tbuckley/cabot-search huggingface dataset:
How the Coronavirus Disease-2019 May Improve Care: Rethinking Cervical Cancer Prevention
Authors: Sarah Feldman, Jennifer S Haas
Journal: JNCI Journal of the National Cancer Institute (2020)

These past months of the coronavirus disease-2019 (COVID-2019) pandemic have given us ample opportunity to reflect on the US health-care system. Despite overwhelming tragedy, it is an opportunity for us to learn and to change. As we postpone routine visits because of the pandemic, we worry about risks for patients who delay cancer screening. We use cervical cancer screening and prevention as an example of how we can use some "lessons learned" from the pandemic to prevent "collateral losses," such as an increase in cancers. COVID-2019-related health-system changes, like the more rapid evaluation of diagnostic tests and vaccines, the transition to compensated virtual care for most counseling and education visits, and broadened access to home services, offer potential benefits to the delivery of cervical cancer screening and prevention. While we detail the case for cervical cancer prevention, many of the issues discussed are generalizable to other preventative measures. It would be a tragedy if the morbidity and mortality of COVID-2019 are multiplied because of additional suffering caused by delayed or deferred cancer screening and diagnostic evaluation-but maybe with creativity and reflection, we can use this pandemic to improve care.
PREDICTORS OF CIRRHOSIS: NON-INVASIVE MRI-BASED LIVERMULTISCAN CAN PREDICT CLINICAL EVENTS IN CIRRHOTIC PATIENTS
Authors: J P Wedd, J Haydek, S Mouchti, D Halliday, M Kelly, S Neubauer, R Banerjee, P Sharma, T Kitajima, J P Norvell
Journal: Hepatology (2019)
Qualitative Assessment of Rapid System Transformation to Primary Care Video Visits at an Academic Medical Center
Authors: Malathi Srinivasan, Steven Asch, Stacie Vilendrer, Samuel Crandall Thomas, Rika Bajra, Linda Barman, Lauren Michelle Edwards, Heather Filipowicz, Lena Giang, Olivia Jee, Megan Mahoney, Ian Nelligan, Anuradha Jayant Phadke, Elise Torres, Maja Artandi
Journal: Annals of Internal Medicine (2020)

The coronavirus disease 2019 pandemic spurred health systems across the world to quickly shift from in-person visits to safer video visits.
Inhibition of Glutaredoxin 5 predisposes Cisplatin-resistant Head and Neck Cancer Cells to Ferroptosis
Authors: Jaewang Lee, Ji Hyeon You, Daiha Shin, Jong-Lyel Roh
Journal: Theranostics (2020)

Rationale: Loss of iron-sulfur cluster function predisposes cancer cells to ferroptosis by upregulating iron-starvation response, but the role of glutaredoxin 5 (GLRX5) silencing in ferroptosis remains unknown. We examined the role of GLRX5 functional loss in promoting ferroptosis in cisplatin-resistant head and neck cancer (HNC) cells. Methods: The effects of sulfasalazine treatment and GLRX5 gene silencing were tested on HNC cell lines and mouse tumor xenograft models. These effects were analyzed concerning cell viability and death, lipid reactive oxygen species (ROS) and mitochondrial iron production, labile iron pool, mRNA/protein expression, and malondialdehyde assays. Results: Cyst(e)ine deprivation, erastin, or sulfasalazine induced ferroptosis in HNC cells, which was relatively less sensitive in cisplatin-resistant HNC cells. Sulfasalazine or cyst(e)ine deprivation-induced ferroptosis resulted from increased lipid peroxidation and intracellular free iron, which were significantly promoted by short-interfering RNA or short hairpin RNA (shRNA) targeting GLRX5 (P<0.05). GLRX5 silencing activated iron-starvation response and boosted up intracellular free iron through the iron-responsive element-binding activity of increased iron regulatory protein (increased transferrin receptor and decreased ferritin). These effects were rescued by resistant GLRX5 cDNA but not by catalytically inactive mutant GLRX5 K101Q. The same results were noted in an in vivo mouse model transplanted with vector or shGLRX5-transduced HNC cells and treated with sulfasalazine. Conclusion: Our data suggest that inhibition of GLRX5 predisposes therapy-resistant HNC cells to ferroptosis.
Serum (1,3)-Beta-d-Glucan has suboptimal performance for the diagnosis of Pneumocystis jirovecii pneumonia in cancer patients and correlates poorly with respiratory burden as measured by quantitative PCR
Authors: Ariel D. Szvalb, Alexandre E. Malek, Ying Jiang, Micah M. Bhatti, Sebastian Wurster, Dimitrios P. Kontoyiannis
Journal: Journal of Infection (2020)
Phase III results of exatecan (DX-8951f) versus gemcitabine (Gem) in chemotherapy-naïve patients with advanced pancreatic cancer (APC)
Authors: P. Cheverton, H. Friess, C. Andras, T. Salek, C. Geddes, G. Bodoky, J. Valle, Y. Humblet
Journal: Journal of Clinical Oncology (2004)

