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Article ; Online: Clinical and Molecular Epidemiology of Staphylococcal Toxic Shock Syndrome in the United Kingdom

Hema Sharma / Debra Smith / Claire E. Turner / Laurence Game / Bruno Pichon / Russell Hope / Robert Hill / Angela Kearns / Shiranee Sriskandan

Emerging Infectious Diseases, Vol 24, Iss 2, Pp 258-

2018 Volume 266

Abstract: Staphylococcal toxic shock syndrome (TSS) was originally described in menstruating women and linked to TSS toxin 1 (TSST-1)–producing Staphylococcus aureus. Using UK national surveillance data, we ascertained clinical, molecular and superantigenic ... ...

Abstract	Staphylococcal toxic shock syndrome (TSS) was originally described in menstruating women and linked to TSS toxin 1 (TSST-1)–producing Staphylococcus aureus. Using UK national surveillance data, we ascertained clinical, molecular and superantigenic characteristics of TSS cases. Average annual TSS incidence was 0.07/100,000 population. Patients with nonmenstrual TSS were younger than those with menstrual TSS but had the same mortality rate. Children <16 years of age accounted for 39% of TSS cases, most caused by burns and skin and soft tissue infections. Nonmenstrual TSS is now more common than menstrual TSS in the UK, although both types are strongly associated with the tst+ clonal complex (CC) 30 methicillin-sensitive S. aureus lineage, which accounted for 49.4% of all TSS and produced more TSST-1 and superantigen bioactivity than did tst+ CC30 methicillin-resistant S. aureus strains. Better understanding of this MSSA lineage and infections in children could focus interventions to prevent TSS in the future.
Keywords	staphylococcal toxic shock syndrome ; bacteria ; MRSA and other staphylococci ; Staphylococcus aureus ; TSST-1 ; CC30 ; Medicine ; R ; Infectious and parasitic diseases ; RC109-216
Subject code	610
Language	English
Publishing date	2018-02-01T00:00:00Z
Publisher	Centers for Disease Control and Prevention
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Optimisation of laboratory methods for whole transcriptomic RNA analyses in human left ventricular biopsies and blood samples of clinical relevance.

Kerrie L Ford / Maryam Anwar / Rachael Heys / Eltayeb Mohamed Ahmed / Massimo Caputo / Laurence Game / Barnaby C Reeves / Prakash P Punjabi / Gianni D Angelini / Enrico Petretto / Costanza Emanueli

PLoS ONE, Vol 14, Iss 3, p e

2019 Volume 0213685

Abstract: This study aimed to optimise techniques for whole transcriptome and small RNA analyses on clinical tissue samples from patients with cardiovascular disease. Clinical samples often represent a particular challenge to extracting RNA of sufficient quality ... ...

Abstract	This study aimed to optimise techniques for whole transcriptome and small RNA analyses on clinical tissue samples from patients with cardiovascular disease. Clinical samples often represent a particular challenge to extracting RNA of sufficient quality for robust RNA sequencing analysis, and due to availability, it is rarely possible to optimise techniques on the samples themselves. Therefore, we have used equivalent samples from pigs undergoing cardiopulmonary bypass surgery to test different protocols for optimal RNA extraction, and then validated the protocols in human samples. Here we present an assessment of the quality and quantity of RNA obtained using a variety of commercially-available RNA extraction kits on both left ventricular biopsies and blood plasma. RNA extraction from these samples presents different difficulties; left ventricular biopsies are small and fibrous, while blood plasma has a low RNA content. We have validated our optimised extraction techniques on human clinical samples collected as part of the ARCADIA (Association of non-coding RNAs with Coronary Artery Disease and type 2 Diabetes) cohort study, resulting in successful whole transcriptome and small RNA sequencing of human left ventricular tissue.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Low Dose Iron Treatments Induce a DNA Damage Response in Human Endothelial Cells within Minutes.

Inês G Mollet / Dilipkumar Patel / Fatima S Govani / Adam Giess / Koralia Paschalaki / Manikandan Periyasamy / Elaine C Lidington / Justin C Mason / Michael D Jones / Laurence Game / Simak Ali / Claire L Shovlin

PLoS ONE, Vol 11, Iss 2, p e

2016 Volume 0147990

Abstract: Spontaneous reports from patients able to report vascular sequelae in real time, and recognition that serum non transferrin bound iron may reach or exceed 10μmol/L in the blood stream after iron tablets or infusions, led us to hypothesize that ... ...

