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  1. AU="De Neck, Simon"
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  1. Article: Toxoplasmosis in Zoo Animals: A Retrospective Pathology Review of 126 Cases.

    Denk, Daniela / De Neck, Simon / Khaliq, Shannon / Stidworthy, Mark F

    Animals : an open access journal from MDPI

    2022  Volume 12, Issue 5

    Abstract: Toxoplasma ... ...

    Abstract Toxoplasma gondii
    Language English
    Publishing date 2022-03-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606558-7
    ISSN 2076-2615
    ISSN 2076-2615
    DOI 10.3390/ani12050619
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Toxoplasmosis in Zoo Animals: A Retrospective Pathology Review of 126 Cases

    Denk, Daniela / De Neck, Simon / Khaliq, Shannon / Stidworthy, Mark F.

    Animals. 2022 Mar. 01, v. 12, no. 5

    2022  

    Abstract: Toxoplasma gondii is an extremely successful zoonotic protozoan parasite that has been demonstrated in a wide range of endo- and poikilothermic species. Although infection is widespread amongst domestic animals, overt disease other than abortion in small ...

    Abstract Toxoplasma gondii is an extremely successful zoonotic protozoan parasite that has been demonstrated in a wide range of endo- and poikilothermic species. Although infection is widespread amongst domestic animals, overt disease other than abortion in small ruminants is sporadic. This survey evaluates toxoplasmosis in zoo animals based on a systematic review of pathology archive material (n = 33,506 submissions) over a 16-year study period. A total of 126 submissions, deriving from 32 zoos, two educational facilities and two private owners, were included in the study, based on gross lesions, cytological, histological and immunohistological diagnosis of toxoplasmosis. Clinical history, signalment, annual distribution and post-mortem findings were evaluated. A total of 31 species (mammalian 97%/avian 3%) were represented in the study material. Ring-tailed lemurs, slender tailed meerkats, Pallas’ cats, and squirrel monkeys were most affected. An unusual outbreak occurred in Asian small-clawed otters, in which toxoplasmosis has not been reported to date. Clinically, animals over 12 months of age presented with non-specific symptoms (anorexia, weight loss, lethargy, debilitation), neurological, gastrointestinal or respiratory signs and sudden death. Systemic disease predominated, with a propensity for encephalitis in meerkats and Pallas’ cats and systemic disease involving lymphoid tissues in ring-tailed lemurs. Cases in the UK occurred year-round, with species-specific peaks and increases between August and November. This study reinforces the importance of toxoplasmosis as a significant cause of sporadic and epizootic mortalities in a wide range of zoo animals. Feral cat control is crucial to reduce infection pressure.
    Keywords Lemuridae ; Protozoa ; Suricata ; Toxoplasma gondii ; anorexia ; death ; encephalitis ; epizootic diseases ; gastrointestinal system ; histology ; parasites ; squirrels ; surveys ; systematic review ; toxoplasmosis ; weight loss ; zoos
    Language English
    Dates of publication 2022-0301
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2606558-7
    ISSN 2076-2615
    ISSN 2076-2615
    DOI 10.3390/ani12050619
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: The Stereotypic Response of the Pulmonary Vasculature to Respiratory Viral Infections: Findings in Mouse Models of SARS-CoV-2, Influenza A and Gammaherpesvirus Infections.

    De Neck, Simon / Penrice-Randal, Rebekah / Clark, Jordan J / Sharma, Parul / Bentley, Eleanor G / Kirby, Adam / Mega, Daniele F / Han, Ximeng / Owen, Andrew / Hiscox, Julian A / Stewart, James P / Kipar, Anja

    Viruses

    2023  Volume 15, Issue 8

    Abstract: The respiratory system is the main target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 19 (COVID-19) where acute respiratory distress syndrome is considered the leading cause of death. Changes in ... ...

