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1,906 results on '"J., Marie"'

1. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Aqeilan, Rami I, Arama, Eli, Baehrecke, Eric H, Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A, Bartek, Jiri, Bazan, Nicolas G, Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Marco E, Blagosklonny, Mikhail V, Blander, J Magarian, Blandino, Giovanni, Blomgren, Klas, Borner, Christoph, Bortner, Carl D, Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, Thomas, Damgaard, Rune Busk, Calin, George A, Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chen, Guo-Qiang, Chen, Quan, Chen, Youhai H, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M, Dawson, Valina L, De Maria, Ruggero, De Strooper, Bart, Debatin, Klaus-Michael, Deberardinis, Ralph J, Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Engeland, Kurt, Fimia, Gian Maria, Galassi, Claudia, Ganini, Carlo, Garcia-Saez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J Marie, Haupt, Ygal, He, Sudan, Heery, David M, Hengartner, Michael O, Hetz, Claudio, Hildeman, David A, Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J, and Kanneganti, Thirumala-Devi

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Good Health and Well Being, Animals, Humans, Apoptosis, Cell Death, Caspases, Carcinogenesis, Mammals, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

2. Development and validation of an integrative pan-solid tumor predictor of PD-1/PD-L1 blockade benefit

Author

Tomlins, Scott A., Khazanov, Nickolay A., Bulen, Benjamin J., Hovelson, Daniel H., Shreve, Melissa J., Lamb, Laura E., Matrana, Marc R., Burkard, Mark E., Yang, Eddy Shih-Hsin, Edenfield, William Jeffery, Dees, E. Claire, Onitilo, Adedayo A., Thompson, Michael, Buchschacher, Jr, Gary L., Miller, Alan M., Menter, Alexander, Parsons, Benjamin, Wassenaar, Timothy, Hwang, Leon C., Suga, J. Marie, Siegel, Robert, Irvin, Jr, William, Nair, Suresh, Slim, Jennifer N., Misleh, Jamal, Khatri, Jamil, Masters, Gregory, Thomas, Sachdev, Safa, Malek, Anderson, Daniel M., Kwiatkowski, Kat, Mitchell, Khalis, Hu-Seliger, Tina, Drewery, Stephanie, Fischer, Andrew, Plouffe, Komal, Czuprenski, Eric, Hipp, Jennifer, Reeder, Travis, Vakil, Hana, Johnson, D. Bryan, and Rhodes, Daniel R.

Published
2023
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3. Cryptococcus neoformans rapidly invades the murine brain by sequential breaching of airway and endothelial tissues barriers, followed by engulfment by microglia

Author

Vanessa I. Francis, Corin Liddle, Emma Camacho, Madhura Kulkarni, Samuel R. S. Junior, Jamie A. Harvey, Elizabeth R. Ballou, Darren D. Thomson, Gordon D. Brown, J. Marie Hardwick, Arturo Casadevall, Jonathan Witton, and Carolina Coelho

Subjects
microglia, Cryptococcus neoformans, blood-brain barrier, Microbiology, QR1-502
Abstract

ABSTRACTCryptococcus neoformans causes lethal meningitis and accounts for approximately 10%–15% of AIDS-associated deaths worldwide. There are major gaps in our understanding of how this fungus invades the mammalian brain. To investigate the dynamics of C. neoformans tissue invasion, we mapped fungal localization and host cell interactions in infected brain, lung, and upper airways using mouse models of systemic and airway infection. To enable this, we developed an in situ imaging pipeline capable of measuring large volumes of tissue while preserving anatomical and cellular information by combining thick tissue sections, tissue clarification, and confocal imaging. We confirm high fungal burden in mouse upper airway after nasal inoculation. Yeast in turbinates were frequently titan cells, with faster kinetics than reported in mouse lungs. Importantly, we observed one instance of fungal cells enmeshed in lamina propria of the upper airways, suggesting penetration of airway mucosa as a possible route of tissue invasion and dissemination to the bloodstream. We extend previous literature positing bloodstream dissemination of C. neoformans, by finding viable fungi in the bloodstream of mice a few days after intranasal infection. As early as 24 h post systemic infection, the majority of C. neoformans cells traversed the blood-brain barrier, and were engulfed or in close proximity to microglia. Our work presents a new method for investigating microbial invasion, establishes that C. neoformans can breach multiple tissue barriers within the first days of infection, and demonstrates microglia as the first cells responding to C. neoformans invasion of the brain.IMPORTANCECryptococcal meningitis causes 10%–15% of AIDS-associated deaths globally. Still, brain-specific immunity to cryptococci is a conundrum. By employing innovative imaging, this study reveals what occurs during the first days of infection in brain and in airways. We found that titan cells predominate in upper airways and that cryptococci breach the upper airway mucosa, which implies that, at least in mice, the upper airways are a site for fungal dissemination. This would signify that mucosal immunity of the upper airway needs to be better understood. Importantly, we also show that microglia, the brain-resident macrophages, are the first responders to infection, and microglia clusters are formed surrounding cryptococci. This study opens the field to detailed molecular investigations on airway immune response, how fungus traverses the blood-brain barrier, how microglia respond to infection, and ultimately how microglia monitor the blood-brain barrier to preserve brain function.

Published
2024
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5. Beth Levine in memoriam

Author

An, Zhenyi, Ballabio, Andrea, Bennett, Lynda, Boya, Patricia, Cecconi, Francesco, Chiang, Wei-Chung, Codogno, Patrice, Colombo, Maria Isabel, Cuervo, Ana Maria, Debnath, Jayanta, Deretic, Vojo, Dikic, Ivan, Dionne, Keith, Dong, Xiaonan, Elazar, Zvulun, Galluzzi, Lorenzo, Gentile, Frank, Griffin, Diane E, Hansen, Malene, Hardwick, J Marie, He, Congcong, Huang, Shu-Yi, Hurley, James, Jackson, William T, Jozefiak, Cindy, Kitsis, Richard N, Klionsky, Daniel J, Kroemer, Guido, Meijer, Alfred J, Melendez, Alicia, Melino, Gerry, Mizushima, Noboru, Murphy, Leon O, Nixon, Ralph, Orvedahl, Anthony, Pattingre, Sophie, Piacentini, Mauro, Reggiori, Fulvio, Ross, Theodora, Rubinsztein, David C, Ryan, Kevin, Sadoshima, Junichi, Schreiber, Stuart L, Scott, Frederick, Sebti, Salwa, Shiloh, Michael, Shoji, Sanae, Simonsen, Anne, Smith, Haley, Sumpter, Kathryn M, Thompson, Craig B, Thorburn, Andrew, Thumm, Michael, Tooze, Sharon, Vaccaro, Maria I, Virgin, Herbert W, Wang, Fei, White, Eileen, Xavier, Ramnik J, Yoshimori, Tamotsu, Yuan, Junying, Yue, Zhenyu, and Zhong, Qing

Subjects
Biochemistry and Cell Biology, Biological Sciences, Biochemistry & Molecular Biology, Biochemistry and cell biology
Published
2020

