tbuckley/cabot-search huggingface dataset:
Association of Prior Antibiotic Treatment With Survival and Response to Immune Checkpoint Inhibitor Therapy in Patients With Cancer
Authors: David J. Pinato, Sarah Howlett, Diego Ottaviani, Heather Urus, Aisha Patel, Takashi Mineo, Cathryn Brock, Danielle Power, Olivia Hatcher, Alison Falconer, Manasi Ingle, Anna Brown, Dorothy Gujral, Sarah Partridge, Naveed Sarwar, Michael Gonzalez, Maggie Bendle, Conrad Lewanski, Thomas Newsom-Davis, Elias Allara, Mark Bower
Journal: JAMA Oncology (2019)

Gut dysbiosis impairs response to immune checkpoint inhibitors (ICIs) and can be caused by broad-spectrum antibiotic (ATB) therapy.To evaluate whether there is an association between ATB therapy administered concurrently (cATB) or prior (pATB) to ICI therapy and overall survival (OS) and treatment response to ICI therapy in patients with cancer treated with ICIs in routine clinical practice.This prospective, multicenter, cohort study conducted at 2 tertiary academic referral centers recruited 196 patients with cancer who received ICI therapy between January 1, 2015, and April 1, 2018, in routine clinical practice rather than clinical trials.Overall survival calculated from the time of ICI therapy commencement and radiologic response to ICI treatment defined using the Response Evaluation Criteria in Solid Tumors (version 1.1), with disease refractory to ICI therapy defined as progressive disease 6 to 8 weeks after the first ICI dose without evidence of pseudoprogression.Among 196 patients (137 men and 59 women; median [range] age, 68 [27-93] years) with non-small cell lung cancer (n = 119), melanoma (n = 38), and other tumor types (n = 39), pATB therapy (HR, 7.4; 95% CI, 4.3-12.8; P < .001), but not cATB therapy (HR, 0.9; 95% CI, 0.5-1.4; P = .76), was associated with worse OS (2 vs 26 months for pATB therapy vs no pATB therapy, respectively) (hazard ratio [HR], 7.4; 95% CI, 4.2-12.9) and a higher likelihood of primary disease refractory to ICI therapy (21 of 26 [81%] vs 66 of 151 [44%], P < .001). Overall survival in patients with non-small cell lung cancer (2.5 vs 26 months, P < .001), melanoma (3.9 vs 14 months, P < .001), and other tumor types (1.1 vs 11, P < .001) was consistently worse in those who received pATBs vs those who did not. Multivariate analyses confirmed that pATB therapy (HR, 3.4; 95% CI, 1.9-6.1; P < .001) and response to ICI therapy (HR, 8.2; 95% CI, 4.0-16.9; P < .001) were associated with OS independent of tumor site, disease burden, and performance status.Despite being limited by sample size, geographic origin, and the lack of correlative analyses on patients' gut microbiota, this study suggests that pATB therapy but not cATB therapy is associated with a worse treatment response and OS in unselected patients treated with ICIs in routine clinical practice. Mechanistic studies are urgently required to investigate ATB-mediated alterations of gut microbiota as a determinant of poorer outcome following ICI treatment.
Correction to: De novo and inherited TCF20 pathogenic variants are associated with intellectual disability, dysmorphic features, hypotonia, and neurological impairments with similarities to Smith–Magenis syndrome
Authors: Francesco Vetrini, Shane McKee, Jill A. Rosenfeld, Mohnish Suri, Andrea M. Lewis, Kimberly Margaret Nugent, Elizabeth Roeder, Rebecca O. Littlejohn, Sue Holder, Wenmiao Zhu, Joseph T. Alaimo, Brett Graham, Jill M. Harris, James B. Gibson, Matthew Pastore, Kim L. McBride, Makanko Komara, Lihadh Al-Gazali, Aisha Al Shamsi, Elizabeth A. Fanning, Klaas J. Wierenga, Daryl A. Scott, Ziva Ben-Neriah, Vardiella Meiner, Hanoch Cassuto, Orly Elpeleg, J. Lloyd Holder Jr, Lindsay C. Burrage, Laurie H. Seaver, Lionel Van Maldergem, Sonal Mahida, Janet S. Soul, Margaret Marlatt, Ludmila Matyakhina, Julie Vogt, June-Anne Gold, Soo-Mi Park, Vinod Varghese, Anne K. Lampe, Ajith Kumar, Melissa Lees, Muriel Holder-Espinasse, Vivienne McConnell, Birgitta Bernhard, Ed Blair, Victoria Harrison, Donna M. Muzny, Richard A. Gibbs, Sarah H. Elsea, Jennifer E. Posey, Weimin Bi, Seema Lalani, Fan Xia, Yaping Yang, Christine M. Eng, James R. Lupski, Pengfei Liu
Journal: Genome Medicine (2019)

