tbuckley/cabot-search huggingface dataset:
CCR5 is Associated With Immune Cell Infiltration and Prognosis of Lung Cancer
Authors: Jia Zhang, Jinhai Wang, Zhenyuan Qian, Yong Han
Journal: Journal of Thoracic Oncology (2019)

Recently, a scientist named He Jiankui from China claims to have created the world's first genetically edited babies by eliminating the C-C motif chemokine receptor 5 (gene/pseudogene) (CCR5) using the genome-editing technology of clustered regularly interspaced short palindromic repeats (CRISPR). CCR5 is an important co-receptor for HIV to enter host cells and defective alleles of this gene will lead to HIV infection resistance.1Joubert B.R. Nora F. Victor M. et al.Regulation of CCR5 expression in human placenta: insights from a study of mother-to-child transmission of HIV in Malawi.PloS One. 2010; 5: e9212Crossref PubMed Scopus (13) Google Scholar The researcher hopes these CRISPR babies would be resistant to HIV. However, because this DNA change can pass to future generations and the molecular function of CCR5 in human has never been clarified, there could be potential side-effects. In this study, several publicly available datasets were obtained and reanalyzed.2Li T. Fan J. Wang B. et al.TIMER: a web server for comprehensive analysis of tumor-infiltrating immune cells.Cancer Res. 2017; 77: e108-e110Crossref PubMed Scopus (0) Google Scholar, 3Győrffy B. Surowiak P. Budczies J. et al.Online survival analysis software to assess the prognostic value of biomarkers using transcriptomic data in non-small-cell lung cancer.PloS One. 2013; 8: e82241Crossref PubMed Scopus (1230) Google Scholar The upper row of Figure 1 indicates that CCR5 was positively correlated with overall survival of patients with lung cancer (n = 1926, Log rank p < 0.0001), lung adenocarcinoma (n = 720, Log rank p < 0.0001), lung squamous cell carcinoma (n = 524, Log rank p = 0.019), liver cancer (n = 364, Log rank p = 0.0043), rectal cancer (n = 165, Log rank p = 0.0002), breast cancer (n = 1402, Log rank p = 0.0002), and cervical cancer (n = 304, Log rank p = 0.0028). Further analyses show that CCR5 was significantly associated with B cell, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, dendritic cell infiltration in both lung adenocarcinoma, and lung squamous cell carcinoma (p < 0.0001) (detailed statistical analysis results are shown in Fig. 1). In summary, CCR5 is a promising prognostic biomarker for several cancer types including lung cancer because of its association with immune cell infiltration. This study was supported by the National Natural Science Foundation of China (81702774), Zhejiang Provincial Administration of Traditional Chinese Medicine (NO.2016ZB018), and the Natural Science Foundation of Zhejiang Province (No. LY17H160065; No.LQ18H160023; LY15H160045). Drs. Zhang and Wang contributed equally to this work.
DIPG-15. PNOC-003: CLINICAL IMPACT OF A PRECISION MEDICINE STRATEGY FOR CHILDREN WITH DIFFUSE INTRINSIC PONTINE GLIOMA
Authors: Sabine Mueller, Cassie Kline, Lindsay Kilburn, Winnie S Liang, Payal Jain, Nalin Gupta, Eshini Panditharatna, Kellie Nazemi, Suresh N Magge, John Crawford, Anu Banerjee, Roger Packer, Alison Roos, Bo Zhang, Yuankun Zhu, Mariam Aboian, Benita Tamrazi, Joanna Philips, David Solomon, Annette Molinaro, John Kuhn, Sara A Byron, Javad Nazarian, Adam Resnick, Michael Berens, Michael Prados
Journal: Neuro-Oncology (2019)