6. Development and validation of an integrative pan-solid tumor predictor of PD-1/PD-L1 blockade benefit

Author

Scott A. Tomlins, Nickolay A. Khazanov, Benjamin J. Bulen, Daniel H. Hovelson, Melissa J. Shreve, Laura E. Lamb, Marc R. Matrana, Mark E. Burkard, Eddy Shih-Hsin Yang, William Jeffery Edenfield, E. Claire Dees, Adedayo A. Onitilo, Michael Thompson, Gary L. Buchschacher, Alan M. Miller, Alexander Menter, Benjamin Parsons, Timothy Wassenaar, Leon C. Hwang, J. Marie Suga, Robert Siegel, William Irvin, Suresh Nair, Jennifer N. Slim, Jamal Misleh, Jamil Khatri, Gregory Masters, Sachdev Thomas, Malek Safa, Daniel M. Anderson, Kat Kwiatkowski, Khalis Mitchell, Tina Hu-Seliger, Stephanie Drewery, Andrew Fischer, Komal Plouffe, Eric Czuprenski, Jennifer Hipp, Travis Reeder, Hana Vakil, D. Bryan Johnson, and Daniel R. Rhodes

Subjects
Medicine
Abstract

Tomlins et al. develop an Immunotherapy Response Score (IRS) to predict clinical benefit from checkpoint inhibition across solid tumors. IRS integrates TMB and gene expression, is evaluable from FFPE material, and is predictive for real-world progression-free survival and overall survival in patients receiving PD-1/PD-L1 blockade therapy.

Published
2023
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7. Galleria mellonella immune melanization is fungicidal during infection

Author

Daniel F. Q. Smith, Quigly Dragotakes, Madhura Kulkarni, J. Marie Hardwick, and Arturo Casadevall

Subjects
Biology (General), QH301-705.5
Abstract

Real-time imaging of fungal infection and tissue clearing in the wax moth, Galleria mellonella, help evaluate the role of melanin in the insect host immune response to fungal pathogens.

Published
2022
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8. The cellular mechanisms associated with the anesthetic and neuroprotective properties of xenon: a systematic review of the preclinical literature

Author

Steven McGuigan, Daniel J. Marie, Liam J. O'Bryan, Francisco J. Flores, Lisbeth Evered, Brendan Silbert, and David A. Scott

Subjects
xenon, anesthesia, neuroprotection, NMDA receptor, ligand gated channels, cell signal cascade, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

IntroductionXenon exhibits significant neuroprotection against a wide range of neurological insults in animal models. However, clinical evidence that xenon improves outcomes in human studies of neurological injury remains elusive. Previous reviews of xenon's method of action have not been performed in a systematic manner. The aim of this review is to provide a comprehensive summary of the evidence underlying the cellular interactions responsible for two phenomena associated with xenon administration: anesthesia and neuroprotection.MethodsA systematic review of the preclinical literature was carried out according to the PRISMA guidelines and a review protocol was registered with PROSPERO. The review included both in vitro models of the central nervous system and mammalian in vivo studies. The search was performed on 27th May 2022 in the following databases: Ovid Medline, Ovid Embase, Ovid Emcare, APA PsycInfo, and Web of Science. A risk of bias assessment was performed utilizing the Office of Health Assessment and Translation tool. Given the heterogeneity of the outcome data, a narrative synthesis was performed.ResultsThe review identified 69 articles describing 638 individual experiments in which a hypothesis was tested regarding the interaction of xenon with cellular targets including: membrane bound proteins, intracellular signaling cascades and transcription factors. Xenon has both common and subtype specific interactions with ionotropic glutamate receptors. Xenon also influences the release of inhibitory neurotransmitters and influences multiple other ligand gated and non-ligand gated membrane bound proteins. The review identified several intracellular signaling pathways and gene transcription factors that are influenced by xenon administration and might contribute to anesthesia and neuroprotection.DiscussionThe nature of xenon NMDA receptor antagonism, and its range of additional cellular targets, distinguishes it from other NMDA antagonists such as ketamine and nitrous oxide. This is reflected in the distinct behavioral and electrophysiological characteristics of xenon. Xenon influences multiple overlapping cellular processes, both at the cell membrane and within the cell, that promote cell survival. It is hoped that identification of the underlying cellular targets of xenon might aid the development of potential therapeutics for neurological injury and improve the clinical utilization of xenon.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier: 336871.

Published
2023
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10. Persuasiveness and Sensitivity to Witnessing Conditions Depend on How Testimony is Presented

Author

Hicks, J. Marie and Clark, Steven E.

Abstract

The present experiment examined the persuasiveness (measured primarily by proportions of guilty verdicts) of the testimony of a single eyewitness as a function of witnessing conditions and method of presenting the testimony--via a Video or Audio recording or a written Transcript or Summary. Proportions of guilty verdicts showed little variation across presentation methods when witnessing conditions were relatively good, but were higher for Video and Audio presentations than for Transcript and Summary presentations when witnessing conditions were relatively poor. These results combined to show a decrease in sensitivity to witnessing conditions for Video and Audio presentations relative to Transcript and Summary presentations. These results were accounted for by a simple weighted cues model.

Published
2021
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12. KCTD7 deficiency defines a distinct neurodegenerative disorder with a conserved autophagy‐lysosome defect

Author

Metz, Kyle A, Teng, Xinchen, Coppens, Isabelle, Lamb, Heather M, Wagner, Bart E, Rosenfeld, Jill A, Chen, Xianghui, Zhang, Yu, Kim, Hee Jong, Meadow, Michael E, Wang, Tim Sen, Haberlandt, Edda D, Anderson, Glenn W, Leshinsky‐Silver, Esther, Bi, Weimin, Markello, Thomas C, Pratt, Marsha, Makhseed, Nawal, Garnica, Adolfo, Danylchuk, Noelle R, Burrow, Thomas A, Jayakar, Parul, McKnight, Dianalee, Agadi, Satish, Gbedawo, Hatha, Stanley, Christine, Alber, Michael, Prehl, Isabelle, Peariso, Katrina, Ong, Min Tsui, Mordekar, Santosh R, Parker, Michael J, Crooks, Daniel, Agrawal, Pankaj B, Berry, Gerard T, Loddenkemper, Tobias, Yang, Yaping, Maegawa, Gustavo HB, Aouacheria, Abdel, Markle, Janet G, Wohlschlegel, James A, Hartman, Adam L, and Hardwick, J Marie