It was highlighted that the original article [1] contained a typographical error in the Results section. Subject 17 was incorrectly cited as Subject 1. This Correction article shows the revised statement. The original article has been updated.
Predicting Response to Immunosuppressive Therapy in Childhood Aplastic Anemia.
Authors: Nao Yoshida, Hiroshi Yagasaki, Yoshiyuki Kosaka, Ryoji Kobayashi, Hiromasa Yabe, Takashi Kaneko, Masahiro Tsuchida, Akira Ohara, Tatsutoshi Nakahata, Seiji Kojima
Journal: Blood (2008)
Trump administration restricts dietary science in new food guidelines
Authors: Owen Dyer
Journal: BMJ (2019)

The US Department of Health and Human Services and Department of Agriculture are limiting the science that can be considered in framing the upcoming 2020 US dietary guidelines, restricting for the first time the topics that can be considered by the guidelines committee.

Updated every five years, the guidelines set the terms for school meals and government assisted food programmes. Many producers follow them, in part so that they can participate in this roughly $100bn market.

The guidelines have been shrouded in controversy for some time. In 2015 a BMJ investigation found that the guideline advisory committee’s processes to protect against bias were inadequate.1 …
Improving Access to Kidney Transplantation
Authors: L. Ebony Boulware, Virginia Wang, Neil R. Powe
Journal: JAMA (2019)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 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
GPR124 facilitates pericyte polarization and migration by regulating the formation of filopodia during ischemic injury
Authors: Dan-Yang Chen, Ning-He Sun, Ya-Ping Lu, Ling-Juan Hong, Tian-Tian Cui, Cheng-Kun Wang, Xing-Hui Chen, Shuai-Shuai Wang, Li-Li Feng, Wei-Xing Shi, Kohji Fukunaga, Zhong Chen, Ying-Mei Lu, Feng Han
Journal: Theranostics (2019)

Prolonged occlusion of multiple microvessels causes microvascular injury. G protein-coupled receptor 124 (GPR124) has been reported to be required for maintaining central nervous system (CNS) angiogenesis and blood-brain barrier integrity. However, the molecular mechanisms by which GPR124 regulates pericytes during ischemia have remained elusive. Methods: A microsphere embolism-induced ischemia model was used to evaluate the expression of GPR124 following microsphere embolism. Immunocytochemistry and stochastic optical reconstruction microscopy imaging were used to assess the expression and distribution of GPR124 in human brain vascular pericytes (HBVPs) and after the treatment with 3-morpholino-sydnonimine (SIN-1) or oxygen-glucose deprivation (OGD). The effect of GPR124 knockdown or overexpression on HBVP migration was analyzed in vitro using wound healing assays and a microfluidic device. GPR124 loss-of-function studies were performed in HBVPs and HEK293 cells using CRISPR-Cas9-mediated gene deletion. Time-lapse imaging was used to assess dynamic changes in the formation of filopodia in an individual cell. Finally, to explore the functional domains required for GPR124 activity, deletion mutants were constructed for each of the N-terminal domains. Results: GPR124 expression was increased in pericytes following microsphere embolism. Morphological analysis showed localization of GPR124 to focal adhesions where GPR124 bound directly to the actin binding protein vinculin and upregulated Cdc42. SIN-1 or OGD treatment redistributed GPR124 to the leading edges of HBVPs where GPR124 signaling was required for pericyte filopodia formation and directional migration. Partial deletion of GPR124 domains decreased SIN-1-induced filopodia formation and cell migration. Conclusion: Taken together, our results provide the first evidence for a role of GPR124 in pericyte migration under ischemic conditions and suggest that GPR124 was essential for Cdc42 activation and filopodia formation.
Abstract 11094: Erythroferrone Can Diagnose Acute Decompensated Heart Failure in Patients Presenting With Breathlessness
Authors: Sarah Appleby, Janice Chew-Harris, Richard Troughton, Mark Richards, Christopher Pemberton
Journal: Circulation (2018)

Introduction: Iron deficiency is the most common nutritional disorder worldwide. It is estimated to be present in 50-60% of chronic heart failure patients; contributing to a significant increase in...
Neurodevelopment of HIV-exposed uninfected children in South Africa: outcomes from an observational birth cohort study
Authors: Catherine J Wedderburn, Shunmay Yeung, Andrea M Rehman, Jacob A M Stadler, Raymond T Nhapi, Whitney Barnett, Landon Myer, Diana M Gibb, Heather J Zar, Dan J Stein, Kirsten A Donald
Journal: The Lancet Child & Adolescent Health (2019)

