SRB/SLEEC (Solid Rocket Booster/Shingle Lap Extendible Exit Cone) feasibility study, volume 1

A preliminary design and analysis was completed for a SLEEC (Shingle Lap Extendible Exit Cone) which could be incorporated on the Space Transportation System (STS) Solid Rocket Booster (SRB). Studies were completed which predicted weights and performance increases and development plans were prepared for the full-scale bench and static test of SLEEC. In conjunction with the design studies, a series of supporting analyses were performed to assure the validity and feasibility of performance, fabrication, cost, and reliability for the selected design. The feasibility and required amounts of bench, static firing, and flight tests considered necessary for the successful incorporation of SLEEC on the Shuttle SRBs were determined. Preliminary plans were completed which define both a follow on study effort and a development program

How Forbes 200 Companies Create and use Mission Statements

Small publicly-held firms included on the Forbes 200 list were surveyed to determine their usage of mission statements. Survey results reveal that most of these firms have developed mission statements, which usually include main company purposes, key business objectives, company identity, and other guiding principles. Most of the mission statements result from a group effort, although less than half of the firms formally seek employee input in the development process. CEOs are generally pleased with the results yielded by their mission statements, giving highest marks for providing direction to managers and helping employees focus. The lowest mark is given to improving employee morale, suggesting that more work is needed to help mission statements foster a sense of mission. Effective mission statements include/our major steps: (a) development, (b) distribution, (c) integration, and (d) evaluation. This article provides guidelines for each of these steps

The 1997 Clark Landfill Failure at Indiana Harbor Works LTV Steel Company, East Chicago, Indiana

A rapid failure of approximately 900,000 cubic yards of fill and lake bed foundation soil occurred sometime between 7:00 a.m. and 8:00 a.m., on August 6, 1997. The 45-acre landfill was approximately 100 feet higher than Lake Michigan and slid on a layer of weak silty clay located 55 to 60 feet below the water surface of Lake Michigan. The horizontally-translating slide mass nearly blocked the operating intake flume to the No. 2 Intake Pump House for the steel mill cooling water. Figure 1 shows the plan location of the slide mass and scarp location. The slide mass extended approximately 1,000 feet from the southwest fill area to a location east of the cofferdam that holds an oil boom along the south side of the landfill next to the intake flume. Pre-failure and failure conditions with estimated slide plane location and scarp geometry for failure sections A-A, B-B and C-C are shown on Figures 2 through 4. The slide extended 200 to 300 feet north from the flume up to a 30- to 40-foot high scarp. The slide mass moved approximately a a 30- to 40-foot high scarp. The slide mass moved approximately 30 feet into the canal and moved the cofferdam structure at least 10 feet south. In fact, the slide mass filled more than 400 feet of the 25-foot-deep, by 140-foot-wide flume and nearly blocked the flume with only 3 to 4 feet of water flowing when the channel was 20 to 25 feet deep

Tissue Inhibitor of Metalloproteinase–3 (TIMP-3) induces FAS dependent apoptosis in human vascular smooth muscle cells

Over expression of Tissue Inhibitor of Metalloproteinases-3 (TIMP-3) in vascular smooth muscle cells (VSMCs) induces apoptosis and reduces neointima formation occurring after saphenous vein interposition grafting or coronary stenting. In studies to address the mechanism of TIMP-3-driven apoptosis in human VSMCs we find that TIMP-3 increased activation of caspase-8 and apoptosis was inhibited by expression of Cytokine response modifier A (CrmA) and dominant negative FAS-Associated protein with Death Domain (FADD). TIMP-3 induced apoptosis did not cause mitochondrial depolarisation, increase activation of caspase-9 and was not inhibited by over-expression of B-cell Lymphoma 2 (Bcl2), indicating a mitochondrial independent/type-I death receptor pathway. TIMP-3 increased levels of the First Apoptosis Signal receptor (FAS) and depletion of FAS with shRNA showed TIMP-3-induced apoptosis was FAS dependent. TIMP-3 induced formation of the Death-Inducing Signalling Complex (DISC), as detected by immunoprecipitation and by immunofluorescence. Cellular-FADD-like IL-1 converting enzyme-Like Inhibitory Protein (c-FLIP) localised with FAS at the cell periphery in the absence of TIMP-3 and this localisation was lost on TIMP-3 expression with c-FLIP adopting a perinuclear localisation. Although TIMP-3 inhibited FAS shedding, this did not increase total surface levels of FAS but instead increased FAS levels within localised regions at the cell surface. A Disintegrin And Metalloproteinase 17 (ADAM17) is inhibited by TIMP-3 and depletion of ADAM17 with shRNA significantly decreased FAS shedding. However ADAM17 depletion did not induce apoptosis or replicate the effects of TIMP-3 by increasing localised clustering of cell surface FAS. ADAM17-depleted cells could activate caspase-3 when expressing levels of TIMP-3 that were otherwise sub-apoptotic, suggesting a partial role for ADAM17 mediated ectodomain shedding in TIMP-3 mediated apoptosis. We conclude that TIMP-3 induced apoptosis in VSMCs is highly dependent on FAS and is associated with changes in FAS and c-FLIP localisation, but is not solely dependent on shedding of the FAS ectodomain

Treatment of estrogen-induced dermatitis with omalizumab

In 1945, Drs Bernhard Zondek and Yehuda Bromberg demonstrated intradermal treatment with estrone and estradiol benzoate induced urticarial lesions in some patients.1 Fifty years later, Shelley et al,2 who introduced the concept of progesterone dermatitis several decades prior, defined estrogen dermatitis based on studies of 7 women with premenstrual flares of skin eruptions including papulovesicular, urticarial, or eczematous lesions or generalized pruritus. Previously described therapies for estrogen dermatitis include estrogen desensitization, tamoxifen, leuprolide, and oophorectomy.3 Here we report a case of estrogen-induced dermatitis successfully treated with omalizumab

Horace H. Comstock, John Kean, and William Baker with Norman Little, August 2, 1836

Indenture for the sale of land in Saginaw, Michigan from Norman Little to Horace H. Comstock, John Kean, and William Baker.https://digitalcommons.kean.edu/lhc_1830s/1112/thumbnail.jp