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4. Phase 1 trial of intrapleural LTI-01; single chain urokinase in complicated parapneumonic effusions or empyema

Author

Beckert, Lutz, Brockway, Ben, Simpson, Graham, Southcott, Anne Marie, Lee, YC Gary, Rahman, Najib, Light, Richard W, Shoemaker, Steven, Gillies, John, Komissarov, Andrey A, Florova, Galina, Ochran, Timothy, Bradley, William, Ndetan, Harrison, Singh, Karan P, Sarva, Krishna, and Idell, Steven

Subjects
Patient Safety, Clinical Research, Infectious Diseases, Clinical Trials and Supportive Activities, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Adult, Aged, Aged, 80 and over, Empyema, Pleural, Female, Humans, Injections, Intralesional, Male, Middle Aged, Pleural Effusion, Thrombolytic Therapy, Treatment Outcome, Urokinase-Type Plasminogen Activator, Bacterial infections, Clinical Trials, Fibrosis
Abstract

Current dosing of intrapleural fibrinolytic therapy (IPFT) in adults with complicated parapneumonic effusion (CPE) / empyema is empiric, as dose-escalation trials have not previously been conducted. We hypothesized that LTI-01 (scuPA), which is relatively resistant to PA inhibitor-1 (PAI-1), would be well-tolerated. This was an open-label, dose-escalation trial of LTI-01 IPFT at 50,000-800,000 IU daily for up to 3 days in adults with loculated CPE/empyema and failed pleural drainage. The primary objective was to evaluate safety and tolerability, and secondary objectives included assessments of processing and bioactivity of scuPA in blood and pleural fluid (PF), and early efficacy. LTI-01 was well tolerated with no bleeding, treatment-emergent adverse events or surgical referrals (n=14 subjects). uPA antigen increased in PFs at 3 hours after LTI-01 (p

Published
2019

8. Effect of Obstructive Sleep Apnea Treatment on Renal Function in Patients with Cardiovascular Disease

Author

Loffler, Kelly A., Heeley, Emma, Freed, Ruth, Anderson, Craig S., Brockway, Ben, Corbett, Alastair, Chang, Catherina L., Douglas, James A., Ferrier, Katherine, Graham, Neil, Hamilton, Garun S., Hlavac, Michael, McArdle, Nigel, McLachlan, John, Mukherjee, Sutapa, Naughton, Matthew T., Thien, Francis, Young, Alan, Grunstein, Ronald R., Palmer, Lyle J., Woodman, Richard J., Hanly, Patrick J., and McEvoy, Doug R.

Published
2017
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9. Essential Features of an Interstitial Lung Disease Multidisciplinary Meeting: An International Delphi Survey

