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  1. Article ; Online: The development and impact of an app for a smart drug interaction reminder system.

    Lee, Hung-Fu / Liao, Pei-Hung

    Technology and health care : official journal of the European Society for Engineering and Medicine

    2023  Volume 32, Issue 3, Page(s) 1595–1608

    Abstract: Background: Improved access to media and medical knowledge has elicited stronger public health awareness.: Objective: This study developed a smart drug interaction reminder system for patients to increase knowledge and reduce nurse workload.: ... ...

    Abstract Background: Improved access to media and medical knowledge has elicited stronger public health awareness.
    Objective: This study developed a smart drug interaction reminder system for patients to increase knowledge and reduce nurse workload.
    Methods: This study used a single-group pre-test/post-test design and applied mining techniques to analyze the weight and probability of interaction among various medicines. Data were collected from 258 participants at a teaching hospital in northern Taiwan using convenience sampling. An app was used to give patients real-time feedback to obtain access to information and remind them of their health issues. In addition to guiding the patients on medications, this app measured the nurses' work satisfaction and patients' knowledge of drug interaction.
    Results: The results indicate that using information technology products to assist the app's real-time feedback system promoted nurses' work satisfaction, improved their health education skills, and helped patients to better understand drug interactions.
    Conclusion: Using information technology to provide patients with real-time inquiring functions has a significant effect on nurses' load reduction. Thus, smart drug interaction reminder system apps can be considered suitable nursing health education tools and the SDINRS app can be integrated into quantitative structure-activity relationship intelligence in the future.
    MeSH term(s) Humans ; Mobile Applications ; Reminder Systems ; Female ; Male ; Taiwan ; Adult ; Drug Interactions ; Middle Aged ; Health Knowledge, Attitudes, Practice ; Job Satisfaction ; Patient Education as Topic/methods
    Language English
    Publishing date 2023-10-13
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1159961-3
    ISSN 1878-7401 ; 0928-7329
    ISSN (online) 1878-7401
    ISSN 0928-7329
    DOI 10.3233/THC-230650
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The Effect of S-Allyl L-Cysteine on Retinal Ischemia: The Contributions of MCP-1 and PKM2 in the Underlying Medicinal Properties.

    Chao, Windsor Wen-Jin / Chao, Howard Wen-Haur / Lee, Hung-Fu / Chao, Hsiao-Ming

    International journal of molecular sciences

    2024  Volume 25, Issue 2

    Abstract: Retinal ischemia plays a vital role in vision-threatening retinal ischemic disorders, such as diabetic retinopathy, age-related macular degeneration, glaucoma, etc. The aim of this study was to investigate the effects of S-allyl L-cysteine (SAC) and its ... ...

    Abstract Retinal ischemia plays a vital role in vision-threatening retinal ischemic disorders, such as diabetic retinopathy, age-related macular degeneration, glaucoma, etc. The aim of this study was to investigate the effects of S-allyl L-cysteine (SAC) and its associated therapeutic mechanism. Oxidative stress was induced by administration of 500 μM H
    MeSH term(s) Rats ; Animals ; Rats, Wistar ; Cysteine/pharmacology ; Cysteine/therapeutic use ; Hydrogen Peroxide/therapeutic use ; Reperfusion Injury/drug therapy ; Retinal Diseases/drug therapy ; Ischemia/drug therapy ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Anti-Inflammatory Agents/therapeutic use ; Glaucoma/drug therapy
    Chemical Substances S-allylcysteine (81R3X99M15) ; Cysteine (K848JZ4886) ; Hydrogen Peroxide (BBX060AN9V) ; Neuroprotective Agents ; Anti-Inflammatory Agents
    Language English
    Publishing date 2024-01-22
    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/ijms25021349
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Transient receptor potential vanilloid 1 inhibition reduces brain damage by suppressing neuronal apoptosis after intracerebral hemorrhage.

    Chen, Chien-Cheng / Ke, Chia-Hua / Wu, Chun-Hu / Lee, Hung-Fu / Chao, Yuan / Tsai, Min-Chien / Shyue, Song-Kun / Chen, Szu-Fu

    Brain pathology (Zurich, Switzerland)

    2024  , Page(s) e13244

    Abstract: Intracerebral hemorrhage (ICH) induces a complex sequence of apoptotic cascades and inflammatory responses, leading to neurological impairment. Transient receptor potential vanilloid 1 (TRPV1), a nonselective cation channel with high calcium permeability, ...

