LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Erweiterte Suche

Suchergebnis

Treffer 1 - 8 von insgesamt 8

Suchoptionen

  1. Artikel ; Online: Are your IT staff ready for the pandemic-driven insider threat?

    Chapman, Phil

    Network Security

    Abstract: As this article is being written it's mid-March. The situation likely will have changed significantly by the time you read this, as it does by the day and even the hour. The World Health Organisation (WHO) has declared Covid-19 to be a global pandemic ... ...

    Abstract As this article is being written it's mid-March. The situation likely will have changed significantly by the time you read this, as it does by the day and even the hour. The World Health Organisation (WHO) has declared Covid-19 to be a global pandemic and the UK Government has stepped up its response from the ‘contain’ to the ‘delay’ phase. Public spaces and transport are noticeably quieter and many workplaces are getting emptier as staff members work from home. The Covid-19 pandemic and consequent lockdowns are hitting businesses hard. And as workforces move to remote working, IT departments are under pressure. At the same time, cyber criminals are exploiting the pandemic, with rises in phishing and other forms of attacks. The cyber security workforce, already suffering a skills crisis, may lack the soft skills required to effectively tackle these issues, many of which could be solved if the industry didn't rely so heavily on recruiting graduates and rather looked towards hiring apprentices, argues Phil Chapman of Firebrand Training.
    Schlagwörter covid19
    Verlag Elsevier; PMC
    Dokumenttyp Artikel ; Online
    DOI 10.1016/s1353-4858(20)30042-8
    Datenquelle COVID19

    Kategorien

  2. Artikel ; Online: Survival of Head and Neck Cancer Cells Relies upon LZK Kinase-Mediated Stabilization of Mutant p53.

    Edwards, Zoe C / Trotter, Eleanor W / Torres-Ayuso, Pedro / Chapman, Phil / Wood, Henry M / Nyswaner, Katherine / Brognard, John

    Cancer research

    2017  Band 77, Heft 18, Seite(n) 4961–4972

    Abstract: Head and neck squamous cell carcinoma (HNSCC) includes epithelial cancers of the oral and nasal cavity, larynx, and pharynx and accounts for ∼350,000 deaths per year worldwide. Smoking-related HNSCC is associated with few targetable mutations but is ... ...

    Abstract Head and neck squamous cell carcinoma (HNSCC) includes epithelial cancers of the oral and nasal cavity, larynx, and pharynx and accounts for ∼350,000 deaths per year worldwide. Smoking-related HNSCC is associated with few targetable mutations but is defined by frequent copy-number alteration, the most common of which is gain at 3q. Critical 3q target genes have not been conclusively determined for HNSCC. Here, we present data indicating that
    Mesh-Begriff(e) Animals ; Apoptosis ; Biomarkers, Tumor ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Cell Proliferation ; Female ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/pathology ; Humans ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mutant Proteins/chemistry ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Mutation/genetics ; Protein Stability ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Xenograft Model Antitumor Assays
    Chemische Substanzen Biomarkers, Tumor ; Mutant Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53 ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K13 protein, human (EC 2.7.11.25)
    Sprache Englisch
    Erscheinungsdatum 2017-09-15
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-17-0267
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  3. Artikel ; Online: Combinatorial CRISPR screen identifies fitness effects of gene paralogues.

    Thompson, Nicola A / Ranzani, Marco / van der Weyden, Louise / Iyer, Vivek / Offord, Victoria / Droop, Alastair / Behan, Fiona / Gonçalves, Emanuel / Speak, Anneliese / Iorio, Francesco / Hewinson, James / Harle, Victoria / Robertson, Holly / Anderson, Elizabeth / Fu, Beiyuan / Yang, Fengtang / Zagnoli-Vieira, Guido / Chapman, Phil / Del Castillo Velasco-Herrera, Martin /
    Garnett, Mathew J / Jackson, Stephen P / Adams, David J

    Nature communications

    2021  Band 12, Heft 1, Seite(n) 1302

    Abstract: Genetic redundancy has evolved as a way for human cells to survive the loss of genes that are single copy and essential in other organisms, but also allows tumours to survive despite having highly rearranged genomes. In this study we CRISPR screen 1191 ... ...

