Report on payments made subsequent to recipients’ dates of death under the Medicaid program administered by the Department of Human Services for the period July 1, 2006 through December 31, 2008

Report on payments made subsequent to recipients’ dates of death under the Medicaid program administered by the Department of Human Services for the period July 1, 2006 through December 31, 2008

Hereditary hepatic and systemic amyloidosis caused by a new deletion/insertion mutation in the apolipoprotein AI gene.

We report a Spanish family with autosomal-dominant non-neuropathic hereditary amyloidosis with a unique hepatic presentation and death from liver failure, usually by the sixth decade. The disease is caused by a previously unreported deletion/insertion mutation in exon 4 of the apolipoprotein AI (apoAI) gene encoding loss of residues 60-71 of normal mature apoAI and insertion at that position of two new residues, ValThr. Affected individuals are heterozygous for this mutation and have both normal apoAI and variant molecules bearing one extra positive charge, as predicted from the DNA sequence. The amyloid fibrils are composed exclusively of NH2-terminal fragments of the variant, ending mainly at positions corresponding to residues 83 and 92 in the mature wild-type sequence. Amyloid fibrils derived from the other three known amyloidogenic apoAI variants are also composed of similar NH2-terminal fragments. All known amyloidogenic apoAI variants carry one extra positive charge in this region, suggesting that it may be responsible for their enhanced amyloidogenicity. In addition to causing a new phenotype, this is the first deletion mutation to be described in association with hereditary amyloidosis and it significantly extends the value of the apoAI model for investigation of molecular mechanisms of amyloid fibrillogenesis.

Special investigation of the City of Truro for the period January 1, 2003 through February 18, 2009

Special investigation of the City of Truro for the period January 1, 2003 through February 18, 2009

Biodiversity study of arthropods collected on rat carrion in Yaounde, Cameroon: first study on forensic entomology in Central Africa

The first investigation of arthropods associated with carrion in Cameroon was carried out within the campus of the University of Yaounde I (Cameroon) from 17thJanuary to 3rd April 2008. Carcasses of rats (Rattus norvegicus Berkenhout, 1769 var WISTAR) were exposed to colonization by the local fauna of arthropods. The invading organisms were collected daily during the study period. 2287 individuals of arthropod belonging to 3 classes, 16 orders, 37 families and 7 subfamilies were identified. The insects assessed were mainly Diptera, Coleoptera and Acari. This study illustrates the high diversity of the necroentomofauna in Cameroon and provides an insight approximation into the succession pattern of invading insect and a weekly estimation of the time of death.

BIRO1, a cell-permeable BH3 peptide, promotes mitochondrial fragmentation and death of retinoblastoma cells.

Retinoblastoma is the most common pediatric intraocular neoplasm. While retinoblastoma development requires the inactivation of both alleles of the retinoblastoma tumor suppressor gene (RB1) in the developing retina, additional genomic changes are involved in tumor progression, which progressively lead to resistance of tumor cells to death. Therapeutics acting at very downstream levels of death signaling pathways should therefore be interesting in killing retinoblastoma cells. The BH3-only proteins promote apoptosis by modulating the interaction between the pro- and antiapoptotic members of the BCL2 protein family, and this effect can be recapitulated by the BH3 domains. This report analyzes the effect of various BH3 peptides, corresponding to different BH3-only proteins, on two retinoblastoma cell lines, Y79 and WERI-Rb, as well as on the photoreceptor cell line 661W. The BH3 peptide BIRO1, derived from the BCL2L11 death domain, was very effective in promoting Y79 and WERI-Rb cell death without affecting the 661W photoreceptor cells. This cell death was efficient even in absence of BAX and was shown to be caspase independent. While ROS production or AIF release was not detected from mitochondria of treated cells, BIRO1 initiated mitochondria fragmentation in a short period of time following treatment. IMPLICATIONS: The BIRO1 peptide is highly effective at killing retinoblastoma cells and has potential as a peptidomimetic.