Author

Teoh, Alan K. Y., primary, Holland, Anne E., additional, Morisset, Julie, additional, Flaherty, Kevin R., additional, Wells, Athol U., additional, Walsh, Simon L. F., additional, Glaspole, Ian, additional, Wuyts, Wim A., additional, Corte, Tamera J., additional, Adamali, Huzaifa, additional, Allam, J. Shirine, additional, Antillon, Sofia, additional, Antoniou, Katherina M., additional, Athanazio, Rodrigo, additional, Avdeev, Sergey, additional, Averyanov, Alexander, additional, Azuma, Arata, additional, Baldi, Bruno, additional, Balestro, Elisabetta, additional, Bascom, Rebecca, additional, Bastiampillai, Shalini, additional, Beckert, Lutz, additional, Behr, Jü¨ergen, additional, Beirne, Paul, additional, Bennett, David, additional, Borie, Raphael, additional, Bouros, Demosthenes, additional, Brockway, Ben, additional, Brown, Kevin, additional, Callejas González, Francisco Javier, additional, Castillo, Diego, additional, Chaves, Ronald Chacon, additional, Chambers, Daniel, additional, Chapman, Sally, additional, Chaudhuri, Nazia, additional, Collard, Harold, additional, Cottin, Vincent, additional, Crestani, Bruno, additional, Davidsen, Jesper Rømhild, additional, Dhasmana, Devesh J., additional, Dhooria, Sahajal, additional, Enghelmayer, Juan Ignacio, additional, Fabro, Alexandre Todorovic, additional, Garcha, Puneet, additional, Goh, Nicole, additional, Gomez, Alejandro, additional, Grainge, Christopher, additional, Handa, Tomohiro, additional, Huie, Tristan, additional, Hunninghake, Gary, additional, Inoue, Yoshikazu, additional, Jo, Helen, additional, Johannson, Kerri, additional, Jonkers, Rene, additional, Judge, Eoin, additional, Kabasakal, Yasemin, additional, Dourado, Leticia Kawano, additional, Keir, Gregory, additional, Khalil, Nasreen, additional, Khor, Yet Hong, additional, Biggs, Melissa King, additional, Kokosi, Maria, additional, Kondoh, Yasuhiro, additional, Kouranos, Vasillis, additional, Kreuter, Michael, additional, Lederer, David, additional, Low, Su Ying, additional, Quernheim, Joachim Mü¨ller, additional, Maher, Toby, additional, Mancuzo, Eliane, additional, Margaritopoulos, George, additional, Mason, Carol, additional, Mazeini, Mariano, additional, Mogulkoc, Nesrin, additional, Molina, Maria, additional, Moodley, Yuben, additional, Morais, António, additional, Nambiar, Anoop, additional, Noth, Imre, additional, Nunes, Hilario, additional, Ogura, Takashi, additional, Okutan, Oguzhan, additional, Patel, Nina, additional, Pereira, Carlos, additional, Piotrowski, Wojciech, additional, Poletti, Venerino, additional, Quadrelli, Silvia, additional, Radzikowska, Elzbieta, additional, Ortega, Pilar Rivera, additional, Ryerson, Christopher J., additional, Salinas, Mauricio, additional, Sanchez, Rafaela, additional, Savas, Recep, additional, Selman, Moises, additional, Shifren, Adrian, additional, Soares, Maria Raquel, additional, Sobh, Eman, additional, Song, Jin Woo, additional, Spagnolo, Paolo, additional, Sterclova, Martina, additional, Strambu, Irina, additional, Strek, Mary E., additional, Suda, Takafumi, additional, Tabaj, Gabriela, additional, Trkanjec, Jasna Tekavec, additional, Akyil, Fatma Tokgoz, additional, Toma, Claudia, additional, Tomic, Rade, additional, Tomioka, Hiromi, additional, Traila, Daniel, additional, Troy, Lauren, additional, Trukillo, Sergio, additional, Tzouvelekis, Argyrios, additional, Vancheri, Carlo, additional, Varela, Brenda Elena, additional, Varone, Francesco, additional, Vasakova, Martina, additional, Veitch, Elizabeth, additional, Zygmunt, Vanesa Vicens, additional, Wessendorf, Thomas, additional, Westall, Glen, additional, Wijsenbeek, Marlies, additional, Wilsher, Margaret L., additional, Wrobel, Jeremy, additional, Fukuda, Cesar Yoshito, additional, and Zappala, Chris, additional

Published
2022
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17. Long‐term follow‐up after intrapleural tPA/DNase therapy for pleural infection.

Author

Popowicz, Natalia D., Piccolo, Francesco, Yap, Elaine, Wong, Conroy, Brockway, Ben, Smith, Nicola A., Sullivan, Cameron, Musk, Arthur W., and Lee, Y.C. Gary

Subjects
GRAM'S stain, TISSUE plasminogen activator, CORONARY artery bypass, CHEST pain
Abstract

