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  • Journal article
    Hewitt RJ, Bartlett EC, Ganatra R, Butt H, Kouranos V, Chua F, Kokosi M, Molyneaux PL, Desai SR, Wells AU, Jenkins RG, Renzoni EA, Kemp S, Devaraj A, George PMet al., 2022,

    Lung cancer screening provides an opportunity for early diagnosis and treatment of interstitial lung disease

    , THORAX, ISSN: 0040-6376
  • Journal article
    Molyneaux PL, Fahy WA, Byrne AJ, Braybrooke R, Saunders P, Toshner R, Albers G, Chua F, Renzoni EA, Wells AU, Karkera Y, Oballa E, Saini G, Nicholson AG, Jenkins G, Maher TMet al., 2022,

    CYFRA 21-1 predicts progression in IPF: a prospective longitudinal analysis of the PROFILE cohort

    , American Journal of Respiratory and Critical Care Medicine, Vol: 205, Pages: 1440-1448, ISSN: 1073-449X

    OBJECTIVES: Idiopathic pulmonary fibrosis (IPF) is a progressive and inevitably fatal condition for which there are a lack of effective biomarkers to guide therapeutic decision making. RATIONALE: To determine the relationship between serum levels of the cytokeratin fragment CYFRA 21-1 and disease progression and mortality in individuals with IPF enrolled in the PROFILE study. METHODS: CYFRA 21-1 was identified by immunohistochemistry in samples of human lung. Concentrations of CYFRA 21-1 were measured using an Elisa-based assay in serum, collected at baseline, 1- and 3-months, from 491 individuals with an incident diagnosis of IPF enrolled in the PROFILE study and from 100 control subjects. Study subjects were followed for a minimum of 3 years. MEASUREMENTS AND MAIN RESULTS: CYFRA 21-1 localises to hyperplastic epithelium in IPF lung. CYFRA 21-1 levels were significantly higher in IPF subjects compared to healthy controls in both discovery (n=132) (control 0.96±0.81 ng/mL versus IPF; 2.34±2.15 ng/mL, p < 0.0001) and validation (n=359) (control; 2.21±1.54 ng/mL and IPF; 4.13±2.77 ng/mL, p<0.0001) cohorts. Baseline levels of CYFRA 21-1 distinguished individuals at risk of 12-month disease progression (C-statistic 0.70 (95% CI 0.61-0.79), p < 0.0001) and were predictive of overall-mortality (HR 1.12 (1.06-1.19) per 1 ng/mL increase in CYFRA 21-1, p=0.0001). Furthermore, 3-month change in levels of CYFRA 21-1 separately predicted 12-month and overall survival in both the discovery and validation cohorts. CONCLUSIONS: CYFRA 21-1, a marker of epithelial damage and turnover, has the potential to be an important prognostic and therapeutic biomarker in individuals with IPF.

  • Journal article
    Allen RJ, Stockwell A, Oldham JM, Guillen-Guio B, Schwartz DA, Maher TM, Flores C, Noth I, Yaspan BL, Jenkins RG, Wain Let al., 2022,

    Genome-wide association study across five cohorts identifies five novel loci associated with idiopathic pulmonary fibrosis

    , THORAX, Vol: 77, Pages: 829-833, ISSN: 0040-6376
  • Journal article
    Kraven LM, Taylor AR, Molyneaux PL, Maher T, McDonough J, Mura M, Yang I, Schwartz DA, Huang Y, Noth I, Ma SF, Yeo AJ, Fahy WA, Jenkins G, Wain Let al., 2022,

    Cluster analysis of transcriptomic datasets to identify endotypes of idiopathic pulmonary fibrosis

