Motor Vehicle Accident Fatalities for the Week Ending, May 12, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, May 19, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, May 26, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, June 2, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, June 9, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, June 16, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, June 23, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, June 30, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, July 14, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, July 28, 2006

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

Motor Vehicle Accident Fatalities for the Week Ending, July 21, 2006

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

La dénervation rénale unilatérale et le système kallikréine-bradykinine rénal chez le rat [Unilateral renal denervation and the renal kallikrein-bradykinin system in the rat].

AIM: The antihypertensive effect of renal denervation in hypertensive patients is partially explained by increased tubular natriuresis. To study the possible contribution of the kallikrein-kinin system (KKS) to this natriuretic effect in rats, we measured kallikrein activity (KA) and bradykinin concentrations (BK) in plasma and tissues. METHODS: To measure KA, we adapted and validated an enzymatic assay that cleaves para-nitroaniline (pNA) from the tripeptide H-D-Pro-Phe-Arg-pNA. The coefficients of variation (CV) within- and between-assays were less than 8% for plasma and tissue KA (plasma n=6 and 13; tissue n=4). Linear results for serially diluted samples confirmed the assay specificity. Tissue BK determinations were based on an established assay for plasma BK: tissue was homogenized and kinins extracted in ethanol, and BK was isolated by high-performance (HPLC) liquid chromatography and quantitated by radioimmunassay. Within- and between-assay CV for plasma BK were 18% (n=8 and n=35, respectively) and for BK in various tissues less than 16% (n=5-8). RESULTS: In male Wistar rats (n=3), plasma BK was 8.2±6.6 fmol/mL (mean±SD), and tissue BK (fmol/g) in 14 tested organs varied between brain (14±3) and submaxillary gland (521±315). Six days after left-sided unilateral renal denervation, left renal tissue BK (89±9) was not different from right renal BK (75±23). Similarly, KA was comparable in the two kidneys (left 18.0±1.5, right 15.8±1.4μkat/g). CONCLUSION: Any possible effect of unilateral renal denervation on the kidney's KKS would have to be bilateral.

Motor Vehicle Accident Fatalities for the Week Ending, August 4, 2006

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

Selective toxicity of the general anesthetic propofol for GABAergic neurons in rat brain cell cultures.

The intravenous, short-acting general anesthetic propofol was applied to three-dimensional (aggregating) cell cultures of fetal rat telencephalon. Both the clinically used formulation (Disoprivan, ICI Pharmaceuticals, Cheshire, England) and the pure form (2,6-diisopropylphenol) were tested at two different periods of brain development: immature brain cell cultures prior to synaptogenesis and at the time of intense synapses and myelin formation. At both time periods and for clinically relevant concentrations and time of exposure (i.e., concentrations > or = 2.0 micrograms/ml for 8 hr), propofol caused a significant decrease of glutamic acid decarboxylase activity. This effect persisted after removal of the drug, suggesting irreversible structural changes in GABAergic neurons. The gamma-aminobutyric acid type A (GABAA) blocking agents bicuculline and picrotoxin partially attenuated the neurotoxic effect of propofol in cultures treated at the more mature phase of development. This protective effect was not observed in the immature brain cells. The present data suggest that propofol may cause irreversible lesions to GABAergic neurons when given at a critical phase of brain development. In contrast, glial cells and myelin appeared resistant even to high doses of propofol.

Motor Vehicle Accident Fatalities for the Week Ending, August 11, 2006

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