Publications by authors named "Alex Barrett"

2 Publications

  • Page 1 of 1

T2*-weighted MRI produces viable fetal "Black-Bone" contrast with significant benefits when compared to current sequences.

Br J Radiol 2021 Jul 21;94(1123):20200940. Epub 2021 May 21.

Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, UK.

Objectives: Fetal "black bone" MRI could be useful in the diagnosis of various skeletal conditions during pregnancy without exposure to ionizing radiation. Previously suggested susceptibility-weighted imaging (SWI) is not available in the suggested form on all scanners leading to long imaging times that are susceptible to motion artefacts. We aimed to assess if an optimized T2*-weighted GRE sequence can provide viable "black bone" contrast and compared it to other sequences in the literature.

Methods: A retrospective study was conducted on 17 patients who underwent fetal MRI. Patients were imaged with an optimized T2*-weighted GRE sequence, as well as at least one other "black-bone" sequence. Image quality was scored by four blinded observers on a five-point scale.

Results: The T2*-weighted GRE sequence offered adequate to excellent image quality in 63% of cases and scored consistently higher than the three other comparison sequences when comparing images from the same patient. Image quality was found to be dependent on gestational age with good image quality achieved on almost all patients after 26 weeks.

Conclusions: T2*-weighted GRE imaging can provide adequate fetal "black bone" contrast and performs at least as well as other sequences in the literature due to good bone to soft tissue contrast and minimal motion artefacts.

Advances In Knowledge: T2*-weighted fetal "black-bone" imaging can provide excellent bone to soft tissue contrast without using ionizing radiation. It is as good as other "black bone" sequences and may be simpler and more widely implemented, with less motion artefacts.
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http://dx.doi.org/10.1259/bjr.20200940DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8248208PMC
July 2021

Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression.

Nat Med 2016 05 18;22(5):497-505. Epub 2016 Apr 18.

Center for Bioengineering and Tissue Regeneration, Department of Surgery, University of California, San Francisco, San Francisco, California, USA.

Fibrosis compromises pancreatic ductal carcinoma (PDAC) treatment and contributes to patient mortality, yet antistromal therapies are controversial. We found that human PDACs with impaired epithelial transforming growth factor-β (TGF-β) signaling have high epithelial STAT3 activity and develop stiff, matricellular-enriched fibrosis associated with high epithelial tension and shorter patient survival. In several KRAS-driven mouse models, both the loss of TGF-β signaling and elevated β1-integrin mechanosignaling engaged a positive feedback loop whereby STAT3 signaling promotes tumor progression by increasing matricellular fibrosis and tissue tension. In contrast, epithelial STAT3 ablation attenuated tumor progression by reducing the stromal stiffening and epithelial contractility induced by loss of TGF-β signaling. In PDAC patient biopsies, higher matricellular protein and activated STAT3 were associated with SMAD4 mutation and shorter survival. The findings implicate epithelial tension and matricellular fibrosis in the aggressiveness of SMAD4 mutant pancreatic tumors and highlight STAT3 and mechanics as key drivers of this phenotype.
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http://dx.doi.org/10.1038/nm.4082DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860133PMC
May 2016
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