    , Thorax, ISSN: 0040-6376

    Background Considerable clinical heterogeneity in idiopathic pulmonary fibrosis (IPF) suggests the existence of multiple disease endotypes. Identifying these endotypes would improve our understanding of the pathogenesis of IPF and could allow for a biomarker-driven personalised medicine approach. We aimed to identify clinically distinct groups of patients with IPF that could represent distinct disease endotypes.Methods We co-normalised, pooled and clustered three publicly available blood transcriptomic datasets (total 220 IPF cases). We compared clinical traits across clusters and used gene enrichment analysis to identify biological pathways and processes that were over-represented among the genes that were differentially expressed across clusters. A gene-based classifier was developed and validated using three additional independent datasets (total 194 IPF cases).Findings We identified three clusters of patients with IPF with statistically significant differences in lung function (p=0.009) and mortality (p=0.009) between groups. Gene enrichment analysis implicated mitochondrial homeostasis, apoptosis, cell cycle and innate and adaptive immunity in the pathogenesis underlying these groups. We developed and validated a 13-gene cluster classifier that predicted mortality in IPF (high-risk clusters vs low-risk cluster: HR 4.25, 95% CI 2.14 to 8.46, p=3.7×10−5).Interpretation We have identified blood gene expression signatures capable of discerning groups of patients with IPF with significant differences in survival. These clusters could be representative of distinct pathophysiological states, which would support the theory of multiple endotypes of IPF. Although more work must be done to confirm the existence of these endotypes, our classifier could be a useful tool in patient stratification and outcome prediction in IPF.

  • Journal article
    Fabbri L, Moss S, Khan FA, Chi W, Xia J, Robinson K, Smyth AR, Jenkins G, Stewart Iet al., 2022,

    Parenchymal lung abnormalities following hospitalisation for COVID-19 and viral pneumonitis: a systematic review and meta-analysis

    , Thorax, ISSN: 0040-6376

    Introduction Persisting respiratory symptoms in COVID-19 survivors may be related to development of pulmonary fibrosis. We assessed the proportion of chest CT scans and pulmonary function tests consistent with parenchymal lung disease in the follow-up of people hospitalised with COVID-19 and viral pneumonitis.Methods Systematic review and random effects meta-analysis of proportions using studies of adults hospitalised with SARS-CoV-2, SARS-CoV, MERS-CoV or influenza pneumonia and followed up within 12 months. Searches performed in MEDLINE and Embase. Primary outcomes were proportion of radiological sequelae on CT scans; restrictive impairment; impaired gas transfer. Heterogeneity was explored in meta-regression.Results Ninety-five studies (98.9% observational) were included in qualitative synthesis, 70 were suitable for meta-analysis including 60 SARS-CoV-2 studies with a median follow-up of 3 months. In SARS-CoV-2, the overall estimated proportion of inflammatory sequelae was 50% during follow-up (0.50; 95% CI 0.41 to 0.58; I2=95%), fibrotic sequelae were estimated in 29% (0.29; 95% CI 0.22 to 0.37; I2=94.1%). Follow-up time was significantly associated with estimates of inflammatory sequelae (−0.036; 95% CI −0.068 to –0.004; p=0.029), associations with fibrotic sequelae did not reach significance (−0.021; 95% CI −0.051 to 0.009; p=0.176). Impaired gas transfer was estimated at 38% of lung function tests (0.38 95% CI 0.32 to 0.44; I2=92.1%), which was greater than restrictive impairment (0.17; 95% CI 0.13 to 0.23; I2=92.5%), neither were associated with follow-up time (p=0.207; p=0.864).Discussion Sequelae consistent with parenchymal lung disease were observed following COVID-19 and other viral pneumonitis. Estimates should be interpreted with caution due to high heterogeneity, differences in study casemix and initial severity.

