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1. Momentum-space imaging of ultra-thin electron liquids in delta-doped silicon

Author

Constantinou, Procopios, Stock, Taylor J. Z., Crane, Eleanor, Kölker, Alexander, van Loon, Marcel, Li, Juerong, Fearn, Sarah, Bornemann, Henric, D'Anna, Nicolò, Fisher, Andrew J., Strocov, Vladimir N., Aeppli, Gabriel, Curson, Neil J., and Schofield, Steven R.

Subjects
Condensed Matter - Materials Science, Condensed Matter - Mesoscale and Nanoscale Physics, Quantum Physics
Abstract

Two-dimensional dopant layers ($\delta$-layers) in semiconductors provide the high-mobility electron liquids (2DELs) needed for nanoscale quantum-electronic devices. Key parameters such as carrier densities, effective masses, and confinement thicknesses for 2DELs have traditionally been extracted from quantum magnetotransport. In principle, the parameters are immediately readable from the one-electron spectral function that can be measured by angle-resolved photoemission spectroscopy (ARPES). Here, buried 2DEL $\delta$-layers in silicon are measured with soft X-ray (SX) ARPES to obtain detailed information about their filled conduction bands and extract device-relevant properties. This study takes advantage of the larger probing depth and photon energy range of SX-ARPES relative to vacuum ultraviolet (VUV) ARPES to accurately measure the $\delta$-layer electronic confinement. The measurements are made on ambient-exposed samples and yield extremely thin ($\approx 1$ $nm$) and dense ($\approx$ $10^{14}$ $cm^2$) 2DELs. Critically, this method is used to show that $\delta$-layers of arsenic exhibit better electronic confinement than $\delta$-layers of phosphorus fabricated under identical conditions., Comment: Published in Advanced Science as a Research Article

Published
2023
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10. FXR inhibition may protect from SARS-CoV-2 infection by reducing ACE2

Author

Brevini, Teresa, Maes, Mailis, Webb, Gwilym J., John, Binu V., Fuchs, Claudia D., Buescher, Gustav, Wang, Lu, Griffiths, Chelsea, Brown, Marnie L., Scott, III, William E., Pereyra-Gerber, Pehuén, Gelson, William T. H., Brown, Stephanie, Dillon, Scott, Muraro, Daniele, Sharp, Jo, Neary, Megan, Box, Helen, Tatham, Lee, Stewart, James, Curley, Paul, Pertinez, Henry, Forrest, Sally, Mlcochova, Petra, Varankar, Sagar S., Darvish-Damavandi, Mahnaz, Mulcahy, Victoria L., Kuc, Rhoda E., Williams, Thomas L., Heslop, James A., Rossetti, Davide, Tysoe, Olivia C., Galanakis, Vasileios, Vila-Gonzalez, Marta, Crozier, Thomas W. M., Bargehr, Johannes, Sinha, Sanjay, Upponi, Sara S., Fear, Corrina, Swift, Lisa, Saeb-Parsy, Kourosh, Davies, Susan E., Wester, Axel, Hagström, Hannes, Melum, Espen, Clements, Darran, Humphreys, Peter, Herriott, Jo, Kijak, Edyta, Cox, Helen, Bramwell, Chloe, Valentijn, Anthony, Illingworth, Christopher J. R., Dahman, Bassam, Bastaich, Dustin R., Ferreira, Raphaella D., Marjot, Thomas, Barnes, Eleanor, Moon, Andrew M., Barritt, IV, Alfred S., Gupta, Ravindra K., Baker, Stephen, Davenport, Anthony P., Corbett, Gareth, Gorgoulis, Vassilis G., Buczacki, Simon J. A., Lee, Joo-Hyeon, Matheson, Nicholas J., Trauner, Michael, Fisher, Andrew J., Gibbs, Paul, Butler, Andrew J., Watson, Christopher J. E., Mells, George F., Dougan, Gordon, Owen, Andrew, Lohse, Ansgar W., Vallier, Ludovic, and Sampaziotis, Fotios

Published
2023
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13. Nucleoside Analogs in ADAR Guide Strands Enable Editing at 5′-G A Sites.

