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Article ; Online: What language is the language-ready brain ready for?: Comment on "Towards a Computational Comparative Neuroprimatology: Framing the language-ready brain" by Michael A. Arbib.

Croft, William

2016 Volume 16, Page(s) 66–68

MeSH term(s)	Animals ; Brain ; Humans ; Language ; Macaca
Language	English
Publishing date	2016-03
Publishing country	Netherlands
Document type	Journal Article ; Comment
ZDB-ID	2148883-6
ISSN	1873-1457 ; 1571-0645
ISSN (online)	1873-1457
ISSN	1571-0645
DOI	10.1016/j.plrev.2016.02.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Killer whales.

Weiss, Michael N / Croft, Darren P

Current biology : CB

2023 Volume 33, Issue 12, Page(s) R668–R670

Abstract: Michael Weiss and Darren Croft introduce Orcas (Orcinus orca) also known as killer whales. ...

Abstract	Michael Weiss and Darren Croft introduce Orcas (Orcinus orca) also known as killer whales.
MeSH term(s)	Animals ; Whale, Killer
Language	English
Publishing date	2023-06-20
Publishing country	England
Document type	Journal Article
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2023.03.004
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Article ; Online: TNF-like weak inducer of apoptosis inhibition is comparable to IL-13 blockade in ameliorating atopic dermatitis inflammation.

Gupta, Rinkesh K / Miller, Jacqueline / Croft, Michael

Allergy

2023 Volume 79, Issue 1, Page(s) 116–127

Abstract: Background: Targeting IL-13 is highly efficacious in patients with Th2-biased atopic dermatitis (AD), but inhibition of other inflammatory molecules might also limit disease. We investigated the importance of the TNF family cytokine TNF-like weak ... ...

Abstract	Background: Targeting IL-13 is highly efficacious in patients with Th2-biased atopic dermatitis (AD), but inhibition of other inflammatory molecules might also limit disease. We investigated the importance of the TNF family cytokine TNF-like weak inducer of apoptosis (TWEAK; TNFSF12) to keratinocyte dysregulation and the pathogenesis of AD in mice and also tested if blocking TWEAK has a similar therapeutic effect as targeting IL-13. Methods: Conditional knockout mice lacking Fn14 (TNFRSF12A), the receptor for TWEAK, only in keratinocytes, were repetitively sensitized with house dust mite allergen and analyzed for AD-like skin inflammation. To determine the translational potential, wild-type mice with AD were therapeutically treated with anti-TWEAK and/or anti-IL-13 antibodies, and skin inflammation was assessed. Results: Mice deficient in Fn14 in keratinocytes were resistant to developing maximal clinical features of AD, exhibiting reduced epidermal hyperplasia and dermal thickening, less skin infiltration of immune cells, and downregulated inflammatory gene expression. Moreover, therapeutic neutralization of TWEAK in wild-type mice with AD reduced all of the pathological features to a comparable extent as blocking IL-13. Conclusions: The activity of TWEAK in keratinocytes contributes to AD development, and neutralizing TWEAK represents a future potential therapeutic option in human AD similar to targeting IL-13.
MeSH term(s)	Humans ; Animals ; Mice ; Interleukin-13 ; Dermatitis, Atopic/drug therapy ; TWEAK Receptor/genetics ; TWEAK Receptor/metabolism ; Inflammation/metabolism ; Apoptosis ; Mice, Knockout
Chemical Substances	Interleukin-13 ; TWEAK Receptor
Language	English
Publishing date	2023-08-31
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.15879
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Article ; Online: Agonism of 4-1BB for immune therapy: a perspective on possibilities and complications.

Salek-Ardakani, Shahram / Zajonc, Dirk M / Croft, Michael

Frontiers in immunology

2023 Volume 14, Page(s) 1228486

Abstract: Costimulatory receptors on immune cells represent attractive targets for immunotherapy given that these molecules can increase the frequency of individual protective immune cell populations and their longevity, as well as enhance various effector ... ...

