tbuckley/cabot-search huggingface dataset:
Left Atrial Appendage Occlusion: Analyzing Factors for Peridevice Leak with Dual-Occlusive Devices
Authors: Heyder Omran
Journal: Clinical Cardiology and Cardiovascular Interventions (2024)

Background: This study examines factors influencing peridevice leak (PDL) in patients treated with the Amplatzer Amulet Occluder for left atrial appendage occlusion (LAAO). Materials and Methods: A retrospective analysis was conducted on 217 patients who underwent successful LAAO with the Amplatzer Amulet Occluder due to atrial fibrillation and anticoagulation contraindications. Follow-up transesophageal echocardiography (TEE) was performed 1-3 months post-procedure to detect PDL and analyze related procedural and anatomical factors. Results: PDL occurred in 42% of patients, predominantly mild (&lt;3 mm). Key factors associated with increased PDL risk included occluder compression &lt;12%, off-axis device positioning, and device size ≥25 mm. Baseline patient characteristics and procedural details did not significantly impact PDL rates. Conclusion: For optimal LAAO outcomes, pre- and periprocedural assessment of LAA size and device positioning is crucial. Ensuring occluder compression above 15% may minimize PDL risks, especially for larger devices.
The use of large language models in detecting Chinese ultrasound report errors
Authors: Yuqi Yan, Kai Wang, Bojian Feng, Jincao Yao, Tian Jiang, Zhiyan Jin, Yin Zheng, Yahan Zhou, Chen Chen, Lin Sui, Xiayi Chen, Yanhong Du, Jie Yang, Qianmeng Pan, Lingyan Zhou, Vicky Yang Wang, Ping Liang, Dong Xu
Journal: npj Digital Medicine (2025)

This retrospective study evaluated the efficacy of large language models (LLMs) in improving the accuracy of Chinese ultrasound reports. Data from three hospitals (January-April 2024) including 400 reports with 243 errors across six categories were analyzed. Three GPT versions and Claude 3.5 Sonnet were tested in zero-shot settings, with the top two models further assessed in few-shot scenarios. Six radiologists of varying experience levels performed error detection on a randomly selected test set. In zero-shot setting, Claude 3.5 Sonnet and GPT-4o achieved the highest error detection rates (52.3% and 41.2%, respectively). In few-shot, Claude 3.5 Sonnet outperformed senior and resident radiologists, while GPT-4o excelled in spelling error detection. LLMs processed reports faster than the quickest radiologist (Claude 3.5 Sonnet: 13.2 s, GPT-4o: 15.0 s, radiologist: 42.0 s per report). This study demonstrates the potential of LLMs to enhance ultrasound report accuracy, outperforming human experts in certain aspects.
The selective sorting of miR-4432 into endothelial extracellular vesicles is controlled by a specific RNA binding protein: New Insights in the pathophysiology of venous malformations
Authors: Stanislovas S Jankauskas, Fahimeh Varzideh, Emanuele Farroni, Pasquale Mone, Urna Kansakar, Gaetano Santulli
Journal: British Journal of Dermatology (2025)
Sorafenib enhanced the function of myeloid-derived suppressor cells in hepatocellular carcinoma by facilitating PPARα-mediated fatty acid oxidation
Authors: Chunxiao Li, Liting Xiong, Yuhan Yang, Ping Jiang, Junjie Wang, Mengyuan Li, Shuhua Wei, Suqing Tian, Yuexuan Wang, Mi Zhang, Jie Tang
Journal: Molecular Cancer (2025)

Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME). Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing. MDSCs were analyzed for chemotaxis, immunosuppressive functions, fatty acid oxidation (FAO), and PPARα expression. The impact of sorafenib on tumor growth, MDSC infiltration, differentiation, and immunosuppressive function was assessed, alongside the modulation of these processes by PPARα. Here, we revealed increased infiltration and enhanced function of MDSCs in TME after treatment with sorafenib. Moreover, our results indicated that sorafenib induced the accumulation of MDSCs mediated by CCR2, and pharmacological blockade of CCR2 markedly reduced MDSCs migration and tumor growth. Mechanistically, sorafenib promoted the effect and fatty acid uptake ability of MDSCs and modulated peroxisome proliferator-activated receptor α (PPARα)-mediated fatty acid oxidation (FAO). In addition, tumor-bearing mice fed a high-fat diet (HFD) at the beginning of sorafenib administration had worse outcomes than mice fed a regular diet. Genetic deficiency of PPARα weakens the effect of sorafenib on MDSCs in mice with HCC. Pharmacological inhibition of PPARα has a synergistic anti-tumor effect with sorafenib, which is attenuated by the inhibition of MDSCs. Mechanistically, sorafenib significantly inhibited the differentiation of macrophages by upregulating PPARα expression and suppressing the PU.1-CSF1R pathway. Overall, our study demonstrated that sorafenib enhanced the function of MDSCs by facilitating PPARα-mediated FAO and further augmenting sorafenib resistance, which sheds light on dietary management and improves the therapeutic response in HCC.
