tbuckley/cabot-search huggingface dataset:
Eating Keto, Vegan Diets Rewired Immune System Within 2 Weeks
Authors: Emily Harris
Journal: JAMA (2024)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Gut microbiota regulates host melatonin production through epithelial cell MyD88
Authors: Bingnan Liu, Lijuan Fan, Youxia Wang, Hao Wang, Yuqi Yan, Shuai Chen, Ifen Hung, Chunxue Liu, Hong Wei, Liangpeng Ge, Wenkai Ren
Journal: Gut Microbes (2024)

Melatonin has various physiological effects, such as the maintenance of circadian rhythms, anti-inflammatory functions, and regulation of intestinal barriers. The regulatory functions of melatonin in gut microbiota remodeling have also been well clarified; however, the role of gut microbiota in regulating host melatonin production remains poorly understood. To address this, we studied the contribution of gut microbiota to host melatonin production using gut microbiota-perturbed models. We demonstrated that antibiotic-treated and germ-free mice possessed diminished melatonin levels in the serum and elevated melatonin levels in the colon. The influence of the intestinal microbiota on host melatonin production was further confirmed by fecal microbiota transplantation. Notably, Lactobacillus reuteri (L. R) and Escherichia coli (E. coli) recapitulated the effects of gut microbiota on host melatonin production. Mechanistically, L. R and E. coli activated the TLR2/4/MyD88/NF-κB signaling pathway to promote expression of arylalkylamine N-acetyltransferase (AANAT, a rate-limiting enzyme for melatonin production), and MyD88 deficiency in colonic epithelial cells abolished the influence of intestinal microbiota on colonic melatonin production. Collectively, we revealed a specific underlying mechanism of gut microbiota to modulate host melatonin production, which might provide novel therapeutic ideas for melatonin-related diseases.
IL-10-Engineered Human CD4+ Tr1 Cells Eliminate Myeloid Leukemia in an HLA Class I-Dependent Mechanism
Authors: Grazia Locafaro, Grazia Andolfi, Fabio Russo, Luca Cesana, Antonello Spinelli, Barbara Camisa, Fabio Ciceri, Angelo Lombardo, Attilio Bondanza, Maria Grazia Roncarolo, Silvia Gregori
Journal: Molecular Therapy (2024)

(Molecular Therapy 25, 2254–2269; October 2017) In the originally published version of this article, there is an error in Figure 8A, where there is a duplication of the mouse pictures at day 5 and day 7. The error occurred during the editing of Figure 8A and does not affect the overall conclusion of the paper. A corrected version of the figure is provided below. The authors apologize for this error and any confusion this may have caused. IL-10-Engineered Human CD4+ Tr1 Cells Eliminate Myeloid Leukemia in an HLA Class I-Dependent MechanismLocafaro et al.Molecular TherapyJuly 4, 2017In BriefTr1 cells are generated by overexpressing IL-10 in CD4+ T cells (CD4IL-10). In this issue of Molecular Therapy, Locafaro et al. (2017) show that CD4IL-10 cells kill myeloid leukemia in an HLA class I-dependent mechanism, mediate anti-tumor and anti-leukemic effects, and contribute to GvL while preventing GvHD in humanized mice. Full-Text PDF Open Access
A cigarette filter-derived biomimetic cardiac niche for myocardial infarction repair
Authors: Guofeng Tang, Zhentao Li, Chengbin Ding, Jiang Zhao, Xianglong Xing, Yan Sun, Xiaozhong Qiu, Leyu Wang
Journal: Bioactive Materials (2024)

