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Book: Jack, die Bärenklaue

Krusow, Major von / Krusow, ... von / Merkel, Johannes / Richter, Dieter

eine Erzählung aus dem wilden Westen

(Sammlung alter Kinderbücher ; Bd. 4)

1979

Author's details	Major von Krusow. Neu hrsg. von Johannes Merkel und Dieter Richter
Series title	Sammlung alter Kinderbücher ; Bd. 4
Size	188 S, Ill.
Edition	Reprint der Ausg. Berlin 1897
Publisher	Weismann
Publishing place	München
Document type	Book
Note	In Fraktur ; Im Anhang: In finstern und blutigen Gründen : das Indianerbuch als Jugendmassenlektüre. Der Herr Major von Krusow
Accompanying material	Ill
ISBN	3921040574 ; 9783921040577
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Staphylococcus scratches its itch.

Major, Jack / Naik, Shruti

Cell

2023 Volume 186, Issue 24, Page(s) 5201–5202

Abstract: Itch exacerbates infection and inflammation-associated skin pathology. In this issue of Cell, Deng et al. identify a V8 protease released by Staphylococcus aureus triggering itch via neuronal protease-activated receptor 1. In so doing, they uncover ... ...

Abstract	Itch exacerbates infection and inflammation-associated skin pathology. In this issue of Cell, Deng et al. identify a V8 protease released by Staphylococcus aureus triggering itch via neuronal protease-activated receptor 1. In so doing, they uncover profound consequences of microbial neurosensory modulation and the ensuing scratch-induced tissue damage that potentiates infection.
MeSH term(s)	Humans ; Inflammation/microbiology ; Peptide Hydrolases ; Pruritus/microbiology ; Staphylococcus aureus ; Staphylococcal Infections/microbiology ; Staphylococcal Infections/pathology
Chemical Substances	Peptide Hydrolases (EC 3.4.-)
Language	English
Publishing date	2023-11-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2023.10.027
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Article ; Online: An ace model for SARS-CoV-2 infection.

Major, Jack / Wack, Andreas

The Journal of experimental medicine

2020 Volume 217, Issue 12

Abstract: Developing effective in vivo models for SARS-CoV-2 infection is crucial for mechanistic studies of COVID-19 disease progression. In this issue of JEM, Israelow et al. (https://doi.org/10.1084/jem.20201241) generate a model that supports SARS-CoV-2 ... ...

Abstract	Developing effective in vivo models for SARS-CoV-2 infection is crucial for mechanistic studies of COVID-19 disease progression. In this issue of JEM, Israelow et al. (https://doi.org/10.1084/jem.20201241) generate a model that supports SARS-CoV-2 infection in mice, which they use to characterize type I IFN-driven pulmonary inflammation.
MeSH term(s)	Animals ; Betacoronavirus ; COVID-19 ; Coronavirus Infections ; Interferon Type I ; Mice ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2 ; Severe Acute Respiratory Syndrome
Chemical Substances	Interferon Type I
Keywords	covid19
Language	English
Publishing date	2020-09-15
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20201748
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Article ; Online: An ace model for SARS-CoV-2 infection

Major, Jack / Wack, Andreas

Journal of Experimental Medicine

2020 Volume 217, Issue 12

Abstract	Developing effective in vivo models for SARS-CoV-2 infection is crucial for mechanistic studies of COVID-19 disease progression. In this issue of JEM, Israelow et al. (https://doi.org/10.1084/jem.20201241) generate a model that supports SARS-CoV-2 infection in mice, which they use to characterize type I IFN–driven pulmonary inflammation.
Keywords	Immunology ; Immunology and Allergy ; covid19
Language	English
Publisher	Rockefeller University Press
Publishing country	us
Document type	Article ; Online
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20201748
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation.

Crotta, Stefania / Villa, Matteo / Major, Jack / Finsterbusch, Katja / Llorian, Miriam / Carmeliet, Peter / Buescher, Joerg / Wack, Andreas

Nature communications

2023 Volume 14, Issue 1, Page(s) 721

Abstract: Epithelial tissues provide front-line barriers shielding the organism from invading pathogens and harmful substances. In the airway epithelium, the combined action of multiciliated and secretory cells sustains the mucociliary escalator required for ... ...

