Cleanroom Energy Optimization Methods

The design and operation of semiconductor cleanrooms play an important role in the advancement of many of today's technology needs as the use of microelectronic products become engrained in our society. Cleanroom construction has averaged double-digit growth through the 1990's and into early 2000. Advances in factory technology have placed demands on all aspects of cleanroom design, construction, materials, and so on. Much of this growth has been centered in hot climate of the sunbelt. Energy efficiency has not been a high priority for the semiconductor industry in the past, since costs related to this issue have historically represented a relatively small percentage of overall operating costs. From a Semiconductor Industry website in October 2001: “Slashing energy consumption has become an unquestioned semiconductor industry goal.” Semiconductor Industry Association's International Technology Roadmap for Semiconductors has energy goals on the roadmap for power per unit of silicon processed; the World Semiconductor Council has policies for energy reduction, numerous publications, workshops, and seminars touting need for energy reduction. There is no longer any question that cutting energy usage makes good business sense, especially given rate increases being experienced in many parts of the country. This paper will present some of the methods being used by a multi-national semiconductor company to change the way they design and build cleanrooms with a focus on resource conservation, energy conservation methods, and cost of ownership. Various clean air and energy management scenarios will be compared with their potential for energy savings

Building Energy Use and Conservation in Cycle VIII of the Texas Institutional Conservation Program

Sixty-two technical assistance (energy audit) reports by twelve different consulting firms representing fifteen independent school districts, nine hospitals, and five colleges have been reviewed to assess energy use characteristics and recommended energy saving measures. Such measures include both maintenance and operation (H&O) measures (generally regarded as "low-cost, no-cost") and energy conservation (ECH) measures (generally more expensive and requiring outside skills). Implementation cost, annual savings of energy and costs, and paybacks were reported for all M&Os and ECHs. Measures were broken down by the consulting firms according to energy use characteristics and categories, and it was determined that average costs for electricity and gas, before implementation of M&Os and ECHs, were $0.0596/KWH and$4.85/MMBTU respectively. The total implementation cost and projected annual savings for the M&Os are $73,000 and$223,000 respectively, yielding a four-month payback. The corresponding results for implementation of ECHs are $2,232,000 and$555,000, resulting in a four-year payback. Also, some obvious problems in the preparation of technical assistance reports along with the general background and implementation of the Institutional Conservation Program in Texas, resulting from the National Energy Act of 1978, are discussed

The use of gamma-irradiation and ultraviolet-irradiation in the preparation of human melanoma cells for use in autologous whole-cell vaccines

<p>Abstract</p> <p>Background</p> <p>Human cancer vaccines incorporating autologous tumor cells carry a risk of implantation and subsequent metastasis of viable tumor cells into the patient who is being treated. Despite the fact that the melanoma cell preparations used in a recent vaccine trial (Mel37) were gamma-irradiated (200 Gy), approximately 25% of the preparations failed quality control release criteria which required that the irradiated cells incorporate ³H-thymidine at no more than 5% the level seen in the non-irradiated cells. We have, therefore, investigated ultraviolet (UV)-irradiation as a possible adjunct to, or replacement for gamma-irradiation.</p> <p>Methods</p> <p>Melanoma cells were gamma- and/or UV-irradiated. ³H-thymidine uptake was used to assess proliferation of the treated and untreated cells. Caspase-3 activity and DNA fragmentation were measured as indicators of apoptosis. Immunohistochemistry and Western blot analysis was used to assess antigen expression.</p> <p>Results</p> <p>UV-irradiation, either alone or in combination with gamma-irradiation, proved to be extremely effective in controlling the proliferation of melanoma cells. In contrast to gamma-irradiation, UV-irradiation was also capable of inducing significant levels of apoptosis. UV-irradiation, but not gamma-irradiation, was associated with the loss of tyrosinase expression. Neither form of radiation affected the expression of gp100, MART-1/MelanA, or S100.</p> <p>Conclusion</p> <p>These results indicate that UV-irradiation may increase the safety of autologous melanoma vaccines, although it may do so at the expense of altering the antigenic profile of the irradiated tumor cells.</p