Cell implantation offers an appealing avenue for heart repair after myocardial infarction (MI). Nevertheless, the implanted cells are subjected to the aberrant myocardial niche, which inhibits cell survival and maturation, posing significant challenges to the ultimate therapeutic outcome. The functional cardiac patches (CPs) have been proved to construct an elastic conductive, antioxidative, and angiogenic microenvironment for rectifying the aberrant microenvironment of the infarcted myocardium. More importantly, inducing implanted cardiomyocytes (CMs) adapted to the anisotropic arrangement of myocardial tissue by bioengineered structural cues within CPs are more conducive to MI repair. Herein, a functional Cig/(TA-Cu) CP served as biomimetic cardiac niche was fabricated based on structural anisotropic cigarette filter by modifying with tannic acid (TA)-chelated Cu2+ (TA-Cu complex) via a green method. This CP possessed microstructural anisotropy, electrical conductivity and mechanical properties similar to natural myocardium, which could promote elongation, orientation, maturation, and functionalization of CMs. Besides, the Cig/(TA-Cu) CP could efficiently scavenge reactive oxygen species, reduce CM apoptosis, ultimately facilitating myocardial electrical integration, promoting vascular regeneration and improving cardiac function. Together, our study introduces a functional CP that integrates multimodal cues to create a biomimetic cardiac niche and provides an effective strategy for cardiac repair.
Editorial Expression of Concern: Hyperbaric oxygen therapy reduces the toll-like receptor signaling pathway in multiple organ failures
Authors: Barbara Rinaldi, Salvatore Cuzzocrea, Maria Donniacuo, Annalisa Capuano, Donatella Di Palma, Francesco Imperatore, Emanuela Mazzon, Rosanna Di Paola, Loredana Sodano, Francesco Rossi
Journal: Intensive Care Medicine (2024)
Advocating action against the climate crisis: the role of the health professional
Authors: Shweta Narayan
Journal: BMJ (2024)

Advocating action against the climate crisis: the role of the health professionalHealth professionals should look back on the rich history of advocacy to drive engagement with the climate debate, writes Shweta Narayan Shweta Narayan, 1The role of the health professional is varied and broad.In its scope there is a pivotal role to play in influencing policy, challenging social norms, and championing transformative change.Health professionals have a unique ability to examine current issues through the lens of public health and disseminate this information to the wider public, be it mapping diseases with epidemic potential, organising for women's rights, helping to prevent nuclear war, or advocating for racial equity.
Two regulatory T cell populations in the visceral adipose tissue shape systemic metabolism
Authors: Santiago Valle Torres, Kevin Man, Tarek Elmzzahi, Darya Malko, David Chisanga, Yang Liao, Melanie Prout, Caitlin A. Abbott, Adelynn Tang, Jian Wu, Matthias Becker, Teisha Mason, Vanessa Haynes, Carlson Tsui, Mehrnoush Hadaddzadeh Shakiba, Doaa Hamada, Kara Britt, Joanna R. Groom, Shaun R. McColl, Wei Shi, Matthew J. Watt, Graham Le Gros, Bhupinder Pal, Marc Beyer, Ajithkumar Vasanthakumar, Axel Kallies
Journal: Nature Immunology (2024)
Entinostat, nivolumab and ipilimumab for women with advanced HER2-negative breast cancer: a phase Ib trial
Authors: Evanthia.T. Roussos Torres, Won J. Ho, Ludmila Danilova, Joseph A. Tandurella, James Leatherman, Christine Rafie, Chenguang Wang, Adam Brufsky, Patricia LoRusso, Vincent Chung, Yuan Yuan, Melinda Downs, Ashley O’Connor, Sarah M. Shin, Alexei Hernandez, Elizabeth L. Engle, Richard Piekarz, Howard Streicher, Zahra Talebi, Michelle A. Rudek, Qingfeng Zhu, Robert A. Anders, Ashley Cimino-Mathews, Elana J. Fertig, Elizabeth M. Jaffee, Vered Stearns, Roisin M. Connolly
Journal: Nature Cancer (2024)
Author Correction: Tumor cell-specific bioluminescence platform to identify stroma-induced changes to anticancer drug activity
Authors: Douglas. W McMillin, Jake Delmore, Ellen Weisberg, Joseph. M Negri, Corey. D Geer, Steffen Klippel, Nicholas Mitsiades, Robert. L Schlossman, Nikhil. C Munshi, Andrew. L Kung, James. D Griffin, Paul. G Richardson, Kenneth. C Anderson, Constantine. S Mitsiades
Journal: Nature Medicine (2024)

