tbuckley/cabot-search huggingface dataset:
AB0043 Anti-filaggrin autoantibodies are not predictive of radiological progression in rheumatoid arthritis (ra) – results of a 3-year longitudinal prospective study from a population based-recruitment of 127 ra
Authors: O Vittecoq, B Inçaurgarat, S Pouplin, J Legoedec, O Letourneur, D Rolland, G Gervasi, K Krzanowska, JF Ménard, A Gayet, M Jolivet, F Tron, X Le Loët
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> <h3>Objectives</h3> To evaluate the predictive value of autoantibodies (Ab) directed against citrullinated recombinant rat filaggrin (ACRFA) detected by a new ELISA for prognosis in a cohort of community cases of RA. <h3>Methods</h3> 127 patients (mean age: 50.5 yr, F/M: 2.9) with early RA (median disease duration: 2 yr) were enrolled prospectively in 1996 (T1), primarily from a population based-recruitment (80%), and were followed until 1999 (T2). At T1 were tested rheumatoid factors determined by the latex fixation test (LFT) and anti-filaggrin Abs identified by different assays, i.e. anti-keratin Ab (AKA), and anti-perinuclear factor (APF) by indirect immunofluorescence, ACRFA by an ELISA test whose results are expressed as the difference of OD values given by sera tested against the citrullinated and non-citrullinated forms of filaggrin. At T1 and T2: radiographs of the hands and wrists. Prognosis was defined by (1) radiological damage (van der Heijde modified Sharp method) at T2; (2) progression of radiological damage between T1 and T2. <h3>Results</h3> At T1: RA had mild activity (Ritchie articular index: 11/78, mean CRP: 15 mg/l), mild functional disability (HAQ: 0.8/3), mild X-ray destruction (Sharp: 9.2/280); 96% of patients were treated at T1 (DMARDs: 95%; prednisone: 72%); frequency of LFT, AKA, APF and ACRFA were respectively: 50%, 33%, 45% and 45%. At T2: total Sharp score: 22.8/280. The only parameter at T1 associated with a higher Sharp score at T2 (p = 0.03) and particularly with a more important radiological progression (p = 0.03) was the LFT. <h3>Conclusion</h3> Whatever the method used, indirect immunofluorescence or ELISA, anti-filaggrin do not allow to predict radiological damage in community cases of RA of limited duration.
Optimized gene engineering of murine CAR-T cells reveals the beneficial effects of IL-15 coexpression
Authors: Evripidis Lanitis, Giorgia Rota, Paris Kosti, Catherine Ronet, Aodrenn Spill, Bili Seijo, Pedro Romero, Denarda Dangaj, George Coukos, Melita Irving
Journal: The Journal of Experimental Medicine (2020)

Limited clinical benefit has been demonstrated for chimeric antigen receptor (CAR) therapy of solid tumors, but coengineering strategies to generate so-called fourth-generation (4G) CAR-T cells are advancing toward overcoming barriers in the tumor microenvironment (TME) for improved responses. In large part due to technical challenges, there are relatively few preclinical CAR therapy studies in immunocompetent, syngeneic tumor-bearing mice. Here, we describe optimized methods for the efficient retroviral transduction and expansion of murine T lymphocytes of a predominantly central memory T cell (TCM cell) phenotype. We present a bicistronic retroviral vector encoding both a tumor vasculature–targeted CAR and murine interleukin-15 (mIL-15), conferring enhanced effector functions, engraftment, tumor control, and TME reprogramming, including NK cell activation and reduced presence of M2 macrophages. The 4G-CAR-T cells coexpressing mIL-15 were further characterized by up-regulation of the antiapoptotic marker Bcl-2 and lower cell-surface expression of the inhibitory receptor PD-1. Overall, this work introduces robust tools for the development and evaluation of 4G-CAR-T cells in immunocompetent mice, an important step toward the acceleration of effective therapies reaching the clinic.
Palbociclib Prevents CDK4/6 Dependent-Myeloproliferation and Myelofibrosis
Authors: Helene Duparc, Delphine Muller, Ileana Antony-Debre, Caroline Marty, Najet Debili, Jean-Luc Villeval, Isabelle Plo, William Vainchenker, Laure Gilles, Hana Raslova
Journal: Blood (2020)
Microscopy and Bacteriology. A Manual for Students and Practitioners.
