tbuckley/cabot-search huggingface dataset:
Anisakis hypersensitivity in Italy: prevalence and clinical features: a multicenter study
Journal: Allergy (2011)

To cite this article: AAITO-IFIACI Anisakis Consortium. Anisakis hypersensitivity in Italy: prevalence and clinical features: a multicenter study. Allergy 2011; 66: 1563–1569. Background: Anisakis simplex (As), a parasite in fish, is able to sensitize humans via the alimentary tract. The prevalence of hypersensitivity and allergy to As outside the Iberian peninsula has not been investigated so far. We investigated Anisakis hypersensitivity in different areas of Italy. Methods: Consecutive subjects seen at 34 Italian allergy centers from October to December 2010 were investigated both by specific interview and by skin prick test (SPT) with As extract. Results: A total of 10 570 subjects were screened, of which 474 (4.5%) scored positive on Anisakis SPT and 66 of these (14% of those sensitized; 0.6% of the studied population) had a history of As allergy. Marinated anchovies were the most frequent cause of allergic reactions. Thirty-four (52%) patients were mono-sensitized to Anisakis. Sensitization rate showed marked geographic differences (range: 0.4–12.7%), being highest along the Adriatic and Tyrrhenian coasts, where homemade marinated anchovies are an age-old tradition. In inland centers in northern Italy, the prevalence was directly related to the number of inhabitants. The analysis of the impact of immigration on the prevalence of Anisakis hypersensitivity showed that about 60% of sensitized subjects in Milano and Torino came from southern Italy or from non-European countries. Conclusions: Anisakis hypersensitivity and allergy are mainly a matter of dietary habits. Areas where marinated anchovies are popular can be considered as 'endemic' for this type of food allergy, whereas immigration and, possibly, new or imported trendy food styles, such as eating raw fish carpaccios or sushi, are a major causative factor in big cities of inland zones.
Exposure-response of olaratumab for survival outcomes and safety when combined with doxorubicin in soft tissue sarcoma (STS) patients
Authors: R. Jones, G. Mo, J.R. Baldwin, R.D. Nichols, R.L. Ilaria, I. Conti, D.M. Cronier, W.D. Tap
Journal: Annals of Oncology (2016)
Extreme Trait Whole-Genome Sequencing Identifies <i>PTPRO</i> as a Novel Candidate Gene in Emphysema with Severe Airflow Obstruction
Authors: Josiah E. Radder, Yingze Zhang, Alyssa D. Gregory, Shibing Yu, Neil J. Kelly, Joseph K. Leader, Naftali Kaminski, Frank C. Sciurba, Steven D. Shapiro
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Genetic association studies in chronic obstructive pulmonary disease have primarily tested for association with common variants, the results of which explain only a portion of disease heritability. Because rare variation is also likely to contribute to susceptibility, we used whole-genome sequencing of subjects with clinically extreme phenotypes to identify genomic regions enriched for rare variation contributing to chronic obstructive pulmonary disease susceptibility.To identify regions of rare genetic variation contributing to emphysema with severe airflow obstruction.We identified heavy smokers that were resistant (n = 65) or susceptible (n = 64) to emphysema with severe airflow obstruction in the Pittsburgh Specialized Center of Clinically Oriented Research cohort. We filtered whole-genome sequencing results to include only rare variants and conducted single variant tests, region-based tests across the genome, gene-based tests, and exome-wide tests.We identified several suggestive associations with emphysema with severe airflow obstruction, including a suggestive association of all rare variation in a region within the gene ZNF816 (19q13.41; P = 4.5 × 10-6), and a suggestive association of nonsynonymous coding rare variation in the gene PTPRO (P = 4.0 × 10-5). Association of rs61754411, a rare nonsynonymous variant in PTPRO, with emphysema and obstruction was demonstrated in all non-Hispanic white individuals in the Pittsburgh Specialized Center of Clinically Oriented Research cohort. We found that cells containing this variant have decreased signaling in cellular pathways necessary for survival and proliferation.PTPRO is a novel candidate gene in emphysema with severe airflow obstruction, and rs61754411 is a previously unreported rare variant contributing to emphysema susceptibility. Other suggestive candidate genes, such as ZNF816, are of interest for future studies.
