tbuckley/cabot-search huggingface dataset:
ACHIEVEMENT OF EUROPEAN SOCIETY OF GASTROINTESTINAL ENDOSCOPY (ESGE) PERFORMANCE MEASURES: OBSERVATIONS FROM THE EUROPEAN COLONOSCOPY QUALITY INVESTIGATION (ECQI) QUESTIONNAIRE
Authors: C Spada, A Agrawal, P Amaro, L Brink, W Fischbach, M Hünger, R Jover, U Kinnunen, A Koulaouzidis, A Ono, Á Patai, S Pecere, L Petruzziello, E Toth, B Amlani, JF Riemann
Journal: Endoscopy (2019)

To investigate the quality of colonoscopy in current clinical practice, through the use of online questionnaires, compared with recently published European Society of Gastrointestinal Endoscopy (ESGE) key performance measures.
IMMU-23. TARGETING THE CD200 CHECKPOINT TO ENHANCE IMMUNOTHERAPY FOR CNS TUMORS
Authors: Christopher Moertel, G Elizabeth Pluhar, Elisabet Ampudia-Mesias, Zhengming Xiong, Christopher A Pennell, Susan K Rathe, David A Largaespada, Michael R Olin
Journal: Neuro-Oncology (2019)

Numerous clinical trials targeting immune checkpoints have failed to enhance survival in patients with CNS tumors. We are targeting a unique checkpoint, CD200, which controls the immune system through paired inhibitory and activation receptors. The CD200 checkpoint interferes with tumor-immune interactions through secretion of CD200 from tumors inducing an immunosuppressive environment and up regulation of CD200 in tumor-associated vascular endothelial cells, creating an immunological blood brain barrier. We are targeting the activation receptor with a peptide ligand (CD200AR-L) that activates antigen-presenting cells and enhances dendritic cell maturation, resulting in antigen specific T cell cytokine production. Directing the immune system requires introduction of an antigen such as autologous or allogeneic brain tumor lysate for non-immunogenic tumors such as CNS tumors. Treatment with CD200AR-L significantly extends survival in two murine glioma models. Additionally, an ongoing pilot study treating companion dogs with high-grade glioma using a canine specific CD200 peptide ligand in combination with an autologous tumor lysate vaccine increased median survival to 330 days, compared to 194 days with lysate alone. Currently, 41% of the dogs are alive; the longest living dog is now 810 days post-surgery. 28% of dogs died of non-tumor related deaths. In contrast, 100% of the dogs in the tumor lysate-only group died of tumor recurrence. We have developed human CD200 peptide ligands that enhance cytokine secretion, dendritic cell maturation, and antigen-specific immune response in vitro. In addition, we have shown that a ligand targeting the activation receptor (CD200AR-L) results in down regulation of PD-1. We have also demonstrated that the use of a CD200AR-L resulted in a significant survival benefit in a murine breast carcinoma model. In this light, CD200AR-L may be a powerful immunotherapy platform for other solid tumors. This innovative research may provide a significant breakthrough for the field of cancer immunotherapy.
HS (反常性痤疮) 管理的 BAD 指南 2018
Authors: J.R. Ingram, F. Collier, D. Brown, T. Burton, J. Burton, M.F. Chin, N. Desai, T.E.E. Goodacre, V. Piguet, A.E. Pink, L.S. Exton, M.F. Mohd Mustapa
Journal: British Journal of Dermatology (2019)

化脓性汗腺炎是一种影响年轻人的长期皮肤病,会导致皮肤褶皱部位(例如腋窝和腹股沟)多处发生脓肿。脓肿是疼痛性的,会流浓,随疾病进展可形成永久性瘢痕。因此,它对生活质量有较大影响。每 100 个英国人中就约有 1 人患有 HS,此病倾向于在青壮年发病。英国皮肤病学会委任了一个 HS 指南开发小组,该小组由信息专家、HS 患者和看护者以及英国医生(包括皮肤科医生、皮肤科护士、整形外科医生和全科医生)组成。要求来自英国的这一小组基于对证据的系统评价提供治疗推荐意见。使用推荐意见分级评估、制订和评价 (GRADE) 系统将这些证据转化为推荐意见。通过搜索数据库鉴定出了近 3000 条证据记录。全科医生和医院诊所为 HS 管理提供的初始推荐意见包括:提供患者信息宣传册、记录基线疾病严重程度、测量疼痛和治疗(如需要)、测量生活质量、记录皮损数量和提供伤口敷料(如需要)。应筛选患者有无心血管疾病风险因素,以及有无抑郁和焦虑。如需要,还应为患者提供戒烟和体重管理转诊。推荐阶梯式的医学治疗,从口服四环素开始,之后联合克林霉素和利福平、阿维 A(男性和未孕女性)、氨苯砜,如果需要,进展到注射阿达木单抗。大范围切除和一系列闭合方法的手术治疗被放在医学治疗途径的末尾,反映了英国的当前实践和证据的相对缺乏。还纳入了未来研究的推荐意见和稽查标准。
Abstract 11577: Systemic Inflammatory Burden in Heart Failure with Preserved Ejection Fraction induced Pulmonary Hypertension Compared to Pulmonary Arterial Hypertension
Authors: Jason N Salamon, Jeremy Mazurek, Wajeeha Saeed, Ronald Zolty
Journal: Circulation (2012)

