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2. Age and frailty are independently associated with increased covid-19 mortality and increased care needs in survivors: results of an international multi-centre study

Author

Alsahab, Mustafa, Beishon, Lucy, Brown, Bryony, Burn, Elinor, Burton, Jenni K, Cox, Natalie, Dani, Melanie, Elhadi, Muhammed, Freshwater, Sarah, Gaunt, Victoria, Gordon, Adam, Goujon, Marie, Hale, Matthew, Hughes, Terry, Jackson, Thomas A, Jelley, Benjamin, Khan, Asma, Khiroya, Heena, Lal, Rajni, Madden, Katy, Magill, Laura, Masoli, Jane, Masud, Tahir, McCluskey, Lauren, McNeela, Natalie, Mohammedseid-Nurhussien, Awolkhier, Moorey, Hannah, Lochlainn, Mary Ni, Nirantharakumar, Krishnarajah, Okoth, Kelvin, Osuafor, Christopher N, Patterson, Katherine, Pearson, Grace M E, Perry, Rita, Pettitt, Michala, Pigott, Jennifer, Pinkney, Thomas, Quinn, Terence, Reynolds, Abigail, Richardson, Sarah, Sanyal, Nik, Seed, Adam, Sleeman, Isobel, Soo, Chee, Steves, Claire, Strain, W David, Taylor, Joanne, Torsney, Kelli, Welch, Carly, Wilson, Daisy, Witham, Miles, Elazeem, Hossam Aldein S Abd, Abdelhafez, Mohammed H, Abdelmalak, Amir, Abdelwahab, Omar A, Abdulhadi, Osama M A S, Adewole, Olubayode, Ahmad, Mohammed, Ahmed, Eltayeb A, Ahmed, Hazem, Ahmed, Islam A, Akcay, Mertcan, Akdeniz, Yeşim, Akın, Emrah, Akladious, Carolyn, Alessandri, Francesco, Ali, Ali, Aljafari, Abdulmalek, Aljafari, Abdulmoiz, Al-Sadawi, Mohammed, Al-Sodani, Lobna, Altintoprak, Fatih, Amaratungaz, Gitanjali, Amer, Jocelyn, Amini, Sylvia, Amir, Taha, Anandarajah, Cheran, Anders, Rachael, Ansari, Muhammed H, Appiah, Kingsley, Atia, Jolene, Atkin, Catherine, Aujayeb, Avinash, Awad, Elsayed M, Azab, Mohammed A, Azam, Mohammad T, Aziz, Sally, Azzam, Ahmed Y, Babar, Laxmi, Babb, Laura, Badh, Manpreet, Baguneid, Clare, Bailey, Emily, Baili, Efstratia, Baldwin, Sarah, Baloyiannis, Ioannis, Bannerjee, Moulinath, Barnard, Anna, Barra, Fabio, Bashir, Hannah, Bawor, Monica, Bayhan, Zülfü, Belcher, James, Belgamwar, Ravindra, Bentley, Corrina, Birchenough, Amy, Bo, Yen Nee J, Boden, Hayley R, Bouhuwaish, Ahmad, Brachini, Gioia, Bremner, Laura, Bridgwater, Hannah, Bryant, Catherine, Budd, Gabrielle, Budd, Sharon, Budzikoski, Adam, Bulla, Reem, Buondonno, Antonio, Burden, Nicole, Butt, Hejab, Capoglu, Recayi, Caracostea, Andra, Cardoso, Rifa, Carr, Alexis, Carrasco-Prats, Milagros, Cattel, Caterina, Ceccarelli, Giancarlo, Cecere, Giuseppe, Charalabopoulos, Alexandros, Charsley, Evelyn, Cheney-Lowe, Hannah, Chevallier, Theodore, Choudhry, Asad J, Ciccarone, Flavia, Cicerchia, Pierfranco M, Cirillo, Bruno, Collins, Fatma D, Comerford, Victoria, Cordie, Ahmed, Coulter, Siobhan, Coulthard, Nick, Cox, Catrin, Cox, Victoria, Crowe, Andrew, Cullen, Jack, Cummings, Jean, Cunningham, Niamh, Curley, Daniel, Currie, Hannah, Daly, Madeleine, Darley, Jay, Dattani, Nikhita, Davakis, Spyridon, Davies, Rowan, De