4005 Background: Ensiv (Exatecan) is a novel hexacyclic, water-soluble, topoisomerase-1 inhibitor. Ensiv has single-agent and combination activity with Gem in APC (D'Adamo, et al. ProcASCO, 2001; O'Reilly, et al. ProcASCO, 2002). Methods: A multi-centre randomised phase III trial comparing Ensiv with gemcitabine in APC has been completed. Eligibility included KPS ≥ 60%; locally advanced or metastatic disease; no prior chemotherapy. Patients (pts) were randomised in a 1:1 ratio to Ensiv (0.5 mg/m2 daily x 5 q3w) or gemcitabine (1000 mg/m2 weekly x 7 then 1 week rest, then weekly x 3 q4w). Treatment continued until disease progression or intolerable toxicity. Primary endpoint was overall survival (OS). Study was powered to demonstrate a 50% increase in OS from 5.1 to 7.65 months. Analysis will be conducted based on 263 events (deaths) having occurred. An independent data safety monitoring board monitored the trial. Results: Altogether, an Intent To Treat (ITT) population of 339 pts (Ensiv 169, Gem 170) were randomised at 67 sites between July 2001 and Jan 2003. Of these 330 (165 Ensiv; 165 Gem) received treatment. Demographic factors were well balanced for age, sex, PS and disease extent. In the ITT population for Ensiv 139 pts died and 30 were censored (gem 137; 33) at data cut-off following the 263 event ocurrence as prescribed in the statistical analysis plan. Survival: Median Survival Times (MST) were Ensiv 151 days; Gem 197 days), 6-month Survival rates Ensiv 44.1%; Gem 51.1%, and 12-month Survival rates Ensiv 17.9%; Gem 22.1%. Response rates seen were: Ensiv 0CR, 1PR, 75 SD; Gem 3CR, 10PR, 78 SD. Median Time to Tumor Progression (TTP) was; Ensiv 85 days; Gem 132 days. Gem was superior to Ensiv in both weight loss and pain worsening ( weight loss; Ensiv 69 days vs Gem 114 days; pain VAS; 112 days vs 236 days; analgesic consumption increase; 69 days vs 114 days) as well as in QOL evaluation. Treatment emergent toxicities are tabulated below: Conclusions: Single agent Ensiv did not show the expected increase in survival or clinical benefit over gemcitabine in this study Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Daiichi Pharmaceuticals UK Ltd Daiichi Pharmaceuticals
If You Build It, They Will Come
Authors: Justin Lowenthal, Sharon Gerecht
Journal: Circulation Research (2020)

odeling of myocardial physiology in vitro has advanced considerably in recent years, with stem cell-based approaches to generating cardiomyocytes (CMs) and supportive vascular/stromal cells advancing in tandem with novel methods to engineer biomimetic microenvironments. 1-3However, achieving macroscopic structural hierarchy and tissue-level function-such as vascularized cardiac tissues mimicking cardiac conduction and chamber pumping behaviorcontinues to be challenging.This roadblock has impaired efforts to use in vitro models of cardiac physiology and disease for mechanistic studies, as platforms for drug discovery, and as precursors for translational applications.
Locus-Specific Differential DNA Methylation and Urinary Arsenic: An Epigenome-Wide Association Study in Blood among Adults with Low-to-Moderate Arsenic Exposure
Authors: Anne K. Bozack, Arce Domingo-Relloso, Karin Haack, Mary V. Gamble, Maria Tellez-Plaza, Jason G. Umans, Lyle G. Best, Joseph Yracheta, Matthew O. Gribble, Andres Cardenas, Kevin A. Francesconi, Walter Goessler, Wan-Yee Tang, M. Daniele Fallin, Shelley A. Cole, Ana Navas-Acien
Journal: Environmental Health Perspectives (2020)