Background: High sensitivity C-reactive protein (hs-CRP) is a robust and reproducible marker of inflammation. Heart failure with preserved ejection fraction (HFpEF) is a common cause of secondary p...
Acute Intermittent Porphyria: Novel Etiologic and Pathogenic Therapies Based on RNA Transfer to the Liver
Authors: Jesus Prieto, Gloria Gonzalez‐Aseguinolaza
Journal: Hepatology (2019)

Prieto, Jesus M.D., Ph.D.1; Gonzalez‐Aseguinolaza, Gloria Ph.D.1Editor(s): Corey, Kathleen E.2; Malhi, Harmeet3 Author Information
Abstract 13917: Post-systolic Shortening in the Ischemic Myocardium is Attenuated in Multivessel Disease
Authors: Daisuke Sakurai, Toshihiko Asanuma, Kasumi Masuda, Masamichi Oka, Koichiro Kotani, Katsuji Inoue, Satoshi Nakatani
Journal: Circulation (2015)

Background: Post-systolic shortening (PSS) is myocardial shortening that occurs after end-systole and is considered as a sensitive marker of myocardial ischemia. Empirically, PSS in patients with multivessel disease is smaller than that in those with single vessel disease. Although this seems to be due to a decrease of difference in contraction between the ischemic and the surrounding myocardium, no study has elucidated it. We investigated the relationship between PSS and the difference of contraction between the ischemic and surrounding myocardium in an animal model which underwent left anterior descending coronary artery (LAD) occlusion (single vessel disease model) followed by left circumflex coronary artery (LCx) occlusion (multivessel disease model). Methods: In 7 open-chest dogs, left ventricular short-axis images (GE Vivid E9) and hemodynamic data were acquired at 3 conditions: (1) at baseline, (2) during LAD occlusion, and (3) during both LAD and LCx occlusion. Circumferential strains were analyzed in 6 segments by speckle tracking software. The amplitude of PSS (ε PSS ) and end-systolic strain (ε ES ) were measured and the difference of ε ES between a segment perfused by the LAD and the average of the other 5 segments was calculated (Δε ES ). Results: In the LAD segment, dyskinetic motion and PSS occurred during LAD occlusion but they were paradoxically attenuated during both LAD and LCx occlusion. ε PSS significantly correlated with Δε ES (r=0.95, p&lt;0.05). Although ε PSS significantly decreased during both occlusion compared to LAD occlusion, ε PSS corrected by Δε ES (ε PSS /Δε ES ) did not decrease (figure). Conclusions: PSS in the ischemic myocardium was attenuated when the surrounding myocardium also became ischemic. The difference of contraction between the ischemic and the surrounding myocardium at end-systole seems to be a determinant of the amplitude of PSS. A parameter ε PSS /Δε ES may be useful for assessing ischemia in patients with multivessel disease.
Systemic Mastocytosis with Associated Acute Myeloid Leukemia (SM-AML): a Poor-Risk Multi-Mutated Disease That Follows a Distinct Diagnostic Algorithm and Requires High-Dose Stem Cell-Targeting Therapy
Authors: Mohamad Jawhar, Sebastian Kreil, Juliana Schwaab, Khalid Shoumariyeh, Lambert L.F. Span, Stephan Fuhrmann, Nicole Naumann, Florian Nolte, Daniela Heidenreich, Nadine Z. Müller, Hans-Peter Horny, Karl Sotlar, Torsten Haferlach, Boris Kubuschok, Karsten Spiekermann, Michael Heuser, Georgia Metzgeroth, Alice Fabarius, Stefan Klein, Wolf-Karsten Hofmann, Nicholas C.P. Cross, Manja Meggendorfer, Hanneke Kluin-Nelemans, Wolfgang R. Sperr, Peter Valent, Andreas Reiter
Journal: Blood (2017)
Sirukumab and adalimumab reduce power Doppler ultrasound signal in patients with rheumatoid arthritis by 4 weeks in a phase III trial
Authors: Kristen Sweet, Bidisha Dasgupta, Dick de Vries, Ian Gourley, Benjamin Hsu, Matthew J Loza, Peter C Taylor
Journal: Annals of the Rheumatic Diseases (2019)