    Abstract Genetic redundancy has evolved as a way for human cells to survive the loss of genes that are single copy and essential in other organisms, but also allows tumours to survive despite having highly rearranged genomes. In this study we CRISPR screen 1191 gene pairs, including paralogues and known and predicted synthetic lethal interactions to identify 105 gene combinations whose co-disruption results in a loss of cellular fitness. 27 pairs influence fitness across multiple cell lines including the paralogues FAM50A/FAM50B, two genes of unknown function. Silencing of FAM50B occurs across a range of tumour types and in this context disruption of FAM50A reduces cellular fitness whilst promoting micronucleus formation and extensive perturbation of transcriptional programmes. Our studies reveal the fitness effects of FAM50A/FAM50B in cancer cells.
    Mesh-Begriff(e) Animals ; Apoptosis ; CRISPR-Cas Systems ; Cell Line, Tumor ; Clustered Regularly Interspaced Short Palindromic Repeats ; DNA-Binding Proteins/genetics ; Gene Knockout Techniques ; Genome ; Heterografts ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Proteins/genetics ; RNA-Binding Proteins/genetics ; Transcriptome
    Chemische Substanzen DNA-Binding Proteins ; FAM50A protein, human ; FAM50B protein, human ; Proteins ; RNA-Binding Proteins
    Sprache Englisch
    Erscheinungsdatum 2021-02-26
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-21478-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  4. Buch: Recycle your bass

    Chapman, Phil

    a guide to handling and releasing your catch

    (Educational bulletin ; no. 2)

    1990  

    Verfasserangabe by Phil Chapman
    Serientitel Educational bulletin ; no. 2
    Schlagwörter Bass fishing ; Fishing
    Sprache Englisch
    Umfang [10] p. :, col. ill. ;, 28 cm.
    Verlag Division of Fisheries, Florida Game & Fresh Water Fish Commission
    Erscheinungsort Tallahassee
    Dokumenttyp Buch
    Anmerkung Cover title.
    Datenquelle NAL Katalog (AGRICOLA)

    Zusatzmaterialien

    Kategorien

  5. Artikel ; Online: Exogenous glucose oxidation is reduced with carbohydrate feeding during exercise after starvation.

    Rowlands, David S / Johnson, Nathan A / Thomson, Jasmine A / Chapman, Phil / Stannard, Stephen R

    Metabolism: clinical and experimental

    2009  Band 58, Heft 8, Seite(n) 1161–1169

    Abstract: Lean healthy individuals are characterized by the ability to rapidly adapt metabolism to acute changes in substrate availability and metabolic rate. However, in glucose-intolerance/insulin-resistant conditions, such as that induced by starvation, the ... ...

    Abstract Lean healthy individuals are characterized by the ability to rapidly adapt metabolism to acute changes in substrate availability and metabolic rate. However, in glucose-intolerance/insulin-resistant conditions, such as that induced by starvation, the flexibility of tissues to rapidly respond to change in substrate availability is diminished. We asked whether the conundrum of increased glucose demand by the contracting skeletal muscle during prolonged exercise and the glucose intolerance of starvation would result in the obstruction of oxidative disposal of ingested (13)C-labeled glucose during exercise. Seven lean, healthy, physically active individuals (2 women, 5 men) completed a randomized crossover study comparing the effects of the normal-fed condition vs a 67-hour water-only fast on the metabolic response to carbohydrate ingestion during 80 minutes of exercise at 56% of maximum oxygen uptake. Compared with the normal condition, fasting resulted in a large overall increase in the rate of fat oxidation (mean effect, 71%; 95% confidence limit, +/-22%) and moderate reductions in both exogenous (-54%, +/-10%) and endogenous (-40%, +/-19%) glucose oxidation rates during exercise. Over the course of exercise, fat oxidation was impermeable to change in the fasting condition, but increased moderately (33%, +/-19%) in the normal condition. These changes were associated with a large increase in plasma free fatty-acid concentration (120%, +/-64%) and a moderate increase in blood lactate concentration (58%, +/-50%). In contrast, large reductions in resting blood glucose (-21%, +/-14%) and moderate reductions in plasma insulin concentrations (-47%, +/-26%) were observed in the fast condition; but this effect was reversed for glucose (30%, +/- 24%) and negated for insulin by the end of exercise. To conclude, a 67-hour fast leads to an impermeable increase in fat oxidation, suppression of both exogenous and endogenous carbohydrate oxidation, and a metabolic response consistent with resistance to contraction-induced exogenous glucose uptake and oxidation.
    Mesh-Begriff(e) Adult ; Blood Glucose/metabolism ; Carbon Isotopes ; Cross-Over Studies ; Dietary Carbohydrates/administration & dosage ; Dietary Carbohydrates/metabolism ; Ergometry ; Exercise ; Female ; Glucose/administration & dosage ; Glucose/metabolism ; Glucose Intolerance/metabolism ; Humans ; Lipid Peroxidation ; Male ; Oxidation-Reduction ; Oxygen Consumption ; Starvation ; Time Factors
    Chemische Substanzen Blood Glucose ; Carbon Isotopes ; Dietary Carbohydrates ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2009-08
    Erscheinungsland United States
    Dokumenttyp Clinical Trial ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2009.03.016
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  6. Artikel ; Online: Software for the Integration of Multiomics Experiments in Bioconductor.

