tbuckley/cabot-search huggingface dataset:
Antigenicity comparison of SARS‐CoV‐2 Omicron sublineages with other variants contained multiple mutations in RBD
Authors: Qianqian Li, Mengyi Zhang, Ziteng Liang, Li Zhang, Xi Wu, Chaoying Yang, Yimeng An, Jincheng Tong, Shuo Liu, Tao Li, Qianqian Cui, Jianhui Nie, Jiajing Wu, Weijin Huang, Youchun Wang
Journal: MedComm (2022)

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants, particularly those with multiple mutations in receptor-binding domain (RBD), pose a critical challenge to the efficacy of coronavirus disease 2019 (COVID-19) vaccines and therapeutic neutralizing monoclonal antibodies (mAbs). Omicron sublineages BA.1, BA.2, BA.3, as well as the recent emergence of C.1.2, B.1.630, B.1.640.1, and B.1.640.2, have multiple mutations in RBD and may lead to severe neutralizing antibody evasion. It is urgent to evaluate the antigenic change of the above seven variants against mAbs and sera from guinea pigs immunized with variants of concern (VOCs) (Alpha, Beta, Gamma, Delta, Omicron) and variants of interest (VOIs) (Lambda, Mu) immunogens. Only seven out of the 24 mAbs showed no reduction in neutralizing activity against BA.1, BA.2, and BA.3. However, among these seven mAbs, the neutralization activity of XGv337 and XGv338 against C.1.2, B.1.630, B.1.640.1, and B.1.640.2 were decreased. Therefore, only five neutralizing mAbs showed no significant change against these seven variants. Using VOCs and VOIs as immunogens, we found that the antigenicity of variants could be divided into three clusters, and each cluster showed similar antigenicity to different immunogens. Among them, D614G, B.1.640.1, and B.1.630 formed a cluster, C.1.2 and B.1.640.2 formed a cluster, and BA.1, BA.2, and BA.3 formed a cluster.
Autoantibodies against NCAM1 from patients with schizophrenia cause schizophrenia-related behavior and changes in synapses in mice
Authors: Hiroki Shiwaku, Shingo Katayama, Kanoh Kondo, Yuri Nakano, Hikari Tanaka, Yuki Yoshioka, Kyota Fujita, Haruna Tamaki, Hironao Takebayashi, Omi Terasaki, Yukihiro Nagase, Teruyoshi Nagase, Tetsuo Kubota, Kinya Ishikawa, Hitoshi Okazawa, Hidehiko Takahashi
Journal: Cell Reports Medicine (2022)

From genetic and etiological studies, autoimmune mechanisms underlying schizophrenia are suspected; however, the details remain unclear. In this study, we describe autoantibodies against neural cell adhesion molecule (NCAM1) in patients with schizophrenia (5.4%, cell-based assay; 6.7%, ELISA) in a Japanese cohort (n = 223). Anti-NCAM1 autoantibody disrupts both NCAM1-NCAM1 and NCAM1-glial cell line-derived neurotrophic factor (GDNF) interactions. Furthermore, the anti-NCAM1 antibody purified from patients with schizophrenia interrupts NCAM1-Fyn interaction and inhibits phosphorylation of FAK, MEK1, and ERK1 when introduced into the cerebrospinal fluid of mice and also reduces the number of spines and synapses in frontal cortex. In addition, it induces schizophrenia-related behavior in mice, including deficient pre-pulse inhibition and cognitive impairment. In conclusion, anti-NCAM1 autoantibodies in patients with schizophrenia cause schizophrenia-related behavior and changes in synapses in mice. These antibodies may be a potential therapeutic target and serve as a biomarker to distinguish a small but treatable subgroup in heterogeneous patients with schizophrenia.
Eliminating predictable DNA off-target effects of cytosine base editor by using dual guiders including sgRNA and TALE
Authors: Jizeng Zhou, Yang Liu, Yuhui Wei, Shuwen Zheng, Shixue Gou, Tao Chen, Yang Yang, Ting Lan, Min Chen, Yuan Liao, Quanjun Zhang, Chengcheng Tang, Yu Liu, Yunqin Wu, Xiaohua Peng, Minghui Gao, Junwei Wang, Kun Zhang, Liangxue Lai, Qingjian Zou
Journal: Molecular Therapy (2022)