Salt‐inducible kinase 2 confers radioresistance in colorectal cancer by facilitating homologous recombination repair
Authors: Yuan Meng, Shuo Li, Da‐Shan Lu, Xue Chen, Lu Li, You‐fa Duan, Gao‐yuan Wang, Wenlin Huang, Ran‐yi Liu
Journal: MedComm (2025)

Abstract Resistance to radiotherapy remains a critical barrier in treating colorectal cancer (CRC), particularly in cases of locally advanced rectal cancer (LARC). To identify key kinases involved in CRC radioresistance, we employed a kinase‐targeted CRISPR‐Cas9 library screen. This approach aimed to identify potential kinase inhibitors as radiosensitizers. Our screening identified salt‐inducible kinase 2 (SIK2) as a critical factor in CRC radioresistance. Increased SIK2 expression correlated with reduced tumor regression and poorer outcomes in LARC patients undergoing neoadjuvant chemoradiotherapy. The depletion of SIK2 significantly enhanced radiation‐induced apoptosis and tumor regression. Mechanistically, SIK2 interacts with valosin‐containing protein (VCP), promoting its hyperphosphorylation. This modification improves VCP's capacity to extract K48‐linked ubiquitin‐conjugated proteins from chromatin, thus aiding the recruitment of RPA and RAD51 to DNA damage sites. This mechanism strengthens homologous recombination–mediated DNA repair, which contributes to radioresistance. Importantly, ARN‐3236, a SIK2 inhibitor, markedly sensitized CRC cells to radiation both in vivo and in vitro, providing a potential strategy to overcome radioresistance. In summary, our findings reveal a novel mechanism by which SIK2 contributes to the radioresistance of CRC, proposing SIK2 as a potential therapeutic target with its inhibitor significantly enhancing CRC radiotherapy efficacy.
Dimethyl fumarate alleviate hepatic ischemia–reperfusion injury through suppressing cGAS‐STING signaling
Authors: Yi Xiong, Jiawen Chen, Kun Li, Wei Liang, Jinwen Song, Xiusheng Qiu, Baoyu Zhang, Dongbo Qiu, Yunfei Qin
Journal: MedComm (2025)

Hepatic ischemia-reperfusion (I/R) injury frequently occurs during the perioperative phase of liver surgery. Inappropriate activation of STING signaling can trigger excessive inflammation response to aggravate hepatic I/R injury. Dimethyl fumarate (DMF) is an FDA-approved immunomodulatory drug used to treat multiple sclerosis and psoriasis due to its notable anti-inflammation properties. However, the mechanism and targets of DMF in immunomodulation remain unclear. Here, we found that DMF suppresses cGAS-STING activation induced by HSV-1, hering testis DNA, and mitochondrial DNA in a variety of cells. DMF significantly reduces hepatic I/R injury and inhibits cGAS-STING pathway activation in mice. The alleviating effect of DMF on hepatic I/R injury was negligible in STING-knockout mice. Mechanistically, DMF directly inhibits STING activation via an autophagy-independent pathway, and the immunocoprecipitation experiment showed that DMF inhibited STING recruitment of downstream TBK1 and IRF3. Our study found that DMF protects liver I/R injury by inhibiting the STING pathway and may be a potential target of this disease.
