Anti-cancer activity of 5-O-alkyl 1,4-imino-1,4-dideoxyribitols.

New derivatives of 1,4-dideoxy-1,4-imino-D-ribitol have been prepared and evaluated for their cytotoxicity on solid and haematological malignancies. 1,4-Dideoxy-5-O-[(9Z)-octadec-9-en-1-yl]-1,4-imino-D-ribitol (13, IC(50) ∼2 μM) and its C(18)-analogues (IC(50) <10 μM) are cytotoxic toward SKBR3 (breast cancer) cells. 13 also inhibits (IC(50) ∼8 μM) growth of JURKAT cells.

IoWoman, July/August 2002, Vol. 32, no.4

Newsletter for the Iowa Commission on the Status of Women.

Biliverdin inhibits Toll-like receptor-4 (TLR4) expression through nitric oxide-dependent nuclear translocation of biliverdin reductase.

The cellular response to an inflammatory stressor requires a proinflammatory cellular activation followed by a controlled resolution of the response to restore homeostasis. We hypothesized that biliverdin reductase (BVR) by binding biliverdin (BV) quells the cellular response to endotoxin-induced inflammation through phosphorylation of endothelial nitric oxide synthase (eNOS). The generated NO, in turn, nitrosylates BVR, leading to nuclear translocation where BVR binds to the Toll-like receptor-4 (TLR4) promoter at the Ap-1 sites to block transcription. We show in macrophages that BV-induced eNOS phosphorylation (Ser-1177) and NO production are mediated in part by Ca(2+)/calmodulin-dependent kinase kinase. Furthermore, we show that BVR is S-nitrosylated on one of three cysteines and that this posttranslational modification is required for BVR-mediated signaling. BV-induced nuclear translocation of BVR and inhibition of TLR4 expression is lost in macrophages derived from Enos(-/-) mice. In vivo in mice, BV provides protection from acute liver damage and is dependent on the availability of NO. Collectively, we elucidate a mechanism for BVR in regulating the inflammatory response to endotoxin that requires eNOS-derived NO and TLR4 signaling in macrophages.

VIP Connection Newsletter, August 2001, Vol. 1, no. 4

Iowa Lottery Authority Player Information Newsletter

Lottery Action, July 22-August 4, 2002, Vol. 9 no. 14

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, November 4-17, 2002, Vol. 9, no. 21

Newsletter for Iowa Lottery

Lottery Action, April 21-May 4, 2003, Vol. 10, no. 8

Iowa Lottery Authority Retailer Information Newsletter

4/1/1920, crue de la Seine, ravitaillement de pain dans une rue d'Asnières [19 rue Dussourd] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57513

Lottery Action, February 24-March 9 2003, Vol. 10, no. 4

Newsletter for Iowa Lottery

4/1/1920, stade Bergeyre, équipe Section Paloise : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57492

ERPN, Enterprise Resource Planning Newsletter, May/June 2001, Vol.1, no.4

Newsletter for Information Technology Department

Iowa 100% E News, May/June 2001, Vol.1, no.4

Newsletter for Information Technology Department

Managing IT, April/May 2002. Vol.2, No.4

Newsletter for Information Technology Department

The orphan receptor CRF2-4 is an essential subunit of the interleukin 10 receptor.

The orphan receptor CRF2-4 is a member of the class II cytokine receptor family (CRF2), which includes the interferon receptors, the interleukin (IL) 10 receptor, and tissue factor. CRFB4, the gene encoding CRF2-4, is located within a gene cluster on human chromosome 21 that comprises three interferon receptor subunits. To elucidate the role of CRF2-4, we disrupted the CRFB4 gene in mice by means of homologous recombination. Mice lacking CRF2-4 show no overt abnormalities, grow normally, and are fertile. CRF2-4 deficient cells are normally responsive to type I and type II interferons, but lack responsiveness to IL-10. By approximately 12 wk of age, the majority of mutant mice raised in a conventional facility developed a chronic colitis and splenomegaly. Thus, CRFB4 mutant mice recapitulate the phenotype of IL-10-deficient mice. These findings suggest that CRF2-4 is essential for IL-10-mediated effects and is a subunit of the IL-10 receptor.