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  1. Book: Targeting oral cancer

    Fribley, Andrew

    2016  

    Author's details Andrew M. Fribley ed
    Keywords Cancer Stem Cells ; Molecular Signaling ; UPR ; Biomarkers ; Surgical Management ; Chemotherapy ; Human Papillomavirus
    Language English
    Size X, 302 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place Cham u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT018924057
    ISBN 978-3-319-27645-8 ; 978-3-319-27647-2 ; 3-319-27645-X ; 3-319-27647-6
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2016 A 733 available for loan (reading room) Lesesaal EG

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  2. Article ; Online: HTS Identification of Activators and Inhibitors of Endoplasmic Reticulum (ER) Stress and the Unfolded Protein Response (UPR).

    Ghafouri, Mehrnoosh / Gauss, Chester B / Fribley, Andrew M

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2378, Page(s) 317–327

    Abstract: The identification of small molecules and natural product extracts that enhance or interfere with the productivity of protein folding in the endoplasmic reticulum (ER) has the potential to improve a wide variety of human pathologies. Every protein that ... ...

    Abstract The identification of small molecules and natural product extracts that enhance or interfere with the productivity of protein folding in the endoplasmic reticulum (ER) has the potential to improve a wide variety of human pathologies. Every protein that is destined for a lysosome, integral to the cell membrane, or secreted, is folded, post-translationally modified, and exported to the cytoplasm from the ER-Golgi complex. The following protocols have successfully employed several high-fidelity cell-based luciferase high-throughput screens (HTS) to identify activators and inhibitors of ER stress and the unfolded protein response (UPR).
    MeSH term(s) Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Chaperone BiP ; Endoplasmic Reticulum Stress ; Humans ; Protein Folding ; Unfolded Protein Response
    Chemical Substances Endoplasmic Reticulum Chaperone BiP
    Language English
    Publishing date 2022-01-05
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1732-8_20
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: The Mechanisms of Zinc Action as a Potent Anti-Viral Agent: The Clinical Therapeutic Implication in COVID-19.

    Prasad, Ananda S / Malysa, Agnes / Bepler, Gerold / Fribley, Andrew / Bao, Bin

    Antioxidants (Basel, Switzerland)

    2022  Volume 11, Issue 10

    Abstract: The pandemic of COVID-19 was caused by a novel coronavirus termed as SARS-CoV2 and is still ongoing with high morbidity and mortality rates in the whole world. The pathogenesis of COVID-19 is highly linked with over-active immune and inflammatory ... ...

    Abstract The pandemic of COVID-19 was caused by a novel coronavirus termed as SARS-CoV2 and is still ongoing with high morbidity and mortality rates in the whole world. The pathogenesis of COVID-19 is highly linked with over-active immune and inflammatory responses, leading to activated cytokine storm, which contribute to ARDS with worsen outcome. Currently, there is no effective therapeutic drug for the treatment of COVID-19. Zinc is known to act as an immune modulator, which plays an important role in immune defense system. Recently, zinc has been widely considered as an anti-inflammatory and anti-oxidant agent. Accumulating numbers of studies have revealed that zinc plays an important role in antiviral immunity in several viral infections. Several early clinical trials clearly indicate that zinc treatment remarkably decreased the severity of the upper respiratory infection of rhinovirus in humans. Currently, zinc has been used for the therapeutic intervention of COVID-19 in many different clinical trials. Several clinical studies reveal that zinc treatment using a combination of HCQ and zinc pronouncedly reduced symptom score and the rates of hospital admission and mortality in COVID-19 patients. These data support that zinc might act as an anti-viral agent in the addition to its anti-inflammatory and anti-oxidant properties for the adjuvant therapeutic intervention of COVID-19.
    Language English
    Publishing date 2022-09-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11101862
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: Targeting oral cancer

    Fribley, Andrew M

    2016  

    Author's details Andrew M. Fribley, editor
    MeSH term(s) Mouth Neoplasms/drug therapy ; Antineoplastic Agents/therapeutic use ; Molecular Targeted Therapy
    Language English
    Size x, 302 pages :, color illustrations
    Document type Book
    ISBN 9783319276458 ; 9783319276472 ; 331927645X ; 3319276476
    Database Catalogue of the US National Library of Medicine (NLM)

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  5. Article ; Online: Lipopolysaccharide induces placental mitochondrial dysfunction in murine and human systems by reducing MNRR1 levels via a TLR4-independent pathway.

    Purandare, Neeraja / Kunji, Yusef / Xi, Yue / Romero, Roberto / Gomez-Lopez, Nardhy / Fribley, Andrew / Grossman, Lawrence I / Aras, Siddhesh

    iScience

    2022  Volume 25, Issue 11, Page(s) 105342

    Abstract: Mitochondria play a key role in placental growth and development, and mitochondrial dysfunction is associated with inflammation in pregnancy pathologies. However, the mechanisms whereby placental mitochondria sense inflammatory signals are unknown. ... ...

