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Book ; Thesis: Protektiver Effekt von 6-Shogaol, Ellagsäure und Myrrhe auf die intestinale epitheliale Barriere

Lüttig, Julia / Püschel, Gerhard

2016

Abstract: Viele bioaktive Pflanzeninhaltsstoffe bzw. Pflanzenmetabolite besitzen antiinflammatorische Eigenschaften. Diese versprechen ein hohes Potential für den Einsatz in der Phytotherapie bzw. Prävention von chronisch-entzündlichen Darmerkrankungen (CED). Eine ...

Title variant	Protective effect of 6-shogaol, ellagic acid and myrrh on intestinal epithelial barrier
Author's details	Julia Lüttig, Ökotrophologin (MSc.)
Abstract	Viele bioaktive Pflanzeninhaltsstoffe bzw. Pflanzenmetabolite besitzen antiinflammatorische Eigenschaften. Diese versprechen ein hohes Potential für den Einsatz in der Phytotherapie bzw. Prävention von chronisch-entzündlichen Darmerkrankungen (CED). Eine intestinale Barrieredysfunktion ist ein typisches Charakteristikum von CED Patienten, die dadurch an akuter Diarrhoe leiden. In dieser Arbeit werden die Pflanzenkomponenten 6-Shogaol, Ellagsäure und Myrrhe an den intestinalen Kolonepithelzellmodellen HT-29/B6 und Caco-2 auf ihr Potential hin, die intestinale Barriere zu stärken bzw. eine Barrieredysfunktion zu verhindern, untersucht. Hauptschwerpunkt der Analysen ist die parazelluläre Barrierefunktion und die Regulation der dafür entscheidenden Proteinfamilie der Tight Junctions (TJs), der Claudine. Die Barrierefunktion wird durch Messung des transepithelialen Widerstands (TER) und der Fluxmessung in der Ussing-Kammer bestimmt. Dazu werden die HT-29/B6- und Caco-2-Monolayer mit den Pflanzenkomponenten (6-Shogaol, Ellagsäure, Myrrh…
Language	German
Size	IX, 108 Blätter, Illustrationen, Diagramme, 30 cm
Publishing place	Potsdam
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Dissertation, Universität Potsdam, 2016
HBZ-ID	HT019991073
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
2019 E 269	order for loan	Magazin

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Book: Taschenlehrbuch Biochemie

Püschel, Gerhard

70 Tabellen

2011

Title variant	Biochemie
Author's details	Gerhard Püschel
Keywords	Biochemistry ; Biochemie
Subject	Biologische Chemie
Language	German
Size	XVIII, 908 S. : zahlr. Ill. und graph. Darst.
Publisher	Thieme
Publishing place	Stuttgart u.a.
Publishing country	Germany
Document type	Book
HBZ-ID	HT016715471
ISBN	978-3-13-148691-2 ; 3-13-148691-0
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

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2009 A 9933	order for loan	Magazin
2011 A 2560	order for loan	Magazin

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Book ; Online ; Thesis: Insulin resistance in Cancer cachexia and Metabolic Syndrome: Role of insulin activated macrophages and miRNA-21-5p

Camargo, Rodolfo Gonzalez / Seelaender, Marilia / Püschel, Gerhard

2016

Abstract: The ever-increasing fat content in Western diet, combined with decreased levels of physical activity, greatly enhance the incidence of metabolic-related diseases. Cancer cachexia (CC) and Metabolic syndrome (MetS) are both multifactorial highly complex ... ...

