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Article ; Online: Proenkephalin A 119-159, a Possible Early Biomarker of Acute Kidney Injury in Complex Endovascular Aortic Repair: a Single Centre Observational, Cross Sectional Study.

Walczak-Wieteska, Paulina / Zuzda, Konrad / Szczęsna, Karolina / Ziętalewicz, Joanna / Andruszkiewicz, Paweł / Małyszko, Jolanta

European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery

2024

Language	English
Publishing date	2024-03-12
Publishing country	England
Document type	Journal Article
ZDB-ID	1225869-6
ISSN	1532-2165 ; 1078-5884
ISSN (online)	1532-2165
ISSN	1078-5884
DOI	10.1016/j.ejvs.2024.01.084
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Zs.A 2283: 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)
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Article ; Online: Proenkephalin A 119-159 (penKid) - a novel biomarker and its quantification on the Nexus IB10 POC system for assessing kidney function.

Cobb, Jared / Szczesna, Karolina / Schulze, Axel / Ngo, Huy / Doyle, McKenna / Do, Tyler / Vu, Minh / Nguyen, John / Löffler, Julia / Borshchivska, Maryna / Bergmann, Deborah / Shin, Elizabeth / Hartmann, Tobias / Gruson, Damien

Clinical chemistry and laboratory medicine

2023 Volume 61, Issue 7, Page(s) e121–e125

MeSH term(s)	Humans ; Biomarkers ; Kidney ; Glomerular Filtration Rate
Chemical Substances	proenkephalin ; Biomarkers
Language	English
Publishing date	2023-01-13
Publishing country	Germany
Document type	Letter
ZDB-ID	1418007-8
ISSN	1437-4331 ; 1434-6621 ; 1437-8523
ISSN (online)	1437-4331
ISSN	1434-6621 ; 1437-8523
DOI	10.1515/cclm-2022-1187
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Article ; Online: Analytical performance evaluation of bioactive adrenomedullin on point-of-care platform.

Joshi, Netra / Löffler, Julia / Szczesna, Karolina / Do, Tyler / Vu, Minh / Cobb, Jared / Ngo, Huy / Nguyen, John / Carbone, Vincenzo / Bergmann, Deborah / Shin, Elizabeth / Hartmann, Tobias / Gruson, Damien

Clinical chemistry and laboratory medicine

2022 Volume 61, Issue 1, Page(s) e13–e16

MeSH term(s)	Humans ; Adrenomedullin ; Point-of-Care Systems ; Intensive Care Units ; Prospective Studies
Chemical Substances	Adrenomedullin (148498-78-6)
Language	English
Publishing date	2022-09-19
Publishing country	Germany
Document type	Letter
ZDB-ID	1418007-8
ISSN	1437-4331 ; 1434-6621 ; 1437-8523
ISSN (online)	1437-4331
ISSN	1434-6621 ; 1437-8523
DOI	10.1515/cclm-2022-0638
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Article: Generation of Cholinergic and Dopaminergic Interneurons from Human Pluripotent Stem Cells as a Relevant Tool for In Vitro Modeling of Neurological Disorders Pathology and Therapy.

Ochalek, Anna / Szczesna, Karolina / Petazzi, Paolo / Kobolak, Julianna / Dinnyes, Andras

Stem cells international

2016 Volume 2016, Page(s) 5838934

Abstract: The cellular and molecular bases of neurological diseases have been studied for decades; however, the underlying mechanisms are not yet fully elucidated. Compared with other disorders, diseases of the nervous system have been very difficult to study ... ...

