tbuckley/cabot-search huggingface dataset:
Functionalized BP@(Zn+Ag)/EPLA Nanofibrous Scaffolds Fabricated by Cryogenic 3D Printing for Bone Tissue Engineering
Authors: Shunyu Chen, Zhoucheng Qiu, Lihua Zhao, Xiaojing Huang, Xiufeng Xiao
Journal: Advanced Healthcare Materials (2024)

Abstract This study fabricates a functionalized scaffold by cryogenic three‐dimensional (3D) printing using an aminated poly‐L‐lactic acid (EPLA) solution containing nanosilver/zinc‐coated black phosphorus (BP@(Zn+Ag)) nanocomposites. The nanocomposites are prepared by a green method of in situ photodeposition of silver and zinc nanoparticles (AgNPs and ZnNPs) on BP nanosheets (BPNs) under visible light irradiation without any chemical reductant. Scanning electron microscope (SEM) and X‐ray energy dispersive spectrometer (EDS) confirm the uniform distribution of BP@(Zn+Ag) nanoparticles in the EPLA nanofibrous matrix. The in vitro tests show that the fabricated BP@(Zn+Ag)/EPLA nanofibrous scaffold exhibits excellent antibacterial activity (over 96%) against E. coli and S. aureus, as well as enhanced cell viability and osteogenic activity to facilitate the growth and differentiation of osteoblasts. The in vivo rat calvarial defect model also demonstrates that the BP@(Zn+Ag)/EPLA nanofibrous scaffold promotes new bone tissue formation around the implant site. Therefore, the prepared multifunctional 3D printed BP@(Zn+Ag)/EPLA nanofibrous scaffold has great potential for bone tissue engineering (BTE) applications.
A case of missing fingerprints
Authors: Mark Eisner, Neil Rajan
Journal: British Journal of Dermatology (2024)

Congenital adermatoglyphia (a lack of fingerprints) is seen with variants in SMARCAD1 and can be associated with an increased risk of cutaneous squamous cell carcinoma. Here we demonstrate adermatoglyphia in a patient with Huriez syndrome and compare with an unaffected volunteer.
Life’s Essential 8, genetic susceptibility and the risk of psoriatic disease: a prospective cohort study
Authors: Fujun Ouyang, Honghao Yang, Zhenghong Di, Jiahao Hu, Yuan Ding, Chao Ji, Yashu Liu, Liangkai Chen, Yang Xia
Journal: British Journal of Dermatology (2024)

Abstract Background Psoriatic disease (PsD) is closely associated with cardiovascular (CV) disease. The Life’s Essential 8 (LE8) score is a new metric to assess CV health (CVH), where a higher score indicates better CVH. However, the longitudinal association between LE8 score and the risk of PsD remains uncertain. Objectives To investigate, in a cohort study, the association between LE8 score, genetic susceptibility and the risk of PsD. Methods This cohort study included 261 642 participants in the UK Biobank without PsD at baseline. LE8 comprises eight indicators: diet, physical activity, nicotine exposure, sleep health, body mass index, blood lipids, blood glucose and blood pressure. Cox proportional hazard models were used to examine the association between participants’ LE8 scores, genetic risk of PsD and the risk of PsD. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated. Results During an average follow-up of 12.3 years, 1501 participants developed PsD. Compared with participants with low LE8 scores, the HRs of developing PsD for those with moderate and high LE8 scores were 0.51 (95% CI 0.43–0.59) and 0.34 (95% CI 0.27–0.42) after adjustments, respectively. Dose–response analysis revealed a linear negative association between continuous LE8 score and the risk of developing PsD (P &amp;lt; 0.001), with no evidence of nonlinear association detected. Genetic susceptibility to PsD did not modify this association (P­interaction = 0.63). Subgroup analyses revealed that women had a more pronounced beneficial association between LE8 scores and PsD risk (P­interaction = 0.02). Conclusions Our study suggests that a higher LE8 score, regardless of genetic risk, is associated with a lower risk of PsD, particularly in women. Consequently, maintaining good CVH status is recommended to prevent PsD and assess associated risks.
Severity of COVID-19 sub-lineages XBB/XBB 1.5/XBB1.16, EG.5.1. and JN.1. in England
Authors: Catherine Quinot, Freja Kirsebom, Nick Andrews, Julia Stowe, Mary Ramsay, Gavin Dabrera, Meaghan Kall, Jamie Lopez Bernal, Alex Allen
Journal: The Lancet Regional Health - Europe (2024)
Author Correction: Inhibition of lysine acetyltransferase KAT6 in ER+HER2− metastatic breast cancer: a phase 1 trial
Authors: Toru Mukohara, Yeon Hee Park, David Sommerhalder, Kan Yonemori, Erika Hamilton, Sung-Bae Kim, Jee Hyun Kim, Hiroji Iwata, Toshinari Yamashita, Rachel M. Layman, Monica Mita, Timothy Clay, Yee Soo Chae, Catherine Oakman, Fengting Yan, Gun Min Kim, Seock-Ah Im, Geoffrey J. Lindeman, Hope S. Rugo, Marlon Liyanage, Michelle Saul, Christophe Le Corre, Athanasia Skoura, Li Liu, Meng Li, Patricia M. LoRusso
Journal: Nature Medicine (2024)

