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  1. Article ; Online: Experimental models for assaying microvascular endothelial cell pathophysiology in stroke.

    Camós, Susanna / Mallolas, Judith

    Molecules (Basel, Switzerland)

    2010  Volume 15, Issue 12, Page(s) 9104–9134

    Abstract: It is important to understand the molecular mechanisms underlying neuron death following stroke in order to develop effective neuroprotective strategies. Since studies on human stroke are extremely limited due to the difficulty in collecting post-mortem ... ...

    Abstract It is important to understand the molecular mechanisms underlying neuron death following stroke in order to develop effective neuroprotective strategies. Since studies on human stroke are extremely limited due to the difficulty in collecting post-mortem tissue at different time points after the onset of stroke, brain ischaemia research focuses on information derived from in-vitro models of neuronal death through ischaemic injury [1]. This review aims to provide an update on the different in-vitro stroke models with brain microvascular endothelial cells that are currently being used. These models provide a physiologically relevant tool to screen potential neuroprotective drugs in stroke and to study the molecular mechanisms involved in brain ischaemia.
    MeSH term(s) Animals ; Brain Ischemia/drug therapy ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Brain Ischemia/physiopathology ; Cell Death ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Humans ; Microvessels/metabolism ; Microvessels/pathology ; Microvessels/physiopathology ; Models, Cardiovascular ; Neurons/metabolism ; Neurons/pathology ; Neuroprotective Agents/therapeutic use ; Stroke/drug therapy ; Stroke/metabolism ; Stroke/pathology ; Stroke/physiopathology
    Chemical Substances Neuroprotective Agents
    Language English
    Publishing date 2010-12-10
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules15129104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Experimental Models for Assaying Microvascular Endothelial Cell Pathophysiology in Stroke

    Susanna Camós / Judith Mallolas

    Molecules, Vol 15, Iss 12, Pp 9104-

    2010  Volume 9134

    Abstract: It is important to understand the molecular mechanisms underlying neuron death following stroke in order to develop effective neuroprotective strategies. Since studies on human stroke are extremely limited due to the difficulty in collecting post-mortem ... ...

    Abstract It is important to understand the molecular mechanisms underlying neuron death following stroke in order to develop effective neuroprotective strategies. Since studies on human stroke are extremely limited due to the difficulty in collecting post-mortem tissue at different time points after the onset of stroke, brain ischaemia research focuses on information derived from in-vitro models of neuronal death through ischaemic injury [1]. This review aims to provide an update on the different in-vitro stroke models with brain microvascular endothelial cells that are currently being used. These models provide a physiologically relevant tool to screen potential neuroprotective drugs in stroke and to study the molecular mechanisms involved in brain ischaemia.
    Keywords neuroprotection ; blood brain barrier ; brain endothelial cells ; cerebral ischaemia ; angiogenesis ; Organic chemistry ; QD241-441
    Language English
    Publishing date 2010-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: A polymorphism in the promoter region of the survivin gene is related to hemorrhagic transformation in patients with acute ischemic stroke.

    Mallolas, Judith / Rodríguez, Rocío / Gubern, Carme / Camós, Susanna / Serena, Joaquín / Castellanos, Mar

    Neuromolecular medicine

    2014  Volume 16, Issue 4, Page(s) 856–861

    Abstract: Hemorrhagic transformation (HT) of cerebral infarction is a common and serious occurrence following acute ischemic stroke. The expression of survivin, a member of the inhibitor of apoptosis protein family, has been shown to increase after cerebral ... ...

