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  1. Article ; Online: Deciphering the cytokine fingerprint of macrophage activation syndrome.

    Henderson, Lauren A

    The Lancet. Rheumatology

    2021  Volume 3, Issue 8, Page(s) e535–e538

    Language English
    Publishing date 2021-06-08
    Publishing country England
    Document type Journal Article
    ISSN 2665-9913
    ISSN (online) 2665-9913
    DOI 10.1016/S2665-9913(21)00180-6
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  2. Article ; Online: HLH treatment: smarter, not harder.

    Henderson, Lauren A / Degar, Barbara A

    Blood

    2022  Volume 139, Issue 24, Page(s) 3453–3455

    MeSH term(s) Child ; Humans ; Lymphohistiocytosis, Hemophagocytic/diagnosis ; Lymphohistiocytosis, Hemophagocytic/therapy ; Nitriles ; Pyrazoles ; Pyrimidines
    Chemical Substances Nitriles ; Pyrazoles ; Pyrimidines ; ruxolitinib (82S8X8XX8H)
    Language English
    Publishing date 2022-06-16
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022016421
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  3. Article ; Online: A Bullseye for Children With Systemic Juvenile Idiopathic Arthritis.

    Henderson, Lauren A

    Arthritis & rheumatology (Hoboken, N.J.)

    2019  Volume 71, Issue 7, Page(s) 1030–1033

    MeSH term(s) Arthritis, Juvenile ; Child ; Follow-Up Studies ; Humans ; Immunosuppressive Agents ; Receptors, Interleukin-1
    Chemical Substances Immunosuppressive Agents ; Receptors, Interleukin-1
    Language English
    Publishing date 2019-05-27
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.40867
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  4. Article ; Online: Clinical features of multisystem inflammatory syndrome in children.

    Roberts, Jordan E / Henderson, Lauren A

    Current opinion in rheumatology

    2021  Volume 33, Issue 5, Page(s) 378–386

    Abstract: Purpose of review: To review diagnosis, clinical characteristics and treatment of multisystem inflammatory syndrome in children (MIS-C) associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).: Recent findings: MIS-C emerged in ... ...

    Abstract Purpose of review: To review diagnosis, clinical characteristics and treatment of multisystem inflammatory syndrome in children (MIS-C) associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
    Recent findings: MIS-C emerged in spring 2020 as a hyperinflammatory syndrome following SARS-CoV-2 exposure in children. Despite growing awareness of MIS-C, diagnosis remains challenging due to the range of phenotypes and severity. Fever accompanied by shock, cardiac dysfunction, gastrointestinal symptoms, or mucocutaneous signs suggestive of Kawasaki disease, especially in the presence of known or suspected coronavirus disease 2019 exposure, should trigger consideration of MIS-C. However, clinical presentations are highly varied and may overlap with other infectious diseases. Clinicians must maintain a high index of suspicion for MIS-C and be aware that patients may develop coronary artery aneurysms and myocarditis even with few or no Kawasaki disease symptoms. More precise diagnostic criteria and specific biomarkers are needed to aid diagnosis. Intravenous immunoglobulin (IVIG) is first-line therapy, and steroids should be considered as initial adjunctive treatment for patients with severe manifestations or other risk factors. Prompt treatment is essential, as patients may worsen acutely, though overall prognosis is reassuring.
    Summary: MIS-C associated with SARS-CoV-2 has varied clinical manifestations. Clinicians must be aware of the common presentation and potential for decompensation and cardiac sequalae to guide appropriate evaluation and treatment.
    MeSH term(s) COVID-19 ; Humans ; Mucocutaneous Lymph Node Syndrome/diagnosis ; Mucocutaneous Lymph Node Syndrome/epidemiology ; Mucocutaneous Lymph Node Syndrome/therapy ; SARS-CoV-2 ; Systemic Inflammatory Response Syndrome
    Language English
    Publishing date 2021-07-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1045317-9
    ISSN 1531-6963 ; 1040-8711
    ISSN (online) 1531-6963
    ISSN 1040-8711
    DOI 10.1097/BOR.0000000000000818
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  5. Article ; Online: Dr. Degar et al reply.

    Degar, Barbara A / Halyabar, Olha / Hazen, Melissa M / Henderson, Lauren A

    The Journal of rheumatology

    2022  Volume 50, Issue 7, Page(s) 968–969

    Language English
    Publishing date 2022-11-15
    Publishing country Canada
    Document type Letter ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 194928-7
    ISSN 1499-2752 ; 0315-162X
    ISSN (online) 1499-2752
    ISSN 0315-162X
    DOI 10.3899/jrheum.221078
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  6. Article ; Online: Human cytomegalovirus attenuates AKT activity by destabilizing insulin receptor substrate proteins.

