LIVIVO - Search results -

Search results

Result 1 - 8 of total 8

Search options

Article ; Online: A new mechanism links preamyloid oligomer formation in the myocyte stress response associated with atrial fibrillation.

Pellman, Jason / Sheikh, Farah

Journal of molecular and cellular cardiology

2015 Volume 80, Page(s) 110–113

MeSH term(s)	Aldehydes/pharmacology ; Amyloid/metabolism ; Animals ; Heart Atria/metabolism ; Heart Atria/pathology ; Humans ; Protein Folding/drug effects ; Protein Multimerization
Chemical Substances	Aldehydes ; Amyloid
Language	English
Publishing date	2015-03
Publishing country	England
Document type	Comment ; Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2014.12.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

In stock of ZB MED Cologne/Königswinter

Zs.A 426: 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)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Heritable transcriptional defects from aberrations of nuclear architecture.

Papathanasiou, Stamatis / Mynhier, Nikos A / Liu, Shiwei / Brunette, Gregory / Stokasimov, Ema / Jacob, Etai / Li, Lanting / Comenho, Caroline / van Steensel, Bas / Buenrostro, Jason D / Zhang, Cheng-Zhong / Pellman, David

Nature

2023 Volume 619, Issue 7968, Page(s) 184–192

Abstract: Transcriptional heterogeneity due to plasticity of the epigenetic state of chromatin contributes to tumour evolution, metastasis and drug ... ...

Abstract	Transcriptional heterogeneity due to plasticity of the epigenetic state of chromatin contributes to tumour evolution, metastasis and drug resistance
MeSH term(s)	Humans ; Chromatin/genetics ; Chromatin/metabolism ; Chromosomal Instability ; Chromosomes/genetics ; Clone Cells/metabolism ; DNA Damage/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Micronuclei, Chromosome-Defective ; Neoplasms/genetics ; Neoplasms/pathology ; Single-Cell Gene Expression Analysis ; Transcription, Genetic
Chemical Substances	Chromatin
Language	English
Publishing date	2023-06-07
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/s41586-023-06157-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 26: 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.MG 9: Show issues
Zs.MO 244: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Atrial fibrillation: mechanisms, therapeutics, and future directions.

Pellman, Jason / Sheikh, Farah

Comprehensive Physiology

2015 Volume 5, Issue 2, Page(s) 649–665

Abstract: Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, affecting 1% to 2% of the general population. It is characterized by rapid and disorganized atrial activation leading to impaired atrial function, which can be diagnosed on an EKG by lack ...

Abstract	Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, affecting 1% to 2% of the general population. It is characterized by rapid and disorganized atrial activation leading to impaired atrial function, which can be diagnosed on an EKG by lack of a P-wave and irregular QRS complexes. AF is associated with increased morbidity and mortality and is a risk factor for embolic stroke and worsening heart failure. Current research on AF support and explore the hypothesis that initiation and maintenance of AF require pathophysiological remodeling of the atria, either specifically as in lone AF or secondary to other heart disease as in heart failure-associated AF. Remodeling in AF can be grouped into three categories that include: (i) electrical remodeling, which includes modulation of L-type Ca(2+) current, various K(+) currents and gap junction function; (ii) structural remodeling, which includes changes in tissues properties, size, and ultrastructure; and (iii) autonomic remodeling, including altered sympathovagal activity and hyperinnervation. Electrical, structural, and autonomic remodeling all contribute to creating an AF-prone substrate which is able to produce AF-associated electrical phenomena including a rapidly firing focus, complex multiple reentrant circuit or rotors. Although various remodeling events occur in AF, current AF therapies focus on ventricular rate and rhythm control strategies using pharmacotherapy and surgical interventions. Recent progress in the field has started to focus on the underlying substrate that drives and maintains AF (termed upstream therapies); however, much work is needed in this area. Here, we review current knowledge of AF mechanisms, therapies, and new areas of investigation.
MeSH term(s)	Animals ; Anti-Arrhythmia Agents/therapeutic use ; Atrial Fibrillation/drug therapy ; Atrial Fibrillation/physiopathology ; Forecasting ; Heart Atria/physiopathology ; Heart Conduction System/physiopathology ; Humans ; Models, Cardiovascular
Chemical Substances	Anti-Arrhythmia Agents
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c140047
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Myocyte-fibroblast communication in cardiac fibrosis and arrhythmias: Mechanisms and model systems.

