Effectiveness of Selective Catalytic Reduction (SCR) systems on reducing gaseous emissions from an engine using Diesel and Biodiesel Blends

The aim of this investigation was to quantify organic and inorganic gas emissions from a four-cylinder diesel engine equipped with a urea selective catalytic reduction (SCR) system. Using a bench dynamometer, the emissions from the following mixtures were evaluated using a Fourier transform infrared (FTIR) spectrometer: low-sulfur diesel (LSD), ultralow-sulfur diesel (ULSD), and a blend of 20% soybean biodiesel and 80% ULSD (B20). For all studied fuels, the use of the SCR system yielded statistically significant (p < 0.05) lower NOx emissions. In the case of the LSD and ULSD fuels, the SCR system also significantly reduced emissions of compounds with high photochemical ozone creation potential, such as formaldehyde. However, for all tested fuels, the SCR system produced significantly (p < 0.05) higher emissions of N2O. In the case of LSD, the NH3 emissions were elevated, and in the case of ULSD and B20 fuels, the non-methane hydrocarbon (NMHC) and total hydrocarbon of diesel (HCD) emissions were significantly higher

Introducing the Condor Array Telescope: IV. A possible nova super-remnant surrounding the putative recurrent nova KT Eridani

Just 10 recurrent novae (RNe) - which erupt repeatedly on timescales shorter than one century - are known in our Galaxy. The most extreme RN known (located in the Andromeda galaxy), M31N 2008-12a, undergoes a nova eruption every year, and is surrounded by a vast nova "super-remnant", 134 pc in extent. Simulations predict that all RNe should be surrounded by similar vast shells, but previous searches have failed to detect them. KT Eri has recently been suggested to be a RN, and we have used the Condor Array Telescope to image its environs through multiple narrowband filters. We report the existence of a large (∼ 50 pc diameter), Hα-bright shell centered on KT Eri, exactly as predicted. This strongly supports the claim that KT Eri is the 11th Galactic recurrent nova, and only the second nova known to be surrounded by a super-remnant. SALT spectra of the super-remnant demonstrate that its velocity width is consistent with that of M31-2008-12a

Production of Multiple Brain-Like Ganglioside Species Is Dispensable for Fas-Induced Apoptosis of Lymphoid Cells

Activation of an acid sphingomyelinase (aSMase) leading to a biosynthesis of GD3 disialoganglioside has been associated with Fas-induced apoptosis of lymphoid cells. The present study was undertaken to clarify the role of this enzyme in the generation of gangliosides during apoptosis triggered by Fas ligation. The issue was addressed by using aSMase-deficient and aSMase-corrected cell lines derived from Niemann-Pick disease (NPD) patients. Fas cross-linking elicited a rapid production of large amounts of complex a- and b-series species of gangliosides with a pattern and a chromatographic behavior as single bands reminiscent of brain gangliosides. The gangliosides were synthesized within the first ten minutes and completely disappeared within thirty minutes after stimulation. Noteworthy is the observation that GD3 was not the only ganglioside produced. The production of gangliosides and the onset of apoptotic hallmarks occurred similarly in both aSMase-deficient and aSMase-corrected NPD lymphoid cells, indicating that aSMase activation is not accountable for ganglioside generation. Hampering ganglioside production by inhibiting the key enzyme glucosylceramide synthase did not abrogate the apoptotic process. In addition, GM3 synthase-deficient lymphoid cells underwent Fas-induced apoptosis, suggesting that gangliosides are unlikely to play an indispensable role in transducing Fas-induced apoptosis of lymphoid cells

Polysialic Acid Is Required for Dopamine D2 Receptor-Mediated Plasticity Involving Inhibitory Circuits of the Rat Medial Prefrontal Cortex

Decreased expression of dopamine D2 receptors (D2R), dysfunction of inhibitory neurotransmission and impairments in the structure and connectivity of neurons in the medial prefrontal cortex (mPFC) are involved in the pathogenesis of schizophrenia and major depression, but the relationship between these changes remains unclear. The polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a plasticity-related molecule, may serve as a link. This molecule is expressed in cortical interneurons and dopamine, via D2R, modulates its expression in parallel to that of proteins related to synapses and inhibitory neurotransmission, suggesting that D2R-targeted antipsychotics/antidepressants may act by affecting the plasticity of mPFC inhibitory circuits. To understand the role of PSA-NCAM in this plasticity, rats were chronically treated with a D2R agonist (PPHT) after cortical PSA depletion. PPHT-induced increases in GAD67 and synaptophysin (SYN) neuropil expression were blocked when PSA was previously removed, indicating a role for PSA-NCAM in this plasticity. The number of PSA-NCAM expressing interneuron somata also increased after PPHT treatment, but the percentages of these cells belonging to different interneuronal subpopulations did not change. Cortical pyramidal neurons did not express PSA-NCAM, but puncta co-expressing this molecule and parvalbumin could be found surrounding their somata. PPHT treatment increased the number of PSA-NCAM and parvalbumin expressing perisomatic puncta, but decreased the percentage of parvalbumin puncta that co-expressed SYN. PSA depletion did not block these effects on the perisomatic region, but increased further the number of parvalbumin expressing puncta and increased the percentage of puncta co-expressing SYN and parvalbumin, suggesting that the polysialylation of NCAM may regulate perisomatic inhibition of mPFC principal neurons. Summarizing, the present results indicate that dopamine acting on D2R influences structural plasticity of mPFC interneurons and point to PSA-NCAM as a key player in this remodeling

Differential Regulation of the Excitability of Prefrontal Cortical Fast-Spiking Interneurons and Pyramidal Neurons by Serotonin and Fluoxetine

Serotonin exerts a powerful influence on neuronal excitability. In this study, we investigated the effects of serotonin on different neuronal populations in prefrontal cortex (PFC), a major area controlling emotion and cognition. Using whole-cell recordings in PFC slices, we found that bath application of 5-HT dose-dependently increased the firing of FS (fast spiking) interneurons, and decreased the firing of pyramidal neurons. The enhancing effect of 5-HT in FS interneurons was mediated by 5-HT2 receptors, while the reducing effect of 5-HT in pyramidal neurons was mediated by 5-HT1 receptors. Fluoxetine, the selective serotonin reuptake inhibitor, also induced a concentration-dependent increase in the excitability of FS interneurons, but had little effect on pyramidal neurons. In rats with chronic fluoxetine treatment, the excitability of FS interneurons was significantly increased, while pyramidal neurons remained unchanged. Fluoxetine injection largely occluded the enhancing effect of 5-HT in FS interneurons, but did not alter the reducing effect of 5-HT in pyramidal neurons. These data suggest that the excitability of PFC interneurons and pyramidal neurons is regulated by exogenous 5-HT in an opposing manner, and FS interneurons are the major target of Fluoxetine. It provides a framework for understanding the action of 5-HT and antidepressants in altering PFC network activity