Jet Effects on Cylindrical Afterbodies Housing Sonic and Supersonic Nozzles which Exhaust Against a Supersonic Stream at Angles of Attack from 90 to 180

Jet effects on cylindrical afterbodies housing sonic and supersonic nozzle

Letter from James McDearmon to Aurelia McDearmon, January 5, 1846

Transcript of Letter from James McDearmon to Aurelia McDearmon, January 5, 1846. A brief description of Lindenwood College in 1846

Experimental Investigation of Effects of Primary Jet Flow and Secondary Flow Through a Zero-length Ejector on Base and Boattail Pressures of a Body of Revolution at Free-stream Mach Numbers of 1.62, 1.93, and 2.41

An investigation was made at free-stream Mach numbers of 1.62, 1.93, and 2.41 to determine the effects of a primary jet and secondary air flow on the base pressure and pressures acting over the boattailsurface of a body of revolution for two secondary discharge areas. The Mach numbers of the primary nozzles were 1 and 3.23 with the secondary mass flow being varied from 0 to 10 percent of the primary mass flow. The ratio of jet stagnation temperature to tunnel stagnation temperature was about 0.96. The Reynolds number range of the investigation was from 2.1 x 10(6) to 2.9 x 10(6)based on body length. All testing was conducted with a turbulent boundary layer along the model. This report presents results obtained with zero-length ejector and covers jet static-pressure ratios from the jet-off condition to a maximum of about 128 for the sonic nozzle and to a maximum of about 9 for the supersonic nozzle

ISPD gene mutations are a common cause of congenital and limb-girdle muscular dystrophies

Dystroglycanopathies are a clinically and genetically diverse group of recessively inherited conditions ranging from the most severe of the congenital muscular dystrophies, Walker-Warburg syndrome, to mild forms of adult-onset limb-girdle muscular dystrophy. Their hallmark is a reduction in the functional glycosylation of α-dystroglycan, which can be detected in muscle biopsies. An important part of this glycosylation is a unique O-mannosylation, essential for the interaction of α-dystroglycan with extracellular matrix proteins such as laminin-α2. Mutations in eight genes coding for proteins in the glycosylation pathway are responsible for ∼50% of dystroglycanopathy cases. Despite multiple efforts using traditional positional cloning, the causative genes for unsolved dystroglycanopathy cases have escaped discovery for several years. In a recent collaborative study, we discovered that loss-of-function recessive mutations in a novel gene, called isoprenoid synthase domain containing (ISPD), are a relatively common cause of Walker-Warburg syndrome. In this article, we report the involvement of the ISPD gene in milder dystroglycanopathy phenotypes ranging from congenital muscular dystrophy to limb-girdle muscular dystrophy and identified allelic ISPD variants in nine cases belonging to seven families. In two ambulant cases, there was evidence of structural brain involvement, whereas in seven, the clinical manifestation was restricted to a dystrophic skeletal muscle phenotype. Although the function of ISPD in mammals is not yet known, mutations in this gene clearly lead to a reduction in the functional glycosylation of α-dystroglycan, which not only causes the severe Walker-Warburg syndrome but is also a common cause of the milder forms of dystroglycanopathy