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  1. Book ; Online ; E-Book: The biology of glial cells: recent advances

    Patro, Ishan / Seth, Pankaj / Patro, Nisha / Tandon, Prakash Narain

    2022  

    Author's details Ishan Patro, Pankaj Seth, Nisha Patro, Prakash Narain Tandon editors
    Keywords Neurosciences ; Nervous system—Diseases ; Developmental neurobiology ; Neuroimmunology
    Language English
    Size 1 Online-Ressource (xxxiv, 745 Seiten), Illustrationen, Diagramme
    Publisher Springer
    Publishing place Singapore
    Publishing country Singapore
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021338276
    ISBN 978-981-16-8313-8 ; 9789811683121 ; 981-16-8313-1 ; 9811683123
    DOI 10.1007/978-981-16-8313-8
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Percutaneous Ultrasound-Guided Aspiration of an Intracranial Abscess in a Neonate.

    Seth, Raghav / Yadav, Ajit / Thakur, Anup / Garg, Pankaj / Gupta, Arun

    Journal of vascular and interventional radiology : JVIR

    2024  Volume 35, Issue 4, Page(s) 636–637

    MeSH term(s) Infant, Newborn ; Humans ; Abscess ; Suction ; Ultrasonography ; Ultrasonography, Interventional ; Drainage
    Language English
    Publishing date 2024-03-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1137756-2
    ISSN 1535-7732 ; 1051-0443
    ISSN (online) 1535-7732
    ISSN 1051-0443
    DOI 10.1016/j.jvir.2023.12.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Insights Into the Role of Mortalin in Alzheimer's Disease, Parkinson's Disease, and HIV-1-Associated Neurocognitive Disorders.

    Priyanka / Seth, Pankaj

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 903031

    Abstract: Mortalin is a chaperone protein that regulates physiological functions of cells. Its multifactorial role allows cells to survive pathological conditions. Pharmacological, chemical, and siRNA-mediated downregulation of mortalin increases oxidative stress, ...

    Abstract Mortalin is a chaperone protein that regulates physiological functions of cells. Its multifactorial role allows cells to survive pathological conditions. Pharmacological, chemical, and siRNA-mediated downregulation of mortalin increases oxidative stress, mitochondrial dysfunction leading to unregulated inflammation. In addition to its well-characterized function in controlling oxidative stress, mitochondrial health, and maintaining physiological balance, recent evidence from human brain autopsies and cell culture-based studies suggests a critical role of mortalin in attenuating the damage seen in several neurodegenerative diseases. Overexpression of mortalin provides an important line of defense against accumulated proteins, inflammation, and neuronal loss, a key characteristic feature observed in neurodegeneration. Neurodegenerative diseases are a group of progressive disorders, sharing pathological features in Alzheimer's disease, Parkinson's disease, multiple sclerosis, and HIV-associated neurocognitive disorder. Aggregation of insoluble amyloid beta-proteins and neurofibrillary tangles in Alzheimer's disease are among the leading cause of neuropathology in the brain. Parkinson's disease is characterized by the degeneration of dopamine neurons in substantia nigra pars compacta. A substantial synaptic loss leading to cognitive decline is the hallmark of HIV-associated neurocognitive disorder (HAND). Brain autopsies and cell culture studies showed reduced expression of mortalin in Alzheimer's, Parkinson's, and HAND cases and deciphered the important role of mortalin in brain cells. Here, we discuss mortalin and its regulation and describe how neurotoxic conditions alter the expression of mortalin and modulate its functions. In addition, we also review the neuroprotective role of mortalin under neuropathological conditions. This knowledge showcases the importance of mortalin in diverse brain functions and offers new opportunities for the development of therapeutic targets that can modulate the expression of mortalin using chemical compounds.
    Language English
    Publishing date 2022-07-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.903031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Insights Into the Role of Mortalin in Alzheimer’s Disease, Parkinson’s Disease, and HIV-1-Associated Neurocognitive Disorders

    Priyanka / Pankaj Seth

    Frontiers in Cell and Developmental Biology, Vol

    2022  Volume 10

    Abstract: Mortalin is a chaperone protein that regulates physiological functions of cells. Its multifactorial role allows cells to survive pathological conditions. Pharmacological, chemical, and siRNA-mediated downregulation of mortalin increases oxidative stress, ...