  • Journal article
    Khan F, Howard L, Hearson G, Edwards C, Barber C, Jones S, Wilson AM, Maher TM, Saini G, Stewart I, Jenkins Get al., 2022,

    Clinical utility of home versus hospital spirometry in fibrotic ILD: evaluation following INJUSTIS interim analysis

    , Annals of the American Thoracic Society, Vol: 19, Pages: 506-510, ISSN: 1546-3222
  • Journal article
    Wilkinson AL, John AE, Barrett JW, Gower E, Morrison VS, Man Y, Pun KT, Roper JA, Luckett JC, Borthwick LA, Barksby BS, Burgoyne RA, Barnes R, Fisher AJ, Procopiou PA, Hatley RJD, Barrett TN, Marshall RP, Macdonald SJF, Jenkins RG, Slack RJet al., 2021,

    Pharmacological characterisation of GSK3335103, an oral alpha v beta 6 integrin small molecule RGD-mimetic inhibitor for the treatment of fibrotic disease

    , European Journal of Pharmacology, Vol: 913, Pages: 1-10c, ISSN: 0376-6357

    Fibrosis is the formation of scar tissue due to injury or long-term inflammation and is a leading cause of morbidity and mortality. Activation of the pro-fibrotic cytokine transforming growth factor-β (TGFβ) via the alpha-V beta-6 (αvβ6) integrin has been identified as playing a key role in the development of fibrosis. Therefore, a drug discovery programme to identify an orally bioavailable small molecule αvβ6 arginyl-glycinyl-aspartic acid (RGD)-mimetic was initiated. As part of a medicinal chemistry programme GSK3335103 was identified and profiled in a range of pre-clinical in vitro and in vivo systems. GSK3335103 was shown to bind to the αvβ6 with high affinity and demonstrated fast binding kinetics. In primary human lung epithelial cells, GSK3335103-induced concentration- and time-dependent internalisation of αvβ6 with a rapid return of integrin to the cell surface observed after washout. Following sustained engagement of the αvβ6 integrin in vitro, lysosomal degradation was induced by GSK3335103. GSK3335103 was shown to engage with the αvβ6 integrin and inhibit the activation of TGFβ in both ex vivo IPF tissue and in a murine model of bleomycin-induced lung fibrosis, as measured by αvβ6 engagement, TGFβ signalling and collagen deposition, with a prolonged duration of action observed in vivo. In summary, GSK3335103 is a potent αvβ6 inhibitor that attenuates TGFβ signalling in vitro and in vivo with a well-defined pharmacokinetic/pharmacodynamic relationship. This translates to a significant reduction of collagen deposition in vivo and therefore GSK3335103 represents a potential novel oral therapy for fibrotic disorders.

  • Journal article
    Slack RJ, Macdonald SJF, Roper JA, Jenkins RG, Hatley RJDet al., 2021,

    Emerging therapeutic opportunities for integrin inhibitors

    , NATURE REVIEWS DRUG DISCOVERY, Vol: 21, Pages: 60-78, ISSN: 1474-1776
  • Journal article
    Khan FA, Stewart I, Fabbri L, Moss S, Robinson K, Smyth AR, Jenkins Get al., 2021,

    Systematic review and meta-analysis of anakinra, sarilumab, siltuximab and tocilizumab for COVID-19