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Pediatric, Rare Diseases, Brain Disorders, Batten Disease, Orphan Drug, Genetics, Clinical Research, Neurodegenerative, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Generic health relevance, Neurological, Age of Onset, Autophagy, Child, Preschool, Female, Humans, Infant, Lysosomes, Male, Mutation, Neurodegenerative Diseases, Pedigree, Potassium Channels, Saccharomyces cerevisiae Proteins, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveSeveral small case series identified KCTD7 mutations in patients with a rare autosomal recessive disorder designated progressive myoclonic epilepsy (EPM3) and neuronal ceroid lipofuscinosis (CLN14). Despite the name KCTD (potassium channel tetramerization domain), KCTD protein family members lack predicted channel domains. We sought to translate insight gained from yeast studies to uncover disease mechanisms associated with deficiencies in KCTD7 of unknown function.MethodsNovel KCTD7 variants in new and published patients were assessed for disease causality using genetic analyses, cell-based functional assays of patient fibroblasts and knockout yeast, and electron microscopy of patient samples.ResultsPatients with KCTD7 mutations can exhibit movement disorders or developmental regression before seizure onset, and are distinguished from similar disorders by an earlier age of onset. Although most published KCTD7 patient variants were excluded from a genome sequence database of normal human variations, most newly identified patient variants are present in this database, potentially challenging disease causality. However, genetic analysis and impaired biochemical interactions with cullin 3 support a causal role for patient KCTD7 variants, suggesting deleterious alleles of KCTD7 and other rare disease variants may be underestimated. Both patient-derived fibroblasts and yeast lacking Whi2 with sequence similarity to KCTD7 have impaired autophagy consistent with brain pathology.InterpretationBiallelic KCTD7 mutations define a neurodegenerative disorder with lipofuscin and lipid droplet accumulation but without defining features of neuronal ceroid lipofuscinosis or lysosomal storage disorders. KCTD7 deficiency appears to cause an underlying autophagy-lysosome defect conserved in yeast, thereby assigning a biological role for KCTD7. Ann Neurol 2018;84:774-788.

Published
2018

13. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V, Arama, Eli, Baehrecke, Eric H, Barlev, Nickolai A, Bazan, Nicolas G, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Katiuscia, Blagosklonny, Mikhail V, Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chandel, Navdeep S, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Cohen, Gerald M, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D’Angiolella, Vincenzo, Dawson, Ted M, Dawson, Valina L, De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J, Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M, Dixon, Scott J, Duckett, Colin S, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J Marie, Harris, Isaac S, Hengartner, Michael O, Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J, Juin, Philippe P, Kaiser, William J, Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N, Klionsky, Daniel J, Knight, Richard A, Kumar, Sharad, Lee, Sam W, Lemasters, John J, Levine, Beth, Linkermann, Andreas, Lipton, Stuart A, Lockshin, Richard A, López-Otín, Carlos, Lowe, Scott W, Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, and Manic, Gwenola

Subjects
Biochemistry and Cell Biology, Biological Sciences, Animals, Cell Death, Humans, Lysosomes, Mitochondrial Membrane Transport Proteins, Mitochondrial Permeability Transition Pore, Necrosis, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

14. Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases

Author

Connolly, Niamh MC, Theurey, Pierre, Adam-Vizi, Vera, Bazan, Nicolas G, Bernardi, Paolo, Bolaños, Juan P, Culmsee, Carsten, Dawson, Valina L, Deshmukh, Mohanish, Duchen, Michael R, Düssmann, Heiko, Fiskum, Gary, Galindo, Maria F, Hardingham, Giles E, Hardwick, J Marie, Jekabsons, Mika B, Jonas, Elizabeth A, Jordán, Joaquin, Lipton, Stuart A, Manfredi, Giovanni, Mattson, Mark P, McLaughlin, BethAnn, Methner, Axel, Murphy, Anne N, Murphy, Michael P, Nicholls, David G, Polster, Brian M, Pozzan, Tullio, Rizzuto, Rosario, Satrústegui, Jorgina, Slack, Ruth S, Swanson, Raymond A, Swerdlow, Russell H, Will, Yvonne, Ying, Zheng, Joselin, Alvin, Gioran, Anna, Moreira Pinho, Catarina, Watters, Orla, Salvucci, Manuela, Llorente-Folch, Irene, Park, David S, Bano, Daniele, Ankarcrona, Maria, Pizzo, Paola, and Prehn, Jochen HM

Subjects
Biochemistry and Cell Biology, Biological Sciences, Neurodegenerative, Aging, Acquired Cognitive Impairment, Brain Disorders, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Neurological, Animals, Humans, Mitochondria, Models, Biological, Neurodegenerative Diseases, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Neurodegenerative diseases are a spectrum of chronic, debilitating disorders characterised by the progressive degeneration and death of neurons. Mitochondrial dysfunction has been implicated in most neurodegenerative diseases, but in many instances it is unclear whether such dysfunction is a cause or an effect of the underlying pathology, and whether it represents a viable therapeutic target. It is therefore imperative to utilise and optimise cellular models and experimental techniques appropriate to determine the contribution of mitochondrial dysfunction to neurodegenerative disease phenotypes. In this consensus article, we collate details on and discuss pitfalls of existing experimental approaches to assess mitochondrial function in in vitro cellular models of neurodegenerative diseases, including specific protocols for the measurement of oxygen consumption rate in primary neuron cultures, and single-neuron, time-lapse fluorescence imaging of the mitochondrial membrane potential and mitochondrial NAD(P)H. As part of the Cellular Bioenergetics of Neurodegenerative Diseases (CeBioND) consortium ( www.cebiond.org ), we are performing cross-disease analyses to identify common and distinct molecular mechanisms involved in mitochondrial bioenergetic dysfunction in cellular models of Alzheimer's, Parkinson's, and Huntington's diseases. Here we provide detailed guidelines and protocols as standardised across the five collaborating laboratories of the CeBioND consortium, with additional contributions from other experts in the field.

Published
2018

20. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. [0000-0002-2705-7432], Degterev, Alexei [0000-0002-8240-7132], Del Sal, Giannino [0000-0003-2185-6003], Deshmukh, Mohanish [0000-0002-2597-5862], Di Virgilio, Francesco [0000-0003-3566-1362], Diederich, Marc [0000-0003-0115-4725], Dixon, Scott J. [0000-0001-6230-8199], El-Deiry, Wafik S. [0000-0002-9577-8266], Elrod, John W. [0000-0003-3925-2224], Engeland, Kurt [0000-0003-3525-0440], Fimia, Gian María [0000-0003-4438-3325], Ganini, Carlo [0000-0002-5839-3965], García-Sáez, Ana J. [0000-0002-3894-5945], Garg, Abhishek D. [0000-0002-9976-9922], Garrido, Carmen [0000-0003-1368-1493], Gavathiotis, Evripidis [0000-0001-6319-8331], Ghosh, Sourav [0000-0001-5990-8708], Green, Douglas R. [0000-0002-7332-1417], Gronemeyer, Hinrich [0000-0001-9454-2449}, Häcker, Georg [0000-0003-1058-5746], Hajnóczky, György [0000-0003-3813-2570], Hardwick, J. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. 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[0000-0001-7872-0196], Walczak, Henning [0000-0002-6312-4591], Wallach, David [0000-0003-2724-9757], Wang, Ruoning [0000-0001-9798-8032], Weber, Achim [0000-0003-0073-3637], Yamazaki, Takahiro [0000-0002-7420-4394], Zakeri, Zahra [0000-0003-4386-8072], Zawacka-Pankau, Joanna E. [0000-0002-7415-2942], Zhivotovsky, Boris [0000-0002-2238-3482], Piacentini, Mauro [0000-0003-2919-1296], Kroemer, Guido [0000-0002-9334-4405], Galluzzi, Lorenzo [0000-0003-2257-8500 ], Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Dieter, Adam, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Aqeilan, Rami I., Arama, Eli, Baehrecke, Eric H., Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A., Bartek, Jiri, Bazan, Nicolas G., Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Marco Emilio, Blagosklonny, Mikhail V., Blander, J. Magarian, Blandino, Giovanni, Blomgren, Klas, Bomer, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, T., Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chen, Guo‑Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, B., Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian María, Galassi, Claudia, Ganini, Carlo, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