Predictable DNA off-target effect is one of the major safety concerns for the application of cytosine base editors (CBEs). To eliminate Cas9-dependent DNA off-target effects, we designed a novel effective CBE system with dual guiders by combining CRISPR with transcription activator-like effector (TALE). In this system, Cas9 nickase (nCas9) and cytosine deaminase are guided to the same target site to conduct base editing by single-guide RNA (sgRNA) and TALE, respectively. However, if nCas9 is guided to a wrong site by sgRNA, it will not generate base editing due to the absence of deaminase. Similarly, when deaminase is guided to a wrong site by TALE, base editing will not occur due to the absence of single-stranded DNA. In this way, Cas9- and TALE-dependent DNA off-target effects could be completely eliminated. Furthermore, by fusing TALE with YE1, a cytidine deaminase with minimal Cas9-independent off-target effect, we established a novel CBE that could induce efficient C-to-T conversion without detectable Cas9- or TALE-dependent DNA off-target mutations. Predictable DNA off-target effect is one of the major safety concerns for the application of cytosine base editors (CBEs). To eliminate Cas9-dependent DNA off-target effects, we designed a novel effective CBE system with dual guiders by combining CRISPR with transcription activator-like effector (TALE). In this system, Cas9 nickase (nCas9) and cytosine deaminase are guided to the same target site to conduct base editing by single-guide RNA (sgRNA) and TALE, respectively. However, if nCas9 is guided to a wrong site by sgRNA, it will not generate base editing due to the absence of deaminase. Similarly, when deaminase is guided to a wrong site by TALE, base editing will not occur due to the absence of single-stranded DNA. In this way, Cas9- and TALE-dependent DNA off-target effects could be completely eliminated. Furthermore, by fusing TALE with YE1, a cytidine deaminase with minimal Cas9-independent off-target effect, we established a novel CBE that could induce efficient C-to-T conversion without detectable Cas9- or TALE-dependent DNA off-target mutations.
The Planetary Health Report Card: a student-led initiative to inspire planetary health in medical schools
Authors: Karly Hampshire, Nuzhat Islam, Bennett Kissel, Hannah Chase, Katherine Gundling
Journal: The Lancet Planetary Health (2022)

The warming of our planet and destruction of our ecosystems have created grave new threats to human health, such as food insecurity, physical and mental trauma from extreme weather events, and heat-related illness. In the 21st century, medical schools should be training physicians who, as researchers, can advance evidence-based linkages between environment and health; who, as clinicians, can recognise, prevent, and treat associated diseases; and who, as healers, can advocate for a healthy biosphere as an indelible precondition for a healthy humanity. To address the substantial gap between existing and needed curricular content that reflects the realities of the health impacts of environmental degradation, medical students have developed the Planetary Health Report Card (PHRC), a metric-based tool for evaluating and improving planetary health content in medical schools. The PHRC spans five topic areas-curriculum, research, community outreach and advocacy, support for student-led initiatives, and sustainability. Since its creation in 2019, the PHRC has expanded rapidly to evaluate more than 60 medical schools in five countries. Although evaluation results reveal inadequate engagement in all topic areas, application of the PHRC is already spawning transformative dialogue between students, faculty, and administrators, serving as a platform to advance the curricular innovations that will hopefully fulfil the learning needs of medical students in a rapidly changing world.
Pulmonary delivery nanomedicines towards circumventing physiological barriers: Strategies and characterization approaches
Authors: Wenhao Wang, Zhengwei Huang, Ying Huang, Xuejuan Zhang, Jiayuan Huang, Yingtong Cui, Xiao Yue, Cheng Ma, Fangqin Fu, Wenhua Wang, Chuanbin Wu, Xin Pan
Journal: Advanced Drug Delivery Reviews (2022)
Smoking Quit Rates Among Menthol vs Nonmenthol Smokers: Implications Regarding a US Ban on the Sale of Menthol Cigarettes
Authors: Heather M Munro, Martha J Shrubsole, Wei Zheng, Wanqing Wen, William J Blot
Journal: JNCI Journal of the National Cancer Institute (2022)