In the version of the article initially published, in Extended Data Fig. 1, under "Part 1B", "5 mg QD" originally read "3 dose levels" and "n=9" was missing from that box.There was originally an additional "Cohort 1 (5 mg QD, n=9)" box that has now been removed.Under "Part "2A", the text "fulvestrant 500 mg" originally preceded "(n=35)".In Extended Data Fig. 5, "(confirmed)" has been removed from both graph legends, which originally read "Best overall response (confirmed)".In Extended Data Table 1, the title of Table 1B has been corrected from "PF-07248144 dose and DLT relationship" to "Bayesian Logistic Regression Model: Predicted probability of DLT".
The Safety of Topical versus Oral Steroids in Bullous Pemphigoid: Considerations for Retrospective Analyses
Authors: Kyle T Amber, Ron J Feldman
Journal: British Journal of Dermatology (2024)

Journal Article Accepted manuscript The Safety of Topical versus Oral Steroids in Bullous Pemphigoid: Considerations for Retrospective Analyses Get access Kyle T Amber, Kyle T Amber Department of Dermatology, Rush University Medical Center, Chicago, IL, USA Correspondence: Kyle T. Amber MD, Email:kyle_amber@rush.edu https://orcid.org/0000-0002-2906-2454 Search for other works by this author on: Oxford Academic Google Scholar Ron J Feldman Ron J Feldman Department of Dermatology, Emory University, Atlanta, GA, USA Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, ljae265, https://doi.org/10.1093/bjd/ljae265 Published: 24 June 2024 Article history Received: 14 June 2024 Accepted: 19 June 2024 Published: 24 June 2024
The biological significance of tumor grade, age, enhancement, and extent of resection in IDH-mutant gliomas: How should they inform treatment decisions in the era of IDH inhibitors?
Authors: Martin J van den Bent, Pim J French, Daniel Brat, Joerg C Tonn, Mehdi Touat, Benjamin M Ellingson, Robert J Young, Johan Pallud, Andreas von Deimling, Felix Sahm, Dominique Figarella Branger, Raymond Y Huang, Michael Weller, Ingo K Mellinghoff, Tim F Cloughsey, Jason T Huse, Kenneth Aldape, Guido Reifenberger, Gilbert Youssef, Philipp Karschnia, Houtan Noushmehr, Katherine B Peters, Francois Ducray, Matthias Preusser, Patrick Y Wen
Journal: Neuro-Oncology (2024)

The 2016 and 2021 World Health Organization 2021 Classification of central nervous system tumors have resulted in a major improvement in the classification of isocitrate dehydrogenase (IDH)-mutant gliomas. With more effective treatments many patients experience prolonged survival. However, treatment guidelines are often still based on information from historical series comprising both patients with IDH wild-type and IDH-mutant tumors. They provide recommendations for radiotherapy and chemotherapy for so-called high-risk patients, usually based on residual tumor after surgery and age over 40. More up-to-date studies give a better insight into clinical, radiological, and molecular factors associated with the outcome of patients with IDH-mutant glioma. These insights should be used today for risk stratification and for treatment decisions. In many patients with IDH-mutant grades 2 and 3 glioma, if carefully monitored postponing radiotherapy and chemotherapy is safe, and will not jeopardize the overall outcome of patients. With the INDIGO trial showing patient benefit from the IDH inhibitor vorasidenib, there is a sizable population in which it seems reasonable to try this class of agents before recommending radio-chemotherapy with its delayed adverse event profile affecting quality of survival. Ongoing trials should help to further identify the patients that are benefiting from this treatment.
No benefit from TMZ treatment in glioblastoma with truly unmethylated <i>MGMT</i> promoter: Reanalysis of the CE.6 and the pooled Nordic/NOA-08 trials in elderly glioblastoma patients
Authors: Monika E Hegi, Felix B Oppong, James R Perry, Wolfgang Wick, Roger Henriksson, Norman J Laperriere, Thierry Gorlia, Annika Malmström, Michael Weller
Journal: Neuro-Oncology (2024)