    Abstract Mortalin is a chaperone protein that regulates physiological functions of cells. Its multifactorial role allows cells to survive pathological conditions. Pharmacological, chemical, and siRNA-mediated downregulation of mortalin increases oxidative stress, mitochondrial dysfunction leading to unregulated inflammation. In addition to its well-characterized function in controlling oxidative stress, mitochondrial health, and maintaining physiological balance, recent evidence from human brain autopsies and cell culture–based studies suggests a critical role of mortalin in attenuating the damage seen in several neurodegenerative diseases. Overexpression of mortalin provides an important line of defense against accumulated proteins, inflammation, and neuronal loss, a key characteristic feature observed in neurodegeneration. Neurodegenerative diseases are a group of progressive disorders, sharing pathological features in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and HIV-associated neurocognitive disorder. Aggregation of insoluble amyloid beta-proteins and neurofibrillary tangles in Alzheimer’s disease are among the leading cause of neuropathology in the brain. Parkinson’s disease is characterized by the degeneration of dopamine neurons in substantia nigra pars compacta. A substantial synaptic loss leading to cognitive decline is the hallmark of HIV-associated neurocognitive disorder (HAND). Brain autopsies and cell culture studies showed reduced expression of mortalin in Alzheimer’s, Parkinson’s, and HAND cases and deciphered the important role of mortalin in brain cells. Here, we discuss mortalin and its regulation and describe how neurotoxic conditions alter the expression of mortalin and modulate its functions. In addition, we also review the neuroprotective role of mortalin under neuropathological conditions. This knowledge showcases the importance of mortalin in diverse brain functions and offers new opportunities for the development of therapeutic targets that can modulate the expression of ...
    Keywords mortalin ; HIV-human immunodeficiency virus ; Alzheimer’s disease ; viral infection ; Parkinson’s disease ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Zika virus E protein modulates functions of human brain microvascular endothelial cells and astrocytes: implications on blood-brain barrier properties.

    Kaur, Guneet / Pant, Pallavi / Bhagat, Reshma / Seth, Pankaj

    Frontiers in cellular neuroscience

    2023  Volume 17, Page(s) 1173120

    Abstract: Neurotropic viruses can cross the otherwise dynamically regulated blood-brain barrier (BBB) and affect the brain cells. Zika virus (ZIKV) is an enveloped ... ...

    Abstract Neurotropic viruses can cross the otherwise dynamically regulated blood-brain barrier (BBB) and affect the brain cells. Zika virus (ZIKV) is an enveloped neurotropic
    Language English
    Publishing date 2023-07-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1173120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Interplay Between Zika Virus-Induced Autophagy and Neural Stem Cell Fate Determination.

    Bindu / Pandey, Hriday Shanker / Seth, Pankaj

    Molecular neurobiology

    2023  

    Abstract: The Zika virus (ZIKV) outbreaks and its co-relation with microcephaly have become a global health concern. It is primarily transmitted by a mosquito, but can also be transmitted from an infected mother to her fetus causing impairment in brain development, ...