The Complex Nomenclature of Allergic Diseases and Hypersensitivity Reactions: An Addendum to the <scp>EAACI</scp> Position Paper
Authors: Andrea Szegedi, Zsolt I. Komlósi, Anikó Kapitány, Zsuzsanna Bata‐Csörgő, Gábor Koncz, Attila Bácsi
Journal: Allergy (2025)
Prospective Pharmacokinetic Evaluation of Venetoclax in <scp>AML</scp> Supports Re‐Evaluation of Recommended Dose Adjustments With Azole Antifungals
Authors: Jitesh D. Kawedia, Caitlin R. Rausch, Xiaoqian Liu, Wei Qiao, Courtney D. Dinardo, Naval Daver, Gautam Borthakur, Naveen Pemmaraju, Patrick Reville, Dimitrios P. Kontoyiannis, Nicholas Short, Marina Konopleva, Elias Jabbour, Guillermo Garcia‐Manero, Farhad Ravandi, Hagop Kantarjian, Tapan M. Kadia
Journal: American Journal of Hematology (2025)
<scp><i>TP53</i></scp> Mutations in Myeloproliferative Neoplasms: Context‐Dependent Evaluation of Prognostic Relevance
Authors: Ayalew Tefferi, Maymona Abdelmagid, Giuseppe G. Loscocco, Saubia Fathima, Kebede H. Begna, Aref Al‐Kali, James Foran, Jeanne Palmer, Talha Badar, Mrinal M. Patnaik, Kaaren K. Reichard, Rong He, Cinthya J. Zepeda Mendoza, Mithun Shah, Attilio Orazi, Daniel A. Arber, Animesh Pardanani, Alessandro M. Vannucchi, Devendra Hiwase, Naseema Gangat, Paola Guglielmelli
Journal: American Journal of Hematology (2025)

ABSTRACT The clinical relevance of TP53 mutations ( TP53 MUT ) in myeloproliferative neoplasms (MPN) and their prognostic interaction with MPN subtype designation has not been systematically studied. In the current study, 114 patients with MPN harboring TP53 MUT (VAF ≥ 2%) were evaluated for overall survival (OS), calculated from the time of TP53 MUT detection: chronic phase myelofibrosis (MF‐CP; N = 61); blast‐phase (MPN‐BP; N = 31) or accelerated‐phase (MPN‐AP; N = 16) MPN, and polycythemia vera/essential thrombocythemia (PV/ET; N = 6). Sixty‐five (57%) patients harbored International Consensus Classification (ICC)‐defined multihit TP53 MUT and 56 (49%) monosomal/complex karyotype (MK/CK). Majority of MPN‐BP (90%) and MPN‐AP (81%) while 39% of MF‐CP and none of PV/ET patients harbored multihit TP53 MUT . OS in MPN‐BP and MPN‐AP was equally dismal (median 6 vs. 4.5 months, respectively; p = 1.0), regardless of multihit configuration ( p = 0.44), while OS in TP53 MUT MPN‐BP/AP ( N = 47; median 4 months) was inferior to that of a separate cohort ( N = 49) with TP53 wild‐type MPN‐BP/AP (median 11 months; p &lt; 0.01). OS in MF‐CP was significantly shorter with multihit versus non‐multihit TP53 MUT (median 10 vs. 35 months; HR 2.9; p &lt; 0.01), independent of other MF‐relevant genetic risk factors, including ASXL1/SRSF2/U2AF1 mutations. Multihit TP53 MUT was also associated with inferior survival following allogeneic stem cell transplant (ASCT): median 9 months versus “not reached” in patients with ( N = 9) versus without ( N = 8) multihit TP53 MUT ( p &lt; 0.01). The presence of multihit or non‐multihit TP53 MUT in MPN‐BP/AP or multihit TP53 MUT in MF‐CP is associated with exceptionally poor prognosis and justifies inclusion into the ICC category of “myeloid neoplasms with mutated TP53 .” By contrast, detection of non‐multihit TP53 MUT , by itself, might not endanger short‐term survival in MF‐CP, PV, or ET.
