tbuckley/cabot-search huggingface dataset:
3 Platelet rich plasma for acute achilles tendon rupture: a double-blind, multicentre, randomised, placebo-controlled trial
Authors: DJ Keene, J Alsousou, P Harrison, P Hulley, S Wagland, MM Schlüssel, S Dutton, SE Lamb, K Willett
Journal: British Journal of Sports Medicine (2019)

Aim Slow recovery and disability after Achilles tendon rupture are major challenges. Platelet Rich Plasma (PRP) is an autologous supraphysiological concentration of platelets from whole blood that has demonstrated positive cellular and physiological effects on healing in the laboratory and is widely used in musculoskeletal treatments. However, evidence from adequately powered, robust clinical trials is lacking. We aimed to determine the clinical efficacy of PRP for treatment of acute Achilles tendon rupture. Methods 230 adults starting Achilles rupture non-surgical management within 12 days of injury were randomised to PRP injection or dry needle insertion to the rupture gap, under local anaesthetic. Participants were blinded to study treatment and received standardised rehabilitation. Blinded outcome assessments were at 4, 7, 13, and 24 weeks. The primary outcome was muscle-tendon function assessed by work performed during the heel-rise endurance test (HRET), measured with the Limb Symmetry Index (LSI) (0–100%; 100% denotes full recovery) at 24 weeks. Secondary outcomes were the Achilles Tendon Rupture Score (ATRS), quality of life (SF-12), pain and goal attainment. The trial was prospectively registered. Results Of 230 participants, 114 were allocated to PRP injection (103 received PRP), 116 were allocated to and received placebo. At 24 weeks, 201/230 (87%) completed the HRET and 214/230 (93%) completed patient reported outcomes. Participant characteristics between the groups were similar. There was no difference between groups at 24 weeks in LSI (mean difference = -4.373; 95% CI −11.217 to 2.471; p=0.195). There were no differences in the secondary outcomes and adverse event rates. Conclusion This trial design and standardised PRP preparation secure the first robust clinical trial evidence for PRP in managing Achilles tendon rupture, and suggest that PRP offers no patient benefit. The use of PRP in soft tissue injuries must be questionable unless supported by equally robust evidence indicating positive outcomes.
AB0077 SERUM IL17 CORRELATED WITH INFLAMMATORY CHANGES BUT NOT WITH BONY CHANGES IN BOTH HAND OSTEOARTHRITIS AND RHEUMATOID ARTHRITIS
Authors: Amany Ebaid, Mohammed A. Mortada, Essam Atwa, Noha M. Hammad
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> previous studies showed that serum IL17 is correlated with disease activity in both osteoarthritis and rheumatoid arthritis which may have therapeutic reflections (1,2). Taking in consideration that OA has different pathogenesis and presentations in comparison with RA; it is not known what the source of high serum level of IL17 in both diseases is? <h3>Objectives</h3> To evaluate the association of IL17 serum level with musculoskeletal ultrasound (MSK US) findings and clinical disease activity in Rheumatoid Arthritis (RA) and hand Osteoarthritis (OA) patients. <h3>Methods</h3> It is a randomized controlled clinical trial, which was done in the period between June 2017 and June 2018. The total number of the included subjects was 120 in 3 equal groups (RA, OA and control). All subject was subjected to serum IL17 level measurement. MSK US (of both wrists, MCPs, PIPs and DIPs) was done to all patients in RA and OA groups to. Disease activity was measured by disease activity score (DAS28) for RA patients. Visual analogue scale for pain (VAS) was obtained from patients in RA and OA groups. Functional assessment was done using health assessment questionnaire (HAQ) for RA patients and the Australian/Canadian (AUSCAN) Osteoarthritis Hand Index for OA patients <h3>Results</h3> Serum levels of IL17 were significantly higher (p&lt;0.0001) in both RA group and OA (141.37±51.09 and 151.69±23.13) group in comparison to control group (32.46±20.71). The serum level of IL17 was correlated with disease activity parameters (DAS28 &amp; VAS for RA and VAS for OA) both RA and OA groups. As regards ultrasonographic findings, serum IL17 levels were correlated with the presence of synovitis in both RA and OA groups. Ultrasonographic detected bony changes (erosions and osteophytes) were not correlated with serum level of IL17 in neither RA nor OA group. As regards functional assessment, serum level of IL17 was correlated with HAQ in RA group but not correlated with AUSCAN in OA group. <h3>Conclusion</h3> Serum level of IL17 was correlated with inflammatory changes detected by US and not correlated with bonny changes (erosions and osteophytes). According to the results of this study, the inflammatory process is the source of increased level of IL17in OA and RA. <h3>References</h3> [1] PLoS One. 2017; 12(6): e0178879. [2] Ther Adv Musculoskelet Dis. 2013Apr; 5(2): 77–94. <h3>Disclosure of Interests</h3> None declared
Pro-Angiogenic Macrophage Phenotype to Promote Myocardial Repair
Authors: Bartolo Ferraro, Giovanna Leoni, Rabea Hinkel, Steffen Ormanns, Nicole Paulin, Almudena Ortega-Gomez, Joana R. Viola, Renske de Jong, Dario Bongiovanni, Tarik Bozoglu, Sanne L. Maas, Michele D’Amico, Thorsten Kessler, Tanja Zeller, Michael Hristov, Chris Reutelingsperger, Hendrik B. Sager, Yvonne Döring, Matthias Nahrendorf, Christian Kupatt, Oliver Soehnlein
Journal: Journal of the American College of Cardiology (2019)