Author

Manjunath, Aashrita, Cheng, Jeff, Campbell, Kristen B, Jacobsen, Casey S., Mendoza, Herra G., Bierbaum, Leila, Jauregui-Matos, Victorio, Doherty, Erin E., Fisher, Andrew J., and Beal, Peter A.

Subjects
CATALYTIC RNA, DOUBLE-stranded RNA, RNA editing, SUBSTRATES (Materials science), NUCLEOTIDES
Abstract

Adenosine Deaminases Acting on RNA (ADARs) are members of a family of RNA editing enzymes that catalyze the conversion of adenosine into inosine in double-stranded RNA (dsRNA). ADARs' selective activity on dsRNA presents the ability to correct mutations at the transcriptome level using guiding oligonucleotides. However, this approach is limited by ADARs' preference for specific sequence contexts to achieve efficient editing. Substrates with a guanosine adjacent to the target adenosine in the 5′ direction (5′-GA) are edited less efficiently compared to substrates with any other canonical nucleotides at this position. Previous studies showed that a G/purine mismatch at this position results in more efficient editing than a canonical G/C pair. Herein, we investigate a series of modified oligonucleotides containing purine or size-expanded nucleoside analogs on guide strands opposite the 5′-G (−1 position). The results demonstrate that modified adenosine and inosine analogs enhance editing at 5′-GA sites. Additionally, the inclusion of a size-expanded cytidine analog at this position improves editing over a control guide bearing cytidine. High-resolution crystal structures of ADAR:/RNA substrate complexes reveal the manner by which both inosine and size-expanded cytidine are capable of activating editing at 5′-GA sites. Further modification of these altered guide sequences for metabolic stability in human cells demonstrates that the incorporation of specific purine analogs at the −1 position significantly improves editing at 5′-GA sites. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Altered TMPRSS2 usage by SARS-CoV-2 Omicron impacts infectivity and fusogenicity

Author

Meng, Bo, Abdullahi, Adam, Ferreira, Isabella A. T. M., Goonawardane, Niluka, Saito, Akatsuki, Kimura, Izumi, Yamasoba, Daichi, Gerber, Pehuén Pereyra, Fatihi, Saman, Rathore, Surabhi, Zepeda, Samantha K., Papa, Guido, Kemp, Steven A., Ikeda, Terumasa, Toyoda, Mako, Tan, Toong Seng, Kuramochi, Jin, Mitsunaga, Shigeki, Ueno, Takamasa, Shirakawa, Kotaro, Takaori-Kondo, Akifumi, Brevini, Teresa, Mallery, Donna L., Charles, Oscar J., Bowen, John E., Joshi, Anshu, Walls, Alexandra C., Jackson, Laurelle, Martin, Darren, Smith, Kenneth G. C., Bradley, John, Briggs, John A. G., Choi, Jinwook, Madissoon, Elo, Meyer, Kerstin B., Mlcochova, Petra, Ceron-Gutierrez, Lourdes, Doffinger, Rainer, Teichmann, Sarah A., Fisher, Andrew J., Pizzuto, Matteo S., de Marco, Anna, Corti, Davide, Hosmillo, Myra, Lee, Joo Hyeon, James, Leo C., Thukral, Lipi, Veesler, David, Sigal, Alex, Sampaziotis, Fotios, Goodfellow, Ian G., Matheson, Nicholas J., Sato, Kei, and Gupta, Ravindra K.