OBJECTIVE: We evaluated the impact on overall survival at 12 months (OS12) of a personalized therapy plan based on tumor/germline whole exome (WES) and tumor RNA sequencing (RNAseq) of diffuse intrinsic pontine glioma (DIPG). METHODS: We enrolled newly diagnosed DIPG patients ≤ 25 years of age. Tumors were sequenced and drug selection was performed using a custom drug-matching pipeline and pharmacopeia. A personalized treatment strategy using up to 4 FDA-approved drugs was determined by a specialized tumor board with target of 21 business days from biopsy. Patients were followed for adverse events (AEs) and OS12. Circulating tumor DNA (ctDNA) was collected at diagnosis and with surveillance MRIs. Xenograft development and cell culture expansion were attempted for each patient. RESULTS: Nineteen patients (6 females; median age 6 years; range 4–25 years) followed therapy recommendations. Average mapped coverages for WES were 490X (tumor) and 194X (germline). An average of 245,951,030 total mapped reads was achieved for tumor RNA. Panobinostat was the most commonly recommended drug (n=12; 63%). The multi-agent therapy plan was well tolerated with mainly grade 1/2 AEs. Grade 3/4 AEs were predominantly hematologic, including thrombocytopenia (n=13; 22%) and neutropenia (n=16; 27%). The OS12 did not significantly differ from historical controls (OS12 0.47; 95% CI 0.24, 0.70) or from a feasibility cohort that did not follow tumor board recommendations (OS12 0.66; 95% CI 0.36, 0.97; p=0.34). Fourteen DIPG cell lines were established. CtDNA analysis at diagnosis confirmed the H3K27M mutation in 16/20 patients, known to harbor H3K27M in tumor. CONCLUSION: A multi-agent therapy recommendation based on WES and RNAseq analysis of DIPG tumors is feasible; however, there is no demonstrated impact on clinical outcome. This is likely due to lack of efficacious FDA-approved drugs that target key mutations in DIPG, as well as molecular evolution of these tumors.
Epithelial dysregulation in obese severe asthmatics with gastro-oesophageal reflux
Authors: Jeanne-Marie Perotin, James P.R. Schofield, Susan J. Wilson, Jonathan Ward, Joost Brandsma, Fabio Strazzeri, Aruna Bansal, Xian Yang, Anthony Rowe, Julie Corfield, Rene Lutter, Dominick E. Shaw, Per S. Bakke, Massimo Caruso, Barbro Dahlén, Stephen J. Fowler, Ildikó Horváth, Peter Howarth, Norbert Krug, Paolo Montuschi, Marek Sanak, Thomas Sandström, Kai Sun, Ioannis Pandis, Charles Auffray, Bertrand De Meulder, Diane Lefaudeux, John H. Riley, Ana R. Sousa, Sven-Erik Dahlen, Ian M. Adcock, Kian Fan Chung, Peter J. Sterk, Paul J. Skipp, Jane E. Collins, Donna E. Davies, Ratko Djukanović
Journal: European Respiratory Journal (2019)

<b>Stratification of severe asthma on the basis of bronchial epithelial gene expression identified a subset whose endotype is defined by marked epithelial dysregulation associated with obesity, gastro-oesophageal reflux and proton pump inhibitors</b>http://bit.ly/2EeKv23
Abstract 15565: A New Non-Invasive Method for the Detection of Local Inflammation Atherosclerotic Lesions: an Experimental Study with Microwave Radiometry
Authors: Maria Drakopoulou, Konstantinos Toutouzas, Charalampia Nikoloaou, Archontoula Michelongona, Andreas Synetos, George Agrogiannis, Efstratios Patsouris, Elias Siores, Haralampos Grassos, Christodoulos Stefanadis
Journal: Circulation (2011)

Background: The presence of inflammatory cells is considered a histological hallmark of vulnerable atherosclerotic lesions. Intravascular thermography (IVT) is the only method currently available, ...
MEDU-46. SONIC HEDGEHOG SPEEDS UP DNA REPLICATION AND CAUSES CANCER-INITIATING MUTATIONS
Authors: Lukas Tamayo-Orrego, David Gallo, Amandine Bemmo, Sushmetha Mohan, Samer Salameh, Frederic Racicot, Grant Brown, Frederic Charron
Journal: Neuro-Oncology (2019)

