tbuckley/cabot-search huggingface dataset:
TMOD-02. CHARACTERIZATION OF THE TUMOR IMMUNE MICROENVIRONMENT IN A PEDIATRIC HIGH GRADE GLIOMA MOUSE MODEL HARBORING THE H3.3-G34R MUTATION
Authors: Maria Garcia Fabiani, Santiago Haase, Padma Kadiyala, Mahmoud Alghamri, Andrea Comba, Felipe Nuñez, Matthew Whalen, Pedro Lowenstein, Maria Castro
Journal: Neuro-Oncology (2019)

Pediatric high grade gliomas (pHGGs) have a median survival (MS) of 9–15 months, are the most common malignant brain tumors in children and no significant improvement in the MS of these patients has been registered in decades. Thus, a representative in vivo model to study this tumor is critical. Recurrent mutations in genes encoding histones H3.3 and H3.1 have been described, which are distinctive of pHGGs. We aimed to establish a mouse model for pHGG harboring the mutation H3.3 G34R, which co-occurs with inactivating mutations in ATRX and TP53. To induce HGG, we used the Sleeping Beauty transposase system in which tumors are induced intrinsically in the mouse brain after injection of plasmids harboring the desired genetic alterations. The WT-H3.3 group pHGGs are generated after the injection of 4 plasmids, i.e., expressing mutated NRAS-G12V (activating mutation) + short hairpins against Tp53 and Atrx + the mutated histone H3.3-G34R (H3.3-G34R group). As controls, we injected plasmids overexpressing mutated NRAS-G12V + short hairpins against Tp53 and Atrx (WT-H3.3 group). H3.3-G34R group have longer MS when compared to the WT-H3.3 group (p<0.0001). We performed RNA-Sequencing of two cell populations from the tumors: one enriched in immune cells and other enriched in tumor cells. RNA-Seq of tumor cells yielded 233 differentially expressed genes between these two groups (p<0.05). GSEA of the upregulated genes in H3.3-G34R group showed significant GOs related to immune response regulation. We next studied the tumor microenvironment (TME) to determine the distinctive immune cell populations, at the phenotypic and functional levels. We observed that the H3.3-G34R TME was less populated with myeloid-derived suppressor cells, which could explain in part its longer MS compared to the WT-H3.3 control group. This information will be harnessed to uncover altered immune signaling pathways in pHGG and develop immune mediated-therapies specific for the H3.3-G34R pHGG subtype.
DIPG-19. REVERSAL OF CANCER GENE EXPRESSION IDENTIFIES NOVEL THERAPEUTICS FOR DIFFUSE INTRINSIC PONTINE GLIOMA
Authors: Guisheng Zhao, Patrick Newbury, William Zeng, Daniel Muldoon, Benjamin S Glicksberg, Anita Wen, Ke Liu, Bin Chen, Theodore Nicolaides
Journal: Neuro-Oncology (2019)

INTRODUCTION: Diffuse intrinsic pontine glioma (DIPG) is an aggressive type of brainstem cancer that targets young children. Complete resection is not possible, and chemotherapy and radiotherapy are currently only palliative. To identify potential therapeutic agents, we used a recently developed computational pipeline to perform an in silico screen for novel drugs. We then tested the identified drugs against a panel of patient-derived DIPG cell lines. METHODS: We used a systematic computational approach with publicly available databases of gene expression signatures in DIPG, as well as gene expression data of cancer cell lines before and after treatment in conjunction with a massive library of clinically available drugs. We identified three drug hits with the ability to reverse a DIPG gene signature to one that matches normal tissue background. We used three DIPG cell lines (SF8628, DIPG4, DIPG-NYU) along with immortalized normal human astrocytes (NHA) as control to test these drugs. Flow cytometry, immunoblot analysis, viability assays, and RNA-Seq before and after drug treatment were performed. In vivo experiments are currently underway. RESULTS: All three drugs showed potency against the primary DIPG4 cell line compared to NHA control. Triptolide showed the most potency against primary DIPG cell lines bearing H3K27M mutations (SF8628 and DIPG4, with IC50’s in the nanomolar range after 72 hours treatment), while the effect on DIPG cell line without H3K27M mutation (DIPG-NYU) was less potent. Immunoblot data also suggested a correlation between drug potency and H3K27M levels in these cell lines. CONCLUSION: Using a computational approach, we identified clinically available drugs with the ability to reverse DIPG gene expression signatures and significantly decreased the growth rate of primary DIPG cells in vitro. This novel approach can repurpose drugs and significantly decrease the cost and time normally required in drug discovery.
Expected Monetary Impact of Oncotype DX Score-Concordant Systemic Breast Cancer Therapy Based on the TAILORx Trial
Authors: Angela Mariotto, Jinani Jayasekerea, Valentina Petkov, Clyde B Schechter, Lindsey Enewold, Kathy J Helzlsouer, Eric J Feuer, Jeanne S Mandelblatt
Journal: JNCI Journal of the National Cancer Institute (2019)