Published
2022
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16. Pharmacological characterisation of GSK3335103, an oral αvβ6 integrin small molecule RGD-mimetic inhibitor for the treatment of fibrotic disease

Author

Wilkinson, Alex L., John, Alison E., Barrett, John W., Gower, E., Morrison, Valerie S., Man, Yim, Pun, K. Tao, Roper, James A., Luckett, Jeni C., Borthwick, Lee A., Barksby, Ben S., Burgoyne, Rachel A., Barnes, Rory, Fisher, Andrew J., Procopiou, Panayiotis A., Hatley, Richard J.D., Barrett, Tim N., Marshall, Richard P., Macdonald, Simon J.F., Jenkins, R. Gisli, and Slack, Robert J.

Published
2021
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18. The circadian clock protein REVERBα inhibits pulmonary fibrosis development

Author

Cunningham, Peter S., Meijer, Peter, Nazgiewicz, Alicja, Anderson, Simon G., Borthwick, Lee A., Bagnall, James, Kitchen, Gareth B., Lodyga, Monika, Begley, Nicola, Venkateswaran, Rajamiyer V., Shah, Rajesh, Mercer, Paul F., Durrington, Hannah J., Henderson, Neil C., Piper-Hanley, Karen, Fisher, Andrew J., Chambers, Rachel C., Bechtold, David A., Gibbs, Julie E., Loudon, Andrew S., Rutter, Martin K., Hinz, Boris, Ray, David W., and Blaikley, John F.

Published
2020

20. Novel delivery of cellular therapy to reduce ischemia reperfusion injury in kidney transplantation

Author

Thompson, Emily R., Bates, Lucy, Ibrahim, Ibrahim K., Sewpaul, Avinash, Stenberg, Ben, McNeill, Andrew, Figueiredo, Rodrigo, Girdlestone, Tom, Wilkins, Georgina C., Wang, Lu, Tingle, Samuel J., Scott III, William E., de Paula Lemos, Henrique, Mellor, Andrew L., Roobrouck, Valerie D., Ting, Anthony E., Hosgood, Sarah A., Nicholson, Michael L., Fisher, Andrew J., Ali, Simi, Sheerin, Neil S., and Wilson, Colin H.

Published
2021
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21. Directed Evolution of a Selective and Sensitive Serotonin Sensor via Machine Learning

Author

Unger, Elizabeth K., Keller, Jacob P., Altermatt, Michael, Liang, Ruqiang, Matsui, Aya, Dong, Chunyang, Hon, Olivia J., Yao, Zi, Sun, Junqing, Banala, Samba, Flanigan, Meghan E., Jaffe, David A., Hartanto, Samantha, Carlen, Jane, Mizuno, Grace O., Borden, Phillip M., Shivange, Amol V., Cameron, Lindsay P., Sinning, Steffen, Underhill, Suzanne M., Olson, David E., Amara, Susan G., Temple Lang, Duncan, Rudnick, Gary, Marvin, Jonathan S., Lavis, Luke D., Lester, Henry A., Alvarez, Veronica A., Fisher, Andrew J., Prescher, Jennifer A., Kash, Thomas L., Yarov-Yarovoy, Vladimir, Gradinaru, Viviana, Looger, Loren L., and Tian, Lin

Published
2020
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22. c-Rel orchestrates energy-dependent epithelial and macrophage reprogramming in fibrosis

Author

Leslie, Jack, Macia, Marina García, Luli, Saimir, Worrell, Julie C., Reilly, William J., Paish, Hannah L., Knox, Amber, Barksby, Ben S., Gee, Lucy M., Zaki, Marco Y. W., Collins, Amy L., Burgoyne, Rachel A., Cameron, Rainie, Bragg, Charlotte, Xu, Xin, Chung, Git W., Brown, Colin D. A., Blanchard, Andrew D., Nanthakumar, Carmel B., Karsdal, Morten, Robinson, Stuart M., Manas, Derek M., Sen, Gourab, French, Jeremy, White, Steven A., Murphy, Sandra, Trost, Matthias, Zakrzewski, Johannes L., Klein, Ulf, Schwabe, Robert F., Mederacke, Ingmar, Nixon, Colin, Bird, Tom, Teuwen, Laure-Anne, Schoonjans, Luc, Carmeliet, Peter, Mann, Jelena, Fisher, Andrew J., Sheerin, Neil S., Borthwick, Lee A., Mann, Derek A., and Oakley, Fiona

