Motor Vehicle Accident Fatalities for the Week Ending, December 22, 2006

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

Progress of the Building Project for the Motor Vehicle Division, 2006

Pursuant to Section 1 of House File 466 of the 81st General Assembly, the Iowa Department of Transportation (DOT) is required to make quarterly reports to the Legislative Council regarding the progress of the building project for the Motor Vehicle Division. Progress of the Building Project for the Motor Vehicle Division. A report to the Iowa Legislature, per Section 1 of House File 466 of the 81st General Assembly.

Motor Vehicle Accident Fatalities for the Week Ending, January 26, 2007

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

Motor Vehicle Accident Fatalities for the Week Ending, December 29, 2006

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

Adenosine A2B receptor-mediated leukemia inhibitory factor release from astrocytes protects cortical neurons against excitotoxicity.

ABSTRACT: BACKGROUND: Neuroprotective and neurotrophic properties of leukemia inhibitory factor (LIF) have been widely reported. In the central nervous system (CNS), astrocytes are the major source for LIF, expression of which is enhanced following disturbances leading to neuronal damage. How astrocytic LIF expression is regulated, however, has remained an unanswered question. Since neuronal stress is associated with production of extracellular adenosine, we investigated whether LIF expression in astrocytes was mediated through adenosine receptor signaling. METHODS: Mouse cortical neuronal and astrocyte cultures from wild-type and adenosine A2B receptor knock-out animals, as well as adenosine receptor agonists/antagonists and various enzymatic inhibitors, were used to study LIF expression and release in astrocytes. When needed, a one-way analysis of variance (ANOVA) followed by Bonferroni post-hoc test was used for statistical analysis. RESULTS: We show here that glutamate-stressed cortical neurons induce LIF expression through activation of adenosine A2B receptor subtype in cultured astrocytes and require signaling of protein kinase C (PKC), mitogen-activated protein kinases (MAPKs: p38 and ERK1/2), and the nuclear transcription factor (NF)-κB. Moreover, LIF concentration in the supernatant in response to 5'-N-ethylcarboxamide (NECA) stimulation was directly correlated to de novo protein synthesis, suggesting that LIF release did not occur through a regulated release pathway. Immunocytochemistry experiments show that LIF-containing vesicles co-localize with clathrin and Rab11, but not with pHogrin, Chromogranin (Cg)A and CgB, suggesting that LIF might be secreted through recycling endosomes. We further show that pre-treatment with supernatants from NECA-treated astrocytes increased survival of cultured cortical neurons against glutamate, which was absent when the supernatants were pre-treated with an anti-LIF neutralizing antibody. CONCLUSIONS: Adenosine from glutamate-stressed neurons induces rapid LIF release in astrocytes. This rapid release of LIF promotes the survival of cortical neurons against excitotoxicity.

Motor Vehicle Accident Fatalities for the Week Ending, January 19, 2007

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

A comparison of frailty of primary neurons, embryonic, and aging mouse cortical layers.

Superficial layers I to III of the human cerebral cortex are more vulnerable toward Aβ peptides than deep layers V to VI in aging. Three models of layers were used to investigate this pattern of frailty. First, primary neurons from E14 and E17 embryonic murine cortices, corresponding respectively to future deep and superficial layers, were treated either with Aβ1-42, okadaic acid, or kainic acid. Second, whole E14 and E17 embryonic cortices, and third, in vitro separated deep and superficial layers of young and old C57BL/6J mice, were treated identically. We observed that E14 and E17 neurons in culture were prone to death after the Aβ and particularly the kainic acid treatment. This was also the case for the superficial layers of the aged cortex, but not for the embryonic, the young cortex, and the deep layers of the aged cortex. Thus, the aged superficial layers appeared to be preferentially vulnerable against Aβ and kainic acid. This pattern of vulnerability corresponds to enhanced accumulation of senile plaques in the superficial cortical layers with aging and Alzheimer's disease.