21. Dry Heat: Baking, Roasting, and Broiling

Author

J. Marie Arick, Kendra Zamojski, and Amarat Simonne

Subjects
nutrition, meal preparation, cooking techniques, Agriculture (General), S1-972, Plant culture, SB1-1110, Biology (General), QH301-705.5
Abstract

This publication is the first in a series of documents to complement A Healthy Table Virtual Cooking School. The purpose is to educate the general public on how to safely prepare healthy meals at home. Written by M. Arick, K. Zamojski, and A. Simonne, and published by the UF/IFAS Department of Family, Youth and Community Sciences, November 2021.

Published
2021
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23. Cryptococcus neoformans rapidly invades the murine brain by sequential breaching of airway and endothelial tissues barriers and engulfment by microglia

Author

Francis, Vanessa, primary, Liddle, Corin, additional, Camacho, Emma, additional, Kulkarni, Madhura, additional, Junior, Samuel RS, additional, Harvey, Jamie A, additional, Ballou, Elizabeth R, additional, Thompson, Darren D, additional, Hardwick, J. Marie, additional, Casadevall, Arturo, additional, Witton, Jonathan, additional, and Coelho, Carolina, additional

Published
2023
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25. Facilitating Creative Idea Selection: The Combined Effects of Self-Affirmation, Promotion Focus and Positive Affect

Author

de Buisonjé, David R., Ritter, Simone M., de Bruin, Suze, ter Horst, J. Marie-Louise, and Meeldijk, Arne

Abstract

Generating creative ideas in a brainstorm session `is a crucial part of innovation. However, for actual implementation, the most creative ideas must be selected from a pool of ideas. To date, idea selection has remained relatively unexplored and validated instruments to measure idea selection performance are not systematically employed. This study aimed to improve creative idea selection performance in a field study. In this study, an idea pool of 18 ideas was used, and participants had to select the 5 most creative ideas from the idea pool. Right before participants performed the idea selection task, in the experimental condition, a promotion focus and positive affect was induced in combination with a self-affirmation task. Participants in the control condition performed corresponding filler tasks. The selection of the 5 most creative ideas from the idea pool of 18 ideas was performed individually. Participants in the experimental condition selected ideas that were more creative than did participants in the control condition. These findings provide first evidence that the selection of creative ideas can be enhanced through a combined induction of promotion-focus, positive mood and self-affirmation.

Published
2017
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27. Overall survival in the OlympiA phase III trial of adjuvant olaparib in patients with germline pathogenic variants in BRCA1/2 and high-risk, early breast cancer