    Abstract Intracerebral hemorrhage (ICH) induces a complex sequence of apoptotic cascades and inflammatory responses, leading to neurological impairment. Transient receptor potential vanilloid 1 (TRPV1), a nonselective cation channel with high calcium permeability, has been implicated in neuronal apoptosis and inflammatory responses. This study used a mouse ICH model and neuronal cultures to examine whether TRPV1 activation exacerbates brain damage and neurological deficits by promoting neuronal apoptosis and neuroinflammation. ICH was induced by injecting collagenase in both wild-type (WT) C57BL/6 mice and TRPV1
    Language English
    Publishing date 2024-02-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.13244
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation.

    Lee, Hung-Fu / Chen, Chih Hung / Chang, Che-Feng

    Journal of visualized experiments : JoVE

    2020  , Issue 160

    Abstract: Cerebral contusion is a severe medical problem affecting millions of people worldwide each year. There is an urgent need to understand the pathophysiological mechanism and to develop effective therapeutic strategy for this devastating neurological ... ...

    Abstract Cerebral contusion is a severe medical problem affecting millions of people worldwide each year. There is an urgent need to understand the pathophysiological mechanism and to develop effective therapeutic strategy for this devastating neurological disorder. Intraparenchymal hemorrhage and post-traumatic inflammatory response induced by initial physical impact can aggravate microglia/macrophage activation and neuroinflammation which subsequently worsen brain pathology. We provide here a controlled cortical impact (CCI) protocol that can reproduce experimental cortical contusion in mice by using a pneumatic impactor system to deliver mechanical force with controllable magnitude and velocity onto the dural surface. This preclinical model allows researchers to induce moderately severe focal cerebral contusion in mice and to investigate a wide range of post-traumatic pathological progressions including hemorrhage contusion, microglia/macrophage activation, iron toxicity, axonal injury, as well as short-term and long-term neurobehavioral deficits. The present protocol can be useful for exploring the long-term effects of and potential interventions for cerebral contusion.
    MeSH term(s) Animals ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/pathology ; Cerebral Cortex/pathology ; Contusions/complications ; Contusions/pathology ; Craniotomy ; Disease Models, Animal ; Hemorrhage/complications ; Hemorrhage/pathology ; Inflammation/complications ; Inflammation/pathology ; Male ; Mice, Inbred C57BL ; Myelin Sheath/metabolism ; Stereotaxic Techniques
    Language English
    Publishing date 2020-06-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/61393
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Acute Kahweol Treatment Attenuates Traumatic Brain Injury Neuroinflammation and Functional Deficits.

    Lee, Hung-Fu / Lin, Jhih Syuan / Chang, Che-Feng

    Nutrients

    2019  Volume 11, Issue 10

    Abstract: Traumatic brain injury (TBI) affects millions worldwide with devastating long-term effects on health and cognition. Emerging data suggest that targeting the immune response may offer promising strategies to alleviate TBI outcomes; kahweol, an anti- ... ...

    Abstract Traumatic brain injury (TBI) affects millions worldwide with devastating long-term effects on health and cognition. Emerging data suggest that targeting the immune response may offer promising strategies to alleviate TBI outcomes; kahweol, an anti-inflammatory diterpene that remains in unfiltered coffee, has been shown to be beneficial in neuronal recovery. Here, we examined whether kahweol could alleviate brain trauma-induced injury in a mouse model of TBI and its underlying mechanisms. TBI was induced by controlled cortical impact (CCI) and various doses of kahweol were intraperitoneally administered following injury. Contusion volume, brain edema, neurobehavioral deficits, and protein expression and activity were evaluated in both short-term and long-term recovery. We found that kahweol treatments significantly reduced secondary brain injury and improved neurobehavioral outcomes in TBI mice. These changes were accompanied by the attenuation of proinflammatory cytokine secretion, decreased microglia/macrophage activation, and reduction of neutrophil and leukocyte infiltration. In addition, continuous kahweol treatment further improved short-term TBI outcomes compared to single-dosage. Collectively, our data showed that kahweol protects against TBI by reducing immune responses and may serve as a potential therapeutic intervention for TBI patients.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Brain Injuries, Traumatic/blood ; Brain Injuries, Traumatic/drug therapy ; Brain Injuries, Traumatic/etiology ; Cytokines/drug effects ; Disease Models, Animal ; Diterpenes/pharmacology ; Leukocytes/drug effects ; Macrophages/drug effects ; Mice ; Microglia/drug effects ; Neutrophil Infiltration/drug effects
    Chemical Substances Anti-Inflammatory Agents ; Cytokines ; Diterpenes ; kahweol (6894-43-5)
    Language English
    Publishing date 2019-09-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu11102301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Evaluation of post-stroke spasticity from the subacute to chronic stages: A clinical and neurophysiologic study of motoneuron pool excitability.