Journal: JAMA (1903)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Response to: ‘Correspondence on ‘Machine learning integration of scleroderma histology and gene expression identifies fibroblast polarisation as a hallmark of clinical severity and improvement’’ by Manetti
Authors: Kimberly Showalter, Cynthia Magro, Yaxia Zhang, Robert Spiera, Dana E Orange, Jessica K Gordon
Journal: Annals of the Rheumatic Diseases (2020)

We thank Dr Manetti for his comments regarding the distinctive CD34 positive dermal stromal cell population and their pathological changes in systemic sclerosis (SSc) skin.1–4 One challenge for the field of SSc dermatopathology is a lack of broad consensus regarding the terminology used to describe CD34+ cells.5 Indeed, CD34+ cells have been described as fibrocytes,6 stromal fibroblastic cells,7 dermal dendritic cells,8 fibroblasts5 9–11 and telocytes.3 4 Our work adds to prior observations by noting that skin samples that exhibit a loss of CD34+ cells, gain expression of alpha-smooth muscle actin (aSMA) in a similar microanatomic distribution, specifically the deeper dermis and subcutaneous fat. This pattern of CD34 and aSMA reversed as patients improved clinically and was associated with a gene signature relevant to clinical improvement.12 Our study was not able to conclude whether this polarisation of …
A Functional Profiling of Microenvironmental Factors and Small Molecules Reveals Monocyte Chemoattractant Protein-1 Mediates Drug Resistance in Acute Myeloid Leukemia
Authors: Rucha V Modak, Sara J Gosline, Alisa Damnernsawad, Tamilla Nechiporuk, Ted Laderas, Guanming Wu, Paul Piehowski, Stephen E Kurtz, Christopher A. Eide, Jeffrey W. Tyner, Karin Rodland, Shannon K. McWeeney, Anupriya Agarwal
Journal: Blood (2020)
Frequency and Functional Analysis of Myeloid-Derived Suppressor Cells (MDSCs) in the Peripheral Blood and Bone Marrow of Patients with Chronic Idiopathic Neutropenia (CIN)
Authors: Nikoleta Bizymi, Athina Damianaki, Maria Velegraki, Konstantina Zavitsanou, Anastasios Karasachinidis, Anthie Georgopoulou, Irene Mavroudi, John Sperelakis, George Kontakis, Charalampos Pontikoglou, Helen A. Papadaki
Journal: Blood (2020)
Cardio-Oncology Education and Training
Authors: Jose A. Alvarez-Cardona, Jordan Ray, Joseph Carver, Vlad Zaha, Richard Cheng, Eric Yang, Joshua D. Mitchell, Keith Stockerl-Goldstein, Lavanya Kondapalli, Susan Dent, Anita Arnold, Sherry Ann Brown, Monica Leja, Ana Barac, Daniel J. Lenihan, Joerg Herrmann
Journal: Journal of the American College of Cardiology (2020)
CYP3A inhibitors and impact of these agents on outcomes in patients with acute myeloid leukemia treated with venetoclax plus azacitidine on the VIALE-A study
Authors: Brian A Jonas, Courtney D. Dinardo, Nicola Fracchiolla, Alexander Pristupa, Kenichi Ishizawa, Jie Jin, Marina Konopleva, Yishai Ofran, Pau Montesinos, Tibor Kovacsovics, Jun-Ho Jang, Hagop M. Kantarjian, Wan-Jen Hong, Yinghui Duan, William Ainsworth, Jalaja Potluri, Michael Werner, Anders Erik Svensson, Keith W. Pratz
Journal: Blood (2020)
Incidence and Outcome of Acute Myeloid Leukemia in Peru: An 11-Year Single Center Experience
Authors: Ali Al-kassab-Córdova, Lizbeth Lachira-Yparraguirre, Gustavo Sandival-Ampuero, Katia Roque, Emperatriz Ortega, Sofia Lozano-Ballena, Juan C Haro, Shirley Quintana, Marco Villena, Greenlandia Ferreyros-Brandon, Juan L Garcia-Leon, Cesar Samanez-Figari, Luis Malpica Castillo, Daniel J Enriquez
Journal: Blood (2020)
Characterizing Transcriptional Regulatory Sequences in Coronaviruses and Their Role in Recombination
Authors: Yiyan Yang, Wei Yan, A Brantley Hall, Xiaofang Jiang
Journal: Molecular Biology and Evolution (2020)

Abstract Novel coronaviruses, including SARS-CoV-2, SARS, and MERS, often originate from recombination events. The mechanism of recombination in RNA viruses is template switching. Coronavirus transcription also involves template switching at specific regions, called transcriptional regulatory sequences (TRS). It is hypothesized but not yet verified that TRS sites are prone to recombination events. Here, we developed a tool called SuPER to systematically identify TRS in coronavirus genomes and then investigated whether recombination is more common at TRS. We ran SuPER on 506 coronavirus genomes and identified 465 TRS-L and 3,509 TRS-B. We found that the TRS-L core sequence (CS) and the secondary structure of the leader sequence are generally conserved within coronavirus genera but different between genera. By examining the location of recombination breakpoints with respect to TRS-B CS, we observed that recombination hotspots are more frequently colocated with TRS-B sites than expected.
