10 research outputs found
Knocking combustion observed in a spark-ignition engine with simultaneous direct and Schlieren high-speed motion pictures and pressure records
Analysis of Spark-Ignition Engine Knock as Seen in Photographs Taken at 200,000 Frames Per Second
A motion picture of the development of knock in a spark-ignition engine, is presented, which consists of 20 photographs taken at intervals of 5 microseconds, or at a rate of 200,000 photographs a second, with an equivalent wide-open exposure time of 6.4 microseconds for each photograph. A motion picture of a complete combustion process, including the development of knock, taken at the rate of 40,000 photographs a second is also presented to assist the reader in orienting the photographs of the knock development taken at 200,000 frames per second. The photographs taken at 200,000 frames per second are analyzed and the conclusion is made that the type of knock in the spark-ignition engine involving violent gas vibration originates as self-propagating disturbance starting at a point in the.burn1ig or autoigniting gases and spreading out from that point through the incompletely burned gases at a rate as high as 6800 feet per second, or about twice the speed of sound in the burned gases. Apparent formation of free carbon particles in both the burning and the burned gas is observed within 10 microseconds after passage of the knock disturbance through the gases
The Mediterranean diet: Effects on proteins that mediate fatty acid metabolism in the colon
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/88101/1/j.1753-4887.2011.00439.x.pd
Recommended from our members
NACA Technical Reports
Simultaneous direct and Schlieren photographs at 40,000 frames per second and correlated pressure records were taken of knocking combustion in a special spark-ignition engine to ascertain the intensity of certain end-zone reactions previously noted from Schlieren photography alone. A violent propagated homogeneous autoignition, or a similar phenomenon, previously observed, was again observed. The pressure records show autoignition of varying violence before the passage of a probable detonation wave. Extensive autoignition without occurrence of gas vibrations was seen in one explosion
Recommended from our members
NACA Technical Reports
Report discussing a motion picture of the development of knock in a spark-ignition engine, which consists of 20 photographs taken at intervals of 5 microseconds, or at a rate of 200,000 photographs per second, with an equivalent wide-open exposure time of 6.4 microseconds for each photograph
RAS/RAF pathway activation in gliomas: the result of copy number gains rather than activating mutations.
Contains fulltext :
52893.pdf (publisher's version ) (Closed access)Aberrant RAS/RAF signaling has been reported to be important for many tumor types including gliomas. Activation of the RAS/RAF pathway can result from oncogenic mutations of RAS/RAF itself. However, such mutations have only occasionally been reported in gliomas. In order to further elucidate the role of RAS/RAF pathway activation in a histopathological and genetic spectrum of glioma subtypes (n = 93), we evaluated different types of aberrations in this pathway. Hotspot mutation analysis of BRAF, NRAS, KRAS, and HRAS revealed only two mutations, V600M in BRAF and G10E in NRAS, both occurring in pure oligodendroglial tumors. However, CGH analysis of 87 tumors revealed copy number gains including the above mentioned oncogenes in 38 of the neoplasms (44%) and including the upstream growth factors EGF, PDGF, IGF, FGF, TGF and/or their receptors in 46 tumors (53%). Phosphorylated MAPK (i.e. the activated compound downstream the RAS/RAF pathway) was detected by immunohistochemistry using tissue micro-arrays in the majority of gliomas. Interestingly, a significant correlation was found for nuclear MAPK-P staining and the number of these copy number gains (or= 3). These results indicate that RAS/RAF pathway activation in gliomas is achieved much more frequently by copy number gains including RAS/RAF and/or upstream growth factor (receptor) than by activating RAS/RAF mutations