After publication, concerns were raised regarding the western blot and immunofluorescence images presented in the figures.Specifically:• Fig. 1b Hypoxia + tPA +APC TUNEL image appears to have no background noise.• Fig. 3e and h images appear to contain inconsistent backgrounds and straight line artifacts between bands.• In Fig. 4e, all images appear to contain repeated features.The corresponding author has stated that the issues in Figs. 1 and 3 may have been caused by data compression artifacts.Notably, the quantitative analysis of caspase levels presented in Fig. 3 is not based on the western blots in Fig. 3e, but on enzymatic assays, as indicated in the article.The corresponding author has also determined that the images in Fig. 4e were manipulated, but was unaware of it at the time of publication.
Prognostic value of ferritin in ASCT MM patients: integration with GEP models and ISS series systems
Authors: Wancheng Guo, Yihao Zhan, David Mery, Eric R. Siegel, Fumou Sun, Yan Cheng, Timothy Cody Ashby, Zijun Zhang, Clyde Bailey, Daisy V. Alapat, Hongling Peng, Samer Al Hadidi, Sharmilan Thanendrarajan, Carolina Schinke, Maurizio Zangari, Frits van Rhee, Guido Tricot, John D. Shaughnessy, Fenghuang Zhan
Journal: Blood Cancer Journal (2024)
Inflammatory linear verrucous epidermal nevus should be genotyped to direct treatment and genetic counseling
Authors: Satyamaanasa Polubothu, Melissa Riachi, Paulina Stadnik, Olumide Ogunbiyi, Regula Brändli-Wälchli, Thomas Cullup, Neil J. Sebire, Alan Pittman, Veronica A. Kinsler
Journal: Journal of the American Academy of Dermatology (2024)

Inflammatory linear verrucous epidermal nevus should be genotyped to direct treatment and genetic counselingTo the Editor: Inflammatory linear verrucous epidermal nevus (ILVEN) is a clinical diagnosis based on persistent Blaschko-linear erythematous scaly and usually pruritic lesions.Sixteen patients with a clinical diagnosis of ILVEN as defined by published diagnostic criteria were recruited and consented under Research Ethics Committee approval for phenotypic, histological, and genotypic analysis.At the time of initiating this study in 2014 no genetic causes of ILVEN were known.Causative genetic variants since described are in GJA1, 1 ABCA12 2 , CARD14, 3 PMVK 4 , NSDHL, 4 HRAS 4 and KRT10. 4Disease mechanisms thus far include germline X-linked variants, mosaic variants, and germline first hit with mosaic second hit.Paired blood and affected skin DNA underwent deep whole exome sequencing (WES, mean 250X), n ¼ 14, and if negative, skin DNA underwent targeted sequencing panel R327 (mosaic disorders, UK National Genomic Test Directory), n ¼ 8. Two patients had a negative WES and did not go forward to next generation sequencing panel due to sample limitations.Two patients recruited late in the study had next generation sequencing panel first and did not proceed to WES.We confirm here that ILVEN has multiple monogenic causes, with mutations in NSDHL (n ¼ 2, germline, NSDHL c.613G [ T, p.[G205T ], c.603_604delTG, p.[H201fs*69], both picked up on WES), PMVK (n ¼ 1, mosaic in blood and skin, no second variant detected in the same gene in skin, PMVK c.126delG, p.R42fs, picked up on WES), HRAS (n ¼ 1, mosaic, HRAS c.37G [ C, p.(G13R), picked up on panel, and CARD14 (n ¼ 2, mosaic, these 2 only previously published, 1 both picked up on WES).Ten patients had no pathogenic variants identified and we specifically excluded any variants in all previously described genes.No patients who were negative on WES had genes identified on a subsequent panel, suggesting that variants still unidentified are not in known mosaic genes, or if they are they are unlikely to be
Antibiotics to eradicate Streptococcus pyogenes pharyngeal carriage in asymptomatic children and adults: A systematic review
Authors: Te-Yu Hung, Linny K. Phuong, Anneke Grobler, Steven Y.C. Tong, Pippin Freeth, Asika Pelenda, Katherine B. Gibney, Andrew C. Steer
Journal: Journal of Infection (2024)

Streptococcus pyogenes (S. pyogenes) is a Gram-positive bacteria which causes a spectrum of diseases ranging from asymptomatic infection to life-threatening sepsis. Studies report up to 2000 times greater risk of invasive S. pyogenes disease in close contacts of index cases within 30-days of symptom onset. Despite this, there is variability in the management of asymptomatic carriage of S. pyogenes and those at risk of secondary cases of invasive S. pyogenes infection.
Integrated Single-Cell Transcriptomic Atlas of Human Kidney Endothelial Cells
Authors: Ka Zhang, Hao Kan, Aiqin Mao, Fan Yu, Li Geng, Tingting Zhou, Lei Feng, Xin Ma
Journal: Journal of the American Society of Nephrology (2024)

