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  1. Article: Clinical Trials in Alzheimer's Disease: A Hurdle in the Path of Remedy.

    Oxford, Alexandra E / Stewart, Erica S / Rohn, Troy T

    International journal of Alzheimer's disease

    2020  Volume 2020, Page(s) 5380346

    Abstract: ... test "disease-modifying drugs," i.e., therapeutic agents that specifically modify pathological features ...

    Abstract Human clinical trials seek to ameliorate the disease states and symptomatic progression of illnesses that, as of yet, are largely untreatable according to clinical standards. Ideally, clinical trials test "disease-modifying drugs," i.e., therapeutic agents that specifically modify pathological features or molecular bases of the disease and would presumably have a large impact on disease progression. In the case of Alzheimer's disease (AD), however, this approach appears to have stalled progress in the successful development of clinically useful therapies. For the last 25 years, clinical trials involving AD have centered on beta-amyloid (A
    Language English
    Publishing date 2020-04-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2573333-3
    ISSN 2090-0252 ; 2090-8024
    ISSN (online) 2090-0252
    ISSN 2090-8024
    DOI 10.1155/2020/5380346
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Endothelial Cell Contributions to COVID-19.

    Oxford, Alexandra E / Halla, Fabio / Robertson, Evan B / Morrison, Brad E

    Pathogens (Basel, Switzerland)

    2020  Volume 9, Issue 10

    Abstract: Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual ... ...

    Abstract Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual clinical presentation with regard to other related coronaviruses. Recent reports suggest that SARS-CoV-2, unlike other related viruses, infects and replicates within endothelial cells, which may explain a significant portion of the observed clinical pathology. Likewise, mounting evidence associates vascular and endothelial cell dysfunction with increased mortality. This review focuses on understanding how endothelial cell pathology is caused by SARS-CoV-2 at the molecular and cellular levels and how these events relate to COVID-19. A detailed examination of current knowledge regarding canonical inflammatory reaction pathways as well as alteration of endothelial cell-derived exosomes and transdifferentiation by SARS-CoV-2 is included in this assessment. Additionally, given an understanding of endothelial contributions to COVID-19, potential therapeutic aims are discussed, particularly as would affect endothelial function and pathology.
    Keywords covid19
    Language English
    Publishing date 2020-09-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens9100785
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Neuropathies of Stüve-Wiedemann Syndrome due to mutations in leukemia inhibitory factor receptor (LIFR) gene.

    Oxford, Alexandra E / Jorcyk, Cheryl L / Oxford, Julia Thom

    Journal of neurology & neuromedicine

    2016  Volume 1, Issue 7, Page(s) 37–44

    Abstract: Stüve-Wiedemann syndrome (STWS; OMIM #610559) is a rare disease that results in dysfunction of the autonomic nervous system, which controls involuntary processes such as breathing rate and body temperature. In infants, this can result in respiratory ... ...

    Abstract Stüve-Wiedemann syndrome (STWS; OMIM #610559) is a rare disease that results in dysfunction of the autonomic nervous system, which controls involuntary processes such as breathing rate and body temperature. In infants, this can result in respiratory distress, feeding and swallowing difficulties, and hyperthermic episodes. Individuals may sweat excessively when body temperature is not elevated. Additionally, individuals have reduced ability to feel pain and may lose reflexes such as the corneal reflex that normally causes one to blink, and the patellar reflex resulting in the knee-jerk. STWS usually results in infant mortality, yet some STWS patients survive into early adulthood. STWS is caused by a mutation in the leukemia inhibitory factor receptor (
    Language English
    Publishing date 2016-11-11
    Publishing country United States
    Document type Journal Article
    ISSN 2572-942X
    ISSN 2572-942X
    DOI 10.29245/2572.942x/2016/7.1068
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  4. Article: Endothelial Cell Contributions to COVID-19

    Oxford, Alexandra E / Halla, Fabio / Robertson, Evan B / Morrison, Brad E

    Pathogens. 2020 Sept. 25, v. 9, no. 10

    2020  

    Abstract: Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual ... ...

