tbuckley/cabot-search huggingface dataset:
Interleukin-27 Exerts Its Antitumor Effects by Promoting Differentiation of Hematopoietic Stem Cells to M1 Macrophages
Authors: Yukino Chiba, Izuru Mizoguchi, Junichi Furusawa, Hideaki Hasegawa, Mio Ohashi, Mingli Xu, Toshiyuki Owaki, Takayuki Yoshimoto
Journal: Cancer Research (2017)

The interleukin IL27 promotes expansion and differentiation of hematopoietic stem cells into myeloid progenitor cells. Many tumor-infiltrating myeloid cells exert immunosuppressive effects, but we hypothesized that the myeloid cells induced by IL27 would have antitumor activity. In this study, we corroborated this hypothesis as investigated in two distinct mouse transplantable tumor models. Malignant mouse cells engineered to express IL27 exhibited reduced tumor growth in vivo Correlated with this effect was a significant increase in the number of tumor-infiltrating CD11b+ myeloid cells exhibiting a reduced immunosuppressive activity. Notably, these CD11b+ cells were characterized by an activated M1 macrophage phenotype, on the basis of increased expression of inducible nitric oxide synthase and other M1 biomarkers. In vivo depletion of these cells by administering anti-Gr-1 eradicated the antitumor effects of IL27. When admixed with parental tumors, CD11b+ cells inhibited tumor growth and directly killed the tumor in a nitric oxide-dependent manner. Mechanistically, IL27 expanded Lineage-Sca-1+c-Kit+ cells in bone marrow. Transplant experiments in Ly5.1/5.2 congenic mice revealed that IL27 directly acted on these cells and promoted their differentiation into M1 macrophages, which mobilized into tumors. Overall, our results illustrated how IL27 exerts antitumor activity by enhancing the generation of myeloid progenitor cells that can differentiate into antitumorigenic M1 macrophages.Significance: These findings show how the interleukin IL27 exerts potent antitumor activity by enhancing the generation of myeloid progenitor cells that can differentiate into antitumorigenic M1 macrophages.Cancer Res; 78(1); 182-94. ©2017 AACR.
The Death of Michael Jackson
Authors: Michael Collins
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Antiapoptotic serine protease inhibitors contribute to survival of allergenic T H 2 cells
Authors: Mohamed H. Shamji, Jeff N. Temblay, Wei Cheng, Susan M. Byrne, Ellen Macfarlane, Amy R. Switzer, Natalia D.C. Francisco, Fedina Olexandra, Fabian Jacubczik, Stephen R. Durham, Philip G. Ashton-Rickardt
Journal: Journal of Allergy and Clinical Immunology (2017)
TCT-747 Associations between Stent Diameter and Clinical Outcomes in ACS PCI Using Second Generation Drug-Eluting Stents: From the PROMETHEUS Study
Authors: Abdul Qadeer, Jaya Chandrasekhar, Usman Baber, Samantha Sartori, Zhen Ge, Serdar Farhan, Madhav Sharma, Annapoorna Kini, Sunil Rao, Samir Kapadia, Timothy Henry, Joseph Muhlestein, Mark Effron, William Weintraub, Sandra Weiss, Craig Strauss, Anthony DeFranco, Catalin Toma, Stuart Keller, Brian Baker, Stuart Pocock, Roxana Mehran
Journal: Journal of the American College of Cardiology (2017)
Immediate and Midterm Cardiac Remodeling After Surgical Pulmonary Valve Replacement in Adults With Repaired Tetralogy of Fallot
Authors: Ee Ling Heng, Michael A. Gatzoulis, Anselm Uebing, Babulal Sethia, Hideki Uemura, Gillian C. Smith, Gerhard-Paul Diller, Karen P. McCarthy, Siew Yen Ho, Wei Li, Piers Wright, Veronica Spadotto, Philip J Kilner, Paul Oldershaw, Dudley J. Pennell, Darryl F. Shore, Sonya V. Babu-Narayan
Journal: Circulation (2017)