    Abstract Mitochondria play a key role in placental growth and development, and mitochondrial dysfunction is associated with inflammation in pregnancy pathologies. However, the mechanisms whereby placental mitochondria sense inflammatory signals are unknown. Mitochondrial nuclear retrograde regulator 1 (MNRR1) is a bi-organellar protein responsible for mitochondrial function, including optimal induction of cellular stress-responsive signaling pathways. Here, in a lipopolysaccharide-induced model of systemic placental inflammation, we show that MNRR1 levels are reduced both in mouse placental tissues
    Language English
    Publishing date 2022-10-12
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.105342
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The MNRR1 activator nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice.

    Purandare, Neeraja / Gomez-Lopez, Nardhy / Arenas-Hernandez, Marcia / Galaz, Jose / Romero, Roberto / Xi, Yue / Fribley, Andrew M / Grossman, Lawrence I / Aras, Siddhesh

    Placenta

    2023  Volume 140, Page(s) 66–71

    Abstract: Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently reported that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, ... ...

    Abstract Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently reported that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, or PARK22), an important bi-organellar regulator of cellular function, are reduced in the context of inflammation and that genetic and pharmacological increases in MNRR1 levels can counter the inflammatory profile. Herein, we show that nitazoxanide, a clinically approved drug, is an activator of MNRR1 and abrogates preterm birth in a well-characterized murine model caused by intra-amniotic lipopolysaccharide (LPS) injection.
    MeSH term(s) Infant, Newborn ; Female ; Humans ; Animals ; Mice ; Premature Birth/prevention & control ; Lipopolysaccharides ; Nitro Compounds/adverse effects ; Inflammation/chemically induced ; Amniotic Fluid ; Chorioamnionitis ; DNA-Binding Proteins ; Transcription Factors/genetics
    Chemical Substances Lipopolysaccharides ; nitazoxanide (SOA12P041N) ; Nitro Compounds ; CHCHD2 protein, human ; DNA-Binding Proteins ; Transcription Factors
    Language English
    Publishing date 2023-07-08
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 603951-0
    ISSN 1532-3102 ; 0143-4004
    ISSN (online) 1532-3102
    ISSN 0143-4004
    DOI 10.1016/j.placenta.2023.07.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1578: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Lipopolysaccharide induces placental mitochondrial dysfunction in murine and human systems by reducing MNRR1 levels via a TLR4-independent pathway

    Neeraja Purandare / Yusef Kunji / Yue Xi / Roberto Romero / Nardhy Gomez-Lopez / Andrew Fribley / Lawrence I. Grossman / Siddhesh Aras

    iScience, Vol 25, Iss 11, Pp 105342- (2022)

    2022  

    Abstract: Summary: Mitochondria play a key role in placental growth and development, and mitochondrial dysfunction is associated with inflammation in pregnancy pathologies. However, the mechanisms whereby placental mitochondria sense inflammatory signals are ... ...

    Abstract Summary: Mitochondria play a key role in placental growth and development, and mitochondrial dysfunction is associated with inflammation in pregnancy pathologies. However, the mechanisms whereby placental mitochondria sense inflammatory signals are unknown. Mitochondrial nuclear retrograde regulator 1 (MNRR1) is a bi-organellar protein responsible for mitochondrial function, including optimal induction of cellular stress-responsive signaling pathways. Here, in a lipopolysaccharide-induced model of systemic placental inflammation, we show that MNRR1 levels are reduced both in mouse placental tissues in vivo and in human trophoblastic cell lines in vitro. MNRR1 reduction is associated with mitochondrial dysfunction, enhanced oxidative stress, and activation of pro-inflammatory signaling. Mechanistically, we uncover a non-conventional pathway independent of Toll-like receptor 4 (TLR4) that results in ATM kinase-dependent threonine phosphorylation that stabilizes mitochondrial protease YME1L1, which targets MNRR1. Enhancing MNRR1 levels abrogates the bioenergetic defect and induces an anti-inflammatory phenotype. We therefore propose MNRR1 as an anti-inflammatory therapeutic in placental inflammation.
    Keywords Cell biology ; Human metabolism ; Immunity ; Science ; Q
    Language English
    Publishing date 2022-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Head and neck fracture patterns associated with playground equipment use in the pediatric population.

    Johnson, Jared / Mehta, Neil / Lucas, Jordyn / Chung, Michael T / Hotaling, Jeffrey / Gonik, Nathan / Fribley, Andrew

    International journal of pediatric otorhinolaryngology

    2020  Volume 134, Page(s) 110031

    Language English
    Publishing date 2020-04-01
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 754501-0
    ISSN 1872-8464 ; 0165-5876
    ISSN (online) 1872-8464
    ISSN 0165-5876
    DOI 10.1016/j.ijporl.2020.110031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1507: Show issues Location:
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    Zs.MO 134: Show issues

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  9. Article ; Online: Disparities in impact of nasopharyngeal cancer: An analysis of global health burden.