    Abstract Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual clinical presentation with regard to other related coronaviruses. Recent reports suggest that SARS-CoV-2, unlike other related viruses, infects and replicates within endothelial cells, which may explain a significant portion of the observed clinical pathology. Likewise, mounting evidence associates vascular and endothelial cell dysfunction with increased mortality. This review focuses on understanding how endothelial cell pathology is caused by SARS-CoV-2 at the molecular and cellular levels and how these events relate to COVID-19. A detailed examination of current knowledge regarding canonical inflammatory reaction pathways as well as alteration of endothelial cell-derived exosomes and transdifferentiation by SARS-CoV-2 is included in this assessment. Additionally, given an understanding of endothelial contributions to COVID-19, potential therapeutic aims are discussed, particularly as would affect endothelial function and pathology.
    Keywords Coronavirus infections ; Severe acute respiratory syndrome coronavirus ; endothelial cells ; exosomes ; histology ; knowledge ; mortality ; pathogens ; therapeutics ; viruses
    Language English
    Dates of publication 2020-0925
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    Note NAL-light
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens9100785
    Database NAL-Catalogue (AGRICOLA)

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  5. Article: Endothelial Cell Contributions to COVID-19

    Oxford, Alexandra E. / Halla, Fabio / Robertson, Evan B. / Morrison, Brad E.

    Pathogens

    Abstract: Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive Coronavirus disease 2019 (COVID-19) caused by this virus has unusual ... ...

    Abstract Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive Coronavirus disease 2019 (COVID-19) caused by this virus has unusual clinical presentation with regard to other related coronaviruses Recent reports suggest that SARS-CoV-2, unlike other related viruses, infects and replicates within endothelial cells, which may explain a significant portion of the observed clinical pathology Likewise, mounting evidence associates vascular and endothelial cell dysfunction with increased mortality This review focuses on understanding how endothelial cell pathology is caused by SARS-CoV-2 at the molecular and cellular levels and how these events relate to COVID-19 A detailed examination of current knowledge regarding canonical inflammatory reaction pathways as well as alteration of endothelial cell-derived exosomes and transdifferentiation by SARS-CoV-2 is included in this assessment Additionally, given an understanding of endothelial contributions to COVID-19, potential therapeutic aims are discussed, particularly as would affect endothelial function and pathology
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #798301
    Database COVID19

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  6. Article ; Online: Endothelial Cell Contributions to COVID-19

    Alexandra E. Oxford / Fabio Halla / Evan B. Robertson / Brad E. Morrison

    Pathogens, Vol 9, Iss 785, p

    2020  Volume 785

    Abstract: Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual ... ...

    Abstract Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual clinical presentation with regard to other related coronaviruses. Recent reports suggest that SARS-CoV-2, unlike other related viruses, infects and replicates within endothelial cells, which may explain a significant portion of the observed clinical pathology. Likewise, mounting evidence associates vascular and endothelial cell dysfunction with increased mortality. This review focuses on understanding how endothelial cell pathology is caused by SARS-CoV-2 at the molecular and cellular levels and how these events relate to COVID-19. A detailed examination of current knowledge regarding canonical inflammatory reaction pathways as well as alteration of endothelial cell-derived exosomes and transdifferentiation by SARS-CoV-2 is included in this assessment. Additionally, given an understanding of endothelial contributions to COVID-19, potential therapeutic aims are discussed, particularly as would affect endothelial function and pathology.
    Keywords COVID-19 ; coronavirus ; SARS-CoV-2 ; endothelial ; vascular ; transdifferentiation ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  7. Book ; Online: Endothelial Cell Contributions to COVID-19

    Oxford, Alexandra E. / Halla, Fabio / Robertson, Evan B. / Morrison, Brad E.