Background: Pulmonary valve replacement (PVR) in patients with repaired tetralogy of Fallot provides symptomatic benefit and right ventricular (RV) volume reduction. However, data on the rate of ventricular structural and functional adaptation are scarce. We aimed to assess immediate and midterm post-PVR changes and predictors of reverse remoeling. Methods: Fifty-seven patients with repaired tetralogy of Fallot (age ≥16 y; mean age, 35.8±10.1 y; 38 male) undergoing PVR were prospectively recruited for cardiovascular magnetic resonance performed before PVR (pPVR), immediately after PVR (median, 6 d), and midterm after PVR (mPVR; median, 3 y). Results: There were immediate and midterm reductions in indexed RV end-diastolic volumes and RV end-systolic volumes (RVESVi) (indexed RV end-diastolic volume pPVR versus immediately after PVR versus mPVR, 156.1±41.9 versus 104.9±28.4 versus 104.2±34.4 mL/m 2 ; RVESVi pPVR versus immediately after PVR versus mPVR, 74.9±26.2 versus 57.4±22.7 versus 50.5±21.7 mL/m 2 ; P &lt;0.01). Normal postoperative diastolic and systolic RV volumes (the primary end point) achieved in 70% of patients were predicted by a preoperative indexed RV end-diastolic volume ≤158 mL/m 2 and RVESVi ≤82 mL/m 2 . RVESVi showed a progressive decrease from baseline to immediate to midterm follow-up, indicating ongoing intrinsic RV functional improvement after PVR. Left ventricular ejection fraction improved (pPVR versus mPVR, 59.4±7.6% versus 61.9±6.8%; P &lt;0.01), and right atrial reverse remodeling occurred (pPVR versus mPVR, 15.2±3.4 versus 13.8±3.6 cm 2 /m 2 ; P &lt;0.01). Larger preoperative RV outflow tract scar was associated with a smaller improvement in post-PVR RV/left ventricular ejection fraction. RV ejection fraction and peak oxygen uptake predicted mortality ( P =0.03) over a median of 9.5 years of follow-up. Conclusions: Significant right heart structural reverse remodeling takes place immediately after PVR, followed by a continuing process of further biological remodeling manifested by further reduction in RVESVi. PVR before RVESVi reaches 82 mL/m 2 confers optimal chances of normalization of RV function.
Prognostic Effect and Longitudinal Hemodynamic Assessment of Borderline Pulmonary Hypertension
Authors: Tufik R. Assad, Bradley A. Maron, Ivan M. Robbins, Meng Xu, Shi Huang, Frank E. Harrell, Eric H. Farber-Eger, Quinn S. Wells, Gaurav Choudhary, Anna R. Hemnes, Evan L. Brittain
Journal: JAMA Cardiology (2017)