Clinical trials in rheumatoid arthritis (RA) involve assessment of response by endpoints including composite measures of disease activity. However, many of the components are subjective and insensitive to change and their use in phase III studies necessitates large and costly trials.

In single-centre, or two-centre RA studies, Greyscale ultrasound (GSUS) and power Doppler ultrasound (PDUS) imaging of a limited joint set is an early and reliable indicator of therapeutic response.1–3 However, use of ultrasound (US) endpoints in multicentre clinical trials presents challenges of operator-dependency and variability in image acquisition, even when using the same model and settings of US machine.

We undertook an exploratory multicentre, US substudy, nested within the SIRROUND-H trial,4 to evaluate effects of sirukumab and adalimumab on synovial thickness and vascularity by GSUS and PDUS, respectively, in 41 consenting subjects (online supplementary Table S1) at nine clinical sites. At each site, ultrasonographers blinded to treatment assessed 12 joints (10 metacarpophalangeal (MCP) joints plus wrists) at Weeks 0, 2, 4, 8 and 24. The same model LOGIQ S8 RD US …
LGG-02. A PHASE II PROSPECTIVE TRIAL OF SELUMETINIB IN CHILDREN WITH RECURRENT/PROGRESSIVE PEDIATRIC LOW-GRADE GLIOMA (PLGG) WITH A FOCUS UPON OPTIC PATHWAY/HYPOTHALAMIC TUMORS AND VISUAL ACUITY OUTCOMES: A PEDIATRIC BRAIN TUMOR CONSORTIUM (PBTC) STUDY, PBTC-029B
Authors: Jason Fangusaro, Arzu Onar-Thomas, Tina Young Poussaint, Shengjie Wu, Azra H Ligon, Neal Lindeman, Anu Banerjee, Roger J Packer, Lindsay B Kilburn, Stewart Goldman, Ian F Pollack, Regina I Jakacki, Ibrahim Qaddoumi, Paul G Fisher, Girish Dhall, Patricia Baxter, Susa G Kreissman, Clinton F Stewart, David T W Jones, Stefan M Pfister, Gilbert Vezina, Jessica S Stern, Ashok Panigrahy, Blaise V Jones, Zoltan Patay, Benita Tamrazi, Jeremy Y Jones, Sofia S Haque, David S Enterline, Soonme Cha, Michael J Fisher, Austin Doyle, Malcolm Smith, Maryam Fouladi, Ira J Dunkel
Journal: Neuro-Oncology (2019)

BACKGROUND: Pediatric low-grade glioma (pLGG) is the most common CNS tumor of childhood. Progression-free survival (PFS) is much lower than overall survival emphasizing the need for alternative treatments. In addition, many children suffer functional morbidities such as visual and motor disturbances. Recently, there has been an appropriate prioritization of functional outcomes in children with pLGG. METHODS: We present the results of a PBTC phase II trial evaluating selumetinib, (AZD6244, ARRY-142886) a MEK-1/2 inhibitor, in children with recurrent/progressive pLGG on 2 strata, including visual outcomes. RESULTS: Stratum 3 enrolled Neurofibromatosis type 1 (NF1)-associated pLGG. Ten of 25 (40%) eligible patients had partial response (PR), 14/25 (56%) had stable disease (SD) and 1/25 (4%) had progressive disease (PD); 2-year PFS was 96+4%. Ten patients with optic pathway glioma (OPG) were evaluable for visual acuity (VA) at baseline and 1 year. VA improved in 2/10 patients (20%) and was stable in 8/10 (80%). One patient (10%) had improvement in visual fields (VF) and 9 patients (90%) had stable VF. Stratum 4 included patients with non-NF1-associated recurrent/progressive hypothalamic and OPG. Five of 25 (20%) eligible patients had PR, 16/25 (64%) had SD and 4 (16%) had PD; 2-year PFS was 78+8.5%. Nineteen of 25 patients were evaluable for VA. VA improved in 4/19 patients (21%), was stable in 13/19 (68%) and worsened in 2/19 (11%). Five patients (26%) had improved VF and 14 (74%) had stable VF. The most common toxicities included grade 1/2 CPK elevation, diarrhea, hypoalbuminemia and rash. Rare grade 3 toxicities included elevated CPK, rash and paronychia. CONCLUSIONS: Selumetinib was tolerable and effective in treating children with NF1-associated and sporadic recurrent/progressive hypothalamic and OPG based upon radiographic response and PFS. Twenty-seven of 29 (93%) evaluable patients had stable or improved vision based on VA and VF testing.
Health apps don’t meet GMC advice on good practice
Authors: John Puntis
Journal: BMJ (2019)