Background: Chronic exposure to arsenic (As), a human toxicant and carcinogen, remains a global public health problem. Health risks persist after As exposure has ended, suggesting epigenetic dysregulation as a mechanistic link between exposure and health outcomes. Objectives: We investigated the association between total urinary As and locus-specific DNA methylation in the Strong Heart Study, a cohort of American Indian adults with low-to-moderate As exposure [total urinary As, mean (±SD) μg/g creatinine: 11.7 (10.6)]. Methods: DNA methylation was measured in 2,325 participants using the Illumina MethylationEPIC array. We implemented linear models to test differentially methylated positions (DMPs) and the DMRcate method to identify regions (DMRs) and conducted gene ontology enrichment analysis. Models were adjusted for estimated cell type proportions, age, sex, body mass index, smoking, education, estimated glomerular filtration rate, and study center. Arsenic was measured in urine as the sum of inorganic and methylated species. Results: In adjusted models, methylation at 20 CpGs was associated with urinary As after false discovery rate (FDR) correction (FDR&lt; 0.05). After Bonferroni correction, 5 CpGs remained associated with total urinary As (pBonferroni&lt;0.05), located in SLC7A11, ANKS3, LINGO3, CSNK1D, ADAMTSL4. We identified one DMR on chromosome 11 (chr11:2,322,050-2,323,247), annotated to C11orf2; TSPAN32 genes. Discussion: This is one of the first epigenome-wide association studies to investigate As exposure and locus-specific DNA methylation using the Illumina MethylationEPIC array and the largest epigenome-wide study of As exposure. The top DMP was located in SLC7A11A, a gene involved in cystine/glutamate transport and the biosynthesis of glutathione, an antioxidant that may protect against As-induced oxidative stress. Additional DMPs were located in genes associated with tumor development and glucose metabolism. Further research is needed, including research in more diverse populations, to investigate whether As-related DNA methylation signatures are associated with gene expression or may serve as biomarkers of disease development. https://doi.org/10.1289/EHP6263
Prevention of Hepatitis A Virus Infection in the United States: Recommendations of the Advisory Committee on Immunization Practices, 2020
Authors: Noele P. Nelson, Mark K. Weng, Megan G. Hofmeister, Kelly L. Moore, Mona Doshani, Saleem Kamili, Alaya Koneru, Penina Haber, Liesl Hagan, José R. Romero, Sarah Schillie, Aaron M. Harris
Journal: MMWR Recommendations and Reports (2020)

HEPATITIS A IS A VACCINE-PREVENTABLE, COMMUNICABLE DISEASE OF THE LIVER CAUSED BY THE HEPATITIS A VIRUS (HAV). THE INFECTION IS TRANSMITTED VIA THE FECAL-ORAL ROUTE, USUALLY FROM DIRECT PERSON-TO-PERSON CONTACT OR CONSUMPTION OF CONTAMINATED FOOD OR WATER. HEPATITIS A IS AN ACUTE, SELF-LIMITED DISEASE THAT DOES NOT RESULT IN CHRONIC INFECTION. HAV ANTIBODIES (IMMUNOGLOBULIN G [IGG] ANTI-HAV) PRODUCED IN RESPONSE TO HAV INFECTION PERSIST FOR LIFE AND PROTECT AGAINST REINFECTION; IGG ANTI-HAV PRODUCED AFTER VACCINATION CONFER LONG-TERM IMMUNITY. THIS REPORT SUPPLANTS AND SUMMARIZES PREVIOUSLY PUBLISHED RECOMMENDATIONS FROM THE ADVISORY COMMITTEE ON IMMUNIZATION PRACTICES (ACIP) REGARDING THE PREVENTION OF HAV INFECTION IN THE UNITED STATES. ACIP RECOMMENDS ROUTINE VACCINATION OF CHILDREN AGED 12-23 MONTHS AND CATCH-UP VACCINATION FOR CHILDREN AND ADOLESCENTS AGED 2-18 YEARS WHO HAVE NOT PREVIOUSLY RECEIVED HEPATITIS A (HEPA) VACCINE AT ANY AGE. ACIP RECOMMENDS HEPA VACCINATION FOR ADULTS AT RISK FOR HAV INFECTION OR SEVERE DISEASE FROM HAV INFECTION AND FOR ADULTS REQUESTING PROTECTION AGAINST HAV WITHOUT ACKNOWLEDGMENT OF A RISK FACTOR. THESE RECOMMENDATIONS ALSO PROVIDE GUIDANCE FOR VACCINATION BEFORE TRAVEL, FOR POSTEXPOSURE PROPHYLAXIS, IN SETTINGS PROVIDING SERVICES TO ADULTS, AND DURING OUTBREAKS.
Novel fibrin-fibronectin matrix accelerates mice skin wound healing
Authors: Carlos Poblete Jara, Ou Wang, Thais Paulino do Prado, Ayman Ismail, Frank Marco Fabian, Han Li, Licio A. Velloso, Mark A. Carlson, William Burgess, Yuguo Lei, William H. Velander, Eliana P. Araújo
Journal: Bioactive Materials (2020)

