophil NADPH oxidase that generates superoxide for microbial killing. The p47(phox) subunit plays a critical role in oxidase assembly. Recent studies showed that the p47(phox) Phox homology (PX) domain mediates phosphoinositide binding in vitro and regulates phorbol ester-induced NADPH oxidase activity in a K562 myeloid cell model.

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Chronic granulomatous disease (CGD), an immunodeficiency with recurrent pyogenic infections and granulomatous inflammation, results from loss of phagocyte superoxide production by recessive mutations in any 1 of 4 genes encoding subunits of the phagocyte NADPH oxidase. These include gp91(phox) and p22(phox), which form the membrane-integrated flavocytochrome b, and cytosolic subunits p47(phox) and p67(phox). A fifth subunit, p40(phox), plays an important role in phagocytosis-induced superoxide production via a phox homology (PX) domain that binds to phosphatidylinositol 3-phosphate (PtdIns(3)P).

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The assembly of cytosolic p47(phox) and p67(phox) with flavocytochrome b(558) at the membrane is crucial for activating the leukocyte NADPH oxidase that generates superoxide for microbial killing. p47(phox) and p67(phox) are linked via a high-affinity, tail-to-tail interaction involving a proline-rich region (PRR) and a C-terminal SH3 domain (SH3b), respectively, in their C-termini. This interaction mediates p67(phox) translocation in neutrophils, but is not required for oxidase activity in model systems.

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The phagocyte NADPH oxidase generates superoxide for microbial killing, and includes a membrane-bound flavocytochrome b(558) and cytosolic p67(phox), p47(phox), and p40(phox) subunits that undergo membrane translocation upon cellular activation. The function of p40(phox), which binds p67(phox) in resting cells, is incompletely understood. Recent studies showed that phagocytosis-induced superoxide production is stimulated by p40(phox) and its binding to phosphatidylinositol-3-phosphate (PI3P), a phosphoinositide enriched in membranes of internalized phagosomes.

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Article Synopsis
  • Chronic granulomatous disease (CGD) is a primary immunodeficiency that makes individuals highly susceptible to severe infections due to a malfunction in the NADPH oxidase enzyme in phagocytes.
  • CGD is linked to mutations in any of four genes responsible for different components of the NADPH oxidase, with studies revealing important insights into gene functions and the enzyme's activation.
  • While long-term antibiotic use is crucial for preventing infections, emerging treatments like hematopoietic stem cell transplantation and gene therapy show promise for future management of CGD.
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The role of Leu505 of Nox2 on the NADPH oxidase activation process was investigated. An X-CGD PLB-985 cell line expressing the Leu505Arg Nox2 mutant was obtained, exactly mimicking the phenotype of a previously published X91+-CGD case. In a reconstituted cell-free system (CFS), NADPH oxidase and iodonitrotetrazolium (INT) reductase activities were partially maintained concomitantly with a partial cytosolic factors translocation to the plasma membrane.

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Superoxide produced by the phagocyte reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is essential for host defense. Enzyme activation requires translocation of p67(phox), p47(phox), and Rac-GTP to flavocytochrome b558 in phagocyte membranes. To examine the regulation of phagocytosis-induced superoxide production, flavocytochrome b558, p47(phox), p67(phox), and the FcgammaIIA receptor were expressed from stable transgenes in COS7 cells.

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Assembly of cytosolic factors p67(phox) and p47(phox) with cytochrome b(558) is one of the crucial keys for NADPH oxidase activation. Certain sequences of Nox2 appear to be involved in cytosolic factor interaction. The role of the D-loop (191)TSSTKTIRRS(200) and the C-terminal (484)DESQANHFAVHHDEEKD(500) of Nox2 on oxidase activity and assembly was investigated.

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Chronic granulomatous disease is an inherited disorder in which phagocytes lack a functional NADPH oxidase and so cannot generate superoxide anions (O(2) (-)). The most common form is caused by mutations in CYBB encoding gp91 phox, the heavy chain of flavocytochrome b(558) (XCGD). We investigated 11 male patients and their families suspected of suffering from X-linked CGD.

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Chronic granulomatous disease (CGD) is a rare inherited disorder in which phagocytes lack NADPH oxidase activity. The most common form is caused by mutations in the CYBB gene encoding gp91 phox protein, the heavy chain of cytochrome b(558), which is the redox element of NADPH oxidase. In some rare cases, the mutated gp91 phox is normally expressed but no NADPH oxidase can be detected.

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EGR-1 gene promoter and CDglyTK gene were used to construct the pcDNA3-EGR-CDglyTK recombinant vector, in which CDglyTK gene expression was under the control of EGR-1 gene promoter. Cationic liposome LipofectAMINE was used to transfect plasmids into human hepatoma 7402 cell line. Subsequently, the transfected cells were treated with different doses of gamma-ray.

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