This study, notwithstanding limitations of its approach, provides the first comprehensive evaluation of adult patients at least 12 months following tPA/DNase treatment for pleural infection. Without a comparison group (e.g. those successfully treated without tPA/DNase or those treated with surgery only), it is difficult to determine if residual symptoms or defects are related to tPA/DNase.5,8 Patient recall biases are inevitable in cross-sectional studies. This cross-sectional multicentre cohort study reports, for the first time, long-term clinical, respiratory and functional outcomes >=12 months following tPA/DNase treatment for pleural infection. Keywords: deoxyribonuclease; intrapleural; pleural effusion; respiratory infection; tissue plasminogen activator EN deoxyribonuclease intrapleural pleural effusion respiratory infection tissue plasminogen activator 388 391 4 03/22/21 20210401 NES 210401 Abbreviations CP loss obliteration of costophrenic angle CXR chest radiograph DNase deoxyribonuclease FEV 1 forced expiratory volume in 1 s FVC forced vital capacity IQR interquartile range mMRC modified Medical Research Council QoL quality of life SF-36v2 36-item short form health survey TLC total lung capacity tPA tissue plasminogen activator Intrapleural tissue plasminogen activator/deoxyribonuclease (tPA/DNase) therapy has been rapidly adopted worldwide for treating pleural infection. [Extracted from the article]

Published
2021
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19. Phase I trial of the single-chain urokinase intrapleural LTI-01 in complicated parapneumonic effusions or empyema

Author

Beckert, Lutz, primary, Brockway, Ben, additional, Simpson, Graham, additional, Southcott, Anne Marie, additional, Lee, Y.C. Gary, additional, Rahman, Najib, additional, Light, Richard W., additional, Shoemaker, Steven, additional, Gillies, John, additional, Komissarov, Andrey A., additional, Florova, Galina, additional, Ochran, Timothy, additional, Bradley, William, additional, Ndetan, Harrison, additional, Singh, Karan P., additional, Sarva, Krishna, additional, and Idell, Steven, additional

Published
2019
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20. Expression of Pseudomonas aeruginosa Antibiotic Resistance Genes Varies Greatly during Infections in Cystic Fibrosis Patients

Author

Martin, Lois W., primary, Robson, Cynthia L., additional, Watts, Annabelle M., additional, Gray, Andrew R., additional, Wainwright, Claire E., additional, Bell, Scott C., additional, Ramsay, Kay A., additional, Kidd, Timothy J., additional, Reid, David W., additional, Brockway, Ben, additional, and Lamont, Iain L., additional

Published
2018
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21. Treatable traits can be identified in a severe asthma registry and predict future exacerbations

Author

McDonald, Vanessa M., primary, Hiles, Sarah A., additional, Godbout, Krystelle, additional, Harvey, Erin S., additional, Marks, Guy B., additional, Hew, Mark, additional, Peters, Matthew, additional, Bardin, Philip G., additional, Reynolds, Paul N., additional, Upham, John W., additional, Baraket, Melissa, additional, Bhikoo, Zaheerodin, additional, Bowden, Jeffrey, additional, Brockway, Ben, additional, Chung, Li Ping, additional, Cochrane, Belinda, additional, Foxley, Gloria, additional, Garrett, Jeffrey, additional, Jayaram, Lata, additional, Jenkins, Christine, additional, Katelaris, Constance, additional, Katsoulotos, Gregory, additional, Koh, Mariko S., additional, Kritikos, Vicky, additional, Lambert, Marina, additional, Langton, David, additional, Lara Rivero, Alexis, additional, Middleton, Peter G., additional, Nanguzgambo, Aldoph, additional, Radhakrishna, Naghmeh, additional, Reddel, Helen, additional, Rimmer, Janet, additional, Southcott, Anne Marie, additional, Sutherland, Michael, additional, Thien, Francis, additional, Wark, Peter A.B., additional, Yang, Ian A., additional, Yap, Elaine, additional, and Gibson, Peter G., additional

Published
2018
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22. Identification of treatable traits in a severe asthma registry: prevalence and exacerbation predictors