TAILORx demonstrated that women with node-negative, hormone receptor-positive, HER2-negative breast cancers and Oncotype DX recurrence scores (RS) of 0-25 had similar 9-year outcomes with endocrine vs chemo-endocrine therapy; evidence for women aged 50 years and younger and RS 16-25 was less clear. We estimated how expected changes in practice following the trial might affect US costs in the initial 12 months of care (initial costs).
Differential effects of mesenchymal stem cells on T cells isolated from childhood allergies and autoimmune diseases
Authors: Yih‐Mei Liou, Teng‐Yuan Wei, Thai‐Yen Ling, Sheng‐Chieh Lin, Yao‐Hsu Yang, Bor‐Luen Chiang, Ya‐Hui Chuang
Journal: Allergy (2019)

Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
EPEN-07. EPENDYMOMAS IN INFANCY: UNDERLYING GENETIC ALTERATIONS, HISTOLOGICAL FEATURES AND CLINICAL OUTCOME
Authors: Stephanie Jünger, Martin Mynarek, Evelyn Dörner, Anja zur Mühlen, Stefan Rutkowski, Andre von Bueren, Felipe Andreiuolo, Torsten Pietsch
Journal: Neuro-Oncology (2019)

Young age represents an adverse prognostic factor in children with ependymomas. Their treatment is challenging since beneficial therapeutic options are limited. As ependymomas are considered a biologically heterogeneous group we aimed to characterize infant ependymomas in respect to their histological and genetic features. We analyzed 28 ependymomas in children younger than 18 months at diagnosis treated according to HIT2000-E protocols in which irradiation was postponed until the age of 18 months. All cases underwent neuropathological review, including immunohistochemical characterization. Genome-wide copy number alterations (CNA) were assessed by molecular inversion probe assays and RELA and YAP1 fusions were detected by RT-PCR and sequencing. All infant ependymomas were anaplastic (WHO grade III). Complete resection was accomplished in 57% of cases. 75% of cases were located in the posterior fossa, all of which showing loss of H3-K27me3, characteristic for PFA ependymomas. CNA analysis showed a stable genome in all cases. No gain of chromosome 1q was observed, an adverse prognostic marker in PFA tumors of older children. After a median follow-up of 5.4 years, 71% relapsed, and 43 % died. Seven ependymomas occurred in the supratentorial region of which in only two cases a complete resection could be achieved. Four tumors carried C11orf95-RELA fusions and two cases typical YAP1-MAMLD1 fusions (one case, not analyzable). The RELA-fused cases did not display CDKN2A loss as an adverse indicator of prognosis in this disease entity. Although 43% of infants with supratentorial ependymomas relapsed, all patients survived (median follow-up, 8.0 years). Infant ependymomas seem to consist of three biological entities: supratentorial tumors carrying RELA or YAP fusions and PFA ependymomas. The latter showed a particularly unfavorable outcome even though chromosome 1q gain was not present. Further biological studies are warranted in these neoplasms to identify prognostic markers and suitable targets for a more effective treatment.
Imaging with ultrasound in physical therapy: What is the PT’s scope of practice? A competency-based educational model and training recommendations
Authors: Jackie L Whittaker, Richard Ellis, Paul William Hodges, Cliona OSullivan, Julie Hides, Samuel Fernandez-Carnero, Jose Luis Arias-Buria, Deydre S Teyhen, Maria J Stokes
Journal: British Journal of Sports Medicine (2019)