    Ramos, Marcel / Schiffer, Lucas / Re, Angela / Azhar, Rimsha / Basunia, Azfar / Rodriguez, Carmen / Chan, Tiffany / Chapman, Phil / Davis, Sean R / Gomez-Cabrero, David / Culhane, Aedin C / Haibe-Kains, Benjamin / Hansen, Kasper D / Kodali, Hanish / Louis, Marie S / Mer, Arvind S / Riester, Markus / Morgan, Martin / Carey, Vince /
    Waldron, Levi

    Cancer research

    2018  Band 77, Heft 21, Seite(n) e39–e42

    Abstract: Multiomics experiments are increasingly commonplace in biomedical research and add layers of complexity to experimental design, data integration, and analysis. R and Bioconductor provide a generic framework for statistical analysis and visualization, as ... ...

    Abstract Multiomics experiments are increasingly commonplace in biomedical research and add layers of complexity to experimental design, data integration, and analysis. R and Bioconductor provide a generic framework for statistical analysis and visualization, as well as specialized data classes for a variety of high-throughput data types, but methods are lacking for integrative analysis of multiomics experiments. The MultiAssayExperiment software package, implemented in R and leveraging Bioconductor software and design principles, provides for the coordinated representation of, storage of, and operation on multiple diverse genomics data. We provide the unrestricted multiple 'omics data for each cancer tissue in The Cancer Genome Atlas as ready-to-analyze MultiAssayExperiment objects and demonstrate in these and other datasets how the software simplifies data representation, statistical analysis, and visualization. The MultiAssayExperiment Bioconductor package reduces major obstacles to efficient, scalable, and reproducible statistical analysis of multiomics data and enhances data science applications of multiple omics datasets.
    Mesh-Begriff(e) Computational Biology ; Datasets as Topic ; Genome, Human ; Genomics ; Humans ; Neoplasms/genetics ; Software
    Sprache Englisch
    Erscheinungsdatum 2018-01-03
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-17-0344
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  7. Artikel ; Online: Discrepancies in cancer genomic sequencing highlight opportunities for driver mutation discovery.

    Hudson, Andrew M / Yates, Tim / Li, Yaoyong / Trotter, Eleanor W / Fawdar, Shameem / Chapman, Phil / Lorigan, Paul / Biankin, Andrew / Miller, Crispin J / Brognard, John

    Cancer research

    2014  Band 74, Heft 22, Seite(n) 6390–6396

    Abstract: Cancer genome sequencing is being used at an increasing rate to identify actionable driver mutations that can inform therapeutic intervention strategies. A comparison of two of the most prominent cancer genome sequencing databases from different ... ...