A ban on the sale of menthol cigarettes in the United States is currently under consideration. A justification is that menthol cigarettes are harder to quit, particularly for African American smokers who use menthols much more frequently than White smokers, but epidemiologic data are limited.In a cohort of 16 425 mostly low-income African American and White current cigarette smokers enrolled during 2002-2009, we computed smoking quit and reuptake rates at 3 follow-ups conducted means of 4.6, 7.7, and 11 years after entry. Generalized estimation equations were used to compute odds ratios (ORs) and 95% confidence intervals (CIs) for quitting and resuming smoking for menthol vs nonmenthol smokers adjusted for race, age, education, income, and smoking pack-years.Crude annual quit rates among current smokers were 4.3% for menthol and 4.5% for nonmenthol smokers, with adjusted odds ratios of quitting for menthol vs nonmenthol smokers of 1.01 (95% CI = 0.91 to 1.11) overall, 0.99 (95% CI = 0.87 to 1.12) among African American smokers, and 1.02 (95% CI = 0.88 to 1.20) among White smokers. Crude annual smoking reuptake rates were somewhat higher among menthol smokers (8.4%) than nonmenthol smokers (7.1%), with an adjusted odds ratio of 1.19 (95% CI = 0.97 to 1.47), but net quit rates remained similar (OR = 1.01, 95% CI = 0.90 to 1.13 overall; OR = 1.00, 95% CI = 0.86 to 1.15 among African American participants; and OR = 1.04, 95% CI = 0.87 to 1.24 among White participants).This large-scale prospective survey revealed similar quit rates among menthol and nonmenthol smokers. Results contribute to policy discussions, especially if, as a meta-analysis suggests, lung cancer risk is higher for nonmenthol smokers and a ban leads menthol smokers to switch to nonmenthol cigarettes.
Peptidergic G Protein–Coupled Receptor Regulation of Adrenal Function: Bench to Bedside and Back
Authors: Livia Lenzini, Brasilina Caroccia, Teresa Maria Seccia, Gian Paolo Rossi
Journal: Endocrine Reviews (2022)

Abstract An altered secretion of adrenocortical and adrenomedullary hormones plays a role in the clinical syndromes of primary aldosteronism (PA), Cushing, and pheochromocytoma. Moreover, an altered production of adrenocortical hormones and/or an abnormal release of factors by the adrenal medulla are involved in several other diseases, including high blood pressure, congestive heart failure, liver cirrhosis, nephrotic syndrome, primary reninism, renovascular hypertension, Addison disease, Bartter, Gitelman, and virilization syndromes. Understanding the regulation of adrenal function and the interactions between adrenal cortex and medulla is, therefore, the prerequisite for mechanistic understanding of these disorders. Accumulating evidence indicates that the modulation of adrenal hormone biosynthesis is a process far more complex than originally thought, as it involves several factors, each cooperating with the other. Moreover, the tight vascular and neural interconnections between the adrenal cortex and medulla underlie physiologically relevant autocrine/paracrine interactions involving several peptides. Besides playing a pathophysiological role in common adrenal diseases, these complex mechanisms could intervene also in rare diseases, such as pheochromocytoma concomitant with adrenal Cushing or with PA, and PA co-occurring with Cushing, through mechanisms that remain to be fully understood at the molecular levels. Heterodimerization of G protein–coupled receptors (GPCRs) induced by peptide signaling is a further emerging new modulatory mechanism capable of finely tuning adrenal hormones synthesis and release. In this review we will examine current knowledge on the role of peptides that act via GPCRs in the regulation of adrenal hormone secretion with a particular focus on autocrine-paracrine signals.
Error in Byline
Journal: JAMA Network Open (2022)