Physical therapists employ ultrasound (US) imaging technology for a broad range of clinical and research purposes. Despite this, few physical therapy regulatory bodies guide the use of US imaging, and there are limited continuing education opportunities for physical therapists to become proficient in using US within their professional scope of practice. Here, we (i) outline the current status of US use by physical therapists; (ii) define and describe four broad categories of physical therapy US applications (ie, rehabilitation, diagnostic, intervention and research US); (iii) discuss how US use relates to the scope of high value physical therapy practice and (iv) propose a broad framework for a competency-based education model for training physical therapists in US. This paper only discusses US imaging-not 'therapeutic' US. Thus, 'imaging' is implicit anywhere the term 'ultrasound' is used.
SJS/TEN 中的 PTSD: 患病率和风险因素
Authors: L. Hefez, K. Zaghbib, E. Sbidian, L. Valeyrie‐Allanore, M. Allain, T.A. Duong, A. Colin, F. Bellivier, H. Romano, N. de Prost, K. Chazelas, O. Chosidow, P. Wolkenstein, S. Ingen‐Housz‐Oro
Journal: British Journal of Dermatology (2019)

表皮坏死是一种罕见且严重的综合征,主要因药物反应导致,可引发皮肤和粘膜的严重水疱和脱落。它包括两种综合征,Stevens‐Johnson 综合征 (SJS) 和中毒性表皮坏死 (TEN),具体取决于受累身体表面积的百分比。法国的发病率是 1 到 2 例/百万人。已知这种凶猛且急性疾病有多个长期后果,主要影响皮肤和眼睛,也有心理困扰,称为创伤后应激障碍(PTSD)。但是,在很大程度上 PTSD 的共性和风险因素依然未知。位于法国 Créteil 的 Henri Mondor 医院的国家中毒性大疱疾病基准中心研究团队进行了当前研究。我们旨在评估 PTSD 的患病率和风险因素。我们纳入了 2009 年到 2013 年间 31 例在 SJS/TEN 急性期(即最严重时候)住院的成年患者。所有患者在急性期都由一名心理医生通过若干心理评分进行评估,并视需要出具一种抗焦虑药物羟嗪,之后在 2、6 和 12 个月时再次检查。通过 PTSD 检查清单评分超过 44 分定义创伤后应激的程度。第 6 个月时,PTSD 的患病率为23%。3 名患者在 12 个月时发生了迟发性 PTSD。我们得出结论,在急性期需要系统性的心理评估,且之后必须对该患者进行至少一年的长期重复评估。
ENDOSCOPIC SUBMUCOSAL DISSECTION FOR GASTROINTESTINAL NEUROENDOCRINE TUMORS: A BICENTRIC PROSPECTIVELY COLLECTED WESTERN PRELIMINARY EXPERIENCE
Authors: AM Bucalau, A Murino, D Costa, L Verset, V Huberty, A Telese, N Lazaridis, T Luong, C Toumpanakis, C Martyn, J Deviere, A Lemmers, E Despott
Journal: Endoscopy (2019)

Selected gastrointestinal (GI) neuroendocrine tumors (NETs) are suitable for endoscopic submucosal dissection (ESD) but its efficacy and safety in western countries are limited. The aim of this study is to review two European centers experience of endoscopic treatment of superficial GI NET by ESD.
GENE-04. ESTABLISHING A MOLECULAR PROFILING SERVICE FOR CHILDREN’S CENTRAL NERVOUS SYSTEM TUMORS IN AUSTRALASIA – THE AUSTRALIAN AND NEW ZEALAND CHILDREN’S HAEMATOLOGY AND ONCOLOGY GROUP (ANZCHOG) AIM BRAIN PROJECT
Authors: Christine White, Kathryn Kinross, Robyn Strong, David Jones, Stefan Pfister, Jordan Hansford, Nicholas Gottardo, Elizabeth Algar
Journal: Neuro-Oncology (2019)

