tbuckley/cabot-search huggingface dataset:
OP0101 Comparison of selected disease activity markers in systemic lupus erythematosus
Authors: P Horák, V Ščudla, Z Heřmanová, L Faltýnek, Z Pospíšil, M Budíková
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Systemic lupus erythematosus (SLE) is an autoimmune disorder, which affects multiple organ systems and which aetiology still remains unknown. The newer markers of the disease activity based on the phenomenon of autoantibody formation (anti-nucleosome antibodies), endothelial cell activation or damage (sVCAM-1, sICAM-1, thrombomodulin), activation of T or B cells (the variety of cytokines or their receptors), macrophage activation (neopterin), apoptosis (fas ligand, bcl-2 expression), complement impairment (C1q, complement split products) are lacking a widely accepted consensus on their utility. <h3>Objectives</h3> The objectives of this study was to assess the utility of measurement of thrombomodulin, anti-nucleosome antibodies, sVCAM-1, sICAM-1, neopterin, fas ligand, IL-10, sIL-2R in patients with SLE and to compare them to traditional markers of SLE activity (anti-dsDNA antibodies, C3, C4), ECLAM index of disease activity and to each other. <h3>Methods</h3> The measurement was done during six months period in three consecutive time points in each proband of the 52 patients with SLE. Anti-dsDNA antibodies, thrombomodulin, anti-nucleosome antibodies, sVCAM-1, sICAM-1, neopterin, fas ligand, IL-10, sIL-2R were tested by ELISA methods, C3, C4 components of complement by nefelometry. Pearson correlation test and ANOVA test were used for statistical evaluation of results. <h3>Results</h3> Fas ligand and IL-10 do not correlate significantly with ECLAM index (p &gt; 0.05). The rest of markers shows significant correlation with the disease activity index (p &lt; 0.05). Differences in plasma levels and fluctuation depending on the changes in disease activity index among the subgroups with stable, rising and dicreasing disease activity index are significant in the case of thrombomodulin and anti-dsDNA antibodies (ANOVA p &lt; 0.05). Solubile VCAM-1, s-ICAM-1, sIL-2R, neopterin correlate with ECLAM index (p &lt; 0.05), but their levels do not differ significantly between the subgroups (ANOVA p &gt; 0.05). Levels of anti-nucleosome antibodies correlate with ECLAM index and they are positive also in 21 sera with negative anti-dsDNA titer, but their levels do not differ significantly between the subgroups (ANOVA p &gt; 0.05). <h3>Conclusion</h3> Thrombomodulin and anti-dsDNA antibodies reflect in the best way the changing trend in disease activity. Anti-nucleosome antibody seems to be a promising a marker useful in early diagnosis. Solubile VCAM-1, sICAM-1, neopterin and sIL-2R are interesting molecules playing role in the disease pathogenesis but their practical utility stayes limited. The financial support by IGA ÈR NK 4616–3 OK 10
TBCRC 030: a phase II study of preoperative cisplatin versus paclitaxel in triple-negative breast cancer: evaluating the homologous recombination deficiency (HRD) biomarker
Authors: E.L. Mayer, V. Abramson, R. Jankowitz, C. Falkson, P.K. Marcom, T. Traina, L. Carey, M. Rimawi, J. Specht, K. Miller, V. Stearns, N. Tung, C. Perou, A.L. Richardson, K. Componeschi, L. Trippa, Z. Tan-Wasielewski, K. Timms, I. Krop, A.C. Wolff, E.P. Winer
Journal: Annals of Oncology (2020)
Development of a two-part biomaterial adhesive strategy for annulus fibrosus repair and ex vivo evaluation of implant herniation risk
Authors: Tyler J. DiStefano, Jennifer O. Shmukler, George Danias, Theodor Di Pauli von Treuheim, Warren W. Hom, David A. Goldberg, Damien M. Laudier, Philip R. Nasser, Andrew C. Hecht, Steven B. Nicoll, James C. Iatridis
Journal: Biomaterials (2020)
Antimicrobial resistance in enteric bacteria: current state and next-generation solutions
Authors: M. J. Wallace, S. R. S. Fishbein, G. Dantas
Journal: Gut Microbes (2020)