Abstract Background The treatment of elderly/ frail patients with glioblastoma is a balance between avoiding undue toxicity, while not withholding effective treatment. It remains debated, whether these patients should receive combined chemo-radiotherapy with temozolomide (RT/TMZ→TMZ) regardless of the O6-methylguanine DNA methyltransferase gene promoter (MGMTp) methylation status. MGMT is a well-known resistance factor blunting the treatment effect of TMZ, by repairing the most genotoxic lesion. Epigenetic silencing of the MGMTp sensitizes glioblastoma to TMZ. For risk-adapted treatment, it is of utmost importance to accurately identify patients, who will not benefit from TMZ treatment. Methods Here, we present a reanalysis of the clinical trials CE.6 and the pooled NOA-08 and Nordic trials in elderly glioblastoma patients that compared RT to RT/TMZ→TMZ, or RT to TMZ, respectively. For 687 patients with available MGMTp methylation data, we applied a cutoff discerning truly unmethylated glioblastoma, established in a pooled analysis of 4 clinical trials for glioblastoma, with RT/TMZ→TMZ treatment, using the same quantitative methylation-specific MGMTp PCR assay. Results When applying this restricted cutoff to the elderly patient population, we confirmed that glioblastoma with truly unmethylated MGMTp derived no benefit from TMZ treatment. In the Nordic/NOA-08 trials, RT was better than TMZ, suggesting little or no benefit from TMZ. Conclusions For evidence-based treatment of glioblastoma patients validated MGMTp methylation assays should be used that accurately identify truly unmethylated patients. Respective stratified management of patients will reduce toxicity without compromising outcomes and allow testing of more promising treatment options.
Bioactive Nanotherapeutic Ultrasound Contrast Agent for Concurrent Breast Cancer Ultrasound Imaging and Treatment
Authors: Junyue Fang, Jiabao Tan, Li Lin, Yuan Cao, Rui Xu, Chunhao Lin, Gui He, Xiaoding Xu, Xiaoyun Xiao, Qiongchao Jiang, Phei Er Saw
Journal: Advanced Healthcare Materials (2024)

Contrast-enhanced ultrasound (CEUS) plays a crucial role in cancer diagnosis. The use of ultrasound contrast agents (UCAs) is inevitable in CEUS. However, current applications of UCAs primarily focus on enhancing imaging quality of ultrasound contrast rather than serving as integrated platforms for both diagnosis and treatment in clinical settings. In this study, a novel UCA, termed NPs-DPPA(C
The Gut Microbiota and Diabetes: Research, Translation, and Clinical Applications—2023 <i>Diabetes</i>, <i>Diabetes Care</i>, and <i>Diabetologia</i> Expert Forum
Authors: Mariana Byndloss, Suzanne Devkota, Frank Duca, Jan Hendrik Niess, Max Nieuwdorp, Marju Orho-Melander, Yolanda Sanz, Valentina Tremaroli, Liping Zhao
Journal: Diabetes Care (2024)