Pediatric neuro-oncology has undergone an exciting and dramatic transformation during the past decade. Molecular analyses have identified subtypes of central nervous system (CNS) tumors not distinguishable using traditional histopathological techniques culminating in the integration of molecular and histologic parameters in the 2016 WHO classification. Analysis of thousands of childhood CNS tumor samples by our collaborators at the German Cancer Research Centre and others has revealed each tumour entity comprises multiple sub-types, each with different survival outcomes and disease characteristics. This led to the establishment of the Molecular Neuropathology 2 (MNP2.0) study, which undertakes methylation profiling of CNS tumors to identify these sub-types and is currently recruiting Australasian participants. The Access to Innovative Molecular Profiling for Pediatric Brain Cancers (AIM BRAIN PROject) will provide a local molecular tumor profiling service for pediatric CNS tumors in Australia and New Zealand. To demonstrate clinical specificity and sensitivity, methylation array profiling results generated locally will be cross-validated with those from MNP2.0. The study aims to recruit up to 400 participants from Australia and New Zealand over four years. Recruitment began in November 2017 and to date 47 patients have been enrolled. Of the 17 patients co-enrolled on both AIM BRAIN and MNP2.0 trials, 16 (94%) have concordant results. 30/35 (86%) of reported AIM BRAIN cases have profiling consistent with their histopathological diagnosis, three cases were not classifiable and two cases showed disparate results. Three cases underwent Tumor Board review. The extent to which molecular profiling information impacts clinical decision-making and patient care will also be investigated during the study. Provision of a centralized and accredited molecular profiling service in the Australasian region aims to not only consolidate and streamline diagnostic testing for CNS tumors but to provide a network hub to facilitate communication and research outcomes for clinical scientists, pathologists and oncologists.
GENE-06. DISTINCT MOLECULAR SUBGROUPS OF TUMORS OF THE PINEAL REGION CORRELATE WITH CLINICAL PARAMETERS AND GENETIC ALTERATIONS
Authors: Elke Pfaff, Christian Aichmüller, Martin Sill, Damian Stichel, Matija Snuderl, Matthias A Karajannis, Martin U Schuhmann, Jens Schittenhelm, Martin Hasselblatt, Christian Thomas, Andrey Korshunov, Marina Rhizova, Petra Temming, Brent A Orr, David W Ellison, James M Olson, Eugene Hwang, Katja von Hoff, Martin Mynarek, Stefan Rutkowski, Marc Zapatka, Peter Lichter, Felix Sahm, Andreas von Deimling, Stefan M Pfister, David T W Jones
Journal: Neuro-Oncology (2019)

Tumors arising in the pineal region comprise a spectrum of different entities with distinct clinical and histopathological characteristics. Pineocytoma (PC), pineal parenchymal tumors of intermediate differentiation (PPTID) and papillary tumors of the pineal region (PTPR) mainly occur in adult patients and are low to moderately aggressive neoplasms (WHO °I-III). In contrast, pineoblastoma (PB) are high-grade (WHO °IV) malignancies primarily affecting children and adolescents. Especially for patients with unresectable or metastatic disease or at very young age survival outcomes remain poor despite aggressive multimodal treatment regimen. To date, no therapeutically actionable molecular targets have been identified. A subset of PB occur in patients with cancer predisposition syndromes including DICER1 and RB1 germline mutations, the latter in the context of trilateral retinoblastoma (TLRB). We analyzed a cohort of ~230 pineal tumors of different histologies using genome-wide DNA methylation profiling and copy-number analysis, as well as gene panel sequencing, miRNA sequencing and gene expression profiling. Unsupervised clustering based on DNA methylation profiles revealed clear separation of known histopathological entities (PC, PTPR, PPTID) and, furthermore, distinction of subclasses within these groups. Interestingly, several biologically discrete subgroups emerged within the group of histologically diagnosed PBs or pineal primitive embryonal tumors/PNETs, which displayed distinct clinical associations (e.g. age distribution). RB1 alterations were recurrent in a small subgroup (PB_RB) including TLRBs as well as sporadic PB cases (~60%) showing similarities with retinoblastoma. About 45% of cases in the largest PB subgroup (PB_B) harbored alterations within the miRNA processing pathway (affecting DROSHA, DGCR8 or DICER1) suggesting a central role of altered miRNA biogenesis in the development of this group which showed evidence for global reduction of mature miRNA by miRNA-Seq. With this study, we provide a foundation for further clinical, molecular and functional characterization of PB subgroups.
Banoxantrone (AQ4N), tissue CYP 450 targeted prodrug: The results of a phase I study using an accelerated dose escalation
Authors: J. Sarantopoulos, A. W. Tolcher, A. Wong, S. Goel, M. Beeram, G. Lam, K. Desai, K. Woody, S. Mani, K. P. Papadopoulos
Journal: Journal of Clinical Oncology (2006)