Abstract	Epithelial tissues provide front-line barriers shielding the organism from invading pathogens and harmful substances. In the airway epithelium, the combined action of multiciliated and secretory cells sustains the mucociliary escalator required for clearance of microbes and particles from the airways. Defects in components of mucociliary clearance or barrier integrity are associated with recurring infections and chronic inflammation. The timely and balanced differentiation of basal cells into mature epithelial cell subsets is therefore tightly controlled. While different growth factors regulating progenitor cell proliferation have been described, little is known about the role of metabolism in these regenerative processes. Here we show that basal cell differentiation correlates with a shift in cellular metabolism from glycolysis to fatty acid oxidation (FAO). We demonstrate both in vitro and in vivo that pharmacological and genetic impairment of FAO blocks the development of fully differentiated airway epithelial cells, compromising the repair of airway epithelia. Mechanistically, FAO links to the hexosamine biosynthesis pathway to support protein glycosylation in airway epithelial cells. Our findings unveil the metabolic network underpinning the differentiation of airway epithelia and identify novel targets for intervention to promote lung repair.
MeSH term(s)	Epithelium/metabolism ; Respiratory System ; Epithelial Cells/metabolism ; Cell Differentiation/physiology ; Fatty Acids/metabolism ; Respiratory Mucosa/metabolism
Chemical Substances	Fatty Acids
Language	English
Publishing date	2023-02-13
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/s41467-023-36352-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Computer tomography measurements of the airway and thoracic cavity do not provide support for bronchial conformation as a predisposing factor of left cranial lung lobe torsion in pugs.

Gall, Nick / Butts, Daniel R / Chanoit, Guillaume P / Major, Alison C

Veterinary radiology & ultrasound : the official journal of the American College of Veterinary Radiology and the International Veterinary Radiology Association

2024

Abstract: ... Jack Russell Terriers (JRT) were analyzed. Thoracic height: width ratio (H:W), cross-sectional areas ...

Abstract	The objective of this retrospective clinical study was to determine if airway or thoracic cavity measurements in pugs, particularly the left cranial lung lobe, were significantly different from brachycephalic and mesocephalic control. Thoracic computed tomographic studies of 10 pugs, French bulldogs (FB), and Jack Russell Terriers (JRT) were analyzed. Thoracic height: width ratio (H:W), cross-sectional areas of the left mainstem bronchus (CSA LMB), left cranial lung lobe bronchus (CSA LCrBr), left caudal lung lobe bronchus (CSA LCauBr), CSA LCrBr relative to length (CSA LCrBr/length) and CSA LCauBr/length were measured and adjusted to body weight (/kg). CSA LMB/kg, CSA LCauBr/length/kg, and CSA LCrBr/length /kg were smaller in pugs and FB compared with JRT (P < .05), but no differences were found between pugs and FB. Cross-sectional areas of left cranial lung lobe bronchus /kg and CSA LCauBr/kg were smaller in pugs than JRT (P < .05), but no differences were found between pugs and FB or FB and JRT. No difference was found in thoracic H:W between any breeds. This demonstrated that pugs and FB had significantly narrower bronchi CSA/lengths ratios compared with JRT, but this was not limited to the LCBr. Airway measurements were not significantly different between brachycephalic breeds; therefore, the pugs' predisposition to left cranial lung lobe torsion cannot be solely explained by narrower lower airways.
Language	English
Publishing date	2024-02-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2142058-0
ISSN	1740-8261 ; 1058-8183
ISSN (online)	1740-8261
ISSN	1058-8183
DOI	10.1111/vru.13345
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Endothelial AHR activity prevents lung barrier disruption in viral infection.

