tbuckley/cabot-search huggingface dataset:
Covid-19: Infections in England reached record high in March, finds React study
Authors: Gareth Iacobucci
Journal: BMJ (2022)

Covid-19 infections in England reached an "unprecedented" level last month, with prevalence higher than at any other time during the pandemic, the Real Time Assessment of Community Transmission (React) monitoring study has reported. 1Covid-19 prevalence was 6.37% between 8 and 31 March 2022, based on samples from over 100 000 people.This is more than twice the 2.88% in February 2022 and exceeds the previous high of 4.41% recorded in January 2022 during the peak of the first wave of omicron.Of 4038 positive samples that were sequenced in the latest round of the Imperial College London and Ipsos MORI study, most (3035, 89.7%) were the BA.2 subvariant of omicron."We observed unprecedented levels of SARS-CoV-2 infection in England in March 2022 and an almost complete replacement of omicron BA.1 by BA.2," concluded the study, published as a preprint on 6 April."The high and increasing prevalence in older adults may increase hospital admissions and deaths despite high levels of vaccination," it warned.
Trophoblast antigens, fetal blood cell antigens, and the paradox of fetomaternal tolerance
Authors: Gabrielle Rizzuto, Adrian Erlebacher
Journal: The Journal of Experimental Medicine (2022)

The paradox of fetomaternal tolerance has puzzled immunologists and reproductive biologists alike for almost 70 yr. Even the idea that the conceptus evokes a uniformly tolerogenic immune response in the mother is contradicted by the long-appreciated ability of pregnant women to mount robust antibody responses to paternal HLA molecules and RBC alloantigens such as Rh(D). Synthesizing these older observations with more recent work in mice, we discuss how the decision between tolerance or immunity to a given fetoplacental antigen appears to be a function of whether the antigen is trophoblast derived-and thus decorated with immunosuppressive glycans-or fetal blood cell derived.
TCTAP C-067 “Salvaging Heart and Saving Limb “: Thanks to Gruentzig and Dotter!
Authors: Nagendra Boopathy Senguttuvan, Santhosh Kumar Periyasamy, Manokar Panchanatham, Thoddi Ramamurthy Muralidharan, Vinod Kumar Balakrishnan, Ramesh Sankaran, Preetam Krishnamurthy
Journal: Journal of the American College of Cardiology (2022)
TCTAP A-029 SYNTAX II Score Predicted and Real Life Observed Mortality in Patients With Left Main Coronary Artery Stenosis Who Treated by Percutaneous Coronary Intervention
Authors: Khuyag Batmyagmar, Gankhulug Gansukh, Bum-Erdene Batbayar, Enkhjargal Erdenetsog, Gereltuya Choijiljav, Lkhagvasuren Zundui, Surenjav Chimed
Journal: Journal of the American College of Cardiology (2022)
Clinical Validation of a Virtual Planner for Coronary Interventions Based on Coronary CT Angiography
Authors: Jeroen Sonck, Sakura Nagumo, Bjarne L. Norgaard, Hiromasa Otake, Brian Ko, Jinlong Zhang, Takuya Mizukami, Michael Maeng, Daniele Andreini, Yu Takahashi, Jesper Møller Jensen, Abdul Ihdayhid, Ward Heggermont, Emanuele Barbato, Niya Mileva, Daniel Munhoz, Jozef Bartunek, Adam Updegrove, Amy Collinsworth, Martin Penicka, Lieven Van Hoe, Jonathon Leipsic, Bon-Kwon Koo, Bernard De Bruyne, Carlos Collet
Journal: JACC. Cardiovascular imaging (2022)

