tbuckley/cabot-search huggingface dataset:
o <sup>8</sup> G Site-Specifically Modified tRF-1-AspGTC: A Novel Therapeutic Target and Biomarker for Pulmonary Hypertension
Authors: Junting Zhang, Yiying Li, Yuan Chen, Jianchao Zhang, Zihui Jia, Muhua He, Xueyi Liao, Siyu He, Jin-Song Bian, Xiao-Wei Nie
Journal: Circulation Research (2024)

Hypoxia and oxidative stress contribute to the development of pulmonary hypertension (PH). tRNA-derived fragments play important roles in RNA interference and cell proliferation, but their epitranscriptional roles in PH development have not been investigated. We aimed to gain insight into the mechanistic contribution of oxidative stress-induced 8-oxoguanine in pulmonary vascular remodeling.
Neurotransmitter accumulation and Parkinson's disease‐like phenotype caused by anion channelrhodopsin opto‐controlled astrocytic mitochondrial depolarization in substantia nigra pars compacta
Authors: Sen‐Miao Li, Dian‐Dian Wang, Dan‐Hua Liu, Xiao‐Yan Meng, Zhizhong Wang, Xitong Guo, Qian Liu, Pei‐Pei Liu, Shu‐Ang Li, Songwei Wang, Run‐Zhou Yang, Yuming Xu, Longde Wang, Jian‐Sheng Kang
Journal: MedComm (2024)

Abstract Parkinson's disease (PD) is a mitochondria‐related neurodegenerative disease characterized by locomotor deficits and loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc). Majority of PD research primarily focused on neuronal dysfunction, while the roles of astrocytes and their mitochondria remain largely unexplored. To bridge the gap and investigate the roles of astrocytic mitochondria in PD progression, we constructed a specialized optogenetic tool, mitochondrial‐targeted anion channelrhodopsin, to manipulate mitochondrial membrane potential in astrocytes. Utilizing this tool, the depolarization of astrocytic mitochondria within the SNc in vivo led to the accumulation of γ‐aminobutyric acid (GABA) and glutamate in SNc, subsequently resulting in excitatory/inhibitory imbalance and locomotor deficits. Consequently, in vivo calcium imaging and interventions of neurotransmitter antagonists demonstrated that GABA accumulation mediated movement deficits of mice. Furthermore, 1 h/day intermittent astrocytic mitochondrial depolarization for 2 weeks triggered spontaneous locomotor dysfunction, α‐synuclein aggregation, and the loss of DA neurons, suggesting that astrocytic mitochondrial depolarization was sufficient to induce a PD‐like phenotype. In summary, our findings suggest the maintenance of proper astrocytic mitochondrial function and the reinstatement of a balanced neurotransmitter profile may provide a new angle for mitigating neuronal dysfunction during the initial phases of PD.
A Novel Macrophage Subpopulation Conveys Increased Genetic Risk of Coronary Artery Disease
Authors: Jiahao Jiang, Thomas K. Hiron, Thomas A. Agbaedeng, Yashaswat Malhotra, Edward Drydale, James Bancroft, Esther Ng, Michael E. Reschen, Lucy J. Davison, Chris A. O’Callaghan
Journal: Circulation Research (2024)