Comparative molecular analyses of pancreatic cancer (PC): Younger vs. older patients (pts)
Authors: M. Salem, P. Philip, R. Feldman, J. Hwang, M. Pishvaian, J. Xiu, W. Eldeiry, S. Reddy, Z. Gatalica, N. Trivedi, A. Zareb, B.S. Colton, H. Wang, A. Shields, J. Marshall
Journal: Annals of Oncology (2016)
RBIO-06. CROSSTALK OF ErbB2 WITH LEF1 REGULATES JAGGED1-MEDIATED RADIORESISTANCE IN GLIOBLASTOMA
Authors: Divya Kesanakurti, Jihong Xu, Balveen Kaur, Vinay Puduvalli, Alessandro Canella
Journal: Neuro-Oncology (2016)

ErbB2 (Her2) belongs to the family of EGF receptor tyrosine kinases and plays a vital oncogenic role in several cancers. Gliomas are reported to have aberrant overexpression of ErbB2, but its role in glioma biology and treatment resistance have not been well studied. We have previously reported that ionizing radiation (IR) increases cell invasiveness and radioresistance. In our preliminary studies, we observed that shRNA mediated ErbB2 silencing in glioma cell lines resulted in a significant inhibition of proliferation and invasion which was associated with a suppression of Notch signaling. To examine its role in radioresistance, we treated glioma cells with IR and observed that the cells exhibited a significant increase in invasiveness associated with nuclear translocation of ErbB2 and transcriptional upregulation of the Notch receptor ligand, Jagged-1. To further investigate the relationship between ErbB2 translocation and Notch signaling, we performed immunoprecipitation and transcription factor binding array studies in IR-treated cells which revealed an interesting association of nuclear ErbB2 with the TCF1/LEF1 complex that is known to transcriptionally regulate Jagged-1 expression. In addition, chromatin-binding assays showed recruitment of ErbB2 to putative LEF1 consensus sites of the Jagged-1 promoter, suggesting a potential role for ErbB2 in the transcriptional regulation of Jagged-1 and consequently of Notch signaling after radiation in glioma cells. Further, downregulation of ErbB2 inhibited Notch signaling and decreased IR-induced invasion in these cells. These in vitro findings were further validated in an orthotopic intracranial glioma model that showed significant growth inhibition of intracranial ErbB2.shRNA-tumors compared to controls. Our results suggest a novel role for nuclear ErbB2 in regulating Jagged1/Notch1-signaling mediated cell invasion in IR treated cells, and provide a potential strategy for targeting ErbB2-mediated Notch signaling to overcome radioresistance in gliomas.
Value of Cardiovascular Magnetic Resonance Imaging–Derived Baseline Left Ventricular Ejection Fraction and Volumes for Precise Risk Stratification of Patients With Ischemic Cardiomyopathy
Authors: Ramdas G. Pai, Padmini Varadarajan, Jean L. Rouleau, Amanda L. Stebbins, Eric J. Velazquez, Hussein R. Al-Khalidi, Gerald M. Pohost
Journal: JAMA Cardiology (2017)

This study tests the hypothesis that cardiovascular magnetic resonance–derived left ventricular ejection fraction and volumes would provide improved risk stratification in patients undergoing coronary artery bypass surgery for ischemic cardiomyopathy.
Implications of key differences across 12 KRAS mutation detection technologies and their relevance in clinical practice
Authors: J.L. Sherwood, A. Rettino, H. Brown, A. Schreieck, B. Claes, G. Clark, B. Agrawal, R. Chaston, P. Choppa, A.O.H. Nygren, A. Kohlman
Journal: Annals of Oncology (2016)
Lymph node dissection in early epithelial ovarian cancer (EOC) – Results from a population based study
Authors: J.T. Man, C.C.H. Khoo, B. Gao, S. Fereday, J. Hung, A.O.C.S. Group, P. Harnett, D.D. Bowtell, A. Brand, A. Defazio
Journal: Annals of Oncology (2016)
TET2 Mutations Are Associated with Poor Outcome in Pediatric AML: A Report From the Children's Oncology Group
Authors: Matthew A. Kutny, Todd A. Alonzo, Robert B. Gerbing, Daniel Geraghty, Alan S. Gamis, Beverly Lange, Nyla A. Heerema, Janet Franklin, Susana C. Raimondi, Betsy A. Hirsch, Soheil Meshinchi
Journal: Blood (2011)
