Analysis of form threads using fluteless taps in cast magnesium alloy (AM60)

Threads are used in the most assemblies of industrial products. Commonly, mechanical components need to have threaded parts allowing fast and accurate assemblies and disassemblies. Internal tapping is one of the most demanded machining operations, and threads obtained by forming have been a good alternative. This work investigates the effect of the factors the hole diameter, the forming speed and types of tool on the responses: torque, hardness, fill rate, and thrust force of the form tapping process. The experiments were carried out with three diameters, three forming speeds, and two coatings. The material used was the AM60 alloy due to its high ductility and wide application as head engine. The results revealed torque is more affected by the hole diameter than thrust force, and little hardening occurred using high forming speed with a small diameter. The fill rate of the thread profile was not significantly affected by the intermediate and large diameters. Finally, it can be stated that the recommended hole diameter provided by the tool's supplier can be modified to achieve more accurate thread profiles.     

Effect of Slag Basicity on Phase Equilibria and Selenium and Tellurium Distribution in Magnesia-Saturated Calcium Iron Silicate Slags

New measurements have been made on the phase equilibria of magnesia-saturated CaO-FeO_x-SiO₂ slags at 1573 K (1300 °C) and an oxygen partial pressure of 10⁻⁹ atm. The thermodynamic behavior of selenium (Se) and tellurium (Te) in the slag and the stability of oxide mineral phases within the slag were examined as a function of slag composition. The measured equilibrium distribution of Se and Te between the slag and the copper showed nonlinear dependence on the slag basicity, reaching maxima at CaO/(CaO + SiO₂) ratios of about 0.2 and 1 and a minimum at a ratio of about 0.5. The solubility of the copper oxide in the bulk slag also passed through a minimum value at a ratio of about 0.5. Results from drop-quench experiments confirmed the stability of various oxide solid solution phases at 1573 K (1300 °C) that had virtually no solubility for Se and Te. The deduced capacity of the liquid slag for Se was found to be independent of basicity in relatively basic slags, and decreased sharply as SiO₂ replaced CaO in relatively acidic slags.     

The potential impacts of climate-change policy on freshwater use in thermoelectric power generation

Climate change policy involving a price on carbon would change the mix of power plants and the amount of water they withdraw and consume to generate electricity. We analyze what these changes could entail for electricity generation in the United States under four climate policy scenarios that involve different costs for emitting CO₂ and different technology options for reducing emissions out to the year 2030. The potential impacts of the scenarios on the U.S. electric system are modeled using a modified version of the U.S. National Energy Modeling System and water-use factors for thermoelectric power plants derived from electric utility data compiled by the U.S. Energy Information Administration. Under all the climate-policy scenarios, freshwater withdrawals decline 2–14% relative to a business-as-usual (BAU) scenario of no U.S. climate policy. Furthermore, water use decreases as the price on CO₂ under the climate policies increases. At relatively high carbon prices (>$50/tonne CO₂), however, retrofitting coal plants to capture CO₂ increases freshwater consumption compared to BAU in 2030. Our analysis suggests that climate policies and a carbon price will reduce both electricity generation and freshwater withdrawals compared to BAU unless a substantial number of coal plants are retrofitted to capture CO₂.     

Hypoxia stimulates insulin-like growth factor binding protein 1 (IGFBP-1) gene expression in HepG2 cells: a possible model for IGFBP-1 expression in fetal hypoxia

IGFBP-1 is elevated in fetuses with long-term, chronic hypoxia and intrauterine growth restriction. We investigated the hypothesis that hypoxia regulates IGFBP-1 in the human fetus in vivo and IGFBP-1 gene expression and protein in vitro. Umbilical artery IGFBP-1 levels (mean +/- SEM) from term babies with respiratory acidosis (acute hypoxia), normal babies, and those with mixed respiratory/metabolic acidosis (more profound and prolonged hypoxia) were measured using an immunoradiometric assay. IGFBP-1 levels were similar in normal (n = 12) and acutely hypoxic (n = 6) babies (189.1 +/- 71.8 vs. 175.8 +/- 45.9 ng /ml, respectively, P = 0.789). However, with more profound and prolonged hypoxia (n = 19), IGFBP-1 levels were markedly elevated (470.6 +/- 80.0 ng /ml, P = 0.044). To investigate IGFBP-1 regulation by hypoxia in vitro, HepG2 cells were incubated under hypoxia (pO2 = 2%) and normoxia (pO2 = 20%). IGFBP-1 protein and mRNA increased 8- and 12-fold, respectively, under hypoxic conditions. Hypoxia did not affect protein or mRNA levels of IGFBP-2 or -4. IGFBP-5 and -6 mRNAs, undetectable in control cells, were not induced by hypoxia, whereas minimally expressed IGFBP-3 mRNA increased twofold. Investigation into IGFBP-1 gene structure revealed three potential consensus sequences for the hypoxia response element (HRE) in the first intron. To investigate functionality, a 372-bp fragment of IGFBP-1 intron 1, containing putative HREs, was placed 5' to a heterologous hsp70 promoter in a plasmid using luciferase as a reporter gene. Under hypoxia, reporter gene activity increased up to 30-fold. Mutations in the middle HRE abolished reporter activity in response to hypoxia, suggesting that this HRE is functional in the IGFBP-1 hypoxia response. Cotransfection of HRE reporter genes with a constitutively expressing hypoxia-inducible factor 1 plasmid in HepG2 cells resulted in a fourfold induction of reporter activity, suggesting a role for hypoxia-inducible factor 1 in hypoxia induction of IGFBP-1 gene expression. These data support the hypothesis that hypoxia regulation of IGFBP-1 may be a mechanism operating in the human fetus to restrict insulin-like growth factor-mediated growth in utero under conditions of chronic hypoxia and limited substrate availability.     