Published
2020
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28. Survival in portopulmonary hypertension: Outcomes of the United Kingdom National Pulmonary Arterial Hypertension Registry

Author

Sithamparanathan, Sasiharan, Nair, Arun, Thirugnanasothy, Logan, Coghlan, J. Gerry, Condliffe, Robin, Dimopoulos, Konstantinos, Elliot, Charlie A, Fisher, Andrew J., Gaine, Sean, Gibbs, J. Simon R., Gatzoulis, Michael A., E. Handler, Clive, Howard, Luke S., Johnson, Martin, Kiely, David G., Lordan, James L., Peacock, Andrew J., Pepke-Zaba, Joanna, Schreiber, Benjamin E., Sheares, Karen K.K., Wort, Stephen J., and Corris, Paul A.

Published
2017
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30. Translational pharmacology of an inhaled small molecule αvβ6 integrin inhibitor for idiopathic pulmonary fibrosis

Author

John, Alison E., Graves, Rebecca H., Pun, K. Tao, Vitulli, Giovanni, Forty, Ellen J., Mercer, Paul F., Morrell, Josie L., Barrett, John W., Rogers, Rebecca F., Hafeji, Maryam, Bibby, Lloyd I., Gower, Elaine, Morrison, Valerie S., Man, Yim, Roper, James A., Luckett, Jeni C., Borthwick, Lee A., Barksby, Ben S., Burgoyne, Rachel A., Barnes, Rory, Le, Joelle, Flint, David J., Pyne, Susan, Habgood, Anthony, Organ, Louise A., Joseph, Chitra, Edwards-Pritchard, Rochelle C., Maher, Toby M., Fisher, Andrew J., Gudmann, Natasja Stæhr, Leeming, Diana J., Chambers, Rachel C., Lukey, Pauline T., Marshall, Richard P., Macdonald, Simon J. F., Jenkins, R. Gisli, and Slack, Robert J.

Published
2020
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31. A Split-Lung Ex Vivo Perfusion Model for Time- and Cost-Effective Evaluation of Therapeutic Interventions to the Human Donor Lung.

Author

Chilvers, Nicholas J. S., Gilmour, Jenny, Brown, Marnie L., Bates, Lucy, Chong Yun Pang, Henning Pauli, Dark, John, and Fisher, Andrew J.

Subjects
PERFUSION, PARALLEL electric circuits, LUNGS, PULMONARY edema, BLOOD gases
Abstract

With the ongoing shortage of donor lungs, ex vivo lung perfusion (EVLP) offers the opportunity for objective assessment and potential therapeutic repair of marginal organs. There is a need for robust research on EVLP interventions to increase the number of transplantable organs. The use of human lungs, which have been declined for transplant, for these studies is preferable to animal organs and is indeed essential if clinical translation is to be achieved. However, experimental human EVLP is time-consuming and expensive, limiting the rate at which promising interventions can be assessed. A split-lung EVLP model, which allows stable perfusion and ventilation of two single lungs from the same donor, offers advantages scientifically, financially and in time to yield results. Identical parallel circuits allow one to receive an intervention and the other to act as a control, removing inter-donor variation between study groups. Continuous hemodynamic and airway parameters are recorded and blood gas, perfusate, and tissue sampling are facilitated. Pulmonary edema is assessed directly using ultrasound, and indirectly using the lung tissue wet:dry ratio. Evans blue dye leaks into the tissue and can quantify vascular endothelial permeability. The split-lung ex vivo perfusion model offers a cost-effective, reliable platform for testing therapeutic interventions with relatively small sample sizes. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease

Author

Brightling, Christopher E., Davies, Donna E., Finch, Donna K., Fisher, Andrew J., Gaw, Alasdair, Knox, Alan J., Mayer, Ruth J., Polkey, Michael, Salmon, Michael, Singh, David, Wiegman, Coen H., Michaeloudes, Charalambos, Haji, Gulammehdi, Narang, Priyanka, Clarke, Colin J., Russell, Kirsty E., Bao, Wuping, Pavlidis, Stelios, Barnes, Peter J., Kanerva, Justin, Bittner, Anton, Rao, Navin, Murphy, Michael P., Kirkham, Paul A., Chung, Kian Fan, and Adcock, Ian M.