The BMJ interview: Chris Whitty, England’s chief medical officer, on covid-19
Authors: Fiona Godlee, Mun-Keat Looi
Journal: BMJ (2020)

Never has the role of chief medical officer (CMO) been under such scrutiny. In a rare interview, England's CMO speaks to The BMJ's editor in chief, <b>Fiona Godlee</b>, about the pandemic and what it's like to be a physician in Whitehall
High Transfusion Dependence and Serum Ferritin but Not Transferrin Saturation Predict Inferior Clinical Outcomes in Patients with MDS
Authors: Jennifer Teichman, Michelle Geddes, Nancy Zhu, Mary-Margaret Keating, Mitchell Sabloff, Grace Christou, Brian Leber, Dina Khalaf, Eve St-Hilaire, Nicholas Finn, April Shamy, Karen W.L. Yee, John M. Storring, Thomas J. Nevill, Robert Delage, Mohamed Elemary, Versha Banerji, Lee Mozessohn, Lisa Chodirker, Liying Zhang, Mohammed Siddiqui, Anne Parmentier, Heather A. Leitch, Rena J. Buckstein
Journal: Blood (2020)
Pilot Trial of the My Hematology Oncology Patient Experience (MyHOPE™) for Multiple Myeloma (MM) Digital Solution in Patients with MM
Authors: Noopur S. Raje, Omar Nadeem, Joseph Mikhael, Catherine Ludwig, Amit Agarwal, Judith Inumerable, Teng J. Ong, Sundar Jagannath
Journal: Blood (2020)
A cell-of-origin epigenetic tracer reveals clinically distinct subtypes of high-grade serous ovarian cancer
Authors: Pietro Lo Riso, Carlo Emanuele Villa, Gilles Gasparoni, Andrea Vingiani, Raffaele Luongo, Anna Manfredi, Annemarie Jungmann, Alessia Bertolotti, Francesca Borgo, Annalisa Garbi, Michela Lupia, Pasquale Laise, Vivek Das, Giancarlo Pruneri, Giuseppe Viale, Nicoletta Colombo, Teresa Manzo, Luigi Nezi, Ugo Cavallaro, Davide Cacchiarelli, Jörn Walter, Giuseppe Testa
Journal: Genome Medicine (2020)

Abstract Background High-grade serous ovarian cancer (HGSOC) is a major unmet need in oncology. The remaining uncertainty on its originating tissue has hampered the discovery of molecular oncogenic pathways and the development of effective therapies. Methods We used an approach based on the retention in tumors of a DNA methylation trace (OriPrint) that distinguishes the two putative tissues of origin of HGSOC, the fimbrial (FI) and ovarian surface epithelia (OSE), to stratify HGSOC by several clustering methods, both linear and non-linear. The identified tumor subtypes (FI-like and OSE-like HGSOC) were investigated at the RNAseq level to stratify an in-house cohort of macrodissected HGSOC FFPE samples to derive overall and disease-free survival and identify specific transcriptional alterations of the two tumor subtypes, both by classical differential expression and weighted correlation network analysis. We translated our strategy to published datasets and verified the co-occurrence of previously described molecular classification of HGSOC. We performed cytokine analysis coupled to immune phenotyping to verify alterations in the immune compartment associated with HGSOC. We identified genes that are both differentially expressed and methylated in the two tumor subtypes, concentrating on PAX8 as a bona fide marker of FI-like HGSOC. Results We show that: - OriPrint is a robust DNA methylation tracer that exposes the tissue of origin of HGSOC. - The tissue of origin of HGSOC is the main determinant of DNA methylation variance in HGSOC. - The tissue of origin is a prognostic factor for HGSOC patients. - FI-like and OSE-like HGSOC are endowed with specific transcriptional alterations that impact patients’ prognosis. - OSE-like tumors present a more invasive and immunomodulatory phenotype, compatible with its worse prognostic impact. - Among genes that are differentially expressed and regulated in FI-like and OSE-like HGSOC, PAX8 is a bona fide marker of FI-like tumors. Conclusions Through an integrated approach, our work demonstrates that both FI and OSE are possible origins for human HGSOC, whose derived subtypes are both molecularly and clinically distinct. These results will help define a new roadmap towards rational, subtype-specific therapeutic inroads and improved patients’ care.