Title variant	Resistência à Insulina na Caquexia Associada ao Câncer e na Sindrome Metabólica: Papel dos Macrófagos ativados pela Insulina e do miRNA-21-5p
Author's details	Rodolfo Gonzalez Camargo
Abstract	The ever-increasing fat content in Western diet, combined with decreased levels of physical activity, greatly enhance the incidence of metabolic-related diseases. Cancer cachexia (CC) and Metabolic syndrome (MetS) are both multifactorial highly complex metabolism related syndromes, whose etiology is not fully understood, as the mechanisms underlying their development are not completely unveiled. Nevertheless, despite being considered “opposite sides”, MetS and CC share several common issues such as insulin resistance and low-grade inflammation. In these scenarios, tissue macrophages act as key players, due to their capacity to produce and release inflammatory mediators. One of the main features of MetS is hyperinsulinemia, which is generally associated with an attempt of the β-cell to compensate for diminished insulin sensitivity (insulin resistance).^ There is growing evidence that hyperinsulinemia per se may contribute to the development of insulin resistance, through the establishment of low grade inflammation in insulin responsive tissues, especially in the liver (as insulin is secreted by the pancreas into the portal circulation). The hypothesis of the present study was that insulin may itself provoke an inflammatory response culminating in diminished hepatic insulin sensitivity. To address this premise, firstly, human cell line U937 differentiated macrophages were exposed to insulin, LPS and PGE2. In these cells, insulin significantly augmented the gene expression of the pro-inflammatory mediators IL-1β, IL-8, CCL2, Oncostatin M (OSM) and microsomal prostaglandin E2 synthase (mPGES1), and of the anti-inflammatory mediator IL-10. Moreover, the synergism between insulin and LPS enhanced the induction provoked by LPS in IL-1β, IL-8, IL-6, CCL2 and TNF-α gene.^ When combined with PGE2, insulin enhanced the induction provoked by PGE2 in IL-1β, mPGES1 and COX2, and attenuated the inhibition induced by PGE2 in CCL2 and TNF-α gene expression contributing to an enhanced inflammatory response by both mechanisms. Supernatants of insulin-treated U937 macrophages reduced the insulin-dependent induction of glucokinase in hepatocytes by 50%. Cytokines contained in the supernatant of insulin-treated U937 macrophages also activated hepatocytes ERK1/2, resulting in inhibitory serine phosphorylation of the insulin receptor substrate. Additionally, the transcription factor STAT3 was activated by phosphorylation resulting in the induction of SOCS3, which is capable of interrupting the insulin receptor signal chain. MicroRNAs, non-coding RNAs linked to protein expression regulation, nowadays recognized as active players in the generation of several inflammatory disorders such as cancer and type II diabetes are also of interest.^
Language	English
Size	1 Online-Ressource (104 Blätter)
Publishing place	Universität Potsdam
Publishing country	Germany
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Dissertation, Universität Potsdam, 2016
HBZ-ID	HT019856214
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Discrimination of the Activity of Low-Affinity Wild-Type and High-Affinity Mutant Recombinant BoNT/B by a SIMA Cell-Based Reporter Release Assay.

Neuschäfer-Rube, Frank / Pathe-Neuschäfer-Rube, Andrea / Püschel, Gerhard P

Toxins

2022 Volume 14, Issue 1

Abstract: Botulinum neurotoxin (BoNT) is used for the treatment of a number of ailments. The activity of the toxin that is isolated from bacterial cultures is frequently tested in the mouse lethality assay. Apart from the ethical concerns inherent to this assay, ... ...

Abstract	Botulinum neurotoxin (BoNT) is used for the treatment of a number of ailments. The activity of the toxin that is isolated from bacterial cultures is frequently tested in the mouse lethality assay. Apart from the ethical concerns inherent to this assay, species-specific differences in the affinity for different BoNT serotypes give rise to activity results that differ from the activity in humans. Thus, BoNT/B is more active in mice than in humans. The current study shows that the stimulus-dependent release of a luciferase from a differentiated human neuroblastoma-based reporter cell line (SIMA-hPOMC1-26-Gluc) was inhibited by clostridial and recombinant BoNT/A to the same extent, whereas both clostridial and recombinant BoNT/B inhibited the release to a lesser extent and only at much higher concentrations, reflecting the low activity of BoNT/B in humans. By contrast, the genetically modified BoNT/B-MY, which has increased affinity for human synaptotagmin, and the BoNT/B protein receptor inhibited luciferase release effectively and with an EC50 comparable to recombinant BoNT/A. This was due to an enhanced uptake into the reporter cells of BoNT/B-MY in comparison to the recombinant wild-type toxin. Thus, the SIMA-hPOMC1-26-Gluc cell assay is a versatile tool to determine the activity of different BoNT serotypes providing human-relevant dose-response data.
MeSH term(s)	Bacterial Toxins/genetics ; Bacterial Toxins/pharmacology ; Bacterial Toxins/toxicity ; Biological Assay ; Botulinum Toxins, Type A/genetics ; Botulinum Toxins, Type A/pharmacology ; Botulinum Toxins, Type A/toxicity ; Cell Line ; Humans ; Mutation ; Recombinant Proteins/genetics ; Recombinant Proteins/pharmacology ; Recombinant Proteins/toxicity
Chemical Substances	Bacterial Toxins ; Recombinant Proteins ; rimabotulinumtoxinB (0Y70779M1F) ; Botulinum Toxins, Type A (EC 3.4.24.69)
Language	English
Publishing date	2022-01-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518395-3
ISSN	2072-6651 ; 2072-6651
ISSN (online)	2072-6651
ISSN	2072-6651
DOI	10.3390/toxins14010065
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dietary cholesterol does not break your heart but kills your liver.

Püschel, Gerhard P / Henkel, Janin

Porto biomedical journal

2019 Volume 3, Issue 1, Page(s) e12

Abstract: It is increasingly accepted that dietary cholesterol has a much lower impact on the progression of cardiovascular disease than previously assumed. However, both animal experiments and human studies seem to support the view that dietary cholesterol may ... ...