Antimicrobial resistance is one of the largest threats to global health and imposes substantial burdens in terms of morbidity, mortality, and economic costs. The gut is a key conduit for the genesis and spread of antimicrobial resistance in enteric bacterial pathogens. Distinct bacterial species that cause enteric disease can exist as invasive enteropathogens that immediately evoke gastrointestinal distress, or pathobionts that can arise from established bacterial commensals to inflict dysbiosis and disease. Furthermore, various environmental reservoirs and stressors facilitate the evolution and transmission of resistance. In this review, we present a comprehensive discussion on circulating resistance profiles and gene mobilization strategies of the most problematic species of enteric bacterial pathogens. Importantly, we present emerging approaches toward surveillance of pathogens and their resistance elements as well as promising treatment strategies that can circumvent common resistance mechanisms.
Perturbation of the circadian clock and pathogenesis of NAFLD
Authors: Atish Mukherji, Mayssa Dachraoui, Thomas F. Baumert
Journal: Metabolism (2020)

All living organisms including humans, experience changes in the light exposure generated by the Earth's rotation. In anticipation of this unavoidable geo-physical variability, and to generate an appropriate biochemical response, species of many phyla, including mammals have evolved a nearly 24-hour endogenous timing device known as the circadian clock (CC), which is self-sustained, cell autonomous and is present in every cell type. At the heart of the 'clock' functioning resides the CC-oscillator, an elegantly designed transcriptional-translational feedback system. Notably, the core components of the CC-oscillator not only drive daily rhythmicity of their own synthesis, but also generate circadian phase-specific variability in the expression levels of thousands of target genes through transcriptional, post-transcriptional and post-translational mechanisms. Thereby, this 'clock'-system provides proper chronological coordination in the functioning of cells, tissues and organs. The CC governs many physiologically critical functions. Among these functions, the key role of the CC in maintaining metabolic homeostasis deserves special emphasis. Indeed, the several features of the modern lifestyle (e.g. travel-induced jet lag, rotating shift work, energy-dense food) which, force disruption of circadian rhythms have recently emerged as a major driver to global health problems like obesity, cardiovascular disease and metabolic liver disease such as non-alcoholic fatty liver disease (NAFLD). Here we review, the CC-dependent pathways in different tissues which play critical roles in mediating several critical metabolic functions under physiological conditions and discuss their impact for the development of metabolic disease with a focus on the liver.
Trends in Intensive Care for Patients with COVID-19 in England, Wales, and Northern Ireland
Authors: James C. Doidge, Doug W. Gould, Paloma Ferrando-Vivas, Paul R. Mouncey, Karen Thomas, Manu Shankar-Hari, David A. Harrison, Kathryn M. Rowan
Journal: American Journal of Respiratory and Critical Care Medicine (2020)

Rationale: By describing trends in intensive care for patients with coronavirus disease (COVID-19) we aim to support clinical learning, service planning, and hypothesis generation.Objectives: To describe variation in ICU admission rates over time and by geography during the first wave of the epidemic in England, Wales, and Northern Ireland; to describe trends in patient characteristics on admission to ICU, first-24-hours physiology in ICU, processes of care in ICU and patient outcomes; and to explore deviations in trends during the peak period.Methods: A cohort of 10,741 patients with COVID-19 in the Case Mix Program national clinical audit from February 1 to July 31, 2020, was used. Analyses were stratified by time period (prepeak, peak, and postpeak periods) and geographical region. Logistic regression was used to estimate adjusted differences in 28-day in-hospital mortality between periods.Measurements and Main Results: Admissions to ICUs peaked almost simultaneously across regions but varied 4.6-fold in magnitude. Compared with patients admitted in the prepeak period, patients admitted in the postpeak period were slightly younger but with higher degrees of dependency and comorbidity on admission to ICUs and more deranged first-24-hours physiology. Despite this, receipt of invasive ventilation and renal replacement therapy decreased, and adjusted 28-day in-hospital mortality was reduced by 11.8% (95% confidence interval, 8.7%-15.0%). Many variables exhibited u-shaped or n-shaped curves during the peak.Conclusions: The population of patients with COVID-19 admitted to ICUs, and the processes of care in ICUs, changed over the first wave of the epidemic. After adjustment for important risk factors, there was a substantial improvement in patient outcomes.
Anaphylaxis to drugs: Overcoming mast cell unresponsiveness by fake antigens
Authors: Werner J. Pichler
Journal: Allergy (2020)