Abstract	The cellular and molecular bases of neurological diseases have been studied for decades; however, the underlying mechanisms are not yet fully elucidated. Compared with other disorders, diseases of the nervous system have been very difficult to study mainly due to the inaccessibility of the human brain and live neurons in vivo or in vitro and difficulties in examination of human postmortem brain tissue. Despite the availability of various genetically engineered animal models, these systems are still not adequate enough due to species variation and differences in genetic background. Human induced pluripotent stem cells (hiPSCs) reprogrammed from patient somatic cells possess the potential to differentiate into any cell type, including neural progenitor cells and postmitotic neurons; thus, they open a new area to in vitro modeling of neurological diseases and their potential treatment. Currently, many protocols for generation of various neuronal subtypes are being developed; however, most of them still require further optimization. Here, we highlight accomplishments made in the generation of dopaminergic and cholinergic neurons, the two subtypes most affected in Alzheimer's and Parkinson's diseases and indirectly affected in Huntington's disease. Furthermore, we discuss the potential role of hiPSC-derived neurons in the modeling and treatment of neurological diseases related to dopaminergic and cholinergic system dysfunction.
Language	English
Publishing date	2016-12-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2573856-2
ISSN	1687-9678 ; 1687-966X
ISSN (online)	1687-9678
ISSN	1687-966X
DOI	10.1155/2016/5838934
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Article ; Online: In vitro models of cancer stem cells and clinical applications.

S Franco, Sara / Szczesna, Karolina / Iliou, Maria S / Al-Qahtani, Mohammed / Mobasheri, Ali / Kobolák, Julianna / Dinnyés, András

BMC cancer

2016 Volume 16, Issue Suppl 2, Page(s) 738

Abstract: Cancer cells, stem cells and cancer stem cells have for a long time played a significant role in the biomedical sciences. Though cancer therapy is more effective than it was a few years ago, the truth is that still none of the current non-surgical ... ...

Abstract	Cancer cells, stem cells and cancer stem cells have for a long time played a significant role in the biomedical sciences. Though cancer therapy is more effective than it was a few years ago, the truth is that still none of the current non-surgical treatments can cure cancer effectively. The reason could be due to the subpopulation called "cancer stem cells" (CSCs), being defined as those cells within a tumour that have properties of stem cells: self-renewal and the ability for differentiation into multiple cell types that occur in tumours.The phenomenon of CSCs is based on their resistance to many of the current cancer therapies, which results in tumour relapse. Although further investigation regarding CSCs is still needed, there is already evidence that these cells may play an important role in the prognosis of cancer, progression and therapeutic strategy. Therefore, long-term patient survival may depend on the elimination of CSCs. Consequently, isolation of pure CSC populations or reprogramming of cancer cells into CSCs, from cancer cell lines or primary tumours, would be a useful tool to gain an in-depth knowledge about heterogeneity and plasticity of CSC phenotypes and therefore carcinogenesis. Herein, we will discuss current CSC models, methods used to characterize CSCs, candidate markers, characteristic signalling pathways and clinical applications of CSCs. Some examples of CSC-specific treatments that are currently in early clinical phases will also be presented in this review.
MeSH term(s)	Animals ; Humans ; Mice ; Models, Biological ; Neoplasms/physiopathology ; Neoplastic Stem Cells ; Prognosis ; Signal Transduction
Language	English
Publishing date	2016--30
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-016-2774-3
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Article ; Online: Inhibition of Gsk3b Reduces Nfkb1 Signaling and Rescues Synaptic Activity to Improve the Rett Syndrome Phenotype in Mecp2-Knockout Mice.

Jorge-Torres, Olga C / Szczesna, Karolina / Roa, Laura / Casal, Carme / Gonzalez-Somermeyer, Louisa / Soler, Marta / Velasco, Cecilia D / Martínez-San Segundo, Pablo / Petazzi, Paolo / Sáez, Mauricio A / Delgado-Morales, Raúl / Fourcade, Stephane / Pujol, Aurora / Huertas, Dori / Llobet, Artur / Guil, Sonia / Esteller, Manel

Cell reports

2018 Volume 23, Issue 6, Page(s) 1665–1677

Abstract: Rett syndrome (RTT) is the second leading cause of mental impairment in girls and is currently untreatable. RTT is caused, in more than 95% of cases, by loss-of-function mutations in the methyl CpG-binding protein 2 gene (MeCP2). We propose here a ... ...