Coronary artery disease (CAD), the leading cause of death worldwide, is influenced by both environmental and genetic factors. Although over 250 genetic risk loci have been identified through genome-wide association studies, the specific causal variants and their regulatory mechanisms are still largely unknown, particularly in disease-relevant cell types such as macrophages.
Management of hematological patients requiring emergency chemotherapy in the intensive care unit
Authors: Antoine Lafarge, Dara Chean, Livia Whiting, Raphaël Clere-Jehl, Elie Azoulay, Djamel Mokart, Virginie Lemiale, Laurent Argaud, Dominique Benoit, Naïke Bigé, Magali Bisbal, Emmanuel Canet, Fabrice Bruneel, Alexandre Demoule, Achille Kouatchet, Julien Mayaux, Anne-Sophie Moreau, Saad Nseir, Martine Nyunga, Frédéric Pène, Amélie Seguin, Lara Zafrani, Olfa Hamzaoui, Bruno Mourvillier, Pierre Asfar, David Schnell, Gaëtan Plantefeve, Julio Badie, Nicholas Sedillot, Xavier Wittebole, Jean-Paul Mira, Jean-Philippe Rigaud, Pierre-Louis Declercq, Jean-Pierre Quenot, Frédéric Foret, Djillali Annane, Nicholas Heming, Pierre Bulpa, Patrick M. Honoré, Raphaël Clere-Jehl, Francis Schneider, Jean-Claude Lacherade, Gwenhaël Colin, Christophe Guitton, Olivier Nigeon, Nicolas Grunderbeeck, Bruno François, Christophe Guervilly, Mehran Monchi, Jérôme Roustan, Jean Reignier, Ferhat Meziani, Julie Helms, François Barbier, Toufik Kamel, Grégoire Muller, Nicolas Schryver, Jean-Pierre Frat, Delphine Chatelier, Nicolas Barbarot, François Legay, Charles Vidal, Laurence Dangers, Emmanuelle Mercier, Stephan Ehrmann, Juliette Audibert, Asaël Berger, David Joganah, Jonathan Chelly, Laurent Ducros, Florian Reizine, Agathe Delbove, Florent Bavozet, Paul-Simon Pugliesi, Thomas Maldiney, Shidasp Siami, Jean-François Timsit, Pierre Tissières, Sébastien Gibot, Eric Maury
Journal: Intensive Care Medicine (2024)
Real world study of grass pollen immunotherapy—Similar efficacy of <scp>SCIT</scp> and <scp>SLIT</scp>
Authors: Lone Winther, Anne Caroline Curtz, Zsuzsa Domokos
Journal: Allergy (2024)

Research data are not shared. Data S1: Supporting Information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Alzheimer blood biomarkers: practical guidelines for study design, sample collection, processing, biobanking, measurement and result reporting
Authors: Xuemei Zeng, Yijun Chen, Anuradha Sehrawat, Jihui Lee, Tara K Lafferty, Julia Kofler, Sarah B Berman, Robert A Sweet, Dana L Tudorascu, William E Klunk, Milos D Ikonomovic, Anna Pfister, Henrik Zetterberg, Beth E Snitz, Anne D Cohen, Victor L Villemagne, Tharick A Pascoal, M Llyas Kamboh, Oscar I Lopez, Kaj Blennow, Thomas K Karikari
Journal: Molecular Neurodegeneration (2024)