Abstract	It is increasingly accepted that dietary cholesterol has a much lower impact on the progression of cardiovascular disease than previously assumed. However, both animal experiments and human studies seem to support the view that dietary cholesterol may contribute to the transition from benign steatosis to the potentially fatal non-alcoholic steatohepatitis. Cholesterol esters and cholesterol accumulate in the hepatocyte and impair its function. This leads to oxidative stress and endoplasmic reticulum stress triggering the release of pro-inflammatory cytokines and rendering the hepatocyte more susceptible to apoptotic or necrotic cell death. Kupffer cells group around dying hepatocytes and phagocytose the hepatocyte debris and lipids. In addition, they are exposed to lipid peroxidation products released from hepatocytes. Kupffer cells, thus activated, release pro-inflammatory, chemotactic and profibrotic cytokines that promote inflammation and fibrosis. Therefore, dietary cholesterol may be harmful to the liver, in particular when administered in combination with polyunsaturated fatty acids that favor lipid peroxidation.
Language	English
Publishing date	2019-06-29
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2444-8672
ISSN (online)	2444-8672
DOI	10.1016/j.pbj.0000000000000012
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Conference proceedings: [No title information]

Lieske, Stefanie / Messner, Sophie / Wieloch, Judith / Laurent, Ilona / Püschel, Gerhard P.

Zeitschrift für Gastroenterologie

2023 Volume 61, Issue 01

Event/congress	39. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber, Bochum, 2023-01-27
Language	German
Publishing date	2023-01-01
Publisher	Georg Thieme Verlag
Publishing place	Stuttgart ; New York
Document type	Article ; Conference proceedings
ZDB-ID	201387-3
ISSN	1439-7803 ; 0044-2771 ; 0172-8504
ISSN (online)	1439-7803
ISSN	0044-2771 ; 0172-8504
DOI	10.1055/s-0042-1759987
Database	Thieme publisher's database

In stock of ZB MED Cologne/Königswinter

Zs.A 111: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.A 111/X: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Discrimination of the Activity of Low-Affinity Wild-Type and High-Affinity Mutant Recombinant BoNT/B by a SIMA Cell-Based Reporter Release Assay

Frank Neuschäfer-Rube / Andrea Pathe-Neuschäfer-Rube / Gerhard P. Püschel

Toxins, Vol 14, Iss 65, p

2022 Volume 65

Abstract	Botulinum neurotoxin (BoNT) is used for the treatment of a number of ailments. The activity of the toxin that is isolated from bacterial cultures is frequently tested in the mouse lethality assay. Apart from the ethical concerns inherent to this assay, species-specific differences in the affinity for different BoNT serotypes give rise to activity results that differ from the activity in humans. Thus, BoNT/B is more active in mice than in humans. The current study shows that the stimulus-dependent release of a luciferase from a differentiated human neuroblastoma–based reporter cell line (SIMA-hPOMC1-26-Gluc) was inhibited by clostridial and recombinant BoNT/A to the same extent, whereas both clostridial and recombinant BoNT/B inhibited the release to a lesser extent and only at much higher concentrations, reflecting the low activity of BoNT/B in humans. By contrast, the genetically modified BoNT/B-MY, which has increased affinity for human synaptotagmin, and the BoNT/B protein receptor inhibited luciferase release effectively and with an EC50 comparable to recombinant BoNT/A. This was due to an enhanced uptake into the reporter cells of BoNT/B-MY in comparison to the recombinant wild-type toxin. Thus, the SIMA-hPOMC1-26-Gluc cell assay is a versatile tool to determine the activity of different BoNT serotypes providing human-relevant dose-response data.
Keywords	cell-based assay ; genetically modified BoNT ; BoNT/B uptake ; Medicine ; R
Subject code	570
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals.

Pathe-Neuschäfer-Rube, Andrea / Neuschäfer-Rube, Frank / Püschel, Gerhard P

Toxins

2021 Volume 13, Issue 4

Abstract: The suitability of a newly developed cell-based functional assay was tested for the detection of the activity of a range of neurotoxins and neuroactive pharmaceuticals which act by stimulation or inhibition of calcium-dependent neurotransmitter release. ... ...