Saurabh Jain, MBBS; Peng Yong Sim, MBChB(Hons); Joanne Beckmann, MBBS, MSc; Yanyan Ni, PhD; Nabil Uddin, BMedSci(Hons); Bronia Unwin, BMedSci(Hons); Neil Marlow, DM
Association of Immune Checkpoint Inhibitors With Neurologic Adverse Events
Authors: Muhammad Zain Farooq, Sheeba Ba Aqeel, Prasanth Lingamaneni, Rayli Carolina Pichardo, Aleeza Jawed, Saad Khalid, Shristi Upadhyay Banskota, Pingfu Fu, Ankit Mangla
Journal: JAMA Network Open (2022)

<h3>Importance</h3> Neurologic adverse events (NAEs) due to immune checkpoint inhibitors (ICIs) can be fatal but are underexplored. <h3>Objective</h3> To compare NAEs reported in randomized clinical trials (RCTs) of US Food and Drug Administration–approved ICIs with other forms of chemotherapy and placebo. <h3>Data Sources</h3> Bibliographic databases (Embase, Ovid, MEDLINE, and Scopus data) and trial registries (ClinicalTrials.gov) were searched from inception through March 1, 2020. <h3>Study Selection</h3> Phase II/III RCTs evaluating the use of ICIs were eligible for inclusion. Unpublished trials were excluded from the analysis. <h3>Data Extraction and Synthesis</h3> Two investigators independently performed screening of trials using the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guideline. NAEs were recorded for each arm. Data were pooled using a random-effects model. <h3>Main Outcomes and Measures</h3> The risk of NAEs with ICI use compared with any drug regimen, cytotoxic chemotherapy, and placebo. <h3>Results</h3> A total 39 trials including 23 705 patients were analyzed (16 135 [68.0%] men, 7866 [33.1%] White). The overall risk of a NAE was lower in the ICI group (risk ratio [RR], 0.59; 95% CI, 0.45-0.77) and in the subgroup of RCTs comparing ICI use with chemotherapy (RR, 0.22; 95% CI, 0.13-0.39). In the subgroup of RCTs comparing ICI with placebo, the overall risk of NAE was significantly higher in the ICI group (RR, 1.57; 95% CI, 1.30-1.89). Peripheral neuropathy (RR, 0.30; 95% CI, 0.17-0.51) and dysgeusia (RR, 0.41; 95% CI, 0.27-0.63) were significantly lower in the ICI group. Headache was more common with the use of ICIs (RR, 1.32; 95% CI, 1.10-1.59). In the subgroup analysis of RCTs comparing ICI use with chemotherapy, peripheral neuropathy (RR, 0.09; 95% CI, 0.05-0.17), dysgeusia (RR, 0.42; 95% CI, 0.21-0.85), and paresthesia (RR, 0.29; 95% CI, 0.13-0.67) were significantly lower in the ICI group. RCTs comparing ICIs with placebo showed a higher risk of headache with ICI use (RR, 1.63; 95%, CI, 1.32-2.02). <h3>Conclusions and Relevance</h3> Results of this meta-analysis suggest that the overall risk of NAEs, peripheral neuropathy, and dysgeusia is lower with the use of ICI. When compared with chemotherapy, the overall risk of NAE, peripheral neuropathy, paresthesia, and dysgeusia was lower with ICI use; however, when compared with placebo, the risk of NAEs is higher with the use of ICI.
High-efficiency nonviral CRISPR/Cas9-mediated gene editing of human T cells using plasmid donor DNA
Authors: Soyoung A. Oh, Kate Senger, Shravan Madireddi, Ilseyar Akhmetzyanova, Isabel E. Ishizuka, Somayeh Tarighat, Jerry H. Lo, David Shaw, Benjamin Haley, Sascha Rutz
Journal: The Journal of Experimental Medicine (2022)

