LIVIVO - Suchergebnisse -

Suchergebnis

Treffer 1 - 10 von insgesamt 25

Artikel ; Online: Tlr5

Alajoleen, Razan M / Oakland, David N / Estaleen, Rana / Shakeri, Aida / Lu, Ran / Appiah, Michael / Sun, Sha / Neumann, Jonathan / Kawauchi, Shimako / Cecere, Thomas E / McMillan, Ryan P / Reilly, Christopher M / Luo, Xin M

Frontiers in immunology

2024 Band 15, Seite(n) 1359534

Abstract: Introduction: Leaky gut has been linked to autoimmune disorders including lupus. We previously reported upregulation of anti-flagellin antibodies in the blood of lupus patients and lupus-prone mice, which led to our hypothesis that a leaky gut drives ... ...

Abstract	Introduction: Leaky gut has been linked to autoimmune disorders including lupus. We previously reported upregulation of anti-flagellin antibodies in the blood of lupus patients and lupus-prone mice, which led to our hypothesis that a leaky gut drives lupus through bacterial flagellin-mediated activation of toll-like receptor 5 (TLR5). Methods: We created MRL/ Result: Contrary to our hypothesis that the deletion of Conclusion: Global deletion of
Mesh-Begriff(e)	Animals ; Female ; Humans ; Mice ; Glomerulonephritis/pathology ; Kidney/pathology ; Mice, Inbred MRL lpr ; Proteinuria ; Toll-Like Receptor 5
Chemische Substanzen	Toll-Like Receptor 5 ; Tlr5 protein, mouse
Sprache	Englisch
Erscheinungsdatum	2024-01-30
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1359534
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

Details ▾
- Kostenpflichtig bestellen

Artikel ; Online: The Abca7

Butler, Claire A / Mendoza Arvilla, Adrian / Milinkeviciute, Giedre / Da Cunha, Celia / Kawauchi, Shimako / Rezaie, Narges / Liang, Heidi Y / Javonillo, Dominic / Thach, Annie / Wang, Shuling / Collins, Sherilyn / Walker, Amber / Shi, Kai-Xuan / Neumann, Jonathan / Gomez-Arboledas, Angela / Henningfield, Caden M / Hohsfield, Lindsay A / Mapstone, Mark / Tenner, Andrea J /

LaFerla, Frank M / Mortazavi, Ali / MacGregor, Grant R / Green, Kim N

Alzheimer's & dementia : the journal of the Alzheimer's Association

2024

Abstract: Background: Variants in ABCA7, a member of the ABC transporter superfamily, have been associated with increased risk for developing late onset Alzheimer's disease (LOAD).: Methods: CRISPR-Cas9 was used to generate an Abca7: Results: Abca7: ... ...

Abstract	Background: Variants in ABCA7, a member of the ABC transporter superfamily, have been associated with increased risk for developing late onset Alzheimer's disease (LOAD). Methods: CRISPR-Cas9 was used to generate an Abca7 Results: Abca7 Discussion: Overall, homozygosity for the Abca7 Highlights: ABCA7 recognized as a top 10 risk gene for developing Alzheimer's disease. Loss of function mutations result in increased risk for LOAD. V1613M variant reduces amyloid beta plaque burden in 5xFAD mice. V1613M variant modulates APP processing and trafficking in 5xFAD mice. V1613M variant reduces amyloid beta-associated damage in 5xFAD mice.
Sprache	Englisch
Erscheinungsdatum	2024-03-20
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13783
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Volltext online

Zugriff für angemeldete ZB MED Nutzerinnen und Nutzer

Zusatzmaterialien

Verfügbar in ZB MED Köln/Königswinter

Zs.A 6316: Hefte anzeigen			Standort: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 540: Hefte anzeigen

Über subito bestellen

Details ▾

Artikel ; Online: CRISPR-mediated generation and characterization of a Gaa homozygous c.1935C>A (p.D645E) Pompe disease knock-in mouse model recapitulating human infantile onset-Pompe disease.