Abstract	Rett syndrome (RTT) is the second leading cause of mental impairment in girls and is currently untreatable. RTT is caused, in more than 95% of cases, by loss-of-function mutations in the methyl CpG-binding protein 2 gene (MeCP2). We propose here a molecular target involved in RTT: the glycogen synthase kinase-3b (Gsk3b) pathway. Gsk3b activity is deregulated in Mecp2-knockout (KO) mice models, and SB216763, a specific inhibitor, is able to alleviate the clinical symptoms with consequences at the molecular and cellular levels. In vivo, inhibition of Gsk3b prolongs the lifespan of Mecp2-KO mice and reduces motor deficits. At the molecular level, SB216763 rescues dendritic networks and spine density, while inducing changes in the properties of excitatory synapses. Gsk3b inhibition can also decrease the nuclear activity of the Nfkb1 pathway and neuroinflammation. Altogether, our findings indicate that Mecp2 deficiency in the RTT mouse model is partially rescued following treatment with SB216763.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Cells, Cultured ; Cerebellum/metabolism ; Cerebellum/pathology ; Dendritic Spines/drug effects ; Dendritic Spines/metabolism ; Dendritic Spines/pathology ; Disease Models, Animal ; Glycogen Synthase Kinase 3 beta/antagonists & inhibitors ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Indoles/pharmacology ; Inflammation/pathology ; Longevity ; Maleimides/pharmacology ; Methyl-CpG-Binding Protein 2/deficiency ; Methyl-CpG-Binding Protein 2/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B p50 Subunit/metabolism ; Phenotype ; Protein Kinase Inhibitors/pharmacology ; Rett Syndrome/metabolism ; Rett Syndrome/pathology ; Signal Transduction ; Survival Analysis ; Synapses/metabolism ; Up-Regulation/drug effects
Chemical Substances	Biomarkers ; Indoles ; Maleimides ; Mecp2 protein, mouse ; Methyl-CpG-Binding Protein 2 ; NF-kappa B p50 Subunit ; Protein Kinase Inhibitors ; SB 216763 ; Nfkb1 protein, mouse (147257-52-1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
Language	English
Publishing date	2018-05-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.04.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dysregulation of the long non-coding RNA transcriptome in a Rett syndrome mouse model.

Petazzi, Paolo / Sandoval, Juan / Szczesna, Karolina / Jorge, Olga C / Roa, Laura / Sayols, Sergi / Gomez, Antonio / Huertas, Dori / Esteller, Manel

RNA biology

2013 Volume 10, Issue 7, Page(s) 1197–1203

Abstract: Mecp2 is a transcriptional repressor protein that is mutated in Rett syndrome, a neurodevelopmental disorder that is the second most common cause of mental retardation in women. It has been shown that the loss of the Mecp2 protein in Rett syndrome cells ... ...