Genome engineering of T lymphocytes, the main effectors of antitumor adaptive immune responses, has the potential to uncover unique insights into their functions and enable the development of next-generation adoptive T cell therapies. Viral gene delivery into T cells, which is currently used to generate CAR T cells, has limitations in regard to targeting precision, cargo flexibility, and reagent production. Nonviral methods for effective CRISPR/Cas9-mediated gene knock-out in primary human T cells have been developed, but complementary techniques for nonviral gene knock-in can be cumbersome and inefficient. Here, we report a convenient and scalable nonviral method that allows precise gene edits and transgene integration in primary human T cells, using plasmid donor DNA template and Cas9-RNP. This method is highly efficient for single and multiplex gene manipulation, without compromising T cell function, and is thus valuable for use in basic and translational research.
Dual-aptamer-engineered M1 macrophage with enhanced specific targeting and checkpoint blocking for solid-tumor immunotherapy
Authors: Husun Qian, Yixin Fu, Minkang Guo, Yu Chen, Dian Zhang, Yu Wei, Fangfang Jin, Qian Zeng, Yange Wang, Chengsen Chai, Shijia Ding, Wei Cheng, Tingmei Chen
Journal: Molecular Therapy (2022)

Chimeric antigen receptor T (CAR-T) cell therapy has faced a series of challenges and has shown very little efficacy in solid tumors to date. Although genetically engineered macrophages have achieved definite therapeutic effect in solid tumors, heterogeneous expression of engineered proteins and the potential for toxicity limit further applications. Herein, we propose a nongenetic and simple macrophage cell engineering strategy through glycan metabolic labeling and click reaction for the treatment of solid tumors. The aptamer-engineered M1 macrophage (ApEn-M1) showed enhanced active targeting ability for tumor cells in vitro and in vivo, resulting in significant cytotoxicity effects. Moreover, ApEn-M1 exhibited superior antitumor efficacy in a breast cancer xenograft mouse model and a lung metastasis mouse model of breast cancer. Interestingly, the ApEn-M1 could reprogram the immunity microenvironment by increasing T cell infiltration and enhancing T cell activity in the tumor region. Additionally, the administration of ApEn-M1 showed no obvious systemic side effects. With glycan metabolic labeling, the macrophages could be efficiently labeled with aptamers on the cell surface via click reaction without genetic alteration or cell damage. Hence, this study serves as a proof of concept for cell-surface anchor engineering and expands the range of nongenetic macrophage cell engineering strategies.Graphical abstract
A loss-of-function <i>IFNAR1</i> allele in Polynesia underlies severe viral diseases in homozygotes
Authors: Paul Bastard, Kuang-Chih Hsiao, Qian Zhang, Jeremy Choin, Emma Best, Jie Chen, Adrian Gervais, Lucy Bizien, Marie Materna, Christine Harmant, Maguelonne Roux, Nicola L. Hawley, Daniel E. Weeks, Stephen T. McGarvey, Karla Sandoval, Carmina Barberena-Jonas, Consuelo D. Quinto-Cortés, Erika Hagelberg, Alexander J. Mentzer, Kathryn Robson, Boubacar Coulibaly, Yoann Seeleuthner, Benedetta Bigio, Zhi Li, Gilles Uzé, Sandra Pellegrini, Lazaro Lorenzo, Zineb Sbihi, Sylvain Latour, Marianne Besnard, Tiphaine Adam de Beaumais, Evelyne Jacqz Aigrain, Vivien Béziat, Ranjan Deka, Litara Esera Tulifau, Satupa‘itea Viali, Muagututi‘a Sefuiva Reupena, Take Naseri, Peter McNaughton, Vanessa Sarkozy, Jane Peake, Annaliesse Blincoe, Sarah Primhak, Simon Stables, Kate Gibson, See-Tarn Woon, Kylie Marie Drake, Adrian V.S. Hill, Cheng-Yee Chan, Richard King, Rohan Ameratunga, Iotefa Teiti, Maite Aubry, Van-Mai Cao-Lormeau, Stuart G. Tangye, Shen-Ying Zhang, Emmanuelle Jouanguy, Paul Gray, Laurent Abel, Andrés Moreno-Estrada, Ryan L. Minster, Lluis Quintana-Murci, Andrew C. Wood, Jean-Laurent Casanova
Journal: The Journal of Experimental Medicine (2022)

