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  1. Article ; Online: Involvement of Glycogen Synthase Kinase 3β (GSK3β) in Formation of Phosphorylated Tau and Death of Retinal Ganglion Cells of Rats Caused by Optic Nerve Crush.

    Fukiyama, Yurie / Hirokawa, Takahisa / Takai, Shinji / Kida, Teruyo / Oku, Hidehiro

    Current issues in molecular biology

    2023  Volume 45, Issue 9, Page(s) 6941–6957

    Abstract: Tauopathy is a neurodegenerative condition associated with oligomeric tau formation through abnormal phosphorylation. We previously showed that tauopathy is involved in death of retinal ganglion cells (RGCs) after optic nerve crush (ONC). It has been ... ...

    Abstract Tauopathy is a neurodegenerative condition associated with oligomeric tau formation through abnormal phosphorylation. We previously showed that tauopathy is involved in death of retinal ganglion cells (RGCs) after optic nerve crush (ONC). It has been proposed that glycogen synthase kinase 3β (GSK3β) is involved in the hyperphosphorylation of tau in Alzheimer's disease. To determine the roles of GSK3β in tauopathy-related death of RGCs, lithium chloride (LiCl), a GSK3β inhibitor, was injected intravitreally just after ONC. The neuroprotective effects of LiCl were determined by counting Tuj-1-stained RGCs on day 7. Changes of phosphorylated (ser 396) tau in the retina were determined by Simple Western analysis (WES) on day 3. Retinal GSK3β levels were determined by immunohistochemistry (IHC) and an ELISA. There was a 1.9- and 2.1-fold increase in the levels of phosphorylated tau monomers and dimers on day 3 after ONC. LiCl significantly suppressed the increase in the levels of phosphorylated tau induced by ONC. GSK3β was mainly present in somas of RGCs, and ELISA showed that retinal levels increased to 2.0-fold on day 7. IHC showed that the GSK3β expression increased over time and remained in RGCs that were poorly stained by Tuj-1. The GSK3β and tau expression was colocalized in RGCs. The number of RGCs decreased from 1881 ± 188 (sham control) to 1150 ± 192 cells/mm
    Language English
    Publishing date 2023-08-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2000024-8
    ISSN 1467-3045 ; 1467-3037
    ISSN (online) 1467-3045
    ISSN 1467-3037
    DOI 10.3390/cimb45090438
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  2. Article ; Online: Roscovitine, a Cyclin-Dependent Kinase-5 Inhibitor, Decreases Phosphorylated Tau Formation and Death of Retinal Ganglion Cells of Rats after Optic Nerve Crush.

    Hirokawa, Takahisa / Horie, Taeko / Fukiyama, Yurie / Mimura, Masashi / Takai, Shinji / Kida, Teruyo / Oku, Hidehiro

    International journal of molecular sciences

    2021  Volume 22, Issue 15

    Abstract: Tauopathies are neurodegenerative diseases characterized by abnormal metabolism of misfolded tau proteins and are progressive. Pathological phosphorylation of tau occurs in the retinal ganglion cells (RGCs) after optic nerve injuries. Cyclin-dependent ... ...

    Abstract Tauopathies are neurodegenerative diseases characterized by abnormal metabolism of misfolded tau proteins and are progressive. Pathological phosphorylation of tau occurs in the retinal ganglion cells (RGCs) after optic nerve injuries. Cyclin-dependent kinase-5 (Cdk5) causes hyperphosphorylation of tau. To determine the roles played by Cdk5 in retinal degeneration, roscovitine, a Cdk5 inhibitor, was injected intravitreally after optic nerve crush (ONC). The neuroprotective effect of roscovitine was determined by the number of Tuj-1-stained RGCs on day 7. The change in the levels of phosphorylated tau, calpain-1, and cleaved α-fodrin was determined by immunoblots on day 3. The expression of P35/P25, a Cdk5 activator, in the RGCs was determined by immunohistochemistry. The results showed that roscovitine reduced the level of phosphorylated tau by 3.5- to 1.6-fold. Calpain-1 (2.1-fold) and cleaved α-fodrin (1.5-fold) were increased on day 3, suggesting that the calpain signaling pathway was activated. P35/P25 was accumulated in the RGCs that were poorly stained by Tuj-1. Calpain inhibition also reduced the increase in phosphorylated tau. The number of RGCs decreased from 2191 ± 178 (sham) to 1216 ± 122 cells/mm
    MeSH term(s) Animals ; Cyclin-Dependent Kinase 5/antagonists & inhibitors ; Cyclin-Dependent Kinase 5/physiology ; Optic Nerve Injuries/metabolism ; Optic Nerve Injuries/pathology ; Phosphorylation ; Rats ; Rats, Wistar ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/pathology ; Roscovitine/pharmacology ; Tauopathies/metabolism ; Tauopathies/pathology ; tau Proteins/metabolism
    Chemical Substances Mapt protein, rat ; tau Proteins ; Roscovitine (0ES1C2KQ94) ; Cyclin-Dependent Kinase 5 (EC 2.7.11.1) ; Cdk5 protein, rat (EC 2.7.11.22)
    Language English
    Publishing date 2021-07-28
    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/ijms22158096
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  3. Article ; Online: Roscovitine, a Cyclin-Dependent Kinase-5 Inhibitor, Decreases Phosphorylated Tau Formation and Death of Retinal Ganglion Cells of Rats after Optic Nerve Crush