Report on a special investigation of the City of Crawfordsville for the period July 1, 1999 through February 28, 2009

Report on a special investigation of the City of Crawfordsville for the period July 1, 1999 through February 28, 2009

Report on a special investigation of Oran Township in Fayette County for the period January 1, 2003 through September 22, 2009

Report on a special investigation of Oran Township in Fayette County for the period January 1, 2003 through September 22, 2009

Report on a special investigation of the Rodman Volunteer Fire Department and Park and Recreation Department for the period January 1, 2006 through September 30, 2009

Report on a special investigation of the Rodman Volunteer Fire Department and Park and Recreation Department for the period January 1, 2006 through September 30, 2009

Report on a special investigation of the City of New Albin for the period January 1, 2006 through July 31, 2009

Report on a special investigation of the City of New Albin for the period January 1, 2006 through July 31, 2009

Report on a special investigation of the Cedar Rapids Community School District for the period July 1, 2002 through August 24, 2009

Report on a special investigation of the Cedar Rapids Community School District for the period July 1, 2002 through August 24, 2009

Report on a special investigation of certain collections of the Tama County Clerk of Court and the Tama County Sheriff’s Office for the period January 1, 2007 through August 31, 2009

Report on a special investigation of certain collections of the Tama County Clerk of Court and the Tama County Sheriff’s Office for the period January 1, 2007 through August 31, 2009

Report on a special investigation of Squaw Township for the period April 19, 2001 through March 18, 2009

Report on a special investigation of Squaw Township for the period April 19, 2001 through March 18, 2009

FLIP prevents apoptosis induced by death receptors but not by perforin/granzyme B, chemotherapeutic drugs, and gamma irradiation.

FLICE-inhibitory protein, FLIP (Casper/I-FLICE/FLAME-1/CASH/CLARP/MRIT), which contains two death effector domains and an inactive caspase domain, binds to FADD and caspase-8, and thereby inhibits death receptor-mediated apoptosis. Here, we characterize the inhibitory effect of FLIP on a variety of apoptotic pathways. Human Jurkat T cells undergoing Fas ligand-mediated apoptosis in response to CD3 activation were completely resistant when transfected with FLIP. In contrast, the presence of FLIP did not affect apoptosis induced by granzyme B in combination with adenovirus or perforin. Moreover, the Fas ligand, but not the perforin/granzyme B-dependent lytic pathway of CTL, was inhibited by FLIP. Apoptosis mediated by chemotherapeutic drugs (i.e., doxorubicin, etoposide, and vincristine) and gamma irradiation was not affected by FLIP or the absence of Fas, indicating that these treatments can induce cell death in a Fas-independent and FLIP-insensitive manner.

p53-induced protein with a death domain (PIDD) isoforms differentially activate nuclear factor-kappaB and caspase-2 in response to genotoxic stress

Cells respond to DNA damage in a complex way and the fate of damaged cells depends on the balance between pro- and antiapoptotic signals. This is of crucial importance in cancer as genotoxic stress is implied both in oncogenesis and in classical tumor therapies. p53-induced protein with a death domain (PIDD), initially described as a p53-inducible gene, is one of the molecular switches able to activate a survival or apoptotic program. Two isoforms of PIDD, PIDD (isoform 1) and LRDD (isoform 2), have already been reported and we describe here a third isoform. These three isoforms are differentially expressed in tissues and cell lines. Genotoxic stress only affects PIDD isoform 3 mRNA levels, whereas isoforms 1 and 2 mRNA levels remain unchanged. All isoforms are capable of activating nuclear factor-kappaB in response to genotoxic stress, but only isoform 1 interacts with RIP-associated ICH-1/CED-3 homologous protein with a death domain and activates caspase-2. Isoform 2 counteracts the pro-apoptotic function of isoform 1, whereas isoform 3 enhances it. Thus, the differential splicing of PIDD mRNA leads to the formation of at least three proteins with antagonizing/agonizing functions, thereby regulating cell fate in response to DNA damage

Whose Interest Is Being Served? An Investigation of a Walker City Council Member’s Conflict of Interest, April 15, 2010

The Ombudsman received a complaint concerning Bill Smith, a city council member who is also the Walker Fire Department Chief. The complainant stated that Mr. Smith votes regularly as a city council member on matters before the Walker City Council (Council) pertaining to the Walker Fire Department. These actions were alleged to be conflicts of interest in violation of Iowa law.