Author

McDonald, Vanessa M., primary, Hiles, Sarah A., additional, Godbout, Krystelle, additional, Harvey, Erin S., additional, Marks, Guy B., additional, Hew, Mark, additional, Peters, Matthew, additional, Bardin, Philip, additional, Reynolds, Paul N., additional, Upham, John W., additional, Baraket, Melissa, additional, Bhikoo, Zaheerodin, additional, Bowden, Jeffrey, additional, Brockway, Ben, additional, Chung, Li Ping, additional, Cochrane, Belinda, additional, Foxley, Gloria, additional, Garrett, Jeffrey, additional, Jayaram, Lata, additional, Jenkins, Christine, additional, Katelaris, Constance, additional, Katsoulotos, Gregory, additional, Koh, Mariko S., additional, Kritikos, Vicky, additional, Lambert, Marina, additional, Langton, David, additional, Lara Rivero, Alexis, additional, Middleton, Peter, additional, Nanguzgambo, Aldoph, additional, Radhakrishna, Naghmeh, additional, Reddel, Helen, additional, Rimmer, Janet, additional, Southcott, Anne Marie, additional, Sutherland, Michael, additional, Thien, Francis, additional, Wark, Peter, additional, Yang, Ian A., additional, Yap, Elaine, additional, and Gibson, Peter G., additional

Published
2018
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23. Biallelic variants in EFEMP1in a man with a pronounced connective tissue phenotype

Author

Driver, Sean G. W., Jackson, Meremaihi R., Richter, Konrad, Tomlinson, Paul, Brockway, Ben, Halliday, Benjamin J., Markie, David M., Robertson, Stephen P., and Wade, Emma M.

Abstract

Connective tissue disorders are a spectrum of diseases that affect the integrity of tissues including skin, vasculature, and joints. They are often caused by variants that disrupt genes encoding components of extracellular matrix (ECM). The fibulin glycoproteins are ECM proteins important for integrity of tissues including dermis, retina, fascia, and vasculature. The fibulin family consists of seven members (fibulins-1 to -7) and is defined by a fibulin-type domain at the C-terminus. The family is associated with human diseases, for instance a variant in FBLN1, encoding fibulin-1, is associated with synpolydactyly, while one in EFEMP1, encoding fibulin-3, causes Doyne honeycomb degeneration of the retina. Loss-of-function of fibulins-4 and -5 causes cutis laxa, while variants in fibulins-5 and -6 are associated with age-related macular degeneration. Of note, EFEMP1is not currently associated with any connective tissue disorder. Here we show biallelic loss-of-function variants in EFEMP1in an individual with multiple and recurrent abdominal and thoracic herniae, myopia, hypermobile joints, scoliosis, and thin translucent skin. Fibroblasts from this individual express significantly lower EFEMP1transcript than age-matched control cells. A skin biopsy, visualised using light microscopy, showed normal structure and abundance of elastic fibres. The phenotype of this individual is remarkably similar to the Efemp1knockout mouse model that displays multiple herniae with premature aging and scoliosis. We conclude that loss of EFEMP1function in this individual is the cause of a connective tissue disorder with a novel combination of phenotypic features, and can perhaps explain similar, previously reported cases in the literature.

Published
2020
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24. Treatable traits can be identified in a severe asthma registry and predict future exacerbations.

Author

McDonald, Vanessa M., Hiles, Sarah A., Harvey, Erin S., Wark, Peter A.B., Gibson, Peter G., Upham, John W., Baraket, Melissa, Bhikoo, Zaheerodin, Bowden, Jeffrey, Brockway, Ben, Chung, Li Ping, Cochrane, Belinda, Katelaris, Constance, Godbout, Krystelle, Garrett, Jeffrey, Yap, Elaine, Jayaram, Lata, Southcott, Anne Marie, Katsoulotos, Gregory, and Lara Rivero, Alexis