Paola, Gilda, De Toma, Giorgio, Del Valle-Ruiz, Sergio, Deldar, Benyamin, Demir, Hakan, Desai, Arjun, Desai, Nirali, Devaney, Alice, Dew, Lindsey, Dhesi, Jugdeep, Dias, Maria, Dick, Gordon, Doddamani, Parveen, Dogra, Gurinder, Doll, Tina, Dooley, Hannah C, Dost, Samiullah, Dotchin, Catherine, Dowell, Hannah, Draghita, Ioan M, Dundas, James M, Duranti, Giulia, Dusara, Hiren, Dwivedi, Rajesh, Dyer, Adam H, Eastaugh, Alison, Edwards, Elinor, Elghazaly, Shrouk M, Elmehrath, Ahmed O, Elrick, Hope, El-Shazly, Mostafa, Emery, Alexander, Etchill, Eric W, Evans, Sarah, Evison, Felicity, Fairhead, Cassandra, Faulkner, Margherita, Felska, Agnieszka, Fernandez, Antia, Fernández-Fernández, Pedro V, Ferraiolo, Antonella, Ferrero, Simone, Fiori, Enrico, Firat, Necattin, Fisk, Gracie, Fleck, Anna, Fonsi, Giovanni B, Gabre-Kidan, Alodia, Gallo, Gaetano, Gandhi, Ratnam, Garner, Madeleine, Georgiou, Nikolaos, Gerretsen, Hannah, Ghannam, Nourhan A A, Ghobrial, Andrew, Ghobrial, Hedra, Ghufoor, Zaynub, Gibbon, Jake, Gilbert, Georgia F, Giles, Marie, Giménez-Francés, Clara, Gonullu, Emre, Gray, Amy, Gray, Joshua H, Green, Deirdre, Greene, Charlotte, Griffin, Ellanna, Griffith, Karla, Grubb, Anthony, Guan, Yue, Guerero, Daniel N, Gupta, Ayushi, Gustavino, Claudio, Guzman, Laurenny, Hadreiez, Ahmed K M, Hajiioannou, Jiannis, Hanji, Deevia, Madhavan, Deepthy Hari, Harmantepe, Tarık, Harrison, Patrick, Hart, Barbara, Haslam, Aidan, Haunton, Victoria, Haut, Elliott R, Heinsohn, Torben, Hennah, Lindsay, Hetta, Helal F, Hickman, Alexander, Hobill, Abigail, Hogan, Patrick C P, Hogan, Vesna, Holmes, Elizabeth, Honney, Katie, Hood, Katharine, Hopkinson, Katherine, Howells, Lara, Hrouda, Nicole, Hunsley, Danielle, Hurst, William, Hussein, Rand A, Ibrahim, Mohamed Eltaher A A, Ibtida, Ishmam, Ibukunoluwakitan, Aina, Ishlek, Irem, Iyer, Rishi, Jackson, Karl, Jackson, Rosie, James, Ellen, Jarvis, Hayley, Jeffs, Sophie, Jenko, Nathan, Jeyakumar, Sasha, Kabir, Shahriar, Kainth, Harjinder, Kalloo, Jason, Kanzaria, Akhil, Karapanou, Amalia, Kardaman, Nuha, Karthikeyan, Sandeep, Karunatilleke, Anne, Kelly, Mairead, Kelly, Nicola I, Khalid, Hesham, Khan, Haris, Khan, Muhammad S, King, Matthew, Kneen, Thomas, Kok, Li, Kratochwila, Chiara, Kuzeva, Aneliya, Lapolla, Pierfrancesco, Lau, Rebecca, Law, Kar Yee, Leadbetter, Aimee, Lee, Gabriel, Lee, Helena, Levinson, Gavriella, Lewis, Grace, Liakakos, Theodore, Lim, Stephen, Lis, Danielle, Livesey, Emma, López-Morales, Pedro, Lowes, Lily, Lunt, Eleanor, Lyon, Emily, Madan, Suvira, Majid, Zeinab, Malapati, Harsha, Man, Jade, Mandane, Baguiasri, Manning, Sarah H, Mantoglu, Baris, Martínez-Sanz, Nuria, Marx, William, Masood, Almontacer E