Abstract	Spontaneous reports from patients able to report vascular sequelae in real time, and recognition that serum non transferrin bound iron may reach or exceed 10μmol/L in the blood stream after iron tablets or infusions, led us to hypothesize that conventional iron treatments may provoke acute vascular injury. This prompted us to examine whether a phenotype could be observed in normal human endothelial cells treated with low dose iron.Confluent primary human endothelial cells (EC) were treated with filter-sterilized iron (II) citrate or fresh media for RNA sequencing and validation studies. RNA transcript profiles were evaluated using directional RNA sequencing with no pre-specification of target sequences. Alignments were counted for exons and junctions of the gene strand only, blinded to treatment types.Rapid changes in RNA transcript profiles were observed in endothelial cells treated with 10μmol/L iron (II) citrate, compared to media-treated cells. Clustering for Gene Ontology (GO) performed on all differentially expressed genes revealed significant differences in biological process terms between iron and media-treated EC, whereas 10 sets of an equivalent number of randomly selected genes from the respective EC gene datasets showed no significant differences in any GO terms. After 1 hour, differentially expressed genes clustered to vesicle mediated transport, protein catabolism, and cell cycle (Benjamini p = 0.0016, 0.0024 and 0.0032 respectively), and by 6 hours, to cellular response to DNA damage stimulus most significantly through DNA repair genes FANCG, BLM, and H2AFX. Comet assays demonstrated that 10μM iron treatment elicited DNA damage within 1 hour. This was accompanied by a brisk DNA damage response pulse, as ascertained by the development of DNA damage response (DDR) foci, and p53 stabilization.These data suggest that low dose iron treatments are sufficient to modify the vascular endothelium, and induce a DNA damage response.
Keywords	Medicine ; R ; Science ; Q
Subject code	612
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Philip Webster / Joanna C. Dawes / Hamlata Dewchand / Katalin Takacs / Barbara Iadarola / Bruce J. Bolt / Juan J. Caceres / Jakub Kaczor / Gopuraja Dharmalingam / Marian Dore / Laurence Game / Thomas Adejumo / James Elliott / Kikkeri Naresh / Mohammad Karimi / Katerina Rekopoulou / Ge Tan / Alberto Paccanaro / Anthony G. Uren

Nature Communications, Vol 10, Iss 1, Pp 1-

Subclonal mutation selection in mouse lymphomagenesis identifies known cancer loci and suggests novel candidates

2019 Volume 1

Abstract: The original version of this Article contained an error in the hyperlink for the online repository http://mulvdb.org which was incorrectly given as http://mulv.lms.mrc.ac.uk. This has been corrected in both the PDF and HTML versions of the Article. ...

Abstract	The original version of this Article contained an error in the hyperlink for the online repository http://mulvdb.org which was incorrectly given as http://mulv.lms.mrc.ac.uk. This has been corrected in both the PDF and HTML versions of the Article.
Keywords	Science ; Q
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Nature Communications, Vol 10, Iss 1, Pp 1-

Subclonal mutation selection in mouse lymphomagenesis identifies known cancer loci and suggests novel candidates

2019 Volume 1

Abstract	The original version of this Article contained an error in the hyperlink for the online repository http://mulvdb.org which was incorrectly given as http://mulv.lms.mrc.ac.uk. This has been corrected in both the PDF and HTML versions of the Article.
Keywords	Science ; Q
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Subclonal mutation selection in mouse lymphomagenesis identifies known cancer loci and suggests novel candidates

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 14

Abstract: Evidence implicating cancer drivers can be sparse when limited to clonal events. Here, the authors present a retrovirus driven in vivo lymphomagenesis time course including hundreds of thousands of subclonal mutations and demonstrate the utility of these ...