Plasma fibrinogen (F1) and fibronectin (pFN) polymerize to form a fibrin clot that is both a hemostatic and provisional matrix for wound healing. About 90% of plasma F1 has a homodimeric pair of γ chains (γγF1), and 10% has a heterodimeric pair of γ and more acidic γ' chains (γγ'F1). We have synthesized a novel fibrin matrix exclusively from a 1:1 (molar ratio) complex of γγ'F1 and pFN in the presence of highly active thrombin and recombinant Factor XIII (rFXIIIa). In this matrix, the fibrin nanofibers were decorated with pFN nanoclusters (termed γγ'F1:pFN fibrin). In contrast, fibrin made from 1:1 mixture of γγF1 and pFN formed a sporadic distribution of "pFN droplets" (termed γγF1+pFN fibrin). The γγ'F1:pFN fibrin enhanced the adhesion of primary human umbilical vein endothelium cells (HUVECs) relative to the γγF1+FN fibrin. Three dimensional (3D) culturing showed that the γγ'F1:pFN complex fibrin matrix enhanced the proliferation of both HUVECs and primary human fibroblasts. HUVECs in the 3D γγ'F1:pFN fibrin exhibited a starkly enhanced vascular morphogenesis while an apoptotic growth profile was observed in the γγF1+pFN fibrin. Relative to γγF1+pFN fibrin, mouse dermal wounds that were sealed by γγ'F1:pFN fibrin exhibited accelerated and enhanced healing. This study suggests that a 3D pFN presentation on a fibrin matrix promotes wound healing.
B7-H1 Promotes the Functional Effect of Human Gingiva-Derived Mesenchymal Stem Cells on Collagen-Induced Arthritis Murine Model
Authors: Wenbin Wu, Ze Xiu Xiao, Donglan Zeng, Feng Huang, Julie Wang, Yanying Liu, Joseph A. Bellanti, Nancy Olsen, Song Guo Zheng
Journal: Molecular Therapy (2020)

Recent studies found that mesenchymal stem cells (MSCs), by virtue of their tissue recovery and immunoregulatory properties, have shown a broad prospect for applications in various autoimmune and degenerative diseases. Although the potential therapeutic use of MSCs is considerable, studies and clinical treatment efficacy are preliminary due to the heterogeneity of MSCs. Herein, based on RNA-sequencing (RNA-seq) and single cell sequence properties, we demonstrated that B7-H1 plays an important role in the immunosuppressive function of human gingiva-derived mesenchymal stem cells (GMSCs) in a collagen-induced arthritis murine model that is dependent on STAT3 signaling. Our data offer convincing evidence that B7-H1 expression by GMSCs helps to identify a new subpopulation of MSCs with a greater immunosuppressive property. The approach provides a unique and additional strategy for stem cells-based therapies of autoimmune and other inflammatory diseases. Recent studies found that mesenchymal stem cells (MSCs), by virtue of their tissue recovery and immunoregulatory properties, have shown a broad prospect for applications in various autoimmune and degenerative diseases. Although the potential therapeutic use of MSCs is considerable, studies and clinical treatment efficacy are preliminary due to the heterogeneity of MSCs. Herein, based on RNA-sequencing (RNA-seq) and single cell sequence properties, we demonstrated that B7-H1 plays an important role in the immunosuppressive function of human gingiva-derived mesenchymal stem cells (GMSCs) in a collagen-induced arthritis murine model that is dependent on STAT3 signaling. Our data offer convincing evidence that B7-H1 expression by GMSCs helps to identify a new subpopulation of MSCs with a greater immunosuppressive property. The approach provides a unique and additional strategy for stem cells-based therapies of autoimmune and other inflammatory diseases.
Renin-Angiotensin System Overactivation in Type 2 Diabetes: A Risk for SARS-CoV-2 Infection?
Authors: Abu Saleh Md Moin, Ahmed Al-Qaissi, Thozhukat Sathyapalan, Stephen L. Atkin, Alexandra E. Butler
Journal: Diabetes Care (2020)