Abstract Alzheimer’s disease (AD), the most common form of dementia, remains challenging to understand and treat despite decades of research and clinical investigation. This might be partly due to a lack of widely available and cost-effective modalities for diagnosis and prognosis. Recently, the blood-based AD biomarker field has seen significant progress driven by technological advances, mainly improved analytical sensitivity and precision of the assays and measurement platforms. Several blood-based biomarkers have shown high potential for accurately detecting AD pathophysiology. As a result, there has been considerable interest in applying these biomarkers for diagnosis and prognosis, as surrogate metrics to investigate the impact of various covariates on AD pathophysiology and to accelerate AD therapeutic trials and monitor treatment effects. However, the lack of standardization of how blood samples and collected, processed, stored analyzed and reported can affect the reproducibility of these biomarker measurements, potentially hindering progress toward their widespread use in clinical and research settings. To help address these issues, we provide fundamental guidelines developed according to recent research findings on the impact of sample handling on blood biomarker measurements. These guidelines cover important considerations including study design, blood collection, blood processing, biobanking, biomarker measurement, and result reporting. Furthermore, the proposed guidelines include best practices for appropriate blood handling procedures for genetic and ribonucleic acid analyses. While we focus on the key blood-based AD biomarkers for the AT(N) criteria (e.g., amyloid-beta [Aβ]40, Aβ42, Aβ42/40 ratio, total-tau, phosphorylated-tau, neurofilament light chain, brain-derived tau and glial fibrillary acidic protein), we anticipate that these guidelines will generally be applicable to other types of blood biomarkers. We also anticipate that these guidelines will assist investigators in planning and executing biomarker research, enabling harmonization of sample handling to improve comparability across studies.
Editor's Note: A 13 mer LNA-i-miR-221 Inhibitor Restores Drug Sensitivity in Melphalan-Refractory Multiple Myeloma Cells
Authors: Annamaria Gullà, Maria Teresa Di Martino, Maria Eugenia Gallo Cantafio, Eugenio Morelli, Nicola Amodio, Cirino Botta, Maria Rita Pitari, Santo Giovanni Lio, Domenico Britti, Maria Angelica Stamato, Teru Hideshima, Nikhil C. Munshi, Kenneth C. Anderson, Pierosandro Tagliaferri, Pierfrancesco Tassone
Journal: Clinical Cancer Research (2024)
Correction: Selective Tumor Hypoxia Targeting by Hypoxia-Activated Prodrug TH-302 Inhibits Tumor Growth in Preclinical Models of Cancer
Authors: Jessica D. Sun, Qian Liu, Jingli Wang, Dharmendra Ahluwalia, Damien Ferraro, Yan Wang, Jian-Xin Duan, W. Steve Ammons, John G. Curd, Mark D. Matteucci, Charles P. Hart
Journal: Clinical Cancer Research (2024)
Overcoming Nutrient Stress: Integrin αvβ3-Driven Metabolic Adaptation Supports Tumor Initiation
Authors: Elena Rainero
Journal: Cancer Research (2024)

Abstract Nutrient stress accompanies several stages of tumor progression, including metastasis formation. Metabolic reprogramming is a hallmark of cancer, and it has been associated with stress tolerance and anchorage-independent cell survival. Adaptive responses are required to support cancer cell survival under these conditions. In this issue of Cancer Research, Nam and colleagues showed that the extracellular matrix (ECM) receptor integrin β3 was upregulated in lung cancer cells in response to nutrient starvation, resulting in increased cell survival that was independent from ECM binding. Delving into the molecular mechanisms responsible for this, the authors found that integrin β3 promoted glutamine metabolism and oxidative phosphorylation (OXPHOS) by activating a Src/AMPK/PGC1α signaling pathway. Importantly, in vivo experiments confirmed that OXPHOS inhibition suppressed tumor initiation in an orthotopic model of lung cancer, while β3 knockout completely abrogated tumor initiation. These observations indicate that targeting signaling pathways downstream of αvβ3 could represent a promising therapeutic avenue to prevent lung cancer progression and metastasis. See related article by Nam et al., p. 1630
Long-Term Course of Remission and Recovery in Psychotic Disorders
Authors: Sara Tramazzo, Wenxuan Lian, Olesya Ajnakina, Gabrielle Carlson, Evelyn Bromet, Roman Kotov, Katherine Jonas
Journal: American Journal of Psychiatry (2024)