    Abstract The respiratory system is the main target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 19 (COVID-19) where acute respiratory distress syndrome is considered the leading cause of death. Changes in pulmonary blood vessels, among which an endothelialitis/endotheliitis has been particularly emphasized, have been suggested to play a central role in the development of acute lung injury. Similar vascular changes are also observed in animal models of COVID-19. The present study aimed to determine whether the latter are specific for SARS-CoV-2 infection, investigating the vascular response in the lungs of mice infected with SARS-CoV-2 and other respiratory viruses (influenza A and murine gammaherpesvirus) by in situ approaches (histology, immunohistology, morphometry) combined with RNA sequencing and bioinformatic analysis. Non-selective recruitment of monocytes and T and B cells from larger muscular veins and arteries was observed with all viruses, matched by a comparable transcriptional response. There was no evidence of endothelial cell infection in any of the models. Both the morphological investigation and the transcriptomics approach support the interpretation that the lung vasculature in mice mounts a stereotypic response to alveolar and respiratory epithelial damage. This may have implications for the treatment and management of respiratory disease in humans.
    MeSH term(s) Humans ; Animals ; Mice ; Influenza, Human ; SARS-CoV-2 ; COVID-19 ; Cardiovascular System ; Disease Models, Animal ; Gammaherpesvirinae
    Language English
    Publishing date 2023-07-27
    Publishing country Switzerland
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v15081637
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Hypoxia inducible factors inhibit respiratory syncytial virus infection by modulation of nucleolin expression.

    Zhuang, Xiaodong / Gallo, Giulia / Sharma, Parul / Ha, Jiyeon / Magri, Andrea / Borrmann, Helene / Harris, James M / Tsukuda, Senko / Bentley, Eleanor / Kirby, Adam / de Neck, Simon / Yang, Hongbing / Balfe, Peter / Wing, Peter A C / Matthews, David / Harris, Adrian L / Kipar, Anja / Stewart, James P / Bailey, Dalan /
    McKeating, Jane A

    iScience

    2023  Volume 27, Issue 1, Page(s) 108763

    Abstract: Respiratory syncytial virus (RSV) is a global healthcare problem, causing respiratory illness in young children and elderly individuals. Our knowledge of the host pathways that define susceptibility to infection and disease severity are limited. Hypoxia ... ...

    Abstract Respiratory syncytial virus (RSV) is a global healthcare problem, causing respiratory illness in young children and elderly individuals. Our knowledge of the host pathways that define susceptibility to infection and disease severity are limited. Hypoxia inducible factors (HIFs) define metabolic responses to low oxygen and regulate inflammatory responses in the lower respiratory tract. We demonstrate a role for HIFs to suppress RSV entry and RNA replication. We show that hypoxia and HIF prolyl-hydroxylase inhibitors reduce the expression of the RSV entry receptor nucleolin and inhibit viral cell-cell fusion. We identify a HIF regulated microRNA, miR-494, that regulates nucleolin expression. In RSV-infected mice, treatment with the clinically approved HIF prolyl-hydroxylase inhibitor, Daprodustat, reduced the level of infectious virus and infiltrating monocytes and neutrophils in the lung. This study highlights a role for HIF-signalling to limit multiple aspects of RSV infection and associated inflammation and informs future therapeutic approaches for this respiratory pathogen.
    Language English
    Publishing date 2023-12-18
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.108763
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Regulation of a progenitor gene program by SOX4 is essential for mammary tumor proliferation.

    Roukens, M Guy / Frederiks, Cynthia L / Seinstra, Danielle / Braccioli, Luca / Khalil, Antoine A / Pals, Cornelieke / De Neck, Simon / Bornes, Laura / Beerling, Evelyne / Mokry, Michal / de Bruin, Alain / Westendorp, Bart / van Rheenen, Jacco / Coffer, Paul J

    Oncogene

    2021  Volume 40, Issue 45, Page(s) 6343–6353

    Abstract: In breast cancer the transcription factor SOX4 has been shown to be associated with poor survival, increased tumor size and metastasis formation. This has mostly been attributed to the ability of SOX4 to regulate Epithelial-to-Mesenchymal-Transition (EMT) ...