    Takahisa Hirokawa / Taeko Horie / Yurie Fukiyama / Masashi Mimura / Shinji Takai / Teruyo Kida / Hidehiro Oku

    International Journal of Molecular Sciences, Vol 22, Iss 8096, p

    2021  Volume 8096

    Abstract: Tauopathies are neurodegenerative diseases characterized by abnormal metabolism of misfolded tau proteins and are progressive. Pathological phosphorylation of tau occurs in the retinal ganglion cells (RGCs) after optic nerve injuries. Cyclin-dependent ... ...

    Abstract Tauopathies are neurodegenerative diseases characterized by abnormal metabolism of misfolded tau proteins and are progressive. Pathological phosphorylation of tau occurs in the retinal ganglion cells (RGCs) after optic nerve injuries. Cyclin-dependent kinase-5 (Cdk5) causes hyperphosphorylation of tau. To determine the roles played by Cdk5 in retinal degeneration, roscovitine, a Cdk5 inhibitor, was injected intravitreally after optic nerve crush (ONC). The neuroprotective effect of roscovitine was determined by the number of Tuj-1-stained RGCs on day 7. The change in the levels of phosphorylated tau, calpain-1, and cleaved α-fodrin was determined by immunoblots on day 3. The expression of P35/P25, a Cdk5 activator, in the RGCs was determined by immunohistochemistry. The results showed that roscovitine reduced the level of phosphorylated tau by 3.5- to 1.6-fold. Calpain-1 (2.1-fold) and cleaved α-fodrin (1.5-fold) were increased on day 3, suggesting that the calpain signaling pathway was activated. P35/P25 was accumulated in the RGCs that were poorly stained by Tuj-1. Calpain inhibition also reduced the increase in phosphorylated tau. The number of RGCs decreased from 2191 ± 178 (sham) to 1216 ± 122 cells/mm 2 on day 7, and roscovitine preserved the level at 1622 ± 130 cells/mm 2 . We conclude that the calpain-mediated activation of Cdk5 is associated with the pathologic phosphorylation of tau.
    Keywords tauopathy ; cyclin-dependent kinase 5 (Cdk5) ; roscovitine ; calpain ; optic nerve crush ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2021-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: A Case of Fundus Oculi Albinoticus Diagnosed as Angelman Syndrome by Genetic Testing.

    Fukiyama, Yurie / Tonari, Masahiro / Matsuo, Junko / Oku, Hidehiro / Sugasawa, Jun / Shimakawa, Shuichi / Ogihara, Tohru / Okamoto, Nobuhiko / Ikeda, Tsunehiko

    Case reports in ophthalmology

    2018  Volume 9, Issue 1, Page(s) 102–107

    Abstract: Purpose: To report a case of fundus oculi albinoticus diagnosed as Angelman syndrome (AS) via genetic testing.: Case report: This study reports on a 4-year-old boy. Since he had been having respiratory disturbance since birth, he underwent a complete ...

    Abstract Purpose: To report a case of fundus oculi albinoticus diagnosed as Angelman syndrome (AS) via genetic testing.
    Case report: This study reports on a 4-year-old boy. Since he had been having respiratory disturbance since birth, he underwent a complete physical examination to investigate the cause. The results indicated that he had various brain congenital abnormalities, such as a thin corpus callosum, as well as hydronephrosis, an atrial septal defect, and skin similar to patients with fundus oculi albinoticus. Examination revealed bilateral fundus oculi albinoticus, mild iridic hypopigmentation, optic atrophy, and poor visual tracking. Genetic testing revealed a deletion in the Prader-Willi syndrome/AS region on chromosome 15, and together with the results of methylation analysis, his condition was diagnosed as AS. Follow-up examinations revealed no change in the fundus oculi albinoticus and optic atrophy, nor did they indicate poor visual tracking.
    Conclusions: When fundus oculi albinoticus and optic atrophy are observed in patients with multiple malformations, AS should be considered as a differential diagnosis.
    Language English
    Publishing date 2018-02-01
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2577666-6
    ISSN 1663-2699
    ISSN 1663-2699
    DOI 10.1159/000485964
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Idiopathic remitting seronegative symmetrical synovitis with pitting edema syndrome associated with bilateral pleural and pericardial effusions: a case report.

