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  1. AU="Matthew Mold"
  2. AU="Kroha, H."
  3. AU="Kang Dufour, Mi-Suk"
  4. AU=Andreas S
  5. AU="Eun Kyung Khil"
  6. AU="Mellaerts, B."
  7. AU="Xiang Yao"
  8. AU="Lan, Tao"
  9. AU="Arnaud Rossard"
  10. AU="Huang, Pau-Yi"
  11. AU="Gangxian He"
  12. AU="Stallings, Amy P"
  13. AU="Hardy, Mark A"
  14. AU="Kotrulja, Lena"
  15. AU="Meeremans, Marguerite"
  16. AU="Chen, Yanguang"
  17. AU="Sakizono, Kenji"
  18. AU="Romero-Daza, Nancy"
  19. AU="Jean-Pierre Thomé"
  20. AU=Narayanan Naveen
  21. AU=Azam Faizul
  22. AU="Özdog˘ru, Asil Ali"
  23. AU="Emami, Hajar"
  24. AU="Cimino, R."
  25. AU="Judith R. Stabel"
  26. AU="Takeuchi, Kazuto"
  27. AU="Mirzaei, Samira"
  28. AU="Carolina Salgado"
  29. AU="Mate, Sebastian"
  30. AU="Hou, Tian-Yang Liu"
  31. AU=Nino Gustavo
  32. AU="Lydon, Myra"
  33. AU="Jain, Nibha"
  34. AU="David A Schwartz"
  35. AU="Swart, Jonathan"
  36. AU="Karol, Agnieszka"
  37. AU="Reilly, Brittni"
  38. AU="Arfaatabar, Maryam"
  39. AU="Kumar Pandey, Anand"

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Treffer 1 - 6 von insgesamt 6

Suchoptionen

  1. Artikel ; Online: Intracellular Aluminium in Inflammatory and Glial Cells in Cerebral Amyloid Angiopathy

    Matthew Mold / Jason Cottle / Andrew King / Christopher Exley

    International Journal of Environmental Research and Public Health, Vol 16, Iss 8, p

    A Case Report

    2019  Band 1459

    Abstract: 1) Introduction: In 2006, we reported on very high levels of aluminium in brain tissue in an unusual case of cerebral amyloid angiopathy (CAA). The individual concerned had been exposed to extremely high levels of aluminium in their potable water due to ...

    Abstract (1) Introduction: In 2006, we reported on very high levels of aluminium in brain tissue in an unusual case of cerebral amyloid angiopathy (CAA). The individual concerned had been exposed to extremely high levels of aluminium in their potable water due to a notorious pollution incident in Camelford, Cornwall, in the United Kingdom. The recent development of aluminium-specific fluorescence microscopy has now allowed for the location of aluminium in this brain to be identified. (2) Case Summary: We used aluminium-specific fluorescence microscopy in parallel with Congo red staining and polarised light to identify the location of aluminium and amyloid in brain tissue from an individual who had died from a rare and unusual case of CAA. Aluminium was almost exclusively intracellular and predominantly in inflammatory and glial cells including microglia, astrocytes, lymphocytes and cells lining the choroid plexus. Complementary staining with Congo red demonstrated that aluminium and amyloid were not co-located in these tissues. (3) Discussion: The observation of predominantly intracellular aluminium in these tissues was novel and something similar has only previously been observed in cases of autism. The results suggest a strong inflammatory component in this case and support a role for aluminium in this rare and unusual case of CAA.
    Schlagwörter cerebral amyloid angiopathy ; brain aluminium ; pro-inflammatory cells ; human exposure to aluminium ; Camelford in Cornwall ; Medicine ; R
    Thema/Rubrik (Code) 669
    Sprache Englisch
    Erscheinungsdatum 2019-04-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Aluminium in Brain Tissue in Epilepsy

    Matthew Mold / Jason Cottle / Christopher Exley

    International Journal of Environmental Research and Public Health, Vol 16, Iss 12, p

    A Case Report from Camelford

    2019  Band 2129

    Abstract: 1) Introduction: Human exposure to aluminium is a burgeoning problem. In 1988, the population of the Cornish town of Camelford was exposed to exceedingly high levels of aluminium in their potable water supply. Herein we provide evidence that aluminium ... ...