    , Thorax, Vol: 76, Pages: 907-919, ISSN: 0040-6376

    Background There is accumulating evidence for an overly activated immune response in severe COVID-19, with several studies exploring the therapeutic role of immunomodulation. Through systematic review and meta-analysis, we assess the effectiveness of specific interleukin inhibitors for the treatment of COVID-19.Methods Electronic databases were searched on 7 January 2021 to identify studies of immunomodulatory agents (anakinra, sarilumab, siltuximab and tocilizumab) for the treatment of COVID-19. The primary outcomes were severity on an Ordinal Scale measured at day 15 from intervention and days to hospital discharge. Key secondary endpoints included overall mortality.Results 71 studies totalling 22 058 patients were included, 6 were randomised trials. Most studies explored outcomes in patients who received tocilizumab (60/71). In prospective studies, tocilizumab was associated with improved unadjusted survival (risk ratio 0.83, 95% CI 0.72 to 0.96, I2=0.0%), but conclusive benefit was not demonstrated for other outcomes. In retrospective studies, tocilizumab was associated with less severe outcomes on an Ordinal Scale (generalised OR 1.34, 95% CI 1.10 to 1.64, I2=98%) and adjusted mortality risk (HR 0.52, 95% CI 0.41 to 0.66, I2=76.6%). The mean difference in duration of hospitalisation was 0.36 days (95% CI −0.07 to 0.80, I2=93.8%). There was substantial heterogeneity in retrospective studies, and estimates should be interpreted cautiously. Other immunomodulatory agents showed similar effects to tocilizumab, but insufficient data precluded meta-analysis by agent.Conclusion Tocilizumab was associated with a lower relative risk of mortality in prospective studies, but effects were inconclusive for other outcomes. Current evidence for the efficacy of anakinra, siltuximab or sarilumab in COVID-19 is insufficient, with further studies urgently needed for conclusive findings.

  • Journal article
    Wild JM, Porter JC, Molyneaux PL, George PM, Stewart I, Allen RJ, Aul R, Baillie JK, Barratt SL, Beirne P, Bianchi SM, Blaikley JF, Brooke J, Chaudhuri N, Collier G, Denneny EK, Docherty A, Fabbri L, Gibbons MA, Gleeson F, Gooptu B, Hall IP, Hanley NA, Heightman M, Hillman TE, Johnson SR, Jones MG, Khan F, Lawson R, Mehta P, Mitchell JA, Plate M, Poinasamy K, Quint JK, Rivera-Ortega P, Semple M, Simpson AJ, Smith DJF, Spears M, Spencer LG, Stanel SC, Thickett DR, Thompson AAR, Walsh SLF, Weatherley ND, Weeks ME, Wootton DG, Brightling CE, Chambers RC, Ho L-P, Jacob J, Piper Hanley K, Wain L, Jenkins RGet al., 2021,

    Understanding the burden of interstitial lung disease post-COVID-19: the UK Interstitial Lung Disease-Long COVID Study (UKILD-Long COVID)

    , BMJ Open Respiratory Research, Vol: 8, Pages: 1-10, ISSN: 2052-4439

    Introduction The COVID-19 pandemic has led to over 100 million cases worldwide. The UK has had over 4 million cases, 400 000 hospital admissions and 100 000 deaths. Many patients with COVID-19 suffer long-term symptoms, predominantly breathlessness and fatigue whether hospitalised or not. Early data suggest potentially severe long-term consequence of COVID-19 is development of long COVID-19-related interstitial lung disease (LC-ILD).Methods and analysis The UK Interstitial Lung Disease Consortium (UKILD) will undertake longitudinal observational studies of patients with suspected ILD following COVID-19. The primary objective is to determine ILD prevalence at 12 months following infection and whether clinically severe infection correlates with severity of ILD. Secondary objectives will determine the clinical, genetic, epigenetic and biochemical factors that determine the trajectory of recovery or progression of ILD. Data will be obtained through linkage to the Post-Hospitalisation COVID platform study and community studies. Additional substudies will conduct deep phenotyping. The Xenon MRI investigation of Alveolar dysfunction Substudy will conduct longitudinal xenon alveolar gas transfer and proton perfusion MRI. The POST COVID-19 interstitial lung DiseasE substudy will conduct clinically indicated bronchoalveolar lavage with matched whole blood sampling. Assessments include exploratory single cell RNA and lung microbiomics analysis, gene expression and epigenetic assessment.Ethics and dissemination All contributing studies have been granted appropriate ethical approvals. Results from this study will be disseminated through peer-reviewed journals.Conclusion This study will ensure the extent and consequences of LC-ILD are established and enable strategies to mitigate progression of LC-ILD.