Investigation Into the Timeliness of the Death Notification to the Surviving Spouse of a Motor Vehicle Accident Victim, 2005

Report: #05-02 Kirke C. Quinn, Attorney for Jo Anne Holland, first contacted the Ombudsman by letter dated January 2, 2004. Quinn also addressed his letter to the Governor’s Office, Iowa State Patrol (ISP), and Iowa Department of Public Safety (DPS). Quinn characterized his letter as a complaint against ISP regarding “the method and manner of reporting the death of Ross Holland to his surviving spouse.” According to Quinn, Mrs. Holland “went through hours of misery as a result of the patrol’s inattention to a tragic situation.” On January 7, 2004, the Ombudsman asked ISP Major Gary Hoskins, Supervisor of Field Operations, how ISP and DPS intended to respond to Mr. Quinn’s letter. Major Hoskins stated he would refer Quinn’s letter of complaint to DPS’ Professional Standards Bureau (PSB) for investigation and response. After speaking with Major Hoskins, the Ombudsman told Mr. Quinn that DPS would do an internal investigation and if he were not satisfied with the results he could contact the Ombudsman again. On March 29, 2004, Mr. Quinn contacted the Ombudsman and stated he was not satisfied with DPS’ response. Quinn stated he would send a copy of the response to the Ombudsman, along with a letter stating his outstanding issues and concerns. In his letter to the Ombudsman, dated May 5, Quinn simply stated: “Please find enclosed [a] copy of the letter received from the Department of Public Safety. We think this is an absolute outrage. We welcome your input.”

Motor Vehicle Accident Fatalities for the Week Ending, February 9, 2007

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

Structural and Resting State Functional Connectivity of the Subthalamic Nucleus: Identification of Motor STN Parts and the Hyperdirect Pathway.

Deep brain stimulation (DBS) for Parkinson's disease often alleviates the motor symptoms, but causes cognitive and emotional side effects in a substantial number of cases. Identification of the motor part of the subthalamic nucleus (STN) as part of the presurgical workup could minimize these adverse effects. In this study, we assessed the STN's connectivity to motor, associative, and limbic brain areas, based on structural and functional connectivity analysis of volunteer data. For the structural connectivity, we used streamline counts derived from HARDI fiber tracking. The resulting tracks supported the existence of the so-called "hyperdirect" pathway in humans. Furthermore, we determined the connectivity of each STN voxel with the motor cortical areas. Functional connectivity was calculated based on functional MRI, as the correlation of the signal within a given brain voxel with the signal in the STN. Also, the signal per STN voxel was explained in terms of the correlation with motor or limbic brain seed ROI areas. Both right and left STN ROIs appeared to be structurally and functionally connected to brain areas that are part of the motor, associative, and limbic circuit. Furthermore, this study enabled us to assess the level of segregation of the STN motor part, which is relevant for the planning of STN DBS procedures.

Motor Vehicle Accident Fatalities for the Week Ending, February 16, 2007

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

Mécanismes cellulaires du métabolisme énergétique cérébral: implications pour l'imagerie fonctionnelle

Signals detected with functional brain imaging techniques are based on the coupling of neuronal activity with energy metabolism. Techniques such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) allow the visualization of brain areas that are activated by a variety of sensory, motor or cognitive tasks. Despite the technological sophistication of these brain imaging techniques, the precise mechanisms and cell types involved in coupling and in generating metabolic signals are still debated. Recent experimental data on the cellular and molecular mechanisms that underlie the fluorodeoxyglucose (FDG) - based PET imaging point to a critical role of a particular brain cell type, the astrocytes, in coupling neuronal activity to glucose utilization. Indeed, astrocytes possess receptors and re-uptake sites for a variety of neurotransmitters, including glutamate, the predominant excitatory neurotransmitter in the brain, In addition, astrocytic end-feet, which surround capillaries, are enriched in the specific glucose transporter GLUT-1. These features allow astrocytes to "sense" synaptic activity and to couple it with energy metabolism. In vivo and in vitro data support the following functional model: in response to glutamate released by active neurons, glucose is predominantly taken up by astrocytic end-feet; glucose is then metabolized to lactate which provides a preferred energy substrate for neurons. These data support the notion that astrocytes markedly contribute to the FDG-PET signal.

Motor Vehicle Accident Fatalities for the Week Ending, March 2, 2007

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