Pellman, Jason / Zhang, Jing / Sheikh, Farah

Journal of molecular and cellular cardiology

2016 Volume 94, Page(s) 22–31

Abstract: Development of cardiac fibrosis and arrhythmias is controlled by the activity of and communication between cardiomyocytes and fibroblasts in the heart. Myocyte-fibroblast interactions occur via both direct and indirect means including paracrine mediators, ...

Abstract	Development of cardiac fibrosis and arrhythmias is controlled by the activity of and communication between cardiomyocytes and fibroblasts in the heart. Myocyte-fibroblast interactions occur via both direct and indirect means including paracrine mediators, extracellular matrix interactions, electrical modulators, mechanical junctions, and membrane nanotubes. In the diseased heart, cardiomyocyte and fibroblast ratios and activity, and thus myocyte-fibroblast interactions, change and are thought to contribute to the course of disease including development of fibrosis and arrhythmogenic activity. Fibroblasts have a developing role in modulating cardiomyocyte electrical and hypertrophic activity, however gaps in knowledge regarding these interactions still exist. Research in this field has necessitated the development of unique approaches to isolate and control myocyte-fibroblast interactions. Numerous methods for 2D and 3D co-culture systems have been developed, while a growing part of this field is in the use of better tools for in vivo systems including cardiomyocyte and fibroblast specific Cre mouse lines for cell type specific genetic ablation. This review will focus on (i) mechanisms of myocyte-fibroblast communication and their effects on disease features such as cardiac fibrosis and arrhythmias as well as (ii) methods being used and currently developed in this field.
MeSH term(s)	Animals ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Cell Communication ; Coculture Techniques ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Extracellular Matrix Proteins/metabolism ; Fibroblasts/metabolism ; Fibrosis ; Humans ; In Vitro Techniques ; Models, Biological ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/metabolism
Chemical Substances	Extracellular Matrix Proteins
Language	English
Publishing date	2016-03-18
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2016.03.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 426: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cell junctions in the specialized conduction system of the heart.

Mezzano, Valeria / Pellman, Jason / Sheikh, Farah

Cell communication & adhesion

2014 Volume 21, Issue 3, Page(s) 149–159

Abstract: Anchoring cell junctions are integral in maintaining electro-mechanical coupling of ventricular working cardiomyocytes; however, their role in cardiomyocytes of the cardiac conduction system (CCS) remains less clear. Recent studies in genetic mouse ... ...

Abstract	Anchoring cell junctions are integral in maintaining electro-mechanical coupling of ventricular working cardiomyocytes; however, their role in cardiomyocytes of the cardiac conduction system (CCS) remains less clear. Recent studies in genetic mouse models and humans highlight the appearance of these cell junctions alongside gap junctions in the CCS and also show that defects in these structures and their components are associated with conduction impairments in the CCS. Here we outline current evidence supporting an integral relationship between anchoring and gap junctions in the CCS. Specifically we focus on (1) molecular and ultrastructural evidence for cell-cell junctions in specialized cardiomyocytes of the CCS, (2) genetic mouse models specifically targeting cell-cell junction components in the heart which exhibit CCS conduction defects and (3) human clinical studies from patients with cell-cell junction-based diseases that exhibit CCS electrophysiological defects.
MeSH term(s)	Animals ; Heart Conduction System/cytology ; Heart Conduction System/metabolism ; Humans ; Intercellular Junctions/metabolism ; Mice
Language	English
Publishing date	2014-04-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2065474-1
ISSN	1543-5180 ; 1061-5385 ; 1541-9061
ISSN (online)	1543-5180
ISSN	1061-5385 ; 1541-9061
DOI	10.3109/15419061.2014.905928
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4377: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Desmosomal COP9 regulates proteome degradation in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Liang, Yan / Lyon, Robert C / Pellman, Jason / Bradford, William H / Lange, Stephan / Bogomolovas, Julius / Dalton, Nancy D / Gu, Yusu / Bobar, Marcus / Lee, Mong-Hong / Iwakuma, Tomoo / Nigam, Vishal / Asimaki, Angeliki / Scheinman, Melvin / Peterson, Kirk L / Sheikh, Farah