  • Journal article
    Bui LT, Winters NI, Chung M-I, Joseph C, Gutierrez AJ, Habermann AC, Adams TS, Schupp JC, Poli S, Peter LM, Taylor CJ, Blackburn JB, Richmond BW, Nicholson AG, Rassl D, Wallace WA, Rosas IO, Jenkins RG, Kaminski N, Kropski JA, Banovich NEet al., 2021,

    Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity

    , NATURE COMMUNICATIONS, Vol: 12
  • Journal article
    Hopkinson NS, Jenkins G, Hart N, 2021,

    COVID-19 and what comes after?

    , THORAX, Vol: 76, Pages: 324-325, ISSN: 0040-6376
  • Journal article
    Dhindsa RS, Mattsson J, Nag A, Wang Q, Wain L, Allen R, Wigmore EM, Ibanez K, Vitsios D, Deevi SVV, Wasilewski S, Karlsson M, Lassi G, Olsson H, Muthas D, Monkley S, Mackay A, Murray L, Young S, Haefliger C, Maher TM, Belvisi MG, Jenkins G, Molyneaux PL, Platt A, Petrovski Set al., 2021,

    Identification of a missense variant in SPDL1 associated with idiopathic pulmonary fibrosis

    , Communications Biology, Vol: 4, ISSN: 2399-3642

    Idiopathic pulmonary fibrosis (IPF) is a fatal disorder characterised by progressive, destructive lung scarring. Despite substantial progress, the genetic determinants of this disease remain incompletely defined. Using whole genome and whole exome sequencing data from 752 individuals with sporadic IPF and 119,055 UK Biobank controls, we performed a variant-level exome-wide association study (ExWAS) and gene-level collapsing analyses. Our variant-level analysis revealed a novel association between a rare missense variant in SPDL1 and IPF (NM_017785.5:g.169588475 G > A p.Arg20Gln; p = 2.4 × 10−7, odds ratio = 2.87, 95% confidence interval: 2.03–4.07). This signal was independently replicated in the FinnGen cohort, which contains 1028 cases and 196,986 controls (combined p = 2.2 × 10−20), firmly associating this variant as an IPF risk allele. SPDL1 encodes Spindly, a protein involved in mitotic checkpoint signalling during cell division that has not been previously described in fibrosis. To the best of our knowledge, these results highlight a novel mechanism underlying IPF, providing the potential for new therapeutic discoveries in a disease of great unmet need.

  • Journal article
    Leavy OC, Ma S-F, Molyneaux PL, Maher TM, Oldham JM, Flores C, Noth I, Jenkins RG, Dudbridge F, Wain LV, Allen RJ, Leavy OC, Ma S-F, Molyneaux PL, Maher TM, Oldham JM, Flores C, Noth I, Jenkins RG, Dudbridge F, Wain LV, Allen RJet al., 2020,

    Proportion of idiopathic pulmonary fibrosis risk explained by known Common genetic loci in European populations

    , American Journal of Respiratory and Critical Care Medicine, Vol: 203, Pages: 775-778, ISSN: 1073-449X

    Genome-wide association studies have identified 14 genetic loci associated with susceptibility to idiopathic pulmonary fibrosis (IPF), a devastating lung disease with poor prognosis. Of these, the variant with the strongest association, rs35705950, is located in the promoter region of the MUC5B gene and has a risk allele (T) frequency of 30-35% in IPF cases. Here we present estimates of the proportion of disease liability explained by each of the 14 IPF risk variants as well as estimates of the proportion of cases that can be attributed to each variant. We estimate that rs35705950 explains 5.9-9.4% of disease liability, which is much lower than previously reported estimates. Of every 100,000 individuals with the rs35705950_GG genotype we estimate 30 will have IPF, whereas for every 100,000 individuals with the rs35705950_GT genotype 152 will have IPF. Quantifying the impact of genetic risk factors on disease liability improves our understanding of the underlying genetic architecture of IPF and provides insight into the impact of genetic factors in risk prediction modelling.