Optimal Interval for Detection of Molecular Relapse after Stop of Tyrosine Kinase Inhibitor (TKI) in Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia (Ph+ALL) Caliculated By Kinetics of BCR-ABL Transcripts
Authors: Koichi Miyamura, Masahide Osaki, Tatsunori Goto, Takanobu Morishita, Yukiyasu Ozawa
Journal: Blood (2020)
Mutated Cancer-Related Genes Detected at Diagnosis of CML and a Novel Class of Variant Associated with the Philadelphia Translocation Are Both Independent Predictors of Inferior Outcomes
Authors: Naranie Shanmuganathan, Carol Wadham, Nur Hezrin Shahrin, Daniel Thomson, Jinghua Feng, Verity A Saunders, Ming Lin, Rosalie Kenyon, Rob King, Paul Wang, David M Ross, David T Yeung, Andreas W Schreiber, Timothy P. Hughes, Susan Branford
Journal: Blood (2020)
Overexpression of the OCT-1 Gene Is a Biomarker Associated with Poor Outcomes in Diffuse Large B-Cell Lymphoma (DLBCL) - Data from a Retrospective Cohort from Latin America: Defining a Very High-Risk Clinical-Molecular Subgroup
Authors: Luis Alberto de Padua Covas Lage, Gisele Rodrigues Gouveia, Suzete Cleusa Ferreira, Sheila Aparecida Coelho de Siqueira, Abrahão Elias Hallack Neto, Renata Oliveira Costa, Juliana Pereira
Journal: Blood (2020)
Long-Term Follow up of a Phase II Study of Guadecitabine (SGI-110) in Patients with Higher-Risk Myelodysplastic Syndrome (MDS)
Authors: Kiyomi Morita, Guillermo Montalban Bravo, Koji Sasaki, Kristy R. Bodden, Feng Wang, Prithviraj Bose, Yesid Alvarado, Naval Daver, Gautam Borthakur, Farhad Ravandi, Koichi Takahashi, Elias Jabbour, Courtney D. DiNardo, Naveen Pemmaraju, Tapan M. Kadia, Maro Ohanian, Sherry A. Pierce, Mohammad Azab, Hagop M. Kantarjian, Guillermo Garcia-Manero
Journal: Blood (2020)
Fluorine-18-Fluorodeoxyglucose Positron Emission Tomography for the Assessment of Acute Intestinal GvHD and Prediction of Response to Immunosuppressive Therapy
Authors: Georg Evers, Wolfgang Roll, Jörn Albring, Christian Reicherts, Benjamin Noto, Matthias Weckesser, Georg Lenz, Michael Schäfers, Matthias Stelljes
Journal: Blood (2020)
A Phase I Dose Escalation Study of PT-112 in Patients with Relapsed or Refractory Multiple Myeloma
Authors: Taxiarchis Kourelis, Sikander Ailawadhi, Dan T. Vogl, Dennis Cooper, Tyler D Ames, Christina Y Yim, Matthew R Price, Jose J Jimeno, P. Leif Bergsagel
Journal: Blood (2020)
<i>TET2</i> and <i>DNMT3A</i> Mutations Exert Divergent Effects on DNA Repair and Sensitivity of Leukemia Cells to PARP Inhibitors
Authors: Silvia Maifrede, Bac Viet Le, Margaret Nieborowska-Skorska, Konstantin Golovine, Katherine Sullivan-Reed, Wangisa M.B. Dunuwille, Joseph Nacson, Michael Hulse, Lisa Beatrice Caruso, Zachary Gazze, Zhaorui Lian, Antonella Padella, Kumaraswamy Chitrala, Boris Bartholdy, Ksenia Matlawska-Wasowska, Daniela Di Marcantonio, Giorgia Simonetti, Georg Greiner, Stephen M. Sykes, Peter Valent, Elisabeth M. Paietta, Hugo F Fernandez, Martin S. Tallman, Mark Litzow, Mark D. Minden, Jian Huang, Giovanni Martinelli, George S. Vassiliou, Italo Tempera, Katarzyna Piwocka, Neil Johnson, Grant Challen, Tomasz Skorski
Journal: Blood (2020)