Cancer is a multi-stage disease caused by sequential mutations; however, the molecular mechanism that generates cancer-initiating mutations is not well understood. Using the developing cerebellum as a model system, here we show the molecular mechanism of tumor initiation in Sonic hedgehog medulloblastoma (SHH-MB), a common subtype of the most frequent pediatric brain tumor. The most common initiating event of SHH-MB is Ptch1 loss of heterozygosity (LOH), which occurs in cerebellar granule cell progenitors (GCPs) and leads to preneoplasia formation. Since GCPs proliferate in response to Shh, we tested whether the normal proliferative effects of Shh can lead to genomic instability and DNA lesions responsible for Ptch1 LOH in the SHH-MB cell-of-origin. We found that Shh profoundly alters DNA replication dynamics in GCPs, leading to DNA damage, formation of DNA breaks in S-phase and hyper-recombination. Shh led to DNA helicase loading and activation, resulting in high levels of replication origin firing. Shh-dependent origin firing was required for Shh-induced DNA damage and recombination. Moreover, reducing origin firing decreased recombination and tumor initiation in a pre-clinical model of MB. These results show that reduction of Shh-dependent, DNA replication-associated DNA damage in tumor-prone Ptch1+/- GCPs before cancer initiation is capable of preventing MB-initiating mutations. Thus, we demonstrate that a developmental mitogen can cause cancer-initiating mutations through an increase in origin firing, and attenuating origin firing can prevent cancer initiation.
Utility of Metabolic Parameters on FDG PET/CT in the Classification of Early-Stage Lung Adenocarcinoma
Authors: Shingo Iwano, Shinji Ito, Shinichiro Kamiya, Rintaro Ito, Katsuhiko Kato, Shinji Naganawa
Journal: Clinical Nuclear Medicine (2019)

Purpose This paper aims to explore the role of a metabolic parameter on 18 F-FDG-PET/CT for clinical T-classification in early-stage adenocarcinoma. Patients and Methods One hundred six surgically resected pathological TNM stage (p-stage) 0/I lung adenocarcinomas were retrospectively reviewed. The solid size (SS) measured on thin-section CT and the pathological invasive size (IS) of tumors were recorded. The SUVmax and metabolic tumor volume with SUV ≥1.0 (MTV 1.0 ) derived from PET/CT data were measured on a workstation, and the metabolic tumor diameter with SUV ≥1.0 (MTD 1.0 ) was calculated automatically from MTV 1.0 . For the correlations between the IS and the SS, MTD 1.0 , or SUVmax, Pearson's correlation coefficients were compared using the Meng-Rosenthal-Rubin method. Additionally, the reproducibility between the clinical TNM stage (c-stage), based on the SS or MTD 1.0 , and the p-stage was analyzed using the kappa coefficient (k). Results For the correlations between the IS and the other parameters, Pearson correlation coefficient was 0.630 for the SS, 0.600 for the SUVmax, and 0.725 for MTD 1.0 . MTD 1.0 correlated significantly and more strongly with the IS than the SS and the SUVmax did ( P = 0.040, and P = 0.008, respectively). The reproducibility between p-stage and c-stage based on the SS was moderate (k = 0.529, P &lt; 0.001), whereas that between p-stage and c-stage based on MTD 1.0 was substantial (k = 0.676, P &lt; 0.001). Conclusions MTD 1.0 on FDG-PET/CT was correlated significantly and more strongly with the pathological IS in lung adenocarcinomas than with the SS on thin-section CT. FDG-PET/CT could classify more precisely early-stage lung adenocarcinoma than the presently used T-classification based on thin-section CT findings.
Anti-Ro52 autoantibodies are associated with interstitial lung disease and more severe disease in patients with juvenile myositis
Authors: Sara Sabbagh, Iago Pinal-Fernandez, Takayuki Kishi, Ira N Targoff, Frederick W Miller, Lisa G Rider, Andrew Lee Mammen
Journal: Annals of the Rheumatic Diseases (2019)

