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Selected AbstractsIs the Cell Death in Mesial Temporal Sclerosis Apoptotic?EPILEPSIA, Issue 6 2003Hilmi Uysal Summary: Purpose: Mesial temporal sclerosis (MTS) is characterized by neuronal loss in the hippocampus. Studies on experimental models and patients with intractable epilepsy suggest that apoptosis may be involved in neuronal death induced by recurrent seizures. Methods: We searched evidence for apoptotic cell death in temporal lobes resected from drug-resistant epilepsy patients with MTS by using the terminal deoxynucleotidyl transferase (TdT) and digoxigenin-11-dUTP (TUNEL) method and immunohistochemistry for Bcl-2, Bax, and caspase-cleaved actin fragment, fractin. The temporal lobe specimens were obtained from 15 patients (six women and nine men; mean age, 29 ± 8 years). Results: Unlike that in normal adult brain, we observed Bcl-2 immunoreactivity in some of the remaining neurons dispersed throughout the hippocampus proper as well as in most of the reactive astroglia. Bax immunopositivity was increased in almost all neurons. Fractin immunostaining, an indicator of caspase activity, was detected in ,10% of these neurons. Des pite increased Bax expression and activation of caspases, we could not find evidence for DNA fragmentation by TUNEL staining. We also could not detect typical apoptotic changes in nuclear morphology by Hoechst-33258 or hematoxylin counterstaining. Conclusions: These data suggest that either apoptosis is not involved in cell loss in MTS, or a very slow rate of cell demise may have precluded detecting TUNEL-positive neurons dying through apoptosis. Increased Bax expression and activation of caspases support the latter possibility. [source] A Note on the Spatial Correlation Structure of County-Level Growth in the U.S.JOURNAL OF REGIONAL SCIENCE, Issue 3 2001Christopher H. Wheeler This paper examines the spatial correlation structure of county-level growth across the contiguous United States. Estimated spatial correlograms using data on four different measures of aggregate economic activity,population, employment, income, and earnings,over the period 1984,1994 indicate that cross-county interdependence is limited to relatively short ranges of distance. For each of the measures, the average correlation between the growth rates of two counties approaches zero within a range of approximately 200 miles. Moreover, the rate at which correlations decline with distance is not uniform. Inside of roughly 40 miles correlations show only a very slow rate of decline whereas beyond this range they drop off at a substantially higher rate. [source] Nigrostriatal dysfunction in homozygous and heterozygous parkin gene carriers: An 18F-dopa PET progression study,MOVEMENT DISORDERS, Issue 15 2009Nicola Pavese MD Abstract Little is known about the rate of progression of striatal dysfunction in subjects with parkin -linked parkinsonism. Being a heterozygous parkin gene carrier may confer susceptibility to Parkinson's disease (PD). In a previous 18F-dopa PET study, we reported that 69% of carriers of a single parkin mutation showed subclinical loss of putamen dopaminergic function. Using serial 18F-dopa PET, the present longitudinal study addresses rates of progression of nigrostriatal dysfunction in both compound heterozygous (parkin -linked parkinsonism) and single heterozygous parkin gene carriers. Three symptomatic patients who were compound heterozygotes for parkin gene mutations and six asymptomatic heterozygous carriers were clinically assessed and had 18F-dopa PET at baseline and again after 5 years. The patients with symptomatic parkin showed a mean 0.5% annual reduction in putamen 18F-dopa uptake over 5 years while caudate 18F-dopa uptake declined by a mean annual rate of 2 %. The asymptomatic heterozygote gene carriers showed a mean 0.56% annual reduction in putamen and 0.62 % annual reduction in caudate 18F-dopa uptake. Neurological examination at both baseline and follow-up showed no evidence of parkinsonism. Loss of nigrostriatal dysfunction in parkin -linked parkinsonism occurs at a very slow rate compared to the 9,12% annual loss of putamen 18F-dopa uptake reported for idiopathic PD. Although subclinical reductions of striatal 18F-dopa uptake are common in carriers of a single parkin mutation their slow rate of progression suggests that few if any of these will develop clinical parkinsonism. © 2009 Movement Disorder Society [source] Seasonal variation in enzyme activities and temperature sensitivities in Arctic tundra soilsGLOBAL CHANGE BIOLOGY, Issue 7 2009MATTHEW D. WALLENSTEIN Abstract Arctic soils contain large amounts of organic matter due to very slow rates of detritus decomposition. The first step in decomposition results from the activity of extracellular enzymes produced by soil microbes. We hypothesized that potential enzyme activities are low relative to the large stocks of organic matter in Arctic tundra soils, and that enzyme activity is low at in situ temperatures. We measured the potential activity of six hydrolytic enzymes at 4 and 20 °C on four sampling dates in tussock, intertussock, shrub organic, and shrub mineral soils at Toolik Lake, Alaska. Potential activities of N -acetyl glucosaminidase, ,-glucosidase, and peptidase tended to be greatest at the end of winter, suggesting that microbes produced enzymes while soils were frozen. In general, enzyme activities did not increase during the Arctic summer, suggesting that enzyme production is N-limited during the period when temperatures would otherwise drive higher enzyme activity in situ. We also detected seasonal variations in the temperature sensitivity (Q10) of soil enzymes. In general, soil enzyme pools were more sensitive to temperature at the end of the winter than during the summer. We modeled potential in situ,-glucosidase activities for tussock and shrub organic soils based on measured enzyme activities, temperature sensitivities, and daily soil temperature data. Modeled in situ enzyme activity in tussock soils increased briefly during the spring, then declined through the summer. In shrub soils, modeled enzyme activities increased through the spring thaw into early August, and then declined through the late summer and into winter. Overall, temperature is the strongest factor driving low in situ enzyme activities in the Arctic. However, enzyme activity was low during the summer, possibly due to N-limitation of enzyme production, which would constrain enzyme activity during the brief period when temperatures would otherwise drive higher rates of decomposition. [source] |