This thesis describes the stress corrosion cracking of a series of aluminium bronze alloys and attempts to characterize the cracking in relation to the various mechanisms proposed. The theories of cracking applicable to the aluminium bronze/ammonia system include; the anodic dissolution, the film rupture and the embrittlement theories, which are described in the literature review. The copper aluminium alloy system was selected for investigation as it exhibits a martensite transformation, making the cracking of these alloys in ammonia solutions a usefulful comparison with the cracking of stainless steels in chloride solutions. The study used 'U-bend' specimens stressed in ammonia solution preconcentrated with copper, while the oxidation of the alloys under the same conditions was examined using unstressed specimens. Oxidation in this thesis is taken to mean an anodic dissolution process with or without the formation of a metallic oxide layer. The tests showed three binary alloys to be susceptible to intergranular and transgranular cracking, while two commercial alloys only cracked transgranularly and only in pH = 11 ammonia solution. Stress corrosion conditions gave rise to sharp, narrow cracks traversing all the phases in the alloy with matching features on opposing fracture surfaces, whereas oxidation gave rise to less distinct, more rounded features with a definite phase dependence. Further experiments showed the limited penetration and reactivity of a corrosive solution along narrow cracks. It is concluded that stress corrosion cracking and oxidation occur by different mechanisms and that the mechanism of stress corrosion cracking is unlikely to involve oxidation as a necessary step to cracking. The results of the present study support an embrittlement mechanism of stress corrosion cracking in aluminium bronze alloys.

The epithelial sodium channel (ENaC) is a key regulator of salt homeostasis. The classic ENaC consists of three subunits: α, β and γ, which are highly expressed in the kidney and colon where they mediate electrogenic Na⁺ influx into cells under the tight hormonal regulation of aldosterone. A fourth ENaC subunit named [delta]ENaC also generates Na⁺ influx with the β- and γENaC subunits in Xenopus oocytes. However [delta]ENaC differs to the other subunits in its channel properties and tissue distribution, suggesting that [delta]ENaC may possess a physiological role other than salt regulation. A copper-toxicosis related protein called COMMD1/Murr1 was previously identified to directly interact with [delta]ENaC and downregulate [delta]ENaC activity. COMMD1 is linked with multiple ubiquitination pathways, therefore we hypothesised that COMMD1 directly interacts with [delta]ENaC through novel protein-protein interaction motifs and promotes internalisation of [delta]ENaC from the cell surface through enhanced ubiquitination. With the use of GST pulldown assays and coimmunoprecipitation, it was found that the binding of COMMD1 to [delta]ENaC is mediated by the COMM domain of COMMD1, primarily through amino acids 120-150 of COMMD1. Immunocytochemical studies showed that the intracellular interaction between [delta]ENaC and COMMD1 predominantly occurred in the early and recycling endosomes, suggesting that COMMD1 may promote the retrieval of [delta]ENaC from the cell surface to the intracellular pool. COMMD1 mediated a decrease in the [delta]ENaC cell surface population, as shown by a biotinylation surface labelling assay. This may be driven by an ubiquitin-regulated endocytosis, as COMMD1 increased ubiquitination, but not proteasomal/lysosomal degradation, of [delta]ENaC. COMMD1 may promote [delta]ENaC ubiquitination through the action of the ubiquitin ligase Nedd4-2 as coexpression with Nedd4-2 enhanced the COMMD1-mediated decrease in surface [delta]ENaC expression. This is abolished by the addition of the Nedd4-2 downregulator kinase sgk1, suggesting that COMMD1 may downregulate [delta]ENaC through the Nedd4-2/sgk1 pathway. Surface levels of [delta]ENaC may also be affected by XIAP, a RING domain ubiquitin ligase which is able to decrease the levels of COMMD1. Coimmunoprecipitation of endogenous [delta]ENaC and COMMD1 proteins, and the enhanced colocalisation of endogenous [delta]ENaC in the recycling endosomes with transfected COMMD1, indicate that interaction between transfected [delta]ENaC and COMMD1 reflect the intracellular interactions of the endogenous proteins. Taken together, these findings suggest that COMMD1 downregulates [delta]ENaC activity by promoting the internalisation of surface [delta]ENaC into early and recycling endosomes and this may be mediated by enhanced [delta]ENaC ubiquitination via the ubiquitin ligase Nedd4-2.