Osteotropism of NETs: role of the CXCR4/CXCL12 axis in regulating the EMT process
Authors: M. Cives, V. Simone, F.M. Rizzo, D. Quaresmini, S. D'Oronzo, C. Felici, D. Lovero, F. Silvestris
Journal: Annals of Oncology (2016)
Soluble TREM2 induces inflammatory responses and enhances microglial survival
Authors: Li Zhong, Xiao-Fen Chen, Tingting Wang, Zhe Wang, Chunyan Liao, Zongqi Wang, Ruizhi Huang, Daxin Wang, Xinxiu Li, Linbei Wu, Lin Jia, Honghua Zheng, Meghan Painter, Yuka Atagi, Chia-Chen Liu, Yun-Wu Zhang, John D. Fryer, Huaxi Xu, Guojun Bu
Journal: The Journal of Experimental Medicine (2017)

Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor expressed in microglia in the brain. A soluble form of TREM2 (sTREM2) derived from proteolytic cleavage of the cell surface receptor is increased in the preclinical stages of AD and positively correlates with the amounts of total and phosphorylated tau in the cerebrospinal fluid. However, the physiological and pathological functions of sTREM2 remain unknown. Here, we show that sTREM2 promotes microglial survival in a PI3K/Akt-dependent manner and stimulates the production of inflammatory cytokines depending on NF-κB. Variants of sTREM2 carrying AD risk-associated mutations were less potent in both suppressing apoptosis and triggering inflammatory responses. Importantly, sTREM2 delivered to the hippocampi of both wild-type and Trem2-knockout mice elevated the expression of inflammatory cytokines and induced morphological changes of microglia. Collectively, these data indicate that sTREM2 triggers microglial activation inducing inflammatory responses and promoting survival. This study has implications for the pathogenesis of AD and provides insights into targeting sTREM2 pathway for AD therapy.
Effect of a small-molecule MDM2/MDMX inhibitor on cell cycle arrest and apoptosis in breast cancer cells.
Authors: Qian Qian Geng, En Xiao Li, Dan Feng Dong, Yin Ying Wu, Jie Wang, Yi Li
Journal: Journal of Clinical Oncology (2013)

e22096 Background: The MDM2 inhibitor which disrupted the MDM2-p53 interaction made little effort on the activation of p53 for breast cancer treatments, due to MDMX over expression. Previously a small molecule inhibitor targeting at MDM2 and MDMX had been successfully synthesized. We tested anti-tumor activity of the small molecule MDM2/MDMX inhibitor, compared with nutlin-3α, a well characterized MDM2 inhibitor, in the wild-type (wt) and mutant (mt) p53 breast cancer cell lines. Methods: Human breast cancer cell lines MCF-7 (wt-p53), ZR-7530 (wt-p53), BT-474 (mt-p53) and MDA-MB-231 (mt-p53) were cultured and treated with the small molecule MDM2/MDMX inhibitor, nutlin-3α or phosphate buffer solution (PBS) for 48 hrs separately. MTT for cell viability, FCM for cell cycle arrest and Annexin V FITC/PI for cell apoptosis were performed. The mechanism of antitumor activity of the small molecule MDM2/MDMX inhibitor was determined by Western-Blot analysis. Results: The inhibitor of MDM2 and MDMX inhibited cell growth and induced cell cycle arrest and apoptosis in mt-p53 breast cancer cells while nutlin-3α cannot. In the breast cancer cells with wt-p53, both of them inhibited cell growth, induced cell cycle arrest and apoptosis, but MDM2/MDMX inhibitor was proven to be more effective. Western Blot revealed that there was higher level of p53 expression in breast cancer cells treated with MDM2/MDMX inhibitor than nutlin-3α. The marked increases in p21, Bax and PUMA expressions were abserved in both wt-p53 and mt-p53 breast cancer cells which indicated that the small molecule MDM2/MDMX inhibitor induced cell apoptosis through p21, Bax and PUMA over expressions. Conclusions: The small molecule MDM2/MDMX inhibitor would be able to suppress cell proliferation, induce cell cycle arrest and apoptosis, activate p53 more effective than nutlin-3α in breast cancer cells, no matter with p53 status. P21, Bax and PUMA were involved in the mechanism of apoptosis induction. The inhibitor of targeting at both MDM2 and MDMX will be a novel treatment for breast cancer p53-independent status in the future.