Abstract	The suitability of a newly developed cell-based functional assay was tested for the detection of the activity of a range of neurotoxins and neuroactive pharmaceuticals which act by stimulation or inhibition of calcium-dependent neurotransmitter release. In this functional assay, a reporter enzyme is released concomitantly with the neurotransmitter from neurosecretory vesicles. The current study showed that the release of a luciferase from a differentiated human neuroblastoma-based reporter cell line (SIMA-hPOMC1-26-GLuc cells) can be stimulated by a carbachol-mediated activation of the Gq-coupled muscarinic-acetylcholine receptor and by the Ca
MeSH term(s)	Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Calcium Signaling/drug effects ; Cell Line, Tumor ; Genes, Reporter ; Humans ; Luciferases/genetics ; Luciferases/metabolism ; Muscarinic Agonists/pharmacology ; Muscarinic Antagonists/pharmacology ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Neurotoxins/pharmacology ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; Secretory Vesicles/drug effects ; Secretory Vesicles/genetics ; Secretory Vesicles/metabolism ; Spider Venoms/pharmacology
Chemical Substances	Calcium Channel Blockers ; Calcium Channels ; Muscarinic Agonists ; Muscarinic Antagonists ; Neurotoxins ; Spider Venoms ; alpha-latrotoxin (65988-34-3) ; Pro-Opiomelanocortin (66796-54-1) ; Luciferases (EC 1.13.12.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-03-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518395-3
ISSN	2072-6651 ; 2072-6651
ISSN (online)	2072-6651
ISSN	2072-6651
DOI	10.3390/toxins13040247
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Humanization of the Reaction Specificity of Mouse Alox15b Inversely Modified the Susceptibility of Corresponding Knock-In Mice in Two Different Animal Inflammation Models.

Schäfer, Marjann / Reisch, Florian / Labuz, Dominika / Machelska, Halina / Stehling, Sabine / Püschel, Gerhard P / Rothe, Michael / Heydeck, Dagmar / Kuhn, Hartmut

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: Mammalian arachidonic acid lipoxygenases (ALOXs) have been implicated in the pathogenesis of inflammatory diseases, and its pro- and anti-inflammatory effects have been reported for different ALOX-isoforms. Human ALOX15B oxygenates arachidonic acid to ... ...

Abstract	Mammalian arachidonic acid lipoxygenases (ALOXs) have been implicated in the pathogenesis of inflammatory diseases, and its pro- and anti-inflammatory effects have been reported for different ALOX-isoforms. Human ALOX15B oxygenates arachidonic acid to its 15-hydroperoxy derivative, whereas the corresponding 8-hydroperoxide is formed by mouse Alox15b (Alox8). This functional difference impacts the biosynthetic capacity of the two enzymes for creating pro- and anti-inflammatory eicosanoids. To explore the functional consequences of the humanization of the reaction specificity of mouse
MeSH term(s)	Humans ; Mice ; Female ; Animals ; Arachidonic Acid ; Dextrans ; Inflammation/genetics ; Colitis ; Mammals ; Anti-Inflammatory Agents ; Edema/chemically induced ; Edema/genetics ; Disease Models, Animal
Chemical Substances	Arachidonic Acid (27YG812J1I) ; sodium sulfate (0YPR65R21J) ; Dextrans ; Anti-Inflammatory Agents
Language	English
Publishing date	2023-07-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241311034
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Article ; Online: Knock-in mice expressing a humanized arachidonic acid 15-lipoxygenase (Alox15) carry a partly dysfunctional erythropoietic system.

Reisch, Florian / Heydeck, Dagmar / Schäfer, Marjann / Rothe, Michael / Yang, Jiaxing / Stehling, Sabine / Püschel, Gerhard P / Kuhn, Hartmut

Cellular & molecular biology letters

2023 Volume 28, Issue 1, Page(s) 97

Abstract: Arachidonic acid 15-lipoxygenases (ALOX15) play a role in mammalian erythropoiesis but they have also been implicated in inflammatory processes. Seven intact Alox genes have been detected in the mouse reference genome and the mouse Alox15 gene is ... ...

Abstract	Arachidonic acid 15-lipoxygenases (ALOX15) play a role in mammalian erythropoiesis but they have also been implicated in inflammatory processes. Seven intact Alox genes have been detected in the mouse reference genome and the mouse Alox15 gene is structurally similar to the orthologous genes of other mammals. However, mouse and human ALOX15 orthologs have different functional characteristics. Human ALOX15 converts C
MeSH term(s)	Animals ; Female ; Humans ; Male ; Mice ; Arachidonate 12-Lipoxygenase/genetics ; Arachidonate 15-Lipoxygenase/genetics ; Arachidonic Acid ; Hydrogen Peroxide ; Mammals
Chemical Substances	Alox15 protein, mouse (EC 1.13.11.31) ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33) ; Arachidonic Acid (27YG812J1I) ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2023-11-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2108724-6
ISSN	1689-1392 ; 1689-1392
ISSN (online)	1689-1392
ISSN	1689-1392
DOI	10.1186/s11658-023-00511-3
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