    Abstract (1) Introduction: Human exposure to aluminium is a burgeoning problem. In 1988, the population of the Cornish town of Camelford was exposed to exceedingly high levels of aluminium in their potable water supply. Herein we provide evidence that aluminium played a role in the death of a Camelford resident following development of late-onset epilepsy. (2) Case summary: We have measured the aluminium content of brain tissue in this individual and demonstrated significant accumulations of aluminium in the hippocampus (4.35 (2.80) µg/g dry wt.) and the occipital lobe (2.22 (2.23) µg/g dry wt., mean, SD, n = 5), the latter being associated with abnormal calcifications. Aluminium-specific fluorescence microscopy confirmed the presence of aluminium in both of these tissues and made the consistent observation of aluminium-loaded glial cells in close proximity to aluminium-rich cell/neuronal debris. These observations support an inflammatory component in this case of late-onset epilepsy. Congo red failed to identify any amyloid deposits in any tissue while thioflavin S showed extensive extracellular and intracellular tau pathologies. (3) Discussion: We present the first data showing aluminium in brain tissue in epilepsy and suggest, in light of complementary evidence from scientific literature, the first evidence that aluminium played a role in the advent of this case of late-onset adult epilepsy.
    Schlagwörter aluminium in brain tissue ; epilepsy ; aluminium-specific fluorescence ; occipital calcifications ; tau pathologies ; Camelford in Cornwall ; Medicine ; R
    Thema/Rubrik (Code) 669
    Sprache Englisch
    Erscheinungsdatum 2019-06-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Update on the Inactivation Procedures for the Vaccine Development Prospects of a New Highly Virulent RGNNV Isolate

    Alberto Falco / Melissa Bello-Perez / Rocío Díaz-Puertas / Matthew Mold / Mikolaj Adamek

    Vaccines, Vol 9, Iss 1441, p

    2021  Band 1441

    Abstract: Viral nervous necrosis (VNN) caused by the nervous necrosis virus (NNV) affects a broad range of primarily marine fish species, with mass mortality rates often seen among larvae and juveniles. Its genetic diversification may hinder the effective ... ...

    Abstract Viral nervous necrosis (VNN) caused by the nervous necrosis virus (NNV) affects a broad range of primarily marine fish species, with mass mortality rates often seen among larvae and juveniles. Its genetic diversification may hinder the effective implementation of preventive measures such as vaccines. The present study describes different inactivation procedures for developing an inactivated vaccine against a new NNV isolate confirmed to possess deadly effects upon the European seabass ( Dicentrarchus labrax ), an important Mediterranean farmed fish species that is highly susceptible to this disease. First, an NNV isolate from seabass adults diagnosed with VNN was rescued and the sequences of its two genome segments (RNA1 and RNA2) were classified into the red-spotted grouper NNV (RGNNV) genotype, closely clustering to the highly pathogenic 283.2009 isolate. The testing of different inactivation procedures revealed that the virus particles of this isolate showed a marked resistance to heat (for at least 60 °C for 120 min with and without 1% BSA) but that they were fully inactivated by 3 mJ/cm 2 UV-C irradiation and 24 h 0.2% formalin treatment, which stood out as promising NNV-inactivation procedures for potential vaccine candidates. Therefore, these procedures are feasible, effective, and rapid response strategies for VNN control in aquaculture.
    Schlagwörter viral nervous necrosis ; betanodavirus ; nervous necrosis virus ; autogenous vaccine ; virus inactivation ; virus-inactivated vaccine ; Medicine ; R
    Thema/Rubrik (Code) 590
    Sprache Englisch
    Erscheinungsdatum 2021-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Intracellular tracing of amyloid vaccines through direct fluorescent labelling

    Matthew Mold / Manpreet Kumar / Ambreen Mirza / Emma Shardlow / Christopher Exley

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Band 10

    Abstract: Abstract Alzheimer’s disease is a debilitating neurodegenerative condition that progressively causes synaptic loss and major neuronal damage. Immunotherapy utilising Aβ as an active immunogen or via passive treatment utilising antibodies raised to ... ...

    Abstract Abstract Alzheimer’s disease is a debilitating neurodegenerative condition that progressively causes synaptic loss and major neuronal damage. Immunotherapy utilising Aβ as an active immunogen or via passive treatment utilising antibodies raised to amyloid have shown therapeutic promise. The migratory properties of peripheral blood-borne monocytes and their ability to enter the central nervous system, suggests a beneficial role in mediating tissue damage and neuroinflammation. However, the intrinsic phagocytic properties of such cells have pre-disposed them to internalise misfolded amyloidogenic peptides that could act as seeds capable of nucleating amyloid formation in the brain. Mechanisms governing the cellular fate of amyloid therefore, may prove to be key in the development of future vaccination regimes. Herein, we have developed unequivocal and direct conformation-sensitive fluorescent molecular probes that reveal the intracytoplasmic and intranuclear persistence of amyloid in a monocytic T helper 1 (THP-1) cell line. Use of the pathogenic Aβ42 species as a model antigen in simulated vaccine formulations suggested differing mechanisms of cellular internalisation, in which fibrillar amyloid evaded lysosomal capture, even when co-deposited on particulate adjuvant materials. Taken collectively, direct fluorescent labelling of antigen-adjuvant complexes may serve as critical tools in understanding subsequent immunopotentiation in vaccines directed against amyloidosis and wider dementia.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-02-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Aluminium in Brain Tissue in Multiple Sclerosis

    Matthew Mold / Agata Chmielecka / Maria Raquel Ramirez Rodriguez / Femia Thom / Caroline Linhart / Andrew King / Christopher Exley

    International Journal of Environmental Research and Public Health, Vol 15, Iss 8, p

    2018  Band 1777

    Abstract: Multiple sclerosis (MS) is a devastating and debilitating neurodegenerative disease of unknown cause. A consensus suggests the involvement of both genetic and environmental factors of which the latter may involve human exposure to aluminium. There are no ...