Objectives Anti-Ro52 autoantibodies are associated with more severe interstitial lung disease (ILD) in adult myositis patients with antiaminoacyl transfer (t)RNA synthetase autoantibodies. However, few studies have examined anti-Ro52 autoantibodies in juvenile myositis. The purpose of this study was to define the prevalence and clinical features associated with anti-Ro52 autoantibodies in a large cohort of patients with juvenile myositis. Methods We screened sera from 302 patients with juvenile dermatomyositis (JDM), 25 patients with juvenile polymyositis (JPM) and 44 patients with juvenile connective tissue disease–myositis overlap (JCTM) for anti-Ro52 autoantibodies by ELISA. Clinical characteristics were compared between myositis patients with and without anti-Ro52 autoantibodies. Results Anti-Ro52 autoantibodies were found in 14% patients with JDM, 12% with JPM and 18% with JCTM. Anti-Ro52 autoantibodies were more frequent in patients with antiaminoacyl tRNA synthetase (64%, p&lt;0.001) and anti-MDA5 (31%, p&lt;0.05) autoantibodies. After controlling for the presence of myositis-specific autoantibodies, anti-Ro52 autoantibodies were associated with the presence of ILD (36% vs 4%, p&lt;0.001). Disease course was more frequently chronic, remission was less common, and an increased number of medications was received in anti-Ro52 positive patients. Conclusions Anti-Ro52 autoantibodies are present in 14% of patients with juvenile myositis and are strongly associated with anti-MDA5 and antiaminoacyl tRNA synthetase autoantibodies. In all patients with juvenile myositis, those with anti-Ro52 autoantibodies were more likely to have ILD. Furthermore, patients with anti-Ro52 autoantibodies have more severe disease and a poorer prognosis.
Changing trends in age-adjusted pulmonary fibrosis mortality in the USA: a joinpoint regression analysis
Authors: Evans R. Fernández Pérez
Journal: European Respiratory Journal (2019)

<b>Pulmonary fibrosis mortality rate increased from 1999 until reaching an inflection point in 2004. Subsequently, mortality rates decreased from 2004 to 2017 and concurred with significant downward trends in cardiovascular, pneumonia and influenza mortality.</b>http://bit.ly/2KTFWPE
Figure errors, sloppy science, and fraud: keeping eyes on your data
Authors: Corinne L. Williams, Arturo Casadevall, Sarah Jackson
Journal: Journal of Clinical Investigation (2019)

Recent reports suggest that there has been an increase in the number of retractions and corrections of published articles due to post-publication detection of problematic data. Moreover, fraudulent data and sloppy science have long-term effects on the scientific literature and subsequent projects based on false and unreproducible claims. At the JCI, we have introduced several data screening checks for manuscripts prior to acceptance in an attempt to reduce the number of post-publication corrections and retractions, with the ultimate goal of increasing confidence in the papers we publish.
Lenalidomide in Pretreated Mantle Cell Lymphoma Patients: An Italian Observational Multicenter Retrospective Study in Daily Clinical Practice, the Lenamant Study
Authors: Vittorio Stefoni, Cinzia Pellegrini, Letizia Gandolfi, Luca Baldini, Monica Tani, Emanuele Cencini, Amalia Figuera, Michela Ansuinelli, Elisa Bernocco, Maria Cantonetti, M. Christina Cox, Filippo Ballerini, Chiara Rusconi, Carlo Visco, Luca Arcaini, Angela Fama, Roberto Marasca, Francesco Zaja, Alessia Castellino, Catello Califano, Marina Cavaliere, Guido Gini, Anna Marina Liberati, Gerardo Musuraca, Anna Lucania, Giuseppina Ricciuti, Lisa Argnani, Pier Luigi Zinzani
Journal: Blood (2015)
SIG-02. RATIONAL TARGETING OF PRO-INVASIVE FGFR SIGNALING IN MEDULLOBLASTOMA
Authors: Karthiga Santhana Kumar, Cyrill Brunner, Dominique Bruns, Ryan Byrne, Gisbert Schneider, Matthias Schuster, Oliver Zerbe, Michael Grotzer, Martin Baumgartner
Journal: Neuro-Oncology (2019)

