High-speed imaging of AC corona for voltage measurement

This paper looks at high-speed imaging of AC corona for voltage measuremen

HVAC measurements by corona analysis

This paper looks at HVAC measurements by corona analysi

Induction of nitric oxide synthase in human chondrocytes.

Incubation of human chondrocytes with interleukin-1 beta, tumour necrosis factor or endotoxin induced the expression of NO synthase. The synthesis of NO induced by IL-1 beta was concentration- and time- dependent, occurred after a lag period of approximately 6h and was inhibited by NG-monomethyl-L-arginine, cycloheximide, dexamethasone and hydrocortisone, but not by indomethacin. The activity of NO synthase from activated chondrocytes was not affected by EGTA or by the calmodulin inhibitor W-13. Northern blot analysis, with a rabbit chondrocyte inos probe, showed a 4.4kb positively hybridising band from activated human chondrocytes. Thus, human articular chondrocytes express an inducible NO synthase from the same family as the rabbit chondrocyte and rodent macrophage enzymes. This family appears to vary in terms of in vitro Ca(2+)-dependence and sensitivity to glucocorticoids

Cloning, characterization, and expression of a cDNA encoding an inducible nitric oxide synthase from the human chondrocyte.

Incubation of human articular chondrocytes with interleukin 1 beta results in the time-dependent expression of nitric oxide (NO) synthase. We report here the isolation of a cDNA clone which encodes a protein of 1153 amino acids with a molecular mass of 131,213 Da and a calculated isoelectric point of 7.9. CHO cells transfected with a plasmid harboring this cDNA clone expressed NO synthase activity that was inhibited by some L-arginine analogues. The deduced amino acid sequence of the human chondrocyte inducible NO synthase shows 51% identity and 68% similarity with the endothelial NO synthase and 54% identity and 70% similarity with the neuronal NO synthase. The similarity (88%) between the human chondrocyte NO synthase cDNA sequence and that reported for the murine macrophage suggests that the inducible class of enzyme is conserved between different cell types and across species

Rasagiline Ameliorates Olfactory Deficits in an Alpha-Synuclein Mouse Model of Parkinson's Disease

<div><p>Impaired olfaction is an early pre-motor symptom of Parkinson's disease. The neuropathology underlying olfactory dysfunction in Parkinson's disease is unknown, however α-synuclein accumulation/aggregation and altered neurogenesis might play a role. We characterized olfactory deficits in a transgenic mouse model of Parkinson's disease expressing human wild-type α-synuclein under the control of the mouse α-synuclein promoter. Preliminary clinical observations suggest that rasagiline, a monoamine oxidase-B inhibitor, improves olfaction in Parkinson's disease. We therefore examined whether rasagiline ameliorates olfactory deficits in this Parkinson's disease model and investigated the role of olfactory bulb neurogenesis. α-Synuclein mice were progressively impaired in their ability to detect odors, to discriminate between odors, and exhibited alterations in short-term olfactory memory. Rasagiline treatment rescued odor detection and odor discrimination abilities. However, rasagiline did not affect short-term olfactory memory. Finally, olfactory changes were not coupled to alterations in olfactory bulb neurogenesis. We conclude that rasagiline reverses select olfactory deficits in a transgenic mouse model of Parkinson's disease. The findings correlate with preliminary clinical observations suggesting that rasagiline ameliorates olfactory deficits in Parkinson's disease.</p> </div

Olfactory deficits in the α-syn mouse model of PD.