B, Maughan, Tom, Mawhinney, Jamie, Maxfield, Dominic, Mayer, Jordan, Maynard, Henry, McDonald, Claire, McGovern, Aine, Mclachlan, Sophie, Medina-Manuel, Esther, Meneghini, Simona, Metcalf, Michelle, Millwood-Hargrave, John, Mingoli, Andrea, Miu, Kelvin, Mohamed, Fawsiya, Mohamed, Soha M, Hussein, Aliae A R Mohamed, Mohammad, Abdulkader, Mohammed, Aaliya, Momen, Ahmed A, Moomo, Farhana, Mora-Guzmán, Ismael, Moriarty, Lizzie, Morrin, Hamilton, Morris, Claire, Moss, Nicholas, Moustafa, Mohamed M, Mpoura, Maria, Mubin, Mohammed, Muhtaroglu, Ali, Muir, Georgina, Mulhern, Stephanie, Muller, Daniel, Murphy, Declan C, Muzammil, Bushra, Nadkarni, Varun, Nageh, Mariam Albatoul, NasrEldin, Yasmin K, Nawaz, Wasim, Nguyen, Hanna, Cheallaigh, Cliona Ni, Noar, Alexander, North, Samuel, Nwolu, Favour, O’Docherty, Alice, Odutola, Omoteniola, O’Dwyer, Sinead, Ogochukwu, Olebu, O’Mahony, Catherine, Orlando, Lia, Osterdahl, Marc, Page, Christina, Panayotidis, Ismini, Pancholi, Shivam, Parkin, Jessica, Passby, Lauren C, Pastor-Pérez, Patricia, Patel, Harnish, Patel, Shefali, Penfold, Rose, Perinpanathan, Rupini, Perivoliotis, Konstantinos, Perra, Teresa, Pinkney, Martha, Pinotti, Enrico, Porcu, Alberto, Price, Angeline, Pugliese, Francesco, Puri, Prabhleen, Pytraczyk, Sylvia, Qaiser, Yusra, Qurashi, Maria, Radenkovic, Dina, Rajeswaran, Thurkka, Rapaport, Sarah F, Razzak, Tahmina, Reilly, Lara, Reynolds, Paul, Richardson, Alexandra, Roberts, Amelia, Roberts-Rhodes, Charlotte, Robinson, Tanya, Rocca, Aldo, Ross-Skinner, Emily, Ruiz-Marín, Miguel, Ryall, Rebecca, Saad, Alshaimaa M, Saad, Mahmoud M, Sadiq, Ambreen, Sammarco, Giuseppe, Sampanis, Michail A, Sanghvi, Hazel, Sapienza, Paolo, Sayers, Ross, Scott, Luca, Sen, Michael, Shaban, Mosab A A, Shakespeare, Kathleen T, Shaw, Ellie, Shaw, Hannah, Sheldrake, Jonathan, Sim, Sing Yang, Simonelli, Luigi, Sipsas, Nikolaos V, Sivam, Jarita, Sivarajan, Sri, Smith, Jennifer, Speranza, Fabio, Spice, Claire, Stafford, Amanda, Stambollouian, Katharine, Stevens, Kent A, Stewart, Jack, Stratton, Emma, Street, Hannah, Surtees, Michael, Swinnerton, Emma, Taher, Ahmed S A, Tait, Caroline, Taylor, Amybel, Thake, Miriam, Thin, Katie, Thould, Hannah, Thyn, Thyn, To, Benjaman, Tobiss, Hannah, Toppley, Kathryn, Townsend, Liam, Tullo, Ellen, Tzovaras, George, Umeadi, Anthony, Vaidya, Hrisheekesh, Valero-Soriano, María, Varden, Rosanna, Vergani, Vittoria, Vervoort, Dominique, Vescio, Giuseppina, Vettasseri, Mark, Virk, Madiha, Vyas, Vaishali, Wagland, Joanne, Wallis, Stephanie, Warner, Chloe, Watkins, Eleanor, Watson, Hannah, Webb, Rachael, Welsh, Sarah H, West, Ruth, Whelan, Elisha, Whitney, Julie, Whitsey, Mark, Wilcock, Catherine, Wilkinson, Iain, Williams, David, Williamson, Megan, Willott, Ruth H, Wimalasundera, Mettha, Win, Yu Lelt, Winter, Laura, Worrall, Stephanie, Wright, Rebecca, Yeo, Natalie, Yeung, Eirene, Yigit, Merve, Yildiz, Yasin A, Yusuf, Humza, Zambon, Martina, Zaw, Hein, and Elabedeen, Omar Zein