Author

C.E. Geyer, J.E. Garber, R.D. Gelber, G. Yothers, M. Taboada, L. Ross, P. Rastogi, K. Cui, A. Arahmani, G. Aktan, A.C. Armstrong, M. Arnedos, J. Balmaña, J. Bergh, J. Bliss, S. Delaloge, S.M. Domchek, A. Eisen, F. Elsafy, L.E. Fein, A. Fielding, J.M. Ford, S. Friedman, K.A. Gelmon, L. Gianni, M. Gnant, S.J. Hollingsworth, S.-A. Im, A. Jager, Ó. Þ Jóhannsson, S.R. Lakhani, W. Janni, B. Linderholm, T.-W. Liu, N. Loman, L. Korde, S. Loibl, P.C. Lucas, F. Marmé, E. Martinez de Dueñas, R. McConnell, K.-A. Phillips, M. Piccart, G. Rossi, R. Schmutzler, E. Senkus, Z. Shao, P. Sharma, C.F. Singer, T. Španić, E. Stickeler, M. Toi, T.A. Traina, G. Viale, G. Zoppoli, Y.H. Park, R. Yerushalmi, H. Yang, D. Pang, K.H. Jung, A. Mailliez, Z. Fan, I. Tennevet, J. Zhang, T. Nagy, G.S. Sonke, Q. Sun, M. Parton, M.A. Colleoni, M. Schmidt, A.M. Brufsky, W. Razaq, B. Kaufman, D. Cameron, C. Campbell, A.N.J. Tutt, Paul Sevelda, Ferdinand Haslbauer, Monika Penzinger, Leopold Öhler, Christoph Tinchon, Richard Greil, Sonja Heibl, Rupert Bartsch, Viktor Wette, Christian F. Singer, Claudia Pasterk, Ruth Helfgott, Gunda Pristauz-Telsnigg, Herbert Stöger, Angsar Weltermann, Daniel Egle, Irene Thiel, David Fuchs, Holger Rumpold, Kathrin Strasser-Weippl, Beate Rautenberg, Volkmar Müller, Marcus Schmidt, Stefan Paepke, Mustafa Aydogdu, Christoph Thomssen, Joachim Rom, Christine Mau, Peter Fasching, Uwe-Jochen Göhring, Thorsten Kühn, Stefanie Noeding, Sherko Kümmel, John Hackmann, Elmar Stickeler, Abhishek Joshi, Joanna Dewar, Michael Friedlander, Kelly-Anne Phillips, Yoland Antill, Natasha Woodward, Ehtesham Abdi, Susan Tiley, Mathew George, David Boadle, Annabel Goodwin, Andre van der Westhuizen, George Kannourakis, Nicholas Murray, Nicole McCarthy, Judith Kroep, Maaike de Boer, Joan Heijns, Agnes Jager, Franciscus Erdkamp, Sandra Bakker, Gabe S. Sonke, Amer Sami, John Mackey, Catherine Prady, Andrea Eisen, Christine Desbiens, Erica Patocskai, Cristiano Ferrario, Karen Gelmon, Louise Bordeleau, Haji Chalchal, Saroj Niraula, null ido wolf, Elżbieta Senkus, François Duhoux, null Randal d’Hondt, Sylvie Luce, Daphné t’Kint de Roodenbeke, Konstantinos Papadimitriou, Marleen Borms, Claire Quaghebeur, William Jacot, Etienne Brain, Laurence Venat-Bouvet, Alain Lortholary, Zbigniew Nowecki, Fátima Cardoso, Richard Hayward, Santiago Bella, Mauricio Fernández Lazzaro, Norma Pilnik, Luis E. Fein, Cesar Blajman, Guillermo Lerzo, Mirta Varela, Juan Jose Zarba, Diego Kaen, Maria Victoria Constanzo, Joke Tio, Wulf Siggelkow, Christian Jackisch, Eva Maria Grischke, Dirk Zahm, Sara Tato-Varela, Sabine Schmatloch, Peter Klare, Andrea Stefek, Kerstin Rhiem, Oliver Hoffmann, Mustafa Deryal, Isolde Gröll, Peter Ledwon, Christoph Uleer, Petra Krabisch, Jochem Potenberg, Maren Darsow, Tjoung-Won Park-Simon, Heinz-Gert Höffkes, Till-Oliver Emde, Gerd Graffunder, Oliver Tomé, Dirk Forstmeyer, Jürgen Terhaag, Christoph Salat, Karin Kast, Steffi Weniger, Carsten Schreiber, Bernhard Heinrich, Max Dieterich, Michaela Penelope Wüllner, Raquel Andrés Conejero, José Ángel García Sáenz, Lourdes Calvo Martinez, Angels Arcusa Lanza, Serafín Morales Murillo, Fernando Henao Carrasco, Salvador Blanch Tormo, Isabel Álvarez López, Juan Ignacio Delgado Mingorance, Elena Álvarez Gomez, Marta Santisteban, Josefina Cruz Jurado, Vanesa Quiroga, Manuel Ruiz Borrego, Eduardo Martínez de Dueñas, Jose Enrique Alés Martínez, Juan De la Haba, Noelia Martínez Jañez, Álvaro Rodríguez Lescure, Antonio Antón Torres, Gema Llort Crusades, Santiago González-Santiago, Antonia Marquez Aragones, Ana Laura Ortega, Agusti Barnadas Molins, José Ignacio Chacón López-Muñiz, Miguel Martín Jiménez, Ana Santaballa Bertrán, César Rodríguez, Lucía González Cortijo, Elisabetta Cretella, Laura Cortesi, Enzo Maria Ruggeri, Claudio Verusio, Stefania Gori, Andrea Bonetti, Anna Maria Mosconi, Oskar Johannsson, Guy Jerusalem, Patrick Neven, Tünde Nagy, Graziella Pinotti, Marco A. Colleoni, Antonio Bernardo, Lorenzo Gianni, Eraldo Bucci, Laura Biganzoli, Konstantin Dedes, Urban Novak, Khalil Zaman, Jeremy Braybrooke, Matthew Winter, Daniel Rea, Muireann Kelleher, Sophie Barrett, Stephen Chan, Tamas Hickish, Jane Hurwitz, John Conibear, Apurna Jegannathen, Marina Parton, Andrew Tutt, Rozenn Allerton, Annabel Borley, Anne Armstrong, Ellen Copson, Nicola Levitt, Jean Abraham, Timothy Perren, Rebecca Roylance, Kazushige Ishida, Tatsuya Toyama, Norikazu Masuda, Junichiro Watanabe, Eriko Tokunaga, Takayuki Kinoshita, Yoshiaki Rai, Masahiro Takada, Yasuhiro Yanagita, Rikiya Nakamura, Takahiro Nakayama, Yasuto Naoi, Hiroji Iwata, Seigo Nakamura, Masato Takahashi, Kenjiro Aogi, Koichiro Tsugawa, Hirofumi Mukai, Toshimi Takano, Akihiko Osaki, Nobuaki Sato, Hideko Yamauchi, Yutaka Tokuda, Mitsuya Ito, Takeki Sugimoto, Shakeela W. Bahadur, Patricia A. Ganz, Min J. Lu, Monica M. Mita, James Waisman, Jonathan A. Polikoff, Melinda L. Telli, Samantha A. Seaward, J. Marie Suga, Lara N. Durna, Jennifer Fu Carney, Alex Menter, Ajithkumar Puthillath, Nitin Rohatgi, James H. Feusner, Kristie A. Bobolis, Peter D. Eisenberg, Derrick Wong, Virginia F. Borges, Alexander T. Urquhart, Erin W. Hofstatter, Edward C. McCarron, Claudine Isaacs, Pia Herbolsheimer, Ramya Varadarajan, Adam Raben, Ruby