Key Points We created a comprehensive reference atlas of normal human kidney endothelial cells. We confirmed that endothelial cell types in the human kidney were also highly conserved in the mouse kidney. Background Kidney endothelial cells are exposed to different microenvironmental conditions that support specific physiologic processes. However, the heterogeneity of human kidney endothelial cells has not yet been systematically described. Methods We reprocessed and integrated seven human kidney control single-cell/single-nucleus RNA sequencing datasets of &gt;200,000 kidney cells in the same process. Results We identified five major cell types, 29,992 of which were endothelial cells. Endothelial cell reclustering identified seven subgroups that differed in molecular characteristics and physiologic functions. Mapping new data to a normal kidney endothelial cell atlas allows rapid data annotation and analysis. We confirmed that endothelial cell types in the human kidney were also highly conserved in the mouse kidney and identified endothelial marker genes that were conserved in humans and mice, as well as differentially expressed genes between corresponding subpopulations. Furthermore, combined analysis of single-cell transcriptome data with public genome-wide association study data showed a significant enrichment of endothelial cells, especially arterial endothelial cells, in BP heritability. Finally, we identified M1 and M12 from coexpression networks in endothelial cells that may be deeply involved in BP regulation. Conclusions We created a comprehensive reference atlas of normal human kidney endothelial cells that provides the molecular foundation for understanding how the identity and function of kidney endothelial cells are altered in disease, aging, and between species. Finally, we provide a publicly accessible online tool to explore the datasets described in this work (https://vascularmap.jiangnan.edu.cn).
The dysbiosis of the gut microbiome in spondyloarthritis patients is correlated with both disease activity and HLA‐B27 status
Authors: Yi Zheng, Jun He, Liqi Li
Journal: Arthritis & Rheumatology (2024)

Disclosure Form 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.
The role of programmed death receptor (PD‐)1/PD‐ligand (L)1 in periodontitis and cancer
Authors: Sabine Groeger, Joerg Meyle
Journal: Periodontology 2000 (2024)

Abstract The programmed‐death‐ligand‐1 (PD‐L1) is an immune‐modulating molecule that is constitutively expressed on various immune cells, different epithelial cells and a multitude of cancer cells. It is a costimulatory molecule that may impair T‐cell mediated immune response. Ligation to the programmed‐death‐receptor (PD)‐1, on activated T‐cells and further triggering of the related signaling pathways can induce T‐cells apoptosis or anergy. The upregulation of PD‐L1 in various cancer types, including oral squamous cell carcinomas, was demonstrated and has been linked to immune escape of tumors and poor prognosis. A bidirectional relationship exists between the increased PD‐L1 expression and periodontitis as well as the epithelial–mesenchymal transition (EMT), a process of interconversion of epithelial cells to mesenchymal cells that may induce immune escape of tumors. Interaction between exosomal PD‐L1 and PD‐1 on T‐cells may cause immunosuppression by blocking the activation and proliferation of T‐cells. The efficacy and importance of treatment with PD‐1/PD‐L1 checkpoint inhibitors and their prognostic influence on human cancers was demonstrated. Regarding PD‐1/PD‐L1 checkpoint inhibitors, resistances exist or may develop, basing on various factors. Further investigations of the underlying mechanisms will help to overcome the therapeutic limitations that result from resistances and to develop new strategies for the treatment of cancer.
<scp>Anti‐S100A4</scp> monoclonal antibody treatment ameliorates experimental skin fibrosis and <scp>SSc</scp>‐specific transcriptional signatures in human skin: Comment on the targeting S100A4 is helpful in SSc treatment by <scp>Trinh‐Minh</scp> et al
Authors: An‐Fang Huang, Wang‐Dong Xu
Journal: Arthritis & Rheumatology (2024)

