TWO-STROKE ENGINE BEHAVIOR (SMALL CHAINSAW) OPERATING WITH NON-COMMERCIAL FUEL BLENDS AND DIVERSE LUBRICATION

The paper presents results for experimental tests in a two-stroke internal combustions engine operating on commercial fuel (gasoline and ethanol blends), with different proportions in mineral oil for lubrication purposes. Appropriate instrumentation was used to carry out the measurement of the quantities of interest, namely fuel consumption (g/s), angular velocity (rpm) and emissions (CO2 and NOx). The methodology was based on regulations from INMETRO (motor vehicles energy conversion efficiency) and ABNT (testing of internal combustion engines). Results obtained are analyzed and discussed for the fuel consumption versus angular velocity (g/s x rpm) for each combination fuel blend and lubricating oil (quantities). Main findings are that fuel consumption increases non linearly as angular velocity increases and as lubrication lowers, while emissions decreases as angular velocity increases. Lowest fuel consumption and emissions occurred, respectively, for A25/L1:25 and A25/L1:50 (commercial fuel and standard lubrication)

The endogenous caspase-8 inhibitor c-FLIPL regulates ER morphology and crosstalk with mitochondria

Components of the death receptors-mediated pathways like caspase-8 have been identified in complexes at intracellular membranes to spatially restrict the processing of local targets. In this study, we report that the long isoform of the cellular FLICE-inhibitory protein (c-FLIPL), a well- known inhibitor of the extrinsic cell death initiator caspase-8, localizes at the endoplasmic reticulum (ER) and mitochondria-associated membranes (MAMs). ER morphology was disrupted and ER Ca2+-release as well as ER-mitochondria tethering were decreased in c-FLIP-/- mouse embryonic fibroblasts (MEFs). Mechanistically, c-FLIP ablation resulted in enhanced basal caspase-8 activation and in caspase-mediated processing of the ER-shaping protein reticulon-4 (RTN4) that was corrected by re-introduction of c-FLIPL and caspase inhibition, resulting in the recovery of a normal ER morphology and ER-mitochondria juxtaposition. Thus, the caspase-8 inhibitor c-FLIPL emerges as a component of the MAMs signaling platforms, where caspases appear to regulate ER morphology and ER-mitochondria crosstalk by impinging on ER-shaping proteins like the RTN4

Bags, junctions, and networks of BPS and non-BPS defects

We investigate several models of coupled scalar fields that present discrete Z_2, Z_2 x Z_2, Z_3 and other symmetries. These models support topological domain wall solutions of the BPS and non-BPS type. The BPS solutions are stable, but the stability of the non-BPS solutions may depend on the parameters that specify the models. The BPS and non-BPS states give rise to bags, and also to three-junctions that may allow the presence of networks of topological defects. In particular, we show that the non-BPS defects of a specific model that engenders the Z_3 symmetry give rise to a stable regular hexagonal network of domain walls.Comment: Revtex, 16 pages, 6 ps figures; Shorter version to be published in Phys. Rev.

Exercise and cognitive function: a hypothesis for the association of type II diabetes mellitus and Alzheimer's disease from an evolutionary perspective

The association of type II diabetes mellitus (DM2) with Alzheimer's disease (AD) has received considerable attention in recent years. In the present paper, a hypothesis for this association from an evolutionary perspective, with emphasis on the close interplay between exercise and cognitive function, will be advanced in order to provide a biological rationale for the notion that the fundamental metabolic features of DM2 act in the brain over a protracted time span to induce the neuropathological characteristics of Alzheimer's disease thereby producing cognitive impairment. It is hoped that this hypothesis puts the association of DM2 and AD on firm conceptual grounds from a biological perspective and offers directions for further research