The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), binds to target cells via the angiotensin-converting enzyme 2 (ACE2) receptor found in cells in blood vessels, lungs, heart, intestines, and kidneys.

Type 2 diabetes (T2D) is a risk factor for acquiring SARS-CoV-2 infection and is associated with severe disease, acute respiratory distress syndrome, and increased mortality (1). Patients with diabetes have ACE2 overexpressed in kidneys and the circulation; further, ACE2 expression may be increased in other tissues (for example, in lungs) as a consequence of angiotensin-receptor blocker (ARB) therapy (a treatment widely used for patients with diabetes), potentially increasing susceptibility to SARS-CoV-2 infection. Previously, circulatory renin-angiotensin system (RAS) activity was described in the setting of sustained hyperglycemia in diabetes (2). Here, we hypothesized that acute normalization of glycemia would modulate RAS overactivation in T2D. Therefore, plasma RAS-related protein levels were determined for T2D subjects versus control subjects at baseline and for T2D subjects after 1-h hyperinsulinemic-euglycemic clamp.

A case-control study of T2D and control subjects was approved by the Yorkshire and the Humber Research Ethics Committee, and all study participants signed an informed consent form prior to participation. The clamp was performed as detailed previously (3); all patients underwent a 10-h fast prior to the clamp, but ad libitum water ingestion was encouraged. Patients were admitted 1 h prior to the clamp procedure and remained in a supine position throughout the study. For the T2D subjects, baseline glucose was mean ± SE 7.6 ± 0.4 mmol/L (136.8 ± 7.2 mg/dL) and …
High fractional exhaled nitric oxide levels may predict short‐term worsening of respiratory oscillometry in asthma
Authors: Yoshinari Endo, Toshihiro Shirai, Keita Hirai, Taisuke Akamatsu, Eishi Kato, Hidehiko Furui, Tetsuo Hiramatsu
Journal: Allergy (2020)

The authors have nothing to disclose. 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.
<i>The Cigarette: A Political History</i>—The Past, Present, and Future of US Tobacco
Authors: Robert N. Proctor
Journal: JAMA (2020)

This Arts and Medicine feature reviews a newly published political history of the US tobacco industry, emphasizing the continuing importance of cigarette smoking to illness and death at a time when the novel coronavirus 2019 (COVID-19) pandemic is perceived as the country’s greatest health threat.
Incidence and outcome of Spitzoid tumour of unknown malignant potential (STUMP): an analysis of cases in the Netherlands from 1999 to 2014
Authors: C.G.H. Ruijter, W. Ouwerkerk, E.H. Jaspars, R. Doorn, R.M. Luiten, M.W. Bekkenk, D.C.K.S. Tio
Journal: British Journal of Dermatology (2020)