Subjects
Male, Aging, medicine.medical_specialty, Frail Elderly, COVID-19, delirium, frailty, mortality, transitions of care, Cohort Studies, AcademicSubjects/MED00280, Interquartile range, Internal medicine, medicine, Dementia, Humans, Survivors, Aged, Proportional hazards model, business.industry, SARS-CoV-2, Hazard ratio, Odds ratio, General Medicine, medicine.disease, Confidence interval, frailty,COVID-19, Ageing, Delirium, Female, medicine.symptom, Geriatrics and Gerontology, business, Cohort study, Research Paper
Abstract

Introduction Increased mortality has been demonstrated in older adults with coronavirus disease 2019 (COVID-19), but the effect of frailty has been unclear. Methods This multi-centre cohort study involved patients aged 18 years and older hospitalised with COVID-19, using routinely collected data. We used Cox regression analysis to assess the impact of age, frailty and delirium on the risk of inpatient mortality, adjusting for sex, illness severity, inflammation and co-morbidities. We used ordinal logistic regression analysis to assess the impact of age, Clinical Frailty Scale (CFS) and delirium on risk of increased care requirements on discharge, adjusting for the same variables. Results Data from 5,711 patients from 55 hospitals in 12 countries were included (median age 74, interquartile range [IQR] 54–83; 55.2% male). The risk of death increased independently with increasing age (>80 versus 18–49: hazard ratio [HR] 3.57, confidence interval [CI] 2.54–5.02), frailty (CFS 8 versus 1–3: HR 3.03, CI 2.29–4.00) inflammation, renal disease, cardiovascular disease and cancer, but not delirium. Age, frailty (CFS 7 versus 1–3: odds ratio 7.00, CI 5.27–9.32), delirium, dementia and mental health diagnoses were all associated with increased risk of higher care needs on discharge. The likelihood of adverse outcomes increased across all grades of CFS from 4 to 9. Conclusion Age and frailty are independently associated with adverse outcomes in COVID-19. Risk of increased care needs was also increased in survivors of COVID-19 with frailty or older age.

Published
2021

5. A mutation in the major autophagy gene, WIPI2, associated with global developmental abnormalities

Author

Jelani, Musharraf, primary, Dooley, Hannah C., additional, Gubas, Andrea, additional, Mohamoud, Hussein Sheikh Ali, additional, Khan, Muhammad Tariq Masood, additional, Ali, Zahir, additional, Kang, Changsoo, additional, Rahim, Fazal, additional, Jan, Amin, additional, Vadgama, Nirmal, additional, Khan, Muhammad Ismail, additional, Al-Aama, Jumana Yousuf, additional, Khan, Asifullah, additional, Tooze, Sharon A, additional, and Nasir, Jamal, additional

Published
2019
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6. WIPI2B links PtdIns3P to LC3 lipidation through binding ATG16L1

Author

Dooley, Hannah C, Wilson, Michael I, and Tooze, Sharon A

Subjects
Mice, Phosphatidylinositol Phosphates, Autophagy, Animals, Humans, Membrane Proteins, Carrier Proteins, Lipids, Microtubule-Associated Proteins, Models, Biological, Autophagic Puncta, HeLa Cells, Protein Binding
Abstract

WIPI proteins, phosphatidylinositol 3-phosphate (PtdIns3P) binding proteins with β-propeller folds, are recruited to the omegasome following PtdIns3P production. The functions of the WIPI proteins in autophagosome formation are poorly understood. In a recent study, we reported that WIPI2B directly binds ATG16L1 and functions by recruiting the ATG12-ATG5-ATG16L1 complex to forming autophagosomes during starvation- or pathogen-induced autophagy. Our model of WIPI2 function provides an explanation for the PtdIns3P-dependent recruitment of the ATG12-ATG5-ATG16L1 complex during initiation of autophagy.