Heart failure following myocardial infarction (MI) remains one of the major causes of death worldwide, and its treatment is a crucial challenge of cardiovascular medicine. An attractive therapeutic strategy is to stimulate endogenous mechanisms of myocardial regeneration. This study evaluates the potential therapeutic treatment with annexin A1 (AnxA1) to induce cardiac repair after MI. AnxA1 knockout (AnxA1−/−) and wild-type mice underwent MI induced by ligation of the left anterior descending coronary artery. Cardiac functionality was assessed by longitudinal echocardiographic measurements. Histological, fluorescence-activated cell sorting, dot blot analysis, and in vitro/ex vivo studies were used to assess the myocardial neovascularization, macrophage content, and activity in response to AnxA1. AnxA1−/− mice showed a reduced cardiac functionality and an expansion of proinflammatory macrophages in the ischemic area. Cardiac macrophages from AnxA1−/− mice exhibited a dramatically reduced ability to release the proangiogenic mediator vascular endothelial growth factor (VEGF)–A. However, AnxA1 treatment enhanced VEGF-A release from cardiac macrophages, and its delivery in vivo markedly improved cardiac performance. The positive effect of AnxA1 treatment on cardiac performance was abolished in wild-type mice transplanted with bone marrow derived from Cx3cr1creERT2Vegfflox/flox or in mice depleted of macrophages. Similarly, cardioprotective effects of AnxA1 were obtained in pigs in which full-length AnxA1 was overexpressed by use of a cardiotropic adeno-associated virus. AnxA1 has a direct action on cardiac macrophage polarization toward a pro-angiogenic, reparative phenotype. AnxA1 stimulated cardiac macrophages to release high amounts of VEGF-A, thus inducing neovascularization and cardiac repair.
Abstract P298: Light-to-Moderate Alcohol Consumption and Risk of Abdominal Aortic Aneurysm in the Physicians’ Health Study
Authors: Rajat Singh, Jiaying Chen, Lu Wang, Howard D Sesso, John M Gaziano, Luc Djoussé
Journal: Circulation (2018)

