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The patternable materials have been improved to be high transparency, high resolution, and adaptable for patterning with photolithography, ink‐jet print and imprint. Moreover, combination of high refractive index materials and the patternable technologies led to wider applications for next generation of display industry, such as AR/VR and smart glasses. [ABSTRACT FROM AUTHOR]

Precisely synthesized subnanometer particles of metalsor metaloxides can be prepared using dendritic polyphenyl azomethines as thetemplate. With a goal of their arrays to a surface using a simpleand quick process, such as spin-casting, statistical analyses wereapplied to a nanodot array of the dendrimers to obtain the relationshipbetween the experimental condition and the results such as size, spacing,or its standard deviations. The dot patterns of a single moleculardendrimer on a substrate were able to be predicted with numericalvalues of the experimental parameters associated with the spin coat(concentration of the dendrimer, physical properties of solvent, thespin coating recipe, temperature of the solution, relative humidity(RH))as the inputs for the statistical analysis. [ABSTRACT FROM AUTHOR]

The constitutive activation of the phosphatidylinositol 3-kinase (P13K)/Akt pathway commonly occurs in cancers and is a crucial event in tumorigenesis. Chronic myelogenous leukemia (CML) is characterized by a reciprocal chromosomal translocation (9;22) that generates the Bcr-Abl fusion gene. The P13K/Akt pathway is activated by Bcr-Abl chimera protein and mediates the leukemogenesis in CML. However, the mechanism by which Bcr-Abl activates the P13K/Akt pathway is not completely understood. In the present study, we found that pleckstrin homology domain leucine-rich repeat protein phosphatases 1 and 2 (PHLPP1 and PHLPP2) were depleted in CML cells. We investigated the interaction between PHLPPs and Bcr-Abl in CML cell lines and Bcr-Abl+ progenitor cells from CML patients. The Abl kinase inhibitors and depletion of Bcr-Abl-induced the expression of PHLPP1 and PHLPP2, which dephosphorylated Ser-473 on Akt1, -2, and -3, resulting in inhibited proliferation of CML cells. The reduction of PHLPP1 and PHLPP2 expression by short interfering RNA in CML cells weakened the Abl kinase inhibitor-mediated inhibition of proliferation. In colony-forming unit-granulocyte, erythroid, macrophage, megakaryocyte; colony-forming unit-granulocyte, macrophage; and burst-forming unit-erythroid, treatment with the Abl kinase inhibitors and depletion of Bcr-Abl-induced PHLPP1 and PHLPP2 expression and inhibited colony formation of Bcr-Abl+ progenitor cells, whereas depletion of PHLPP1 and PHLPP2 weakened the inhibition of colony formation activity by the AbI kinase inhibitors in Bcr-Abl+ progenitor cells. Thus, Bcr-Abl represses the expression of PHLPP1 and PHLPP2 and continuously activates Akt1, -2, and -3 via phosphorylation on Ser-473, resulting in the proliferation of CML cells. [ABSTRACT FROM AUTHOR]

Abstract: Double annulation of 1,6-bis(bromomethyl)-1,3,5-cycloheptatriene with diethyl acetonedicarboxylate under basic conditions provided the title cyclooctadecane derivative having formally two 1,3,5-cycloheptatriene moieties. An NMR study of the compound suggested that one moiety stays as a cycloheptatriene form and the other as a norcaradiene form. X-ray crystallographic analysis revealed that two methano bridges have syn- and anti-configurations to the central carbonyl bridge and also showed that one of the moieties having the syn-methano bridge stays a CHT form and the other having the anti-methano bridge stays an NCD form. [Copyright &y& Elsevier]

Abstract: CEM, MOLT4 and SUP-B15 cells were transduced with lentivirus-mediated siRNA KIS gene. The mRNA expressions of KIS were successfully reduced in all cell lines. On the other hand, the mRNA expressions of p27 Kip1 in CEM, MOLT4 and SUP-B15 cells were not affected by the transduction with siRNA KIS gene. We showed that KIS protein directly interacted with p27 Kip1 protein, and reduction of KIS inhibited the S10 phosphorylation of p27 Kip1 in leukemia cells. On these cells transfected with siRNA KIS, the inhibition of S10 phosphorylation of p27 Kip1 was strongly suppressed cell proliferation in a time-dependent manner. Moreover, the inhibition of S10 phosphorylation of p27 Kip1 increased a significant population in G0/G1 fraction. These data demonstrated that the KIS activity was induced during G0/G1, and it promotes cell cycle progression by phosphorylation of S10 on p27 Kip1 . We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62±0.68, 3.27±0.73 and 3.17±0.58, respectively. Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2). This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells. [Copyright &y& Elsevier]

Chronic myelogenous leukemia (CML) is characterized by a reciprocal chromosomal translocation (9;22) that generates the Bcr-AbI fusion gene. The Ras/Raf-1/MEK/ERK pathway is constitutively activated in Bcr-Abl-transformed cells, and Ras activity enhances the oncogenic ability of Bcr-Abl. However, the mechanism by which Bcr-Abl activates the Ras pathway is not completely understood. Raf kinase inhibitor protein (RKIP) inhibits activation of MEK by Raf-1 and its downstream signal transduction, resulting in blocking the MAP kinase pathway. In the present study, we found that RKIP was depleted in CML cells. We investigated the interaction between RKIP and Bcr- Abi in CML cell lines and Bcr-Abl+ progenitor cells from CML patients. The Abl kinase inhibitors and depletion of Bcr-Abl induced the expression of RKIP and reduced the pERK1/2 status, resulting in inhibited proliferation of CML cells. Moreover, RKIP up-regulated cell cycle regulator FoxM1 expression, resulting in G1 arrest via p27Kip1 and p21Cip1 accumulation. In colony-forming unit granulocyte, erythroid, macrophage, megakaryocyte, colony-forming unit-granulocyte macrophage, and burst-forming unit erythroid, treatment with the Abl kinase inhibitors and depletion of Bcr-Abl induced RKIP and reduced FoxM1 expressions, and inhibited colony formation of Bcr-Abl+ progenitor cells, whereas depletion of RKIP weakened the inhibition of colony formation activity by the Abl kinase inhibitors in Bcr-Abl+ progenitor cells. Thus, Bcr-Abl represses the expression of RKIP, continuously activates pERK1/2, and suppresses FoxM1 expression, resulting in proliferation of CML cells. [ABSTRACT FROM AUTHOR]