Abstract	Evidence implicating cancer drivers can be sparse when limited to clonal events. Here, the authors present a retrovirus driven in vivo lymphomagenesis time course including hundreds of thousands of subclonal mutations and demonstrate the utility of these in mapping the selective forces affecting cancer gene loci, including negatively selected mutations.
Keywords	Science ; Q
Language	English
Publishing date	2018-07-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Subclonal mutation selection in mouse lymphomagenesis identifies known cancer loci and suggests novel candidates

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 14

Abstract	Evidence implicating cancer drivers can be sparse when limited to clonal events. Here, the authors present a retrovirus driven in vivo lymphomagenesis time course including hundreds of thousands of subclonal mutations and demonstrate the utility of these in mapping the selective forces affecting cancer gene loci, including negatively selected mutations.
Keywords	Science ; Q
Language	English
Publishing date	2018-07-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Towards clinical molecular diagnosis of inherited cardiac conditions

Xinzhong Li / Andrew J Buckton / Samuel L Wilkinson / Shibu John / Roddy Walsh / Tomas Novotny / Iveta Valaskova / Manu Gupta / Laurence Game / Paul J R Barton / Stuart A Cook / James S Ware

PLoS ONE, Vol 8, Iss 7, p e

a comparison of bench-top genome DNA sequencers.

2013 Volume 67744

Abstract: Molecular genetic testing is recommended for diagnosis of inherited cardiac disease, to guide prognosis and treatment, but access is often limited by cost and availability. Recently introduced high-throughput bench-top DNA sequencing platforms have the ... ...

Abstract	Molecular genetic testing is recommended for diagnosis of inherited cardiac disease, to guide prognosis and treatment, but access is often limited by cost and availability. Recently introduced high-throughput bench-top DNA sequencing platforms have the potential to overcome these limitations.We evaluated two next-generation sequencing (NGS) platforms for molecular diagnostics. The protein-coding regions of six genes associated with inherited arrhythmia syndromes were amplified from 15 human samples using parallelised multiplex PCR (Access Array, Fluidigm), and sequenced on the MiSeq (Illumina) and Ion Torrent PGM (Life Technologies). Overall, 97.9% of the target was sequenced adequately for variant calling on the MiSeq, and 96.8% on the Ion Torrent PGM. Regions missed tended to be of high GC-content, and most were problematic for both platforms. Variant calling was assessed using 107 variants detected using Sanger sequencing: within adequately sequenced regions, variant calling on both platforms was highly accurate (Sensitivity: MiSeq 100%, PGM 99.1%. Positive predictive value: MiSeq 95.9%, PGM 95.5%). At the time of the study the Ion Torrent PGM had a lower capital cost and individual runs were cheaper and faster. The MiSeq had a higher capacity (requiring fewer runs), with reduced hands-on time and simpler laboratory workflows. Both provide significant cost and time savings over conventional methods, even allowing for adjunct Sanger sequencing to validate findings and sequence exons missed by NGS.MiSeq and Ion Torrent PGM both provide accurate variant detection as part of a PCR-based molecular diagnostic workflow, and provide alternative platforms for molecular diagnosis of inherited cardiac conditions. Though there were performance differences at this throughput, platforms differed primarily in terms of cost, scalability, protocol stability and ease of use. Compared with current molecular genetic diagnostic tests for inherited cardiac arrhythmias, these NGS approaches are faster, less expensive, and yet more comprehensive.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Temporal regulation of expression of immediate early and second phase transcripts by endothelin-1 in cardiomyocytes

Cullingford, Timothy E / Alejandro Giraldo / Ali Alsafi / Angela Clerk / Collins Ekere / Georgia Zoumpoulidou / Jayne L Dennis / Laurence Game / Peter H Sugden / Sampsa Pikkarainen / Stephen J Fuller / Thomais Markou / Timothy J Kemp

Genome biology. 2008 Feb., v. 9, no. 2

2008

Abstract: BACKGROUND: Endothelin-1 stimulates Gq protein-coupled receptors to promote proliferation in dividing cells or hypertrophy in terminally differentiated cardiomyocytes. In cardiomyocytes, endothelin-1 rapidly (within minutes) stimulates protein kinase ... ...