Background: Abdominal aortic aneurysm (AAA) is an increasingly recognized cause of morbidity and mortality in the aging US population. While moderate alcohol consumption has been shown to be associated with a lower risk of atherosclerotic macrovascular disease, its relationship with AAA remains inconsistent in previous studies. We therefore sought to elucidate the relationship between alcohol consumption and risk of AAA in a prospective cohort of middle-aged and older men. Methods: Our study included 21,842 male physicians (mean age: 53.7 years) in the Physicians’ Health Study I who reported no history of AAA at baseline. Self-reported information on alcohol consumption and known AAA risk factors including body mass index (BMI), smoking and exercise was obtained on baseline questionnaires. Incidence of clinically diagnosed AAA was assessed via self-reported information on annual questionnaires and validated successfully in a subsample. Cox regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of AAA in each category of alcohol intake. Cubic spline regression was used to assess non-linear trend. Results: During an average follow-up of 23.0 years, 655 cases of newly diagnosed AAA were reported. Compared with men reporting less than one alcoholic drink (combined beer, wine, and liquor) per month, the HR [95% CI] of incident AAA after adjustment for age, BMI, smoking, and exercise was 0.69 [0.50 - 0.95] with one to three drinks per month, 0.80 [0.60 - 1.08] with one drink per week, 0.75 [0.58 - 0.97] with two to four drinks per week, 0.67 [0.49 - 0.90] with five to six drinks per week, 0.77 [0.61 - 0.99] with one drink per day, and 0.73 [0.47 - 1.13] with two or more drinks per day (P, non-linear trend=0.17). Conclusions: In this large cohort of middle-aged and older male physicians, light-to-moderate alcohol consumption was associated with a lower risk of clinically diagnosed AAA.
Utility of Multimodality Intravascular Imaging and the Local Hemodynamic Forces to Predict Atherosclerotic Disease Progression
Authors: Christos V. Bourantas, Lorenz Räber, Antonis Sakellarios, Yashusi Ueki, Thomas Zanchin, Konstantinos C. Koskinas, Kyohei Yamaji, Masanori Taniwaki, Dik Heg, Maria D. Radu, Michail I. Papafaklis, Fanis Kalatzis, Katerina K. Naka, Dimitrios I. Fotiadis, Anthony Mathur, Patrick W. Serruys, Lampros K. Michalis, Hector M. Garcia-Garcia, Alexios Karagiannis, Stephan Windecker
Journal: JACC. Cardiovascular imaging (2019)
Abstract 16731: Megalin Inhibition Regulates Angiotensinogen and Angiotensin II in Mice
Authors: Hong Lu, Deborah Howatt, Anju Balakrishnan, Jing Xiao, Dudley Strickland, Craig Vander Kooi, Adam Mullick, Mark Graham, A.H. Jan Danser, Alan Daugherty
Journal: Circulation (2016)

Objective: Angiotensinogen (AGT) is the unique precursor for generation of angiotensin II (AngII). Megalin interacts with both AGT and AngII in the kidneys. The purpose of this study was to determi...
PS1286 INVASIVE YEAST INFECTIONS IN HEMATOLOGICAL PATIENTS AFTER HEMATOPOIETIC STEM CELL TRANSPLANTATION
Authors: M. Popova, Y. Rogacheva, A. Volkova, I. Markova, A. Frolova, A. Shvetcov, I. Nikolaev, O. Goloshchapov, T. Bykova, O. Paina, A. Gevorgian, E. Darskaya, M. Vladovskaya, S. Bondarenko, I. Moiseev, V. Baykov, L. Zubarovskaya, N. Klimko, B. Afanasyev
Journal: HemaSphere (2019)

Background: Invasive yeast infection is rare invasive fungal disease but associated with high mortality rate in hematological patients. Data on Invasive yeast infection in hematopoietic stem cell transplantation (HSCT) recipients are limited. Aims: The aim of our study was to estimate epidemiology of invasive yeast infections in large HSCT recipients’ cohort for the 10‐year period transplant activity in CIC725. Methods: Between 2008 and 2017 2430 stem cell transplantation have been performed in CIC 725: 1647 allogeneic HSCT and 783 autologous HSCT. A retrospective study included 30 cases of invasive yeast infections in patients with hematological malignances and non‐malignant hematological diseases after HSCT. EORTC/MSG 2008 criteria were used for the diagnosis of proven yeast infections as well as to evaluate response to therapy. Results: Incidence of invasive yeast infections for the 10‐year period of high transplant activity was 1,2%: 1,4% in allo‐HSCT recipients (n = 23), 0,9% – auto‐HSCT (n = 7) predominantly in patients with acute leukemia – 67% (n = 20). The median age was 10 y.o. (range, 1 month‐59 years). In study population allo‐HSCT from unrelated donor was performed in 50% (n = 15), haplo‐HSCT in 27% (n = 8) and auto‐HSCT in 23% (n = 7). In study cohort 30% of patients had no complete remission at the moment of HSCT. As a primary antifungal prophylaxis was used: fluconazole – 37% (n = 11), echinocandins – 13% (n = 4), without prophylaxis – 23% (n = 7); as a secondary prophylaxis – voriconazole in 27% (n = 8). The median day of onset of invasive yeast infections after allo‐HSCT was 109 days (3–1337), auto‐HSCT – 20 days (8–33). The etiology of invasive yeast infections was: Candida spp. – 87% (n = 26), Malassezia furfur – 7% (n = 2), Trichosporon asahii – 3% (n = 1), Cryptococcus spp. – 3% (n = 1). Febrile fever was the main clinical symptom and septic syndrome developed in 60% of cases. OS at 30 days from diagnosis of invasive yeast infection was 63%. The central venous catheter removal was the only factor significantly improved OS at 30 days after invasive yeast infection diagnosis (91% vs 17%, p = 0,001). Summary/Conclusion: Incidence of invasive yeast infections for the 10 years of observation was 1,2%: 1,4% in allo‐HSCT recipients, 0,9% – auto‐HSCT. The main etiology was Candida spp. (87%). Overall survival at 30 days from the diagnosis of invasive yeast infections was 60%. Removing of central venous catheter improved overall survival in hematological patients after HSCT with invasive yeast infections.
Shining a Light on Industry Payments to Health Care Professionals Who Are Not Physicians
Authors: Colette DeJong, Robert Steinbrook
Journal: JAMA Internal Medicine (2019)