    Shen, Heng-Yi / Lin, Jou-Yu / Chen, Chien-Cheng / Lee, Hung-Fu / Chao, Hsien / Lieu, Fu-Kong / Chen, Szu-Fu

    The Chinese journal of physiology

    2022  Volume 65, Issue 3, Page(s) 109–116

    Abstract: Spasticity measured using clinical scales, such as the modified Ashworth scale (MAS), may not sufficiently evaluate the effectiveness of therapeutic interventions and predict prognosis. This study aimed to compare changes in H-reflex excitability in the ... ...

    Abstract Spasticity measured using clinical scales, such as the modified Ashworth scale (MAS), may not sufficiently evaluate the effectiveness of therapeutic interventions and predict prognosis. This study aimed to compare changes in H-reflex excitability in the spastic and unimpaired upper and lower limbs of patients with acute and chronic stroke. We also investigated the relationship between the degree of spasticity as assessed by the MAS and motor neuron pool excitability with by analyzing H-reflex excitability. Sixty adult patients with a first-ever stroke were recruited for this study. MAS scores were recorded in the post-stroke upper and lower limb muscles. H-reflexes and M-responses of the bilateral flexor carpi radialis and soleus were tested by stimulating the median and tibial nerves. The results showed that both the ratio of the maximal size of the H-reflex (Hmax) to the maximal size of the M-response (Mmax) and the ratio of the developmental slope of H-reflex (Hslp) to that of the M-responses (Mslp) were significantly higher on the spastic side than on the unimpaired side for the upper and lower limbs. In contrast, the ratio of the threshold of the H-reflex (Hth) to the threshold of the M-response (Mth) only showed significant differences between the two sides in the upper limbs. The Hslp/Mslp paretic/non-paretic ratio was increased in patients with MAS scores of 2 or 3 compared to MAS scores of 1 for both the upper and lower limbs, whereas the Hmax/Mmax paretic/non-paretic ratio showed significant differences between MAS scores of 2 or 3 and 1 only in the upper limbs. Moreover, in either the spastic or unimpaired sides, there were no significant differences in any of the three motoneuron pool excitability parameters, Hmax/Mmax, Hslp/Mslp, and Hth/Mth, between the shorter chronicity (time post-stroke ≤6 months) and longer chronicity groups (time post-stroke >6 months) for both the upper and lower limbs. These results suggest that Hslp/Mslp could be a potential neurophysiological indicator for evaluating the degree of spasticity in both the upper and lower limbs of patients with hemiplegia. The MAS and Hslp/Mslp characterize clinical and neurophysiologic spasticity, respectively, and could be used as an integrated approach to evaluate and follow up post-stroke spasticity.
    MeSH term(s) Adult ; Humans ; Motor Neurons ; Muscle Spasticity/diagnosis ; Muscle Spasticity/etiology ; Stroke/complications ; Upper Extremity
    Language English
    Publishing date 2022-06-30
    Publishing country India
    Document type Journal Article
    ZDB-ID 966112-8
    ISSN 0304-4920 ; 0300-8525
    ISSN 0304-4920 ; 0300-8525
    DOI 10.4103/0304-4920.348359
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Acute Kahweol Treatment Attenuates Traumatic Brain Injury Neuroinflammation and Functional Deficits

    Lee, Hung-Fu / Lin, Jhih Syuan / Chang, Che-Feng

    Nutrients. 2019 Sept. 27, v. 11, no. 10

    2019  

    Abstract: Traumatic brain injury (TBI) affects millions worldwide with devastating long-term effects on health and cognition. Emerging data suggest that targeting the immune response may offer promising strategies to alleviate TBI outcomes; kahweol, an anti- ... ...