Gut microbiota modulation via fecal microbiota transplantation mitigates hyperoxaluria and calcium oxalate crystal depositions induced by high oxalate diet
Authors: Lingyue An, Shujue Li, Zhenglin Chang, Min Lei, Zhican He, Peng Xu, Shike Zhang, Zheng Jiang, Muhammad Sarfaraz Iqbal, Xinyuan Sun, Hongxing Liu, Xiaolu Duan, Wenqi Wu
Journal: Gut Microbes (2025)

Hyperoxaluria, including primary and secondary hyperoxaluria, is a disorder characterized by increased urinary oxalate excretion and could lead to recurrent calcium oxalate kidney stones, nephrocalcinosis and eventually end stage renal disease. For secondary hyperoxaluria, high dietary oxalate (HDOx) or its precursors intake is a key reason. Recently, accumulated studies highlight the important role of gut microbiota in the regulation of oxalate homeostasis. However, the underlying mechanisms involving gut microbiota and metabolite disruptions in secondary hyperoxaluria remain poorly understood. Here, we investigated the therapeutic efficacy of fecal microbiota transplantation (FMT) sourced from healthy rats fed with standard pellet diet against urinary oxalate excretion, renal damage and calcium oxalate (CaOx) crystal depositions via using hyperoxaluria rat models. We observed dose-dependent increases in urinary oxalate excretion and CaOx crystal depositions due to hyperoxaluria, accompanied by significant reductions in gut microbiota diversity characterized by shifts in Ruminococcaceae_UCG-014 and Parasutterella composition. Metabolomic analysis validated these findings, revealing substantial decreases in key metabolites associated with these microbial groups. Transplanting microbes from healthy rats effectively reduced HDOx-induced urinary oxalate excretion and CaOx crystal depositions meanwhile restoring Ruminococcaceae_UCG-014 and Parasutterella populations and their associated metabolites. Furthermore, FMT treatment could significantly decrease the urinary oxalate excretion and CaOx crystal depositions in rat kidneys via, at least in part, upregulating the expressions of intestinal barrier proteins and oxalate transporters in the intestine. In conclusion, our study emphasizes the effectiveness of FMT in countering HDOx-induced hyperoxaluria by restoring gut microbiota and related metabolites. These findings provide insights on the complex connection between secondary hyperoxaluria caused by high dietary oxalate and disruptions in gut microbiota, offering promising avenues for targeted therapeutic strategies.
T cell immune evasion by SARS-CoV-2 JN.1 escapees targeting two cytotoxic T cell epitope hotspots
Authors: Jinmin Tian, Bingli Shang, Jianing Zhang, Yuanyuan Guo, Min Li, Yuechao Hu, Dan Bai, Junying She, Yang Han, Peipei Guo, Mengkun Huang, Yalan Wang, Maoshun Liu, Jie Zhang, Beiwei Ye, Yaxin Guo, Mengjie Yang, Ying Lin, Ting Zhang, Xin Sun, Xiaoju Yuan, Danni Zhang, Ziqian Xu, Yan Chai, Jianxun Qi, Kefang Liu, Shuguang Tan, Yingze Zhao, Jikun Zhou, Rui Song, George F Gao, Jun Liu
Journal: Nature Immunology (2025)
Population-based, first-tier genomic newborn screening in the maternity ward