Subjects
INHALERS, VOCAL cord dysfunction, ASTHMA
Abstract

Background and objective: A new taxonomic and management approach, termed treatable traits, has been proposed for airway diseases including severe asthma. This study examined whether treatable traits could be identified using registry data and whether particular treatable traits were associated with future exacerbation risk. Methods: The Australasian Severe Asthma Web‐Based Database (SAWD) enrolled 434 participants with severe asthma and a comparison group of 102 participants with non‐severe asthma. Published treatable traits were mapped to registry data fields and their prevalence was described. Participants were characterized at baseline and every 6 months for 24 months. Results: In SAWD, 24 treatable traits were identified in three domains: pulmonary, extrapulmonary and behavioural/risk factors. Patients with severe asthma expressed more pulmonary and extrapulmonary treatable traits than non‐severe asthma. Allergic sensitization, upper‐airway disease, airflow limitation, eosinophilic inflammation and frequent exacerbations were common in severe asthma. Ten traits predicted exacerbation risk; among the strongest were being prone to exacerbations, depression, inhaler device polypharmacy, vocal cord dysfunction and obstructive sleep apnoea. Conclusion: Treatable traits can be assessed using a severe asthma registry. In severe asthma, patients express more treatable traits than non‐severe asthma. Traits may be associated with future asthma exacerbation risk demonstrating the clinical utility of assessing treatable traits. We assessed the prevalence of treatable traits in severe asthma compared with non‐severe asthma, and assessed the relationship between treatable traits and future exacerbation risk. We demonstrate the usefulness of the treatable traits approach in severe asthma and which specific treatable traits are predictive of future asthma attacks. See relatedEditorial [ABSTRACT FROM AUTHOR]

Published
2019
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27. Effect of Inhaled β2-Agonist on Exhaled Nitric Oxide in Chronic Obstructive Pulmonary Disease.

Author

Amer, Mostafa, Cowan, Jan, Gray, Andrew, Brockway, Ben, and Dummer, Jack

Subjects
OBSTRUCTIVE lung diseases, NITRIC oxide, ALPHA adrenoceptors, BRONCHODILATOR agents, EXPIRATORY flow, STEROID drugs, ASTHMA
Abstract

The fractional exhaled nitric oxide measured at an expiratory flow of 50mL/s (FENO50) is a marker of airway inflammation, and high levels are associated with greater response to steroid treatment. In asthma, FENO50 increases with bronchodilation and decreases with bronchoconstriction, the latter potentially causing an underestimate of the degree of airway inflammation when asthma worsens. It is unknown whether the same effect occurs in chronic obstructive lung disease (COPD). Likewise, it is not known whether changes in airway calibre in COPD patients alter flow-independent parameters describing pulmonary nitric oxide exchange, such as the maximal flux of nitric oxide (NO) from the proximal airway compartment (J’awNO) and the distal airway/alveolar concentration of NO (CANO). We recruited 24 patients with COPD and performed FENO analysis at multiple expiratory flows before and after treatment with inhaled β2-agonist bronchodilator therapy. For the 21 patients analysed, FENO50 rose from 17.1 (1.4) ppb (geometric mean (geometric SD)) at baseline, to 19.3 (1.3) ppb after bronchodilator therapy, an increase of 2.2 ppb (95% CI, 0.7–3.6; P = 0.005). There were non-significant changes in flow-independent NO parameters. The change in FENO50 correlated positively with the change in J’awNO (rs = 0.67, P < 0.001; rs = 0.62, P = 0.002 before and after correction for axial back-diffusion respectively) following bronchodilation. Inhaled bronchodilator therapy can increase exhaled nitric oxide measurements in COPD. The standardisation of inhaled bronchodilator therapy before FENO analysis in COPD patients should therefore be considered in both research and clinical settings. [ABSTRACT FROM AUTHOR]

Published
2016
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28. Expression of Pseudomonas aeruginosaAntibiotic Resistance Genes Varies Greatly during Infections in Cystic Fibrosis Patients

Author

Martin, Lois W., Robson, Cynthia L., Watts, Annabelle M., Gray, Andrew R., Wainwright, Claire E., Bell, Scott C., Ramsay, Kay A., Kidd, Timothy J., Reid, David W., Brockway, Ben, and Lamont, Iain L.

Abstract

The lungs of individuals with cystic fibrosis (CF) become chronically infected with Pseudomonas aeruginosathat is difficult to eradicate by antibiotic treatment. Two key P. aeruginosaantibiotic resistance mechanisms are the AmpC β-lactamase that degrades β-lactam antibiotics and MexXYOprM, a three-protein efflux pump that expels aminoglycoside antibiotics from the bacterial cells.

Published
2018
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