Abstract	Mecp2 is a transcriptional repressor protein that is mutated in Rett syndrome, a neurodevelopmental disorder that is the second most common cause of mental retardation in women. It has been shown that the loss of the Mecp2 protein in Rett syndrome cells alters the transcriptional silencing of coding genes and microRNAs. Herein, we have studied the impact of Mecp2 impairment in a Rett syndrome mouse model on the global transcriptional patterns of long non-coding RNAs (lncRNAs). Using a microarray platform that assesses 41,232 unique lncRNA transcripts, we have identified the aberrant lncRNA transcriptome that is present in the brain of Rett syndrome mice. The study of the most relevant lncRNAs altered in the assay highlighted the upregulation of the AK081227 and AK087060 transcripts in Mecp2-null mice brains. Chromatin immunoprecipitation demonstrated the Mecp2 occupancy in the 5'-end genomic loci of the described lncRNAs and its absence in Rett syndrome mice. Most importantly, we were able to show that the overexpression of AK081227 mediated by the Mecp2 loss was associated with the downregulation of its host coding protein gene, the gamma-aminobutyric acid receptor subunit Rho 2 (Gabrr2). Overall, our findings indicate that the transcriptional dysregulation of lncRNAs upon Mecp2 loss contributes to the neurological phenotype of Rett syndrome and highlights the complex interaction between ncRNAs and coding-RNAs.
MeSH term(s)	5' Flanking Region ; Animals ; Cluster Analysis ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Genetic Loci ; Humans ; Male ; Methyl-CpG-Binding Protein 2/genetics ; Methyl-CpG-Binding Protein 2/metabolism ; Mice ; Mice, Knockout ; Protein Binding ; RNA, Long Noncoding/genetics ; Reproducibility of Results ; Rett Syndrome/genetics ; Transcriptome
Chemical Substances	Methyl-CpG-Binding Protein 2 ; RNA, Long Noncoding
Language	English
Publishing date	2013-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1555-8584
ISSN (online)	1555-8584
DOI	10.4161/rna.24286
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The positional identity of iPSC-derived neural progenitor cells along the anterior-posterior axis is controlled in a dosage-dependent manner by bFGF and EGF.

Zhou, Shuling / Ochalek, Anna / Szczesna, Karolina / Avci, Hasan X / Kobolák, Julianna / Varga, Eszter / Rasmussen, Mikkel / Holst, Bjørn / Cirera, Susanna / Hyttel, Poul / Freude, Kristine K / Dinnyés, András

Differentiation; research in biological diversity

2016 Volume 92, Issue 4, Page(s) 183–194

Abstract: Neural rosettes derived from human induced pluripotent stem cells (iPSCs) have been claimed to be a highly robust in vitro cellular model for biomedical application. They are able to propagate in vitro in the presence of mitogens, including basic ... ...

Abstract	Neural rosettes derived from human induced pluripotent stem cells (iPSCs) have been claimed to be a highly robust in vitro cellular model for biomedical application. They are able to propagate in vitro in the presence of mitogens, including basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF). However, these two mitogens are also involved in anterior-posterior patterning in a gradient dependent manner along the neural tube axis. Here, we compared the regional identity of neural rosette cells and specific neural subtypes of their progeny propagated with low and high concentrations of bFGF and EGF. We observed that low concentrations of bFGF and EGF in the culturing system were able to induce forebrain identity of the neural rosettes and promote subsequent cortical neuronal differentiation. On the contrary, high concentrations of these mitogens stimulate a mid-hindbrain fate of the neural rosettes, resulting in subsequent cholinergic neuron differentiation. Thus, our results indicate that different concentrations of bFGF and EGF supplemented during propagation of neural rosettes are involved in altering the identity of the resultant neural cells.
MeSH term(s)	Cell Differentiation/genetics ; Cholinergic Neurons/metabolism ; Epidermal Growth Factor/genetics ; Epidermal Growth Factor/metabolism ; Fibroblast Growth Factor 2/genetics ; Fibroblast Growth Factor 2/metabolism ; Gene Expression Regulation, Developmental ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mitogens/metabolism ; Neural Stem Cells/metabolism ; Neural Tube/growth & development ; Neural Tube/metabolism ; Neurogenesis/genetics
Chemical Substances	Mitogens ; Fibroblast Growth Factor 2 (103107-01-3) ; Epidermal Growth Factor (62229-50-9)
Language	English
Publishing date	2016-10
Publishing country	England
Document type	Journal Article
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2016.06.002
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Article: Dysregulation of the long non-coding RNA transcriptome in a Rett syndrome mouse model

Petazzi, Paolo / Sandoval, Juan / Szczesna, Karolina / Jorge, Olga C / Roa, Laura / Sayols, Sergi / Gomez, Antonio / Huertas, Dori / Esteller, Manel