Relationship of senescence of corn (Zea mays L.) stalk pith, cob parenchyma and first developed leaf tissues to RNA content and synthesis

In stalk parenchyma tissue of WF9 X 38-11 single corn (Zea mays L.), there was a per cell increase in RNA synthesis and a slight increase in total RNA as cells became older. In cob parenchyma tissue of WF9 X 38-11 single cross corn, both total RNA content and RNA synthesis per cell decreased with the age of cells. In first developed leaf tissue of FR43 X FR14A single cross corn, RNA synthesis increased steadily but only slightly over its life span. The pattern of RNA synthesis and destruction in senescing leaf tissue of seedlings and two sources of parenchyma tissue of maturing plants appeared to differ.     

TAG-1 can mediate homophilic binding, but neurite outgrowth on TAG-1 requires an L1-like molecule and beta 1 integrins

Subsets of axons in the embryonic nervous system transiently express the glycoprotein TAG-1, a member of the subfamily of immunoglobulin (Ig)-like proteins that contain both C2 class Ig and fibronectin type III domains. TAG-1 is attached to the cell surface by a glycosylphosphatidylinositol linkage and is secreted by neurons. In vitro studies have shown that substrate-bound TAG-1 promotes neurite outgrowth. We have examined the nature of axonal receptors that mediate the neurite-outgrowth promoting properties of TAG-1. Although TAG-1 can mediate homophilic binding, neurite outgrowth on a substrate of TAG-1 does not depend on the presence of TAG-1 on the axonal surface. Instead, neurite outgrowth on TAG-1 is inhibited by polyclonal antibodies directed against L1 and, independently, by polyclonal and monoclonal antibodies against beta 1-containing integrins. These results provide evidence that TAG-1 can interact with cell surfaces in both a homophilic and heterophilic manner and suggest that neurite extension on TAG-1 requires the function of both integrins and an L1-like molecule.     

Enhanced cyclooxygenase-2 gene expression in alcoholic liver disease in the rat

BACKGROUND & AIMS: Inflammatory stimuli and lipid peroxidation up-regulate cyclooxygenase (COX)-2. This study evaluated the relationship between inflammatory mediators, COX expression, and pathological changes in experimental alcoholic liver disease. METHODS: Rats (5 per group) were fed ethanol and a diet containing saturated fat, corn oil, or fish oil by intragastric infusion. Dextrose isocalorically replaced ethanol in controls. In the first set of experiments, whole livers were analyzed. In the second set of experiments, Kupffer cells, endothelial cells, and hepatocytes were isolated from rats in each group. Pathological analyses and measurements of lipid peroxidation, tumor necrosis factor (TNF)-alpha, COX-1 and COX-2 messenger RNA (mRNA), endotoxin, and liver and plasma thromboxane were performed. RESULTS: Increased expression of COX-2 mRNA was detected in the livers of rats showing necroinflammatory changes. The Kupffer cell was the cell primarily responsible for the increase in COX-2 mRNA level. Increased expression of COX-2 was associated with increased levels of endotoxin, TNF-alpha mRNA, lipid peroxidation, and synthesis of thromboxane. COX-1 mRNA was decreased in Kupffer cells in rats with the most severe liver injury. CONCLUSIONS: Up-regulation of COX-2 in alcoholic liver injury occurred in the presence of proinflammatory stimuli and resulted in increased synthesis of inflammatory and vasoactive eicosanoids. Down-regulation of COX-1 may result in decreased synthesis of cytoprotective eicosanoids and additionally exacerbate liver injury.     

Bayes estimates for immunological progression rates in HIV disease

We develop Bayesian methods for calculating shrinkage estimates of immunological progression rates (for example, CD4 count decline rates) in populations of HIV-infected patients. These methods make the assumption that decline of immunological markers may be modelled as approximately linear on some suitable chosen scale. They are applicable in situations where seroconversion times are unknown and follow-up of patients is variable, with some patients having only sparse measurements of immunological markers. Fitting of models is achieved by Gibbs sampling and CD4 count data from 603 members of the Edinburgh City Hospital Cohort with at least two CD4 determinations are analysed to provide an illustration. It is found that Bayesian shrinkage estimates for CD4 slopes on the square root scale are much more effective predictors of future CD4 counts than the least squares estimates, with respect to squared error loss. Of various shrinkage estimators considered, the most effective corresponds to the simplest model, which can also be fitted using SAS. A characterization of the pattern of CD4 loss in the Edinburgh cohort is obtained (mean rate of decline on root scale-1.61 per annum, standard deviation 1.03) and the effect of various covariates (sex, age, risk category and HLA antigen type) on immunological progression is considered. It is found that homosexual men in Edinburgh and patients with HLA haplotype A1B8DR3 experience significantly faster loss of CD4.