Analysis of CNL of CCSD-MH

Luo, M; Pan, Haojie; Zhao, Yuechun; Zhang, H

doi:10.1201/noe0415451369.ch17

Cited by 2 publications

(2 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These stresses are smaller than those calculated for thermal mismatch of the PZT and substrate at room temperature. This stress relaxation has been noted in other works [22]. The variation of residual stress affects many aspects of generator performance including compliance, strain at failure and resonance frequency.…”

Section: Resultsmentioning

confidence: 87%

Coupling bulge testing and nanoindention to characterize materials properties of bulk micromachined structures

et al. 2005

View full text Add to dashboard Cite

Nanoindentation and the continuous stiffness method was used to obtain the elastic modulus of Pb(Zr x Ti 1)x )O 3 (X:1)XPZT) thin films that can be utilized in high aspect ratio structures. PZT films were deposited onto bulk micromachined silicon wafers by sol-gel deposition and two annealing treatments. Conventional annealing produced films that had an elastic modulus of 80 GPa for both the 52:48 and 40:60 PZT, while a 52:48 PZT deposited using rapid thermal annealing demonstrated a modulus of 70 GPa. These moduli allowed accurate stress measurements of both the composite membranes by bulge testing and also the individual PZT layers by X-ray diffraction. The residual tensile stress in the PZT film ranged from 190 to 400 MPa. Residual stresses were shown to affect both the strain to failure and the resonance frequency of the membrane generators. The applied strain to failure decreased with increasing residual stress. A tungsten underlayer was added to reduce the composite residual stress and increase the compliance, lowering the resonant frequency from 23 to 18 kHz.

show abstract

Section: Resultsmentioning

confidence: 87%

Coupling bulge testing and nanoindention to characterize materials properties of bulk micromachined structures

et al. 2005

View full text Add to dashboard Cite

show abstract

“…The BCR-ABL1 t(9;22) fusion transcript was validated in each cell line, and several other fusions were also observed (including e.g. the known fusion NUP214-XKR3 t(9;22) (26)(27) ) ( Supplementary Table S1). To examine the BCR-ABL1 transcripts for potential drug-resistant point mutations, a custom version of the human hg19 genome was built to incorporate the BCR-ABL1 fusion gene, map the specific fusion transcripts and identify whether point mutations in the gatekeeper residue were associated with inhibitor resistance.…”

Section: Whole Transcriptome Analysis: Resistance Is Mediated By Pathmentioning

confidence: 99%

Multiomic Profiling of Tyrosine Kinase Inhibitor-Resistant K562 Cells Suggests Metabolic Reprogramming To Promote Cell Survival

et al. 2019

View full text Add to dashboard Cite

Resistance to chemotherapy can occur through a wide variety of mechanisms. Resistance to tyrosine kinase inhibitors (TKIs) often arises from kinase mutations-however, "off-target" resistance occurs but is poorly understood. Previously, we established cell line resistance models for three TKIs used in chronic myeloid leukemia treatment, and found that resistance was not attributed entirely to failure of kinase inhibition. Here, we performed global, integrated proteomic and transcriptomic profiling of these cell lines to describe mechanisms of resistance at the protein and gene expression level. We used whole transcriptome sequencing and SWATH-based dataindependent acquisition mass spectrometry (DIA-MS), which does not require isotopic labels and provides quantitative measurements of proteins in a comprehensive, unbiased fashion. The proteomic and transcriptional data were correlated to generate an integrated understanding of the gene expression and protein alterations associated with TKI resistance. We defined mechanisms of resistance and two novel markers, CA1 and alpha-synuclein, that were common to all TKIs tested. Resistance to all of the TKIs was associated with oxidative stress responses, hypoxia signatures, and apparent metabolic reprogramming of the cells. Metabolite profiling and glucose-dependence experiments showed that resistant cells had routed their metabolism through glycolysis (particularly through the pentose phosphate pathway) and exhibited disruptions in mitochondrial metabolism. These experiments are the first to report a global, integrated proteomic, transcriptomic and metabolic analysis of TKI resistance. These data suggest that although the mechanisms are complex, targeting metabolic pathways along with TKI treatment may overcome pan-TKI resistance.

show abstract

Analysis of CNL of CCSD-MH

Cited by 2 publications

References 1 publication

Coupling bulge testing and nanoindention to characterize materials properties of bulk micromachined structures

Coupling bulge testing and nanoindention to characterize materials properties of bulk micromachined structures

Multiomic Profiling of Tyrosine Kinase Inhibitor-Resistant K562 Cells Suggests Metabolic Reprogramming To Promote Cell Survival

Contact Info

Product

Resources

About