Our understanding of IgE-mediated drug allergy relies on the hapten concept, which is well established in inducing adaptive reactions of the immune system to small molecules like drugs. The role of hapten-carrier adducts in re-challenge reactions leading to mast cell degranulation and anaphylaxis is unclear. Based on clinical observations, the speed of adduct formation, skin and in vitro tests to inert drug molecules, a different explanation of IgE-mediated reactions to drugs is proposed: These are (a) A natural role of reduced mast cell (MC) reactivity in developing IgE-mediated reactions to drugs. This MC unresponsiveness is antigen-specific and covers the serum drug concentrations, but allows reactivity to locally higher concentrations. (b) Some non-covalent drug-protein complexes rely on rather affine bindings and have a similar appearance as covalent hapten-protein adducts. Such drug-protein complexes represent so-called "fake antigens," as they are unable to induce immunity, but may react with and cross-link preformed drug-specific IgE. As they are formed very rapidly and in high concentrations, they may cause fulminant MC degranulation and anaphylaxis. (c) The generation of covalent hapten-protein adducts requires hours, either because the formation of covalent bonds requires time or because first a metabolic step for forming a reactive metabolite is required. This slow process of stable adduct formation has the advantage that it may give time to desensitize mast cells, even in already sensitized individuals. The consequences of this new interpretation of IgE-mediated reactions to drugs are potentially wide-reaching for IgE-mediated drug allergy but also allergy in general.
Prevalence of Chronic Disease in Laboratory-Confirmed COVID-19 Cases and U.S. Adults (2017–2018)
Authors: Michael Fang, Dan Wang, Olive Tang, Elizabeth Selvin
Journal: Diabetes Care (2020)

Chronic conditions such as diabetes have been implicated as risk factors for poor prognosis in hospitalized patients with coronavirus disease 2019 (COVID-19), the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (1–3). A 19 June 2020 report from the Centers for Disease Control and Prevention (CDC) found a significant burden of chronic conditions in reported cases of laboratory-confirmed COVID-19 (4). Most case subjects identified from the CDC COVID-19 surveillance reporting were not hospitalized. The current study compares the prevalence of comorbid conditions in the CDC report to population-representative data. Our objective was to examine the extent to which the prevalence of underlying conditions in patients with laboratory-confirmed COVID-19 exceeded what would be expected in similarly aged adults in the general U.S. population.

We estimated the prevalence of four conditions—diabetes, cardiovascular disease, chronic kidney disease, and chronic obstructive pulmonary disease (COPD)—in the general U.S. adult population (aged ≥20 years) using the most recent National Health and Nutrition Examination Survey (NHANES) cycle (2017–2018, n = 4,757). We compared these estimates to those reported among patients with laboratory-confirmed COVID-19 in the CDC’s June 2020 report.

We used definitions of comorbidities designed to most closely approximate those used in the CDC report. We defined cardiovascular disease as a self-reported history of coronary heart disease, heart failure, heart attack, stroke, or hypertension (mean blood pressure …
Optimizing the East African Community’s Medicines Regulatory Harmonization initiative in 2020–2022: A Roadmap for the Future
Authors: Mawien Arik, Emmanuel Bamenyekanye, Adam Fimbo, Joseph Kabatende, Agnes Sitta Kijo, Burhani Simai, Fred Siyoi, Samvel Azatyan, Aggrey Ambali, Emer Cooke, Jane H. Mashingia, John Patrick Mwesigye, Margareth Ndomondo-Sigonda, Hiiti Sillo, Stanley Sonoiya, Paul Tanui, Mike Ward, Thomas Delano
Journal: PLoS Medicine (2020)

The East African Community (EAC)'s Medicines Regulatory Harmonization (MRH) initiative was created to improve access to quality, safe medicines in the region by simplifying the regulatory process while maintaining a high level of rigor.Building on lessons learned since its launch in 2012, the EAC MRH
p53 and Bcl-2 expression in breast and lung carcinoma cells exposed to arsenic trioxide
Authors: Alice Walker, Jacqueline Stevens, Paul Tchounwou
Journal: Cancer Research (2007)

