Footnotes, June, July, August 2007, Vol. 32, no. 6,7, 8

Monthly newsletter of the State Library

Motor Vehicle Accident Fatalities for the Week Ending, September 7, 2007

Record of the Fatalities for Motor Vehicle Accidents in Iowa per week.

Agreed upon procedures report for evaluating compliance with provisions of IowaCare (Project No 11-W-00189/7) within the Iowa Department of Human Services for the year ended June 30, 2006

Agreed upon procedures report for evaluating compliance with provisions of IowaCare (Project No 11-W-00189/7) within the Iowa Department of Human Services for the year ended June 30, 2006

EPI Update, September 7, 2007

Weekly newsletter for Center For Acute Disease Epidemiology of Iowa Department of Public Health.

Rouva Mirjami Töyräs 7/4 1972

Kirje 7.4.1972

Hausjärvi 6.7.1932

Kirje

Neuroprotection by inhibiting the c-Jun N-terminal kinase pathway after cerebral ischemia occurs independently of interleukin-6 and keratinocyte-derived chemokine (KC/CXCL1) secretion.

BACKGROUND: Cerebral ischemia is associated with the activation of glial cells, infiltration of leukocytes and an increase in inflammatory mediators in the ischemic brain and systemic circulation. How this inflammatory response influences lesion size and neurological outcome remains unclear. D-JNKI1, an inhibitor of the c-Jun N-terminal kinase pathway, is strongly neuroprotective in animal models of stroke. Intriguingly, the protection mediated by D-JNKI1 is high even with intravenous administration at very low doses with undetectable drug levels in the brain, pointing to a systemic mode of action, perhaps on inflammation. FINDINGS: We evaluated whether D-JNKI1, administered intravenously 3 h after the onset of middle cerebral artery occlusion (MCAO), modulates secretion of the inflammatory mediators interleukin-6 and keratinocyte-derived chemokine in the plasma and from the spleen and brain at several time points after MCAO. We found an early release of both mediators in the systemic circulation followed by an increase in the brain and went on to show a later systemic increase in vehicle-treated mice. Release of interleukin-6 and keratinocyte-derived chemokine from the spleen of mice with MCAO was not significantly different from sham mice. Interestingly, the secretion of these inflammatory mediators was not altered in the systemic circulation or brain after successful neuroprotection with D-JNKI1. CONCLUSIONS: We demonstrate that neuroprotection with D-JNKI1 after experimental cerebral ischemia is independent of systemic and brain release of interleukin-6 and keratinocyte-derived chemokine. Furthermore, our findings suggest that the early systemic release of interleukin-6 and keratinocyte-derived chemokine may not necessarily predict an unfavorable outcome in this model.

ABD e-News, September 7, 2007

Weekly newsletter

Nuori hiihtäjämestari Markus Sahlberg 7/3 1958

Kirje 7.3.1958

Tasavallan Presidentin radio- ja televisiopuhe 31.7.1970

Puhe

Hki 23/7 1942

Kirje 23.7.1942

Hki 22/7 1942

Kirje 22.7.1942

Angervonniemellä 12.7.1929

Kirje