Objective: Understanding prognosis is critical to anticipating public health needs and providing care to individuals with psychotic disorders. However, the long-term course of remission and recovery remains unclear. In this study, the most common trajectories of illness course are described for a cohort of individuals followed for 25 years since first admission for psychosis. Methods: Participants are from the Suffolk County Mental Health Project, an epidemiological study of first-admission psychosis. Data for the present study was collected from six follow-ups, with 311 individuals assessed at the 25-year follow-up. Common patterns of remission and recovery were assessed in the baseline cohort of 591 individuals and the subsample from the 25-year follow up. Results: In the baseline cohort and the 25-year subsample, the most common trajectory for individuals with schizophrenia spectrum disorders was no remission and no recovery. Among individuals with other psychotic disorders, in both the baseline and 25-year cohorts, the modal pattern was one of intermittent remission and recovery. Individuals with other psychotic disorders were more likely to experience stable remission (15.1%) and stable recovery (21.1%), outcomes that were rare among individuals with schizophrenia spectrum disorders (0% and 0.6%, respectively). Conclusions: The modal longitudinal pattern for individuals with other psychoses is one of multiple transitions into and out of symptomatic and functional recovery. Engagement in a long-term health care plan may help individuals detect and respond to these changes. Sustained remission and recovery are rare among people with schizophrenia spectrum disorders. Efforts should be directed toward developing more effective treatments for this population.
Correction: Chimeric Antigen Receptor T Cells Targeting CD79b Show Efficacy in Lymphoma with or without Cotargeting CD19
Authors: Maria Ormhøj, Irene Scarfò, Maria L. Cabral, Stefanie R. Bailey, Selena J. Lorrey, Amanda A. Bouffard, Ana P. Castano, Rebecca C. Larson, Lauren S. Riley, Andrea Schmidts, Bryan D. Choi, Rikke S. Andersen, Oriane Cédile, Charlotte G. Nyvold, Jacob H. Christensen, Morten F. Gjerstorff, Henrik J. Ditzel, David M. Weinstock, Torben Barington, Matthew J. Frigault, Marcela V. Maus
Journal: Clinical Cancer Research (2024)
Selected Articles from This Issue
Journal: Clinical Cancer Research (2024)

Highlights| May 15 2024 Selected Articles from This Issue Author & Article Information Online ISSN: 1557-3265 Print ISSN: 1078-0432 ©2024 American Association for Cancer Research2024American Association for Cancer Research Clin Cancer Res (2024) 30 (10): 2003. https://doi.org/10.1158/1078-0432.CCR-30-10-HI Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record May 15 2024 Citation Selected Articles from This Issue. Clin Cancer Res 15 May 2024; 30 (10): 2003. https://doi.org/10.1158/1078-0432.CCR-30-10-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Although KRAS mutations are common in patients with colorectal cancer, efforts to target KRAS have had limited success, necessitating the development of additional treatment options. In patients with metastatic colorectal cancer (mCRC) who progress after first-line treatment, further therapy with FOLFIRI and the VEGF-targeting bevacizumab has had modest efficacy. Polo-like kinase 1 (PLK1) levels were found to be increased in relapsed colorectal tumors, suggesting it may contribute to resistance. In a phase Ib clinical study, Ahn and colleagues preclinically and clinically evaluated the PLK inhibitor onvansertib with chemotherapy for treating KRAS-mutant mCRC. Preclinically, the authors demonstrate increased onvansertib activity in KRAS-mutant in vitro models and significant antitumor activity when combined with chemotherapy in vivo. In patients with mCRC, the authors observed partial responses in 44% of patients treated with onvansertib plus FOLFIRI/bevacizumab, with a tolerable safety profile. Early changes in KRAS-mutant circulating tumor DNA levels in... You do not currently have access to this content.
Striking the Balance with a PD-L1×4–1BB Bispecific Antibody
Authors: JongHoon Ha, Adam J. Grippin, Betty Y.S. Kim, Wen Jiang
Journal: Cancer Research (2024)

