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Article: Immunology of Pregnancy and Systemic Consequences.

Menzies, Fiona M

Current topics in microbiology and immunology

2023 Volume 441, Page(s) 253–280

Abstract: Pregnancy is an immunological paradox, with renowned Nobel Prize winning transplantation biologist Sir Peter Brian Medawar being the first to introduce this concept back in 1953. This concept considers how the maternal immune system can tolerate the ... ...

Abstract	Pregnancy is an immunological paradox, with renowned Nobel Prize winning transplantation biologist Sir Peter Brian Medawar being the first to introduce this concept back in 1953. This concept considers how the maternal immune system can tolerate the developing fetus, which is 50% antigenically foreign to the uterus. There have been significant advances in our understanding of the immune system in regulating fertility, pregnancy and in complications of these, and what was once considered a paradox can be seen as a highly evolved system. Indeed, the complexity of the maternal-fetal interface along with our ever-advancing knowledge of immune cells and mediators means that we have a better understanding of these interactions, with gaps still present. This chapter will summarise the key aspects of the role of the immune system at each stage of pregnancy and highlight the recent advances in our knowledge.
MeSH term(s)	Female ; Humans ; Pregnancy/immunology ; Immune System
Language	English
Publishing date	2023-09-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	210099-X
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-031-35139-6_10
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Article ; Online: Effectiveness of germicidal ultraviolet light to inactivate coronaviruses on personal protective equipment to reduce nosocomial transmission.

Camargo, Carolina / Lupien, Andréanne / McIntosh, Fiona / Menzies, Dick / Behr, Marcel A / Sagan, Selena M

Infection control and hospital epidemiology

2021 Volume 43, Issue 7, Page(s) 886–891

Abstract: Objective: To circumvent the need for rationing personal protective equipment (PPE), we explored whether germicidal ultraviolet light (GUV) could be used to inactivate human coronaviruses on PPE, enabling safe reuse.: Design: We performed a ... ...

Abstract	Objective: To circumvent the need for rationing personal protective equipment (PPE), we explored whether germicidal ultraviolet light (GUV) could be used to inactivate human coronaviruses on PPE, enabling safe reuse. Design: We performed a laboratory study to assess the ability of 2 commercially available portable GUV devices to inactivate 2 common cold coronaviruses (HCoV-229E and HCoV-OC43) and severe acute respiratory syndrome coronavirus virus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), on the surface of whole N95 respirators and coupons cut from those respirators. We experimentally contaminated N95 respirators with coronavirus cultures and then assessed viral inactivation after GUV exposure by plaque assay, the median tissue culture infectious dose (TCID Results: We found that GUV could efficiently inactivate coronaviruses on the surface of N95 masks, with an average reduction in viral titers of 5-log for HCoV-229E, 3-log for HCoV-OC43, and 5-log for SARS-CoV-2. In addition, the GUV susceptibility of HCoV-229E was similar on coupons and whole N95 respirators. Conclusions: We demonstrate that diverse human coronaviruses, including SARS-CoV-2, are susceptible to GUV inactivation, and 2 scalable portable GUV devices were effective in inactivating coronaviruses on N95 respirators. Thus, GUV treatment with commercially scalable devices may be an effective method to decontaminate PPE, allowing their safe reuse.
MeSH term(s)	COVID-19/prevention & control ; Cross Infection/prevention & control ; Equipment Reuse ; Humans ; Personal Protective Equipment ; SARS-CoV-2 ; Ultraviolet Rays
Language	English
Publishing date	2021-06-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639378-0
ISSN	1559-6834 ; 0195-9417 ; 0899-823X
ISSN (online)	1559-6834
ISSN	0195-9417 ; 0899-823X
DOI	10.1017/ice.2021.249
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Article ; Online: The role of chemokines and their receptors during protist parasite infections.

Menzies, Fiona M / Macphail, David / Henriquez, Fiona L

Parasitology

2016 Volume 143, Issue 14, Page(s) 1890–1901

Abstract: Protists are a diverse collection of eukaryotic organisms that account for a significant global infection burden. Often, the immune responses mounted against these parasites cause excessive inflammation and therefore pathology in the host. Elucidating ... ...