    Abstract In breast cancer the transcription factor SOX4 has been shown to be associated with poor survival, increased tumor size and metastasis formation. This has mostly been attributed to the ability of SOX4 to regulate Epithelial-to-Mesenchymal-Transition (EMT). However, SOX4 regulates target gene transcription in a context-dependent manner that is determined by the cellular and epigenetic state. In this study we have investigated the loss of SOX4 in mammary tumor development utilizing organoids derived from a PyMT genetic mouse model of breast cancer. Using CRISPR/Cas9 to abrogate SOX4 expression, we found that SOX4 is required for inhibiting differentiation by regulating a subset of genes that are highly activated in fetal mammary stem cells (fMaSC). In this way, SOX4 re-activates an oncogenic transcriptional program that is regulated in many progenitor cell-types during embryonic development. SOX4-knockout organoids are characterized by the presence of more differentiated cells that exhibit luminal or basal gene expression patterns, but lower expression of cell cycle genes. In agreement, primary tumor growth and metastatic outgrowth in the lungs are impaired in SOX4
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; CRISPR-Cas Systems ; Cell Cycle Proteins/genetics ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Lung Neoplasms/secondary ; Mice ; Neoplasm Transplantation ; Organoids/pathology ; Organoids/transplantation ; SOXC Transcription Factors/genetics
    Chemical Substances Cell Cycle Proteins ; SOX4 protein, human ; SOXC Transcription Factors ; Sox4 protein, mouse
    Language English
    Publishing date 2021-09-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-021-02004-z
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2218: Show issues Location:
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  6. Article ; Online: Recombinant SARS-CoV-2 lacking initiating and internal methionine codons within ORF10 is attenuated in vivo

    Gu, Shichun / Bentley, Eleanor G / Milligan, Rachel I / Almuqrin, Abdulaziz M / Sharma, Parul / Kirby, Adam / Mega, Daniele F / Kipar, Anja / Erdmann, Max / Bazire, James / Heesom, Kate J / Lewis, Phillip A / Donovan-Banfield, I'ah / Reston, Charlotte / Webb, Isobel / de Neck, Simon / Dong, Xiaofeng / Hiscox, Julian Alexander / Davidson, Andrew D /
    Stewart, James P / Matthews, David A

    bioRxiv

    Abstract: SARS-CoV-2 has been proposed to encode ORF10 as the 39 terminal gene in the viral genome. However, the potential role and even existence of a functional ORF10 product has been the subject of debate. There are significant structural features in the viral ... ...

    Abstract SARS-CoV-2 has been proposed to encode ORF10 as the 39 terminal gene in the viral genome. However, the potential role and even existence of a functional ORF10 product has been the subject of debate. There are significant structural features in the viral genomic RNA that could, by themselves, explain the retention of the ORF10 nucleotide sequences without the need for a functional protein product. To explore this question further we made two recombinant viruses, firstly a control virus (WT) based on the genome sequence of the original Wuhan isolate and with the inclusion of the early D614G mutation in the Spike protein. We also made a second virus, identical to WT except for two additional changes that replaced the initiating ORF10 start codon and an internal methionine codon for stop codons (ORF10KO). Here we show that the two viruses have apparently identical growth kinetics in a VeroE6 cell line that over expresses TMPRSS2 (VTN cells). However, in A549 cells over expressing ACE2 and TMPRSS2 (A549-AT cells) the ORF10KO virus appears to have a small growth rate advantage. Growth competition experiments were used whereby the two viruses were mixed, passaged in either VTN or A549-AT cells and the resulting output virus was sequenced. We found that in VTN cells the WT virus quickly dominated whereas in the A549-AT cells the ORF10KO virus dominated. We then used a hamster model of SARS-CoV-2 infection and determined that the ORF10KO virus has attenuated pathogenicity (as measured by weight loss). We found an almost 10-fold reduction in viral titre in the lower respiratory tract for ORF10KO vs WT. In contrast, the WT and ORF10KO viruses had similar titres in the upper respiratory tract. Sequencing of viral RNA in the lungs of hamsters infected with ORF10KO virus revealed that this virus frequently reverts to WT. Our data suggests that the retention of a functional ORF10 sequence is highly desirable for SARS-CoV-2 infection of hamsters and affects the virus9s ability to propagate in the lower respiratory tract.
    Keywords covid19
    Language English
    Publishing date 2023-08-07
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2023.08.04.551973
    Database COVID19

