Search

Your search keyword '"Hale, Benjamin"' showing total 221 results
Start Over Author "Hale, Benjamin" Search Limiters Peer Reviewed
221 results on '"Hale, Benjamin"'

9. Proteogenetic drug response profiling elucidates targetable vulnerabilities of myelofibrosis

Author

Wildschut, Mattheus H. E., Mena, Julien, Dördelmann, Cyril, van Oostrum, Marc, Hale, Benjamin D., Settelmeier, Jens, Festl, Yasmin, Lysenko, Veronika, Schürch, Patrick M., Ring, Alexander, Severin, Yannik, Bader, Michael S., Pedrioli, Patrick G. A., Goetze, Sandra, van Drogen, Audrey, Balabanov, Stefan, Skoda, Radek C., Lopes, Massimo, Wollscheid, Bernd, Theocharides, Alexandre P. A., and Snijder, Berend

Published
2023
Full Text
View/download PDF

15. Mechanisms and clinical relevance of the bidirectional relationship of viral infections with metabolic diseases

Author

Perakakis, Nikolaos, Harb, Hani, Hale, Benjamin G, Varga, Zsuzsanna, Steenblock, Charlotte, Kanczkowski, Waldemar, Alexaki, Vasileia Ismini, Ludwig, Barbara, Mirtschink, Peter, Solimena, Michele, Toepfner, Nicole, Zeissig, Sebastian, Gado, Manuel, Abela, Irene Alma, Beuschlein, Felix, Spinas, Giatgen A, Cavelti-Weder, Claudia, Gerber, Philipp A, Huber, Michael, Trkola, Alexandra, Puhan, Milo A, Wong, Wendy Wei-Lynn, Linkermann, Andreas, Mohan, Viswanathan, Lehnert, Hendrik, Nawroth, Peter, Chavakis, Triantafyllos, Mingrone, Geltrude, Wolfrum, Christian, Zinkernagel, Annelies S, and Bornstein, Stefan R

Published
2023
Full Text
View/download PDF

31. MHC class II proteins mediate cross-species entry of bat influenza viruses

Author

Karakus, Umut, Thamamongood, Thiprampai, Ciminski, Kevin, Ran, Wei, Günther, Sira C., Pohl, Marie O., Eletto, Davide, Jeney, Csaba, Hoffmann, Donata, Reiche, Sven, Schinköthe, Jan, Ulrich, Reiner, Wiener, Julius, Hayes, Michael G. B., Chang, Max W., Hunziker, Annika, Yángüez, Emilio, Aydillo, Teresa, Krammer, Florian, Oderbolz, Josua, Meier, Matthias, Oxenius, Annette, Halenius, Anne, Zimmer, Gert, Benner, Christopher, Hale, Benjamin G., García-Sastre, Adolfo, Beer, Martin, Schwemmle, Martin, and Stertz, Silke

Published
2019
Full Text
View/download PDF

36. Absence of Type I Interferon Autoantibodies or Significant Interferon Signature Alterations in Adults With Post–COVID-19 Syndrome.

Author

Achleitner, Martin, Mair, Nina K, Dänhardt, Juliane, Kardashi, Romina, Puhan, Milo A, Abela, Irene A, Toepfner, Nicole, With, Katja de, Kanczkowski, Waldemar, Jarzebska, Natalia, Rodionov, Roman N, Wolf, Christine, Lee-Kirsch, Min Ae, Steenblock, Charlotte, Hale, Benjamin G, and Bornstein, Stefan R

Subjects
TYPE I interferons, AUTOANTIBODIES, COVID-19 pandemic, INTERFERONS, FATIGUE (Physiology), POSTPOLIOMYELITIS syndrome
Abstract

Genetic defects in the interferon (IFN) system or neutralizing autoantibodies against type I IFNs contribute to severe COVID-19. Such autoantibodies were proposed to affect post–COVID-19 syndrome (PCS), possibly causing persistent fatigue for >12 weeks after confirmed SARS-CoV-2 infection. In the current study, we investigated 128 patients with PCS, 21 survivors of severe COVID-19, and 38 individuals who were asymptomatic. We checked for autoantibodies against IFN-α, IFN-β, and IFN-ω. Few patients with PCS had autoantibodies against IFNs but with no neutralizing activity, indicating a limited role of type I IFNs in PCS pathogenesis. In a subset consisting of 28 patients with PCS, we evaluated IFN-stimulated gene activity and showed that it did not correlate with fatigue. In conclusion, impairment of the type I IFN system is unlikely responsible for adult PCS. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

37. A practical framework for ethics assessment in wildlife management decision‐making.

Author

Smith, Christian A., Tantillo, James A., Hale, Benjamin, Decker, Daniel J., Forstchen, Ann B., Pomeranz, Emily F., Lauber, T. Bruce, Schiavone, Michael V., Frohlich, Kipp, Lederle, Patrick E., Benedict, R. Joseph, Hurst, Jeremy, King, Richard, Siemer, William F., and Baumer, Meghan S.

Subjects
APPLIED ethics, CONDUCT of life, DECISION making, WILDLIFE management, TRUST, WESTERN civilization
Abstract

Wildlife professionals lack a framework and process for incorporating ethical considerations in a systematic and transparent way, along with ecological and social science, to support wildlife management decision‐making. We provide such a framework and process based on 3 of the major theoretical branches ethicists have developed in Western culture: consequentialist moral theory, which focuses on consequences and outcomes; principle‐ and rule‐based approaches that deal with what is considered right or wrong; and virtue ethical theory, which considers factors such as character, virtue, and aesthetics. The framework can be used to anticipate the ethical consequences of alternative courses of action or taking no action. If wildlife professionals use this framework as an assessment tool to provide input into decision‐making, resulting decisions will be more transparent, better understood by stakeholders, and more consistent with public trust responsibilities. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

44. Retinoic acid is dispensable for meiotic initiation but required for spermiogenesis in the mammalian testis.

Author

Kirsanov, Oleksandr, Johnson, Taylor A., Niedenberger, Bryan A., Malachowski, Taylor N., Hale, Benjamin J., Qing Chen, Lackford, Brad, Jiajia Wang, Singh, Anukriti, Schindler, Karen, Hermann, Brian P., Guang Hu, and Geyer, Christopher B.