<p><b>A-B: </b><b>Odor detection test. A.</b> Description of the protocol composed of 3 sessions (S). In each 5-min session, mice were exposed to 2 cartridges, one filled with water, the other with increasing odor concentrations from 1∶10⁸ to 1∶10⁴. <b>B.</b> Percentage of time sniffing the odor for the different concentrations. WT mice start detecting the odor at the concentration 1∶10⁶ when percentage of time sniffing the odor is significantly different from the chance level (50%, where mice spent same time sniffing water and odor cartridges) (°°°p<0.001, °°p<0.01, one-sample t-test). α-Syn mice can detect the odor only at 1∶10⁴ (°°°p<0.001, one-sample t-test). At the concentration 1∶10⁶, α-syn mice are significantly impaired compared to WT. N = 10 for each group aged 10–11 months. Statistics: One-sample t-test to compare each value to chance level (50%), (°°°p<0.001, °°p<0.01). Two-way RM ANOVA: odor concentration, p = 0.0001, F(2,36) = 11.96; genotype, p = 0.015, F(1,36) = 7.2; odor concentration×genotype, p = 0.0073, F(2,36) = 5.65; Bonferroni post-hoc (***p<0.001). <b>C-D: Short-term olfactory memory test. C.</b> Description of the protocol composed of 3 sessions (S). Each session consisted of two 5 min-trials (T) where mice are exposed to a novel odor separated by an increasing inter-trial time (ITI) from 60 s to 120 s. <b>D.</b> Percentage of time sniffing the odor during T2 compared to the total time spent sniffing during both trials. WT mice remember the odor during the 2^nd exposure for the 3 ITI tested and their percentage of time sniffing the odor during T2 was significantly different from the chance level (50%, where mice spent same time sniffing the odor during T1 and T2) (°°p<0.01, °°°p<0.001, one-sample t-test). By contrast, short-term olfactory memory of α-syn mice was impaired from an ITI of 120 s (p>0.05, one-sample t-test). However, it was significantly different from chance level at 60 s and 90 s (°°°p<0.001 and °p<0.05 respectively, one-sample t-tests). N = 10 for each group aged 10–11 months. Statistics: One-sample t-test to compare each value to chance level (50%), (°°°p<0.001, °°p<0.01, °p<0.05). <b>E-H: Odor discrimination test. E and G:</b> Social odor discrimination test. <b>E.</b> Description of the protocol composed of 6 habituation trials where mice are exposed to a familiar odor (F, odor of the tested mouse); and one odor discrimination trial, where one familiar odor is replaced by a novel odor (N, another mouse's odor). This test was performed with low or high odor intensities (wood blocks impregnated with mouse's odor for 2 or 7 days respectively). Each trial lasted 2 min and was separated by 1 min. <b>G.</b> Percentage of time sniffing novel odor. For both low and high odor intensities, α-syn mice have impaired odor discrimination with the percentage of time sniffing the odor significantly lower than WT. N = 19–21 for each group aged 10–11 months. Statistics: Two-way RM ANOVA: odor intensity, p = 0.55, F(1,38) = 0.37; genotype, p<0.0001, F(1,38) = 27.1; odor intensity×genotype, p = 0.63, F(1,38) = 0.23; Bonferroni post-hoc (***p<0.001). <b>F and H:</b> Non-social odor discrimination test. <b>F.</b> Description of the protocol based on the same principle of the social odor discrimination test but using non-social odors (lemon and lime). In the 8^th 2 min-trial, an item discrimination trial was added where the usual cartridge, with the novel odor (lime), was replaced by a novel item (a novel type of cartridge associated with the same novel odor, lime). <b>H.</b> Percentage of time sniffing the novel odor during the odor discrimination trial and percentage of time exploring the novel item in the item discrimination trial. α-syn mice had significantly impaired odor discrimination of the social odor. By contrast, the ability to discriminate the novel item was similar between WT and α-syn mice suggesting that the discrimination deficit is specific to olfaction. Statistics: unpaired t-test, non-social odor discrimination p<0.0001, N = 19–21 for each group aged 10–11 months; item discrimination p = 0.16, N = 10 for each group aged 10-11 months (***p<0.001).</p

Behavioral experiments: design and parameters analyzed.

<p><b>A.</b> Experimental design of the behavioral study. <b>B</b>. Olfactory- and control tests and the parameters analyzed from these experiments.</p