    Abstract Traumatic brain injury (TBI) affects millions worldwide with devastating long-term effects on health and cognition. Emerging data suggest that targeting the immune response may offer promising strategies to alleviate TBI outcomes; kahweol, an anti-inflammatory diterpene that remains in unfiltered coffee, has been shown to be beneficial in neuronal recovery. Here, we examined whether kahweol could alleviate brain trauma-induced injury in a mouse model of TBI and its underlying mechanisms. TBI was induced by controlled cortical impact (CCI) and various doses of kahweol were intraperitoneally administered following injury. Contusion volume, brain edema, neurobehavioral deficits, and protein expression and activity were evaluated in both short-term and long-term recovery. We found that kahweol treatments significantly reduced secondary brain injury and improved neurobehavioral outcomes in TBI mice. These changes were accompanied by the attenuation of proinflammatory cytokine secretion, decreased microglia/macrophage activation, and reduction of neutrophil and leukocyte infiltration. In addition, continuous kahweol treatment further improved short-term TBI outcomes compared to single-dosage. Collectively, our data showed that kahweol protects against TBI by reducing immune responses and may serve as a potential therapeutic intervention for TBI patients.
    Keywords animal models ; brain ; brain damage ; cognition ; cytokines ; diterpenoids ; edema ; long term effects ; macrophage activation ; mice ; neuroglia ; neurons ; neutrophils ; patients ; protein synthesis ; secretion ; therapeutics
    Language English
    Dates of publication 2019-0927
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2518386-2
    ISSN 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu11102301
    Database NAL-Catalogue (AGRICOLA)

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  8. Article ; Online: Astaxanthin Ameliorates Ischemic-Hypoxic-Induced Neurotrophin Receptor p75 Upregulation in the Endothelial Cells of Neonatal Mouse Brains.

    Kuo, Min-Hsun / Lee, Hung-Fu / Tu, Yi-Fang / Lin, Li-Hsuan / Cheng, Ya-Yun / Lee, Hsueh-Te

    International journal of molecular sciences

    2019  Volume 20, Issue 24

    Abstract: Ischemic stroke is a leading cause of human death in present times. Two phases of pathological impact occur during an ischemic stroke, namely, ischemia and reperfusion. Both periods include individual characteristic effects on cell injury and apoptosis. ... ...

    Abstract Ischemic stroke is a leading cause of human death in present times. Two phases of pathological impact occur during an ischemic stroke, namely, ischemia and reperfusion. Both periods include individual characteristic effects on cell injury and apoptosis. Moreover, these conditions can cause severe cell defects and harm the blood-brain barrier (BBB). Also, the BBB components are the major targets in ischemia-reperfusion injury. The BBB owes its enhanced protective roles to capillary endothelial cells, which maintain BBB permeability. One of the nerve growth factor (NGF) receptors initiating cell signaling, once activated, is the p75 neurotrophin receptor (p75NTR). This receptor is involved in both the survival and apoptosis of neurons. Although many studies have attempted to explain the role of p75NTR in neurons, the mechanisms in endothelial cells remain unclear. Endothelial cells are the first cells to encounter p75NTR stimuli. In this study, we found the upregulated p75NTR expression and reductive expression of tight junction proteins after in vivo and in vitro ischemia-reperfusion injury. Moreover, astaxanthin (AXT), an antioxidant drug, was utilized and was found to reduce p75NTR expression and the number of apoptotic cells. This study verified that p75NTR plays a prominent role in endothelial cell death and provides a novel downstream target for AXT.
    MeSH term(s) Animals ; Animals, Newborn ; Antioxidants/therapeutic use ; Blotting, Western ; Brain/drug effects ; Brain/metabolism ; Cell Survival/drug effects ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Immunochemistry ; Immunohistochemistry ; In Situ Nick-End Labeling ; Male ; Mice ; Mice, Inbred C57BL ; Receptor, Nerve Growth Factor/metabolism ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Xanthophylls/therapeutic use
    Chemical Substances Antioxidants ; Receptor, Nerve Growth Factor ; Xanthophylls ; astaxanthine (8XPW32PR7I)
    Language English
    Publishing date 2019-12-06
    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/ijms20246168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Anti-inflammatory and neuroprotective effects of triptolide on traumatic brain injury in rats.

    Lee, Hung-Fu / Lee, Tzong-Shyuan / Kou, Yu Ru

    Respiratory physiology & neurobiology

    2012  Volume 182, Issue 1, Page(s) 1–8

    Abstract: Traumatic brain injury (TBI) is characterized by neuroinflammation, brain edema, and cerebral damage leading to impairment of neurobehavioral function. Triptolide (PG-490), a diterpenoid component from Tripterygium wilfordii Hook F., has anti- ... ...

