Technology requirements to be addressed by the NASA Lewis Research Center Cryogenic Fluid Management Facility program

The NASA Lewis Research Center is responsible for the planning and execution of a scientific program which will provide advance in space cryogenic fluid management technology. A number of future space missions were identified that require or could benefit from this technology. These fluid management technology needs were prioritized and a shuttle attached reuseable test bed, the cryogenic fluid management facility (CFMF), is being designed to provide the experimental data necessary for the technology development effort

PVP2008-61205 NATURAL FLAW SHAPE DEVELOPMENT DUE TO STRESS CORROSION CRACKING

ABSTRACT Typical ASME Section XI subcritical cracking analyses assume an idealized flaw shape driven by stress intensity factors developed for semi-elliptical shaped flaws. Recent advanced finite element analyses (AFEA) conducted by both the US NRC and the nuclear industry for long circumferential indications found in the pressurizer nozzle dissimilar metal welds at the Wolf Creek power plant, suggest that the semielliptical flaw assumption may be overly conservative in some cases. The AFEA methodology that was developed allowed the progression of a planar flaw subjected to typical SCC-type growth laws by calculating stress intensity factors at every nodal point along the crack front, and incrementally advancing the crack front in a more natural manner. Typically crack growth analyses increment the semi-elliptical flaw by considering only the stress intensity factor at the deepest and surface locations along the crack front, while keeping the flaw shape semi-elliptical. In this paper, a brief background to the AFEA methodology and the analyses conducted in the Wolf Creek effort will be discussed. In addition, the natural behavior of surface cracks under normal operating conditions (plus welding residual stress) will be investigated and compared to the semi-elliptical assumption. Conclusions on the observation of when semi-elliptical flaw assumptions are appropriate will be made. These observations will add insight into the conservatism of using an idealized flaw shape assumption. INTRODUCTION In October 2006, circumferential indications were located by ultrasonic testing (UT) in three of the pressurizer nozzle dissimilar metal (DM) welds at the Wolf Creek nuclear power plant. The indications located were relatively long circumferential defects in Alloy 82/182 dissimilar metal welds. In one case the flaw was sized at 43% of the circumference and 26% deep. Using ASME Section XI type analyses, Emc 2 and NRC staff estimated the times to both leakage and rupture fo

Determination of the Elastic-Plastic Fracture Mechanics Z-factor for Alloy 182 Weld Metal Flaws for Use

ABSTRACT One of the ways that the ASME Section XI code incorporates elastic-plastic fracture mechanics (EPFM) in the Section XI Appendix C flaw evaluation procedures for circumferential cracks is through a parameter called Z-factor. This parameter allows the simpler limit-load (or net-section-collapse) solutions to be used with a multiplier from EPFM analyses. Traditionally the EPFM solution was determined by using the GE-EPRI Jestimation scheme to determine the maximum load by EPFM, and Z = limit load / EPFM solution. The Z-factor is a function of the material toughness as well as the pipe diameter. With the advent of primary water stress-corrosion cracks (PWSCC) in pressurized water reactor (PWR) dissimilar metal welds (DMW), there is a need to develop Z-factors for Alloy 82/182 nickel-based alloy welds that are susceptible to such cracks. Although there have been Z-factor solutions for cracks in stainless and ferritic pipe butt welds, the DMW are somewhat different in that there is a much lower yield strength material on one side of the weld (typically forged or wrought 304 stainless steel) and on the other side of the weld the low alloy steel has a much higher strength than even the weld metal. This paper shows how 3D finite element analyses were used for a particular pipe size to determine the sensitivity of the crack location in the Alloy 182 weldment (crack in the center of weld, or closer to the stainless or low alloy steel sides), and how an appropriate stress-strain curve was determined for use in the J-estimation schemes. A Z-factor as a function of the pipe diameter was then calculated using the LBB.ENG2 J estimation scheme using the appropriate stress-strain curves from the finite element analysis. The LBB.ENG2 analysis was used rather than the GE-EPRI estimation scheme since it has been found that the LBB.ENG2 analysis is more accurate when compared with full-scale pipe tests. From past work, the GE-EPRI method was found to be the most conservative of the Jestimation schemes in predicting the maximum loads for circumferential flaws when compared to full-scale circumferentially cracked-pipe tests. The proposed Z-factor relationship should be restricted to normal operating temperatures (above 200C) with low H 2 concentrations, where the Alloy 182 weld metal exhibits high toughness. BACKGROUND The occurrence of PWSCC in dissimilar metal pipe butt welds using Alloy 82 and 182 weld metals has been increasing and evaluation procedures are needed in Section XI of the ASME Boiler and Pressure Vessel Code. Article IWB-3640 and Appendix C (2004 Edition) cover elastic-plastic fracture mechanics (EPFM) analyses for ferritic and austenitic stainless steels and their welds. Currently no criterion exists for cracks in Alloy 82/182 weld metals

