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  1. Article: Inhibition of autophagy rescues HT22 hippocampal neurons from erastin-induced ferroptosis.

    Hanke, Nora / Rami, Abdelhaq

    Neural regeneration research

    2022  Volume 18, Issue 7, Page(s) 1548–1552

    Abstract: Ferroptosis is a regulated form of cell death which is considered an oxidative iron-dependent process. The lipid hydroperoxidase glutathione peroxidase 4 prevents the iron ( ... ...

    Abstract Ferroptosis is a regulated form of cell death which is considered an oxidative iron-dependent process. The lipid hydroperoxidase glutathione peroxidase 4 prevents the iron (Fe
    Language English
    Publishing date 2022-12-26
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.360246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cerebral Ischemia Induces Iron Deposit, Ferritin Accumulation, Nuclear Receptor Coactivator 4-depletion, and Ferroptosis.

    Hanke, Nora / Rami, Abdelhaq

    Current neurovascular research

    2022  Volume 19, Issue 1, Page(s) 47–60

    Abstract: Background: The neuronal death upon cerebral ischemia shares not only characteristics of necrosis, apoptosis, and autophagy but also exhibits biochemical and morphological characteristics of ferroptosis. Ferroptosis is a regulated form of cell death ... ...

    Abstract Background: The neuronal death upon cerebral ischemia shares not only characteristics of necrosis, apoptosis, and autophagy but also exhibits biochemical and morphological characteristics of ferroptosis. Ferroptosis is a regulated form of cell death that is considered to be an oxidative iron-dependent process. It is now commonly accepted that iron and free radicals are considered to cause lipid peroxidation as well as the oxidation of proteins and nucleic acids, leading to increased membrane and enzymatic dysfunction and finally contributing to cell death. Although ferroptosis was first described in cancer cells, emerging evidence now links mechanisms of ferroptosis to many different diseases, including cerebral ischemia.
    Methods: The objective of this study was to identify the key players and underlying biochemical pathways of ferroptosis, leading to cell death upon focal cerebral ischemia in mice by using immunofluorescence, Western blotting, histochemistry, and densitometry.
    Results: In this study, we demonstrated that cerebral ischemia induced iron-deposition, downregulated dramatically the expression of the glutathione peroxidase 4 (GPX4), decreased the expression of the nuclear receptor coactivator 4 (NCOA4), and induced inappropriate accumulation of ferritin in the ischemic brain. This supports the hypothesis that an ischemic insult may induce ferroptosis through inhibition of GPX4.
    Conclusion: We conclude that iron excess following cerebral ischemia leads to cell death despite activating compensatory mechanisms for iron homeostasis, as illustrated by the accumulation of ferritins. These data emphasized the presence of a cellular mechanism that allows neuronal cells to buffer iron levels.
    MeSH term(s) Animals ; Brain Ischemia ; Ferritins/metabolism ; Ferroptosis ; Iron/metabolism ; Mice ; Nuclear Receptor Coactivators/metabolism
    Chemical Substances Nuclear Receptor Coactivators ; Ferritins (9007-73-2) ; Iron (E1UOL152H7)
    Language English
    Publishing date 2022-03-29
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2296350-9
    ISSN 1875-5739 ; 1567-2026
    ISSN (online) 1875-5739
    ISSN 1567-2026
    DOI 10.2174/1567202619666220321120954
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Relationship Between Self-Efficacy and Functional Capacity Among Discharged Heart Failure Patients in Jordan.

    Abusafieh, Ahmad Moh'd / Shajrawi, Abedalmajeed Methqal / Al-Smadi, Ahmed Mohammad / Saleh, Akram / Masa'deh, Rami / Ismaile, Samantha / Abdelhaq, Mohammad Jamil

    Dimensions of critical care nursing : DCCN

    2024  Volume 43, Issue 3, Page(s) 136–145

    Abstract: Background: Self-efficacy is an important factor associated with healthy lifestyle changes in heart failure treatment. Functional capacity testing of heart failure patients (HFPs) can stratify prognosis. Reduced functional capacities in HFPs are linked ... ...