Bortezomib Induces Anti-Multiple Myeloma Immune Response Mediated By Cgas/Sting Pathway Activation, Type I Interferon Secretion, and Immunogenic Cell Death: Clinical Application
Authors: Annamaria Gulla, Eugenio Morelli, Mehmet Kemal Samur, Cirino Botta, Teru Hideshima, Giada Bianchi, Mariateresa Fulciniti, Stefano Malvestiti, Rao Prabhala, Srikanth Talluri, Yu-Tzu Tai, Kenneth Wen, Paul G. Richardson, Ruben D. Carrasco, Dharminder Chauhan, Nikhil C. Munshi, Kenneth Anderson
Journal: Blood (2020)
Abstract 238: Single-Cell Transcriptomic Analysis and Patient-Specific IPSCs Reveal Dysregulated Cell Cycle in Coronary Endothelial Cell in Hypoplastic Left Heart Syndrome
Authors: Mingxia Gu, Yifei Miao, Xin Zhou, Lei Tian, Marcy Martin, Timothy J Nelson
Journal: Circulation Research (2020)

Hypoplastic left heart syndrome (HLHS) is a single ventricle congenital heart disease that results in severe underdevelopment of the left ventricle, mitral valve, aortic valve, and ascending aorta. Early serial postmortem examinations also revealed a high rate of coronary anomalies in HLHS, which included multiple ventriculo-coronary arterial connections as well as thick-walled and kinked coronary arteries. A previous study showed that fetal hypoplastic left hearts had a reduced endothelial cell (EC) population and lower capillary density compared with normal hearts. However, the mechanism underlying coronary abnormalities associated with HLHS remains unknown. Thus, we generated induced pluripotent stem cells derived ECs (iPSC-ECs) from three HLHS patients and three age-matched controls. Single Cell RNA-Seq (scRNA-seq) profiling identified both endocardial (NPR3 + /CDH5 + ) and coronary endothelial populations (APLN + /CDH5 + ) from the heterogeneous iPSC-ECs. Intriguingly, a subcluster of the coronary endothelial cells (CECs) with cell cycle arrest was specifically enriched in HLHS patients. Further cell cycle analysis showed that 30.6% of the HLHS cells were trapped in the G1 phase, while the majority of the control CECs entered cell cycle normally. Additionally, the cell cycle differences between control and HLHS was only seen in CECs, not in the endocardial population. To verify our transcriptomic analysis, we applied negative cell sorting (NPR3 - /CDH5 + ) on iPSC-ECs to purify CECs (iCECs) and confirmed that HLHS iCECs showed profound reduction of cell cycle/proliferative genes ( KI67, PCNA, CCNA2, CCNB1 ) and abnormal induction of CCND2 , which is the hallmark of G1 phase. BrdU assays also indicated suppressed proliferation in HLHS iCECs. Furthermore, we profiled the transcriptome from a human heart with an underdevelopment left ventricle (ULV) at single cell resolution. When compared to the normal human heart, pathway enrichment analysis of differentially expressed genes in ULV hearts demonstrated reduced cell proliferation in the CEC subpopulation. Here, we identified that CECs from HLHS patients exerted proliferative defects that can potentially impede the development of vascular/capillary structure and cause related functional deficiencies. Reformation of the coronary defect provides a promising therapeutic strategy to prevent HLHS deterioration.