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  7. Article ; Online: Loss of hepatic SMLR1 causes hepatosteatosis and protects against atherosclerosis due to decreased hepatic VLDL secretion.

    van Zwol, Willemien / Rimbert, Antoine / Wolters, Justina C / Smit, Marieke / Bloks, Vincent W / Kloosterhuis, Niels J / Huijkman, Nicolette C A / Koster, Mirjam H / Tharehalli, Umesh / de Neck, Simon M / Bournez, Colin / Fuh, Marceline M / Kuipers, Jeroen / Rajan, Sujith / de Bruin, Alain / Ginsberg, Henry N / van Westen, Gerard J P / Hussain, M Mahmood / Scheja, Ludger /
    Heeren, Joerg / Zimmerman, Philip / van de Sluis, Bart / Kuivenhoven, Jan Albert

    Hepatology (Baltimore, Md.)

    2022  Volume 78, Issue 5, Page(s) 1418–1432

    Abstract: Background and aims: The assembly and secretion of VLDL from the liver, a pathway that affects hepatic and plasma lipids, remains incompletely understood. We set out to identify players in the VLDL biogenesis pathway by identifying genes that are co- ... ...

    Abstract Background and aims: The assembly and secretion of VLDL from the liver, a pathway that affects hepatic and plasma lipids, remains incompletely understood. We set out to identify players in the VLDL biogenesis pathway by identifying genes that are co-expressed with the MTTP gene that encodes for microsomal triglyceride transfer protein, key to the lipidation of apolipoprotein B, the core protein of VLDL. Using human and murine transcriptomic data sets, we identified small leucine-rich protein 1 ( SMLR1 ), encoding for small leucine-rich protein 1, a protein of unknown function that is exclusively expressed in liver and small intestine.
    Approach and results: To assess the role of SMLR1 in the liver, we used somatic CRISPR/CRISPR-associated protein 9 gene editing to silence murine Smlr1 in hepatocytes ( Smlr1 -LKO). When fed a chow diet, male and female mice show hepatic steatosis, reduced plasma apolipoprotein B and triglycerides, and reduced VLDL secretion without affecting microsomal triglyceride transfer protein activity. Immunofluorescence studies show that SMLR1 is in the endoplasmic reticulum and Cis-Golgi complex. The loss of hepatic SMLR1 in female mice protects against diet-induced hyperlipidemia and atherosclerosis but causes NASH. On a high-fat, high-cholesterol diet, insulin and glucose tolerance tests did not reveal differences in male Smlr1 -LKO mice versus controls.
    Conclusions: We propose a role for SMLR1 in the trafficking of VLDL from the endoplasmic reticulum to the Cis-Golgi complex. While this study uncovers SMLR1 as a player in the VLDL assembly, trafficking, and secretion pathway, it also shows that NASH can occur with undisturbed glucose homeostasis and atheroprotection.
    MeSH term(s) Animals ; Female ; Humans ; Male ; Mice ; Apolipoproteins B/blood ; Atherosclerosis/blood ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/prevention & control ; Leucine ; Lipoproteins, VLDL/biosynthesis ; Lipoproteins, VLDL/blood ; Lipoproteins, VLDL/metabolism ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Small Leucine-Rich Proteoglycans/genetics ; Small Leucine-Rich Proteoglycans/metabolism ; Triglycerides/blood
    Chemical Substances Apolipoproteins B ; Leucine (GMW67QNF9C) ; Lipoproteins, VLDL ; microsomal triglyceride transfer protein ; Small Leucine-Rich Proteoglycans ; Triglycerides
    Language English
    Publishing date 2022-10-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.32709
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
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