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AB0465 EFFICACY AND SAFETY OF IGURATIMOD IN PATIENTS WITH PRIMARY SJOGREN SYNDROME: A FOLLOW-UP STUDY
Authors: Hui Gao, Xiao-Ying Zhang, Xue-Wu Zhang, LI Zhanguo
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background:</h3> Primary Sjogren syndrome (pSS) is a chronic autoimmune disorder affecting 0.2–3% of the population. However, there are currently no effective systemic therapies. Anti-Ro, anti-La and rheumatoid factor(RF) as well as hyper γ-globulinaemia indicate a degree of B cell hyperactivity. In the recent ten years, iguratimod (T-614) has been used to treat RA as a novel immunomodulatory, which functions by suppressing the production of some inflammatory cytokines, as well as reducing immunoglobulin production by acting directly on human B lymphocytes without affecting B lymphocyte proliferation. <h3>Objectives:</h3> We evaluated the effectiveness and safety of iguratimod on pSS patients in this follow up study. <h3>Methods:</h3> A total of 21 pSS patients without severe systemic damage needing corticosteroid were recruited to receive iguratimod 25mg Bid for 12 weeks. <h3>Results:</h3> Among them, 1 patient and 2 patients withdrew because of kidney dysfunction and ineffectiveness. For those 18 patients who finished the follow up, 94.4% were females and average age were 46.5±13.8 year-old with median disease duration of 22.0 (9.8, 58.5) months. Compared with baseline, ESSDAI score, hyperglobulinaemia and ESR was significant decreased after iguratimod treatment (Table). Two of the 18 patients presented with decreased white blood cell count. This side effect ameliorated in one patient after tapering the dose to 25mg Qd and in another patient after 2 weeks without any intervention. <h3>Conclusion:</h3> This is the first follow study of iguratimod in pSS to show benefit with good tolerance. <h3>References</h3> [1] Saraux, A., et al. (2016). "Treatment of primary Sjogren syndrome." Nat Rev Rheumatol 12(8): 456-471. [2] Li, J., et al. (2013). "Efficacy and safety of iguratimod for the treatment of rheumatoid arthritis." Clin Dev Immunol 2013: 310628. [3] Ramos-Casals, M., et al. (2010). "Treatment of primary Sjogren syndrome: a systematic review." JAMA 304(4): 452-460. <h3>Disclosure of Interests:</h3> Hui Gao Grant/research support from: This work was supported by grant from PANDA (Z-2014-06-2-1637)., Xiao-ying Zhang: None declared, Xue-wu Zhang: None declared, Zhanguo Li: None declared
PB1853 IMMUNOREGULATORY CYTOKINES (IL1β‐3954 AND IFNγ‐874) GENE POLYMORPHISMS IN NORTH INDIAN PATIENTS AFFECTED BY ACQUIRED APLASTIC ANEMIA.
Authors: A. Tripathi, S. Shukla
Journal: HemaSphere (2019)