5352  Arsenic is a metalloid that is ubiquitous in the environment. The toxicity of arsenic depends upon its chemical form; the organic forms being usually less harmful the inorganic ones. The primary source of human exposure is through drinking water and food. p53 plays a key role in mediating cell response to various stresses, mainly by inducing or repressing a number of genes involved in cell cycle arrest, senescence, apoptosis, DNA repair, and angiogenesis. p53 exerts its anti-proliferative action by inducing reversible or irreversible (senescence) cell cycle arrest or apoptosis. It may also enhance DNA repair and inhibit angiogenesis. Bcl-2 can act as a pro or anti-apoptotic regulator that is involved in wide variety of cellular activities. The Bcl-2 gene has been implicated in several cancers such as melanoma, breast, prostate and lung. Arsenic has also shown to be cytotoxic and able to induce stress-related genes and proteins in a number of cell lines, mainly of the skin and liver. Although arsenic has been reported to cause DNA damage to liver and hematopoetic cells, its effects on breast and lung cells are not well elucidated. The primary objective of this research is to evaluate the effects of arsenic trioxide on p53 and Bcl-2 expression in breast and lung carcinoma cells. To achieve this goal, breast cancer (MCF-7) and lung cancer (A549) cells were cultured following standard protocols, and exposed to various doses (0, 2, 4, 6, 8, and 10 µg/ml) of arsenic trioxide for 48 h. Protein and western blot analyses were performed using standard protocols. The Western blot analysis revealed an up-regulation of p53 with the exposure of arsenic trioxide, showing a peak expression at 4µg/ml. Experiments on Bcl-2 expression are underway, and it is anticipated that arsenic exposure would induce a its down -regulation in arsenic-treated cells.  Keywords: Arsenic, p53 activation, Bcl-2 repression, MCF-7 and A549 cells  Acknowledgements: This research supported by a grant from NIH-RCMI grant # G12RR13459. We thank Dr. Abdul K. Mohamed, Dean Emeritus, College of Science Engineering and Technology and RCMI Program Director at Jackson State University (JSU) for his support of this research.
AB0129 Is the association sjÖgren’syndrome-spondylarthropathy fortuitous?
Authors: C Scotto di Fazano
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Secondary Sjögren’s syndrome is known to occur with rheumatoid arthritis, systemic lupus erythematosus, but apart from a few cases, has not been reported with spondylarthropathy. <h3>Objectives</h3> To determine the prevalence of Sjögren’s syndrome in spondylarthropathy patients. <h3>Methods</h3> Patients with spondylarthropathy (n = 62) with inflammatory back pain and/or peripheral arthritis were diagnosed as ankylosing spondylitis, undiferentiated spondylarthropathy, psoriatic arthritis and arthritis associated with inflammatory bowel disease. The investigation of sicca symptoms in the spondylarthropathy group and healthy controls (n = 102) was based on a valited questionnaire. Patients with spondylarthropathy with sicca symptomes and/or positive antinuclear antibodies (ANA) were investigated for Sjögren’s syndrome by minor salivary gland biopsy. In the spondylarthropathy group, the laboratory variables were: HLA B27, HLA DR, DQ, anti ENA, serology hepatitis B, C. <h3>Results</h3> In 17/62 patients (11 undifferentiated spondylarthropathy,5 ankylosing spondylitis,16 females,1 male) Sjögren’s syndrome diagnosis by the europeans criteria indicated a frequency of 27,4%. Of 62 spondylarthropathy,12 were ANA positive (19,3%), of whom 5 had Sjögren’s syndrome. ANA were detected in 8/17(47%) patients with Sjögren’s syndrome. Of 62 spondylarthropathy patients,20 had sicca symptoms (32,2%), compared to 3 of 102 (2,9%) controls. HLA B27 is positive in 12/17 patients (70,5%). The results of the study of HLA DR, DQ seem to show an high frequency of HLA DR4, and DQ3 in the association group, but the difference is not significative. <h3>Conclusion</h3> The frequency of Sjögren’s syndrome is 27,4%in the spondylarthropathy group, thus more than in controls. The association Sjögren’s syndrome and spondylarthropathy seems to be not fortuitous, and the HLA class II study seems to show a probable genetic predisposition.
Principles and innovative technologies for decrypting noncoding RNAs: from discovery and functional prediction to clinical application
Authors: Yu-Meng Sun, Yue-Qin Chen
Journal: Journal of Hematology & Oncology (2020)