Major, Jack / Crotta, Stefania / Finsterbusch, Katja / Chakravarty, Probir / Shah, Kathleen / Frederico, Bruno / D'Antuono, Rocco / Green, Mary / Meader, Lucy / Suarez-Bonnet, Alejandro / Priestnall, Simon / Stockinger, Brigitta / Wack, Andreas

Nature

2023 Volume 621, Issue 7980, Page(s) 813–820

Abstract: Disruption of the lung endothelial-epithelial cell barrier following respiratory virus infection causes cell and fluid accumulation in the air spaces and compromises vital gas exchange ... ...

Abstract	Disruption of the lung endothelial-epithelial cell barrier following respiratory virus infection causes cell and fluid accumulation in the air spaces and compromises vital gas exchange function
MeSH term(s)	Animals ; Humans ; Mice ; Apelin/metabolism ; Diet ; Endothelial Cells/metabolism ; Endothelium/cytology ; Endothelium/metabolism ; Epithelial Cells/metabolism ; Erythrocytes/metabolism ; Influenza, Human/immunology ; Influenza, Human/metabolism ; Intestines/metabolism ; Leukocytes/metabolism ; Ligands ; Lung/immunology ; Lung/metabolism ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/metabolism ; Pulmonary Alveoli/immunology ; Pulmonary Alveoli/metabolism ; Receptors, Aryl Hydrocarbon/metabolism
Chemical Substances	AHR protein, human ; Ahr protein, mouse ; Apelin ; APLNR protein, human ; Aplnr protein, mouse ; Ligands ; Receptors, Aryl Hydrocarbon
Language	English
Publishing date	2023-08-16
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06287-y
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Article ; Online: Tissue-specific and interferon-inducible expression of nonfunctional ACE2 through endogenous retroelement co-option.

Ng, Kevin W / Attig, Jan / Bolland, William / Young, George R / Major, Jack / Wrobel, Antoni G / Gamblin, Steve / Wack, Andreas / Kassiotis, George

Nature genetics

2020 Volume 52, Issue 12, Page(s) 1294–1302

Abstract: Angiotensin-converting enzyme 2 (ACE2) is an entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and a regulator of several physiological processes. ACE2 has recently been proposed to be interferon (IFN) inducible, suggesting ... ...

Abstract	Angiotensin-converting enzyme 2 (ACE2) is an entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and a regulator of several physiological processes. ACE2 has recently been proposed to be interferon (IFN) inducible, suggesting that SARS-CoV-2 may exploit this phenomenon to enhance viral spread and questioning the efficacy of IFN treatment in coronavirus disease 2019. Using a recent de novo transcript assembly that captured previously unannotated transcripts, we describe a new isoform of ACE2, generated by co-option of intronic retroelements as promoter and alternative exon. The new transcript, termed MIRb-ACE2, exhibits specific expression patterns across the aerodigestive and gastrointestinal tracts and is highly responsive to IFN stimulation. In contrast, canonical ACE2 expression is unresponsive to IFN stimulation. Moreover, the MIRb-ACE2 translation product is a truncated, unstable ACE2 form, lacking domains required for SARS-CoV-2 binding and is therefore unlikely to contribute to or enhance viral infection.
MeSH term(s)	Angiotensin-Converting Enzyme 2/biosynthesis ; Angiotensin-Converting Enzyme 2/genetics ; Animals ; Cell Line ; Chlorocebus aethiops ; Enzyme Induction ; Gene Expression Profiling ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Viral ; HEK293 Cells ; Humans ; Interferons/metabolism ; Isoenzymes/biosynthesis ; Isoenzymes/genetics ; Protein Stability ; RNA-Seq ; Receptors, Coronavirus/metabolism ; Retroelements/genetics ; SARS-CoV-2/metabolism ; Tissue Distribution ; Vero Cells
Chemical Substances	Isoenzymes ; Receptors, Coronavirus ; Retroelements ; Interferons (9008-11-1) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-020-00732-8
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Article ; Online: Type I and III interferons disrupt lung epithelial repair during recovery from viral infection.