Fatty acid activated PPARγ promotes tumorigenicity of prostate cancer cells by up regulating VEGF via PPAR responsive elements of the promoter.

In previous work, it is suggested that the excessive amount of fatty acids transported by FABP5 may facilitate the malignant progression of prostate cancer cells through a FABP5-PPARγ-VEGF signal transduction axis to increase angiogenesis. To further functionally characterise the FABP5-PPARγ-VEGF signal transduction pathway, we have, in this work, investigated the molecular mechanisms involved in its tumorigenicity promoting role in prostate cancer. Suppression of PPARγ in highly malignant prostate cancer cells produced a significant reduction (up to 53%) in their proliferation rate, invasiveness (up to 89%) and anchorage-independent growth (up to 94%) in vitro. Knockdown of PPARγ gene in PC3-M cells by siRNA significantly reduced the average size of tumours formed in nude mice by 99% and tumour incidence by 90%, and significantly prolonged the latent period by 3.5 fold. Results in this study combined with some previous results suggested that FABP5 promoted VEGF expression and angiogenesis through PPARγ which was activated by fatty acids transported by FABP5. Further investigations showed that PPARγ up-regulated VEGF expression through acting with the PPAR-responsive elements in the promoter region of VEGF gene in prostate cancer cells. Although androgen can modulate VEGF expression through Sp1/Sp3 binding site on VEGF promoter in androgen-dependent prostate cancer cells, this route, disappeared as the cells gradually lost their androgen dependency; was replaced by the FABP5-PPARγ-VEGF signalling pathway. These results suggested that the FABP5-PPARγ-VEGF signal transduction axis, rather than androgen modulated route, may be a more important novel therapeutic target for angiogenesis-suppression treatment of castration resistant prostate cancer

Quantification of Epithelial Cell Differentiation in Mammary Glands and Carcinomas from DMBA- and MNU-Exposed Rats

Rat mammary carcinogenesis models have been used extensively to study breast cancer initiation, progression, prevention, and intervention. Nevertheless, quantitative molecular data on epithelial cell differentiation in mammary glands of untreated and carcinogen-exposed rats is limited. Here, we describe the characterization of rat mammary epithelial cells (RMECs) by multicolor flow cytometry using antibodies against cell surface proteins CD24, CD29, CD31, CD45, CD49f, CD61, Peanut Lectin, and Thy-1, intracellular proteins CK14, CK19, and FAK, along with phalloidin and Hoechst staining. We identified the luminal and basal/myoepithelial populations and actively dividing RMECs. In inbred rats susceptible to mammary carcinoma development, we quantified the changes in differentiation of the RMEC populations at 1, 2, and 4 weeks after exposure to mammary carcinogens DMBA and MNU. DMBA exposure did not alter the percentage of basal or luminal cells, but upregulated CD49f (Integrin α6) expression and increased cell cycle activity. MNU exposure resulted in a temporary disruption of the luminal/basal ratio and no CD49f upregulation. When comparing DMBA- or MNU-induced mammary carcinomas, the RMEC differentiation profiles are indistinguishable. The carcinomas compared with mammary glands from untreated rats, showed upregulation of CD29 (Integrin β1) and CD49f expression, increased FAK (focal adhesion kinase) activation especially in the CD29hi population, and decreased CD61 (Integrin β3) expression. This study provides quantitative insight into the protein expression phenotypes underlying RMEC differentiation. The results highlight distinct RMEC differentiation etiologies of DMBA and MNU exposure, while the resulting carcinomas have similar RMEC differentiation profiles. The methodology and data will enhance rat mammary carcinogenesis models in the study of the role of epithelial cell differentiation in breast cancer