Subjects
TRETINOIN, GERM cell differentiation, TESTIS, MALE models, MEIOSIS
Abstract

Retinoic acid (RA) is the proposed mammalian 'meiosis inducing substance'. However, evidence for this role comes from studies in the fetal ovary, where germ cell differentiation and meiotic initiation are temporally inseparable. In the postnatal testis, these events are separated by more than 1 week. Exploiting this difference, we discovered that, although RA is required for spermatogonial differentiation, it is dispensable for the subsequent initiation, progression and completion of meiosis. Indeed, in the absence of RA, the meiotic transcriptome program in both differentiating spermatogonia and spermatocytes entering meiosis was largely unaffected. Instead, transcripts encoding factors required during spermiogenesis were aberrant during preleptonema, and the subsequent spermatid morphogenesis program was disrupted such that no sperm were produced. Taken together, these data reveal a RA-independent model for male meiotic initiation. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

45. Autoantibodies targeting type I interferons: Prevalence, mechanisms of induction, and association with viral disease susceptibility.

Author

Hale, Benjamin G.

Subjects
TYPE I interferons, VIRUS diseases, DISEASE susceptibility, THYMUS tumors, AUTOANTIBODIES, VACCINATION complications
Abstract

The type I IFN (IFN‐I) system is essential to limit severe viral disease in humans. Thus, IFN‐I deficiencies are associated with serious life‐threatening infections. Remarkably, some rare individuals with chronic autoimmune diseases develop neutralizing autoantibodies (autoAbs) against IFN‐Is thereby compromising their own innate antiviral defenses. Furthermore, the prevalence of anti‐IFN‐I autoAbs in apparently healthy individuals increases with age, such that ∼4% of those over 70 years old are affected. Here, I review the literature on factors that may predispose individuals to develop anti‐IFN‐I autoAbs, such as reduced self‐tolerance caused by defects in the genes AIRE, NFKB2, and FOXP3 (among others), or by generally impaired thymus function, including thymic involution in the elderly. In addition, I discuss the hypothesis that predisposed individuals develop anti‐IFN‐I autoAbs following "autoimmunization" with IFN‐Is generated during some acute viral infections, systemic inflammatory events, or chronic IFN‐I exposure. Finally, I highlight the enhanced susceptibility that individuals with anti‐IFN‐I autoAbs appear to have towards viral diseases such as severe COVID‐19, influenza, or herpes (e.g., varicella‐zoster virus, herpes simplex virus, cytomegalovirus), as well as adverse reactions to live‐attenuated vaccines. Understanding the mechanisms underlying development and consequences of anti‐IFN‐I autoAbs will be key to implementing effective prophylactic and therapeutic measures. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

46. vPIF-1 is an insulin-like antiferroptotic viral peptide.

Author

Belavgeni, Alexia, Maremonti, Francesca, Tonnus, Wulf, Stadtmüller, Marlena, Gavali, Shubhangi, Mallais, Melodie, Flade, Karolin, Brucker, Anne, Becker, Jorunn Naila, Beer, Kristina, Tmava, Mirela, Stumpf, Julian, Gembardt, Florian, Hugo, Christian, Giacca, Mauro, Hale, Benjamin G., Perakakis, Nikolaos, Wei Sha, Pratt, Derek A., and Schally, Andrew V.

Subjects
PEPTIDES, INSULIN-like growth factor receptors, CELL death, INSULIN receptors
Abstract

Iridoviridae, such as the lymphocystis disease virus-1 (LCDV-1) and other viruses, encode viral insulin-like peptides (VILPs) which are capable of triggering insulin receptors (IRs) and insulin-like growth factor receptors. The homology of VILPs includes highly conserved disulfide bridges. However, the binding affinities to IRs were reported to be 200-to 500-fold less effective compared to the endogenous ligands. We therefore speculated that these peptides also have noninsulin functions. Here, we report that the LCDV-1 VILP can function as a potent and highly specific inhibitor of ferroptosis. Induction of cell death by the ferroptosis inducers erastin, RSL3, FIN56, and FINO2 and nonferroptotic necrosis produced by the thioredoxin-reductase inhibitor ferroptocide were potently prevented by LCDV-1, while human insulin had no effect. Fas-induced apoptosis, necroptosis, mitotane-induced cell death and growth hormone-releasing hormone antagonist-induced necrosis were unaffected, suggesting the specificity to ferroptosis inhibition by the LCDV-1 VILP. Mechanistically, we identified the viral C-peptide to be required for inhibition of lipid peroxidation and ferroptosis inhibition, while the human C-peptide exhibited no antiferroptotic properties. In addition, the deletion of the viral C-peptide abolishes radical trapping activity in cell-free systems. We conclude that iridoviridae, through the expression of insulin-like viral peptides, are capable of preventing ferroptosis. In analogy to the viral mitochondrial inhibitor of apoptosis and the viral inhibitor of RIP activation (vIRA) that prevents necroptosis, we rename the LCDV-1 VILP a viral peptide inhibitor of ferroptosis-1. Finally, our findings indicate that ferroptosis may function as a viral defense mechanism in lower organisms. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

49. EDITORS' NOTE

Author

Morrow, Bradford and Hale, Benjamin

Published
2013

Catalog

Books, media, physical & digital resources
See catalog results