    Ramsey, Tam / Hojjat, Houmehr / Yuhan, Brian / Svider, Peter F / Eloy, Jean Anderson / Folbe, Adam J / Raza, Syed Naweed / Fribley, Andrew M

    The Laryngoscope

    2019  Volume 129, Issue 11, Page(s) 2482–2486

    Abstract: Objectives: Nasopharyngeal carcinoma has a unique worldwide racial and geographic distribution. Our objective was to evaluate socioeconomic disparities in the burden of nasopharyngeal cancer (NPC) between endemic and nonendemic regions.: Methods: To ... ...

    Abstract Objectives: Nasopharyngeal carcinoma has a unique worldwide racial and geographic distribution. Our objective was to evaluate socioeconomic disparities in the burden of nasopharyngeal cancer (NPC) between endemic and nonendemic regions.
    Methods: To demonstrate trends regarding societal burden of NPC and socioeconomic development, national disability-adjusted life year (DALY) rates and human development indices (HDI) between 1990 and 2015 were evaluated. Countries were divided based on the endemic versus nonendemic presence of NPC and further analyzed by HDI status as specified by the United Nations Development Program. Gini coefficients and concentration index were used to evaluate global equality in NPC burden over this period.
    Results: Age-standardized DALYs dropped from 36.1 in 1990 to 26.5 in 2015 (26.6% decline) (r = -0.991, P < 0.001). Lower socioeconomic countries harbored greater NPC burden upon controlling by endemic and nonendemic regions, as demonstrated by progressively negative concentration indexes. Health inequality was greater in nonendemic countries than in endemic countries (P < 0.01).
    Conclusion: To our knowledge, this is the first study to investigate socioeconomic-related changes in NPC burden using statistical tools such as the Gini coefficient and concentration index. Although the burden of NPC has steadily decreased, there remain persistent inequalities associated with socioeconomic disparities. Nasopharyngeal cancer burden is more pronounced in countries with lower HDI. Our results reinforce the importance of increasing resources for developing countries and continuing inquiry into the screening, diagnosis, and management of NPC.
    Level of evidence: NA Laryngoscope, 129:2482-2486, 2019.
    MeSH term(s) Adult ; Aged ; Cost of Illness ; Endemic Diseases/statistics & numerical data ; Female ; Global Health/statistics & numerical data ; Health Status Disparities ; Humans ; Male ; Middle Aged ; Nasopharyngeal Neoplasms/epidemiology ; Quality-Adjusted Life Years ; Socioeconomic Factors
    Language English
    Publishing date 2019-03-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80180-x
    ISSN 1531-4995 ; 0023-852X
    ISSN (online) 1531-4995
    ISSN 0023-852X
    DOI 10.1002/lary.27532
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Evidence for Increased Response to Induced Endoplasmic Reticulum Stress in Myeloid Cells in Acquired Aplastic Anemia.

    Sidhu, Alpa / Callaghan, Michael U / Gadgeel, Manisha S / Buck, Steven A / Fribley, Andrew M / Savaşan, Süreyya

    Journal of pediatric hematology/oncology

    2017  Volume 39, Issue 3, Page(s) e163–e166

    Abstract: Autoimmune response targeting the hematopoietic stem cells highlights the current understanding of acquired aplastic anemia (AAA) pathogenesis. Upregulation of the unfolded protein response is the cell's rejoinder to a variety of stresses, which either ... ...

    Abstract Autoimmune response targeting the hematopoietic stem cells highlights the current understanding of acquired aplastic anemia (AAA) pathogenesis. Upregulation of the unfolded protein response is the cell's rejoinder to a variety of stresses, which either result in restoring homeostasis or cell death by increased expression of the transcription factor C/EBP homologous protein. We hypothesized that there is an inherent increased sensitivity to various cellular stressors, including the ones that target endoplasmic reticulum (ER) in AAA leading to a decreased proliferation and potentially contributing to susceptibility to autologous cytotoxicity. Using archived bone marrow aspirate samples, we demonstrate that the culture-expanded AAA myeloid cells have an increased response to ER stress induced by tunicamycin leading to decreased cell proliferation. Within the AAA myeloid samples, we show that the disease status, active versus response to therapy at the time of sampling does not alter the ER stress response. This is the first report, which provides evidence for an inherent defective stress control in the myeloid cells as a possible mechanism of evolution of the disease process in AAA.
    MeSH term(s) Anemia, Aplastic/etiology ; Anemia, Aplastic/pathology ; Anti-Bacterial Agents/pharmacology ; Bone Marrow/pathology ; Cell Death ; Cell Proliferation/drug effects ; Cells, Cultured ; Endoplasmic Reticulum Stress/physiology ; Humans ; Myeloid Cells/pathology ; Tunicamycin/pharmacology ; Unfolded Protein Response
    Chemical Substances Anti-Bacterial Agents ; Tunicamycin (11089-65-9)
    Language English
    Publishing date 2017-03-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1231152-2
    ISSN 1536-3678 ; 1077-4114 ; 0192-8562
    ISSN (online) 1536-3678
    ISSN 1077-4114 ; 0192-8562
    DOI 10.1097/MPH.0000000000000810
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1537: Show issues Location:
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