Abstract Antibody-based immune checkpoint blockade therapy has revolutionized the field of cancer immunotherapy, yet its efficacy remains limited in immunologically cold tumors. Combining checkpoint inhibitors with costimulatory agonists improves tumoricidal activity of T cells but also can lead to off-target hepatotoxicity. Although bispecific antibodies confer tumor selectivity to alleviate undesirable adverse effects, toxicity concerns persist with increased dosing. In this issue of Cancer Research, Yuwen and colleagues introduce ATG-101, a tetravalent PD-L1×4–1BB bispecific antibody with high programmed death ligand 1 (PD-L1) affinity and low 4–1BB affinity, aiming to mitigate hepatotoxicity. ATG-101 demonstrates PD-L1–dependent 4–1BB activation, leading to selective T-cell activation within the tumor microenvironment. ATG-101 exhibits potent antitumor activity, even in large, immunologically cold, and monotherapy-resistant tumor models. Single-cell RNA sequencing reveals significant shifts of immune cell populations in the tumor microenvironment from protumor to antitumor phenotypes following ATG-101 treatment. In cynomolgus monkeys, no serious cytokine storm and hepatotoxicity are observed after ATG-101 treatment, indicating a broad therapeutic window for ATG-101 in cancer treatment. This study highlights the potential of tetravalent bispecific antibodies in cancer immunotherapy, with implications for various antibody-based treatment modalities across different fields. See related article by Yuwen et al., p. 1680
Chest X-ray alone is insufficient for predicting drug-resistant pulmonary tuberculosis
Authors: Ole Skouvig Pedersen, Tetiana Butova, Natalia Borovok, Oleksandra Akymenko, Nadiya Sapelnik, Oleksandr Tantsura, Vitaliy Knysh, Andreas Fløe, Victor Naestholt Dahl, Dmytro Butov
Journal: Clinical Microbiology and Infection (2024)
Genome-Wide Association Study of Treatment-Resistant Depression: Shared Biology With Metabolic Traits
Authors: JooEun Kang, Victor M. Castro, Michael Ripperger, Sanan Venkatesh, David Burstein, Richard Karlsson Linnér, Daniel B. Rocha, Yirui Hu, Drew Wilimitis, Theodore Morley, Lide Han, Rachel Youngjung Kim, Yen-Chen Anne Feng, Tian Ge, Stephan Heckers, Georgios Voloudakis, Christopher Chabris, Panos Roussos, Thomas H McCoy, Colin G. Walsh, Roy H. Perlis, Douglas M. Ruderfer
Journal: American Journal of Psychiatry (2024)

Treatment-resistant depression (TRD) occurs in roughly one-third of all individuals with major depressive disorder (MDD). Although research has suggested a significant common variant genetic component of liability to TRD, with heritability estimated at 8% when compared with non-treatment-resistant MDD, no replicated genetic loci have been identified, and the genetic architecture of TRD remains unclear. A key barrier to this work has been the paucity of adequately powered cohorts for investigation, largely because of the challenge in prospectively investigating this phenotype. The objective of this study was to perform a well-powered genetic study of TRD.
Symptoms as a Predictor of the Placebo-Controlled Efficacy of PCI in Stable Coronary Artery Disease
Authors: Florentina A. Simader, Christopher A. Rajkumar, Michael J. Foley, Fiyyaz Ahmed-Jushuf, Shayna Chotai, Nina Bual, Arif Khokhar, Aisha Gohar, Ioannis Lampadakis, Sashiananthan Ganesananthan, Rachel H. Pathimagaraj, Alexandra Nowbar, John R. Davies, Tom R. Keeble, Peter D. O’Kane, Peter Haworth, Helen Routledge, Tushar Kotecha, James C. Spratt, Rupert Williams, Sukhjinder S. Nijjer, Sayan Sen, Nick Curzen, Manas Sinha, James P. Howard, Graham Cole, Frank E. Harrell, Darrel P. Francis, Matthew J. Shun-Shin, Rasha K. Al-Lamee, Christopher Rajkumar, Michael Foley, Fiyyaz Ahmed-Jushuf, Florentina Simader, Sashiananthan Ganesananthan, Danqi Wang, Muhammad Mohsin, Rachel Pathimagaraj, Krzysztof Macierzanka, Ricardo Petraco, Ramzi Khamis, Graham Cole, James Howard, Jamil Mayet, Darrel Francis, Arif Kokhar, Aisha Gohar, Ioannis Lampadakis, Henry Seligman, Amit Kaura, Sukhjinder Nijjer, Sayan Sen, Punit Ramrakha, Raffi Kaprielian, Iqbal Malik, Masood Khan, Amarjit Sethi, Rodney Foale, Thomas Keeble, Kare Tang, John Davies, Reto Gamma, Gerald Clesham, Jason Dungu, Alamgir Kabir, Shah Mohd Nazri, Peter O’Kane, Jonathan Hinton, Jehangir Din, Alexandra Nowbar, Tushar Kotecha, Peter Haworth, James Spratt, Rupert Williams, Claudia Cosgrove, Pitt Lim, Helen Routledge, Lal Mughal, Jasper Trevelyan, Manas Sinha, Nick Curzen, James Wilkinson, Rohit Sirohi, Alison Calver, John Rawlins, Richard Jabbour, Neil Ruparelia, Joban Sehmi, Tim Kinnaird, Fairoz Abdul, Vasileios Panoulas, David Collier, George Thornton, Afzal Sohaib, Rasha K. Al-Lamee
Journal: Journal of the American College of Cardiology (2024)
Real-World 1-Year Results of Tricuspid Edge-to-Edge Repair From the bRIGHT Study
Authors: Philipp Lurz, Karl-Philipp Rommel, Thomas Schmitz, Raffi Bekeredjian, Georg Nickenig, Helge Möllmann, Ralph Stephan von Bardeleben, Alexander Schmeisser, Iskandar Atmowihardjo, Rodrigo Estevez-Loureiro, Edith Lubos, Megan Heitkemper, Kelli Peterman, Harald Lapp, Erwan Donal
Journal: Journal of the American College of Cardiology (2024)