Low fractional flow reserve (FFR) values after percutaneous coronary intervention (PCI) carry a worse prognosis than high post-PCI FFR values. Therefore, the ability to predict post-PCI FFR might play an important role in procedural planning. Post-PCI FFR values can now be computed from pre-PCI coronary computed tomography angiography (CTA) using the fractional flow reserve derived from coronary computed tomography angiography revascularization planner (FFRCT Planner). The aim of this study was to validate the accuracy of the FFRCT Planner. In this multicenter, investigator-initiated, prospective study, patients with chronic coronary syndromes and significant lesions based on invasive FFR ≤0.80 were recruited. The FFRCT Planner was applied to the fractional flow reserve derived from coronary computed tomography angiography (FFRCT) model, simulating PCI. The primary objective was the agreement between the predicted post-PCI FFR by the FFRCT Planner and measured post-PCI FFR. Accuracy of the FFRCT Planner's luminal dimensions was assessed by using post-PCI optical coherence tomography as the reference. Overall, 259 patients were screened, with 120 patients (123 vessels) included in the final analysis. The mean patient age was 64 ± 9 years, and 24% had diabetes. Measured FFR post-PCI was 0.88 ± 0.06, and the FFRCT Planner FFR was 0.86 ± 0.06 (mean difference: 0.02 ± 0.07 FFR unit; limits of agreement: –0.12 to 0.15). Optical coherence tomography minimal stent area was 5.60 ± 2.01 mm2, and FFRCT Planner minimal stent area was 5.0 ± 2.2 mm2 (mean difference: 0.66 ± 1.21 mm2; limits of agreement: –1.7 to 3.0). The accuracy and precision of the FFRCT Planner remained high in cases with focal and diffuse disease and with low and high calcium burden. The FFRCT-based technology was accurate and precise for predicting FFR after PCI. (Precise Percutaneous Coronary Intervention Plan Study [P3]; NCT03782688)
Association of 2 Social Needs Interventions With Child Emergency Department Use and Hospitalizations
Authors: Matthew S. Pantell, Danielle Hessler, Holly Wing, Philip Herrera, Denisse E. Velazquez, Nancy E. Adler, Laura M. Gottlieb
Journal: JAMA Pediatrics (2022)

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Binding of LAG-3 to stable peptide-MHC class II limits T cell function and suppresses autoimmunity and anti-cancer immunity
Authors: Takumi Maruhashi, Daisuke Sugiura, Il-mi Okazaki, Kenji Shimizu, Takeo K. Maeda, Jun Ikubo, Harunori Yoshikawa, Katsumi Maenaka, Naozumi Ishimaru, Hidetaka Kosako, Tatsuya Takemoto, Taku Okazaki
Journal: Immunity (2022)
Omitted Author, Funding Information, and Study Group Members
Journal: JAMA Network Open (2022)

Ailiana Santosa, MD, MMedSc, PhD; Annika Rosengren, MD, PhD; Chinthanie Ramasundarahettige, MSc; Sumathy Rangarajan, MSc; Sadi Gulec, MD; Jephat Chifamba, DPhil; Scott A. Lear, PhD; Paul Poirier, MD; Karen E. Yeates, MD, MPH; Rita Yusuf, PhD; Andreas Orlandini, MD; Liu Weida, MD; Li Sidong, MSc; Zhu Yibing, PhD; Viswanathan Mohan, MD, PhD, DSc; Manmeet Kaur, PhD; Katarzyna Zatonska, PhD; Noorhassim Ismail, MD; Patricio Lopez-Jaramillo, MD, PhD; Romaina Iqbal, PhD; Lia M. Palileo-Villanueva, MD; Afzalhusein H. Yusufali, MD; Khalid F. AlHabib, MBBS; Salim Yusuf, DPhil
Immunogenicity and early clinical outcome after two or three doses of SARS-CoV-2 mRNA-BNT162b2 vaccine in actively treated cancer patients: results from the prospective observational Vax-On-Third study
Authors: F. Nelli, D. Giannarelli, A. Fabbri, M.A. Silvestri, J. R. Giron Berrios, A. Virtuoso, E. Marrucci, M. Schirripa, M. Mazzotta, A. Onorato, V. Panichi, G. Topini, G. Pessina, F. Natoni, C. Signorelli, M.G. Chilelli, F. Primi, E.M. Ruggeri
Journal: Annals of Oncology (2022)
Type VI secretion system-associated FHA domain protein TagH regulates the hemolytic activity and virulence of Vibrio cholerae
Authors: Guangli Wang, Chan Fan, Hui Wang, Chengyi Jia, Xiaoting Li, Jianru Yang, Tao Zhang, Song Gao, Xun Min, Jian Huang
Journal: Gut Microbes (2022)

The type VI secretion system (T6SS) and hemolysin HlyA are important virulence factors in Vibrio cholerae. The forkhead-associated (FHA) domain is a conserved phosphopeptide binding domain that exists in many regulatory modules. The FHA domain protein-encoding gene is conserved in the T6SS gene cluster and regulates the assembly and secretion of the T6SS. This study shows for the first time that the FHA domain protein TagH plays a role in controlling the hemolytic activity of V. cholerae, in addition to regulating the T6SS. TagH negatively regulates HlyA expression at the transcriptional and post-translational levels. The phosphopeptide binding sites of the FHA domain of TagH play a key role in the regulation of hemolytic activity. The deletion of tagH enhances the intestinal pathogenicity and extraintestinal invasion ability of V. cholerae, which mainly depend on the expression of HlyA. This study provides evidence that helps unravel the novel regulatory role of TagH in HlyA and provides critical insights which will aid in the development of strategies to manage HlyA.
Multimodal therapy strategies based on hydrogels for the repair of spinal cord injury
Authors: Yan Wang, Hong-Qian Lv, Xuan Chao, Wen-Xin Xu, Yun Liu, Gui-Xia Ling, Peng Zhang
Journal: Military Medical Research (2022)