    Biology Faculty Publications and Presentations

    2020  

    Abstract: Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual ... ...

    Abstract Understanding of the clinical, histological and molecular features of the novel coronavirus 2019 (Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)) has remained elusive. Coronavirus disease 2019 (COVID-19) caused by this virus has unusual clinical presentation with regard to other related coronaviruses. Recent reports suggest that SARS-CoV-2, unlike other related viruses, infects and replicates within endothelial cells, which may explain a significant portion of the observed clinical pathology. Likewise, mounting evidence associates vascular and endothelial cell dysfunction with increased mortality. This review focuses on understanding how endothelial cell pathology is caused by SARS-CoV-2 at the molecular and cellular levels and how these events relate to COVID-19. A detailed examination of current knowledge regarding canonical inflammatory reaction pathways as well as alteration of endothelial cell-derived exosomes and transdifferentiation by SARS-CoV-2 is included in this assessment. Additionally, given an understanding of endothelial contributions to COVID-19, potential therapeutic aims are discussed, particularly as would affect endothelial function and pathology.
    Keywords COVID-19 ; coronavirus ; SARS-CoV-2 ; endothelial ; vascular ; transdifferentiation ; Biology ; Immunology and Infectious Disease ; Virology ; covid19
    Subject code 610
    Publishing date 2020-10-01T07:00:00Z
    Publisher ScholarWorks
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  8. Article ; Online: Endoplasmic Reticulum Stress and Unfolded Protein Response in Cartilage Pathophysiology; Contributing Factors to Apoptosis and Osteoarthritis.

    Hughes, Alexandria / Oxford, Alexandra E / Tawara, Ken / Jorcyk, Cheryl L / Oxford, Julia Thom

    International journal of molecular sciences

    2017  Volume 18, Issue 3

    Abstract: Chondrocytes of the growth plate undergo apoptosis during the process of endochondral ossification, as well as during the progression of osteoarthritis. Although the regulation of this process is not completely understood, alterations in the precisely ... ...

    Abstract Chondrocytes of the growth plate undergo apoptosis during the process of endochondral ossification, as well as during the progression of osteoarthritis. Although the regulation of this process is not completely understood, alterations in the precisely orchestrated programmed cell death during development can have catastrophic results, as exemplified by several chondrodystrophies which are frequently accompanied by early onset osteoarthritis. Understanding the mechanisms that underlie chondrocyte apoptosis during endochondral ossification in the growth plate has the potential to impact the development of therapeutic applications for chondrodystrophies and associated early onset osteoarthritis. In recent years, several chondrodysplasias and collagenopathies have been recognized as protein-folding diseases that lead to endoplasmic reticulum stress, endoplasmic reticulum associated degradation, and the unfolded protein response. Under conditions of prolonged endoplasmic reticulum stress in which the protein folding load outweighs the folding capacity of the endoplasmic reticulum, cellular dysfunction and death often occur. However, unfolded protein response (UPR) signaling is also required for the normal maturation of chondrocytes and osteoblasts. Understanding how UPR signaling may contribute to cartilage pathophysiology is an essential step toward therapeutic modulation of skeletal disorders that lead to osteoarthritis.
    MeSH term(s) Age of Onset ; Animals ; Apoptosis ; Arthritis/etiology ; Arthritis/metabolism ; Arthritis/pathology ; Bone Morphogenetic Proteins/metabolism ; Calcification, Physiologic ; Cartilage/metabolism ; Cartilage/pathology ; Chondrocytes/metabolism ; Chondrocytes/pathology ; Chondrogenesis ; Collagen/genetics ; Collagen/metabolism ; Connective Tissue Diseases/etiology ; Connective Tissue Diseases/metabolism ; Connective Tissue Diseases/pathology ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Hearing Loss, Sensorineural/etiology ; Hearing Loss, Sensorineural/metabolism ; Hearing Loss, Sensorineural/pathology ; Humans ; Molecular Targeted Therapy ; Osteoarthritis/epidemiology ; Osteoarthritis/etiology ; Osteoarthritis/metabolism ; Osteoarthritis/pathology ; Osteoblasts/metabolism ; Retinal Detachment/etiology ; Retinal Detachment/metabolism ; Retinal Detachment/pathology ; Unfolded Protein Response
    Chemical Substances Bone Morphogenetic Proteins ; Collagen (9007-34-5)
    Language English
    Publishing date 2017-03-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms18030665
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Endoplasmic Reticulum Stress and Unfolded Protein Response in Cartilage Pathophysiology; Contributing Factors to Apoptosis and Osteoarthritis