    Abstract Cancer genome sequencing is being used at an increasing rate to identify actionable driver mutations that can inform therapeutic intervention strategies. A comparison of two of the most prominent cancer genome sequencing databases from different institutes (Cancer Cell Line Encyclopedia and Catalogue of Somatic Mutations in Cancer) revealed marked discrepancies in the detection of missense mutations in identical cell lines (57.38% conformity). The main reason for this discrepancy is inadequate sequencing of GC-rich areas of the exome. We have therefore mapped over 400 regions of consistent inadequate sequencing (cold-spots) in known cancer-causing genes and kinases, in 368 of which neither institute finds mutations. We demonstrate, using a newly identified PAK4 mutation as proof of principle, that specific targeting and sequencing of these GC-rich cold-spot regions can lead to the identification of novel driver mutations in known tumor suppressors and oncogenes. We highlight that cross-referencing between genomic databases is required to comprehensively assess genomic alterations in commonly used cell lines and that there are still significant opportunities to identify novel drivers of tumorigenesis in poorly sequenced areas of the exome. Finally, we assess other reasons for the observed discrepancy, such as variations in dbSNP filtering and the acquisition/loss of mutations, to give explanations as to why there is a discrepancy in pharmacogenomic studies, given recent concerns with poor reproducibility of data.
    Mesh-Begriff(e) Cell Line, Tumor ; Exome ; Genes, Tumor Suppressor ; Humans ; Mutation ; Neoplasms/genetics ; Oncogenes ; Pharmacogenetics ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; p21-Activated Kinases/genetics
    Chemische Substanzen PAK4 protein, human (EC 2.7.1.11) ; p21-Activated Kinases (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2014-09-25
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-14-1020
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  8. Artikel ; Online: Recurrent MLK4 Loss-of-Function Mutations Suppress JNK Signaling to Promote Colon Tumorigenesis.

    Marusiak, Anna A / Stephenson, Natalie L / Baik, Hayeon / Trotter, Eleanor W / Li, Yaoyong / Blyth, Karen / Mason, Susan / Chapman, Phil / Puto, Lorena A / Read, Jon A / Brassington, Claire / Pollard, Hannah K / Phillips, Chris / Green, Isabelle / Overman, Ross / Collier, Matthew / Testoni, Ewelina / Miller, Crispin J / Hunter, Tony /
    Sansom, Owen J / Brognard, John

    Cancer research

    2015  Band 76, Heft 3, Seite(n) 724–735

    Abstract: MLK4 is a member of the mixed-lineage family of kinases that regulate the JNK, p38, and ERK kinase signaling pathways. MLK4 mutations have been identified in various human cancers, including frequently in colorectal cancer, where their function and ... ...

    Abstract MLK4 is a member of the mixed-lineage family of kinases that regulate the JNK, p38, and ERK kinase signaling pathways. MLK4 mutations have been identified in various human cancers, including frequently in colorectal cancer, where their function and pathobiological importance have been uncertain. In this study, we assessed the functional consequences of MLK4 mutations in colon tumorigenesis. Biochemical data indicated that a majority of MLK4 mutations are loss-of-function (LOF) mutations that can exert dominant-negative effects. In seeking to understand the abrogated activity of these mutants, we elucidated a new MLK4 catalytic domain structure. To determine whether MLK4 is required to maintain tumorigenic phenotypes, we reconstituted its signaling axis in colon cancer cells harboring MLK4-inactivating mutations. We found that restoring MLK4 activity reduced cell viability, proliferation, and colony formation in vitro and delayed tumor growth in vivo. Mechanistic investigations established that restoring the function of MLK4 selectively induced the JNK pathway and its downstream targets, cJUN, ATF3, and the cyclin-dependent kinase inhibitors CDKN1A and CDKN2B. Our work indicates that MLK4 is a novel tumor-suppressing kinase harboring frequent LOF mutations that lead to diminished signaling in the JNK pathway and enhanced proliferation in colon cancer.
    Mesh-Begriff(e) Animals ; Carcinogenesis ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Female ; Humans ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mutation ; Signal Transduction ; Xenograft Model Antitumor Assays
    Chemische Substanzen MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K21 protein, human (EC 2.7.11.25)
    Sprache Englisch
    Erscheinungsdatum 2015-12-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-15-0701-T
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

Zum Seitenanfang