    Abstract The Zika virus (ZIKV) outbreaks and its co-relation with microcephaly have become a global health concern. It is primarily transmitted by a mosquito, but can also be transmitted from an infected mother to her fetus causing impairment in brain development, leading to microcephaly. However, the underlying molecular mechanism of ZIKV-induced microcephaly is poorly understood. In this study, we explored the role of ZIKV non-structural protein NS4A and NS4B in ZIKV pathogenesis in a well-characterized primary culture of human fetal neural stem cells (fNSCs). We observed that the co-transfection of NS4A and NS4B altered the neural stem cell fate by arresting proliferation and inducing premature neurogenesis. NS4A + NS4B transfection in fNSCs increased autophagy and dysregulated notch signaling. Further, it also altered the regulation of downstream genes controlling cell proliferation. Additionally, we reported that 3 methyl-adenine (3-MA), a potent autophagy inhibitor, attenuated the deleterious effects of NS4A and NS4B as evidenced by the rescue in Notch1 expression, enhanced proliferation, and reduced premature neurogenesis. Our attempts to understand the mechanism of autophagy induction indicate the involvement of mitochondrial fission and ROS. Collectively, our findings highlight the novel role of NS4A and NS4B in mediating NSC fate alteration through autophagy-mediated notch degradation. The study also helps to advance our understanding of ZIKV-induced neuropathogenesis and suggests autophagy as a potential target for anti-ZIKV therapeutic intervention.
    Language English
    Publishing date 2023-11-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03704-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Potential role of lncRNA in impairing cellular properties of human neural progenitor cells following exposure to Zika virus E protein.

    Arora, Himali / Prajapati, Bharat / Seth, Pankaj

    Experimental neurology

    2023  Volume 368, Page(s) 114493

    Abstract: Zika virus (ZIKV) infection during the first trimester of the pregnancy may lead to Congenital zika syndrome in the neonates. The viral infection hampers foetal brain development and causes microcephaly. Human neural progenitor cells (hNPCs) play an ... ...

    Abstract Zika virus (ZIKV) infection during the first trimester of the pregnancy may lead to Congenital zika syndrome in the neonates. The viral infection hampers foetal brain development and causes microcephaly. Human neural progenitor cells (hNPCs) play an important role in brain development, however they are highly susceptible to ZIKV infection. In this study, we elucidated the molecular mechanisms that lead to cellular alterations in hNPCs due to ZIKV E-protein. We investigated proliferation, differentiation, migration and inflammation in hNPCs, which may lead to microcephaly. In our study, we found that ZIKV E-protein causes cell cycle arrest, decrease in proliferation and increase in mitotic length of the dividing hNPCs. We observed CyclinD1 and upstream molecules (p21 and p53) of the pathway are dysregulated, and intracellular calcium at basal level as well as upon ATP stimulation were reduced following over expression of ZIKV E-protein. ZIKV E-protein transfected hNPCs exhibited pre-mature differentiation with pro-neural genes upregulated. Furthermore, ZIKV E-protein disrupted migrational properties of hNPCs and caused elevated levels of inflammatory chemokines and cytokines. To gain insights into molecular mechanisms of these effects on hNPCs, we explored the possible involvement of long non coding RNAs in ZIKV neuropathogenesis. We have shortlisted lncRNAs associated with differentially expressed genes from publicly available transcriptomic data and found some of those lncRNAs are differentially expressed upon E-protein transfection of hNPCs. Gene ontology analysis suggest these lncRNAs play an important role in regulation of viral life cycle, host's defence response and cell proliferation.
    MeSH term(s) Pregnancy ; Female ; Infant, Newborn ; Humans ; Zika Virus/genetics ; Zika Virus Infection/metabolism ; Zika Virus Infection/pathology ; RNA, Long Noncoding/genetics ; Microcephaly/pathology ; Transcription Factors ; Stem Cells/metabolism
    Chemical Substances RNA, Long Noncoding ; Transcription Factors
    Language English
    Publishing date 2023-07-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2023.114493
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 184: Show issues Location:
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  8. Article ; Online: Editorial (Thematic Issue: NeuroAIDS: Past, Present and Future).

