Calibration of the Advanced LIGO detectors is the quantification of the detectors’ response to gravitational waves. Gravitational waves incident on the detectors cause phase shifts in the ...interferometer laser light which are read out as intensity fluctuations at the detector output. Understanding this detector response to gravitational waves is crucial to producing accurate and precise gravitational wave strain data. Estimates of binary black hole and neutron star parameters and tests of general relativity require well-calibrated data, as miscalibrations will lead to biased results. We describe the method of producing calibration uncertainty estimates for both LIGO detectors in the first and second observing runs.
Calibration of the Advanced LIGO detectors is the quantification of the detectors' response to gravitational waves. Gravitational waves incident on the detectors cause phase shifts in the ...interferometer laser light which are read out as intensity fluctuations at the detector output. Understanding this detector response to gravitational waves is crucial to producing accurate and precise gravitational wave strain data. Estimates of binary black hole and neutron star parameters and tests of general relativity require well-calibrated data, as miscalibrations will lead to biased results. We describe the method of producing calibration uncertainty estimates for both LIGO detectors in the first and second observing runs.
Human adenocarcinomas commonly harbor mutations in the KRAS and MYC proto-oncogenes and the TP53 tumor suppressor gene. All three genetic lesions are potentially pro-angiogenic, as they sustain ...production of vascular endothelial growth factor (VEGF). Yet Kras-transformed mouse colonocytes lacking p53 formed indolent, poorly vascularized tumors, whereas additional transduction with a Myc-encoding retrovirus promoted vigorous vascularization and growth. In addition, VEGF levels were unaffected by Myc, but enhanced neovascularization correlated with downregulation of anti-angiogenic thrombospondin-1 (Tsp1) and related proteins, such as connective tissue growth factor (CTGF). Both Tsp1 and CTGF are predicted targets for repression by the miR-17-92 microRNA cluster, which was upregulated in colonocytes coexpressing K-Ras and c-Myc. Indeed, miR-17-92 knockdown with antisense 2′-O-methyl oligoribonucleotides partly restored Tsp1 and CTGF expression; in addition, transduction of Ras-only cells with a miR-17-92-encoding retrovirus reduced Tsp1 and CTGF levels. Notably, miR-17-92-transduced cells formed larger, better-perfused tumors. These findings establish a role for microRNAs in non-cell-autonomous Myc-induced tumor phenotypes.
Celotno besedilo
Dostopno za:
DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
PDF