Abstract Spinal cord injury (SCI) is a serious traumatic disease of the central nervous system, which can give rise to the loss of motor and sensory function. Due to its complex pathological mechanism, the treatment of this disease still faces a huge challenge. Hydrogels with good biocompatibility and biodegradability can well imitate the extracellular matrix in the microenvironment of spinal cord. Hydrogels have been regarded as promising SCI repair material in recent years and continuous studies have confirmed that hydrogel-based therapy can effectively eliminate inflammation and promote spinal cord repair and regeneration to improve SCI. In this review, hydrogel-based multimodal therapeutic strategies to repair SCI are provided, and a combination of hydrogel scaffolds and other therapeutic modalities are discussed, with particular emphasis on the repair mechanism of SCI.
Tauopathies: new perspectives and challenges
Authors: Yi Zhang, Kai-Min Wu, Liu Yang, Qiang Dong, Jin-Tai Yu
Journal: Molecular Neurodegeneration (2022)

Abstract Background Tauopathies are a class of neurodegenerative disorders characterized by neuronal and/or glial tau-positive inclusions. Main body Clinically, tauopathies can present with a range of phenotypes that include cognitive/behavioral-disorders, movement disorders, language disorders and non-specific amnestic symptoms in advanced age. Pathologically, tauopathies can be classified based on the predominant tau isoforms that are present in the inclusion bodies (i.e., 3R, 4R or equal 3R:4R ratio). Imaging, cerebrospinal fluid (CSF) and blood-based tau biomarkers have the potential to be used as a routine diagnostic strategy and in the evaluation of patients with tauopathies. As tauopathies are strongly linked neuropathologically and genetically to tau protein abnormalities, there is a growing interest in pursuing of tau-directed therapeutics for the disorders. Here we synthesize emerging lessons on tauopathies from clinical, pathological, genetic, and experimental studies toward a unified concept of these disorders that may accelerate the therapeutics. Conclusions Since tauopathies are still untreatable diseases, efforts have been made to depict clinical and pathological characteristics, identify biomarkers, elucidate underlying pathogenesis to achieve early diagnosis and develop disease-modifying therapies.
Metabolic reservoir cycles in cancer
Authors: Cissy Zhang, Addison Quinones, Anne Le
Journal: Seminars in Cancer Biology (2022)

Cancer cells possess various biological processes to ensure survival and proliferation even under unfavorable conditions such as hypoxia, nutrient deprivation, and oxidative stress. One of the defining hallmarks of cancer cells is their ability to reprogram their metabolism to suit their needs. Building on over a decade of research in the field of cancer metabolism, numerous unique metabolic capabilities are still being discovered in the present day. One recent discovery in the field of cancer metabolism that was hitherto unexpected is the ability of cancer cells to store vital metabolites in forms that can be readily converted to glucose and glutamine for later use. We called these forms "metabolic reservoirs." While many studies have been conducted on storage molecules such as glycogen, triglyceride, and phosphocreatine (PCr), few have explored the concept of "metabolic reservoirs" for cancer as a whole. In this review, we will provide an overview of this concept, the previously known reservoirs including glycogen, triglyceride, and PCr, and the new discoveries made including the newly discovered reservoirs such as N-acetyl-aspartyl-glutamate (NAAG), lactate, and γ- aminobutyric acid (GABA). We will also discuss whether disrupting these reservoir cycles may be a new avenue for cancer treatment.
TCTAP A-001 An Evaluation of a Sirolimus-Eluting Bioadaptor as Compared to a Zotarolimus-Eluting Stent in de Novo Coronary Arteries - “The Bioadaptor RCT Study”
Authors: Shigeru Saito, Holger Nef, Mark Webster, Stefan Verheye
Journal: Journal of the American College of Cardiology (2022)
Cytotoxic granzyme C–expressing ILC1s contribute to antitumor immunity and neonatal autoimmunity
Authors: Briana G. Nixon, Chun Chou, Chirag Krishna, Saïda Dadi, Adam O. Michel, Andrew E. Cornish, Emily R. Kansler, Mytrang H. Do, Xinxin Wang, Kristelle J. Capistrano, Alexander Y. Rudensky, Christina S. Leslie, Ming O. Li
Journal: Science Immunology (2022)