Authors: François Boemer, Kristine Hovhannesyan, Flavia Piazzon, Frédéric Minner, Myriam Mni, Valérie Jacquemin, Davood Mashhadizadeh, Noor Benmhammed, Vincent Bours, Adeline Jacquinet, Julie Harvengt, Saskia Bulk, Vinciane Dideberg, Laura Helou, Leonor Palmeira, Tamara Dangouloff, Serpil Alkan, Christophe Barrea, Paulina Bartoszek, Emeline Bequet, Hedwige Boboli, Romain Bruninx, Laure Collard, Aurore Daron, François-Guillaume Debray, Marie-Françoise Dresse, Jean-Marie Dubru, Iulia Ebetiuc, Benoit Florkin, Caroline Jacquemart, Céline Kempeneers, Nadège Hennuy, Marie-Christine Lebrethon, Marie Leonard, Patricia Leroy, Angélique Lhomme, Jacques Lombet, Sabine Michotte, Ariane Milet, Anne-Simone Parent, Vincent Rigo, Marie-Christine Seghaye, Sandrine Vaessen, Laurent Servais
Journal: Nature Medicine (2025)
An online multidomain lifestyle intervention to prevent cognitive decline in at-risk older adults: a randomized controlled trial
Authors: Henry Brodaty, Tiffany Chau, Megan Heffernan, Jeewani A Ginige, Gavin Andrews, Michael Millard, Perminder S Sachdev, Kaarin J Anstey, Nicola T Lautenschlager, John J McNeil, Louisa Jorm, Nicole A Kochan, Anthony Maeder, Heidi Welberry, Juan Carlo San Jose, Nancy E Briggs, Gordana Popovic, Yorgi Mavros, Carolina Almendrales Rangel, Yian Noble, Sue Radd-Vagenas, Victoria M Flood, Fiona O'Leary, Amit Lampit, Courtney C Walton, Polly Barr, Maria Fiatarone Singh, Michael Valenzuela
Journal: Nature Medicine (2025)
Influence Of Tennis Court Surface On Outcomes Of Circuit Training Among Recreational Tennis Players.
Authors: Ashish Mathew A, T.N. Suresh, S.F.Mariyam Farzana, M Arvind, V Prithiha
Journal: British Journal of Sports Medicine (2019)

The characteristics of tennis game require contrasting velocity, acceleration, deceleration, turns, changeovers, strokes, sprints, sliding and upper arm involvement, making players perform short bursts of high-intensity exercise interspersed with periods of rest or low-intensity activities over a prolonged period. Circuit training was designed to increase muscle strength, endurance and flexibility and significantly reduce workout time. The mechanical properties of clay and acrylic courts vary, which alters the movement patterns and style of play. When low friction and high-friction surfaces are analyzed , high-friction surfaces leads to kinematic changes such as lower attack angles (measured horizontally ), in addition to faster running speeds and movements. To determine the influence of the tennis court surface on the outcomes of circuit training among recreational tennis players. This was an experimental study in which 20 participants were recruited according to the inclusion and exclusion criteria. The pre test results were analyzed via a T test for agility, a 50 yard dash test for speed, a vertical jump test for lower limb strength, wiebe tennis performance strength tests for the forehand and back hand after 8 weeks of the circuit training protocol post test was analyzed . Comparison between pretest and posttest results within groups and between group A and Group B were not statistically significant. This study revealed that there was no significant improvement in either group.