Abstract	Costimulatory receptors on immune cells represent attractive targets for immunotherapy given that these molecules can increase the frequency of individual protective immune cell populations and their longevity, as well as enhance various effector functions. 4-1BB, a member of the TNF receptor superfamily, also known as CD137 and TNFRSF9, is one such molecule that is inducible on several cell types, including T cells and NK cells. Preclinical studies in animal models have validated the notion that stimulating 4-1BB with agonist reagents or its natural ligand could be useful to augment conventional T cell and NK cell immunity to protect against tumor growth and against viral infection. Additionally, stimulating 4-1BB can enhance regulatory T cell function and might be useful in the right context for suppressing autoimmunity. Two human agonist antibodies to 4-1BB have been produced and tested in clinical trials for cancer, with variable results, leading to the production of a wealth of second-generation antibody constructs, including bi- and multi-specifics, with the hope of optimizing activity and selectivity. Here, we review the progress to date in agonism of 4-1BB, discuss the complications in targeting the immune system appropriately to elicit the desired activity, together with challenges in engineering agonists, and highlight the untapped potential of manipulating this molecule in infectious disease and autoimmunity.
MeSH term(s)	Animals ; Humans ; Immunotherapy ; Antibodies ; Autoimmunity ; Killer Cells, Natural ; Longevity
Chemical Substances	Antibodies
Language	English
Publishing date	2023-08-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1228486
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Article ; Online: The evolution of menopause in toothed whales.

Ellis, Samuel / Franks, Daniel W / Nielsen, Mia Lybkær Kronborg / Weiss, Michael N / Croft, Darren P

Nature

2024 Volume 627, Issue 8004, Page(s) 579–585

Abstract: Understanding how and why menopause has evolved is a long-standing challenge across disciplines. Females can typically maximize their reproductive success by reproducing for the whole of their adult life. In humans, however, women cease reproduction ... ...

Abstract	Understanding how and why menopause has evolved is a long-standing challenge across disciplines. Females can typically maximize their reproductive success by reproducing for the whole of their adult life. In humans, however, women cease reproduction several decades before the end of their natural lifespan
MeSH term(s)	Animals ; Female ; Biological Evolution ; Databases, Factual ; Longevity/physiology ; Menopause/physiology ; Models, Biological ; Reproduction/physiology ; Whales/classification ; Whales/physiology ; Humans
Language	English
Publishing date	2024-03-13
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-024-07159-9
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Article ; Online: TNF‐like weak inducer of apoptosis inhibition is comparable to IL‐13 blockade in ameliorating atopic dermatitis inflammation

Gupta, Rinkesh K. / Miller, Jacqueline / Croft, Michael

Allergy. 2024 Jan., v. 79, no. 1, p. 116-127

2024 , Page(s) 116–127

Abstract: BACKGROUND: Targeting IL‐13 is highly efficacious in patients with Th2‐biased atopic dermatitis (AD), but inhibition of other inflammatory molecules might also limit disease. We investigated the importance of the TNF family cytokine TNF‐like weak inducer ...