A phase 1 study of PF-06647020, an antibody-drug conjugate (ADC) targeting protein tyrosine kinase 7 (PTK7), in patients with advanced solid tumors including platinum resistant ovarian cancer (OVCA)
Authors: J.C. Sachdev, M. Maitland, M. Sharma, V. Moreno, V. Boni, S. Kummar, B. Gibson, D. Xuan, T. Joh, E. Powell, A. Jackson-Fisher, M. Damelin, X. Xin, A. Tolcher, E. Calvo
Journal: Annals of Oncology (2016)
Darinaparsin in T-Cell Lymphoma (TCL) and Hodgkin Lymphoma (HL) Cells Lines and SCID Xenograft Mouse Models: Single-Agent Activity and Synergistic Cell Death Combined with a PI3K/mTOR Inhibitor
Authors: Ravi Dashnamoorthy, Savita Bhalla, Jennifer Crombie, Irawati Kandela, Andrew Mazar, Andrew M. Evens
Journal: Blood (2012)
Subcortical brain volume differences in participants with attention deficit hyperactivity disorder in children and adults: a cross-sectional mega-analysis
Authors: Martine Hoogman, Janita Bralten, Derrek P Hibar, Maarten Mennes, Marcel P Zwiers, Lizanne S J Schweren, Kimm J E van Hulzen, Sarah E Medland, Elena Shumskaya, Neda Jahanshad, Patrick de Zeeuw, Eszter Szekely, Gustavo Sudre, Thomas Wolfers, Alberdingk M H Onnink, Janneke T Dammers, Jeanette C Mostert, Yolanda Vives-Gilabert, Gregor Kohls, Eileen Oberwelland, Jochen Seitz, Martin Schulte-Rüther, Sara Ambrosino, Alysa E Doyle, Marie F Høvik, Margaretha Dramsdahl, Leanne Tamm, Theo G M van Erp, Anders Dale, Andrew Schork, Annette Conzelmann, Kathrin Zierhut, Ramona Baur, Hazel McCarthy, Yuliya N Yoncheva, Ana Cubillo, Kaylita Chantiluke, Mitul A Mehta, Yannis Paloyelis, Sarah Hohmann, Sarah Baumeister, Ivanei Bramati, Paulo Mattos, Fernanda Tovar-Moll, Pamela Douglas, Tobias Banaschewski, Daniel Brandeis, Jonna Kuntsi, Philip Asherson, Katya Rubia, Clare Kelly, Adriana Di Martino, Michael P Milham, Francisco X Castellanos, Thomas Frodl, Mariam Zentis, Klaus-Peter Lesch, Andreas Reif, Paul Pauli, Terry L Jernigan, Jan Haavik, Kerstin J Plessen, Astri J Lundervold, Kenneth Hugdahl, Larry J Seidman, Joseph Biederman, Nanda Rommelse, Dirk J Heslenfeld, Catharina A Hartman, Pieter J Hoekstra, Jaap Oosterlaan, Georg von Polier, Kerstin Konrad, Oscar Vilarroya, Josep Antoni Ramos-Quiroga, Joan Carles Soliva, Sarah Durston, Jan K Buitelaar, Stephen V Faraone, Philip Shaw, Paul M Thompson, Barbara Franke
Journal: The Lancet Psychiatry (2017)
Observational study of chondrodermatitis nodularis helicis treated with methyl aminolevulinate photodynamic therapy
Authors: Ana Julia García-Malinis, Lucia Turrión-Merino, Bibiana Pérez-García, David Saceda-Corralo, Antonio Harto-Castaño, Yolanda Gilaberte
Journal: Journal of the American Academy of Dermatology (2017)
OS7.4 Outcome of patients presenting with brain metastasis as first manifestation of cancer
Authors: L. M. Füreder, A. S. Berghoff, B. Gatterbauer, K. Dieckmann, G. Widhalm, J. A. Hainfellner, P. Birner, R. Bartsch, C. C. Zielinski, M. Preusser
Journal: Neuro-Oncology (2016)
Mindfulness-based Stress Reduction (MBSR) in cancer patients: prospective single-centre case-control study (MIND4ME study)
Authors: M. Maur, A. Guida, M.P. Ricchieri, F. Caggia, G. Pontoni, S. Poletti, F. Gavioli, A. Fontana, V. Tarantino, S. Cascinu, R. Ferrari
Journal: Annals of Oncology (2016)
Modulation of Neuronal Nitric Oxide Synthase (NOS1) Sensitized NOS1 -/- Mice to Total Body Irradiaton.