HIV infection is known to cause developmental delay, but the effects of HIV exposure without infection during pregnancy on child development are unclear. We compared the neurodevelopmental outcomes of HIV-exposed uninfected and HIV-unexposed children during their first 2 years of life.
Homocygous PAX5Sequence Mutations Define a Novel Subtype of B Cell Precursor Acute Lymphoblastic Leukemia
Authors: Lorenz Bastian, Michael P Schroeder, Cornelia Eckert, Cornelia Schlee, Jutta Ortiz Tanchez, Sebastian Kämpf, Dimitrios L. Wagner, Veronika Schulze, Konstandina Isaakidis, Alva Rani James, Thomas Burmeister, Stefan Schwartz, Sebastian Vosberg, Stefan Krebs, Helmut Blum, Jochen Hecht, Philipp A. Greif, Michael A. Rieger, Monika Brüggemann, Nicola Goekbuget, Carsten Müller-Tidow, Hubert Serve, Martin Neumann, Claudia D. Baldus
Journal: Blood (2017)
Improved survival of men 50 to 75 years old with acute myeloid leukemia over a 20-year period
Authors: Gunnar Juliusson, Oskar Hagberg, Vladimir Lj Lazarevic, Emma Ölander, Petar Antunovic, Jörg Cammenga, Lovisa Wennström, Lars Möllgård, Mats Brune, Martin Jädersten, Stefan Deneberg, Sören Lehmann, Åsa Rangert Derolf, Martin Höglund
Journal: Blood (2019)
CABG Improves Outcomes in Patients With Ischemic Cardiomyopathy
Authors: Jonathan G Howlett, Amanda Stebbins, Mark C Petrie, Pardeep S Jhund, Serenella Castelvecchio, Alexander Cherniavsky, Carla A Sueta, Ambuj Roy, Ileana L Piña, Raphael Wurm, Mark H Drazner, Bert Andersson, Carmen Batlle, Michele Senni, Lukasz Chrzanowski, Bela Merkely, Peter Carson, Patrice M Desvigne-Nickens, Kerry L Lee, Eric J Velazquez, Hussein R Al-Khalidi
Journal: JACC Heart Failure (2019)
Lymphatic and Hematogenous Dissemination in Patients With Primary Cutaneous Melanoma
Authors: Nikki R. Adler, Grant A. McArthur, Victoria J. Mar
Journal: JAMA Dermatology (2019)

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 Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 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 Dermatology journal
In-Hospital Coronary Revascularization Rates and Post-Discharge Mortality Risk in Non–ST-Segment Elevation Acute Coronary Syndrome
Authors: Héctor Bueno, Xavier Rossello, Stuart J. Pocock, Frans Van de Werf, Chee Tang Chin, Nicolas Danchin, Stephen W.-L. Lee, Jesús Medina, Yong Huo
Journal: Journal of the American College of Cardiology (2019)
Vein-First Ligation Procedure for Lung Cancer Surgery
Authors: Masahiro Yanagiya
Journal: JAMA Surgery (2019)

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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast Publications 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 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 Surgery journal
Equity and diversity in academic medicine: a perspective from the JCI editors
Authors: Linda M.S. Resar, Elizabeth M. Jaffee, Mary Armanios, Sarah Jackson, Nilofer S. Azad, Maureen R. Horton, Mariana J. Kaplan, Marikki Laiho, Marcela V. Maus, Charlotte J. Sumner, Sarah J. Wheelan, Marsha Wills-Karp
Journal: Journal of Clinical Investigation (2019)
Letter by O’Neill and Ohman Regarding Article, “Impella Support for Acute Myocardial Infarction Complicated by Cardiogenic Shock: Matched-Pair IABP-SHOCK II Trial 30-Day Mortality Analysis”
Authors: William W. O’Neill, E. Magnus Ohman
Journal: Circulation (2019)

Whether this is attributable to a better selection of patients, use of the device, or other factors, will only be answered when appropriately sized randomized trials are completed.
Engineered Anti‐GPC3 Immunotoxin, HN3‐ABD‐T20, Produces Regression in Mouse Liver Cancer Xenografts Through Prolonged Serum Retention
Authors: Bryan D. Fleming, Daniel J. Urban, Matthew D. Hall, Thomas Longerich, Tim F. Greten, Ira Pastan, Mitchell Ho
Journal: Hepatology (2019)