This article summarizes the state of the science on the role of the gut microbiota (GM) in diabetes from a recent international expert forum organized by Diabetes, Diabetes Care, and Diabetologia, which was held at the European Association for the Study of Diabetes 2023 Annual Meeting in Hamburg, Germany. Forum participants included clinicians and basic scientists who are leading investigators in the field of the intestinal microbiome and metabolism. Their conclusions were as follows: 1) the GM may be involved in the pathophysiology of type 2 diabetes, as microbially produced metabolites associate both positively and negatively with the disease, and mechanistic links of GM functions (e.g., genes for butyrate production) with glucose metabolism have recently emerged through the use of Mendelian randomization in humans; 2) the highly individualized nature of the GM poses a major research obstacle, and large cohorts and a deep-sequencing metagenomic approach are required for robust assessments of associations and causation; 3) because single-time point sampling misses intraindividual GM dynamics, future studies with repeated measures within individuals are needed; and 4) much future research will be required to determine the applicability of this expanding knowledge to diabetes diagnosis and treatment, and novel technologies and improved computational tools will be important to achieve this goal.
Intraoperative Image Guidance in Orbital and Lacrimal Surgery
Authors: Timothy J. McCulley, Vinay K. Aakalu, Jill A. Foster, Suzanne K. Freitag, Lora R. Dagi Glass, Seanna R. Grob, Jeremiah P. Tao, M. Reza Vagefi, Michael T. Yen, Michael K. Yoon, Stephen J. Kim, Edward J. Wladis
Journal: Ophthalmology (2024)
A Comparison of Gout Flares with the Initiation of Treat‐to‐Target Allopurinol and Febuxostat: A Post‐hoc Analysis of a Randomized Multicenter Trial
Authors: Austin Barry, Lindsay N. Helget, Maria Androsenko, Hongsheng Wu, Bridget Kramer, Jeff A. Newcomb, Mary T. Brophy, Anne Davis‐Karim, Bryant R. England, Ryan Ferguson, Michael H. Pillinger, Tuhina Neogi, Paul M. Palevsky, Tony R. Merriman, James R. O'Dell, Ted R. Mikuls
Journal: Arthritis & Rheumatology (2024)

Initiating urate-lowering therapy (ULT) in gout can precipitate arthritis flares. There have been limited comparisons of flare risk during the initiation and escalation of allopurinol and febuxostat, administered as a treat-to-target strategy with optimal anti-inflammatory prophylaxis.
Amino acid influx via LAT1 regulates iron demand and sensitivity to PPMX-T003 of aggressive natural killer cell leukemia
Authors: Ryo Yanagiya, Yuji Miyatake, Natsumi Watanabe, Takanobu Shimizu, Akane Kanamori, Masaya Ueno, Sachiko Okabe, Joaquim Carreras, Shunya Nakayama, Ami Hasegawa, Kazuaki Kameda, Takeshi Kamakura, So Nakagawa, Takuji Yamauchi, Takahiro Maeda, Keisuke Ishii, Tadashi Matsuura, Hiroshi Handa, Atsushi Hirao, Kenichi Ishizawa, Makoto Onizuka, Tetsuo Mashima, Naoya Nakamura, Kiyoshi Ando, Ai Kotani
Journal: Leukemia (2024)

Abstract Aggressive natural killer cell leukemia (ANKL) is a rare hematological malignancy with a fulminant clinical course. Our previous study revealed that ANKL cells proliferate predominantly in the liver sinusoids and strongly depend on transferrin supplementation. In addition, we demonstrated that liver-resident ANKL cells are sensitive to PPMX-T003, an anti-human transferrin receptor 1 inhibitory antibody, whereas spleen-resident ANKL cells are resistant to transferrin receptor 1 inhibition. However, the microenvironmental factors that regulate the iron dependency of ANKL cells remain unclear. In this study, we first revealed that the anti-neoplastic effect of PPMX-T003 was characterized by DNA double-strand breaks in a DNA replication-dependent manner, similar to conventional cytotoxic agents. We also found that the influx of extracellular amino acids via LAT1 stimulated sensitivity to PPMX-T003. Taken together, we discovered that the amount of extracellular amino acid influx through LAT1 was the key environmental factor determining the iron dependency of ANKL cells via adjustment of their mTOR/Myc activity, which provides a good explanation for the different sensitivity to PPMX-T003 between liver- and spleen-resident ANKL cells, as the liver sinusoid contains abundant amino acids absorbed from the gut.
Corrigendum to “Comparison of baseline patient characteristics in Italian oncology drug monitoring registries and clinical trials: a real-world cross-sectional study” [The Lancet Regional Health – Europe 41 (2024) 100912]
Authors: Maria Lucia Iacovino, Simone Celant, Luca Tomassini, Laura Arenare, Andrea Caglio, Andrea Canciello, Flavio Salerno, Pier Paolo Olimpieri, Susanna Di Segni, Antonella Sferrazza, Maria Carmela Piccirillo, Giordano Domenico Beretta, Carmine Pinto, Livio Blasi, Saverio Cinieri, Luigi Cavanna, Massimo Di Maio, Pierluigi Russo, Francesco Perrone
Journal: The Lancet Regional Health - Europe (2024)