    Abstract Hemorrhagic transformation (HT) of cerebral infarction is a common and serious occurrence following acute ischemic stroke. The expression of survivin, a member of the inhibitor of apoptosis protein family, has been shown to increase after cerebral ischemia. This protein has been mainly located at the microvasculature within the infarcted and peri-infarcted area, so we aimed to investigate whether survivin gene polymorphisms, also known as BIRC5 gene, were associated with HT of cerebral infarction. Polymorphism screening of the BIRC5 gene was performed in 107 patients with a hemispheric ischemic stroke and 93 controls by polymerase chain reaction, single-strand conformation polymorphism and sequencing analysis. Genotype-phenotype correlation was performed in patients. MRI was carried out within 12 h of symptoms onset and at 72 ± 12 h. The presence of HT was determined on the second DWI sequence and classified according to ECASS II criteria. MMP-9 levels were analyzed at admission. Forty-nine patients (45.8%) had HT. The -241 C/T (rs17878467) polymorphism was identified in the promoter region of the survivin gene. The prevalence of the mutant allele (T) was similar in patients and controls (14 vs. 16%, respectively; P = 0.37). However, 9 (29%) patients with allele T had HT compared to 40 (52.6%) of wild-type (P = 0.021). Logistic regression analysis showed that the polymorphism was associated with a lower risk of HT (OR 0.16; 95% CI 0.04-0.65; P = 0.01). The -241 C/T polymorphism in the promoter region of the survivin gene is associated with a lower risk of HT in patients with ischemic stroke. It has recently been reported that the -241 C/T polymorphism increases survivin promoter activity, reinforcing the hypothesis that patients with the mutant allele may have increased survivin expression in the brain. Different mechanisms, including BBB protection by the inhibition or activation of different angiogenic growth factors and the inhibition of apoptosis during angiogenesis, may explain the protective effect of this polymorphism on HT development in ischemic stroke. Further studies are needed to confirm our results and elucidate the mechanisms explaining this effect.
    MeSH term(s) Aged ; Aged, 80 and over ; Alleles ; Blood-Brain Barrier ; Brain Ischemia/complications ; Case-Control Studies ; Cerebral Hemorrhage/epidemiology ; Cerebral Hemorrhage/etiology ; Cerebral Hemorrhage/genetics ; Cerebral Hemorrhage/pathology ; Cerebral Hemorrhage/physiopathology ; Cerebral Infarction/complications ; Comorbidity ; Diffusion Magnetic Resonance Imaging ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/physiology ; Male ; Matrix Metalloproteinase 9/blood ; Middle Aged ; Phenotype ; Polymorphism, Single Nucleotide ; Polymorphism, Single-Stranded Conformational ; Promoter Regions, Genetic/genetics ; Risk ; Risk Factors ; Sequence Analysis, DNA ; Single-Blind Method ; Spain/epidemiology ; Survivin
    Chemical Substances BIRC5 protein, human ; Inhibitor of Apoptosis Proteins ; Survivin ; MMP9 protein, human (EC 3.4.24.35) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
    Language English
    Publishing date 2014-10-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2077809-0
    ISSN 1559-1174 ; 1535-1084
    ISSN (online) 1559-1174
    ISSN 1535-1084
    DOI 10.1007/s12017-014-8333-7
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5818: Show issues Location:
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  4. Article ; Online: Paediatric patients with acute leukaemia and KMT2A (MLL) rearrangement show a distinctive expression pattern of histone deacetylases.

    Vega-García, Nerea / Malatesta, Roberta / Estella, Camino / Pérez-Jaume, Sara / Esperanza-Cebollada, Elena / Torrebadell, Montserrat / Català, Albert / Gassiot, Susanna / Berrueco, Rubén / Ruiz-Llobet, Anna / Alonso-Saladrigues, Anna / Mesegué, Montserrat / Pont-Martí, Sandra / Rives, Susana / Camós, Mireia

    British journal of haematology

    2018  Volume 182, Issue 4, Page(s) 542–553

    Abstract: Histone deacetylase inhibitors (HDACi) had emerged as promising drugs in leukaemia, but their toxicity due to lack of specificity limited their use. Therefore, there is a need to elucidate the role of HDACs in specific settings. The study of HDAC ... ...