Abstract	Protists are a diverse collection of eukaryotic organisms that account for a significant global infection burden. Often, the immune responses mounted against these parasites cause excessive inflammation and therefore pathology in the host. Elucidating the mechanisms of both protective and harmful immune responses is complex, and often relies of the use of animal models. In any immune response, leucocyte trafficking to the site of infection, or inflammation, is paramount, and this involves the production of chemokines, small chemotactic cytokines of approximately 8-10 kDa in size, which bind to specific chemokine receptors to induce leucocyte movement. Herein, the scientific literature investigating the role of chemokines in the propagation of immune responses against key protist infections will be reviewed, focussing on Plasmodium species, Toxoplasma gondii, Leishmania species and Cryptosporidium species. Interestingly, many studies find that chemokines can in fact, promote parasite survival in the host, by drawing in leucocytes for spread and further replication. Recent developments in drug targeting against chemokine receptors highlights the need for further understanding of the role played by these proteins and their receptors in many different diseases.
MeSH term(s)	Animals ; Chemokines/classification ; Chemokines/immunology ; Chemokines/metabolism ; Cryptosporidiosis/drug therapy ; Cryptosporidiosis/immunology ; Cryptosporidiosis/metabolism ; Cryptosporidiosis/parasitology ; Cryptosporidium/drug effects ; Cryptosporidium/immunology ; Host-Parasite Interactions ; Humans ; Malaria/drug therapy ; Malaria/immunology ; Malaria/metabolism ; Malaria/parasitology ; Mice ; Plasmodium/drug effects ; Plasmodium/immunology ; Receptors, Chemokine/chemistry ; Receptors, Chemokine/immunology ; Receptors, Chemokine/metabolism ; Toxoplasma/drug effects ; Toxoplasma/immunology ; Toxoplasmosis/drug therapy ; Toxoplasmosis/immunology ; Toxoplasmosis/metabolism ; Toxoplasmosis/parasitology
Chemical Substances	Chemokines ; Receptors, Chemokine
Language	English
Publishing date	2016-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	207627-5
ISSN	1469-8161 ; 0031-1820
ISSN (online)	1469-8161
ISSN	0031-1820
DOI	10.1017/S0031182016001694
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Article: The role of chemokines and their receptors during protist parasite infections

MENZIES, FIONA M / MACPHAIL, DAVID / HENRIQUEZ, FIONA L

Parasitology. 2016 Dec., v. 143, no. 14

2016

Abstract	Protists are a diverse collection of eukaryotic organisms that account for a significant global infection burden. Often, the immune responses mounted against these parasites cause excessive inflammation and therefore pathology in the host. Elucidating the mechanisms of both protective and harmful immune responses is complex, and often relies of the use of animal models. In any immune response, leucocyte trafficking to the site of infection, or inflammation, is paramount, and this involves the production of chemokines, small chemotactic cytokines of approximately 8–10 kDa in size, which bind to specific chemokine receptors to induce leucocyte movement. Herein, the scientific literature investigating the role of chemokines in the propagation of immune responses against key protist infections will be reviewed, focussing on Plasmodium species, Toxoplasma gondii, Leishmania species and Cryptosporidium species. Interestingly, many studies find that chemokines can in fact, promote parasite survival in the host, by drawing in leucocytes for spread and further replication. Recent developments in drug targeting against chemokine receptors highlights the need for further understanding of the role played by these proteins and their receptors in many different diseases.
Keywords	Cryptosporidium ; Leishmania ; Plasmodium ; Toxoplasma gondii ; animal models ; chemokine receptors ; chemokines ; drugs ; immune response ; inflammation ; leukocytes ; parasites ; protists
Language	English
Dates of publication	2016-12
Size	p. 1890-1901.
Publishing place	Cambridge University Press
Document type	Article
ZDB-ID	207627-5
ISSN	1469-8161 ; 0031-1820
ISSN (online)	1469-8161
ISSN	0031-1820
DOI	10.1017/S0031182016001694
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Leucine regulates autophagy via acetylation of the mTORC1 component raptor.

Son, Sung Min / Park, So Jung / Stamatakou, Eleanna / Vicinanza, Mariella / Menzies, Fiona M / Rubinsztein, David C

Nature communications

2020 Volume 11, Issue 1, Page(s) 3148

Abstract: Macroautophagy ("autophagy") is the main lysosomal catabolic process that becomes activated under nutrient-depleted conditions, like amino acid (AA) starvation. The mechanistic target of rapamycin complex 1 (mTORC1) is a well-conserved negative regulator ...