  • Journal article
    George PM, Barratt SL, Condliffe R, Desai SR, Devaraj A, Forrest I, Gibbons MA, Hart N, Jenkins RG, McAuley DF, Patel BV, Thwaite E, Spencer LGet al., 2020,

    Respiratory follow-up of patients with COVID-19 pneumonia

    , Thorax, Vol: 75, Pages: 1009-1016, ISSN: 0040-6376

    The COVID-19 pandemic has led to an unprecedented surge in hospitalised patients with viral pneumonia. The most severely affected patients are older men, individuals of black and Asian minority ethnicity and those with comorbidities. COVID-19 is also associated with an increased risk of hypercoagulability and venous thromboembolism. The overwhelming majority of patients admitted to hospital have respiratory failure and while most are managed on general wards, a sizeable proportion require intensive care support. The long-term complications of COVID-19 pneumonia are starting to emerge but data from previous coronavirus outbreaks such as severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) suggest that some patients will experience long-term respiratory complications of the infection. With the pattern of thoracic imaging abnormalities and growing clinical experience, it is envisaged that interstitial lung disease and pulmonary vascular disease are likely to be the most important respiratory complications. There is a need for a unified pathway for the respiratory follow-up of patients with COVID-19 balancing the delivery of high-quality clinical care with stretched National Health Service (NHS) resources. In this guidance document, we provide a suggested structure for the respiratory follow-up of patients with clinicoradiological confirmation of COVID-19 pneumonia. We define two separate algorithms integrating disease severity, likelihood of long-term respiratory complications and functional capacity on discharge. To mitigate NHS pressures, virtual solutions have been embedded within the pathway as has safety netting of patients whose clinical trajectory deviates from the pathway. For all patients, we suggest a holistic package of care to address breathlessness, anxiety, oxygen requirement, palliative care and rehabilitation.

  • Journal article
    John AE, Graves RH, Pun KT, Vitulli G, Forty EJ, Mercer PF, Morrell JL, Barrett JW, Rogers RF, Hafeji M, Bibby LI, Gower E, Morrison VS, Man Y, Roper JA, Luckett JC, Borthwick LA, Barksby BS, Burgoyne RA, Barnes R, Le J, Flint DJ, Pyne S, Habgood A, Organ LA, Joseph C, Edwards-Pritchard RC, Maher TM, Fisher AJ, Gudmann NS, Leeming DJ, Chambers RC, Lukey PT, Marshall RP, Macdonald SJF, Jenkins RG, Slack RJet al., 2020,

    Translational pharmacology of an inhaled small molecule alpha v beta 6 integrin inhibitor for idiopathic pulmonary fibrosis

    , Nature Communications, Vol: 11, ISSN: 2041-1723

    The αvβ6 integrin plays a key role in the activation of transforming growth factor-β (TGFβ), a pro-fibrotic mediator that is pivotal to the development of idiopathic pulmonary fibrosis (IPF). We identified a selective small molecule αvβ6 RGD-mimetic, GSK3008348, and profiled it in a range of disease relevant pre-clinical systems. To understand the relationship between target engagement and inhibition of fibrosis, we measured pharmacodynamic and disease-related end points. Here, we report, GSK3008348 binds to αvβ6 with high affinity in human IPF lung and reduces downstream pro-fibrotic TGFβ signaling to normal levels. In human lung epithelial cells, GSK3008348 induces rapid internalization and lysosomal degradation of the αvβ6 integrin. In the murine bleomycin-induced lung fibrosis model, GSK3008348 engages αvβ6, induces prolonged inhibition of TGFβ signaling and reduces lung collagen deposition and serum C3M, a marker of IPF disease progression. These studies highlight the potential of inhaled GSK3008348 as an anti-fibrotic therapy.