Anne E. Deveras, Frances Valdes-Albini, Reshma L. Mahtani, Jane L. Meisel, Bradley T. Sumrall, Cheryl F. Jones, Samuel N. Ofori, Kenneth N.M. Sumida, Mark Karwal, Deborah W. Wilbur, (Joe) Singh, David M. Spector, John Schallenkamp, Douglas E. Merkel, Shelly S. Lo, Pam G. Khosla, Massimo Cristofanilli, Lisa Flaum, Kent F. Hoskins, Melody A. Cobleigh, Elyse A. Lambiase, Olwen M. Hahn, Ira A. Oliff, Bryan A. Faller, James L. Wade, Nafisa D. Burhani, Amaryllis Gil, Harvey E. Einhorn, Anna M.V. Storniolo, Brian K. Chang, Maitri Kalra, Erwin L. Robin, Bilal Ansari, Priyanka Sharma, Shaker R. Dakhil, Richard L. Deming, John T. Cole, David S. Hanson, Augusto C. Ochoa, Judy E. Garber, Harvey Zimbler, Deborah K. Armstrong, Katherine H.R. Tkaczuk, David A. Riseberg, Brian M. O'Connor, Thomas H. Openshaw, Dana Zakalik, Cynthia M. Vakhariya, Anne F. Schott, Michael S. Simon, Thomas J. Doyle, Tareq Al Baghdadi, Amy VanderWoude, Patrick J. Flynn, Richard T. Zera, Bret E.B. Friday, Kathryn J. Ruddy, Ron Smith, null Ademuyiwa, Foluso Olabisi, Robert Ellis, Jay W. Carlson, null Marchello, Benjamin T, Edward A. Levine, Paul K. Marcom, Cameron B. Harkness, Antoinette R. Tan, William J. Charles, Charles S. Kuzma, Shonda Asaad, James E. Radford, Preston D. Steen, Madhu Unnikrishnan, Grant R. Seeger, Kirsten M.H. Leu, Mehmet S. Copur, Ralph J. Hauke, Gamini S. Soori, Bradley A. Arrick, Jennifer G. Reeder, Deborah L. Toppmeyer, Zoneddy R. Dayao, Sylvia Adams, Eleni Andreopoulou, Magnuson Allison, Jesus D. Anampa Mesias, Ruby Sharma, Bhuvaneswari Ramaswamy, Aaron T. Gerds, Robert R. Shenk, Howard M. Gross, Shruti Trehan, Wajeeha Razaq, Abdul H. Mansoor, Christie J. Hilton, Adam M. Brufsky, Chanh Huynh, Nabila Chowdhury, Susan M. Domchek, Elin R. Sigurdson, Terrence P. Cescon, Marc A. Rovito, Albert S. DeNittis, Victor G. Vogel, Thomas B. Julian, L.E. Boyle, Luis Baez-Diaz, Frank J. Brescia, John E. Doster, Robert D. Siegel, Lucas Wong, Tejal Patel, Julie R. Nangia, Catherine A. Jones, George M. Cannon, Harry D. Bear, Hetal Vachhani, Mary Wilkinson, Marie E. Wood, Fengting Yan, Xingwei Sui, Carol M. van Haelst, Jennifer M. Specht, Ying Zhuo, Rubina Qamar, Matthew L. Ryan, Abigail Stockham, Shamsuddin Virani, Arlene A. Gayle, Steven J. Jubelirer, Sobha Kurian, Mohamad A. Salkeni, Niklas Loman, Barbro Linderholm, Gustav Silander, Anna-Lotta Hallbeck, Anna von Wachenfeldt Väppling, Elsa Curtit, Catarina Cardoso, Sofia Braga, Miguel Abreu, Mafalda Casa-Nova, Mónica Nave, Eva María Ciruelos Gil, Judith Balmaña Gelpi, Adela Fernández Ortega, Josep Gumà Padró, Begoña Bermejo de las Heras, María González Cao, Juan Cueva Bañuelos, Jesús Alarcon Company, Gemma Viñas Villaró, Laura García Estevez, Jens Huober, Steffi Busch, Tanja Fehm, Antje Hahn, Andrea Grafe, Thomas Noesselt, Thomas Dewitz, Harald Wagner, Christina Bechtner, Michael Weigel, Hans-Christian Kolberg, Thomas Decker, Jörg Thomalla, Tobias Hesse, Nadia Harbeck, Jan Schröder Jens-Uwe Blohmer, Marc Wolf Sütterlin, Renske Altena, Chang-Fang Chiu, Shin-Cheh Chen, Ming-Feng Hou, Yuan-Ching Chang, Shang-Hung Chen, Shou-Tung Chen, Chiun-Sheng Huang, Dah-Cherng Yeh, Jyh-Cherng Yu, Ling-Ming Tseng, Wei-Pang Chung, Audrey Mailliez, Thierry Petit, Suzette Delaloge, Christelle Lévy, Philippe Dalivoust, Jean-Marc Extra, Marie-Ange Mouret-Reynier, Anne-Claire Hardy-Bessard, Hélène Simon, Tiffenn L'Haridon, Alice Mege, Sylvie Giacchetti, Camille Chakiba-Brugere, Alain Gratet, Virginie Pottier, Jean-Marc Ferrero, Isabelle Tennevet, Christophe Perrin, Jean-Luc Canon, Sofie Joris, Zhimin Shao, Binghe Xu, ZeFei Jiang, Qiang Sun, Kunwei Shen, Da Pang, Jin Zhang, Shui Wang, Hongjian Yang, Ning Liao, Hong Zheng, Peifen Fu, Chuangui Song, Yongsheng Wang, Zhimin Fan, Cuizhi Geng, Olivier Tredan, László Landherr, Bella Kaufman, Rinat Yerushalmi, Beatrice Uziely, Pierfranco Conte, Claudio Zamagni, Giampaolo Bianchini, Michelino De Laurentiis, Carlo Tondini, Vittorio Gebbia, Mariangela Ciccarese, Tomasz Sarosiek, Jacek Mackiewicz, Anna Słowińska, Ewa Kalinka, Tomasz Huzarski, Seock-Ah Im, Kyung Hae Jung, Joo Hyuk Sohn, Jee Hyun Kim, Keun Seok Lee, Yeon Hee Park, Kyoung Eun Lee, Yee Soo Chae, Eun Kyung Cho, Institut Català de la Salut, [Geyer CE Jr] NRG Oncology/NSABP Foundation, Pittsburgh, USA. Department of Medicine, UPMC Hillman Cancer Center, Pittsburgh, USA. [Garber JE] Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA. [Gelber RD] Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA. Harvard T.H. Chan School of Public Health, Boston, USA. Frontier Science Foundation, Boston, USA. [Yothers G] NRG Oncology/NSABP Foundation, Pittsburgh, USA. Department of Biostatistics, University of Pittsburgh, Pittsburgh, USA. [Taboada M] Oncology Biometrics Department, AstraZeneca, Macclesfield, UK. [Ross L] Department of Data Management, Frontier Science (Scotland), Kincraig, Scotland, UK. [Balmaña J] Vall d’Hebron Institute of Oncology (VHIO), Barcelona, Spain. Servei d’Oncologia Mèdica, Vall d’Hebron Hospital Universitari, Barcelona, Spain, Vall d'Hebron Barcelona Hospital Campus, Medical Oncology, Public Health, Virology, Department of Psychology, Education and Child Studies, Internal Medicine, General Practice, and Child and Adolescent Psychiatry / Psychology