Published
2015

8. Assessing Mammalian Autophagy.

Author

Tooze, Sharon A., Dooley, Hannah C., Jefferies, Harold B. J., Joachim, Justin, Judith, Delphine, Lamb, Christopher A., Razi, Minoo, and Wirth, Martina

Published
2015
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11. A mutation in the major autophagy gene, WIPI2, associated with global developmental abnormalities

Author

Musharraf Jelani, Dooley, Hannah C, Gubas, Andrea, Mohamoud, Hussein Sheikh Ali, Khan, Muhammad Tariq Masood, Ali, Zahir, Changsoo Kang, Fazal Rahim, Jan, Amin, Vadgama, Nirmal, Khan, Muhammad Ismail, Al-Aama, Jumana Yousuf, Asifullah Khan, Tooze, Sharon A, and Nasir, Jamal

Subjects
Model organisms, Chemical Biology & High Throughput, Signalling & Oncogenes, Cell Biology, Biochemistry & Proteomics, 3. Good health, Imaging
Abstract

We describe a large consanguineous pedigree from a remote area of Northern Pakistan, with a complex developmental disorder associated with wide-ranging symptoms, including mental retardation, speech and language impairment and other neurological, psychiatric, skeletal and cardiac abnormalities. We initially carried out a genetic study using the HumanCytoSNP-12 v2.1 Illumina gene chip on nine family members and identified a single region of homozygosity shared amongst four affected individuals on chromosome 7p22 (positions 3059377-5478971). We performed whole-exome sequencing on two affected individuals from two separate branches of the extended pedigree and identified a novel nonsynonymous homozygous mutation in exon 9 of the WIPI2 (WD-repeat protein interacting with phosphoinositide 2) gene at position 5265458 (c.G745A;pV249M). WIPI2 plays a critical role in autophagy, an evolutionary conserved cellular pathway implicated in a growing number of medical conditions. The mutation is situated in a highly conserved and critically important region of WIPI2, responsible for binding PI(3)P and PI(3,5)P2, an essential requirement for autophagy to proceed. The mutation is absent in all public databases, is predicted to be damaging and segregates with the disease phenotype. We performed functional studies in vitro to determine the potential effects of the mutation on downstream pathways leading to autophagosome assembly. Binding of the V231M mutant of WIPI2b to ATG16L1 (as well as ATG5-12) is significantly reduced in GFP pull-down experiments, and fibroblasts derived from the patients show reduced WIPI2 puncta, reduced LC3 lipidation and reduced autophagic flux.

12. A mutation in the major autophagy gene, WIPI2, associated with global developmental abnormalities

Author

Musharraf Jelani, Dooley, Hannah C, Gubas, Andrea, Mohamoud, Hussein Sheikh Ali, Khan, Muhammad Tariq Masood, Ali, Zahir, Changsoo Kang, Fazal Rahim, Jan, Amin, Vadgama, Nirmal, Khan, Muhammad Ismail, Al-Aama, Jumana Yousuf, Asifullah Khan, Tooze, Sharon A, and Nasir, Jamal

Subjects
Model organisms, Chemical Biology & High Throughput, Signalling & Oncogenes, Cell Biology, Biochemistry & Proteomics, 3. Good health, Imaging
Abstract