Jackie Applebee is right to be worried about digital promotion of the inverse care law and of unintended consequences,1 including increased costs.2

Despite continuing concerns over Babylon Health’s GP at Hand, the company has been distributing a leaflet to residential addresses in London with the strapline: “Get well now.” In …
A Recurrent Activating Missense Mutation in Waldenström Macroglobulinemia Affects the DNA Binding of the ETS Transcription Factor SPI1 and Enhances Proliferation
Authors: Damien Roos-Weil, Camille Decaudin, Marine Armand, Véronique Della-Valle, M'boyba K. Diop, Hussein Ghamlouch, Virginie Ropars, Cécile Hérate, Diane Lara, Eric Durot, Rima Haddad, Elena Mylonas, Frederik Damm, Francoise Pflumio, Bilyana Stoilova, Marlen Metzner, Olivier Elemento, Philippe Dessen, Valérie Camara-Clayette, François-Loïc Cosset, Els Verhoeyen, Véronique Leblond, Vincent Ribrag, Pascale Cornillet-Lefebvre, Philippe Rameau, Nabih Azar, Frédéric Charlotte, Pierre Morel, Jean-Baptiste Charbonnier, Paresh Vyas, Thomas Mercher, Said Aoufouchi, Nathalie Droin, Christel Guillouf, Florence Nguyen-Khac, Olivier A. Bernard
Journal: Cancer Discovery (2019)

The ETS-domain transcription factors divide into subfamilies based on protein similarities, DNA-binding sequences, and interaction with cofactors. They are regulated by extracellular clues and contribute to cellular processes, including proliferation and transformation. ETS genes are targeted through genomic rearrangements in oncogenesis. The PU.1/SPI1 gene is inactivated by point mutations in human myeloid malignancies. We identified a recurrent somatic mutation (Q226E) in PU.1/SPI1 in Waldenström macroglobulinemia, a B-cell lymphoproliferative disorder. It affects the DNA-binding affinity of the protein and allows the mutant protein to more frequently bind and activate promoter regions with respect to wild-type protein. Mutant SPI1 binding at promoters activates gene sets typically promoted by other ETS factors, resulting in enhanced proliferation and decreased terminal B-cell differentiation in model cell lines and primary samples. In summary, we describe oncogenic subversion of transcription factor function through subtle alteration of DNA binding leading to cellular proliferation and differentiation arrest. SIGNIFICANCE: The demonstration that a somatic point mutation tips the balance of genome-binding pattern provides a mechanistic paradigm for how missense mutations in transcription factor genes may be oncogenic in human tumors.This article is highlighted in the In This Issue feature, p. 681.
TMOD-10. REPLICATION REPAIR DEFICIENT MOUSE MODELS PROVIDE INSIGHT ON HYPERMUTANT BRAIN TUMOURS AND COMBINATIONAL IMMUNOTHERAPY
Authors: Melissa Galati, Taylor Bridge, Sumedha Sudhaman, Dana Elshaer, Ayse Ercan, Lazar Joksimovic, Miki Gams, Karl Hodel, Tatiana Lipman, Iram Siddiqui, Richard de Borja, Victoria Forster, Alberto Martin, Eric Bouffet, Adam Shlien, Cynthia Guidos, Zachary Pursell, Cynthia Hawkins, Uri Tabori
Journal: Neuro-Oncology (2019)