    Abstract Background: Self-efficacy is an important factor associated with healthy lifestyle changes in heart failure treatment. Functional capacity testing of heart failure patients (HFPs) can stratify prognosis. Reduced functional capacities in HFPs are linked to a poor heart failure prognosis. Limited research has examined the potential relationship between self-efficacy and functional capacity.
    Aim: The aims of this study were to assess self-efficacy level and functional capacity among HFPs after hospitalization, and examine whether there is a relationship between them.
    Methods: A descriptive correlational design was used. A convenience sample of 220 HFPs was recruited from 2 hospitals in Jordan. The Arabic version of Cardiac Self-Efficacy Questionnaire was used to assess self-efficacy, the 6-Minute Walking Test (6-MWT) was used to assess functional capacity, and the Borg rating of perceived exertion scale (Borg Scale) was used to assess exertion during 6-MWT.
    Result: The sample included 46.8% male (n = 103) and 53.2% female (n = 117). The mean age was 52.66 ± 8.91 years. Most of the HFPs were categorized based on New York Heart Association classification as class I, 35.9% (n = 79), and class II, 41.4% (n = 91). The mean ejection fraction was 41.46 ± 9.44. The global self-efficacy was moderate (32.98 ± 9.92), and the mean score for the 6-MWT was 494.35 ± 143.37. The Borg Scale mean was 10.94 ± 3.34. In addition, there was a positive relationship between self-efficacy and 6-MWT (r = 0.63, n = 220, P = .01).
    Conclusion: This study provides baseline data for further research on treatment of HFPs, and the development of evidence-based tailored health interventions to maintain and improve self-efficacy and functional capacity among these service users. Moreover, replicated researches can test the study results considering different methodologies, such as using objective functional capacity tool and longer follow-up periods.
    MeSH term(s) Humans ; Male ; Female ; Adult ; Middle Aged ; Exercise Test/methods ; Patient Discharge ; Self Efficacy ; Jordan ; Heart Failure
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 632780-1
    ISSN 1538-8646 ; 0730-4625
    ISSN (online) 1538-8646
    ISSN 0730-4625
    DOI 10.1097/DCC.0000000000000633
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 2895: Show issues Location:
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  4. Book ; Online ; Thesis: Refraktives und visuelles Ergebnis nach Neuausrichtung von rotierten torischen Intraokularlinsen

    Sartory, Tsvetina Georgieva [Verfasser] / Rami, Abdelhaq [Akademischer Betreuer] / Brandes, Ralf [Akademischer Betreuer] / Hengerer, Fritz [Akademischer Betreuer] / Shajari, Mehdi [Gutachter] / Kohnen, Thomas [Gutachter]

    2024  

    Author's details Tsvetina Georgieva Sartory ; Gutachter: Mehdi Shajari, Thomas Kohnen ; Abdelhaq Rami, Ralf Brandes, Fritz Hengerer
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek Johann Christian Senckenberg
    Publishing place Frankfurt am Main
    Document type Book ; Online ; Thesis
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  5. Article: Exacerbated Age-Related Hippocampal Alterations of Microglia Morphology, β-Amyloid and Lipofuscin Deposition and Presenilin Overexpression in

    Börner, Jan Hendrik / Rawashdeh, Oliver / Rami, Abdelhaq

    Antioxidants (Basel, Switzerland)

    2021  Volume 10, Issue 9

    Abstract: In humans, alterations of circadian rhythms and autophagy are linked to metabolic, cardiovascular and neurological dysfunction. Autophagy constitutes a specific form of cell recycling in many eukaryotic cells. Aging is the principal risk factor for the ... ...

    Abstract In humans, alterations of circadian rhythms and autophagy are linked to metabolic, cardiovascular and neurological dysfunction. Autophagy constitutes a specific form of cell recycling in many eukaryotic cells. Aging is the principal risk factor for the development of neurodegenerative diseases. Thus, we assume that both the circadian clock and autophagy are indispensable to counteract aging. We have previously shown that the hippocampus of
    Language English
    Publishing date 2021-08-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10091330
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  6. Article ; Online: Inhibition of Autophagy Potentiated Hippocampal Cell Death Induced by Endoplasmic Reticulum Stress and its Activation by Trehalose Failed to be Neuroprotective.

    Halbe, Luisa / Rami, Abdelhaq

    Current neurovascular research

    2019  Volume 16, Issue 1, Page(s) 3–11

    Abstract: Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where ... ...

    Abstract Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate.
    Materials and methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability.
    Results and conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.
    MeSH term(s) Animals ; Autophagy/drug effects ; Autophagy/physiology ; Cell Death/drug effects ; Cell Death/physiology ; Cell Line, Transformed ; Cell Survival/drug effects ; Cell Survival/physiology ; Dose-Response Relationship, Drug ; Endoplasmic Reticulum Stress/drug effects ; Endoplasmic Reticulum Stress/physiology ; Hippocampus/cytology ; Hippocampus/drug effects ; Hippocampus/metabolism ; Mice ; Neuroprotective Agents/pharmacology ; Trehalose/pharmacology
    Chemical Substances Neuroprotective Agents ; Trehalose (B8WCK70T7I)
    Language English
    Publishing date 2019-02-01
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2296350-9
    ISSN 1875-5739 ; 1567-2026
    ISSN (online) 1875-5739
    ISSN 1567-2026
    DOI 10.2174/1567202616666190131155834
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    In stock of ZB MED Cologne/Königswinter

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  7. Book ; Online ; Thesis: Die Konsequenzen der zeitspezifischen Deletion von Neuroligin 2 für die synaptische Übertragung, Plastizität und neuronale Exzitabilität im Gyrus Dentatus von adulten Mäusen

    Frank, Franziska [Verfasser] / Jedlicka, Peter [Gutachter] / Rami, Abdelhaq [Gutachter]

    2021  

    Author's details Franziska Frank ; Gutachter: Peter Jedlicka, Abdelhaq Rami
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek Johann Christian Senckenberg
    Publishing place Frankfurt am Main
    Document type Book ; Online ; Thesis
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  8. Book ; Online ; Thesis: Physical activity and health during the SARS-CoV2 pandemic