Treatment of hepatocellular carcinomas using our glypican-3 (GPC3)-targeting human nanobody (HN3) immunotoxins causes potent tumor regression by blocking protein synthesis and down-regulating the Wnt signaling pathway. However, immunogenicity and a short serum half-life may limit the ability of immunotoxins to transition to the clinic.To address these concerns, we engineered HN3-based immunotoxins to contain various deimmunized Pseudomonas exotoxin (PE) domains. This included HN3-T20, which was modified to remove T-cell epitopes and contains a PE domain II truncation. We compared them to our previously reported B-cell deimmunized immunotoxin (HN3-mPE24) and our original HN3-immunotoxin with a wild-type PE domain (HN3-PE38). All of our immunotoxins displayed high affinity to human GPC3, with HN3-T20 having a KD value of 7.4 nM. HN3-T20 retained 73% enzymatic activity when compared with the wild-type immunotoxin in an adenosine diphosphate-ribosylation assay. Interestingly, a real-time cell growth inhibition assay demonstrated that a single dose of HN3-T20 at 62.5 ng/mL (1.6 nM) was capable of inhibiting nearly all cell proliferation during the 10-day experiment. To enhance HN3-T20's serum retention, we tested the effect of adding a streptococcal albumin-binding domain (ABD) and a llama single-domain antibody fragment specific for mouse and human serum albumin. For the detection of immunotoxin in mouse serum, we developed a highly sensitive enzyme-linked immunosorbent assay and found that HN3-ABD-T20 had a 45-fold higher serum half-life than HN3-T20 (326 minutes vs. 7.3 minutes); consequently, addition of an ABD resulted in HN3-ABD-T20-mediated tumor regression at 1 mg/kg.These data indicate that ABD-containing deimmunized HN3-T20 immunotoxins are high-potency therapeutics ready to be evaluated in clinical trials for the treatment of liver cancer.
Galectin 3 protects from cisplatin-induced acute kidney injury by promoting TLR-2-dependent activation of IDO1/Kynurenine pathway in renal DCs
Authors: Vladislav Volarevic, Bojana Simovic Markovic, Marina Gazdic Jankovic, Bojana Djokovic, Nemanja Jovicic, C. Randall Harrell, Crissy Fellabaum, Valentin Djonov, Nebojsa Arsenijevic, Miodrag L. Lukic
Journal: Theranostics (2019)

Strategies targeting cross-talk between immunosuppressive renal dendritic cells (DCs) and T regulatory cells (Tregs) may be effective in treating cisplatin (CDDP)-induced acute kidney injury (AKI).Galectin 3 (Gal-3), expressed on renal DCs, is known as a crucial regulator of immune response in the kidneys.In this study, we investigated the role of Gal-3 for DCs-mediated expansion of Tregs in the attenuation of CDDP-induced AKI.Methods: AKI was induced in CDDP-treated wild type (WT) C57BL/6 and Gal-3 deficient (Gal-3 -/-) mice.Biochemical, histological analysis, enzyme-linked immunosorbent assay (ELISA), immunohistochemistry, real-time PCR, magnetic cell sorting, flow cytometry and intracellular staining of renal-infiltrated immune cells were used to determine the differences between CDDP-treated WT and Gal-3 -/-mice.Newly synthesized selective inhibitor of Gal-3 (Davanat) was used for pharmacological inhibition of Gal-3.Recombinant Gal-3 was used to demonstrate the effects of exogenously administered soluble Gal-3 on AKI progression.Pam3CSK4 was used for activation of Toll-like receptor (TLR)-2 in DCs.Cyclophosphamide or anti-CD25 antibody were used for the depletion of Tregs.1-Methyl Tryptophan (1-MT) was used for pharmacological inhibition of Indoleamine 2,3-dioxygenase-1 (IDO1) in TLR-2-primed DCs which were afterwards used in passive transfer experiments.Results: CDDP-induced nephrotoxicity was significantly more aggravated in Gal-3 -/-mice.Significantly reduced number of immunosuppressive TLR-2 and IDO1-expressing renal DCs, lower serum levels of KYN, decreased presence of IL-10-producing Tregs and significantly higher number of inflammatory IFN-γ and IL-17-producing neutrophils, Th1 and Th17 cells were observed in the CDDP-injured kidneys of Gal-3 -/-mice.Pharmacological inhibitor of Gal-3 aggravated CDDP-induced AKI in WT animals while recombinant Gal-3 attenuated renal injury and inflammation in CDDP-treated Gal-3 -/-mice.CDDP-induced apoptosis, driven by Bax and caspase-3, was aggravated in Gal-3 -/-animals and in WT mice that received Gal-3 inhibitor (CDDP+Davanat-treated mice).Recombinant Gal-3 managed to completely attenuate CDDP-induced apoptosis in CDDP-injured kidneys of Gal-3 -/-mice.Genetic deletion as well as pharmacological inhibition of Gal-3 in renal DCs remarkably reduced TLR-2-dependent activation of IDO1/KYN pathway in these cells diminishing their capacity to prevent transdifferentiation of Tregs in inflammatory Th1 and Th17 cells.Additionally, Tregs generated by Gal-3 deficient DCs were not able to suppress production of IFN-γ and IL-17 in activated neutrophils.TLR-2-primed DCs significantly enhanced capacity of Tregs for attenuation of CDDP-induced AKI and inflammation and expression of Ivyspring International
Adipose tissue–derived WNT5A regulates vascular redox signaling in obesity via USP17/RAC1-mediated activation of NADPH oxidases
Authors: Ioannis Akoumianakis, Fabio Sanna, Marios Margaritis, Ileana Badi, Nadia Akawi, Laura Herdman, Patricia Coutinho, Harry Fagan, Alexios S. Antonopoulos, Evangelos K. Oikonomou, Sheena Thomas, Amy P. Chiu, Surawee Chuaiphichai, Christos P. Kotanidis, Constantinos Christodoulides, Mario Petrou, George Krasopoulos, Rana Sayeed, Lei Lv, Ashley Hale, Meisam Naeimi Kararoudi, Eileen McNeill, Gillian Douglas, Sarah George, Dimitris Tousoulis, Keith M. Channon, Charalambos Antoniades
Journal: Science Translational Medicine (2019)