Replication repair deficiency (RRD) is the leading cause of hypermutant brain tumours in children. RRD is caused by defects in one of four mismatch repair (MMR) genes—PMS2, MSH6, MLH1, and MSH2—as well as mutations in the exonuclease “proofreading” domains of either DNA polymerase ε (POLE) or δ (POLD1). Such tumours are often resistant to common therapeutic agents and animal models are needed to study RRD in vivo and test novel therapies like immune checkpoint inhibitors (ICIs). We initially engineered a Pole mutant mouse model harbouring the clinically relevant S459F mutation (PoleS459F). PoleS459F mice succumbed to various lethal cancers that mirrored the genomic landscape of POLE mutant human tumours. PoleS459F tumours were hypermutant (~170 mutations/Mb by whole exome sequencing), harboured mutational signature 10 (caused by POLE proofreading loss), and exhibited subclonal characteristics consistent with POLE-driven mutagenesis. PoleS459F tumours were not preventable by mono-ICI therapy and were exacerbated by combinational α-PD1 and α-CTLA4 therapy. To model RRD brain tumours specifically, we combined PoleS459F mice with conditional Msh2 knockout (Msh2LoxP) and Nestin-cre mice. Nestin-cre+Msh2LoxP/LoxPPoleS459F/+ mice rapidly succumbed to tumours between 8.6 and 12.4 weeks with 100% penetrance. Tumours developed in the cerebellum and histologically resembled human medulloblastoma. Importantly, tumours exhibited hallmark “ultrahypermutation” (~399 mutations/Mb) and analysis of mutational signatures revealed the presence of signature 14 (characteristic of combined MMR and POLE-proofreading loss). These tumours are transplantable and grow efficiently in syngeneic animals despite their high mutational load and presumed immunogenicity. This first mouse model of immunocompetent, hypermutant brain tumors can be used to uncover unique characteristics of RRD tumour evolution and allow for immune based therapeutic preclinical testing. Experiments to assess combinational ICIs and other therapeutic interventions will be presented.
Efficacy and Safety of Firibastat, A First-in-Class Brain Aminopeptidase A Inhibitor, in Hypertensive Overweight Patients of Multiple Ethnic Origins
Authors: Keith C. Ferdinand, Fabrice Balavoine, Bruno Besse, Henry R. Black, Stephanie Desbrandes, Howard C. Dittrich, Shawna D. Nesbitt
Journal: Circulation (2019)

Background: Despite existing therapy, successful control of hypertension in the United States is estimated at less than 50%. In blacks, hypertension occurs earlier, is more severe, controlled less often and has a higher morbidity and mortality than in whites. Blacks are also less responsive to monotherapy with angiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 blockers. Obesity, higher salt-sensitivity and low plasma renin activity are possible reasons of this poor blood pressure (BP) control, especially in blacks. The aim of the study was to assess efficacy and safety of firibastat, a first-in-class aminopeptidase A inhibitor preventing conversion of brain angiotensin-II into angiotensin-III, in BP lowering in a high-risk diverse hypertensive population. Methods: Two hundred fifty-six overweight or obese hypertensive patients, including 54% black and Hispanic individuals, were enrolled in a multicenter, open-label, phase II study. After a 2-week wash-out period, subjects received firibastat for 8 weeks (250 mg BID orally for 2 weeks, then 500 mg BID if automated office blood pressure (AOBP) &gt;140/90 mm Hg; hydrochlorothiazide 25 mg QD was added after 1 month if AOBP ≥160/110 mm Hg). The primary end point was change from baseline in systolic AOBP after 8 weeks of treatment, and secondary end points include diastolic AOBP, 24-hour mean ambulatory BP and safety. Results: Firibastat lowered systolic AOBP by 9.5 mm Hg ( P &lt;0.0001) and diastolic AOBP by 4.2 mm Hg ( P &lt;0.0001). 85% of the subjects did not receive hydrochlorothiazide and were treated with firibastat alone. Significant BP reduction was found across all subgroups regardless age, sex, body mass index, or race. Systolic AOBP decreased by 10.2 mm Hg ( P &lt;0.0001) in obese patients, by 10.5 mm Hg ( P &lt;0.0001) in blacks, and 8.9 mm Hg ( P &lt;0.0001) in nonblacks. Most frequent adverse events were headaches (4%) and skin reactions (3%). No angioedema was reported. No change in potassium, sodium, and creatinine blood level were observed. Conclusions: Our results demonstrate the efficacy of firibastat in lowering BP in a high-risk diverse population where monotherapy with angiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 blockers may be less effective and support the strategy to further investigate firibastat in subjects with difficult-to-treat or potentially resistant hypertension. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique Identifier: NCT03198793.
THER-11. BMI-1 MODULATION IMPAIRS DNA DAMAGE RESPONSE AND SENSITIZES DIPG CELLS TO IONIZING RADIATION
Authors: Shiva Senthil Kumar, Satarupa Sengupta, Marla Weetall, John Baird, Rachid Drissi
Journal: Neuro-Oncology (2019)