    Wilke, Jan [Verfasser] / Groneberg, Jan David Alexander [Akademischer Betreuer] / Groneberg, Jan David Alexander [Gutachter] / Rami, Abdelhaq [Gutachter] / Woll, Alexander [Gutachter]

    2023  

    Author's details Jan Wilke ; Gutachter: Jan David Alexander Groneberg, Abdelhaq Rami, Alexander Woll ; Betreuer: Jan David Alexander Groneberg
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Universitätsbibliothek Johann Christian Senckenberg
    Publishing place Frankfurt am Main
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  9. Article: Exacerbated Age-Related Hippocampal Alterations of Microglia Morphology, β-Amyloid and Lipofuscin Deposition and Presenilin Overexpression in Per1−/−-Mice

    Börner, Jan Hendrik / Rawashdeh, Oliver / Rami, Abdelhaq

    Antioxidants. 2021 Aug. 24, v. 10, no. 9

    2021  

    Abstract: In humans, alterations of circadian rhythms and autophagy are linked to metabolic, cardiovascular and neurological dysfunction. Autophagy constitutes a specific form of cell recycling in many eukaryotic cells. Aging is the principal risk factor for the ... ...

    Abstract In humans, alterations of circadian rhythms and autophagy are linked to metabolic, cardiovascular and neurological dysfunction. Autophagy constitutes a specific form of cell recycling in many eukaryotic cells. Aging is the principal risk factor for the development of neurodegenerative diseases. Thus, we assume that both the circadian clock and autophagy are indispensable to counteract aging. We have previously shown that the hippocampus of Per1⁻/⁻-mice exhibits a reduced autophagy and higher neuronal susceptibility to ischemic insults compared to wild type (WT). Therefore, we chose to study the link between aging and loss of clock gene Per1⁻/⁻-mice. Young and aged C3H- and Per1⁻/⁻-mice were used as models to analyze the hippocampal distribution of Aβ42, lipofuscin, presenilin, microglia, synaptophysin and doublecortin. We detected several changes in the hippocampus of aged Per1⁻/⁻-mice compared to their wild type littermates. Our results show significant alterations of microglia morphology, an increase in Aβ42 deposition, overexpression of presenilin, decrease in synaptophysin levels and massive accumulation of lipofuscin in the hippocampus of 24-month-old Per1⁻/⁻-mice, without alteration of adult neurogenesis. We suggest that the marked lipofuscin accumulation, Aβ42 deposition, and overexpression of presenilin-2 observed in our experiments may be some of the consequences of the slowed autophagy in the hippocampus of aged Per1⁻/⁻-mice. This may lead during aging to excessive accumulation of misfolded proteins which may, consequently, result in higher neuronal vulnerability.
    Keywords adults ; autophagy ; circadian clocks ; genes ; hippocampus ; neurogenesis ; neuroglia ; neurons ; risk factors
    Language English
    Dates of publication 2021-0824
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10091330
    Database NAL-Catalogue (AGRICOLA)

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  10. Article ; Online: Upregulation of Beclin 1 in the ischemic penumbra.

    Rami, Abdelhaq

    Autophagy

    2007  Volume 4, Issue 2, Page(s) 227–229

    Abstract: Here we discuss the probable role of autophagy in cerebral ischemia based on our own recent data and the literature. We examined the protein level of Beclin 1 (Bcl-2 interacting protein) and microtubule-associated protein 1 light chain 3 (LC3) which were ...

    Abstract Here we discuss the probable role of autophagy in cerebral ischemia based on our own recent data and the literature. We examined the protein level of Beclin 1 (Bcl-2 interacting protein) and microtubule-associated protein 1 light chain 3 (LC3) which were previously found to promote autophagy. We found a dramatic elevation in Beclin 1 levels and LC3 in the penumbra of rats challenged by cerebral ischemia. We found also that a subpopulation of Beclin 1-upregulating cells is also expressing the active form of caspase-3, and that all Beclin 1 upregulating cells display dense staining of LC3. Neuronal cells that overexpress Beclin 1 may exhibit damaged DNA but without changes in nuclear morphology, which indicates that not all the Beclin 1-upregulating cells are predestined to die. We conclude that the cell death in the penumbra bears a resemblance not only to necrosis, apoptosis, or a compromise between the two, but exhibits also biochemical and morphological characteristics of autophagic cell death. The question that constantly arises, however, is whether autophagic activity in damaged cells is the cause of death or is actually an attempt to prevent it as a part of an endogenous neuroprotective response.
    MeSH term(s) Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Autophagy/genetics ; Beclin-1 ; Biomarkers/metabolism ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Cell Death ; Cerebral Cortex/metabolism ; Microtubule-Associated Proteins/metabolism ; Models, Biological ; Protein Transport ; Rats ; Up-Regulation
    Chemical Substances Apoptosis Regulatory Proteins ; Beclin-1 ; Becn1 protein, rat ; Biomarkers ; LC3 protein, rat ; Microtubule-Associated Proteins
    Language English
    Publishing date 2007-11-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.5339
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    Zs.A 6741: Show issues Location:
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