Background: The etiopathogenesis of Acquired aplastic anemia is not clear. However immune mediated mechanisms are implicated in the genesis of this disease. Aims: The purpose of the study was to evaluate the polymorphisms in cytokine ( IL1β‐3954 and IFN‐γ 874 ) genes in patients with acquired Aplastic Anemia (AA). Methods: In this observational case‐control study, 120 cases of AA &amp; 120 healthy controls were taken under the standard criteria of Camitta's et al for AA. Genotyping for IL1β‐3954 and IFN‐γ 874 was performed using polymerase chain reaction and restriction fragment length polymorphism (PCR‐RFLP). Peripheral venous blood was collected in EDTA vial from all participants and DNA was extracted. Primer sequences of IL1β‐3954 and IFNγ‐ 874 genes were used under specific PCR conditions. PCR products were then digested with restriction enzymes at 37 °C for overnight. The digested products were run for gel electrophoresis and gel images were taken using the gel doc. Results: The frequency of homozygous (TT) variant genotypes of IL‐1β‐3954 was significantly associated with the higher susceptibility of developing AA when compared with the healthy controls (OR = 2.35, 95% CI = 1.10‐5.00, p = 0.0383). The mutant allele frequency (T) of IFN‐γ 874 showed a significant association with the lower susceptibility of developing AA when compared with the healthy controls (OR = 5.89, 95% CI = 3.97‐8.74, p = 0.0001). Summary/Conclusion: These findings suggest that IL‐1β‐3954 and IFN‐γ 874 gene polymorphisms may be implicated in the pathophysiology of Alastic Anemia.
PS1290 HEPARIN‐ANALOGUE SEVUPARIN INHIBITS STREPTOCOCCUS‐INDUCED VASCULAR HYPERPERMEABILITY THROUGH NEUTRALIZING NEUTROPHIL‐DERIVED PROTEINS
Authors: M. Wahlgren, J. Rasmuson, E. Kenne, O. Soehnlein, L. Lindbom
Journal: HemaSphere (2019)

Background: Acute lung injury (ALI) and respiratory distress can develop as a consequence of sepsis with pathogens such as Group A streptococcus (GAS) including S. pyogenes . In the pathogenesis of sepsis‐associated ALI, plasma exudation and leukocyte accumulation in the lungs are central events, and endothelial barrier disruption brought on by degranulation of neutrophil‐derived proteins is considered a causative factor. Heparin and heparin derivatives have been suggested as novel therapeutics in sepsis on the basis of their pleiotropic anti‐inflammatory effects. Aims: Here, we study wheter sevuparin, a heparinoid wihich lacks anticoagulant activity, affects neutrophil‐induced lung plasma leakage. Methods: A murine model of systemic inflammation evoked by heat‐killed GAS and furthermore, we utilized human neutrophils and endothelial cell monolayers Results: We demonstrate that sevuparin inhibits hkGAS‐induced endothelial barrier disruption by neutralizing the activity of neutrophil‐derived proteins. By mass spectrometry of neutrophil secretion we identify candidate proteins, including serprocidins, S100 proteins and histone H4, that interact with sevuparin and that are responsible for the disruptive effect on endothelial integrity. Summary/Conclusion: Collectively, our results corroborate the role of neutrophil‐derived proteins in vascular hyperpermeability caused by Group A streptococci, and suggest sevuparin as a potential therapeutic in acute neutrophilic inflammation.
Killer Meiotic Drive and Dynamic Evolution of the wtf Gene Family
Authors: Michael T Eickbush, Janet M Young, Sarah E Zanders
Journal: Molecular Biology and Evolution (2019)

Natural selection works best when the two alleles in a diploid organism are transmitted to offspring at equal frequencies. Despite this, selfish loci known as meiotic drivers that bias their own transmission into gametes are found throughout eukaryotes. Drive is thought to be a powerful evolutionary force, but empirical evolutionary analyses of drive systems are limited by low numbers of identified meiotic drive genes. Here, we analyze the evolution of the wtf gene family of Schizosaccharomyces pombe that contains both killer meiotic drive genes and suppressors of drive. We completed assemblies of all wtf genes for two S. pombe isolates, as well as a subset of wtf genes from over 50 isolates. We find that wtf copy number can vary greatly between isolates and that amino acid substitutions, expansions and contractions of DNA sequence repeats, and nonallelic gene conversion between family members all contribute to dynamic wtf gene evolution. This work demonstrates the power of meiotic drive to foster rapid evolution and identifies a recombination mechanism through which transposons can indirectly mobilize meiotic drivers.