Robust mucosal SARS-CoV-2-specific T cells effectively combat COVID-19 and establish polyfunctional resident memory in patient lungs
Authors: Airu Zhu, Zhao Chen, Qihong Yan, Mei Jiang, Xuesong Liu, Zhengtu Li, Na Li, Chunli Tang, Wenhua Jian, Jiangping He, Lan Chen, Jinling Cheng, Canjie Chen, Tian Tang, Zhiwei Xu, Qingtao Hu, Fang Li, Yanqun Wang, Jing Sun, Zhen Zhuang, Liyan Wen, Jianfen Zhuo, Donglan Liu, Yanjun Zhang, Xiaofang Huang, Suxiang Li, Qiuhui Zeng, Fangli Chen, Liang Zhou, Dongdong Liu, Changhao Zhong, Yu Chen, Shiyue Li, Kangli Liang, Na Zhong, Xinmei Zhang, Jiekai Chen, Xiaobo Chen, Yonghao Xu, Nanshan Zhong, Jingxian Zhao, Jincun Zhao
Journal: Nature Immunology (2025)
The architecture of the human default mode network explored through cytoarchitecture, wiring and signal flow
Authors: Casey Paquola, Margaret Garber, Stefan Frässle, Jessica Royer, Yigu Zhou, Shahin Tavakol, Raul Rodriguez-Cruces, Donna Gift Cabalo, Sofie Valk, Simon Eickhoff, Daniel S. Margulies, Alan Evans, Katrin Amunts, Elizabeth Jefferies, Jonathan Smallwood, Boris C. Bernhardt
Journal: Nature Neuroscience (2025)

Abstract The default mode network (DMN) is implicated in many aspects of complex thought and behavior. Here, we leverage postmortem histology and in vivo neuroimaging to characterize the anatomy of the DMN to better understand its role in information processing and cortical communication. Our results show that the DMN is cytoarchitecturally heterogenous, containing cytoarchitectural types that are variably specialized for unimodal, heteromodal and memory-related processing. Studying diffusion-based structural connectivity in combination with cytoarchitecture, we found the DMN contains regions receptive to input from sensory cortex and a core that is relatively insulated from environmental input. Finally, analysis of signal flow with effective connectivity models showed that the DMN is unique amongst cortical networks in balancing its output across the levels of sensory hierarchies. Together, our study establishes an anatomical foundation from which accounts of the broad role the DMN plays in human brain function and cognition can be developed.
Associations between common genetic variants and income provide insights about the socio-economic health gradient
Authors: Hyeokmoon Kweon, Casper A. P. Burik, Yuchen Ning, Rafael Ahlskog, Charley Xia, Erik Abner, Yanchun Bao, Laxmi Bhatta, Tariq O. Faquih, Maud de Feijter, Paul Fisher, Andrea Gelemanović, Alexandros Giannelis, Jouke-Jan Hottenga, Bita Khalili, Yunsung Lee, Ruifang Li-Gao, Jaan Masso, Ronny Myhre, Teemu Palviainen, Cornelius A. Rietveld, Alexander Teumer, Renske M. Verweij, Emily A. Willoughby, Esben Agerbo, Sven Bergmann, Dorret I. Boomsma, Anders D. Børglum, Ben M. Brumpton, Neil Martin Davies, Tõnu Esko, Scott D. Gordon, Georg Homuth, M. Arfan Ikram, Magnus Johannesson, Jaakko Kaprio, Michael P. Kidd, Zoltán Kutalik, Alex S. F. Kwong, James J. Lee, Annemarie I. Luik, Per Magnus, Pedro Marques-Vidal, Nicholas G. Martin, Dennis O. Mook-Kanamori, Preben Bo Mortensen, Sven Oskarsson, Emil M. Pedersen, Ozren Polašek, Frits R. Rosendaal, Melissa C. Smart, Harold Snieder, Peter J. van der Most, Peter Vollenweider, Henry Völzke, Gonneke Willemsen, Jonathan P. Beauchamp, Thomas A. DiPrete, Richard Karlsson Linnér, Qiongshi Lu, Tim T. Morris, Aysu Okbay, K. Paige Harden, Abdel Abdellaoui, W. David Hill, Ronald de Vlaming, Daniel J. Benjamin, Philipp D. Koellinger
Journal: Nature Human Behaviour (2025)

Abstract We conducted a genome-wide association study on income among individuals of European descent ( N = 668,288) to investigate the relationship between socio-economic status and health disparities. We identified 162 genomic loci associated with a common genetic factor underlying various income measures, all with small effect sizes (the Income Factor). Our polygenic index captures 1–5% of income variance, with only one fourth due to direct genetic effects. A phenome-wide association study using this index showed reduced risks for diseases including hypertension, obesity, type 2 diabetes, depression, asthma and back pain. The Income Factor had a substantial genetic correlation (0.92, s.e. = 0.006) with educational attainment. Accounting for the genetic overlap of educational attainment with income revealed that the remaining genetic signal was linked to better mental health but reduced physical health and increased risky behaviours such as drinking and smoking. These findings highlight the complex genetic influences on income and health.