Crk and CrkL adaptor proteins: networks for physiological and pathological signaling

The Crk adaptor proteins (Crk and CrkL) constitute an integral part of a network of essential signal transduction pathways in humans and other organisms that act as major convergence points in tyrosine kinase signaling. Crk proteins integrate signals from a wide variety of sources, including growth factors, extracellular matrix molecules, bacterial pathogens, and apoptotic cells. Mounting evidence indicates that dysregulation of Crk proteins is associated with human diseases, including cancer and susceptibility to pathogen infections. Recent structural work has identified new and unusual insights into the regulation of Crk proteins, providing a rationale for how Crk can sense diverse signals and produce a myriad of biological responses

Inhibition of focal adhesion kinase suppresses the adverse phenotype of endocrine-resistant breast cancer cells and improves endocrine response in endocrine-sensitive cells

International audienceAcquired resistance to endocrine therapy in breast cancer is a major clinical problem. Previous reports have demonstrated that cell models of acquired endocrine resistance have altered cell–matrix adhesion and a highly migratory phenotype, features which may impact on tumour spread in vivo. Focal adhesion kinase (FAK) is an intracellular kinase that regulates signalling pathways central to cell adhesion, migration and survival and its expression is frequently deregulated in breast cancer. In this study, we have used the novel FAK inhibitor PF573228 to address the role of FAK in the development of endocrine resistance. Whilst total-FAK expression was similar between endocrine-sensitive and endocrine-resistant MCF7 cells, FAK phosphorylation status (Y397 or Y861) was altered in resistance. PF573228 promoted a dose-dependent inhibition of FAK phosphorylation at Y397 but did not affect other FAK activation sites (pY407, pY576 and pY861). Endocrine-resistant cells were more sensitive to these inhibitory effects versus MCF7 (mean IC for FAK pY397 inhibition: 0.43 μM, 0.05 μM and 0.13 μM for MCF7, TamR and FasR cells, respectively). Inhibition of FAK pY397 was associated with a reduction in TamR and FasR adhesion to, and migration over, matrix components. PF573228 as a single agent (0–1 μM) did not affect the growth of MCF7 cells or their endocrine-resistant counterparts. However, treatment of endocrine-sensitive cells with PF573228 and tamoxifen combined resulted in greater suppression of proliferation versus single agent treatment. Together these data suggest the importance of FAK in the process of endocrine resistance, particularly in the development of an aggressive, migratory cell phenotype and demonstrate the potential to improve endocrine response through combination treatment

BCAR3 Regulates Src/p130Cas Association, Src Kinase Activity, and Breast Cancer Adhesion Signaling*

The nonreceptor protein-tyrosine kinase c-Src is frequently overexpressed and/or activated in a variety of cancers, including those of the breast. Several heterologous binding partners of c-Src have been shown to regulate its catalytic activity by relieving intramolecular autoinhibitory interactions. One such protein, p130Cas (Cas), is expressed at high levels in both breast cancer cell lines and breast tumors, providing a potential mechanism for c-Src activation in breast cancers. The Cas-binding protein BCAR3 (breast cancer antiestrogen resistance-3) is expressed at high levels in invasive breast cancer cell lines, and this molecule has previously been shown to coordinate with Cas to increase c-Src activity in COS-1 cells. In this study, we show for the first time using gain- and loss-of-function approaches that BCAR3 regulates c-Src activity in the endogenous setting of breast cancer cells. We further show that BCAR3 regulates the interaction between Cas and c-Src, both qualitatively as well as quantitatively. Finally, we present evidence that the coordinated activity of these proteins contributes to breast cancer cell adhesion signaling and spreading. Based on these data, we propose that the c-Src/Cas/BCAR3 signaling axis is a prominent regulator of c-Src activity, which in turn controls cell behaviors that lead to aggressive and invasive breast tumor phenotypes