Kan, Shih-Hsin / Huang, Jeffrey Y / Harb, Jerry / Rha, Allisandra / Dalton, Nancy D / Christensen, Chloe / Chan, Yunghang / Davis-Turak, Jeremy / Neumann, Jonathan / Wang, Raymond Y

Scientific reports

2022 Band 12, Heft 1, Seite(n) 21576

Abstract: Pompe disease, an autosomal recessive disorder caused by deficient lysosomal acid α-glucosidase (GAA), is characterized by accumulation of intra-lysosomal glycogen in skeletal and oftentimes cardiac muscle. The c.1935C>A (p.Asp645Glu) variant, the most ... ...

Abstract	Pompe disease, an autosomal recessive disorder caused by deficient lysosomal acid α-glucosidase (GAA), is characterized by accumulation of intra-lysosomal glycogen in skeletal and oftentimes cardiac muscle. The c.1935C>A (p.Asp645Glu) variant, the most frequent GAA pathogenic mutation in people of Southern Han Chinese ancestry, causes infantile-onset Pompe disease (IOPD), presenting neonatally with severe hypertrophic cardiomyopathy, profound muscle hypotonia, respiratory failure, and infantile mortality. We applied CRISPR-Cas9 homology-directed repair (HDR) using a novel dual sgRNA approach flanking the target site to generate a Gaa
Mesh-Begriff(e)	Animals ; Humans ; Infant ; Mice ; alpha-Glucosidases/genetics ; alpha-Glucosidases/metabolism ; Cardiomyopathy, Hypertrophic/genetics ; Cardiomyopathy, Hypertrophic/metabolism ; Cardiomyopathy, Hypertrophic/pathology ; Disease Models, Animal ; Glucan 1,4-alpha-Glucosidase ; Glycogen/metabolism ; Glycogen Storage Disease Type II/genetics ; Glycogen Storage Disease Type II/metabolism ; Glycogen Storage Disease Type II/pathology ; Muscle, Skeletal/metabolism
Chemische Substanzen	alpha-Glucosidases (EC 3.2.1.20) ; Glucan 1,4-alpha-Glucosidase (EC 3.2.1.3) ; Glycogen (9005-79-2)
Sprache	Englisch
Erscheinungsdatum	2022-12-14
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-25914-8
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Artikel ; Online: Early embryonic lethality in complex I associated p.L104P Nubpl mutant mice.

Cheng, Cheng / Cleak, James / Weiss, Lan / Cater, Heather / Stewart, Michelle / Wells, Sara / Columbres, Rod Carlo / Shmara, Alyaa / Morato Torres, C Alejandra / Zafar, Faria / Schüle, Birgitt / Neumann, Jonathan / Hatchwell, Eli / Kimonis, Virginia

Orphanet journal of rare diseases

2022 Band 17, Heft 1, Seite(n) 386

Abstract: Background: Variants in the mitochondrial complex I assembly factor, NUBPL are associated with a rare cause of complex I deficiency mitochondrial disease. Patients affected by complex I deficiency harboring homozygous NUBPL variants typically have ... ...