The Journal of clinical investigation

2021 Volume 131, Issue 11

Abstract: Dysregulated protein degradative pathways are increasingly recognized as mediators of human disease. This mechanism may have particular relevance to desmosomal proteins that play critical structural roles in both tissue architecture and cell-cell ... ...

Abstract	Dysregulated protein degradative pathways are increasingly recognized as mediators of human disease. This mechanism may have particular relevance to desmosomal proteins that play critical structural roles in both tissue architecture and cell-cell communication, as destabilization/breakdown of the desmosomal proteome is a hallmark of genetic-based desmosomal-targeted diseases, such as the cardiac disease arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). However, no information exists on whether there are resident proteins that regulate desmosomal proteome homeostasis. Here, we uncovered a cardiac constitutive photomorphogenesis 9 (COP9) desmosomal resident protein complex, composed of subunit 6 of the COP9 signalosome (CSN6), that enzymatically restricted neddylation and targeted desmosomal proteome degradation. CSN6 binding, localization, levels, and function were affected in hearts of classic mouse and human models of ARVD/C affected by desmosomal loss and mutations, respectively. Loss of desmosomal proteome degradation control due to junctional reduction/loss of CSN6 and human desmosomal mutations destabilizing junctional CSN6 were also sufficient to trigger ARVD/C in mice. We identified a desmosomal resident regulatory complex that restricted desmosomal proteome degradation and disease.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Arrhythmogenic Right Ventricular Dysplasia/genetics ; Arrhythmogenic Right Ventricular Dysplasia/metabolism ; COP9 Signalosome Complex/genetics ; COP9 Signalosome Complex/metabolism ; Desmosomes/genetics ; Desmosomes/metabolism ; Desmosomes/pathology ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Mice, Knockout ; Proteolysis ; Proteome/genetics ; Proteome/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cops6 protein, mouse ; Proteome ; COP9 Signalosome Complex (EC 3.4.19.12)
Language	English
Publishing date	2021-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Video-Audio Media
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI137689
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ua VI Zs.184: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Using wastewater-based analysis to monitor the effects of legalized retail sales on cannabis consumption in Washington State, USA.

Burgard, Daniel A / Williams, Jason / Westerman, Danielle / Rushing, Rosie / Carpenter, Riley / LaRock, Addison / Sadetsky, Jane / Clarke, Jackson / Fryhle, Heather / Pellman, Melissa / Banta-Green, Caleb J

Addiction (Abingdon, England)

2019 Volume 114, Issue 9, Page(s) 1582–1590

Abstract: Aims: To perform a wastewater-based analysis to explore the impact of newly legalized retail cannabis sales on its use and to determine if this approach could estimate the size of the legal market place, which began 1 August 2014 in the study area.: ... ...