    Abstract Traumatic brain injury (TBI) is characterized by neuroinflammation, brain edema, and cerebral damage leading to impairment of neurobehavioral function. Triptolide (PG-490), a diterpenoid component from Tripterygium wilfordii Hook F., has anti-inflammatory properties. Whether triptolide has neuroprotective functions when treating TBI is unclear. To investigate this possibility, Sprague-Dawley rats were treated with triptolide immediately after TBI had been induced by a controlled cortical impact procedure or after a sham procedure. TBI produced neuroinflammation when measured on day 1 after TBI, induced cerebral damage when measured on day 1 and day 3, and impaired neurobehavioral functioning over a 28-day observation period. Triptolide suppressed TBI-induced increases in contusion volume, cell apoptosis, edema and the levels of various pro-inflammatory mediators in the brain. Thriptolide reversed the TBI-induced decrease in brain levels of anti-inflammatory cytokine interleukin-10. Importantly, triptolide improved neurobehavioral outcomes regarding motor, sensory, reflex and balance function. We conclude that triptolide confers neuroprotection against TBI, at least in part, via its anti-inflammatory activity.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/therapeutic use ; Apoptosis/drug effects ; Brain Edema/drug therapy ; Brain Injuries/drug therapy ; Disease Models, Animal ; Diterpenes/therapeutic use ; Epoxy Compounds/therapeutic use ; Inflammation Mediators/physiology ; Male ; Neurons/drug effects ; Neuroprotective Agents/therapeutic use ; Phenanthrenes/therapeutic use ; Rats ; Rats, Sprague-Dawley ; Recovery of Function/drug effects
    Chemical Substances Anti-Inflammatory Agents ; Diterpenes ; Epoxy Compounds ; Inflammation Mediators ; Neuroprotective Agents ; Phenanthrenes ; triptolide (19ALD1S53J)
    Language English
    Publishing date 2012-06-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2077867-3
    ISSN 1878-1519 ; 1569-9048
    ISSN (online) 1878-1519
    ISSN 1569-9048
    DOI 10.1016/j.resp.2012.01.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Increased GABAergic inhibitory function against ischemic long-term potentiation in the CA1 region of the hippocampus

    Chu, Ming-Chia / Lee, Jing-Ying / Lee, Hung-Fu / Chu, Kai-Wen / Wu, Han-Fang / Lee, Chi-Wei / Lin, Chia-Hsien / Tang, Chih-Wei / Lin, Hui-Ching

    Biochemical and biophysical research communications. 2020 May 28, v. 526, no. 2

    2020  

    Abstract: Potentiation of N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory synaptic plasticity around 1 h after brief exposure to anoxia/aglycemia is called ischemic long-term potentiation (iLTP), which is considered a pathological form of synaptic ... ...

    Abstract Potentiation of N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory synaptic plasticity around 1 h after brief exposure to anoxia/aglycemia is called ischemic long-term potentiation (iLTP), which is considered a pathological form of synaptic response during the early phase of ischemic stroke. It is known that GABAergic inhibitory transmission is also an important molecular process involved in synaptic plasticity and learning memory. However, whether GABAergic transmission is involved in iLTP and early-phase plasticity in ischemic stroke remains unknown. In this study, iLTP was found to be induced in the hippocampal Schaffer-collateral pathway by exposure to oxygen glucose deprivation (OGD). Western blot analysis was conducted to analyze excitatory synaptic receptors and inhibitory synaptic receptors following OGD. The β3 subunit of the GABAA receptor (GABAAR) was markedly reduced, whereas the GluN2B subunit of the NMDAR was increased in the hippocampal area in the OGD group. Using extracellular recording, we demonstrated that application of GABAAR agonist midazolam could abolish the hippocampal iLTP. Moreover, midazolam had no significant effect on the increase in NMDAR subunit GluN2B, but ameliorated the reduction in the β3 subunit of GABAAR after OGD. In summary, our results indicated that hippocampal GABAAR reduction promoted synaptic potentiation after OGD. Activation of GABAergic inhibitory transmission function could inhibit iLTP; thus, modulation of GABAergic function is a protective treatment method in the acute phase of synaptic plasticity in ischemic stroke.
    Keywords Western blotting ; agonists ; glucose ; hippocampus ; hypoxia ; memory ; neuroplasticity ; oxygen ; plasticity ; research ; stroke
    Language English
    Dates of publication 2020-0528
    Size p. 491-496.
    Publishing place Elsevier Inc.
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2020.03.111
    Database NAL-Catalogue (AGRICOLA)

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