Spitz naevi are spindle and epithelioid cell melanocytic proliferations that Sophie Spitz first described in 1948 as juvenile melanomas [1]. The broader group of Spitzoid proliferations is thought to comprise a biological spectrum with benign Spitz naevi, intermediate lesions and malignant Spitzoid melanomas. Intermediate lesions are known by various synonyms such as atypical Spitz tumours (AST) and Spitzoid tumours of unknown malignant potential (STUMP). These intermediate lesions share features of both Spitz naevi and Spitzoid melanomas. Subsequently they represent a diagnostic grey zone and a clinically challenging group [2, 3]. Biological behaviour and clinical course of this intermediate group still remains largely unknown. This results in a clinical challenge regarding the management of AST/STUMP. In an earlier study on Spitzoid proliferations in children and adolescents Bartenstein et al. reported that Spitzoid proliferations very frequently have benign outcomes [3].
Discovery of regulatory noncoding variants in individual cancer genomes by using cis-X
Authors: Yu Liu, Chunliang Li, Shuhong Shen, Xiaolong Chen, Karol Szlachta, Michael N. Edmonson, Ying Shao, Xiaotu Ma, Judith Hyle, Shaela Wright, Bensheng Ju, Michael C. Rusch, Yanling Liu, Benshang Li, Michael Macias, Liqing Tian, John Easton, Maoxiang Qian, Jun J. Yang, Shaoyan Hu, A. Thomas Look, Jinghui Zhang
Journal: Nature Genetics (2020)
T-Cell Dynamics in Chronic Lymphocytic Leukemia under Different Treatment Modalities
Authors: Anna Vardi, Elisavet Vlachonikola, Despoina Papazoglou, Fotis Psomopoulos, Kostantia Kotta, Nikolaos Ioannou, Chrysi Galigalidou, Katerina Gemenetzi, Kostantinos Pasentsis, Maria Kotouza, Evdoxia Koravou, Lydia Scarfó, Michail Iskas, Niki Stavroyianni, Paolo Ghia, Achilles Anagnostopoulos, Anastasia Kouvatsi, Alan G. Ramsay, Kostas Stamatopoulos, Anastasia Chatzidimitriou
Journal: Clinical Cancer Research (2020)

Abstract Purpose: Using next-generation sequencing (NGS), we recently documented T-cell oligoclonality in treatment-naïve chronic lymphocytic leukemia (CLL), with evidence indicating T-cell selection by restricted antigens. Experimental Design: Here, we sought to comprehensively assess T-cell repertoire changes during treatment in relation to (i) treatment type [fludarabine-cyclophosphamide-rituximab (FCR) versus ibrutinib (IB) versus rituximab-idelalisib (R-ID)], and (ii) clinical response, by combining NGS immunoprofiling, flow cytometry, and functional bioassays. Results: T-cell clonality significantly increased at (i) 3 months in the FCR and R-ID treatment groups, and (ii) over deepening clinical response in the R-ID group, with a similar trend detected in the IB group. Notably, in constrast to FCR that induced T-cell repertoire reconstitution, B-cell receptor signaling inhibitors (BcRi) preserved pretreatment clones. Extensive comparisons both within CLL as well as against T-cell receptor sequence databases showed little similarity with other entities, but instead revealed major clonotypes shared exclusively by patients with CLL, alluding to selection by conserved CLL-associated antigens. We then evaluated the functional effect of treatments on T cells and found that (i) R-ID upregulated the expression of activation markers in effector memory T cells, and (ii) both BcRi improved antitumor T-cell immune synapse formation, in marked contrast to FCR. Conclusions: Taken together, our NGS immunoprofiling data suggest that BcRi retain T-cell clones that may have developed against CLL-associated antigens. Phenotypic and immune synapse bioassays support a concurrent restoration of functionality, mostly evident for R-ID, arguably contributing to clinical response.
Open letter from UK based academic scientists to the secretaries of state for digital, culture, media and sport and for health and social care regarding the need for independent funding for the prevention and treatment of gambling harms
Authors: Heather Wardle, James Banks, Paul Bebbington, Lindsey Blank, Henrietta Bowden Jones OBE, Stephanie Bramley, Christopher Bunn, Emma Casey, Rebecca Cassidy, Samuel R Chamberlain, James Close, Nathan Critchlow, Fiona Dobbie, Carolyn Downs, Simon Dymond, Emanuele Fino, Elizabeth Goyder, Cindy Gray, Mark Griffiths, Peter Grindrod, Lee Hogan, Alice Hoon, Kate Hunt, Richard James, Bev John, Jill Manthorpe, Jim McCambridge, David McDaid, Martin McKee, Sally McManus, Antony Moss, Caroline Norrie, David J Nutt, Jim Orford, Rob Pryce, Richard Purves, Gerda Reith, Amanda Roberts, Emmert Roberts, Gareth Roderique-Davies, Jim Rogers, Robert D Rogers, Stephen Sharman, John Strang, Richard Tunney, John Turner, Robert West, David Zendle
Journal: BMJ (2020)

Open letter from UK based academic scientists to the secretaries of state for digital, culture, media and sport and for health and social care regarding the need for independent funding for the prevention and treatment of gambling harms.