  • Journal article
    Molyneaux PL, Smith JJ, Saunders P, Chua F, Wells AU, Renzoni EA, Nicholson AG, Fahy WA, Jenkins RG, Maher TMet al., 2020,

    Bronchoalveolar lavage is safe and well tolerated in individuals with idiopathic pulmonary fibrosis: an analysis of the PROFILE study

    , American Journal of Respiratory and Critical Care Medicine, Vol: 203, Pages: 136-139, ISSN: 1073-449X
  • Journal article
    Leavy O, Ma S-F, Molyneaux P, Maher T, Oldham J, Flores C, Noth I, Jenkins G, Dudbridge F, Wain L, Allen Ret al., 2020,

    Proportion of idiopathic pulmonary fibrosis risk explained by known genetic loci

    Genome-wide association studies have identified 14 genetic loci associated with susceptibility to idiopathic pulmonary fibrosis (IPF), a devastating lung disease with poor prognosis. Of these, the variant with the strongest association, rs35705950, is located in the promoter region of the MUC5B gene and has a risk allele (T) frequency of 30-35% in IPF cases. Here we present estimates of the proportion of disease liability explained by each of the 14 IPF risk variants as well as estimates of the proportion of cases that can be attributed to each variant. We estimate that rs35705950 explains 5.9-9.4% of disease liability, which is much lower than previously reported estimates. Of every 100,000 individuals with the rs35705950_GG genotype we estimate 30 will have IPF, whereas for every 100,000 individuals with the rs35705950_GT genotype 152 will have IPF. Quantifying the impact of genetic risk factors on disease liability improves our understanding of the underlying genetic architecture of IPF and provides insight into the impact of genetic factors in risk prediction modelling.

  • Journal article
    Sultan Z, Graça I, Li Y, Lima S, Peeva LG, Kim D, Ebrahim MAA, Rinaldi R, Livingston Aet al., 2019,

    Membrane fractionation of liquors from lignin-first biorefining

    , ChemSusChem, Vol: 12, Pages: 1203-1212, ISSN: 1864-5631

    For the purposing of each lignin fraction in the lignin liquors, the development of separation strategies to fractionate the lignin streams by MW ranges constitutes a timely challenge to be tackled. Herein, membrane separation was applied to the refining of lignin streams obtained from a lignin-first biorefining process based on H-transfer reactions catalyzed by Raney Ni, using 2-propanol as a part of the lignin extraction liquor and as an H-donor. A two-stage membrane cascade was considered to separate and concentrate the monophenol-rich fraction from the CUB liquor. Building on the experimental results, an economic evaluation of the potential of membrane separation for the refining of lignin streams was undertaken. The membrane performance represents the bottleneck of the costs associated with the separation process. Accordingly, we present a detailed analysis of future developments in the performance required to debottleneck the utilization of membrane separation for lignin refining.

  • Journal article
    Dong R, Liu R, Gaffney P, Schaepertoens M, Marchetti P, Williams C, Chen R, Livingston Aet al., 2019,

    Sequence-defined multifunctional polyethers via liquid-phase synthesis with molecular sieving

    , Nature Chemistry, Vol: 11, Pages: 136-145, ISSN: 1755-4330

    Synthetic chemists have devoted tremendous effort towards the production of precision synthetic polymers with defined sequences and specific functions. However, the creation of a general technology that enables precise control over monomer sequence, with efficient isolation of the target polymers, is highly challenging. Here, we report a robust strategy for the production of sequence-defined synthetic polymers through a combination of liquid-phase synthesis and selective molecular sieving. The polymer is assembled in solution with real-time monitoring to ensure couplings proceed to completion, on a three-armed star-shaped macromolecule to maximize efficiency during the molecular sieving process. This approach is applied to the construction of sequence-defined polyethers, with side-arms at precisely defined locations that can undergo site-selective modification after polymerization. Using this versatile strategy, we have introduced structural and functional diversity into sequence-defined polyethers, unlocking their potential for real-life applications in nanotechnology, healthcare and information storage.

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