The metastatic potential of tumors depends in part on their response to growth factors available in the tumor microenvironment. We addressed how micro-environmental cues control tumor cell invasion in pediatric medulloblastoma (MB). We show that bFGF promotes MB tumor cell invasion through FGF receptor (FGFR) in vitro and that pharmacological blockade of FGFR represses brain tissue infiltration in vivo. TGF-ß regulates pro-migratory bFGF function in a context-dependent manner. Under low bFGF, the non-canonical TGF-ß pathway causes ROCK activation and cortical translocation of ERK1/2, which antagonizes FGFR signaling by inactivating FGFR substrate 2 (FRS2), and promotes a contractile, non-motile phenotype. Under high bFGF, negative feedback regulation of FRS2 by bFGF-induced ERK1/2 causes repression of the FGFR pathway. Under these conditions, TGF-ß counters inactivation of FRS2 and restores pro-invasive signaling [1]. These findings pinpoint coincidence detection of bFGF and TGF-ß signaling by FRS2 as a mechanism that controls tumor cell invasion and identified targeting of FRS2 as a rational strategy to abrogate aberrant FGFR signaling independent of kinase inhibition. Using computer-assisted compound discovery, we screened chemical libraries for potential small molecule inhibitors of the interaction between FGFR and FRS2. Using functional testing, we selected potential hits that block invasion comparable to current small molecule FGFR kinase inhibitors and that bind FRS2 in the relevant domain. Thus, our study provides first evidence of rationally discovered, precisely acting small molecule interaction inhibitors with the potential to effectively target pro-invasive signaling in MB and other FGFR-driven cancers. 1. Santhana Kumar K et al. Cell Rep. 2018; 23: 3798–812
Mechanical Skin Injury Promotes Food Anaphylaxis by Driving Intestinal Mast Cell Expansion
Authors: Juan-Manuel Leyva-Castillo, Claire Galand, Christy Kam, Oliver Burton, Michael Gurish, Melissa A. Musser, Jeffrey D. Goldsmith, Elizabeth Hait, Samuel Nurko, Frank Brombacher, Chen Dong, Fred D. Finkelman, Richard T. Lee, Steven Ziegler, Isaac Chiu, K. Frank Austen, Raif S. Geha
Journal: Immunity (2019)
Novel therapeutic approach with <scp>PAC</scp> ‐14028 cream, a <scp>TRPV</scp> 1 antagonist, for patients with mild‐to‐moderate atopic dermatitis
Authors: P.I. Song, C.A. Armstrong
Journal: British Journal of Dermatology (2019)

Linked Article: Lee et al. Br J Dermatol 2019; 180: 1030‐1038.
Branched-chain amino acids impact health and lifespan indirectly via amino acid balance and appetite control
Authors: Samantha M. Solon-Biet, Victoria C. Cogger, Tamara Pulpitel, Devin Wahl, Ximonie Clark, Elena E. Bagley, Gabrielle C. Gregoriou, Alistair M. Senior, Qiao-Ping Wang, Amanda E. Brandon, Ruth Perks, John O’Sullivan, Yen Chin Koay, Kim Bell-Anderson, Melkam Kebede, Belinda Yau, Clare Atkinson, Gunbjorg Svineng, Tim Dodgson, Jibran A. Wali, Matthew D. W. Piper, Paula Juricic, Linda Partridge, Adam J. Rose, David Raubenheimer, Gregory J. Cooney, David G. Le Couteur, Stephen J. Simpson
Journal: Nature Metabolism (2019)
Abstract 17242: Paradoxical Impact of Decreased Low-Density Lipoprotein Cholesterol Level at Baseline on Long-Term Prognosis in Patients With Acute Coronary Syndrome
Authors: Takuya Nakahashi, Hayato Tada, Kenji Sakata, Hidenobu Terai, Yuki Horita, Masatoshi Ikeda, Masanobu Namura, Masayuki Takamura, Masa-aki Kawashiri, Masakazu Yamagishi
Journal: Circulation (2017)

Introduction: Although statin thetapy is beneficial in the setting of acute coronary syndrome (ACS), a substantial proportion of patients with ACS still do not receive the guideline-recommended lip...
Broad-spectrum antibiotic use and poor outcomes in community-onset pneumonia: a cohort study
Authors: Brandon J. Webb, Jeff Sorensen, Al Jephson, Ian Mecham, Nathan C. Dean
Journal: European Respiratory Journal (2019)