Pulmonary hypertension (PH) is diagnosed by a mean pulmonary arterial pressure (mPAP) value of at least 25 mm Hg during right heart catheterization (RHC). While several studies have demonstrated increased mortality in patients with mPAP less than that threshold, little is known about the natural history of borderline PH. To test the hypothesis that patients with borderline PH have decreased survival compared with patients with lower mPAP and frequently develop overt PH and to identify clinical correlates of borderline PH. Retrospective cohort study from 1998 to 2014 at Vanderbilt University Medical Center, comprising all patients undergoing routine RHC for clinical indication. We extracted demographics, clinical data, invasive hemodynamics, echocardiography, and vital status for all patients. Patients with mPAP values of 18 mm Hg or less, 19 to 24 mm Hg, and at least 25 mm Hg were classified as reference, borderline PH, and PH, respectively. Mean pulmonary arterial pressure. Our primary outcome was all-cause mortality after adjusting for clinically relevant covariates in a Cox proportional hazards model. Our secondary outcome was the diagnosis of overt PH in patients initially diagnosed with borderline PH. Both outcomes were determined prior to data analysis. We identified 4343 patients (mean [SD] age, 59 [15] years, 51% women, and 86% white) among whom the prevalence of PH and borderline PH was 62% and 18%, respectively. Advanced age, features of the metabolic syndrome, and chronic heart and lung disease were independently associated with a higher likelihood of borderline PH compared with reference patients in a logistic regression model. After adjusting for 34 covariates in a Cox proportional hazards model, borderline PH was associated with increased mortality compared with reference patients (hazard ratio, 1.31; 95% CI, 1.04-1.65; P = .001). The hazard of death increased incrementally with higher mPAP, without an observed threshold. In the 70 patients with borderline PH who underwent a repeated RHC, 43 (61%) had developed overt PH, with a median increase in mPAP of 5 mm Hg (interquartile range, -1 to 11 mm Hg; P < .001). Borderline PH is common in patients undergoing RHC and is associated with significant comorbidities, progression to overt PH, and decreased survival. Small increases in mPAP, even at values currently considered normal, are independently associated with increased mortality. Prospective studies are warranted to determine whether early intervention or closer monitoring improves clinical outcomes in these patients.
Tripartite motif-containing (TRIM) 21 negatively regulates intestinal mucosal inflammation through inhibiting TH1/TH17 cell differentiation in patients with inflammatory bowel diseases
Authors: Guangxi Zhou, Wei Wu, Lin Yu, Tianming Yu, Wenjing Yang, Ping Wang, Xiaoping Zhang, Yingzi Cong, Zhanju Liu
Journal: Journal of Allergy and Clinical Immunology (2017)
Pro-Inflammatory CXCR3 Impairs Mitochondrial Function in Experimental Non-Alcoholic Steatohepatitis
Authors: Jinghua Du, Xiang Zhang, Juqiang Han, Kwan Man, Yanquan Zhang, Eagle SH Chu, Yuemin Nan, Jun Yu
Journal: Theranostics (2017)

Mitochondrial dysfunction plays a crucial role in the development of non-alcoholic steatohepatitis (NASH).However, the regulator of mitochondrial dysfunction in the pathogenesis of NASH is still largely unclear.CXCR3 is an essential pro-inflammatory factor in chronic liver diseases.We explored the significance of CXCR3 in regulating mitochondrial function during NASH development in animal models and cultured hepatocytes.Methods: The effects of CXCR3 on mitochondrial function were evaluated by genetic knockout or pharmacological inhibition in mouse models and in vitro.The ultrastructural changes of mitochondria were assessed by transmission electron microscopy (TEM).Hepatic levels of mitochondrial reactive oxygen species (ROS), DNA damage, membrane potential and ATP were examined.Results: CXCR3 ablation by genetic knockout or pharmacological inhibition in mice protected against NASH development by influencing mitochondrial function.Similarly, depletion of CXCR3 reduced steatohepatitis injury in cultured hepatocytes.TEM analysis revealed that liver mitochondrial integrity was much improved in CXCR3 knockout (CXCR3 -/-) compared to wildtype (WT) mice.In agreement with this, impaired mitochondrial function was pronounced in WT mice compared to CXCR3 -/-mice, evidenced by increased protein expression of dynamic-related protein-1 (DRP1) and fission-1 (FIS1) and decreased protein expression of mitofusin-1 (MFN1).Mitochondrial dysfunction was induced in AML-12 hepatocytes by methionine and choline deficient medium and in HepG2 cells by palmitic acid.The impaired mitochondrial function in both cell lines was evidenced by reduced membrane potential and ATP content, and by increased mitochondrial ROS accumulation and DNA damage.However, CXCR3 knockdown by siCXCR3 significantly diminished the mitochondrial dysfunction in both AML-12 and HepG2 hepatocytes.In addition, inhibition of CXCR3 by CXCR3 specific antagonists SCH546738 and AMG487 restored mitochondrial function and inhibited mitochondrial-dependent apoptosis in the liver of WT mice fed with methionine and choline deficient diet.Conclusion: CXCR3 induces mitochondrial dysfunction, which contributes to the pathogenesis of steatohepatitis.Pharmacologic blockade of CXCR3 prevents mitochondrial dysfunction and restores the severity of steatohepatitis, indicating a potential clinical impact for controlling the disease.
Re: Robert J. Motzer, Alain Ravaud, Jean-Jacques Patard, et al. Adjuvant Sunitinib for High-risk Renal Cell Carcinoma After Nephrectomy: Subgroup Analyses and Updated Overall Survival Results. Eur Urol 2018;73:62–8
Authors: Francesco Massari, Vincenzo Di Nunno, Andrea Ardizzoni
Journal: European Urology (2017)
Liver Reptin/RUVBL2 controls glucose and lipid metabolism with opposite actions on mTORC1 and mTORC2 signalling
Authors: Joaquim Javary, Nathalie Allain-Courtois, Nicolas Saucisse, Pierre Costet, Capucine Heraud, Fadila Benhamed, Rémi Pierre, Corinne Bure, Nestor Pallares-Lupon, Marcio Do Cruzeiro, Catherine Postic, Daniela Cota, Pierre Dubus, Jean Rosenbaum, Samira Benhamouche-Trouillet
Journal: Gut (2017)