    Yanamoto, Shozaburo / Fukae, Jiro / Fukiyama, Yurie / Fujioka, Shinsuke / Ouma, Shinji / Tsuboi, Yoshio

    Journal of medical case reports

    2016  Volume 10, Page(s) 198

    Abstract: Background: Remitting seronegative symmetrical synovitis with pitting edema syndrome is characterized by symmetrical synovitis with pitting edema in the dorsum of the hands or feet. Most cases of remitting seronegative symmetrical synovitis with pitting ...

    Abstract Background: Remitting seronegative symmetrical synovitis with pitting edema syndrome is characterized by symmetrical synovitis with pitting edema in the dorsum of the hands or feet. Most cases of remitting seronegative symmetrical synovitis with pitting edema syndrome are idiopathic, but some are secondary to malignancy, autoimmune disease, or neurodegenerative disorders. Pleural and pericardial effusions are unusual complications in idiopathic remitting seronegative symmetrical synovitis with pitting edema syndrome.
    Case presentation: A 74-year-old Japanese woman presented to our hospital with arthralgia and pitting edema in her feet. She had pain in multiple joints, peripheral edema, and a markedly elevated erythrocyte sedimentation rate. Enhanced computed tomography and laboratory data showed no evidence of malignancy. These findings suggested that she had idiopathic remitting seronegative symmetrical synovitis with pitting edema syndrome. She also developed respiratory distress because of bilateral pleural and pericardial effusions. Laboratory data showed that serum vascular endothelial growth factor and interleukin-6 were significantly elevated. After administration of steroids, her pleural and pericardial effusions decreased and finally disappeared. Furthermore, vascular endothelial growth factor and interleukin-6 decreased when the pleural and pericardial effusions disappeared.
    Conclusions: Here we report the case of a patient with idiopathic remitting seronegative symmetrical synovitis with pitting edema syndrome associated with life-threatening complications, including bilateral pleural and pericardial effusions during the course of the illness, which led to respiratory failure and atrial fibrillation. Elevated vascular endothelial growth factor and interleukin-6 may be associated with the cause of pleural and pericardial effusions in idiopathic remitting seronegative symmetrical synovitis with pitting edema syndrome.
    MeSH term(s) Adrenal Cortex Hormones/therapeutic use ; Aged ; Diagnosis, Differential ; Edema/complications ; Edema/diagnosis ; Edema/drug therapy ; Female ; Humans ; Pericardial Effusion/complications ; Pericardial Effusion/diagnosis ; Pericardial Effusion/drug therapy ; Pleural Effusion/complications ; Pleural Effusion/diagnosis ; Pleural Effusion/drug therapy ; Syndrome ; Synovitis/complications ; Synovitis/diagnosis ; Synovitis/drug therapy
    Chemical Substances Adrenal Cortex Hormones
    Language English
    Publishing date 2016-07-20
    Publishing country England
    Document type Case Reports ; Journal Article
    ZDB-ID 2269805-X
    ISSN 1752-1947 ; 1752-1947
    ISSN (online) 1752-1947
    ISSN 1752-1947
    DOI 10.1186/s13256-016-0983-7
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  6. Article: Complete Recovery from Blindness in Case of Compressive Optic Neuropathy due to Unruptured Anterior Cerebral Artery Aneurysm.

    Fukiyama, Yurie / Oku, Hidehiro / Hashimoto, Yusuke / Nishikawa, Yuko / Tonari, Masahiro / Sugasawa, Jun / Miyachi, Shigeru / Ikeda, Tsunehiko

    Case reports in ophthalmology

    2017  Volume 8, Issue 1, Page(s) 157–162

    Abstract: It is not common for an isolated visual symptom to be the first indication of an aneurysm compressing the optic nerve. The compression can lead to blindness, and a recovery from the blindness is rare. We report a female with a left painless optic ... ...