Abstract	Background: Variants in the mitochondrial complex I assembly factor, NUBPL are associated with a rare cause of complex I deficiency mitochondrial disease. Patients affected by complex I deficiency harboring homozygous NUBPL variants typically have neurological problems including seizures, intellectual disability, and ataxia associated with cerebellar hypoplasia. Thus far only 19 cases have been reported worldwide, and no treatment is available for this rare disease. Methods: To investigate the pathogenesis of NUBPL-associated complex I deficiency, and for translational studies, we generated a knock-in mouse harboring a patient-specific variant Nubpl c.311T>C; p. L104P reported in three families. Results: Similar to Nubpl global knockout mice, the Nubpl p. L104P homozygous mice are lethal at embryonic day E10.5, suggesting that the Nubpl p. L104P variant is likely a hypomorph allele. Given the recent link between Parkinson's disease and loss-of-function NUBPL variants, we also explored aging-related behaviors and immunocytochemical changes in Nubpl hemizygous mice and did not find significant behavioral and pathological changes for alpha-synuclein and oxidative stress markers . Conclusion: Our data suggest that homozygotes with Nubpl variants, similar to the null mice, are lethal, and heterozygotes are phenotypically and neuropathologically normal. We propose that a tissue-specific knockout strategy is required to establish a mouse model of Nubpl-associated complex I deficiency disorder for future mechanistic and translational studies.
Mesh-Begriff(e)	Animals ; Mice ; alpha-Synuclein ; Mitochondrial Proteins/genetics ; Mutation ; Electron Transport Complex I/metabolism ; Mice, Knockout
Chemische Substanzen	alpha-Synuclein ; Mitochondrial Proteins ; Electron Transport Complex I (EC 7.1.1.2)
Sprache	Englisch
Erscheinungsdatum	2022-10-24
Erscheinungsland	England
Dokumenttyp	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-022-02446-y
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Artikel ; Online: Holocnemus pluchei (Araneae, Pholcidae) in Getränke- und Baumärkten in Deutschland

Reiser, Nils / Neumann, Jonathan

Arachnologische Mitteilungen, Vol 48, Pp 24-

2014 Band 27

Abstract: Some colonies of spiders belonging to the Mediterranean cellar spider Holocnemus pluchei (Scopoli, 1763), were found in both beverage and do-it-yourself stores in Germany. Among these are the first records of H. pluchei in Berlin, Hamburg, Lower Saxony ... ...

Abstract	Some colonies of spiders belonging to the Mediterranean cellar spider Holocnemus pluchei (Scopoli, 1763), were found in both beverage and do-it-yourself stores in Germany. Among these are the first records of H. pluchei in Berlin, Hamburg, Lower Saxony and Mecklenburg-Western Pomerania.
Schlagwörter	imported species ; synanthropic spider ; Zoology ; QL1-991
Sprache	Deutsch
Erscheinungsdatum	2014-12-01T00:00:00Z
Verlag	Arachnologische Gesellschaft (ARAGES)
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

Volltext online

Volltext online

Zusatzmaterialien

Fernleihe an ZB MED

Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Artikel ; Online: BIN1

Garcia-Agudo, Laura Fernandez / Shi, Zechuan / Smith, Ian F / Kramár, Enikö A / Tran, Katelynn / Kawauchi, Shimako / Wang, Shuling / Collins, Sherilyn / Walker, Amber / Shi, Kai-Xuan / Neumann, Jonathan / Liang, Heidi Yahan / Da Cunha, Celia / Milinkeviciute, Giedre / Morabito, Samuel / Miyoshi, Emily / Rezaie, Narges / Gomez-Arboledas, Angela / Arvilla, Adrian Mendoza /

Ghaemi, Daryan Iman / Tenner, Andrea J / LaFerla, Frank M / Wood, Marcelo A / Mortazavi, Ali / Swarup, Vivek / MacGregor, Grant R / Green, Kim N

Alzheimer's & dementia : the journal of the Alzheimer's Association

2024 Band 20, Heft 4, Seite(n) 2922–2942

Abstract: Introduction: The BIN1 coding variant rs138047593 (K358R) is linked to Late-Onset Alzheimer's Disease (LOAD) via targeted exome sequencing.: Methods: To elucidate the functional consequences of this rare coding variant on brain amyloidosis and ... ...