2011 Background: AQ4N was rationally designed to have anti-tumor activity following bioreduction by tissue cytochrome P450 to AQ4, an active DNA topoisomerase II inhibitor. Preclinical studies demonstrated AQ4N selectively targets lymphoid tissues and hypoxic tumor tissues. This study assessed the maximum tolerated dose (MTD), pharmacokinetic (PK), and pharmacodynamic (PD) of repeated weekly dosing of AQ4N in patients (pts) with advanced cancers. Methods: AQ4N was administered IV on Days 1, 8, and 15 of a 28-day cycle in the following dose cohorts 12, 24, 48, 96, 192, 384, 768, and 1200 mg/m 2 . Accelerated titration design 2B was employed and the MTD was defined by ≤ 33% of 6 pts with a drug-related dose limiting toxicity (DLT). Response was assessed every 8 weeks by RECIST. Results: 16 pts were enrolled. A single pt per cohort was treated up to 384 mg/m 2 . At 1200 mg/m 2 , 2 of 5 pts experienced a DLT (Grade 5 respiratory distress and Grade 3 fatigue). A total of 5 pts were treated without toxicity at the 768 mg/m 2 , and established this dose as MTD. One pt in the 1200 mg/m 2 cohort died during the trial from acute complications of metastatic soft tissue sarcoma and respiratory distress. The most common adverse events (AE) observed were fatigue (63%), anorexia (38%), nausea (38%), vomiting (38%), peripheral edema (25%), and diarrhea (25%). 6 pts experienced 8 serious AEs. Anticipated blue coloration of skin and body fluids was observed. One pt (48 mg/m 2 ) with renal cancer has had stable disease for &gt; 12 months. The PK was linear over all doses studied. At 768 mg/m 2 (n=4), the Day 1 AQ4N C max was 99.8 ± 27.0 μg/mL, AUC 0- ∞ was 259.5 ± 67.8 μg·h/mL, and T 1/2 was 3.9 ± 0.7 h (range 3.1–4.8 h). A predictable dose-related and exposure related decrease in lymphocytes and neutrophils were observed. Conclusions: AQ4N is well tolerated when administered on a weekly schedule. AQ4N levels sufficient for anti-neoplastic activity in pre-clinical models are achieved with weekly dosing at 768 mg/m 2 . AQ4N monotherapy and combination trials with chemo- and radiation therapy are planned. [Table: see text]
IGF1R as druggable target mediating PI3K-δ inhibitor resistance in a murine model of chronic lymphocytic leukemia
Authors: Annika Scheffold, Billy Michael Chelliah Jebaraj, Eugen Tausch, Johannes Bloehdorn, Paolo Ghia, Anella Yahiaoui, Anna Dolnik, Tamara Jacqueline Blätte, Lars Bullinger, Rashmi Priyadharshini Dheenadayalan, Li Li, Christof Schneider, Shih-Shih Chen, Nicholas Chiorazzi, Sascha Dietrich, Martina Seiffert, Stacey Tannheimer, Hartmut Döhner, Daniel Mertens, Stephan Stilgenbauer
Journal: Blood (2019)
Abstract 14281: Predictors of Fatigue in the Presence of Coronary Heart Disease
Authors: Ann L Eckhardt, Holli A DeVon, Mariann R Piano, Catherine J Ryan, Julie J Zerwic
Journal: Circulation (2013)

Background: Fatigue may be an important warning sign before an acute myocardial infarction (AMI). Prior to establishing the importance of fatigue in AMI, it is critical to examine the presence of f...
LGG-03. NEW INSIGHTS INTO PEDIATRIC LOW-GRADE GLIOMAS IN SAUDI ARABIA REVEALED THROUGH GENETIC PROFILING SINGLE CENTER EXPERIENCE
Authors: Nahla Ali Mobark, Musa Alharpi, Maqsood Ahmad, Ayman Al-Banyan, Fahad E Alotabi, Malak Abedalthagafi
Journal: Neuro-Oncology (2019)