[This corrects the article DOI: 10.1016/j.lanepe.2024.100912.].
Corrigendum to “Consensus recommendation for prenatal, neonatal and postnatal management of congenital cytomegalovirus infection from the European congenital infection initiative (ECCI)” [The Lancet Regional Health – Europe 40 (2024) 100892]
Authors: Marianne Leruez-Ville, Christos Chatzakis, Daniele Lilleri, Daniel Blazquez-Gamero, Ana Alarcon, Nicolas Bourgon, Ina Foulon, Jacques Fourgeaud, Anna Gonce, Christine E Jones, Paul Klapper, André Krom, Tiziana Lazzarotto, Hermione Lyall, Paulo Paixao, Vassiliki Papaevangelou, Elisabeth Puchhammer, George Sourvinos, Pamela Vallely, Yves Ville, Ann Vossen
Journal: The Lancet Regional Health - Europe (2024)

[This corrects the article DOI: 10.1016/j.lanepe.2024.100892.].
Early pregnancy HbA1c as the first screening test for gestational diabetes: results from three prospective cohorts
Authors: Ponnusamy Saravanan, Mohan Deepa, Zain Ahmed, Uma Ram, Tarakeswari Surapaneni, Sailaja Devi Kallur, Papa Desari, Seshadri Suresh, Ranjit Mohan Anjana, Wesley Hannah, Chockalingam Shivashri, Saite Hemavathy, Nithya Sukumar, Wycliffe K Kosgei, Astrid Christoffersen-Deb, Vincent Kibet, John N Hector, Gertrude Anusu, Nigel Stallard, Yonas Ghebremichael-Weldeselassie, Norman Waugh, Sonak D Pastakia, Viswanathan Mohan
Journal: The Lancet Diabetes & Endocrinology (2024)
Single-cell epigenomic reconstruction of developmental trajectories from pluripotency in human neural organoid systems
Authors: Fides Zenk, Jonas Simon Fleck, Sophie Martina Johanna Jansen, Bijan Kashanian, Benedikt Eisinger, Małgorzata Santel, Jean-Samuel Dupré, J. Gray Camp, Barbara Treutlein
Journal: Nature Neuroscience (2024)

Abstract Cell fate progression of pluripotent progenitors is strictly regulated, resulting in high human cell diversity. Epigenetic modifications also orchestrate cell fate restriction. Unveiling the epigenetic mechanisms underlying human cell diversity has been difficult. In this study, we use human brain and retina organoid models and present single-cell profiling of H3K27ac, H3K27me3 and H3K4me3 histone modifications from progenitor to differentiated neural fates to reconstruct the epigenomic trajectories regulating cell identity acquisition. We capture transitions from pluripotency through neuroepithelium to retinal and brain region and cell type specification. Switching of repressive and activating epigenetic modifications can precede and predict cell fate decisions at each stage, providing a temporal census of gene regulatory elements and transcription factors. Removing H3K27me3 at the neuroectoderm stage disrupts fate restriction, resulting in aberrant cell identity acquisition. Our single-cell epigenome-wide map of human neural organoid development serves as a blueprint to explore human cell fate determination.
A high-density 1,024-channel probe for brain-wide recordings in non-human primates
Authors: Yang Liu, Huilin Jia, Hongji Sun, Shengyi Jia, Ziqian Yang, Ao Li, Anqi Jiang, Yuji Naya, Cen Yang, Shengyuan Xue, Xiaojian Li, Bingyan Chen, Jingjun Zhu, Chenghao Zhou, Minning Li, Xiaojie Duan
Journal: Nature Neuroscience (2024)
Transcriptomic analysis of intestine following administration of a transglutaminase 2 inhibitor to prevent gluten-induced intestinal damage in celiac disease
Authors: Valeriia Dotsenko, Bernhard Tewes, Martin Hils, Ralf Pasternack, Jorma Isola, Juha Taavela, Alina Popp, Jani Sarin, Heini Huhtala, Pauliina Hiltunen, Timo Zimmermann, Ralf Mohrbacher, Roland Greinwald, Knut E. A. Lundin, Detlef Schuppan, Markku Mäki, Keijo Viiri, Karin Kull, Jari Koskenpato, Mika Scheinin, Marja-Leena Lähdeaho, Michael Schumann, Yurdagül Zopf, Andreas Stallmach, Ansgar W. Lohse, Stefano Fusco, Jost Langhorst, Helga Paula Török, Valerie Byrnes, Juozas Kupcinskas, Øistein Hovde, Jørgen Jahnsen, Luc Biedermann, Jonas Zeitz
Journal: Nature Immunology (2024)