    Alexandria Hughes / Alexandra E. Oxford / Ken Tawara / Cheryl L. Jorcyk / Julia Thom Oxford

    International Journal of Molecular Sciences, Vol 18, Iss 3, p

    2017  Volume 665

    Abstract: Chondrocytes of the growth plate undergo apoptosis during the process of endochondral ossification, as well as during the progression of osteoarthritis. Although the regulation of this process is not completely understood, alterations in the precisely ... ...

    Abstract Chondrocytes of the growth plate undergo apoptosis during the process of endochondral ossification, as well as during the progression of osteoarthritis. Although the regulation of this process is not completely understood, alterations in the precisely orchestrated programmed cell death during development can have catastrophic results, as exemplified by several chondrodystrophies which are frequently accompanied by early onset osteoarthritis. Understanding the mechanisms that underlie chondrocyte apoptosis during endochondral ossification in the growth plate has the potential to impact the development of therapeutic applications for chondrodystrophies and associated early onset osteoarthritis. In recent years, several chondrodysplasias and collagenopathies have been recognized as protein-folding diseases that lead to endoplasmic reticulum stress, endoplasmic reticulum associated degradation, and the unfolded protein response. Under conditions of prolonged endoplasmic reticulum stress in which the protein folding load outweighs the folding capacity of the endoplasmic reticulum, cellular dysfunction and death often occur. However, unfolded protein response (UPR) signaling is also required for the normal maturation of chondrocytes and osteoblasts. Understanding how UPR signaling may contribute to cartilage pathophysiology is an essential step toward therapeutic modulation of skeletal disorders that lead to osteoarthritis.
    Keywords chondrocyte ; osteoarthritis ; endoplasmic reticulum (ER) stress ; unfolded protein response ; endochondral ossification ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 612
    Language English
    Publishing date 2017-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  10. Article ; Online: A Fragment of Apolipoprotein E4 Leads to the Downregulation of a CXorf56 Homologue, a Novel ER-Associated Protein, and Activation of BV2 Microglial Cells.

    Pollock, Tanner B / Mack, Jacob M / Day, Ryan J / Isho, Noail F / Brown, Raquel J / Oxford, Alexandra E / Morrison, Brad E / Hayden, Eric J / Rohn, Troy T

    Oxidative medicine and cellular longevity

    2019  Volume 2019, Page(s) 5123565

    Abstract: Despite the fact that harboring the apolipoprotein E4 ( ...

    Abstract Despite the fact that harboring the apolipoprotein E4 (
    MeSH term(s) Animals ; Apolipoprotein E4/genetics ; Apolipoprotein E4/metabolism ; Astrocytes/cytology ; Astrocytes/physiology ; Cells, Cultured ; Cytokines/metabolism ; Gene Expression Regulation ; Humans ; Mice ; Microglia/cytology ; Microglia/physiology ; Peptide Fragments/genetics ; Peptide Fragments/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Apolipoprotein E4 ; Cytokines ; Mamld1 protein, mouse ; Peptide Fragments ; Transcription Factors
    Language English
    Publishing date 2019-05-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2019/5123565
    Database MEDical Literature Analysis and Retrieval System OnLINE

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