RNA biology. 2013 July 1, v. 10, no. 7

2013

Abstract	Mecp2 is a transcriptional repressor protein that is mutated in Rett syndrome, a neurodevelopmental disorder that is the second most common cause of mental retardation in women. It has been shown that the loss of the Mecp2 protein in Rett syndrome cells alters the transcriptional silencing of coding genes and microRNAs. Herein, we have studied the impact of Mecp2 impairment in a Rett syndrome mouse model on the global transcriptional patterns of long non-coding RNAs (lncRNAs). Using a microarray platform that assesses 41,232 unique lncRNA transcripts, we have identified the aberrant lncRNA transcriptome that is present in the brain of Rett syndrome mice. The study of the most relevant lncRNAs altered in the assay highlighted the upregulation of the AK081227 and AK087060 transcripts in Mecp2-null mice brains. Chromatin immunoprecipitation demonstrated the Mecp2 occupancy in the 5′-end genomic loci of the described lncRNAs and its absence in Rett syndrome mice. Most importantly, we were able to show that the overexpression of AK081227 mediated by the Mecp2 loss was associated with the downregulation of its host coding protein gene, the gamma-aminobutyric acid receptor subunit Rho 2 (Gabrr2). Overall, our findings indicate that the transcriptional dysregulation of lncRNAs upon Mecp2 loss contributes to the neurological phenotype of Rett syndrome and highlights the complex interaction between ncRNAs and coding-RNAs.
Keywords	animal models ; behavior disorders ; brain ; chromatin immunoprecipitation ; gamma-aminobutyric acid ; gamma-aminobutyric acid receptors ; gene expression regulation ; gene overexpression ; genes ; genomics ; loci ; messenger RNA ; mice ; microRNA ; microarray technology ; non-coding RNA ; phenotype ; repressor proteins ; transcription (genetics) ; transcriptome ; women
Language	English
Dates of publication	2013-0701
Size	p. 1197-1203.
Publishing place	Taylor & Francis
Document type	Article
ISSN	1555-8584
DOI	10.4161/rna.24286
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Circadian cycle-dependent MeCP2 and brain chromatin changes.

Martínez de Paz, Alexia / Sanchez-Mut, Jose Vicente / Samitier-Martí, Mireia / Petazzi, Paolo / Sáez, Mauricio / Szczesna, Karolina / Huertas, Dori / Esteller, Manel / Ausió, Juan

PloS one

2015 Volume 10, Issue 4, Page(s) e0123693

Abstract: Methyl CpG binding protein 2 (MeCP2) is a chromosomal protein of the brain, very abundant especially in neurons, where it plays an important role in the regulation of gene expression. Hence it has the potential to be affected by the mammalian circadian ... ...

Abstract	Methyl CpG binding protein 2 (MeCP2) is a chromosomal protein of the brain, very abundant especially in neurons, where it plays an important role in the regulation of gene expression. Hence it has the potential to be affected by the mammalian circadian cycle. We performed expression analyses of mice brain frontal cortices obtained at different time points and we found that the levels of MeCP2 are altered circadianly, affecting overall organization of brain chromatin and resulting in a circadian-dependent regulation of well-stablished MeCP2 target genes. Furthermore, this data suggests that alterations of MeCP2 can be responsible for the sleeping disorders arising from pathological stages, such as in autism and Rett syndrome.
MeSH term(s)	Animals ; Brain/metabolism ; CLOCK Proteins/metabolism ; Cerebral Cortex/metabolism ; Chromatin/metabolism ; Circadian Rhythm/genetics ; Gene Expression Regulation, Developmental ; Methyl-CpG-Binding Protein 2/metabolism ; Mice ; Mice, Inbred C57BL ; Promoter Regions, Genetic/genetics
Chemical Substances	Chromatin ; Methyl-CpG-Binding Protein 2 ; CLOCK Proteins (EC 2.3.1.48)
Language	English
Publishing date	2015-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0123693
Database	MEDical Literature Analysis and Retrieval System OnLINE

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