Customer Focus Newsletter, July-August, 2010, Vol. 7, no.4

A bi-monthly bulletin to keep the department/agency management teams of state government better informed. We hope to consolidate most of the service update messages we send throughout the month and keep you updated about the work of the Customer Councils. If yours is one of the many departments who participated in the second annual DAS customer satisfaction survey recently, we thank you for taking the time to give us this important feedback. We look forward to sharing survey results with you, and pledge to consider responses carefully as we work to determine benchmarks and set future priorities.

RAGBRAI Learn about the Land; Day 7, July 2010

The University of Iowa Office of the State Archaeologist and Team Archaeology are back on RAGBRAI for our third year of Archaeology on the Road, and pleased to partner this year with the IDNR: Geological and Water Survey and the U.S. Geological Survey under the theme “Human and Natural History Partners.” Archaeology on the Road brings you the unique cultural history and prehistory of Iowa on the RAGBRAI route, pointing out interesting and significant archaeological sites and sharing Iowa’s past along the way. Look for our booth at Expo and then again on Days 1, 5 and 6 on the route, and also keep an eye out for our Team Archaeology

Fiscal Update, September 7, 2010

The Fiscal Division newsletter, published weekly during session and periodically during the interim.

Customer Focus Newsletter, September-October, 2010, Vol. 7, no.5

A bi-monthly bulletin to keep the department/agency management teams of state government better informed. We hope to consolidate most of the service update messages we send throughout the month and keep you updated about the work of the Customer Councils. If yours is one of the many departments who participated in the second annual DAS customer satisfaction survey recently, we thank you for taking the time to give us this important feedback. We look forward to sharing survey results with you, and pledge to consider responses carefully as we work to determine benchmarks and set future priorities.

Footnotes, July-August-September 2010, Vol.35, no.7-9

Monthly newsletter of State Library

Iowa Board of Nursing Annual Report FY 10 (7/1/09 - 6/30/20)

The Iowa Bord of Nursing Annual Report includes information on legislation, rule changes and statistics related to all aspects of board business: licensing, education, continuing education, enforcement, administrative changes, financial report, general nursing demographics.

Secure and Prepared Newsletter, October 7, 2010, Vol. 6, no. 19

A bi-weekly newsletter for those involved in the fields of homeland security and/or emergency management

Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding

Cellular prion protein (PrPC) is a glycosyl-phosphatidylinositol¿anchored glycoprotein. When mutated or misfolded, the pathogenic form (PrPSC) induces transmissible spongiform encephalopathies. In contrast, PrPC has a number of physiological functions in several neural processes. Several lines of evidence implicate PrPC in synaptic transmission and neuroprotection since its absence results in an increase in neuronal excitability and enhanced excitotoxicity in vitro and in vivo. Furthermore, PrPC has been implicated in the inhibition of N-methyl-D-aspartic acid (NMDA)¿mediated neurotransmission, and prion protein gene (Prnp) knockout mice show enhanced neuronal death in response to NMDA and kainate (KA). In this study, we demonstrate that neurotoxicity induced by KA in Prnp knockout mice depends on the c-Jun N-terminal kinase 3 (JNK3) pathway since Prnpo/oJnk3o/o mice were not affected by KA. Pharmacological blockage of JNK3 activity impaired PrPC-dependent neurotoxicity. Furthermore, our results indicate that JNK3 activation depends on the interaction of PrPC with postsynaptic density 95 protein (PSD-95) and glutamate receptor 6/7 (GluR6/7). Indeed, GluR6¿PSD-95 interaction after KA injections was favored by the absence of PrPC. Finally, neurotoxicity in Prnp knockout mice was reversed by an AMPA/KA inhibitor (6,7-dinitroquinoxaline-2,3-dione) and the GluR6 antagonist NS-102. We conclude that the protection afforded by PrPC against KA is due to its ability to modulate GluR6/7-mediated neurotransmission and hence JNK3 activation.