Published
2015
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41. Momentum‐Space Imaging of Ultra‐Thin Electron Liquids in δ‐Doped Silicon.

Author

Constantinou, Procopios, Stock, Taylor J. Z., Crane, Eleanor, Kölker, Alexander, van Loon, Marcel, Li, Juerong, Fearn, Sarah, Bornemann, Henric, D'Anna, Nicolò, Fisher, Andrew J., Strocov, Vladimir N., Aeppli, Gabriel, Curson, Neil J., and Schofield, Steven R.

Subjects
LIQUID silicon, SOFT X rays, PHOTOELECTRON spectroscopy, CONDUCTION bands, NANOELECTROMECHANICAL systems, CARRIER density, ELECTRONS, MOMENTUM transfer
Abstract

Two‐dimensional dopant layers (δ‐layers) in semiconductors provide the high‐mobility electron liquids (2DELs) needed for nanoscale quantum‐electronic devices. Key parameters such as carrier densities, effective masses, and confinement thicknesses for 2DELs have traditionally been extracted from quantum magnetotransport. In principle, the parameters are immediately readable from the one‐electron spectral function that can be measured by angle‐resolved photoemission spectroscopy (ARPES). Here, buried 2DEL δ‐layers in silicon are measured with soft X‐ray (SX) ARPES to obtain detailed information about their filled conduction bands and extract device‐relevant properties. This study takes advantage of the larger probing depth and photon energy range of SX‐ARPES relative to vacuum ultraviolet (VUV) ARPES to accurately measure the δ‐layer electronic confinement. The measurements are made on ambient‐exposed samples and yield extremely thin (< 1 nm) and dense (≈1014 cm−2) 2DELs. Critically, this method is used to show that δ‐layers of arsenic exhibit better electronic confinement than δ‐layers of phosphorus fabricated under identical conditions. [ABSTRACT FROM AUTHOR]

Published
2023
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42. Identification of a protein expression signature distinguishing early from organising diffuse alveolar damage in COVID-19 patients.

Author

Ashwin, Helen, Milross, Luke, Wilson, Julie, Majo, Joaquim, Tsz Hang Lee, Jimmy, Calder, Grant, Hunter, Bethany, James, Sally, Lagos, Dimitris, Signoret, Nathalie, Filby, Andrew, Bayraktar, Omer Ali, Fisher, Andrew J., and Kaye, Paul M.

Subjects
PROTEOMICS, COVID-19, PROTEIN expression, MYELOID-derived suppressor cells
Published
2023
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49. Downregulation of MALAT1 is a hallmark of tissue and peripheral proliferative T cells in COVID-19.

Author

Dey, Shoumit, Ashwin, Helen, Milross, Luke, Hunter, Bethany, Majo, Joaquim, Filby, Andrew J, Fisher, Andrew J, Kaye, Paul M, and Lagos, Dimitris

Subjects
T cells, COVID-19 pandemic, LINCRNA, GENE expression, TH1 cells
Abstract