We describe a large consanguineous pedigree from a remote area of Northern Pakistan, with a complex developmental disorder associated with wide-ranging symptoms, including mental retardation, speech and language impairment and other neurological, psychiatric, skeletal and cardiac abnormalities. We initially carried out a genetic study using the HumanCytoSNP-12 v2.1 Illumina gene chip on nine family members and identified a single region of homozygosity shared amongst four affected individuals on chromosome 7p22 (positions 3059377-5478971). We performed whole-exome sequencing on two affected individuals from two separate branches of the extended pedigree and identified a novel nonsynonymous homozygous mutation in exon 9 of the WIPI2 (WD-repeat protein interacting with phosphoinositide 2) gene at position 5265458 (c.G745A;pV249M). WIPI2 plays a critical role in autophagy, an evolutionary conserved cellular pathway implicated in a growing number of medical conditions. The mutation is situated in a highly conserved and critically important region of WIPI2, responsible for binding PI(3)P and PI(3,5)P2, an essential requirement for autophagy to proceed. The mutation is absent in all public databases, is predicted to be damaging and segregates with the disease phenotype. We performed functional studies in vitro to determine the potential effects of the mutation on downstream pathways leading to autophagosome assembly. Binding of the V231M mutant of WIPI2b to ATG16L1 (as well as ATG5-12) is significantly reduced in GFP pull-down experiments, and fibroblasts derived from the patients show reduced WIPI2 puncta, reduced LC3 lipidation and reduced autophagic flux.

13. Assessing mammalian autophagy.

Author

Tooze SA, Dooley HC, Jefferies HB, Joachim J, Judith D, Lamb CA, Razi M, and Wirth M

Subjects
Animals, Blotting, Western, Humans, Lysosomes metabolism, Microscopy, Fluorescence, Microtubule-Associated Proteins metabolism, Phagosomes metabolism, Autophagy physiology
Abstract

Autophagy (self-eating) is a highly conserved, vesicular pathway that cells use to eat pieces of themselves, including damaged organelles, protein aggregates or invading pathogens, for self-preservation and survival (Choi et al., N Engl J Med 368:651-662, 2013; Lamb et al., Nat Rev Mol Cell Biol 14:759-774, 2013). Autophagy can be delineated into three major vesicular compartments (the phagophore, autophagosome, autolysosome, see Fig. 1). The initial stages of the pathway involve the formation of phagophores (also called isolation membranes), which are open, cup-shaped membranes that expand and sequester the cytosolic components, including organelles and aggregated proteins or intracellular pathogens. Closure of the phagophore creates an autophagosome, which is a double-membrane vesicle. Fusion of the autophagosome with the lysosome, to form an autolysosome, delivers the content of the autophagosome into the lysosomal lumen and allows degradation to occur.Autophagy is a dynamic process that is initiated within 15 min of amino acid starvation in cell culture systems (Köchl et al., Traffic 7:129-145, 2006) and is likely to occur as rapidly in vivo (Mizushima et al., J Cell Biol 152:657-668, 2001). To initiate studies on the formation of the autophagosomes, and trafficking to and from the autophagic pathway, an ideal starting approach is to do a morphological analysis in fixed cells. Additional validation of the morphological data can be obtained using simple Western blot analysis. Here we describe the most commonly used morphological technique to study autophagy, in particular, using the most reliable marker, microtubule-associated protein 1A/1B-light chain 3 (LC3). In addition, we describe a second immunofluorescence assay to determine if autophagy is being induced, using an antibody to WD repeat domain, phosphoinositide interacting 2 (WIPI2), an effector of the phosphatidylinositol (3)-phosphate (PI3P) produced during autophagosome formation.

Published
2015
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14. WIPI2B links PtdIns3P to LC3 lipidation through binding ATG16L1.

Author

Dooley HC, Wilson MI, and Tooze SA

Subjects
Animals, Autophagy, HeLa Cells, Humans, Mice, Models, Biological, Protein Binding, Carrier Proteins metabolism, Lipids chemistry, Membrane Proteins metabolism, Microtubule-Associated Proteins metabolism, Phosphatidylinositol Phosphates metabolism
Abstract

WIPI proteins, phosphatidylinositol 3-phosphate (PtdIns3P) binding proteins with β-propeller folds, are recruited to the omegasome following PtdIns3P production. The functions of the WIPI proteins in autophagosome formation are poorly understood. In a recent study, we reported that WIPI2B directly binds ATG16L1 and functions by recruiting the ATG12-ATG5-ATG16L1 complex to forming autophagosomes during starvation- or pathogen-induced autophagy. Our model of WIPI2 function provides an explanation for the PtdIns3P-dependent recruitment of the ATG12-ATG5-ATG16L1 complex during initiation of autophagy.

Published
2015
Full Text
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