Community Action In Iowa Annual Report, 2001

Iowa Division of Community Action Agencies Annual Report

Community Action In Iowa Annual Report, 2002

Iowa Division of Community Action Agencies Annual Report

Community Action In Iowa Annual Report, 1999

Iowa Division of Community Action Agencies Annual Report

Bortezomib reverses the proliferative and antiapoptotic effect of neuropeptides on prostate cancer cells.

Objectives:  Neuropeptides are important signal initiators in advanced prostate cancer, partially acting through activation of nuclear factor kappa B. Central to nuclear factor kappa B regulation is the ubiquitin-proteasome system, pharmacological inhibition of which has been proposed as an anticancer strategy. We investigated the putative role of the proteasome inhibitor bortezomib in neuropeptides signaling effects on prostate cancer cells. Methods:  Human prostate cancer cell lines, LNCaP and PC-3, were used to examine cell proliferation, levels of proapoptotic (caspase-3, Bad) and cell cycle regulatory proteins (p53, p27, p21), as well as total and phosphorylated Akt and p44/42 mitogen-activated protein kinase proteins. Furthermore, 20S proteasome activity, subcellular localization of nuclear factor kappa B and transcription of nuclear factor kappa B target genes, interleukin-8 and vascular endothelial growth factor, were assessed. Results:  Neuropeptides (endothelin-1, bombesin) increased cell proliferation, whereas bortezomib decreased proliferation and induced apoptosis, an effect maintained after cotreatment with neuropeptides. Bad, p53, p21 and p27 were downregulated by neuropeptides in PC-3, and these effects were reversed with the addition of bortezomib. Neuropeptides increased proteasomal activity and nuclear factor kappa B levels in PC-3, and these effects were prevented by bortezomib. Interleukin-8 and vascular endothelial growth factor transcripts were induced after neuropeptides treatment, but downregulated by bortezomib. These results coincided with the ability of bortezomib to reduce mitogen-activated protein kinase signaling in both cell lines. Conclusions:  These findings are consistent with bortezomib-mediated abrogation of neuropeptides-induced proliferative and antiapoptotic signaling. Thus, the effect of the drug on the neuropeptides axis needs to be further investigated, as neuropeptide action in prostate cancer might entail involvement of the proteasome.

Lottery Action, July 26 - August 8, 2004, Vol. 11, no. 14

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, August 9-22, 2004, Vol. 11, no. 15

Iowa Lottery Authority Retailer Information Newsletter

Affirmative Action in Iowa, September 2003

This report is prepared pursuant to Iowa Code Section 19B.5. This Section required The Department of Administrative Services shall submit a report on the condition of affirmative action, diversity, and multicultural programs in state agencies covered by subsection 1 by September 30 of each year to the governor and the general assembly. Subsection 1 requires the head of each state agency to submit annual report of the affirmative action accomplishments of that agency to the Department of Administrative services.

Lottery Action, August 23-September 9, 2004, Vol. 11, no. 16

Iowa Lottery Retailer Newsletter

Lottery Action, September 27-October 10, 2004, Vol. 11, no. 18

Iowa Lottery Retailer Newsletter

Lottery Action, October 11-24, 2004, Vol. 11, no. 19

Iowa Lottery Retailer Newsletter

Lottery Action, October 25-November 14, 2004, Vol. 11, no. 20

Iowa Lottery Retailer Newsletter

Affirmative Action in Iowa, September 2004

This report is prepared pursuant to Iowa Code Section 19B.5, requiring the Department of Administrative Services to submit a report on the condition of affirmative action, diversity, and multicultural programs in state agencies by September 30 of each year to the governor and the general assembly. Additionally, the report summarizes the annual reports of the affirmative action accomplishments submitted to the Department of Administrative Services by agency directors.

Altered growth in male peroxisome proliferator-activated receptor gamma (PPARgamma) heterozygous mice: involvement of PPARgamma in a negative feedback regulation of growth hormone action.

The peroxisome proliferator-activated receptor gamma (PPARgamma) plays a major role in fat tissue development and physiology. Mutations in the gene encoding this receptor have been associated to disorders in lipid metabolism. A thorough investigation of mice in which one PPARgamma allele has been mutated reveals that male PPARgamma heterozygous (PPARgamma +/-) mice exhibit a reduced body size associated with decreased body weight, reflecting lean mass reduction. This phenotype is reproduced when treating the mice with a PPARgamma- specific antagonist. Monosodium glutamate treatment, which induces weight gain and alters body growth in wild-type mice, further aggravates the growth defect of PPARgamma +/- mice. The levels of circulating GH and that of its downstream effector, IGF-I, are not altered in mutant mice. However, the IGF-I mRNA level is decreased in white adipose tissue (WAT) of PPARgamma +/- mice and is not changed by acute administration of recombinant human GH, suggesting an altered GH action in the mutant animals. Importantly, expression of the gene encoding the suppressor of cytokine signaling-2, which is an essential negative regulator of GH signaling, is strongly increased in the WAT of PPARgamma +/- mice. Although the relationship between the altered GH signaling in WAT and reduced body size remains unclear, our results suggest a novel role of PPARgamma in GH signaling, which might contribute to the metabolic disorder affecting insulin signaling in PPARgamma mutant mice.

Lottery Action, November 15-28, 2004, Vol. 11, no. 12

Iowa Lottery Retailer Newsletter