Abstract Transglutaminase 2 (TG2) plays a pivotal role in the pathogenesis of celiac disease (CeD) by deamidating dietary gluten peptides, which facilitates antigenic presentation and a strong anti-gluten T cell response. Here, we elucidate the molecular mechanisms underlying the efficacy of the TG2 inhibitor ZED1227 by performing transcriptional analysis of duodenal biopsies from individuals with CeD on a long-term gluten-free diet before and after a 6-week gluten challenge combined with 100 mg per day ZED1227 or placebo. At the transcriptome level, orally administered ZED1227 effectively prevented gluten-induced intestinal damage and inflammation, providing molecular-level evidence that TG2 inhibition is an effective strategy for treating CeD. ZED1227 treatment preserved transcriptome signatures associated with mucosal morphology, inflammation, cell differentiation and nutrient absorption to the level of the gluten-free diet group. Nearly half of the gluten-induced gene expression changes in CeD were associated with the epithelial interferon-γ response. Moreover, data suggest that deamidated gluten-induced adaptive immunity is a sufficient step to set the stage for CeD pathogenesis. Our results, with the limited sample size, also suggest that individuals with CeD might benefit from an HLA-DQ2 / HLA-DQ8 stratification based on gene doses to maximally eliminate the interferon-γ-induced mucosal damage triggered by gluten.
Deep learning-based prediction of one-year mortality in Finland is an accurate but unfair aging marker
Authors: Andrius Vabalas, Tuomo Hartonen, Pekka Vartiainen, Sakari Jukarainen, Essi Viippola, Rodosthenis S. Rodosthenous, Aoxing Liu, Sara Hägg, Markus Perola, Andrea Ganna
Journal: Nature Aging (2024)

Abstract Short-term mortality risk, which is indicative of individual frailty, serves as a marker for aging. Previous age clocks focused on predicting either chronological age or longer-term mortality. Aging clocks predicting short-term mortality are lacking and their algorithmic fairness remains unexamined. We developed a deep learning model to predict 1-year mortality using nationwide longitudinal data from the Finnish population (FinRegistry; n = 5.4 million), incorporating more than 8,000 features spanning up to 50 years. We achieved an area under the curve (AUC) of 0.944, outperforming a baseline model that included only age and sex (AUC = 0.897). The model generalized well to different causes of death (AUC &gt; 0.800 for 45 of 50 causes), including coronavirus disease 2019, which was absent in the training data. Performance varied among demographics, with young females exhibiting the best and older males the worst results. Extensive prediction fairness analyses highlighted disparities among disadvantaged groups, posing challenges to equitable integration into public health interventions. Our model accurately identified short-term mortality risk, potentially serving as a population-wide aging marker.
Spatiotemporally responsive cascade bilayer microneedles integrating local glucose depletion and sustained nitric oxide release for accelerated diabetic wound healing
Authors: Yongnian Zeng, Chenyuan Wang, Jiapeng Lei, Xue Jiang, Kai Lei, Yinli Jin, Tianshu Hao, Wen Zhang, Jianying Huang, Wei Li
Journal: Acta Pharmaceutica Sinica B (2024)

High glucose level, bacterial infection, and persistent inflammation within the microenvironment are key factors contributing to the delay of diabetic ulcers healing, while traditional therapeutic methods generally fail to address these issues simultaneously. Here, we present a spatiotemporally responsive cascade bilayer microneedle (MN) patch for accelerating diabetic wound healing