Abstract	Introduction: The BIN1 coding variant rs138047593 (K358R) is linked to Late-Onset Alzheimer's Disease (LOAD) via targeted exome sequencing. Methods: To elucidate the functional consequences of this rare coding variant on brain amyloidosis and neuroinflammation, we generated BIN1 Results: The presence of the BIN1 Discussion: The BIN1 K358R variant modulates amyloid pathology in 5xFAD mice, attenuates the astrocytic and oligodendrocytic responses to amyloid plaques, decreases damage markers, and elevates synaptic densities. Highlights: BIN1 rs138047593 (K358R) coding variant is associated with increased risk of LOAD. BIN1 K358R variant increases amyloid plaque load in 12-month-old 5xFAD mice. BIN1 K358R variant dampens astrocytic and oligodendrocytic response to plaques. BIN1 K358R variant decreases neuronal damage in 5xFAD mice. BIN1 K358R upregulates synaptic densities and modulates synaptic transmission.
Mesh-Begriff(e)	Animals ; Mice ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Amyloid beta-Peptides ; Disease Models, Animal ; Mice, Transgenic ; Neuroglia/pathology ; Plaque, Amyloid/pathology ; Humans
Chemische Substanzen	Amyloid beta-Peptides ; BIN1 protein, human
Sprache	Englisch
Erscheinungsdatum	2024-03-09
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13767
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Volltext online

Zugriff für angemeldete ZB MED Nutzerinnen und Nutzer

Zusatzmaterialien

Verfügbar in ZB MED Köln/Königswinter

Zs.A 6316: Hefte anzeigen			Standort: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 540: Hefte anzeigen

Über subito bestellen

Details ▾

Artikel ; Online: Interneuron Dysfunction in a New Mouse Model of SCN1A GEFS.

Das, Antara / Zhu, Bingyao / Xie, Yunyao / Zeng, Lisha / Pham, An T / Neumann, Jonathan C / Safrina, Olga / Benavides, Daniel R / MacGregor, Grant R / Schutte, Soleil S / Hunt, Robert F / O'Dowd, Diane K

eNeuro

2021 Band 8, Heft 2

Abstract: Advances in genome sequencing have identified over 1300 mutations in ... ...

Abstract	Advances in genome sequencing have identified over 1300 mutations in the
Mesh-Begriff(e)	Animals ; Interneurons ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; NAV1.1 Voltage-Gated Sodium Channel/genetics ; Seizures/genetics ; Seizures, Febrile
Chemische Substanzen	NAV1.1 Voltage-Gated Sodium Channel ; Scn1a protein, mouse
Sprache	Englisch
Erscheinungsdatum	2021-04-12
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0394-20.2021
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Artikel ; Online: Aliens in Europe

Huber, Bernhard A. / Neumann, Jonathan / Grabolle, Arno / Hula, Vladimír

Arachnologische Mitteilungen, Vol 53, Pp 12-

updates on the distributions of Modisimus culicinus and Micropholcus fauroti (Araneae, Pholcidae)

2017 Band 18

Abstract: The pholcid spiders Modisimus culicinus (Simon, 1893) and Micropholcus fauroti (Simon, 1887) are pantropical species that have spread around the world at least several decades ago. Here we present numerous new records for both species, most of which fall ...

Abstract	The pholcid spiders Modisimus culicinus (Simon, 1893) and Micropholcus fauroti (Simon, 1887) are pantropical species that have spread around the world at least several decades ago. Here we present numerous new records for both species, most of which fall into the expected latitudes, i.e. between the Tropics of Cancer and Capricorn (93% and 87% of records respectively). However, we also report the first records for M. culicinus from Central Europe (Germany and Czech Republic, >50°N) and the first European record for M. fauroti from outside of Belgium (Germany). The fact that in both species several specimens have been found at more than one locality suggests that they may already be in the stage of establishment and spreading in Europe. Finally, we present an updated identification key to the genera of Pholcidae in Europe.
Schlagwörter	alien ; harmless ; invasive ; pantropical ; synanthropic ; Zoology ; QL1-991
Thema/Rubrik (Code)	590
Sprache	Deutsch
Erscheinungsdatum	2017-04-01T00:00:00Z
Verlag	Arachnologische Gesellschaft (ARAGES)
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

Volltext online

Volltext online

Zusatzmaterialien

Fernleihe an ZB MED

Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Artikel ; Online: First record of the exotic spitting spider Scytodes fusca (Araneae, Scytodidae) in Central Europe from Germany and Slovakia

Šestáková, Anna / Černecká, Ľudmila / Neumann, Jonathan / Reiser, Nils

Arachnologische Mitteilungen, Vol 47, Pp 1-

2014 Band 6

Abstract: The spitting spider Scytodes fusca Walckenaer, 1837 is recorded for the first time in Central Europe from both Germany and Slovakia. The species was found in two localities, within the Botanical Garden in Bratislava (Slovakia), specifically from a heated ...