Authors: Brandon Stone, Malolan Rajagopalan, Jean-Claude Rwigema, Umar Salimi, Medical, Tracy Dixon, Darcy Franicola, Julie Goff, Michael W. Epperly, Anthony Bauer, Joel Greenberger
Journal: Blood (2009)
GENT-21. ATRX DEFICIENCY PROMOTES INVASION AND ALTERS THE DIFFERENTIATION CAPACITY OF GLIOMA CELLS OF ORIGIN BY DYSREGULATING GENOME-WIDE CHROMATIN ACCESSIBILITY AND MODULATING TRANSCRIPTIONAL PROGRAMS
Authors: Carla Danussi, Promita Bose, Prasanna Parthasarathy, Pedro Silberman, Sevin Turcan, David Picketts, Timothy Chan, Jason Huse
Journal: Neuro-Oncology (2016)

Comprehensive genomic profiling in cancer continues to reveal frequent alterations in epigenetic regulators, firmly implicating chromatin biology in the oncogenic process. Inactivating mutations in the SWI/SNF family member ATRX invariably pair with mutations in TP53 and IDH1/2 and represent defining molecular alterations in diffusely infiltrating gliomas. So far, ATRX deficiency has been linked to a wide spectrum of physiological dysfunction, including aberrant gene regulation, abnormal telomere maintenance, genomic instability, and aneuploidy, but the molecular mechanism(s) by which ATRX deficiency promotes oncogenesis are still largely unknown. To understand the role of Atrx loss-of-function mutations in gliomagenesis, we inactivated Atrx in Tp53-/- murine neuroepithelial progenitor cells (NPCs), which have been implicated as potential glioma cells of origin by several prior studies. Interestingly, Atrx loss induced NPCs to stop growing as neurospheres and adopt an adherent phenotype, while also exhibiting significantly increased cellular motility by transwell migration assay, the latter an established pathogenic feature of diffusely infiltrating gliomas. Moreover, when cultured in differentiation conditions, Atrx deficient cells displayed upregulation of astrocyte markers and downregulation of neuronal and oligodendrocyte markers, suggesting that Atrx directly regulates NPCs differentiation state and potential. Notably, the observed phenotypes correlated with altered gene expression profiles involving molecular networks implicated in development, regulation of signal transduction and cellular motility and invasion. Integrating these transcriptional changes with shifts in chromatin accessibility occurring with Atrx deficiency and genome-wide Atrx distribution, as determined by ChIP-seq, revealed highly significant spatial correlations between differentially expressed genes, regions of altered chromatin compaction, and genomic sites normally occupied by Atrx. Taken together, these findings demonstrate that Atrx deficiency induces widespread disruptions in chromatin organization, which in turn lead to dramatic shifts in gene expression and acquisition of disease-relevant phenotypes in putative glioma cells of origin.
Evaluation of Genotoxicity of Chromatin Modifying Agents Expanded Hematopoietic Graft in a Non-Human Primate Model.
Authors: Simona Taioli, Benjamin Petro, Sujata Gaitonde, John G. Quigley, Valerie Lindgren, Manuel Borce, Karen Sweiss, Damiano Rondelli, Nadim Mahmud
Journal: Blood (2012)
Regulation of FANCL by Glycogen Synthase Kinase-3beta Links the Fanconi anemia pathway to Self Renewal and Survival Signals
Authors: Kim-Hien T. Dao, Michael D. Rotelli, Jane E. Yates, Brieanna Brown, Juha Rantala, Keaney Rathbun, Jeffrey W Tyner, Brian J. Druker, Grover C. Bagby
Journal: Blood (2012)
Patterns of Primary Treatment, Trial Participation and Survival in Adult Acute Myeloid Leukemia: A Nationwide Population-Based Study Among Patients Diagnosed in the Netherlands from 1989 to 2012
Authors: Avinash G Dinmohamed, Otto Visser, Yvette van Norden, Nicole MA Blijlevens, Jan J. Cornelissen, Gerwin A Huls, Peter C Huijgens, Pieter Sonneveld, Arjan A van de Loosdrecht, Gert J Ossenkoppele, Bob Löwenberg, Mojca Jongen-Lavrencic
Journal: Blood (2014)
Intraclonal Heterogeneity Associates with Clonal Stability in Multiple Myeloma
Authors: Noemi Puig, Isabel Conde, Cristina Jimenez, Maria E Sarasquete, Ana Balanzategui, Miguel Alcoceba, Jonathan Quintero, Carmen Chillon, Elena Sebastian, Rocío Corral, Luis Marín, Norma C Gutiérrez, Maria-Victoria Mateos, Marcos Gonzalez-Diaz, Jesus F. San Miguel, Ramon Garcia-Sanz
Journal: Blood (2014)
Health-related quality-of-life (HRQOL) impact of dabrafenib (D) and trametinib (T) vs BRAF inhibitor (BRAFi) monotherapy by lactate dehydrogenase (LDH) in patients (pts) with BRAF V600–mutant melanoma
Authors: J.J. Grob, C. Robert, G.V. Long, D. Stroyakovskiy, E. Levchenko, V. Chiarion-Sileni, K. Flaherty, P. Nathan, A. Ribas, M. Davies, J. Zhang, L. Chen, B. Mookerjee, S. Redhu, D. Schadendorf
Journal: Annals of Oncology (2016)
Internal Tandem Duplication Mutations of Flt3 (ITD-Flt3) up-Regulate p21 WAF1/CDKN1 Protein That Negatively Regulates Aberrant Proliferation of Hematopoietic Cells Induced by ITD-Flt3.