Adipose-secreted WNT5A triggers vascular disease in obesity, activating vascular smooth muscle cell migration by an NADPH oxidase–dependent mechanism.
Characteristics and Role of Lenalidomide Therapy in Patients with Myelodysplastic/Myeloproliferative Neoplasm with Ring Sideroblasts and Thrombocytosis
Authors: Kiran Naqvi, Koji Sasaki, Guillermo Montalban-Bravo, Michael S Teach, Sherry A. Pierce, Hagop M. Kantarjian, Guillermo Garcia-Manero
Journal: Blood (2018)
Abstract 8269: Cysteine Protease Cathepsin K: A New Biomarker in Patients with Atrial Fibrillation
Authors: Masaya Fujita, Xian Wu Cheng, Yasuya Inden, Naoki Yoshida, Kazuhisa Kitamura, Masayuki Shimano, Kenji Okumura, Toyoaki Murohara
Journal: Circulation (2011)

Background. The cysteine protease cathepsin K is one of the most potent mammalian collagenases and elastases. It is overexpressed in cardiovascular tissues in response to injury, and is regulated by pro-inflammatory stimuli. Atrial remodeling in atrial fibrillation (AF) involves extensive extracellular matrix (ECM) remodeling that requires collagenolysis and elastolysis. We hypothesized that plasma levels of cathepsin K could be an important biomarker for atrial remodeling in AF patients receiving ablation therapy. Methods and Results. We examined a total of 156 subjects with paroxysmal AF (PAF) and 67 with chronic AF (CAF), as well as 21 individuals free from atrial disease. Plasma cathepsin K, interleukin-1β (IL-1β), high-sensitivity C-reactive protein (CRP), intact amino-terminal peptide of procollagen type I (I-PINP, as a marker of collagen type I synthesis), carboxyl-terminal telopeptide of collagen type I (ICTP, as a marker of collagen type I degradation), and lipid protein profiles were measured. Serum cathepsin K levels were significantly higher in patients with AF than in those without AF (AF vs. non-AF: 20.8 ± 3.5 ng/mL vs. 6.1 ± 0.8 ng/mL, P &lt; 0.01). Patients with AF had higher levels of IL-1β, CRP, and ICTP than those without AF ( P &lt; 0.05). After subgrouping the AF patients into those with PAF or CAF, we found that patients with CAF had higher levels of cathepsin K and IL-1β than those with PAF ( P &lt; 0.05). Although a Spearman's correlation test showed that plasma cathepsin K correlated significantly with IL-1β ( P &lt; 0.01), ICTP ( P &lt; 0.05) and left atrial diameter ( P &lt; 0.05), and correlated weakly with I-PINP ( P = 0.08), serum cathepsin K levels remained significantly higher in AF patients than in non-AF patients in a multiple linear regression test after adjusting for all of these confounders (P &lt; 0.01). Conclusions. Our findings suggest that circulating cathepsin K represents a novel potential marker of atrial remodeling and therapeutic efficacy and that augmented cathepsin K, IL-1β, and ICTP levels could provide an underlying inflammation-induced proteolytic mechanism of atrial remodeling in cases of AF.