Objective The AAA+ ATPase Reptin is overexpressed in hepatocellular carcinoma and preclinical studies indicate that it could be a relevant therapeutic target. However, its physiological and pathophysiological roles in vivo remain unknown. This study aimed to determine the role of Reptin in mammalian adult liver. Design and results We generated an inducible liver-specific Reptin knockout ( Repin LKO ) mouse model. Following Reptin invalidation, mice displayed decreased body and fat mass, hypoglycaemia and hypolipidaemia. This was associated with decreased hepatic mTOR protein abundance. Further experiments in primary hepatocytes demonstrated that Reptin maintains mTOR protein level through its ATPase activity. Unexpectedly, loss or inhibition of Reptin induced an opposite effect on mTORC1 and mTORC2 signalling, with: (1) strong inhibition of hepatic mTORC1 activity, likely responsible for the reduction of hepatocytes cell size, for decreased de novo lipogenesis and cholesterol transcriptional programmes and (2) enhancement of mTORC2 activity associated with inhibition of the gluconeogenesis transcriptional programme and hepatic glucose production. Consequently, the role of hepatic Reptin in the pathogenesis of insulin resistance (IR) and non-alcoholic fatty liver disease consecutive to a high-fat diet was investigated. We found that Reptin deletion completely rescued pathological phenotypes associated with IR, including glucose intolerance, hyperglycaemia, hyperlipidaemia and hepatic steatosis. Conclusion We show here that the AAA +ATPase Reptin is a regulator of mTOR signalling in the liver and global glucido-lipidic homeostasis. Inhibition of hepatic Reptin expression or activity represents a new therapeutic perspective for metabolic syndrome.
Peripheral and local predictive immune signatures identified in a phase II trial of ipilimumab with carboplatin/paclitaxel in unresectable stage III or stage IV melanoma
Authors: Rahima Jamal, Réjean Lapointe, Eftihia Cocolakis, Paméla Thébault, Shirin Kazemi, Jennifer E. Friedmann, Jeanne Dionne, Jean-François Cailhier, Karl Bélanger, Jean-Pierre Ayoub, Huy Le, Caroline Lambert, Jida El-Hajjar, Léon C. van Kempen, Alan Spatz, Wilson H. Miller
Journal: Journal for ImmunoTherapy of Cancer (2017)

Checkpoint blockade with ipilimumab provides long-term survival to a significant proportion of patients with metastatic melanoma. New approaches to increase survival and to predict which patients will benefit from treatment are needed. This phase II trial combined ipilimumab with carboplatin/paclitaxel (CP) to assess its safety, efficacy, and to search for peripheral and tumor-based predictive biomarkers.
Recovery of Left Atrial Contractile Function After Maze Surgery in Persistent Longstanding Atrial Fibrillation
Authors: Yasir Abu-Omar, Benjamin S. Thorpe, Carol Freeman, Christine Mills, Victoria E.A. Stoneman, Deepa Gopalan, Bushra Rana, Tomasz J. Spyt, Linda D. Sharples, Samer A.M. Nashef
Journal: Journal of the American College of Cardiology (2017)
Hamstring muscle injuries in elite football: translating research into practice
Authors: Matthew Buckthorpe, Mo Gimpel, Steve Wright, Thomas Sturdy, Matthew Stride
Journal: British Journal of Sports Medicine (2017)