    Abstract Histone deacetylase inhibitors (HDACi) had emerged as promising drugs in leukaemia, but their toxicity due to lack of specificity limited their use. Therefore, there is a need to elucidate the role of HDACs in specific settings. The study of HDAC expression in childhood leukaemia could help to choose more specific HDACi for selected candidates in a personalized approach. We analysed HDAC1-11, SIRT1, SIRT7, MEF2C and MEF2D mRNA expression in 211 paediatric patients diagnosed with acute leukaemia. There was a global overexpression of HDACs, while specific HDACs correlated with clinical and biological features, and some even predicted outcome. Thus, some HDAC and MEF2C profiles probably reflected the lineage and the maturation of the blasts and some profiles identified specific oncogenic pathways active in the leukaemic cells. Specifically, we identified a distinctive signature for patients with KMT2A (MLL) rearrangement, with high HDAC9 and MEF2D expression, regardless of age, KMT2A partner and lineage. Moreover, we observed an adverse prognostic value of HDAC9 overexpression, regardless of KMT2A rearrangement. Our results provide useful knowledge on the complex picture of HDAC expression in childhood leukaemia and support the directed use of specific HDACi to selected paediatric patients with acute leukaemia.
    MeSH term(s) Acute Disease ; Adolescent ; Child ; Child, Preschool ; Female ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Leukemic ; Gene Rearrangement ; Histone Deacetylase Inhibitors/administration & dosage ; Histone Deacetylases/biosynthesis ; Histone-Lysine N-Methyltransferase/biosynthesis ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Infant ; Infant, Newborn ; Leukemia/drug therapy ; Leukemia/enzymology ; Leukemia/genetics ; Male ; Myeloid-Lymphoid Leukemia Protein/biosynthesis ; Myeloid-Lymphoid Leukemia Protein/genetics ; Retrospective Studies
    Chemical Substances Histone Deacetylase Inhibitors ; KMT2A protein, human ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2018-07-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.15436
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    Uh III Zs.182: Show issues Location:
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  5. Article: The Acute Optic Neuritis Network (ACON): Study protocol of a non-interventional prospective multicenter study on diagnosis and treatment of acute optic neuritis.

    Asseyer, Susanna / Asgari, Nasrin / Bennett, Jeffrey / Bialer, Omer / Blanco, Yolanda / Bosello, Francesca / Camos-Carreras, Anna / Carnero Contentti, Edgar / Carta, Sara / Chen, John / Chien, Claudia / Chomba, Mashina / Dale, Russell C / Dalmau, Josep / Feldmann, Kristina / Flanagan, Eoin P / Froment Tilikete, Caroline / Garcia-Alfonso, Carolina / Havla, Joachim /
    Hellmann, Mark / Kim, Ho Jin / Klyscz, Philipp / Konietschke, Frank / La Morgia, Chiara / Lana-Peixoto, Marco / Leite, Maria Isabel / Levin, Netta / Levy, Michael / Llufriu, Sara / Lopez, Pablo / Lotan, Itay / Lugaresi, Alessandra / Marignier, Romain / Mariotto, Sara / Mollan, Susan P / Ocampo, Cassandra / Cosima Oertel, Frederike / Olszewska, Maja / Palace, Jacqueline / Pandit, Lekha / Peralta Uribe, José Luis / Pittock, Sean / Ramanathan, Sudarshini / Rattanathamsakul, Natthapon / Saiz, Albert / Samadzadeh, Sara / Sanchez-Dalmau, Bernardo / Saylor, Deanna / Scheel, Michael / Schmitz-Hübsch, Tanja / Shifa, Jemal / Siritho, Sasitorn / Sperber, Pia S / Subramanian, Prem S / Tiosano, Alon / Vaknin-Dembinsky, Adi / Mejia Vergara, Alvaro Jose / Wilf-Yarkoni, Adi / Zarco, Luis Alfonso / Zimmermann, Hanna G / Paul, Friedemann / Stiebel-Kalish, Hadas

    Frontiers in neurology

    2023  Volume 14, Page(s) 1102353

    Abstract: Optic neuritis (ON) often occurs at the presentation of multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD). The recommended treatment of high-dose ... ...