Abstract	BACKGROUND: Endothelin-1 stimulates Gq protein-coupled receptors to promote proliferation in dividing cells or hypertrophy in terminally differentiated cardiomyocytes. In cardiomyocytes, endothelin-1 rapidly (within minutes) stimulates protein kinase signaling, including extracellular-signal regulated kinases 1/2 (ERK1/2; though not ERK5), with phenotypic/physiological changes developing from approximately 12 h. Hypertrophy is associated with changes in mRNA/protein expression, presumably consequent to protein kinase signaling, but the connections between early, transient signaling events and developed hypertrophy are unknown. RESULTS: Using microarrays, we defined the early transcriptional responses of neonatal rat cardiomyocytes to endothelin-1 over 4 h, differentiating between immediate early gene (IEG) and second phase RNAs with cycloheximide. IEGs exhibited differential temporal and transient regulation, with expression of second phase RNAs within 1 h. Of transcripts upregulated at 30 minutes encoding established proteins, 28 were inhibited >50% by U0126 (which inhibits ERK1/2/5 signaling), with 9 inhibited 25-50%. Expression of only four transcripts was not inhibited. At 1 h, most RNAs (approximately 67%) were equally changed in total and polysomal RNA with approximately 17% of transcripts increased to a greater extent in polysomes. Thus, changes in expression of most protein-coding RNAs should be reflected in protein synthesis. However, approximately 16% of transcripts were essentially excluded from the polysomes, including some protein-coding mRNAs, presumably inefficiently translated. CONCLUSION: The phasic, temporal regulation of early transcriptional responses induced by endothelin-1 in cardiomyocytes indicates that, even in terminally differentiated cells, signals are propagated beyond the primary signaling pathways through transcriptional networks leading to phenotypic changes (that is, hypertrophy). Furthermore, ERK1/2 signaling plays a major role in this response.
Keywords	cardiomyocytes ; cycloheximide ; endothelins ; gene regulatory networks ; genes ; hypertrophy ; messenger RNA ; microarray technology ; phenotype ; phosphotransferases (kinases) ; polyribosomes ; protein synthesis ; rats ; receptors ; signal transduction ; transcription (genetics) ; translation (genetics)
Language	English
Dates of publication	2008-02
Size	p. 1894.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6914 ; 1465-6906
ISSN (online)	1474-760X ; 1465-6914
ISSN	1465-6906
DOI	10.1186/gb-2008-9-2-r32
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Kcnn4 Is a Regulator of Macrophage Multinucleation in Bone Homeostasis and Inflammatory Disease

Heeseog Kang / Audrey Kerloc’h / Maxime Rotival / Xiaoqing Xu / Qing Zhang / Zelpha D’Souza / Michael Kim / Jodi Carlson Scholz / Jeong-Hun Ko / Prashant K. Srivastava / Jonathan R. Genzen / Weiguo Cui / Timothy J. Aitman / Laurence Game / James E. Melvin / Adedayo Hanidu / Janice Dimock / Jie Zheng / Donald Souza /

Aruna K. Behera / Gerald Nabozny / H. Terence Cook / J.H. Duncan Bassett / Graham R. Williams / Jun Li / Agnès Vignery / Enrico Petretto / Jacques Behmoaras

Cell Reports, Vol 8, Iss 4, Pp 1210-

2014 Volume 1224

Abstract: Macrophages can fuse to form osteoclasts in bone or multinucleate giant cells (MGCs) as part of the immune response. We use a systems genetics approach in rat macrophages to unravel their genetic determinants of multinucleation and investigate their role ...

Abstract	Macrophages can fuse to form osteoclasts in bone or multinucleate giant cells (MGCs) as part of the immune response. We use a systems genetics approach in rat macrophages to unravel their genetic determinants of multinucleation and investigate their role in both bone homeostasis and inflammatory disease. We identify a trans-regulated gene network associated with macrophage multinucleation and Kcnn4 as being the most significantly trans-regulated gene in the network and induced at the onset of fusion. Kcnn4 is required for osteoclast and MGC formation in rodents and humans. Genetic deletion of Kcnn4 reduces macrophage multinucleation through modulation of Ca2+ signaling, increases bone mass, and improves clinical outcome in arthritis. Pharmacological blockade of Kcnn4 reduces experimental glomerulonephritis. Our data implicate Kcnn4 in macrophage multinucleation, identifying it as a potential therapeutic target for inhibition of bone resorption and chronic inflammation.
Keywords	Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2014-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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