Disclosure form 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.
SLC25A51 decouples the mitochondrial NAD+/NADH ratio to control proliferation of AML cells
Authors: Mu-Jie Lu, Jonathan Busquets, Valeria Impedovo, Crystal N. Wilson, Hsin-Ru Chan, Yu-Tai Chang, William Matsui, Stefano Tiziani, Xiaolu A. Cambronne
Journal: Cell Metabolism (2024)
Recombinant Human Keratinocyte Growth Factor Ameliorates Cancer Treatment‐Induced Oral Mucositis on a Chip
Authors: Khanh L. Ly, May Rajtboriraks, Ahmed Elgerbi, Xiaolong Luo, Christopher B. Raub
Journal: Advanced Healthcare Materials (2024)

Abstract Oral mucositis (OM) is a severe complication of cancer therapies caused by off‐target cytotoxicity. Palifermin, which is recombinant human keratinocyte growth factor (KGF), is currently the only mitigating treatment available to a subset of OM patients. This study used a previously established model of oral mucositis on a chip (OM‐OC) comprised of a confluent human gingival keratinocytes (GIE) layer attached to a basement membrane‐lined subepithelial layer consisting of human gingival fibroblasts (HGF) and human dermal microvascular endothelial cells (HMEC) on a stable collagen I gel. Cisplatin, radiation, and combined treatments are followed by a recovery period in the OM‐OC to determine possible cellular and molecular mechanisms of OM under effects of KGF. Cancer treatments affected the keratinocyte layer, causing death and epithelial barrier loss. Both keratinocytes and subepithelial cells died rapidly, as evidenced by propidium iodide staining. In response to radiation exposure, cell death occurred in the apical epithelial layer, predominantly, within 24h. Cisplatin exposure predominantly promoted death of basal epithelial cells within 32‐36h. Presence of KGF in OM‐OC protected tissues from damage caused by cancer treatments in a dose‐dependent manner, being more effective at 10 ng/mL. As verified by F‐actin staining and the Alamar Blue assay, KGF contributed to epithelial survival and induced proliferation of GIE and HGF as well as HMEC within 120h. When the expression of eighty inflammatory cytokines is evaluated at OM induction (Day 12) and resolution (Day 18) stages in OM‐OC, some cytokines are identified as potential novel therapeutic targets. In comparison with chemoradiation exposure, KGF treatment showed a trend to decrease IL‐8 and TNF‐a expression at Day 12 and 18, and TGF‐β1 at Day 18 in OM‐OC. Taken together, these findings support the utility of OM‐OC as a platform to model epithelial damage and evaluate molecular mechanisms following OM treatment.
Gut microbiota-derived trimethylamine N-Oxide: a novel target for the treatment of preeclampsia
Authors: Jiayi Wang, Yajie Gao, Shuaijun Ren, Jialin Li, Siqian Chen, Jiating Feng, Bing He, Yuping Zhou, Rongrong Xuan
Journal: Gut Microbes (2024)

Pre-eclampsia (PE) is the most common complication of pregnancy and seriously threatens the health and safety of the mother and child. Studies have shown that an imbalance in gut microbiota can affect the progression of PE. Trimethylamine N-oxide (TMAO) is an intestinal microbiota-derived metabolite that is thought to be involved in the occurrence of PE; however, its causal relationship and mechanism remain unclear. In this clinical cohort study, including 28 patients with eclampsia and 39 matched healthy controls, fecal samples were collected for 16S rRNA gene sequencing, and serum was collected for targeted metabolomics research. The results showed that the level of TMAO and the abundance of its source bacteria had significantly increased in patients with PE, and were positively correlated with the clinical progression of PE. Fecal microbiota transplantation (FMT) was applied to an antibiotic-depleted-treated mouse model and targeted inhibition of TMAO. The results of the FMT experiment revealed that mice that received fecal microbiota transplantation from patients with PE developed typical PE symptoms and increased oxidative stress and inflammatory damage, both of which were reversed by 3,3-Dimethyl-1-butanol (DMB), a TMAO inhibitor, which also improved pregnancy outcomes in the model mice. Similar results were obtained in the classical NG-Nitroarginine methyl ester (L-NAME) induced PE mouse model. Mechanistically, TMAO promotes the progression of PE by regulating inflammatory and oxidative stress-related signaling pathways, affecting the migration and angiogenesis of vascular endothelial cells, as well as the migration and invasion of trophoblast cells. Our results reveal the role and mechanism of gut microbiota and TMAO in the progression of PE, provides new ideas for exploring the pathogenesis and therapeutic targets of PE, and determines the potential application value of TMAO as a target for PE intervention.