Abstract	The spitting spider Scytodes fusca Walckenaer, 1837 is recorded for the first time in Central Europe from both Germany and Slovakia. The species was found in two localities, within the Botanical Garden in Bratislava (Slovakia), specifically from a heated greenhouse with high humidity, and the 'Tropical Islands', a tropical holiday resort in Krausnick (Germany). It seems that this Pantropical species has probably been introduced here along with imported plants. A description of diagnostic characters, as well as figures, is given.
Schlagwörter	artificial tropical ecosystem ; botanical garden ; first record ; introduced species ; Zoology ; QL1-991
Sprache	Deutsch
Erscheinungsdatum	2014-05-01T00:00:00Z
Verlag	Arachnologische Gesellschaft (ARAGES)
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

Volltext online

Volltext online

Zusatzmaterialien

Fernleihe an ZB MED

Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Artikel: Systematic Phenotyping and Characterization of the 3xTg-AD Mouse Model of Alzheimer's Disease.

Frontiers in neuroscience

2022 Band 15, Seite(n) 785276

Abstract: Animal models of disease are valuable resources for investigating pathogenic mechanisms and potential therapeutic interventions. However, for complex disorders such as Alzheimer's disease (AD), the generation and availability of innumerous distinct ... ...

Abstract	Animal models of disease are valuable resources for investigating pathogenic mechanisms and potential therapeutic interventions. However, for complex disorders such as Alzheimer's disease (AD), the generation and availability of innumerous distinct animal models present unique challenges to AD researchers and hinder the success of useful therapies. Here, we conducted an in-depth analysis of the 3xTg-AD mouse model of AD across its lifespan to better inform the field of the various pathologies that appear at specific ages, and comment on drift that has occurred in the development of pathology in this line since its development 20 years ago. This modern characterization of the 3xTg-AD model includes an assessment of impairments in long-term potentiation followed by quantification of amyloid beta (Aβ) plaque burden and neurofibrillary tau tangles, biochemical levels of Aβ and tau protein, and neuropathological markers such as gliosis and accumulation of dystrophic neurites. We also present a novel comparison of the 3xTg-AD model with the 5xFAD model using the same deep-phenotyping characterization pipeline and show plasma NfL is strongly driven by plaque burden. The results from these analyses are freely available via the AD Knowledge Portal (https://modeladexplorer.org/). Our work demonstrates the utility of a characterization pipeline that generates robust and standardized information relevant to investigating and comparing disease etiologies of current and future models of AD.
Sprache	Englisch
Erscheinungsdatum	2022-01-24
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2021.785276
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

Zusatzmaterialien

Über subito bestellen

Details ▾
- Kostenpflichtig bestellen

Zum Seitenanfang

Zusatzmaterialien

Kategorien

Über subito bestellen

Volltext online

Zusatzmaterialien

Kategorien

Verfügbar in ZB MED Köln/Königswinter

Über subito bestellen

Zusatzmaterialien

Kategorien

Über subito bestellen

Zusatzmaterialien

Kategorien

Über subito bestellen

Volltext online

Zusatzmaterialien

Kategorien

Fernleihe an ZB MED

Volltext online

Zusatzmaterialien

Kategorien

Verfügbar in ZB MED Köln/Königswinter

Über subito bestellen

Zusatzmaterialien

Kategorien

Über subito bestellen

Volltext online

Zusatzmaterialien

Kategorien

Fernleihe an ZB MED

Volltext online

Zusatzmaterialien

Kategorien

Fernleihe an ZB MED

Zusatzmaterialien

Kategorien

Über subito bestellen