This paper investigates the effect of mesophase separation on the crystallization behavior of olefin block copolymers (OBCs) with different octene contents, which were synthesized by chain shuttling technology. Crystallization always occurs simultaneously but competitively with mesophase separation in OBCs. Because of the reason that the crystallization temperature is lower than the mesophase separation temperature for the OBCs, the mesophase separation can start first; large portions of the crystallizable hard blocks are confined in the mesophase-separated domains and could not contribute to the formation of radial lamellar stacks. In addition, the mesophase separation creates a stereo-hindrance effect; crystal lamellae could only grow through the interstitial space between the dispersed domains. As a result, large and compact crystals could not be formed. As the octene content increased in the sample, mesophase separation becomes more and more dominant, and the crystal morphology degrades sharply from spherulites to fragmentary lamella structures. It is found that increasing the annealing time during development of the mesophase-separated structure has a similar effect to increasing the octene content in the sample. However, all of the OBCs can form nearly the same crystalline morphology if the mesophase separation is suppressed, from which we can postulate that the nature of crystallization due to the crystallizable hard blocks in OBCs should be similar.

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Cited2 is a transcriptional modulator involved in various biologic processes including fetal liver hematopoiesis. In the present study, the function of Cited2 in adult hematopoiesis was investigated in conditional knockout mice. Deletion of Cited2 using Mx1-Cre resulted in increased hematopoietic stem cell (HSC) apoptosis, loss of quiescence, and increased cycling, leading to a severely impaired reconstitution capacity as assessed by 5-fluorouracil treatment and long-term transplantation. Transcriptional profiling revealed that multiple HSC quiescence-and hypoxia-related genes such as Egr1, p57, and Hes1 were affected in Cited2-deficient HSCs. Because Cited2 is a negative regulator of HIF-1, which is essential for maintaining HSC quiescence, and because we demonstrated previously that decreased HIF-1␣ gene dosage partially rescues both cardiac and lens defects caused by Cited2 deficiency, we generated Cited2 and HIF-1␣ doubleknockout mice. Additional deletion of HIF-1␣ in Cited2-knockout BM partially rescued impaired HSC quiescence and reconstitution capacity. At the transcriptional level, deletion of HIF-1␣ restored expression of p57 and Hes1 but not Egr1 to normal levels. Our results suggest that Cited2 regulates HSC quiescence through both HIF-1-dependent and HIF-1-independent pathways. (Blood. 2012;119(12):2789-2798) IntroductionHematopoietic stem cells (HSCs) are thought to be localized in the hypoxic microenvironment of the BM and remain quiescent or differentiate into multiple blood cell lineages. Several factors have been found to regulate HSC quiescence in either a cell-intrinsic (eg, p21, p57, Bmi1, Egr1, GATA2, Gfi1, Pbx1, and others) or a cell-extrinsic (eg, Tie2/Angpt1, c-Mpl/Tpo, CXCR4/CXCL12, and others) manner.CBP/p300-interacting transactivator with glutamic acid (E) and aspartic acid (D)-rich tail 2 (Cited2), a member of the Cited family of transcriptional modulators, is a cytokine-inducible gene 1 that plays various roles during mouse development. [2][3][4][5][6] In particular, Cited2 plays an important role in fetal liver hematopoiesis, which is supported by severely impaired fetal liver HSC function and decreased expression of genes known to be essential for hematopoiesis in Cited2-deficient fetal liver HSC/progenitors. 7 Cited2 has also been implicated in tumor cell invasion and progression. 8,9 Cited2 is a negative regulator of hypoxia-inducible factor 1 (HIF-1). Bhattacharya et al first demonstrated in vitro that Cited2 competes with HIF-1␣ for binding to p300-CH1 and inhibits HIF-1-mediated transactivation. 10 Bakker et al also showed that FOXO3a inhibits HIF-1-induced apoptosis by stimulating the transcription of Cited2, which reduces the expression of the pro-apoptotic HIF-1 target genes NIX (also called "Bnip3l") and RTP801 (also called "Ddit4"). 11 In our previous studies, we showed that deletion of HIF-1␣ partially rescues defects in heart and lens caused by Cited2 deficiency. 4,12 In addition, at the structural level, Freedman et al revealed that Cited2 and HIF-1␣ share a conserved...

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