    Abstract Optic neuritis (ON) often occurs at the presentation of multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD). The recommended treatment of high-dose corticosteroids for ON is based on a North American study population, which did not address treatment timing or antibody serostatus. The Acute Optic Neuritis Network (ACON) presents a global, prospective, observational study protocol primarily designed to investigate the effect of time to high-dose corticosteroid treatment on 6-month visual outcomes in ON. Patients presenting within 30 days of the inaugural ON will be enrolled. For the primary analysis, patients will subsequently be assigned into the MS-ON group, the aquapotin-4-IgG positive ON (AQP4-IgG+ON) group or the MOG-IgG positive ON (MOG-IgG+ON) group and then further sub-stratified according to the number of days from the onset of visual loss to high-dose corticosteroids (
    Trial registration: ClinicalTrials.gov, identifier: NCT05605951.
    Language English
    Publishing date 2023-02-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2023.1102353
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  6. Article ; Online: miRNA expression is modulated over time after focal ischaemia: up-regulation of miR-347 promotes neuronal apoptosis.

    Gubern, Carme / Camós, Susanna / Ballesteros, Iván / Rodríguez, Rocío / Romera, Víctor G / Cañadas, Roberto / Lizasoain, Ignacio / Moro, María A / Serena, Joaquín / Mallolas, Judith / Castellanos, Mar

    The FEBS journal

    2013  Volume 280, Issue 23, Page(s) 6233–6246

    Abstract: Despite the large number of molecules reported as being over-expressed after ischaemia, little is known regarding their regulation. miRNAs are potent post-transcriptional regulators of gene expression, and reports have shown differentially miRNA ... ...

    Abstract Despite the large number of molecules reported as being over-expressed after ischaemia, little is known regarding their regulation. miRNAs are potent post-transcriptional regulators of gene expression, and reports have shown differentially miRNA expression in response to focal cerebral ischaemia. The present study analysed miRNA expression from acute to late phases of ischaemia to identify specific ischaemia-related miRNAs, elucidate their role, and identify potential targets involved in stroke pathophysiology. Of 112 miRNAs, 32 showed significant changes and different expression profiles. In addition to the previously reported differentially expressed miRNAs, new ischaemia-regulated miRNAs have been found, including miR-347. Forty-seven genes involved in brain functions or related to ischaemia are predicted to be potential targets of the differentially expressed miRNAs after middle cerebral artery occlusion. Analysis of four of these targets (Acsl4, Arf3, Btg2 and Dpysl5) showed them to be differentially regulated by ischaemia at the transcriptional or post-transcriptional level. Acsl4, Bnip3l and Phyhip, potential targets of miR-347, were up-regulated after miR-347 over-expression, inducing neuronal apoptotic death. Our findings suggest that miR-347 plays an important role in regulating neuronal cell death, identify Acsl4 as a new protein requiring study in ischaemia, and provide an important resource for future functional studies of miRNAs after ischaemia.
    MeSH term(s) ADP-Ribosylation Factors/genetics ; ADP-Ribosylation Factors/metabolism ; Animals ; Apoptosis ; Biomarkers/metabolism ; Blotting, Western ; Cells, Cultured ; Coenzyme A Ligases/genetics ; Coenzyme A Ligases/metabolism ; Gene Expression Profiling ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Ischemia/genetics ; Ischemia/metabolism ; Ischemia/pathology ; Male ; MicroRNAs/genetics ; Neurons/metabolism ; Neurons/pathology ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances BTG2 protein, rat ; Biomarkers ; Immediate-Early Proteins ; MicroRNAs ; RNA, Messenger ; Tumor Suppressor Proteins ; Arf3 protein, rat (EC 3.6.1.-) ; ADP-Ribosylation Factors (EC 3.6.5.2) ; Acsl4 protein, rat (EC 6.2.1.-) ; Coenzyme A Ligases (EC 6.2.1.-)
    Language English
    Publishing date 2013-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.12546
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 260: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  7. Article ; Online: Oct-2 transcription factor binding activity and expression up-regulation in rat cerebral ischaemia is associated with a diminution of neuronal damage in vitro.