OBJECTIVE: Gliomas account for ≥ 50% of childhood central nervous neoplasms and can be subdivided into low-grade (LGG) and high grade gliomas (HGG). We performed comprehensive genomic profiling on 20 Saudi pediatric LGG (pLGG) patients to identify tumor associated genetic abnormalities. The identification of these events can inform prognostic, and therapeutic decision-making. METHODS: This retrospective study was performed on 20 children (<16 y) newly diagnosed with pathologically confirmed LGG. We reviewed the molecular, clinical and therapeutic aspects and the treatment outcome of pLGG patients. Next generation sequencing was performed using the Oncomine Comprehensive Assay v3 system from formalin-fixed paraffin embedded (FFPE) tumor samples. Data were analyzed using the SPSS statistical package version 23. RESULTS: We detected genomic alterations (GAs) in all of the tumors, averaging 4.52 ± 2.11 GAs per patient. BRAF was the most commonly altered gene (75.0%, 15/20 cases). Other frequently mutated genes included ATM 15% (3/20), RNF43 15 % (3/20), RAD51C 20% (4/20) and Notch2 20% (4/20). Casually altered genes (observed in less than 3 patients) included FANCD2, FGFR1, BRCA2, CDC4, KIF5B, RET, AKAP, SLX4, MSH6, NTRK, CCDC170, MLH1, AGK, PDGFRB, EIF3B,FGFR2, CDKN2A/B, PTCH1, SETD2, SLX4, MSH6 NTRK and CDK4. Interestingly, we identified a novel gene fusion of GOPC (Fig)-ROS1 in a 10-year old patient that lacked BRAF fusions. Midline tumor analysis revealed a left parietal mass with vasogenic edema. The patient received surgical resection with excellent postoperative recovery and no neurological deficit. No adjuvant chemotherapy or radiation therapy was required and the patient is stable with no tumor recurrence. CONCLUSIONS: We provide comprehensive genomic profiling of Saudi pLGGs that promote diagnostic accuracy and enhance clinical decision-making. Additionally, GOPC1-ROS1 may be a biomarker to identify pLGG patients that will benefit from Target therapy
Collaborative systematic review of the randomised trials of organised in-patient (stroke unit) care after stroke.
Authors: K Asplund, P Berman, C Blomstrand, M Dennis, J Douglas, T Erila, M Garraway, E Hamrin, G Hankey, M Ilmavirta, B Indredavik, L Kalra, M Kaste, P Langhorne, H Rodgers, J Sivenius, J Slattery, R Stevens, A Svensson, C Warlow, B Williams, S WoodDauphinee
Journal: BMJ (1997)
Clinical and immunological features in a cohort of patients with partial DiGeorge syndrome followed at a single center
Authors: Giuliana Giardino, Nesrine Radwan, Patra Koletsi, Deborah M. Morrogh, Stuart Adams, Winnie Ip, Austen Worth, Alison Jones, Imke Meyer-Parsonson, H. Bobby Gaspar, Kimberly Gilmour, E. Graham Davies, Fani Ladomenou
Journal: Blood (2019)
Valine 11 and phenylalanine 13 have a greater impact on the T-cell response to citrullinated peptides than the 70–74 shared epitope of the DRB1 molecule in macaques
Authors: Samuel Bitoun, Pierre Roques, Bernard Maillere, Roger Le Grand, Xavier Mariette
Journal: Annals of the Rheumatic Diseases (2019)

Objectives Various rheumatoid arthritis (RA) HLA-DRB-1 risk haplotypes have been regrouped under the shared epitope (SE) in position 70–74. The presence of Valine in position 11 (Val11) and phenylalanine in position 13 (Phe13) are also associated with RA, but it is impossible to differentiate their role compared with the SE since they are in strong linkage disequilibrium (LD) in humans. Similar to humans, certain macaques express the SE (H6). We analysed the effect of various DRB1 haplotypes on T-cell response to citrullinated peptides (Cit-P) in macaques. Methods Six H6 and six non-H6 macaques were immunized with four Cit-P. T-cell response was assessed using Interferon γ enzyme-linked immunospot. Results Animals developed a specific anti-Cit-P T-cell response. Surprisingly, H6 animals had a significantly lower T-cell response than non-H6. In macaques, the 70–74 SE and the Val11 are on separate haplotypes. Presence of Val11 was strongly associated with the anti-Cit-P T-cell response, whatever the 70–74 sequence was. This response was amplified in case of presence of Phe13. Conclusion The absence of LD between Val11 and SE in macaques allowed us to demonstrate that the most important HLA positions to induce a T-cell response against Cit-P were Val11 and Phe13 and not the 70–74 SE.
Physical Inactivity Is a Risk Factor for Primary Ventricular Fibrillation
Authors: Gaetano M. De Ferrari, Veronica Dusi, Marta Ruffinazzi, Vincenzo Gionti, Luisa Cacciavillani, Patrizia Noussan, Valerio Zacà, Tommaso Sanna, Lia Crotti, Peter J. Schwartz
Journal: Journal of the American College of Cardiology (2019)