Abstract	Macroautophagy ("autophagy") is the main lysosomal catabolic process that becomes activated under nutrient-depleted conditions, like amino acid (AA) starvation. The mechanistic target of rapamycin complex 1 (mTORC1) is a well-conserved negative regulator of autophagy. While leucine (Leu) is a critical mTORC1 regulator under AA-starved conditions, how Leu regulates autophagy is poorly understood. Here, we describe that in most cell types, including neurons, Leu negatively regulates autophagosome biogenesis via its metabolite, acetyl-coenzyme A (AcCoA). AcCoA inhibits autophagy by enhancing EP300-dependent acetylation of the mTORC1 component raptor, with consequent activation of mTORC1. Interestingly, in Leu deprivation conditions, the dominant effects on autophagy are mediated by decreased raptor acetylation causing mTORC1 inhibition, rather than by altered acetylation of other autophagy regulators. Thus, in most cell types we examined, Leu regulates autophagy via the impact of its metabolite AcCoA on mTORC1, suggesting that AcCoA and EP300 play pivotal roles in cell anabolism and catabolism.
MeSH term(s)	Acetyl Coenzyme A/metabolism ; Acetylation ; Animals ; Autophagosomes ; Autophagy/physiology ; Cell Line ; E1A-Associated p300 Protein/metabolism ; Humans ; Leucine/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Primary Cell Culture ; Regulatory-Associated Protein of mTOR/metabolism ; Starvation/metabolism
Chemical Substances	Regulatory-Associated Protein of mTOR ; Acetyl Coenzyme A (72-89-9) ; E1A-Associated p300 Protein (EC 2.3.1.48) ; EP300 protein, human (EC 2.3.1.48) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Leucine (GMW67QNF9C)
Language	English
Publishing date	2020-06-19
Publishing country	England
Document type	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/s41467-020-16886-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A Comprehensive Profile of Chemokine Gene Expression in the Tissues of the Female Reproductive Tract in Mice.

Menzies, Fiona M / Oldham, Rachel S / Waddell, Carolann / Nelson, Scott M / Nibbs, Robert J B

Immunological investigations

2019 Volume 49, Issue 3, Page(s) 264–286

Abstract: Homeostatic leukocyte trafficking into and within the female reproductive tract (FRT) contributes to fertility and reproductive health. It is unclear how this process is regulated in the anatomically distinct reproductive tissues, or whether the genes ... ...

Abstract	Homeostatic leukocyte trafficking into and within the female reproductive tract (FRT) contributes to fertility and reproductive health. It is unclear how this process is regulated in the anatomically distinct reproductive tissues, or whether the genes involved are affected by cyclical changes in reproductive hormones. In tissues such as skin and intestine, mouse studies have defined evolutionarily conserved molecular mechanisms for tissue-specific homing, interstitial positioning, and leukocyte egress. Chemokine family members are invariably involved, with the chemokine expression profile of a tissue regulating leukocyte content. Reproductive tissues (ovary, vagina, cervix, uterine horn) of 8 week old virgin female C57BL/6 mice (
MeSH term(s)	Animals ; Chemokines/genetics ; Estrous Cycle/immunology ; Female ; Gene Expression Profiling ; Genitalia, Female/cytology ; Genitalia, Female/metabolism ; Leukocytes/metabolism ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/metabolism ; Organ Specificity/immunology
Chemical Substances	Chemokines
Language	English
Publishing date	2019-08-20
Publishing country	England
Document type	Journal Article
ZDB-ID	632565-8
ISSN	1532-4311 ; 0882-0139
ISSN (online)	1532-4311
ISSN	0882-0139
DOI	10.1080/08820139.2019.1655573
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Article ; Online: LC3-II Tagging and Western Blotting for Monitoring Autophagic Activity in Mammalian Cells.

Streeter, Anne / Menzies, Fiona M / Rubinsztein, David C

Methods in molecular biology (Clifton, N.J.)

2015 Volume 1303, Page(s) 161–170

Abstract: The autophagosome-associated protein LC3-II is commonly used as a marker of autophagic activity within cells, but its levels are affected by both formation and degradation of autophagosomes. This can make the significance of altered LC3-II levels ... ...

Abstract	The autophagosome-associated protein LC3-II is commonly used as a marker of autophagic activity within cells, but its levels are affected by both formation and degradation of autophagosomes. This can make the significance of altered LC3-II levels ambiguous. Here we describe the method of Bafilomycin A1 blotting, in which the degradation of autophagosomes is prevented in cultured cells, allowing the causes of altered LC3-II levels to be determined.
MeSH term(s)	Autophagy/drug effects ; Blotting, Western/methods ; HeLa Cells ; Humans ; Macrolides/pharmacology ; Microtubule-Associated Proteins/metabolism ; Proteolysis/drug effects
Chemical Substances	MAP1LC3A protein, human ; Macrolides ; Microtubule-Associated Proteins ; bafilomycin A1 (88899-55-2)
Language	English
Publishing date	2015-07-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-2627-5_8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Compromised autophagy and neurodegenerative diseases.