    Seth, Pankaj

    Current HIV research

    2016  Volume 14, Issue 5, Page(s) 372

    MeSH term(s) Acquired Immunodeficiency Syndrome ; Humans
    Language English
    Publishing date 2016-10-14
    Publishing country Netherlands
    Document type Introductory Journal Article
    ZDB-ID 2192348-6
    ISSN 1873-4251 ; 1570-162X
    ISSN (online) 1873-4251
    ISSN 1570-162X
    DOI 10.2174/1570162x1405161027113704
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6102: Show issues Location:
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  9. Article ; Online: Hypoxia-Induced miR-101 Impairs Endothelial Barrier Integrity Through Altering VE-Cadherin and Claudin-5.

    Shukla, Astha / Bhardwaj, Utkarsh / Apoorva / Seth, Pankaj / Singh, Sunit K

    Molecular neurobiology

    2023  Volume 61, Issue 3, Page(s) 1807–1817

    Abstract: Stroke is a life-threatening medical condition across the world that adversely affects the integrity of the blood-brain barrier (BBB). The brain microvascular endothelial cells are the important constituent of the BBB. These cells line the blood vessels ... ...

    Abstract Stroke is a life-threatening medical condition across the world that adversely affects the integrity of the blood-brain barrier (BBB). The brain microvascular endothelial cells are the important constituent of the BBB. These cells line the blood vessels and form a semipermeable barrier. Disruptions in adherens junction and tight junction proteins of brain microvascular endothelial cells compromise the integrity of BBB. The Vascular Endothelial (VE)-cadherin is an integral adherens junction protein required for the establishment and maintenance of the endothelial barrier integrity. This study aims to investigate the role of miRNA in hypoxia-induced endothelial barrier disruption. In this study, brain endothelial cells were exposed to hypoxic conditions for different time points. Western blotting, overexpression and knockdown of miRNA, real-time PCR, TEER, and sodium fluorescein assay were used to examine the effect of hypoxic conditions on brain endothelial cells. Hypoxic exposure was validated using HIF-1α protein. Exposure to hypoxic conditions resulted to a significant decrease in endothelial barrier resistance and an increase in sodium fluorescein migration across the endothelial barrier. Reduction in endothelial barrier resistance demonstrated compromised barrier integrity, whereas the increase in migration of sodium fluorescein across the barrier indicated the increase in barrier permeability. The present study revealed microRNA-101 decreases the expression of VE-cadherin and claudin-5 in brain endothelial cells exposed to the hypoxic conditions.
    MeSH term(s) Humans ; Endothelial Cells/metabolism ; Claudin-5/genetics ; Claudin-5/metabolism ; Fluorescein/metabolism ; Fluorescein/pharmacology ; Cadherins/genetics ; Cadherins/metabolism ; Blood-Brain Barrier/metabolism ; Hypoxia/metabolism ; MicroRNAs/metabolism ; Antigens, CD
    Chemical Substances cadherin 5 ; Claudin-5 ; Fluorescein (TPY09G7XIR) ; Cadherins ; MicroRNAs ; MIRN101 microRNA, human ; Antigens, CD
    Language English
    Publishing date 2023-09-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03662-8
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    Zs.A 2411: Show issues Location:
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  10. Article ; Online: Acute liver failure: a rare presentation of an adult-onset Still's disease.

    Mathur, Aadhar / Seth, Arihant / Gangwal, Pankaj / Pahadiya, Hans Raj / Mathur, Ajay / Goyal, Laxmikant

    Journal of gastrointestinal and liver diseases : JGLD

    2023  Volume 32, Issue 3, Page(s) 414–416

    MeSH term(s) Adult ; Humans ; Still's Disease, Adult-Onset/complications ; Still's Disease, Adult-Onset/diagnosis ; Still's Disease, Adult-Onset/drug therapy ; Liver Failure, Acute/diagnosis ; Liver Failure, Acute/etiology
    Language English
    Publishing date 2023-09-29
    Publishing country Romania
    Document type Case Reports ; Letter ; Comment
    ZDB-ID 2427021-0
    ISSN 1842-1121 ; 1841-8724
    ISSN (online) 1842-1121
    ISSN 1841-8724
    DOI 10.15403/jgld-5032
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    Zs.A 3825: Show issues Location:
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