Severe tricuspid regurgitation (TR) is known to be associated with poor quality of life and increased risk of death when left untreated.
Clinical characteristics and outcomes of respiratory syncytial virus-associated ARF in immunocompetent patients: A seven-year experience at a tertiary hospital in France
Authors: David Mokrani, Quentin Le Hingrat, Michaël Thy, Christophe Choquet, Véronique Joly, Sylvie Lariven, Christophe Rioux, Laurène Deconinck, Paul Loubet, Thomas Papo, Bruno Crestani, Vincent Bunel, Lila Bouadma, Antoine Khalil, Laurence Armand-Lefèvre, Agathe Raynaud-Simon, Jean-François Timsit, François-Xavier Lescure, Yazdan Yazdanpanah, Diane Descamps, Nathan Peiffer-Smadja
Journal: Journal of Infection (2024)
Risk-adjusted Screening for Prostate Cancer—Defining the Low-risk Group by Data from the PROBASE Trial
Authors: Agne Krilaviciute, Rudolf Kaaks, Petra Seibold, Maxime de Vrieze, Jale Lakes, Jan Philipp Radtke, Markus Kuczyk, Nina N Harke, Jürgen Debus, Christoph A Fink, Kathleen Herkommer, Jürgen E Gschwend, Valentin H Meissner, Axel Benner, Glen Kristiansen, Boris Hadaschik, Christian Arsov, Lars Schimmöller, Gerald Antoch, Frederik L Giesel, Marcus Makowski, Frank Wacker, Heinz-Peter Schlemmer, Nikolaus Becker, Peter Albers
Journal: European Urology (2024)

Risk-adjusted screening for prostate cancer (PCa) aims to reduce harms by less frequent retesting, especially in men at a low risk of PCa. Definitions of low risk are based mainly on studies in men starting screening at age 55-60 yr.
CRISPR-Cas13d screens identify KILR, a breast cancer risk-associated lncRNA that regulates DNA replication and repair
Authors: Lu Wang, Mainá Bitar, Xue Lu, Sebastien Jacquelin, Sneha Nair, Haran Sivakumaran, Kristine M. Hillman, Susanne Kaufmann, Rebekah Ziegman, Francesco Casciello, Harsha Gowda, Joseph Rosenbluh, Stacey L. Edwards, Juliet D. French
Journal: Molecular Cancer (2024)

Long noncoding RNAs (lncRNAs) have surpassed the number of protein-coding genes, yet the majority have no known function. We previously discovered 844 lncRNAs that were genetically linked to breast cancer through genome-wide association studies (GWAS). Here, we show that a subset of these lncRNAs alter breast cancer risk by modulating cell proliferation, and provide evidence that a reduced expression on one lncRNA increases breast cancer risk through aberrant DNA replication and repair.