Authors: Mariko Abe, Louis M. Pelus, Takeshi Taketani, Seiji Yamaguchi, Seiji Fukuda
Journal: Blood (2009)
A Multicentre Phase I/II Study of TAS-102 with nintedanib in patients with metastatic colorectal cancer refractory to standard therapies (N-task force: EPOC1410)
Authors: K. Yamazaki, Y. Kuboki, E. Shinozaki, H. Hara, Y. Komatsu, T. Nishina, K. Yamaguchi, S. Yuki, H. Bando, M. Asayama, T. Tsushima, S. Hamauchi, H. Nakatsumi, T. Kajiwara, M. Wakabayashi, S. Nomura, A. Sato, T. Doi, A. Ohtsu, T. Yoshino
Journal: Annals of Oncology (2017)
P06.01 Correlating fluorescence and conventional MRI with proliferation markers in glioblastoma
Authors: F. T. Rasul, T. Al-Mayhani
Journal: Neuro-Oncology (2016)

Glioblastoma is the commonest primary brain cancer and is associated with a devastating prognosis. Median survival is just 14 months with surgery, chemoradiotherapy. Tumour heterogeneity likely underlies poor prognosis and treatment resistance. We sought to correlate imaging and biological features of tumour heterogeneity. We used contrast enhancement on conventional MRI and fluorescence as markers for proliferation in glioblastoma. We quantified the expression of three cell surface receptors CD133, EGFR and NG2 in fluorescent positive and fluorescent negative areas using flow cytometry. We also quantified the expression of these three cell surface receptors according to their contrast enhancement status (positive or negative). Eight patients with histologically confirmed glioblastoma were studied. Nineteen tumour samples were acquired. We found a statistically significant correlation between fluorescence and expression of all three cell surface receptors (CD 133 p-value = 0.015 (p <0.05), EGFR p-value = 0.035, NG2 p-value 0.015). We observed a statistically non-significant decrease in expression of all three cell surface receptors in contrast enhancing areas of tumour. Flourescence may be used as a guide to identify areas of high proliferation in glioblastoma. Contrast enhancement does not identify areas of high proliferation. Further work is required to confirm these findings.
A High Proportion of CD4+CD25+ Lymphocytes Associates with a Risk of aGvHD and Inversely Correlate with Proportions of CMV and EBV Specific CD8+ Cells in Blood.
Authors: Andrzej Lange, Dorota Dlubek, Daria Drabczak-Skrzypek, Emilia Jaskula, Dorota Duda
Journal: Blood (2006)
Effect of a condolence letter on grief symptoms among relatives of patients who died in the ICU: a randomized clinical trial
Authors: Nancy Kentish-Barnes, Sylvie Chevret, Benoît Champigneulle, Marina Thirion, Virginie Souppart, Marion Gilbert, Olivier Lesieur, Anne Renault, Maïté Garrouste-Orgeas, Laurent Argaud, Marion Venot, Alexandre Demoule, Olivier Guisset, Isabelle Vinatier, Gilles Troché, Julien Massot, Samir Jaber, Caroline Bornstain, Véronique Gaday, René Robert, Jean-Philippe Rigaud, Raphaël Cinotti, Mélanie Adda, François Thomas, Laure Calvet, Marion Galon, Zoé Cohen-Solal, Alain Cariou, Elie Azoulay
Journal: Intensive Care Medicine (2017)