    Abstract Multiple sclerosis (MS) is a devastating and debilitating neurodegenerative disease of unknown cause. A consensus suggests the involvement of both genetic and environmental factors of which the latter may involve human exposure to aluminium. There are no data on the content and distribution of aluminium in human brain tissue in MS. The aluminium content of brain tissue from 14 donors with a diagnosis of MS was determined by transversely heated graphite furnace atomic absorption spectrometry. The location of aluminium in the brain tissue of two donors was investigated by aluminium-specific fluorescence microscopy. The aluminium content of brain tissue in MS was universally high with many tissues bearing concentrations in excess of 10 μg/g dry wt. (10 ppm) and some exceeding 50 ppm. There were no statistically significant relationships between brain lobes, donor age or donor gender. Aluminium-specific fluorescence successfully identified aluminium in brain tissue in both intracellular and extracellular locations. The association of aluminium with corpora amylacea suggests a role for aluminium in neurodegeneration in MS.
    Schlagwörter multiple sclerosis ; human exposure to aluminium ; human brain tissue ; TH GFAAS ; aluminium-specific fluorescence ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2018-08-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel: Al adjuvants can be tracked in viable cells by lumogallion staining

    Mile, Irene / Andreas Svensson / Anna Darabi / Håkan Eriksson / Matthew Mold / Peter Siesjö

    Journal of Immunological Methods. 2015 July, v. 422

    2015  

    Abstract: The mechanism behind the adjuvant effect of aluminum salts is poorly understood notwithstanding that aluminum salts have been used for decades in clinical vaccines. In an aqueous environment and at a nearly neutral pH, the aluminum salts form particulate ...

    Abstract The mechanism behind the adjuvant effect of aluminum salts is poorly understood notwithstanding that aluminum salts have been used for decades in clinical vaccines. In an aqueous environment and at a nearly neutral pH, the aluminum salts form particulate aggregates, and one plausible explanation of the lack of information regarding the mechanisms could be the absence of an efficient method of tracking phagocytosed aluminum adjuvants and thereby the intracellular location of the adjuvant.In this paper, we want to report upon the use of lumogallion staining enabling the detection of phagocytosed aluminum adjuvants inside viable cells. Including micromolar concentrations of lumogallion in the culture medium resulted in a strong fluorescence signal from cells that had phagocytosed the aluminum adjuvant. The fluorescence appeared as spots in the cytoplasm and by confocal microscopy and co-staining with probes presenting fluorescence in the far-red region of the spectrum, aluminum adjuvants could to a certain extent be identified as localized in acidic vesicles, i.e., lysosomes.Staining and detection of intracellular aluminum adjuvants was achieved not only by diffusion of lumogallion into the cytoplasm, thereby highlighting the presence of the adjuvant, but also by pre-staining the aluminum adjuvant prior to incubation with cells. Pre-staining of aluminum adjuvants resulted in bright fluorescent particulate aggregates that remained fluorescent for weeks and with only a minor reduction of fluorescence upon extensive washing or incubation with cells. Both aluminum oxyhydroxide and aluminum hydroxyphosphate, two of the most commonly used aluminum adjuvants in clinical vaccines, could be pre-stained with lumogallion and were easily tracked intracellularly after incubation with phagocytosing cells.Staining of viable cells using lumogallion will be a useful method in investigations of the mechanisms behind aluminum adjuvants' differentiation of antigen-presenting cells into inflammatory cells. Information will be gained regarding the phagosomal pathways and the events inside the phagosomes, and thereby the ultimate fate of phagocytosed aluminum adjuvants could be resolved.
    Schlagwörter adjuvants ; aluminum ; antigen-presenting cells ; cell viability ; confocal microscopy ; culture media ; fluorescence ; pH ; phagocytosis ; phagosomes ; salts ; staining ; vaccines ; washing
    Sprache Englisch
    Erscheinungsverlauf 2015-07
    Umfang p. 87-94.
    Erscheinungsort Elsevier B.V.
    Dokumenttyp Artikel
    ZDB-ID 120142-6
    ISSN 1872-7905 ; 0022-1759
    ISSN (online) 1872-7905
    ISSN 0022-1759
    DOI 10.1016/j.jim.2015.04.008
    Datenquelle NAL Katalog (AGRICOLA)

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