Footnotes April/May 2002, Vol.26, no.4/5

Monthly newsletter of the State Library

Footnotes April 2000, Vol.24, no.4

Monthly newsletter of the State Library of Iowa

IDED Quick News, December 4, 2002

Newsletter for Economic Development

Oeuvres de J.-P. Florian.... Vol. 4

Comprend : Vie de J.-P. Florian

Factum pour François de La Salle, sieur de Clochet, tant pour lui que pour Louis et Suzanne de La Salle, ses neveu et nièce mineurs, et Salomon de La Salle, sieur de Puyrichard,... tous lesdits de La Salle enfants et petits-enfants et héritiers de défunt Jacques de La Salle et de Françoise Penigaud, leur mère,... demandeurs en lettres de rescision du 4 juin 1631,... contre damoiselle Catherine Penigaud, veuve de Barthélemy de Pivert des Gittons, sieur de Chenay...

[Factum. La Salle, Jacques de (Héritiers). 1631?]

Iowa Developments, November 2002, Vol.11 No.4

Report of iowa development for Economic Development

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