Abstract Noncoding RNAs (ncRNAs) are a large segment of the transcriptome that do not have apparent protein-coding roles, but they have been verified to play important roles in diverse biological processes, including disease pathogenesis. With the development of innovative technologies, an increasing number of novel ncRNAs have been uncovered; information about their prominent tissue-specific expression patterns, various interaction networks, and subcellular locations will undoubtedly enhance our understanding of their potential functions. Here, we summarized the principles and innovative methods for identifications of novel ncRNAs that have potential functional roles in cancer biology. Moreover, this review also provides alternative ncRNA databases based on high-throughput sequencing or experimental validation, and it briefly describes the current strategy for the clinical translation of cancer-associated ncRNAs to be used in diagnosis.
Abstract 12340: Utilization and Outcomes of Catheter-directed Thrombolysis for Acute Pulmonary Embolism: A Nationwide Cohort Study
Authors: Sebastian E Beyer, Colby Shanafelt, Duane S Pinto, Jeffrey Weinstein, Herbert D Aronow, Ido Weinberg, Robert W Yeh, Eric A Secemsky, Brett Carroll
Journal: Circulation (2019)

Introduction: Catheter-directed thrombolysis (CDT) may improve short-term effectiveness and safety in selected patients with acute pulmonary embolism (PE) who have high-risk features and a treatmen...
Preparedness for Residency
Authors: Jennifer N. Choi, Dimitrios Stefanidis, Gary L. Dunnington
Journal: JAMA Surgery (2020)

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AB0030 QUANTIFICATION OF CD27+ MEMORY B-CELLS IN RHEUMATOID ARTHRITISPATIENTS TREATED WITH RITUXIMAB
Authors: Arianna Gatti, Laura Castelnovo, Paola Faggioli, Antonio Tamburello, Alfredo Maria Lurati, Antonella Laria, Bruno Brando, Antonino Mazzone
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background:</h3> Rituximab (RTX) is being increasingly used in treatment of several autoimmune diseases, including Rheumatoid Arthritis (RA).RTX induces a deep depletion of all peripheral B-Cell subsets (memory and naïve B-cells). During the B-Cell repopulation phase, occurring approximately after 3 months of RTX administration, B-precursors and naïve cells reappear.Several studies have shown that relapsing RA patients are characterized by a relative expansion of memory B cells during the B-Cell repopulation phase <h3>Objectives:</h3> The aim of this study was to quantify the memory B-Cell compartment in RA patients with different disease activity scores, evaluated by DAS28, during RTX treatment <h3>Methods:</h3> 26 RA patients under RTX treatment were studied. At the end of th treatment 8/26 showed high-to-moderate activity risk (median DAS28=4.8) and 18 low activity risk or remission (median DAS28=2.69). After a median of 3 months from last RTX infusion, B-Cell subsets (precursors, naïve, memory B cells and plasma cells) were quantified in peripheral blood by flow cytometry, using a panel of 8 markers (CD3, CD4, CD8, CD19, CD20, CD27, CD38 and CD45). B naïve cells were identified as CD19+ CD20+ CD27-, B memory cells were identified as CD19+ CD20+ CD27+, plasma cells as CD19+ CD38++ CD27++ CD20- and B precursors as CD19+ CD38++ CD20- CD27-, respectively. Percent and absolute values were calculated for each subset. In adition 10 healthy subjects were included as negative control group (NC). <h3>Results:</h3> The median percent and absolute values of B naïve cells, B memory cells and plasma cells identified in NC, non-responder RA patients with high/moderate disease activity and responder RA patients with low disease activity or in remission are reported in Table 1. The virtual absence of peripheral B-Cell was defined as &lt;0.1 B-Cell/μL. In the responder group, 5/18 cases showed absolute B-Cell levels &lt;0.1 cell/μL, while only in 1/8 of the non responder group a similar B-Cell depletion was found. The memory B-Cell% was significantly higher in non responder than in responders (p&lt;0.05); the memory B-Cell level in non responders was similar to that of the NC group. <h3>Conclusion:</h3> We used a sensitive and easily applicable flow cytometric multicolor panel that allowed the accurate and standardized identification and enumeration of peripheral blood B-Cell subsets. As reported by other studies, higher levels of memory B-Cells were found in non responder RA patients treated by RTX, approaching those of healthy individuals. <h3>References</h3> [1] Lòpez J. Clin Exp Rheumatol2018; Dec 19. Sellam J. Arthritis Rheum 2011; 63: 3692-3701.Dass S. Arthritis Rheum2008; 58: 2993-2999 <h3>Disclosure of Interests:</h3> None declared
Esophageal Stenting as Bridge Therapy to Direct Intrahepatic Portocaval Shunt for Refractory Variceal Bleeding
Authors: Kristel K. Leung, Paul D. James, Arash Jaberi, Gideon M. Hirschfield
Journal: Hepatology (2020)

Leung, Kristel K.; James, Paul D.; Jaberi, Arash; Hirschfield, Gideon M. Author Information