Subjects
Neoplasms::Neoplasms by Site::Breast Neoplasms [DISEASES], Medicaments antineoplàstics - Ús terapèutic, Otros calificadores::Otros calificadores::/farmacoterapia [Otros calificadores], Breast Neoplasms, Other subheadings::Other subheadings::/drug therapy [Other subheadings], olaparib, Article, breast cancer, SDG 3 - Good Health and Well-being, BRCA1/2, células::células germinativas [ANATOMÍA], Humans, Other subheadings::/therapeutic use [Other subheadings], Cells::Germ Cells [ANATOMY], neoplasias::neoplasias por localización::neoplasias de la mama [ENFERMEDADES], Otros calificadores::/uso terapéutico [Otros calificadores], BRCA1 Protein, PARP inhibition, acciones y usos químicos::acciones farmacológicas::usos terapéuticos::antineoplásicos [COMPUESTOS QUÍMICOS Y DROGAS], adjuvant therapy, Hematology, Cèl·lules germinals, Germ Cells, Oncology, Mama - Càncer - Tractament, Phthalazines, Female, Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [CHEMICALS AND DRUGS]
Abstract

Adjuvant therapy; Breast cancer; Olaparib Terapia adyuvante; Cáncer de mama; Olaparib Teràpia adjuvant; Càncer de mama; Olaparib Background The randomized, double-blind OlympiA trial compared 1 year of the oral poly(adenosine diphosphate-ribose) polymerase inhibitor, olaparib, to matching placebo as adjuvant therapy for patients with pathogenic or likely pathogenic variants in germline BRCA1 or BRCA2 (gBRCA1/2pv) and high-risk, human epidermal growth factor receptor 2-negative, early breast cancer (EBC). The first pre-specified interim analysis (IA) previously demonstrated statistically significant improvement in invasive disease-free survival (IDFS) and distant disease-free survival (DDFS). The olaparib group had fewer deaths than the placebo group, but the difference did not reach statistical significance for overall survival (OS). We now report the pre-specified second IA of OS with updates of IDFS, DDFS, and safety. Patients and methods One thousand eight hundred and thirty-six patients were randomly assigned to olaparib or placebo following (neo)adjuvant chemotherapy, surgery, and radiation therapy if indicated. Endocrine therapy was given concurrently with study medication for hormone receptor-positive cancers. Statistical significance for OS at this IA required P < 0.015. Results With a median follow-up of 3.5 years, the second IA of OS demonstrated significant improvement in the olaparib group relative to the placebo group [hazard ratio 0.68; 98.5% confidence interval (CI) 0.47-0.97; P = 0.009]. Four-year OS was 89.8% in the olaparib group and 86.4% in the placebo group (Δ 3.4%, 95% CI −0.1% to 6.8%). Four-year IDFS for the olaparib group versus placebo group was 82.7% versus 75.4% (Δ 7.3%, 95% CI 3.0% to 11.5%) and 4-year DDFS was 86.5% versus 79.1% (Δ 7.4%, 95% CI 3.6% to 11.3%), respectively. Subset analyses for OS, IDFS, and DDFS demonstrated benefit across major subgroups. No new safety signals were identified including no new cases of acute myeloid leukemia or myelodysplastic syndrome. Conclusion With 3.5 years of median follow-up, OlympiA demonstrates statistically significant improvement in OS with adjuvant olaparib compared with placebo for gBRCA1/2pv-associated EBC and maintained improvements in the previously reported, statistically significant endpoints of IDFS and DDFS with no new safety signals. Funding for this work, which was conducted as a collaborative partnership among the Breast International Group, NRG Oncology, Frontier Science, AstraZeneca, and Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, NJ, U.S.A. (MSD), was provided by the National Institutes of Health (grant numbers: U10CA 180868, UG1CA 189867, and U10CA 180822) and by AstraZeneca as part of an alliance between AstraZeneca and MSD. Provision of olaparib and placebo was from AstraZeneca.

Published
2022
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33. Optimal FOPI-FOPD controller design for rotary inverted pendulum system using grey wolves' optimization technique

Author

Muhannad A. Hasan, Ahmed A. Oglah, and Mehdi J. Marie

Subjects
optimization technique, RIP system, integer and fractional order PI-PD controllers, Electrical and Electronic Engineering
Abstract

The rotary inverted pendulum (RIP) has been used in various control application areas. This system can be represented as two degree of freedom (2-DOF), consisting of a rotating arm and rotating pendulum rod. RIP is an excellent example of designing a single-input multi-output (SIMO) system. Due to unstable RIP system dynamics, and its nonlinear model, multiple control techniques have been used to control this system. This paper uses integer and fractional order proportional integral-proportional derivative (PI-PD) controllers to stabilize the pendulum in the vertical direction. Constrained optimization approaches, such as the grey wolf optimization (GWO) methodology, are utilized to estimate the parametric values of the controllers. The simulation results showed that the fractional order PI-PD controller outperforms the integer order PI-PD controller with and without disturbance signal existence. A multiple results comparison has illustrated the superiority of fractional order controller over a previous work.

Published
2023

40. Wireless Network Control System for Electro Stati Precipitator in Cement Plants

Author

Mehdi J. Marie, Khalaf S. Gaied, and Ahmed R. Ajel

Subjects
Chemical engineering, TP155-156, Engineering (General). Civil engineering (General), TA1-2040
Abstract

Wireless control networks (WCNs), based on distributed control systems of wireless sensor and actuator networks, integrate four technologies: control, computer network and wireless communications. Electrostatic precipitator (ESP) in cement plants reduces the emissions from rotary kiln by 99.8% approximately. It is an important thing to change the existing systems (wireline) to wireless because of dusty and hazardous environments. In this paper, we designed a wireless control system for ESP using Truetime 2 beta 6 simulator, depending on the mathematical model that have been built using identification toolbox of Matlab v7.1.1. We also study the effect ofusing wireless network on performance and stability of the closed loop control system. Simulation results of WCN for ESP show smooth operation with a little bit of perturbation between transient and steady state region.

Published
2018
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41. Data from Syndecan-2 Affects the Basal and Chemotherapy-Induced Apoptosis in Osteosarcoma

Author

Dominique Modrowski, Pierre J. Marie, Pierre Levillain, Natacha Entz-Werle, Céline Bazille, Olivia Fromigué, and Armelle Orosco

Abstract

Syndecans are transmembrane heparan sulfate proteoglycans controlling cell adhesion, migration, and proliferation. We previously showed that syndecan-2 is involved in the control of apoptosis in cultured osteosarcoma cells. These data led us to the hypothesis that syndecan-2 may play a role in the apoptotic signaling in bone tumors. We immunohistochemically analyzed tissue sections from biopsies from 21 patients with well-characterized osteosarcoma. These tissues expressed low levels of syndecan-2 compared with osteoblasts and osteocytes in normal bone. Cultured human osteosarcoma cells also produced lower mRNA levels of syndecan-2 than normal osteoblastic cells. Moreover, the presence of syndecan-2 correlated with spontaneous apoptosis in osteosarcoma tissues as assessed by detection of DNA fragmentation in situ. Overexpression of syndecan-2 resulted in decreased number of migrating and invading U2OS osteosarcoma cells in Matrigel. In addition, overexpression of syndecan-2 sensitized human osteosarcoma cells to chemotherapy-induced apoptosis, increasing the response to methotrexate, doxorubicin, and cisplatin. Consistently, knockdown of the proteoglycan using stable transfection with a plasmid coding small interfering RNA resulted in inhibition of chemotherapy-induced apoptosis. Analysis of syndecan-2 expression both in biopsies and in corresponding postchemotherapy-resected tumors, as well as in cells treated with methotrexate or doxorubicin, showed that the cytotoxic action of chemotherapy can be associated with an increase in syndecan-2. These results provide support for a tumor-suppressor function for syndecan-2 and suggest that dysregulation of apoptosis may be related to abnormal syndecan-2 expression or induction in osteosarcoma. Moreover, our data identify syndecan-2 as a new factor mediating the antioncogenic effect of chemotherapeutic drugs. [Cancer Res 2007;67(8):3708–14]

Published
2023
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43. Suppression of Steady-state, but not Stimulus-induced NF-κB Activity Inhibits Alphavirus-induced Apoptosis

Author

Lin, Kuo-I, DiDonato, Joseph A, Hoffmann, Alexander, Hardwick, J Marie, and Ratan, Rajiv R

Subjects
Genetics, Vector-Borne Diseases, Prevention, Cancer, 3T3 Cells, Acetylcysteine, Animals, Antiviral Agents, Apoptosis, DNA-Binding Proteins, Genetic Vectors, Hydrogen Peroxide, I-kappa B Proteins, Mice, NF-KappaB Inhibitor alpha, NF-kappa B, NF-kappa B p50 Subunit, Rats, Sindbis Virus, Staurosporine, Time Factors, Transcription Factor RelA, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Recent studies have established cell type- specific, proapoptotic, or antiapoptotic functions for the transcription factor NF-kappaB. In each of these studies, inhibitors of NF-kappaB activity have been present before the apoptotic stimulus, and so the role of stimulus- induced NF-kappaB activation in enhancing or inhibiting survival could not be directly assessed. Sindbis virus, an alphavirus, induces NF-kappaB activation and apoptosis in cultured cell lines. To address whether Sindbis virus- induced NF-kappaB activation is required for apoptosis, we used a chimeric Sindbis virus that expresses a superrepressor of NF-kappaB activity. Complete suppression of virus-induced NF-kappaB activity neither prevents nor potentiates Sindbis virus-induced apoptosis. In contrast, inhibition of NF-kappaB activity before infection inhibits Sindbis virus-induced apoptosis. Our results demonstrate that suppression of steady-state, but not stimulus-induced NF-kappaB activity, regulates expression of gene products required for Sindbis virus-induced death. Furthermore, we show that in the same cell line, NF-kappaB can be proapoptotic or antiapoptotic depending on the death stimulus. We propose that the role of NF-kappaB in regulating apoptosis is determined by the death stimulus and by the timing of modulating NF-kappaB activity relative to the death stimulus.