    Camós, Susanna / Gubern, Carme / Sobrado, Mónica / Rodríguez, Rocío / Romera, Víctor G / Moro, María Ángeles / Lizasoain, Ignacio / Serena, Joaquín / Mallolas, Judith / Castellanos, Mar

    Neuromolecular medicine

    2013  Volume 16, Issue 2, Page(s) 332–349

    Abstract: Brain plasticity provides a mechanism to compensate for lesions produced as a result of stroke. The present study aims to identify new transcription factors (TFs) following focal cerebral ischaemia in rat as potential therapeutic targets. A transient ... ...

    Abstract Brain plasticity provides a mechanism to compensate for lesions produced as a result of stroke. The present study aims to identify new transcription factors (TFs) following focal cerebral ischaemia in rat as potential therapeutic targets. A transient focal cerebral ischaemia model was used for TF-binding activity and TF-TF interaction profile analysis. A permanent focal cerebral ischaemia model was used for the transcript gene analysis and for the protein study. The identification of TF variants, mRNA analysis, and protein study was performed using conventional polymerase chain reaction (PCR), qPCR, and Western blot and immunofluorescence, respectively. Rat cortical neurons were transfected with small interfering RNA against the TF in order to study its role. The TF-binding analysis revealed a differential binding activity of the octamer family in ischaemic brain in comparison with the control brain samples both in acute and late phases. In this study, we focused on Oct-2 TF. Five of the six putative Oct-2 transcript variants are expressed in both control and ischaemic rat brain, showing a significant increase in the late phase of ischaemia. Oct-2 protein showed neuronal localisation both in control and ischaemic rat brain cortical slices. Functional studies revealed that Oct-2 interacts with TFs involved in important brain processes (neuronal and vascular development) and basic cellular functions and that Oct-2 knockdown promotes neuronal injury. The present study shows that Oct-2 expression and binding activity increase in the late phase of cerebral ischaemia and finds Oct-2 to be involved in reducing ischaemic-mediated neuronal injury.
    MeSH term(s) Animals ; Brain Damage, Chronic/etiology ; Brain Damage, Chronic/genetics ; Brain Damage, Chronic/pathology ; Brain Damage, Chronic/prevention & control ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cerebral Infarction/genetics ; Cerebral Infarction/metabolism ; Cerebral Infarction/pathology ; Chromatin Immunoprecipitation ; Disease Progression ; Gene Expression Profiling ; Infarction, Middle Cerebral Artery/genetics ; Infarction, Middle Cerebral Artery/metabolism ; Infarction, Middle Cerebral Artery/pathology ; Ischemic Attack, Transient/genetics ; Ischemic Attack, Transient/metabolism ; Male ; Models, Animal ; Nerve Tissue Proteins/biosynthesis ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Neurons/metabolism ; Octamer Transcription Factor-2/biosynthesis ; Octamer Transcription Factor-2/genetics ; Octamer Transcription Factor-2/physiology ; Protein Binding ; RNA Interference ; RNA, Messenger/biosynthesis ; RNA, Small Interfering/pharmacology ; Rats ; Rats, Inbred F344 ; Transcription, Genetic ; Up-Regulation
    Chemical Substances Nerve Tissue Proteins ; Octamer Transcription Factor-2 ; Pou2f2 protein, rat ; RNA, Messenger ; RNA, Small Interfering
    Language English
    Publishing date 2013-11-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2077809-0
    ISSN 1559-1174 ; 1535-1084
    ISSN (online) 1559-1174
    ISSN 1535-1084
    DOI 10.1007/s12017-013-8279-1
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