Mitochondrial dysfunction in inflammatory bowel disease alters intestinal epithelial metabolism of hepatic acylcarnitines
Authors: Sarah A. Smith, Sayaka A. Ogawa, Lillian Chau, Kelly A. Whelan, Kathryn E. Hamilton, Jie Chen, Lu Tan, Eric Z. Chen, Sue Keilbaugh, Franz Fogt, Meenakshi Bewtra, Jonathan Braun, Ramnik J. Xavier, Clary B. Clish, Barry Slaff, Aalim M. Weljie, Frederic D. Bushman, James D. Lewis, Hongzhe Li, Stephen R. Master, Michael J. Bennett, Hiroshi Nakagawa, Gary D. Wu
Journal: Journal of Clinical Investigation (2020)

As the interface between the gut microbiota and the mucosal immune system, there has been great interest in the maintenance of colonic epithelial integrity through mitochondrial oxidation of butyrate, a short-chain fatty acid produced by the gut microbiota. Herein, we showed that the intestinal epithelium could also oxidize long-chain fatty acids, and that luminally delivered acylcarnitines in bile could be consumed via apical absorption by the intestinal epithelium, resulting in mitochondrial oxidation. Finally, intestinal inflammation led to mitochondrial dysfunction in the apical domain of the surface epithelium that may reduce the consumption of fatty acids, contributing to higher concentrations of fecal acylcarnitines in murine Citrobacter rodentium–induced colitis and human inflammatory bowel disease. These results emphasized the importance of both the gut microbiota and the liver in the delivery of energy substrates for mitochondrial metabolism by the intestinal epithelium.
Effects of carbon-based nanomaterials on vascular endothelia under physiological and pathological conditions: interactions, mechanisms and potential therapeutic applications
Authors: Yanli Zhang, Yulin Zhang, Junrong Wu, Jia Liu, Yiyuan Kang, Chen Hu, Xiaoli Feng, Wenjing Liu, Haiyun Luo, Aijie Chen, Lili Chen, Longquan Shao
Journal: Journal of Controlled Release (2020)
Genome-Wide Transcriptome Analysis Identifies Molecular Patterns of FDG-PET/CT Biomarkers in MM Patients from the Cassiopet Study
Authors: Jean-Baptiste Alberge, Bastien Jamet, Clement Bailly, Cyrille Touzeau, Jonathan Cruard, Thomas Carlier, Caroline Bodet-Milin, Michel Cherel, Philippe Moreau, Stephane Minvielle, Francoise Kraeber-Bodere
Journal: Blood (2020)
Abstract 275: <i>In Vitro</i> Inflammatory Assays for Decellularized Xenogeneic Heart Valves
Authors: Mitchell Vedepo, Kyra Flores, Jeffrey Jacot
Journal: Circulation Research (2020)

Intro: There is great interest in a decellularized xenogeneic heart valve for valve replacement due to the shortage of human tissue available for implant. However, decellularized xenografts have a poor clinical history due to incomplete antigen removal. The inflammatory potential of decellularized heart valves can be evaluated in vitro using assays that measure antigen presence and cytokine production by cultured human macrophages. This study tests the inflammatory potential of porcine aortic valves before and after decellularization. Methods: Decellularization was confirmed by histology and DNA quantification. Enzyme linked immunosorbent assays (ELISAs) tested for inflammatory potential using pooled human serum as a primary antibody. Additional tissue samples were cultured with THP-1 derived macrophages and the production of monocyte chemoattractant protein-1 (MCP-1) was measured. Results: Decellularization resulted in 99% removal of DNA. The decellularized valve conduit was found to be 2.49% as inflammatory as native tissue (Figure 1). Human macrophages cultured with native tissue produced approximately 10-fold more MCP-1 compared to decellularized tissue. Impact: The in vitro assays described quantify a reduced inflammatory response for decellularized heart valves. Future use of these assays can be used to further decrease the inflammatory potential, increasing the safety of decellularized xenogeneic heart valves.