Abstract	BACKGROUND: Targeting IL‐13 is highly efficacious in patients with Th2‐biased atopic dermatitis (AD), but inhibition of other inflammatory molecules might also limit disease. We investigated the importance of the TNF family cytokine TNF‐like weak inducer of apoptosis (TWEAK; TNFSF12) to keratinocyte dysregulation and the pathogenesis of AD in mice and also tested if blocking TWEAK has a similar therapeutic effect as targeting IL‐13. METHODS: Conditional knockout mice lacking Fn14 (TNFRSF12A), the receptor for TWEAK, only in keratinocytes, were repetitively sensitized with house dust mite allergen and analyzed for AD‐like skin inflammation. To determine the translational potential, wild‐type mice with AD were therapeutically treated with anti‐TWEAK and/or anti‐IL‐13 antibodies, and skin inflammation was assessed. RESULTS: Mice deficient in Fn14 in keratinocytes were resistant to developing maximal clinical features of AD, exhibiting reduced epidermal hyperplasia and dermal thickening, less skin infiltration of immune cells, and downregulated inflammatory gene expression. Moreover, therapeutic neutralization of TWEAK in wild‐type mice with AD reduced all of the pathological features to a comparable extent as blocking IL‐13. CONCLUSIONS: The activity of TWEAK in keratinocytes contributes to AD development, and neutralizing TWEAK represents a future potential therapeutic option in human AD similar to targeting IL‐13.
Keywords	allergens ; apoptosis ; atopic dermatitis ; dust mites ; gene expression ; humans ; hyperplasia ; inflammation ; interleukin-13 ; keratinocytes ; neutralization ; pathogenesis ; therapeutics
Language	English
Dates of publication	2024-01
Size	p. 116-127
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.15879
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Global Expanded Access Program for Pemigatinib in Patients with Previously Treated Locally Advanced or Metastatic Cholangiocarcinoma and Fibroblast Growth Factor Receptor Gene Alterations.

Lindley, Anouk / Prager, Gerald / Bitzer, Michael / Burn, Timothy C / Lihou, Christine F / Croft, Elisabeth

Cancer research and treatment

2024

Abstract: Purpose: Pemigatinib is a fibroblast growth factor receptor-2 (FGFR2) inhibitor approved for use in patients with previously treated cholangiocarcinoma (CCA) and FGFR2 fusions or rearrangements. This ongoing global Expanded Access Program (EAP) allows ... ...

Abstract	Purpose: Pemigatinib is a fibroblast growth factor receptor-2 (FGFR2) inhibitor approved for use in patients with previously treated cholangiocarcinoma (CCA) and FGFR2 fusions or rearrangements. This ongoing global Expanded Access Program (EAP) allows physicians in regions where pemigatinib is not commercially available to request pemigatinib for patients with locally advanced or metastatic CCA who, in the physician's opinion, could benefit from pemigatinib treatment. Materials and methods: Eighty-nine patients from Europe, North America, and Israel were treated from January 2020 through September 2021. Results: Patients had FGFR gene fusions (68.5%), rearrangements (12.4%), translocations (5.6%), amplifications (2.2%), and other alterations (11.2%). Median duration of treatment in the EAP was 4.0 months (range, 0.1-13.6). The most frequently reported adverse event (AE) was hyperphosphatemia (22.5%); the most common serious AE was cholangitis (3.4%). Treatment discontinuation was associated with reports of AEs for seven patients (7.9%). AEs associated with pemigatinib were consistent with those observed in clinical trials. Conclusion: Efficacy was not assessed in this EAP. However, some patients remained on treatment for up to a year, suggesting that they observed a benefit from treatment. Patients with CCA should undergo molecular testing to identify those who could benefit from targeted treatments such as pemigatinib.
Language	English
Publishing date	2024-02-07
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2133613-1
ISSN	2005-9256 ; 1598-2998
ISSN (online)	2005-9256
ISSN	1598-2998
DOI	10.4143/crt.2023.1197
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Article ; Online: Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine.

Liu, Hsin Yu / Altman, Amnon / Canonigo-Balancio, Ann J / Croft, Michael

Journal of visualized experiments : JoVE

2023 , Issue 192

Abstract: Fms-like tyrosine kinase 3 ligand (Flt3L) is a hematopoietic cytokine that promotes the survival and differentiation of dendritic cells (DCs). It has been used in tumor vaccines to activate innate immunity and enhance antitumor responses. This protocol ... ...

