XAFS Characterization of Active Fe Species in Fe2O3-SiO2 Catalyst for Styrene Dimerization

α-メチルスチレン二量化反応に活性を示す鉄ゾル－ゲル法にて調製した鉄シリカ触媒をX線回折およびX線吸収分光法により評価した．触媒中鉄種の存在状態は仕込みSi /Fe 比に依存し，100 以上では四面体FeOxCl4-x種，50以下ではα-Fe2O3 凝集種が主成分であり，その存在比をXANES解析により求めた．シリカマトリクスに捕捉された孤立FeOxCl4-x が活性種として機能し，固体酸性質を発現する機構について論じた．　Iron ion-promoted silica solid acid catalysts active for α-methylstyrene dimerization were characterized by XRD and Fe K-edge XANES/EXAFS spectroscopic techniques. The possible active species were proposed. The 1 mol % of iron to Si was incorporated in catalyst samples, which was prepared by sol-gel process using iron chloride and tetraethylorthsilicate (TEOS) as the sources. The incorporated trivalent iron species were characterized as tetrahedral FeOxCl4-x , and excess loaded species were aggregated to form α-Fe2O3 during drying process at 403 K. The fraction of [FeOxCl4-x], [FeCl6] and [FeO6] species in the catalyst samples were determined by the least-squares analysis of XANES

Aortic thrombus in a patient with myeloproliferative thrombocytosis, successfully treated by pharmaceutical therapy: a case report

<p>Abstract</p> <p>Introduction</p> <p>Thrombosis in myeloproliferative thrombocytosis occurs usually in the microvessels and medium-sized arteries and veins and only rarely in the aorta. Aortic thrombosis is usually treated with thrombectomy. Reported here is a rare case that was treated pharmacologically.</p> <p>Case presentation</p> <p>A 60-year-old Japanese woman presented with numbness of both lower extremities. Her platelet count was 1787 × 10³/μl. Through bone marrow examination, we diagnosed her condition as myelodysplastic and/or myeloproliferative disorder-unclassifiable. Abdominal ultrasonography and computed tomographic scan revealed aortic thrombosis. Her platelet count was controlled with hydroxyurea and ranimustine. Aspirin and ticlopidine improved the numbness in both lower limbs on the second day. Aortic thrombosis was not observed in a computed tomographic scan on the seventh day.</p> <p>Conclusion</p> <p>For aortic thrombosis, surgical management is usually adopted, but pharmacological management is also an option because of its immediate curative effects.</p

Human AK2 links intracellular bioenergetic redistribution to the fate of hematopoietic progenitors

AK2 is an adenylate phosphotransferase that localizes at the intermembrane spaces of the mitochondria, and its mutations cause a severe combined immunodeficiency with neutrophil maturation arrest named reticular dysgenesis (RD). Although the dysfunction of hematopoietic stem cells (HSCs) has been implicated, earlier developmental events that affect the fate of HSCs and/or hematopoietic progenitors have not been reported. Here, we used RD-patient-derived induced pluripotent stem cells (iPSCs) as a model of AK2-deficient human cells. Hematopoietic differentiation from RD-iPSCs was profoundly impaired. RD-iPSC-derived hemoangiogenic progenitor cells (HAPCs) showed decreased ATP distribution in the nucleus and altered global transcriptional profiles. Thus, AK2 has a stage-specific role in maintaining the ATP supply to the nucleus during hematopoietic differentiation, which affects the transcriptional profiles necessary for controlling the fate of multipotential HAPCs. Our data suggest that maintaining the appropriate energy level of each organelle by the intracellular redistribution of ATP is important for controlling the fate of progenitor cells

c-Kit-Mediated Functional Positioning of Stem Cells to Their Niches Is Essential for Maintenance and Regeneration of Adult Hematopoiesis

The mechanism by which hematopoietic stem and progenitor cells (HSPCs) through interaction with their niches maintain and reconstitute adult hematopoietic cells is unknown. To functionally and genetically track localization of HSPCs with their niches, we employed novel mutant loxPs, lox66 and lox71 and Cre-recombinase technology to conditionally delete c-Kit in adult mice, while simultaneously enabling GFP expression in the c-Kit-deficient cells. Conditional deletion of c-Kit resulted in hematopoietic failure and splenic atrophy both at steady state and after marrow ablation leading to the demise of the treated adult mice. Within the marrow, the c-Kit-expressing GFP+ cells were positioned to Kit ligand (KL)-expressing niche cells. This c-Kit-mediated cellular adhesion was essential for long-term maintenance and expansion of HSPCs. These results lay the foundation for delivering KL within specific niches to maintain and restore hematopoiesis