Menzies, Fiona M / Fleming, Angeleen / Rubinsztein, David C

Nature reviews. Neuroscience

2015 Volume 16, Issue 6, Page(s) 345–357

Abstract: Most neurodegenerative diseases that afflict humans are associated with the intracytoplasmic deposition of aggregate-prone proteins in neurons and with mitochondrial dysfunction. Autophagy is a powerful process for removing such proteins and for ... ...

Abstract	Most neurodegenerative diseases that afflict humans are associated with the intracytoplasmic deposition of aggregate-prone proteins in neurons and with mitochondrial dysfunction. Autophagy is a powerful process for removing such proteins and for maintaining mitochondrial homeostasis. Over recent years, evidence has accumulated to demonstrate that upregulation of autophagy may protect against neurodegeneration. However, autophagy dysfunction has also been implicated in the pathogenesis of various diseases. This Review summarizes the progress that has been made in our understanding of how perturbations in autophagy are linked with neurodegenerative diseases and the potential therapeutic strategies resulting from the modulation of this process.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Neurodegenerative Diseases/physiopathology
Language	English
Publishing date	2015-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2034150-7
ISSN	1471-0048 ; 1471-0048 ; 1471-003X
ISSN (online)	1471-0048
ISSN	1471-0048 ; 1471-003X
DOI	10.1038/nrn3961
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Zs.MG 47: Show issues

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Article ; Online: Leucine regulates autophagy via acetylation of the mTORC1 component raptor

Sung Min Son / So Jung Park / Eleanna Stamatakou / Mariella Vicinanza / Fiona M. Menzies / David C. Rubinsztein

Nature Communications, Vol 11, Iss 1, Pp 1-

2020 Volume 13

Abstract: Leucine is a critical amino acid that inhibits autophagy. Here, the authors show that the leucine inhibits autophagy in most cell types, predominantly via its catabolite acetyl CoA, which drives acetylation of raptor, which activates mTORC1, a negative ... ...

Abstract	Leucine is a critical amino acid that inhibits autophagy. Here, the authors show that the leucine inhibits autophagy in most cell types, predominantly via its catabolite acetyl CoA, which drives acetylation of raptor, which activates mTORC1, a negative regulator of this catabolic process.
Keywords	Science ; Q
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: α-Catenin levels determine direction of YAP/TAZ response to autophagy perturbation.

Pavel, Mariana / Park, So Jung / Frake, Rebecca A / Son, Sung Min / Manni, Marco M / Bento, Carla F / Renna, Maurizio / Ricketts, Thomas / Menzies, Fiona M / Tanasa, Radu / Rubinsztein, David C

Nature communications

2021 Volume 12, Issue 1, Page(s) 1703

Abstract: The factors regulating cellular identity are critical for understanding the transition from health to disease and responses to therapies. Recent literature suggests that autophagy compromise may cause opposite effects in different contexts by either ... ...

Abstract	The factors regulating cellular identity are critical for understanding the transition from health to disease and responses to therapies. Recent literature suggests that autophagy compromise may cause opposite effects in different contexts by either activating or inhibiting YAP/TAZ co-transcriptional regulators of the Hippo pathway via unrelated mechanisms. Here, we confirm that autophagy perturbation in different cell types can cause opposite responses in growth-promoting oncogenic YAP/TAZ transcriptional signalling. These apparently contradictory responses can be resolved by a feedback loop where autophagy negatively regulates the levels of α-catenins, LC3-interacting proteins that inhibit YAP/TAZ, which, in turn, positively regulate autophagy. High basal levels of α-catenins enable autophagy induction to positively regulate YAP/TAZ, while low α-catenins cause YAP/TAZ activation upon autophagy inhibition. These data reveal how feedback loops enable post-transcriptional determination of cell identity and how levels of a single intermediary protein can dictate the direction of response to external or internal perturbations.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy/physiology ; Cells, Cultured ; Epithelial Cells ; Feedback, Physiological ; Humans ; Mice ; Microtubule-Associated Proteins/metabolism ; Mutation ; Protein Binding ; Protein Interaction Domains and Motifs/genetics ; Signal Transduction ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcriptional Coactivator with PDZ-Binding Motif Proteins ; YAP-Signaling Proteins ; alpha Catenin/chemistry ; alpha Catenin/genetics ; alpha Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Trans-Activators ; Transcription Factors ; Transcriptional Coactivator with PDZ-Binding Motif Proteins ; WWTR1 protein, human ; YAP-Signaling Proteins ; YAP1 protein, human ; alpha Catenin
Language	English
Publishing date	2021-03-17
Publishing country	England
Document type	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/s41467-021-21882-1
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