Graduation date: 1983

Graduation date: 1998

The median-times-to-failure (t₅₀’s) for straight dual-damascene via-terminated copper interconnect structures, tested under the same conditions, depend on whether the vias connect down to underlaying leads (metal 2, M2, or via-below structures) or connect up to overlaying leads (metal 1, M1, or via-above structures). Experimental results for a variety of line lengths, widths, and numbers of vias show higher t₅₀’s for M2 structures than for analogous M1 structures. It has been shown that despite this asymmetry in lifetimes, the electromigration drift velocity is the same for these two types of structures, suggesting that fatal void volumes are different in these two cases. A numerical simulation tool based on the Korhonen model has been developed and used to simulate the conditions for void growth and correlate fatal void sizes with lifetimes. These simulations suggest that the average fatal void size for M2 structures is more than twice the size of that of M1 structures. This result supports an earlier suggestion that preferential nucleation at the Cu/Si₃N₄ interface in both M1 and M2 structures leads to different fatal void sizes, because larger voids are required to span the line thickness in M2 structures while smaller voids at the base of vias can cause failures in M1 structures. However, it is also found that the fatal void sizes corresponding to the shortest-times-to-failure (STTF’s) are similar for M1 and M2, suggesting that the voids that lead to the shortest lifetimes occur at or in the vias in both cases, where a void need only span the via to cause failure. Correlation of lifetimes and critical void volumes provides a useful tool for distinguishing failure mechanisms. / Singapore-MIT Alliance (SMA)

Thesis (M.S.)--Ohio State University, 1984. / Includes bibliographical references (leaves 227-231). Available online via OhioLINK's ETD Center

Thesis (Ph. D.)--Oregon Graduate Center, 1979.

In contrast to traditional stamp shaping techniques, tube hydroforming is a realively new shaping technique. But there are still a lack of engineering parameters, mold designs data bases and technique knowledge in this area. This research conducts various tube hydraulic bulge forming experiments, using hydraulic bulge forming testing machines. The pressure and bulge height for UNS C26800 zinc-copper tubing and AISI 1215 carbon steel tubing are measured. The above data are substituted into a hydraulic pressure bulge mathematic model to derive UNS C26800 zinc-copper and AISI 1215 carbon-steel tubes flow stress parameters of initial yielding stress £m0¡Bcoefficient K value and contingency index n value. Moreover, tensile test of the above materials are conducted to the material¡¦s £m0¡BK and n values. then proceed with a comparison of the two sets of statistics. In bulge tests, UNS C26800 zinc-copper tube annealed with temperatures of 300¢J and 500¢J and the not-yet annealing AISI 1215 carbon-steel tube without annealing are used. Additionally, finite element package software is used to simulate the bulge-height and forming pressure. From the comparisons of experimental and analytic results, the deformation mechanisms of tube during the bulge-shaping discussed.

Hepatocellular carcinoma (HCC) is one of the most prevalent cancers in Taiwan. Copper-zinc superoxide dismutase (SOD1) is widely distributed and comprises 90% of the total superoxide dismutase (SOD), which catalyzes the conversion of superoxide to hydrogen peroxide. Reduced expression of antioxidant enzymes, particularly SOD1, has been identified in human hepatoma specimens and cell lines. However, it remains unclear how SOD1 expression affected the tumorigenic processes of hepatoma cells. Expression analysis of an array of human HCC cell lines revealed that SOD1 protein levels were down regulated in poorly differentiated SK-Hep-1 cells. Adenovirus-mediated SOD1 expression increased the SOD1 protein level by 30-40% of control. In addition, SOD1 gene transfer decreased the cellular O2 ¡V level yet increased the H2O2 production. SOD1 overexpression significantly reduced the proliferation, motility, and anchorage-independent growth of SK-Hep-1 cells, but had no effect on the secretion of matrix metalloproteinase-2 (MMP-2) and MMP-9. SOD1 restoration inhibited the proliferation of SK-Hep-1 cells through induction of cell cycle arrest, which was associated with decreased expression of cyclin A, cyclin D1, cdk1, cdk4 and upregulation of p21Cip1 and p27kip1. Besides, SOD1 overexpression also inhibited the nuclear factor £e B (NF-£eB) activities, thereby attenuating the proliferation and migration of SK-Hep-1 cells. In conclusion, SOD1 restoration attenuated the tumorigenicity of hepatoma cells.

A sustainable electroless copper coating process was developed for plating automotive fasteners shaped from AISI 9255 low carbon, high silicon steel. The objective was to minimize the ionic and organic species present in each step of the plating process. A sulfuric acid solution inhibited with quinine was defined to clean the steel prior to plating. The corrosivity of the solution was examined through electrochemical and weight loss measurements to evaluate the efficiency of the cleaning process at high temperatures and high acid concentrations. An electroless copper coating process was then developed using a simple copper sulfate chemistry inhibited with quinine to extend the possible operating window. Finally, benzotriazole was evaluated as a possible anti-oxidant coating. Accelerated thioacetamide corrosion tests were used to evaluate the corrosion inhibition of benzotriazole on copper coatings.