Question Is broad-spectrum antibiotic use associated with poor outcomes in community-onset pneumonia after adjusting for confounders? Methods We performed a retrospective, observational cohort study of 1995 adults with pneumonia admitted from four US hospital emergency departments. We used multivariable regressions to investigate the effect of broad-spectrum antibiotics on 30-day mortality, length of stay, cost and Clostridioides difficile infection (CDI). To address indication bias, we developed a propensity score using multilevel (individual provider) generalised linear mixed models to perform inverse-probability of treatment weighting (IPTW) to estimate the average treatment effect in the treated. We also manually reviewed a sample of mortality cases for antibiotic-associated adverse events. Results 39.7% of patients received broad-spectrum antibiotics, but drug-resistant pathogens were recovered in only 3%. Broad-spectrum antibiotics were associated with increased mortality in both the unweighted multivariable model (OR 3.8, 95% CI 2.5–5.9; p&lt;0.001) and IPTW analysis (OR 4.6, 95% CI 2.9–7.5; p&lt;0.001). Broad-spectrum antibiotic use by either analysis was also associated with longer hospital stay, greater cost and increased CDI. Healthcare-associated pneumonia was not associated with mortality independent of broad-spectrum antibiotic use. In manual review we identified antibiotic-associated events in 17.5% of mortality cases. Conclusion Broad-spectrum antibiotics appear to be associated with increased mortality and other poor outcomes in community-onset pneumonia.
The impact of carbapenemase-producing Enterobacteriaceae colonization on infection risk after liver transplantation: a prospective observational cohort study
Authors: M. Giannella, M. Bartoletti, C. Campoli, M. Rinaldi, S. Coladonato, R. Pascale, S. Tedeschi, S. Ambretti, F. Cristini, F. Tumietto, A. Siniscalchi, V. Bertuzzo, M.C. Morelli, M. Cescon, A.D. Pinna, R. Lewis, P. Viale
Journal: Clinical Microbiology and Infection (2019)
Use of Platelet-Rich Plasma Injection for Rejuvenation of Photoaged Facial Skin?
Authors: Miloš D. Pavlovic, Michael D. Loubser
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
FRI0053 Steroids restore the impaired ceruloplamin ferroxidase activity in synovial fluid of rheumatoid arthritis
Authors: V Livshitz, AM Nahir
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Ceruloplasmin (CP) is an acute phase reactant with significant antioxidative activity. In rheumatoid arthritis (RA), joint destruction continues in spite of high levels of CP in the synovial fluid (SF). The antioxidative activity of CP correlates with its ferroxidase I activity (FerrI). The biology role of the recently discovered ferroxidase II (FerrII) is unknown. <h3>Objectives</h3> The present study was aimed to find the effect of drug therapy on CP levels and CP ferroxidase activity in RA SF and to compare it to SF nitrite levels, which indicate the degree of the inflammatory process. <h3>Methods</h3> SF was collected from 75 RA patients who were: w/o drug therapy (UT). with NSAIDs and disease modifying drugs (DMD), mainly MTX who had no steroid in the last 3 months (NST). with low dose steroids (=/ &lt; 10 mg Prednisone) + DMD ST). SF of osteoarthritic (OA) patients served as control. For CP levels Ravin’s method was used.<sup>1</sup> For CP ferroxidase activity Johnson’s method was used.<sup>2</sup> For FerrII activity Johnson’s method in the presence of sodium azide. FerrI activity was calculated: Total-FerrII. For nitrite levels Ding’s method was used.<sup>3</sup> <h3>Results</h3> Inspite of drug therapy and nitrite level similar to OA, CP and total ferroxidase activity remained high in all RA groups. FerrI/FerrII ratio was significantly abnrmal in RA without steroids. Low dose steroids restored FerrI/FerrII ratio to levels seen in OA. <h3>Conclusion</h3> Low dose steroid therapy in RA did not reduce SF ceruloplasmin concentration, but restored FerrI/FerrII ratio to normal levels. <h3>References</h3> Ravin HA. J Lab Clin Med. 1961;58:161–8 Johnson DA, <i>et al</i>. Clin Chem. 1967;13:142–9 Ding AH, <i>et al</i>. J Immunol. 1998;141:2407–13