    Abstract It is not common for an isolated visual symptom to be the first indication of an aneurysm compressing the optic nerve. The compression can lead to blindness, and a recovery from the blindness is rare. We report a female with a left painless optic neuropathy caused by an unruptured anterior cerebral artery aneurysm. The patient had a temporal hemianopic visual field defect, which progressed to blindness in the left eye, while the right visual function was not affected. A coil embolization of the aneurysm completely restored her visual acuity to 20/20. These findings suggest that aneurysmal lesions should be ruled out in case of unilateral optic neuropathy with hemianopic visual field defects and progressive visual loss.
    Language English
    Publishing date 2017-03-07
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2577666-6
    ISSN 1663-2699
    ISSN 1663-2699
    DOI 10.1159/000458753
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  7. Article: A Case of Fundus Oculi Albinoticus Diagnosed as Angelman Syndrome by Genetic Testing

    Fukiyama, Yurie / Tonari, Masahiro / Matsuo, Junko / Oku, Hidehiro / Sugasawa, Jun / Shimakawa, Shuichi / Ogihara, Tohru / Okamoto, Nobuhiko / Ikeda, Tsunehiko

    Case Reports in Ophthalmology

    2018  Volume 9, Issue 1, Page(s) 108–113

    Abstract: Purpose: To report a case of fundus oculi albinoticus diagnosed as Angelman syndrome (AS) via genetic testing. Case Report: This study reports on a 4-year-old boy. Since he had been having respiratory disturbance since birth, he underwent a complete ... ...

    Institution Department of Ophthalmology, Osaka Medical College, Takatsuki-City, Japan
    Department of Pediatrics, Osaka Medical College, Takatsuki-City, Japan
    Department of Neonatology, Osaka Medical College, Takatsuki-City, Japan
    Department of Medical Genetics, Osaka Women’s and Children’s Hospital, Izumi-City, Japan
    Abstract Purpose: To report a case of fundus oculi albinoticus diagnosed as Angelman syndrome (AS) via genetic testing. Case Report: This study reports on a 4-year-old boy. Since he had been having respiratory disturbance since birth, he underwent a complete physical examination to investigate the cause. The results indicated that he had various brain congenital abnormalities, such as a thin corpus callosum, as well as hydronephrosis, an atrial septal defect, and skin similar to patients with fundus oculi albinoticus. Examination revealed bilateral fundus oculi albinoticus, mild iridic hypopigmentation, optic atrophy, and poor visual tracking. Genetic testing revealed a deletion in the Prader-Willi syndrome/AS region on chromosome 15, and together with the results of methylation analysis, his condition was diagnosed as AS. Follow-up examinations revealed no change in the fundus oculi albinoticus and optic atrophy, nor did they indicate poor visual tracking. Conclusions: When fundus oculi albinoticus and optic atrophy are observed in patients with multiple malformations, AS should be considered as a differential diagnosis.
    Keywords Angelman syndrome ; Fundus oculi albinoticus ; Optic atrophy ; Congenital anomaly ; Chromosome 15
    Language English
    Publishing date 2018-02-01
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Case Report ; This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC).
    ZDB-ID 2577666-6
    ISSN 1663-2699 ; 1663-2699
    ISSN (online) 1663-2699
    ISSN 1663-2699
    DOI 10.1159/000485964
    Database Karger publisher's database

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  8. Article: Complete Recovery from Blindness in Case of Compressive Optic Neuropathy due to Unruptured Anterior Cerebral Artery Aneurysm

    Fukiyama, Yurie / Oku, Hidehiro / Hashimoto, Yusuke / Nishikawa, Yuko / Tonari, Masahiro / Sugasawa, Jun / Miyachi, Shigeru / Ikeda, Tsunehiko

    Case Reports in Ophthalmology

    2017  Volume 8, Issue 1, Page(s) 157–162

    Abstract: It is not common for an isolated visual symptom to be the first indication of an aneurysm compressing the optic nerve. The compression can lead to blindness, and a recovery from the blindness is rare. We report a female with a left painless optic ... ...

    Institution Department of Ophthalmology, Osaka Medical College, Osaka, Japan
    Department of Neurosurgery, Osaka Medical College, Osaka, Japan
    Abstract It is not common for an isolated visual symptom to be the first indication of an aneurysm compressing the optic nerve. The compression can lead to blindness, and a recovery from the blindness is rare. We report a female with a left painless optic neuropathy caused by an unruptured anterior cerebral artery aneurysm. The patient had a temporal hemianopic visual field defect, which progressed to blindness in the left eye, while the right visual function was not affected. A coil embolization of the aneurysm completely restored her visual acuity to 20/20. These findings suggest that aneurysmal lesions should be ruled out in case of unilateral optic neuropathy with hemianopic visual field defects and progressive visual loss.
    Keywords Compressive optic neuropathy ; Hemianopic visual field defects ; Anterior cerebral artery aneurysm
    Language English
    Publishing date 2017-03-07
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Case Report ; This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC).
    ZDB-ID 2577666-6
    ISSN 1663-2699 ; 1663-2699
    ISSN (online) 1663-2699
    ISSN 1663-2699
    DOI 10.1159/000458753
    Database Karger publisher's database

    Full text online

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