Innate lymphocytes are integral components of the cellular immune system that can coordinate host defense against a multitude of challenges and trigger immunopathology when dysregulated. Natural killer (NK) cells and innate lymphoid cells (ILCs) are innate immune effectors postulated to functionally mirror conventional cytotoxic T lymphocytes and helper T cells, respectively. Here, we showed that the cytolytic molecule granzyme C was expressed in cells with the phenotype of type 1 ILCs (ILC1s) in mouse liver and salivary gland. Cell fate-mapping and transfer studies revealed that granzyme C-expressing innate lymphocytes could be derived from ILC progenitors and did not interconvert with NK cells, ILC2s, or ILC3s. Granzyme C defined a maturation state of ILC1s. These granzyme C-expressing ILC1s required the transcription factors T-bet and, to a lesser extent, Eomes and support from transforming growth factor-β (TGF-β) signaling for their maintenance in the salivary gland. In a transgenic mouse breast cancer model, depleting ILC1s caused accelerated tumor growth. ILC1s gained granzyme C expression following interleukin-15 (IL-15) stimulation, which enabled perforin-mediated cytotoxicity. Constitutive activation of STAT5, a transcription factor regulated by IL-15, in granzyme C-expressing ILC1s triggered lethal perforin-dependent autoimmunity in neonatal mice. Thus, granzyme C marks a cytotoxic effector state of ILC1s, broadening their function beyond "helper-like" lymphocytes.
Acute seizures and status epilepticus in immune effector cell associated neurotoxicity syndrome (ICANS)
Authors: Jacqui-Lyn Saw, M. Hasib Sidiqi, Michael Ruff, Sara Hocker, Hassan Alkhateeb, Stephen M. Ansell, N. Nora Bennani, David Dingli, Suzanne R. Hayman, Patrick B. Johnston, Prashant Kapoor, Saad J. Kenderian, Taxiarchis V. Kourelis, Shaji K. Kumar, Jonas Paludo, Mithun V. Shah, Mustaqeem A. Siddiqui, Rahma Warsame, Allison Rosenthal, Marie Grill, Januario E. Castro, Jason Siegel, Zaid H. Abdel Rahman, Mohamed A. Kharfan-Dabaja, Elson So, Yi Lin
Journal: Blood Cancer Journal (2022)
Clinical Biology of the Pituitary Adenoma
Authors: Shlomo Melmed, Ursula B Kaiser, M Beatriz Lopes, Jerome Bertherat, Luis V Syro, Gerald Raverot, Martin Reincke, Gudmundur Johannsson, Albert Beckers, Maria Fleseriu, Andrea Giustina, John A H Wass, Ken K Y Ho
Journal: Endocrine Reviews (2022)

Abstract All endocrine glands are susceptible to neoplastic growth, yet the health consequences of these neoplasms differ between endocrine tissues. Pituitary neoplasms are highly prevalent and overwhelmingly benign, exhibiting a spectrum of diverse behaviors and impact on health. To understand the clinical biology of these common yet often innocuous neoplasms, we review pituitary physiology and adenoma epidemiology, pathophysiology, behavior, and clinical consequences. The anterior pituitary develops in response to a range of complex brain signals integrating with intrinsic ectodermal cell transcriptional events that together determine gland growth, cell type differentiation, and hormonal production, in turn maintaining optimal endocrine health. Pituitary adenomas occur in 10% of the population; however, the overwhelming majority remain harmless during life. Triggered by somatic or germline mutations, disease-causing adenomas manifest pathogenic mechanisms that disrupt intrapituitary signaling to promote benign cell proliferation associated with chromosomal instability. Cellular senescence acts as a mechanistic buffer protecting against malignant transformation, an extremely rare event. It is estimated that fewer than one-thousandth of all pituitary adenomas cause clinically significant disease. Adenomas variably and adversely affect morbidity and mortality depending on cell type, hormone secretory activity, and growth behavior. For most clinically apparent adenomas, multimodal therapy controlling hormone secretion and adenoma growth lead to improved quality of life and normalized mortality. The clinical biology of pituitary adenomas, and particularly their benign nature, stands in marked contrast to other tumors of the endocrine system, such as thyroid and neuroendocrine tumors.
TCTAP A-028 Predicted and Observed Mortality at 10-Year in Patients With Bifurcation Lesion in the SYNTAX Trial
Authors: Kai Ninomiya, Patrick W. Serruys, Shinichiro Masuda, Francesco Burzotta, Marie-Claude Morice, Michael J. Mack, David R. Holmes, Yoshinobu Onuma
Journal: Journal of the American College of Cardiology (2022)
Dose Addition in the Induction of Craniofacial Malformations in Zebrafish Embryos Exposed to a Complex Mixture of Food-Relevant Chemicals with Dissimilar Modes of Action
Authors: Leo T.M. Van Der Ven, Paul Van Ommeren, Edwin P. Zwart, Eric R. Gremmer, Hennie M. Hodemaekers, Harm J. Heusinkveld, Jacob D. van Klaveren, Emiel Rorije
Journal: Environmental Health Perspectives (2022)