Globally, autosomal recessive IFNAR1 deficiency is a rare inborn error of immunity underlying susceptibility to live attenuated vaccine and wild-type viruses. We report seven children from five unrelated kindreds of western Polynesian ancestry who suffered from severe viral diseases. All the patients are homozygous for the same nonsense IFNAR1 variant (p.Glu386*). This allele encodes a truncated protein that is absent from the cell surface and is loss-of-function. The fibroblasts of the patients do not respond to type I IFNs (IFN-α2, IFN-ω, or IFN-β). Remarkably, this IFNAR1 variant has a minor allele frequency &amp;gt;1% in Samoa and is also observed in the Cook, Society, Marquesas, and Austral islands, as well as Fiji, whereas it is extremely rare or absent in the other populations tested, including those of the Pacific region. Inherited IFNAR1 deficiency should be considered in individuals of Polynesian ancestry with severe viral illnesses.
Pulse Oximetry for Monitoring Patients with Covid-19 at Home — A Pragmatic, Randomized Trial
Authors: Kathleen C Lee, Anna U Morgan, Krisda H Chaiyachati, David A Asch, Ruiying A Xiong, David Do, Austin S Kilaru, Doreen Lam, Andrew Parambath, Ari B Friedman, Zachary F Meisel, Christopher K Snider, Deena L Chisholm, Sheila Kelly, Jessica E Hemmons, Dina Abdel-Rahman, Jeffrey Ebert, Medha Ghosh, Julianne Reilly, Christina J O'Malley, Lauren Hahn, Nancy M Mannion, Ann M Huffenberger, Susan McGinley, Mohan Balachandran, Neda Khan, Judy A Shea, Nandita Mitra, M Kit Delgado
Journal: New England Journal of Medicine (2022)
Reply to Dr. Chung and colleagues
Authors: Parag Dashatwar, Vishnu Biradar, Amol Bapaye
Journal: Endoscopy (2022)

See also: Letter to the editor re initial experience with per-rectal endoscopic myotomy for Hirschsprungʼs diseaseEndoscopy 2022; 54(05): 525-525DOI: 10.1055/a-1762-5456
Stagnant US Mammography Rates and the Influence of COVID-19
Authors: Melissa Suran
Journal: JAMA (2022)

Kevin C. Oeffinger, MD; Elizabeth T. H. Fontham, MPH, DrPH; Ruth Etzioni, PhD; Abbe Herzig, PhD; James S. Michaelson, PhD; Ya-Chen Tina Shih, PhD; Louise C. Walter, MD; Timothy R. Church, PhD; Christopher R. Flowers, MD, MS; Samuel J. LaMonte, MD; Andrew M. D. Wolf, MD; Carol DeSantis, MPH; Joannie Lortet-Tieulent, MSc; Kimberly Andrews; Deana Manassaram-Baptiste, PhD; Debbie Saslow, PhD; Robert A. Smith, PhD; Otis W. Brawley, MD; Richard Wender, MD
Calorie and Time Restriction in Weight Loss
Authors: Blandine Laferrère, Satchidananda Panda
Journal: New England Journal of Medicine (2022)

Weight loss with calorie restriction is the recommended approach for treatment of obesity, but this approach is resource-intensive and difficult to sustain over time.1 Time-restricted eating is a potentially low-cost and sustainable lifestyle in which daily intake of calories is restricted to a consistent time period of less than 10 hours without explicit attempts to modify diet composition or reduce calories. Chronic disruption of the circadian rhythm increases the risk of obesity and metabolic diseases. Restricting the window of time for eating sustains circadian rhythms and improves metabolism by prolonging the daily fast, which in turn activates cellular pathways that . . .
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Authors: Valencia Long
Journal: JAMA Oncology (2022)

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Epigenetic modifier gene mutations in chronic myeloid leukemia (CML) at diagnosis are associated with risk of relapse upon treatment discontinuation
Authors: Shady Adnan Awad, Oscar Brück, Naranie Shanmuganathan, Timo Jarvinen, Hanna Lähteenmäki, Jay Klievink, Hazem Ibrahim, Soili Kytölä, Perttu Koskenvesa, Timothy P. Hughes, Susan Branford, Matti Kankainen, Satu Mustjoki
Journal: Blood Cancer Journal (2022)