Hamstring muscle injuries (HMI) are consistently the most prevalent time-loss injury in football and are prone to reoccurrence.1 We note the disconnection between evidence-based recommendations and the HMI prevention programmes adopted in elite clubs.2 For example, only 11% of elite level football teams surveyed fully use the Nordic Hamstring Programme.3 

Why don’t elite sports medicine teams adopt evidence-based practices?4 The aim of this editorial is not only to share our experience of HMI prevention and demonstrate that elite clubs do consider the research on HMI, but also place this alongside other factors which, although may not yet be ‘evidenced based’, have theoretical merit and clinically observed benefits in the prevention of HMIs within elite football. We feel there is an overemphasis placed on isolated strength capacity in HMI management within the recommended research, with a lack of focus on contextual factors. Furthermore, there is typically limited consideration of how the muscle functions during the mechanisms in which it is typically used and injured. Our aim is not to discredit current evidence-based strategies (eg, Nordic Hamstring Programme), but we share five additional …
TCT-704 Intravascular Ultrasound Analysis of Intraplaque Versus Subintimal Tracking in Percutaneous Intervention for Coronary Chronic Total Occlusions: One Year Outcomes
Authors: Jake Cleaman, Matthew Finn, Lei Song, Akiko Maehara, Sanjog Kalra, Justin Fried, Jeffrey Moses, Manish Parikh, Ajay Jayant Kirtane, Michael Collins, Tamim Nazif, Khady Fall, Philip Green, Candido Batres, Ziad Ali, Martin Leon, Gary Mintz
Journal: Journal of the American College of Cardiology (2017)
Hepatic leukocyte immunoglobulin‐like receptor B4 (LILRB4) attenuates nonalcoholic fatty liver disease via SHP1‐TRAF6 pathway
Authors: Yao Lu, Zhou Jiang, Haijiang Dai, Rujia Miao, Jingxian Shu, Haotian Gu, Xing Liu, Zhijun Huang, Guoping Yang, Alex F. Chen, Hong Yuan, Ying Li, Jingjing Cai
Journal: Hepatology (2017)

Nonalcoholic fatty liver disease (NAFLD) is an increasingly prevalent liver pathology characterized by hepatic steatosis and commonly accompanied by systematic inflammation and metabolic disorder. Despite an accumulating number of studies, no pharmacological strategy is available to treat this condition in the clinic. In this study, we applied extensive gain- and loss-of-function approaches to identify the key immune factor leukocyte immunoglobulin-like receptor B4 (LILRB4) as a negative regulator of NAFLD. The hepatocyte-specific knockout of LILRB4 (LILRB4-HKO) exacerbated high-fat diet-induced insulin resistance, glucose metabolic imbalance, hepatic lipid accumulation, and systematic inflammation in mice, whereas LILRB4 overexpression in hepatocytes showed a completely opposite phenotype relative to that of LILRB4-HKO mice when compared with their corresponding controls. Further investigations of molecular mechanisms demonstrated that LILRB4 recruits SHP1 to inhibit TRAF6 ubiquitination and subsequent inactivation of nuclear factor kappa B and mitogen-activated protein kinase cascades. From a therapeutic perspective, the overexpression of LILRB4 in a genetic model of NAFLD, ob/ob mice, largely reversed the inherent hepatic steatosis, inflammation, and metabolic disorder. Targeting hepatic LILRB4 to improve its expression or activation represents a promising strategy for the treatment of NAFLD as well as related liver and metabolic diseases. (Hepatology 2018;67:1303-1319).
TCT-542 Incidence and Predictors of Left Ventricular Negative Remodeling after MitraClip treatment in patients with Functional Mitral Regurgitation
Authors: Cosmo Godino, Andrea Scotti, Maurizio Taramasso, Marianna Adamo, Marco Russo, Carlo Andrea Pivato, Luca Arrigoni, Luca Baldetti, Barbara Bellini, Alberto Cappelletti, Stefano Stella, Gabriele Fragasso, Matteo Montorfano, Eustachio Agricola, Alberto Margonato, Francesco Maisano, Federica Ettori, Antonio Colombo
Journal: Journal of the American College of Cardiology (2017)
TCT-666 Long-term Clinical Impact of Percutaneous Coronary Intervention with the Retrograde Approach for Chronic Total Occlusive Lesions
Authors: Osung Kwon, Pil Hyung Lee, Seung-Whan Lee, Kyusup Lee, Ungjeong Do, Cheol Hyun Lee, Do-yoon Kang, Jung-Min Ahn, Duk-Woo Park, Soo-Jin Kang, Young-Hak Kim, Cheol Whan Lee, Seong-Wook Park, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2017)
3-Year Clinical Outcomes With Everolimus-Eluting Bioresorbable Coronary Scaffolds
Authors: Dean J. Kereiakes, Stephen G. Ellis, Christopher Metzger, Ronald P. Caputo, David G. Rizik, Paul S. Teirstein, Marc R. Litt, Annapoorna Kini, Ameer Kabour, Steven O. Marx, Jeffrey J. Popma, Robert McGreevy, Zhen Zhang, Charles Simonton, Gregg W. Stone
Journal: Journal of the American College of Cardiology (2017)
Prevenzione della rosolia congenita nella Regione Europea dell'OMS : l'obiettivo per il 2010
Authors: J. S. Spika, F X Hanon, S Wassilak, R G Pebody, N Emiroglu
Journal: Eurosurveillance (2004)