Major, Jack / Crotta, Stefania / Llorian, Miriam / McCabe, Teresa M / Gad, Hans Henrik / Priestnall, Simon L / Hartmann, Rune / Wack, Andreas

Science (New York, N.Y.)

2020 Volume 369, Issue 6504, Page(s) 712–717

Abstract: Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-α and IFN-β) and III (IFN-λ) interferons are host-produced antiviral cytokines. Prolonged IFN-α and IFN-β responses can lead to harmful ...

Abstract	Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-α and IFN-β) and III (IFN-λ) interferons are host-produced antiviral cytokines. Prolonged IFN-α and IFN-β responses can lead to harmful proinflammatory effects, whereas IFN-λ mainly signals in epithelia, thereby inducing localized antiviral immunity. In this work, we show that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-λ driving these effects most potently. IFN-induced protein p53 directly reduces epithelial proliferation and differentiation, which increases disease severity and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN production aggravates viral infection by impairing lung epithelial regeneration. Timing and duration are therefore critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disease 2019 (COVID-19).
MeSH term(s)	Alveolar Epithelial Cells/immunology ; Alveolar Epithelial Cells/pathology ; Animals ; Apoptosis ; Bronchoalveolar Lavage Fluid/immunology ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Cytokines/administration & dosage ; Cytokines/immunology ; Cytokines/metabolism ; Female ; Influenza A Virus, H3N2 Subtype ; Interferon Type I/administration & dosage ; Interferon Type I/metabolism ; Interferon Type I/pharmacology ; Interferon-alpha/administration & dosage ; Interferon-alpha/metabolism ; Interferon-alpha/pharmacology ; Interferon-beta/administration & dosage ; Interferon-beta/metabolism ; Interferon-beta/pharmacology ; Interferons/administration & dosage ; Interferons/metabolism ; Interferons/pharmacology ; Lung/pathology ; Male ; Mice ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/metabolism ; Orthomyxoviridae Infections/pathology ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/metabolism ; Receptors, Interferon/genetics ; Receptors, Interferon/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Cytokines ; IFNLR1 protein, mouse ; Interferon Type I ; Interferon-alpha ; Receptors, Interferon ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; interferon type III ; interferon-lambda protein, mouse ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferon-beta (77238-31-4) ; Interferons (9008-11-1)
Keywords	covid19
Language	English
Publishing date	2020-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.abc2061
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Article ; Online: Visible Signs of Concussion and Cognitive Screening in Community Sports.

Reyes, Jonathan / Mitra, Biswadev / Makdissi, Michael / Clifton, Patrick / Nguyen, Jack V K / Harcourt, Peter / Howard, Teresa S / Cameron, Peter A / Rosenfeld, Jeffrey V / Major, Brendan P / Willmott, Catherine

Journal of neurotrauma

2021 Volume 39, Issue 1-2, Page(s) 122–130

Abstract: Video surveillance and detection of players with visible signs of concussion by experienced medical staff facilitates rapid on-field screening of suspected concussion in professional sports. This method, however has not been validated in community sports ...

Abstract	Video surveillance and detection of players with visible signs of concussion by experienced medical staff facilitates rapid on-field screening of suspected concussion in professional sports. This method, however has not been validated in community sports where video footage is unavailable. This study aimed to explore the utility of visible signs of concussion to identify players with decrements in performance on concussion screening measures. In this observational prospective cohort study, personnel with basic training observed live matches across a season (60 matches) of community male and female Australian football for signs of concussion outlined in the community-based Head Injury Assessment form (HIAf). Players identified to have positive signs of concussion (CoSign+) following an impact were compared with players without signs (CoSign-). Outcome measures, the Sport Concussion Assessment Tool (SCAT3) and Cogstate, were administered at baseline and post-match. CoSign+ (
MeSH term(s)	Female ; Humans ; Male ; Athletic Injuries/diagnosis ; Athletic Injuries/epidemiology ; Australia ; Brain Concussion/psychology ; Cognition ; Prospective Studies ; Team Sports
Language	English
Publishing date	2021-04-21
Publishing country	United States
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2020.7425
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