T cells play key protective but also pathogenic roles in COVID-19. We studied the expression of long non-coding RNAs (lncRNAs) in COVID-19 T-cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic non-coding RNA MALAT1 was the most highly transcribed lncRNA in T cells, with Th1 cells demonstrating the lowest and CD8+ resident memory cells the highest MALAT1 expression, amongst CD4+ and CD8+ T-cells populations, respectively. We then identified gene signatures that covaried with MALAT1 in single T cells. A significantly higher number of transcripts correlated negatively with MALAT1 than those that correlated. Enriched functional annotations of the MALAT1- anti-correlating gene signature included processes associated with T-cell activation such as cell division, oxidative phosphorylation, and response to cytokine. The MALAT1 anti-correlating gene signature shared by both CD4+ and CD8+ T-cells marked dividing T cells in both the lung and blood of COVID-19 patients. Focussing on the tissue, we used an independent patient cohort of post-mortem COVID-19 lung samples and demonstrated that MALAT1 suppression was indeed a marker of MKI67+ proliferating CD8+ T cells. Our results reveal MALAT1 suppression and its associated gene signature are a hallmark of human proliferating T cells. T cells play important roles in the body's response to COVID-19. We found gene signatures anti-correlating to MALAT1 expression as a marker of proliferating CD4+ Th1 and CD8+ exhausted sub-populations. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Identification of a broadly fibrogenic macrophage subset induced by type 3 inflammation.

Author

Fabre, Thomas, Barron, Alexander M. S., Christensen, Stephen M., Asano, Shoh, Bound, Kathryn, Lech, Matthew P., Wadsworth II, Marc H., Chen, Xiao, Wang, Chang, Wang, Ju, McMahon, James, Schlerman, Franklin, White, Alexis, Kravarik, Kellie M., Fisher, Andrew J., Borthwick, Lee A., Hart, Kevin M., Henderson, Neil C., Wynn, Thomas A., and Dower, Ken

Abstract

Macrophages are central orchestrators of the tissue response to injury, with distinct macrophage activation states playing key roles in fibrosis progression and resolution. Identifying key macrophage populations found in human fibrotic tissues could lead to new treatments for fibrosis. Here, we used human liver and lung single-cell RNA sequencing datasets to identify a subset of CD9+TREM2+ macrophages that express SPP1, GPNMB, FABP5, and CD63. In both human and murine hepatic and pulmonary fibrosis, these macrophages were enriched at the outside edges of scarring and adjacent to activated mesenchymal cells. Neutrophils expressing MMP9, which participates in the activation of TGF-β1, and the type 3 cytokines GM-CSF and IL-17A coclustered with these macrophages. In vitro, GM-CSF, IL-17A, and TGF-β1 drive the differentiation of human monocytes into macrophages expressing scar-associated markers. Such differentiated cells could degrade collagen IV but not collagen I and promote TGF-β1–induced collagen I deposition by activated mesenchymal cells. In murine models blocking GM-CSF, IL-17A or TGF-β1 reduced scar-associated macrophage expansion and hepatic or pulmonary fibrosis. Our work identifies a highly specific macrophage population to which we assign a profibrotic role across species and tissues. It further provides a strategy for unbiased discovery, triage, and preclinical validation of therapeutic targets based on this fibrogenic macrophage population. Fibrogenic fiend: Macrophages are key players in responding to tissue injury, and specific macrophage subsets can drive fibrosis progression or resolution. Fabre et al. showed that CD9+TREM2+ macrophages further defined by expression of SPP1, GPNMB, FABP5, and CD63 can mediate fibrosis. Analysis of human and murine hepatic and pulmonary fibrosis samples revealed accumulation of these macrophages near scar sites and proximal to activated mesenchymal cells. These macrophages also clustered with MMP9-expressing neutrophils that secreted GM-CSF and IL-17A and drove TGF-β1 activation. In vitro analysis revealed that GM-CSF, IL-17A, and TGF-β1 can promote differentiation of these macrophages, which are unable to degrade collagen I and contribute to collagen I–associated fibrosis. Blockade of GM-CSF, IL-17A, or TGF-β1 in mice was sufficient to limit fibrosis. These findings highlight a critical role for fibrogenic macrophages in this pathological process. —CNF [ABSTRACT FROM AUTHOR]

Published
2023
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