Background: Humans are exposed to combinations of chemicals. In cumulative risk assessment (CRA), regulatory bodies such as the European Food Safety Authority consider dose addition as a default and sufficiently conservative approach. The principle of dose addition was confirmed previously for inducing craniofacial malformations in zebrafish embryos in binary mixtures of chemicals with either similar or dissimilar modes of action (MOAs). Objectives: In this study, we explored a workflow to select and experimentally test multiple compounds as a complex mixture with each of the compounds at or below its no observed adverse effect level (NOAEL), in the same zebrafish embryo model. Methods: Selection of candidate compounds that potentially induce craniofacial malformations was done using in silico methods—structural similarity, molecular docking, and quantitative structure–activity relationships—applied to a database of chemicals relevant for oral exposure in humans via food (EuroMix inventory, n=1,598). A final subselection was made manually to represent different regulatory fields (e.g., food additives, industrial chemicals, plant protection products), different chemical families, and different MOAs. Results: A final selection of eight compounds was examined in the zebrafish embryo model, and craniofacial malformations were observed in embryos exposed to each of the compounds, thus confirming the developmental toxicity as predicted by the in silico methods. When exposed to a mixture of the eight compounds, each at its NOAEL, substantial craniofacial malformations were observed; according to a dose–response analysis, even embryos exposed to a 7-fold dilution of this mixture still exhibited a slight abnormal phenotype. The cumulative effect of the compounds in the mixture was in accordance with dose addition (added doses of the individual compounds after adjustment for relative potencies), despite different MOAs of the compounds involved. Discussion: This case study of a complex mixture inducing craniofacial malformations in zebrafish embryos shows that dose addition can adequately predicted the cumulative effect of a mixture of multiple substances at low doses, irrespective of the (expected) MOA. The applied workflow may be useful as an approach for CRA in general. https://doi.org/10.1289/EHP9888
Strand asymmetry influences mismatch resolution during single-strand annealing
Authors: Victoria O. Pokusaeva, Aránzazu Rosado Diez, Lorena Espinar, Albert Torelló Pérez, Guillaume J. Filion
Journal: Genome biology (2022)

Abstract Background Biases of DNA repair can shape the nucleotide landscape of genomes at evolutionary timescales. The molecular mechanisms of those biases are still poorly understood because it is difficult to isolate the contributions of DNA repair from those of DNA damage. Results Here, we develop a genome-wide assay whereby the same DNA lesion is repaired in different genomic contexts. We insert thousands of barcoded transposons carrying a reporter of DNA mismatch repair in the genome of mouse embryonic stem cells. Upon inducing a double-strand break between tandem repeats, a mismatch is generated if the break is repaired through single-strand annealing. The resolution of the mismatch showed a 60–80% bias in favor of the strand with the longest 3′ flap. The location of the lesion in the genome and the type of mismatch had little influence on the bias. Instead, we observe a complete reversal of the bias when the longest 3′ flap is moved to the opposite strand by changing the position of the double-strand break in the reporter. Conclusions These results suggest that the processing of the double-strand break has a major influence on the repair of mismatches during single-strand annealing.
Inflammation targeted nanomedicines: Patents and applications in cancer therapy
Authors: Thaggikuppe Krishnamurthy Praveen, Hosahalli Veerabhadrappa Gangadharappa, Amr Selim Abu Lila, Afrasim Moin, Khalid Mehmood, Kamsagara Linganna Krishna, Talib Hussain, Ahmed Alafnan, Shazi Shakil, Syed Mohd Danish Rizvi
Journal: Seminars in Cancer Biology (2022)