Published
1998

44. Similar evolutionary trajectories in an environmental Cryptococcus neoformans isolate after human and murine infection

Author

Sephton-Clark, Poppy, primary, McConnell, Scott A., additional, Grossman, Nina, additional, Baker, Rosanna P., additional, Dragotakes, Quigly, additional, Fan, Yunfan, additional, Fu, Man Shun, additional, Gerbig, Gracen, additional, Greengo, Seth, additional, Hardwick, J. Marie, additional, Kulkarni, Madhura, additional, Levitz, Stuart M., additional, Nosanchuk, Joshua D., additional, Shoham, Shmuel, additional, Smith, Daniel F. Q., additional, Stempinski, Piotr, additional, Timp, Winston, additional, Wear, Maggie P., additional, Cuomo, Christina A., additional, and Casadevall, Arturo, additional

Published
2023
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45. Similar evolutionary trajectories in an environmental

Author

Poppy, Sephton-Clark, Scott A, McConnell, Nina, Grossman, Rosanna P, Baker, Quigly, Dragotakes, Yunfan, Fan, Man Shun, Fu, Gracen, Gerbig, Seth, Greengo, J Marie, Hardwick, Madhura, Kulkarni, Stuart M, Levitz, Joshua D, Nosanchuk, Shmuel, Shoham, Daniel F Q, Smith, Piotr, Stempinski, Winston, Timp, Maggie P, Wear, Christina A, Cuomo, and Arturo, Casadevall

Abstract

A pet cockatoo was the suspected source of

Published
2023

47. Do Fungi Undergo Apoptosis-Like Programmed Cell Death?

Author

J. Marie Hardwick

Subjects
apoptosis, cell death, cell-autonomous, fungi, mycoptosis, necroptosis, Microbiology, QR1-502
Abstract

ABSTRACT This question of whether fungi undergo apoptosis-like programmed cell death can be separated into two questions. One question is about applying the term "apoptosis" to fungi, and the other is a more challenging question of whether fungi have evolved mechanisms that inflict self-injury. The answers to both questions depend on the definitions applied to “apoptosis” and “programmed cell death.” Considering how these and other cell death terms originated and are currently defined for animals, some confusion arises when the terms are applied to fungi. While it is difficult to defend the concept of fungal apoptosis, the more interesting issue is whether fungi will eventually be found to encode programmed or extemporaneous self-destructive processes, as suggested by intriguing new findings.

Published
2018
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48. Whi2 is a conserved negative regulator of TORC1 in response to low amino acids.

Author

Xianghui Chen, Guiqin Wang, Yu Zhang, Margaret Dayhoff-Brannigan, Nicola L Diny, Mingjun Zhao, Ge He, Cierra N Sing, Kyle A Metz, Zachary D Stolp, Abdel Aouacheria, Wen-Chih Cheng, J Marie Hardwick, and Xinchen Teng

Subjects
Genetics, QH426-470
Abstract

Yeast WHI2 was originally identified in a genetic screen for regulators of cell cycle arrest and later suggested to function in general stress responses. However, the function of Whi2 is unknown. Whi2 has predicted structure and sequence similarity to human KCTD family proteins, which have been implicated in several cancers and are causally associated with neurological disorders but are largely uncharacterized. The identification of conserved functions between these yeast and human proteins may provide insight into disease mechanisms. We report that yeast WHI2 is a new negative regulator of TORC1 required to suppress TORC1 activity and cell growth specifically in response to low amino acids. In contrast to current opinion, WHI2 is dispensable for TORC1 inhibition in low glucose. The only widely conserved mechanism that actively suppresses both yeast and mammalian TORC1 specifically in response to low amino acids is the conserved SEACIT/GATOR1 complex that inactivates the TORC1-activating RAG-like GTPases. Unexpectedly, Whi2 acts independently and simultaneously with these established GATOR1-like Npr2-Npr3-Iml1 and RAG-like Gtr1-Gtr2 complexes, and also acts independently of the PKA pathway. Instead, Whi2 inhibits TORC1 activity through its binding partners, protein phosphatases Psr1 and Psr2, which were previously thought to only regulate amino acid levels downstream of TORC1. Furthermore, the ability to suppress TORC1 is conserved in the SKP1/BTB/POZ domain-containing, Whi2-like human protein KCTD11 but not other KCTD family members tested.

Published
2018
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49. Potent anti-seizure effects of D-leucine

Author

Adam L. Hartman, Polan Santos, Kenneth J. O'Riordan, Carl E. Stafstrom, and J. Marie Hardwick

Subjects
Amino acids, Epilepsy, Kainic acid, Preclinical testing, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

There are no effective treatments for millions of patients with intractable epilepsy. High-fat ketogenic diets may provide significant clinical benefit but are challenging to implement. Low carbohydrate levels appear to be essential for the ketogenic diet to work, but the active ingredients in dietary interventions remain elusive, and a role for ketogenesis has been challenged. A potential antiseizure role of dietary protein or of individual amino acids in the ketogenic diet is understudied. We investigated the two exclusively ketogenic amino acids, L-leucine and L-lysine, and found that only L-leucine potently protects mice when administered prior to the onset of seizures induced by kainic acid injection, but not by inducing ketosis. Unexpectedly, the D-enantiomer of leucine, which is found in trace amounts in the brain, worked as well or better than L-leucine against both kainic acid and 6 Hz electroshock-induced seizures. However, unlike L-leucine, D-leucine potently terminated seizures even after the onset of seizure activity. Furthermore, D-leucine, but not L-leucine, reduced long-term potentiation but had no effect on basal synaptic transmission in vitro. In a screen of candidate neuronal receptors, D-leucine failed to compete for binding by cognate ligands, potentially suggesting a novel target. Even at low doses, D-leucine suppressed ongoing seizures at least as effectively as diazepam but without sedative effects. These studies raise the possibility that D-leucine may represent a new class of anti-seizure agents, and that D-leucine may have a previously unknown function in eukaryotes.

Published
2015
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