L'Ufficio Regionale per l'Europa dell'Organizzazione Mondiale della Sanita (OMS) ha recentemente pubblicato un piano strategico e linee guida per la sorveglianza di morbillo e rosolia congenita. La strategia da la priorita alle attivita di controllo del morbillo ma incoraggia anche l'introduzione della vaccinazione antirosolia quando la copertura vaccinale per il morbillo sara superiore al 90%; nel frattempo molti paesi dell'Europa occidentale con livelli di copertura vaccinale per il morbillo sub-ottimali stanno gia usando il vaccino combinato contro morbillo, parotite e rosolia (MPR). Le donne di questi paesi corrono un rischio molto elevato di avere un bambino con sindrome da rosolia congenita. L'obiettivo dell'OMS e di migliorare la sorveglianza di rosolia e sindrome da rosolia congenita al fine di ottenere informazioni affidabili sul carico di queste malattie e di fare prendere coscienza a coloro che debbono prendere decisioni di politica sanitaria della necessita di sostenere la strategia di lotta contro la rosolia dell'Ufficio Regionale per l'Europa dell'OMS.
Azithromycin reduced exacerbations and improved QoL in symptomatic asthma despite inhaled maintenance therapy
Authors: Matthew B. Stanbrook
Journal: Annals of Internal Medicine (2017)

Source Citation Gibson PG, Yang IA, Upham JW, et al. Effect of azithromycin on asthma exacerbations and quality of life in adults with persistent uncontrolled asthma (AMAZES): a randomised, double-blind, placebo-controlled trial. Lancet. 2017;390:659-68. 28687413
TCT-3 Outcomes of Left Main Revascularization in Patients with Acute Coronary Syndrome vs. Stable Angina: Analysis from the EXCEL Trial
Authors: Serge Doucet, Marc Jolicoeur, Patrick Serruys, Michael Ragosta, Werner Scholtz, Yiran Zhang, Joseph Sabik, Thomas McAndrew, A. Pieter Kappetein, Gregg Stone
Journal: Journal of the American College of Cardiology (2017)
Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Is a New Biomarker for Mantle Cell Lymphoma: Expression, Localization, and Phosphorylation Study
Authors: Tomas Stopka, Jarmila Vargova, Karina Vargova, Nina Dusilkova, Vojtech Kulvait, Vit Pospisil, Jiri Zavadil, Marek Trneny, Pavel Klener
Journal: Blood (2016)