Abstract	Fms-like tyrosine kinase 3 ligand (Flt3L) is a hematopoietic cytokine that promotes the survival and differentiation of dendritic cells (DCs). It has been used in tumor vaccines to activate innate immunity and enhance antitumor responses. This protocol demonstrates a therapeutic model using cell-based tumor vaccine consisting of Flt3L-expressing B16-F10 melanoma cells along with phenotypic and functional analysis of immune cells in the tumor microenvironment (TME). Procedures for cultured tumor cell preparation, tumor implantation, cell irradiation, tumor size measurement, intratumoral immune cell isolation, and flow cytometry analysis are described. The overall goal of this protocol is to provide a preclinical solid tumor immunotherapy model, and a research platform to study the relationship between tumor cells and infiltrating immune cells. The immunotherapy protocol described here can be combined with other therapeutic modalities, such as immune checkpoint blockade (anti-CTLA-4, anti-PD-1, anti-PD-L1 antibodies) or chemotherapy in order to improve the cancer therapeutic effect of melanoma.
MeSH term(s)	Animals ; Humans ; Melanoma, Experimental/therapy ; Cancer Vaccines ; Dendritic Cells ; Immunotherapy/methods ; Cytokines ; Vaccination ; Tumor Microenvironment
Chemical Substances	Cancer Vaccines ; Cytokines
Language	English
Publishing date	2023-02-24
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/64082
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Article ; Online: Contribution of circulatory cells to asthma exacerbations and lung tissue-resident CD4 T cell memory.

Sethi, Gurupreet S / Gracias, Donald / Croft, Michael

Frontiers in immunology

2022 Volume 13, Page(s) 951361

Abstract: Tissue-resident memory CD4 T cells (Trm) are thought to be a major contributor to asthma relapse, but the role of circulatory T cells in asthma exacerbations or to maintaining the population of lung Trm cells is not fully understood. Here, we used a ... ...

Abstract	Tissue-resident memory CD4 T cells (Trm) are thought to be a major contributor to asthma relapse, but the role of circulatory T cells in asthma exacerbations or to maintaining the population of lung Trm cells is not fully understood. Here, we used a house dust mite allergen-based murine model of asthma relapse, and monitored the development of lung effector/Trm phenotype CD44
MeSH term(s)	Allergens ; Animals ; Asthma/pathology ; CD4-Positive T-Lymphocytes ; Fingolimod Hydrochloride/pharmacology ; Immunologic Memory ; Lung ; Mice ; Pneumonia/pathology ; Recurrence
Chemical Substances	Allergens ; Fingolimod Hydrochloride (G926EC510T)
Language	English
Publishing date	2022-07-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.951361
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Article ; Online: Realigning the LIGHT signaling network to control dysregulated inflammation.

Ware, Carl F / Croft, Michael / Neil, Garry A

The Journal of experimental medicine

2022 Volume 219, Issue 7

Abstract: Advances in understanding the physiologic functions of the tumor necrosis factor superfamily (TNFSF) of ligands, receptors, and signaling networks are providing deeper insight into pathogenesis of infectious and autoimmune diseases and cancer. LIGHT ( ... ...

Abstract	Advances in understanding the physiologic functions of the tumor necrosis factor superfamily (TNFSF) of ligands, receptors, and signaling networks are providing deeper insight into pathogenesis of infectious and autoimmune diseases and cancer. LIGHT (TNFSF14) has emerged as an important modulator of critical innate and adaptive immune responses. LIGHT and its signaling receptors, herpesvirus entry mediator (TNFRSF14), and lymphotoxin β receptor, form an immune regulatory network with two co-receptors of herpesvirus entry mediator, checkpoint inhibitor B and T lymphocyte attenuator, and CD160. Deciphering the fundamental features of this network reveals new understanding to guide therapeutic development. Accumulating evidence from infectious diseases points to the dysregulation of the LIGHT network as a disease-driving mechanism in autoimmune and inflammatory reactions in barrier organs, including coronavirus disease 2019 pneumonia and inflammatory bowel diseases. Recent clinical results warrant further investigation of the LIGHT regulatory network and application of target-modifying therapeutics for disease intervention.
MeSH term(s)	COVID-19 ; Humans ; Inflammation ; Receptors, Tumor Necrosis Factor, Member 14 ; Signal Transduction ; T-Lymphocytes
Chemical Substances	Receptors, Tumor Necrosis Factor, Member 14
Language	English
Publishing date	2022-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20220236
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