Diffuse intrinsic pontine glioma (DIPG) is a poor-prognosis brain tumor with no effective curative therapy. We previously identified BMI-1 as a potential therapeutic target in DIPG*. We have shown that BMI-1 is highly expressed in DIPG tumors and patient-derived cells regardless of histone subtype. In the present study, we used PTC596, a potent BMI-1 modulator recently entered into clinical trials. PTC596 treatment results in post-translational modification of BMI-1, affecting its downstream target H2AK119 mono-ubiquitination levels. BMI-1 has been shown to be one of the early proteins recruited to DNA damage sites during the process of DNA damage response (DDR). In DIPG cells treated with PTC596, we observed time and concentration dependent increase in both γH2AX phosphorylation levels and foci formation, indicating DNA double strand breaks (DSBs). Cell cycle analysis, cleaved caspase-3 and γH2AX staining showed a sequence of events leading to apoptosis of DIPG cells treated with PTC596. Moreover, the kinetics of DDR was impaired in DIPG cells treated with ionizing radiation (IR) in combination with PTC596. Both the foci formation and resolution were delayed resulting in further reduction in cell viability compared with either treatment alone. Our results suggest that PTC596-induced modulation of BMI-1 sensitizes DIPG cells to IR. This is the first report providing evidence supporting the effectiveness of IR in combination with BMI-1 modulation to treat DIPG. *Kumar, S.S. et al. BMI-1 is a Potential Therapeutic Target in Diffuse Intrinsic Pontine Glioma. Oncotarget 2017.
Non-accidental harms (‘abuse’) in athletes with impairment (‘para athletes’): a state-of-the-art review
Authors: Yetsa A Tuakli-Wosornu, Qisi Sun, Mark Gentry, Kimberly E Ona Ayala, Fiona C Doolan, Taylor D Ottesen, Blake Caldwell, Nida Naushad, Patrick Huang, Sandi Kirby
Journal: British Journal of Sports Medicine (2019)

Objective Para athletes reap significant health benefits from sport but are vulnerable to non-accidental harms. Little is known about the types and impacts of non-accidental harms Para athletes face. In this literature review, we summarise current knowledge and suggest priorities for future research related to non-accidental harms in Para athletes. Design Six electronic databases were searched between August and September 2017. 2245 articles were identified in the initial title/abstract review, and 202 records were selected for full-text review following preliminary screening. Two independent examiners evaluated each full text, and eight citations were selected based on inclusion/exclusion criteria. Data sources MEDLINE, Embase, PsycInfo, Cumulative Index to Nursing and Allied Health Literature, Scopus and Academic Search Premier. Eligibility criteria for selecting studies Inclusion criteria: (A) human participants; (B) written in English; (C) descriptive, cohort and case series, case–control, qualitative, mixed methods studies and all clinical trials; and (D) data pertain to harassment/abuse of youth, recreational, collegiate, national-level and/or elite-level athletes with a physical and/or intellectual impairment. Results Most studies focused on young, visually impaired athletes and approximately half of all studies described high rates of bullying and its social implications. One study confirmed remarkably high rates of psychological, physical and sexual harms in Para athletes, compared with able-bodied peers. Conclusions Bullying in young, visually impaired athletes is described most commonly in the available literature. Due to the limited amount of data, the prevalence of non-accidental harms in Para athletes remains unclear and information on trends over time is similarly unavailable.
CXCR5+CD8+ T cells are a distinct functional subset with an antitumor activity
Authors: Fuliang Chu, Haiyan S Li, Xindong Liu, Jingjing Cao, Wencai Ma, Ying Ma, Jinsheng Weng, Zheng Zhu, Xiaoyun Cheng, Zhiqiang Wang, Jingwei Liu, Zi Yang Jiang, Amber U Luong, Weiyi Peng, Jing Wang, Kumudha Balakrishnan, Cassian Yee, Chen Dong, Richard Eric Davis, Stephanie S Watowich, Sattva S Neelapu
Journal: Leukemia (2019)