Abstract	Aims: To perform a wastewater-based analysis to explore the impact of newly legalized retail cannabis sales on its use and to determine if this approach could estimate the size of the legal market place, which began 1 August 2014 in the study area. Design: Laboratory study of raw wastewater samples collected and analyzed over the 3-year period from 2014 to 2016. Setting and participants: Samples obtained from the two wastewater treatment plants that serviced a municipality of 200 000 people in the state of Washington, USA. Measurements: Quantitative analysis of 24-hour composite influent samples for the metabolite of the active ingredient in cannabis, 11-nor-9-Carboxy-Δ9-tetrahydrocannabinol (THC-COOH) were performed by liquid chromatography coupled to mass spectrometry. Findings: Wastewater estimates for THC-COOH increased by 9% per quarter, suggesting a doubling in cannabis consumption from 1 December 2013 to 31 December 2016. State-sold THC increased at nearly 70% per quarter, while stores operated from 1 August 2014 to 31 December 2016. Estimating the proportion of the total cannabis market supplied by state-regulated cannabis from these data is not currently achievable. Conclusion: A wastewater-based measure of cannabis consumption suggests a significant increase in consumption in Washington, USA following legalization, and that legal sales appear to have displaced a large portion of the illicit market.
MeSH term(s)	Chromatography, Liquid ; Commerce/legislation & jurisprudence ; Dronabinol/analogs & derivatives ; Dronabinol/analysis ; Humans ; Marijuana Use/epidemiology ; Marijuana Use/legislation & jurisprudence ; Marijuana Use/trends ; Mass Spectrometry ; Washington/epidemiology ; Wastewater-Based Epidemiological Monitoring
Chemical Substances	11-nor-delta(9)-tetrahydrocannabinol-9-carboxylic acid (4TPC9E4A32) ; Dronabinol (7J8897W37S)
Language	English
Publishing date	2019-06-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1141051-6
ISSN	1360-0443 ; 0965-2140
ISSN (online)	1360-0443
ISSN	0965-2140
DOI	10.1111/add.14641
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 551: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Extracellular matrix remodeling in atrial fibrosis: mechanisms and implications in atrial fibrillation.

Pellman, Jason / Lyon, Robert C / Sheikh, Farah

Journal of molecular and cellular cardiology

2009 Volume 48, Issue 3, Page(s) 461–467

Abstract: Atrial fibrosis has been strongly associated with the presence of heart diseases/arrhythmias, including congestive heart failure (CHF) and atrial fibrillation (AF). Inducibility of AF as a result of atrial fibrosis has been the subject of intense recent ... ...

Abstract	Atrial fibrosis has been strongly associated with the presence of heart diseases/arrhythmias, including congestive heart failure (CHF) and atrial fibrillation (AF). Inducibility of AF as a result of atrial fibrosis has been the subject of intense recent investigation since it is the most commonly encountered arrhythmia in adults and can substantially increase the risk of premature death. Rhythm and rate control drugs as well as surgical interventions are used as therapies for AF; however, increased attention has been diverted to mineralocorticoid receptor (MR) antagonists including spironolactone as potential therapies for human AF because of their positive effects on reducing atrial fibrosis and associated AF in animal models. Spironolactone has been shown to exert positive effects in human patients with heart failure; however, the mechanisms and effects in human atrial fibrosis and AF remain undetermined. This review will discuss and highlight developments on (i) the relationship between atrial fibrosis and AF, (ii) spironolactone, as a drug targeted to atrial fibrosis and AF, as well as (iii) the distinct and common mechanisms important for regulating atrial and ventricular fibrosis, inclusive of the key extracellular matrix regulatory proteins involved.
MeSH term(s)	Angiotensin II Type 1 Receptor Blockers/therapeutic use ; Animals ; Atrial Fibrillation/drug therapy ; Atrial Fibrillation/metabolism ; Atrial Fibrillation/physiopathology ; Extracellular Matrix/metabolism ; Fibrosis/drug therapy ; Fibrosis/metabolism ; Fibrosis/physiopathology ; Heart Atria/metabolism ; Heart Atria/pathology ; Heart Atria/physiopathology ; Humans ; Signal Transduction/drug effects ; Spironolactone/therapeutic use
Chemical Substances	Angiotensin II Type 1 Receptor Blockers ; Spironolactone (27O7W4T232)
Language	English
Publishing date	2009-09-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2009.09.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 426: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito