66 research outputs found

    Measurement of the Coefficient of Thermal Expansion of Superconducting Thin Films Using Powder X-Ray Diffraction

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    The High Density Electronics Center (HiDEC) at the University of Arkansas, Fayetteville is developing the technology for High Temperature Superconductor Multi-Chip Modules (HTSC-MCM\u27s). As part of this work, we are looking at the mechanical properties of HTSC materials. An important mechanical property which influences the mechanical integrity of the hybrid MCMis the coefficient of thermal expansion (CTE) of the HTSC films. As a first step in developing a procedure for the determination of the CTE of HTSC materials, the lattice parameters and the CTE of an alpha-alumina substrate have been determined by powder x-ray diffraction technique. An extension of this technique applicable to HTSC materials is presented

    Hotspot ESR1 mutations are multimodal and contextual modulators of breast cancer metastasis

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    Constitutively active estrogen receptor α (ER/ESR1) mutations have been identified in approximately one-third of ER+ metastatic breast cancers. Although these mutations are known as mediators of endocrine resistance, their potential role in promoting metastatic disease has not yet been mechanistically addressed. In this study, we show the presence of ESR1 mutations exclusively in distant but not local recurrences in five independent breast cancer cohorts. In concordance with transcriptomic profiling of ESR1-mutant tumors, genome-edited ESR1 Y537S and D538G-mutant cell models exhibited a reprogrammed cell adhesive gene network via alterations in desmosome/gap junction genes and the TIMP3/MMP axis, which functionally conferred enhanced cell–cell contacts while decreasing cell-extracellular matrix adhesion. In vivo studies showed ESR1-mutant cells were associated with larger multicellular circulating tumor cell (CTC) clusters with increased compactness compared with ESR1 wild-type CTCs. These preclinical findings translated to clinical observations, where CTC clusters were enriched in patients with ESR1-mutated metastatic breast cancer. Conversely, context-dependent migratory phenotypes revealed cotargeting of Wnt and ER as a vulnerability in a D538G cell model. Mechanistically, mutant ESR1 exhibited noncanonical regulation of several metastatic pathways, including secondary transcriptional regulation and de novo FOXA1-driven chromatin remodeling. Collectively, these data provide evidence for ESR1 mutation–modulated metastasis and suggest future therapeutic strategies for targeting ESR1-mutant breast cancer

    Characterization of Corrosion Products in RTPF and All-Aluminum Microchannel Heat Exchangers

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    Failure Analysis of Al 356-T6 Clutch Lever

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    Application of Fourier transform infrared spectroscopy in cement Alkali quantification

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    Investigation of Failed Pin Carrier Plate for the Anti-Rotation Device in a Motor

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