    Domma, Anthony J / Henderson, Lauren A / Goodrum, Felicia D / Moorman, Nathaniel J / Kamil, Jeremy P

    Journal of virology

    2023  Volume 97, Issue 10, Page(s) e0056323

    Abstract: Importance: Human cytomegalovirus (HCMV) requires inactivation of AKT to efficiently replicate, yet how AKT is shut off during HCMV infection has remained unclear. We show that UL38, an HCMV protein that activates mTORC1, is necessary and sufficient to ... ...

    Abstract Importance: Human cytomegalovirus (HCMV) requires inactivation of AKT to efficiently replicate, yet how AKT is shut off during HCMV infection has remained unclear. We show that UL38, an HCMV protein that activates mTORC1, is necessary and sufficient to destabilize insulin receptor substrate 1 (IRS1), a model insulin receptor substrate (IRS) protein. Degradation of IRS proteins in settings of excessive mTORC1 activity is an important mechanism for insulin resistance. When IRS proteins are destabilized, PI3K cannot be recruited to growth factor receptor complexes, and hence, AKT membrane recruitment, a rate limiting step in its activation, fails to occur. Despite its penchant for remodeling host cell signaling pathways, our results reveal that HCMV relies upon a cell-intrinsic negative regulatory feedback loop to inactivate AKT. Given that pharmacological inhibition of PI3K/AKT potently induces HCMV reactivation from latency, our findings also imply that the expression of UL38 activity must be tightly regulated within latently infected cells to avoid spontaneous reactivation.
    MeSH term(s) Humans ; Cytomegalovirus/physiology ; Insulin Receptor Substrate Proteins/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/metabolism ; Protein Stability ; Proteolysis ; Insulin Resistance ; Feedback, Physiological ; Virus Activation ; Virus Latency
    Chemical Substances Insulin Receptor Substrate Proteins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; UL38 protein, human herpesvirus-5
    Language English
    Publishing date 2023-09-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/jvi.00563-23
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    Zs.A 609: Show issues Location:
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  7. Article ; Online: Cannabidiol Safety Data: A Systematic Mapping Study.

    Henderson, Rayetta G / Franke, Kara S / Payne, Lauren E / Franzen, Allison

    Cannabis and cannabinoid research

    2022  Volume 8, Issue 1, Page(s) 34–40

    Abstract: Robust assessment of potential adverse outcomes is needed to determine a safe cannabidiol (CBD) intake level for consumer use. To assist in identifying knowledge gaps and inform future decision making regarding systematic development of health-based ... ...

    Abstract Robust assessment of potential adverse outcomes is needed to determine a safe cannabidiol (CBD) intake level for consumer use. To assist in identifying knowledge gaps and inform future decision making regarding systematic development of health-based benchmarks, we have developed the first systematic map of the safety-related information available for CBD in the peer-reviewed literature. Literature searching conducted according to a published protocol yielded a total of 4186 unique titles and abstracts published through 2020. These were screened using DistillerSR for studies that evaluated at least one potential health outcome following exposure to CBD and/or other hemp-derived substances. Additional categorization was conducted for a subset of 1001 studies in which CBD was administered alone. Studies that investigated CBD most frequently reported on neurological outcomes (532), carcinogenic outcomes (129), and pharmacokinetics (118). Less frequently studied categories included developmental and reproductive, hepatic, and gastrointestinal outcomes. The primary outcomes associated with the most adverse events reported in the literature were neurological (13) and developmental and reproductive (12). Based on the studies identified, reproductive and developmental toxicity was identified as a data gap that warrants conducting a well-designed, guideline-compliant reproductive toxicity study on CBD. In addition, immune outcomes were noted as a potential emerging research area for CBD. This systematic map provides an important baseline from which to identify topics that may be suitable for further research related to the safe use of CBD. Implications for future potential work and limitations of the mapping exercise are discussed.
    MeSH term(s) Cannabidiol/adverse effects ; Liver ; Cannabis
    Chemical Substances Cannabidiol (19GBJ60SN5)
    Language English
    Publishing date 2022-10-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2867624-5
    ISSN 2378-8763 ; 2578-5125
    ISSN (online) 2378-8763
    ISSN 2578-5125
    DOI 10.1089/can.2022.0100
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  8. Article ; Online: Macrophage Activation Syndrome and Secondary Hemophagocytic Lymphohistiocytosis in Childhood Inflammatory Disorders: Diagnosis and Management.

    Henderson, Lauren A / Cron, Randy Q

    Paediatric drugs

    2019  Volume 22, Issue 1, Page(s) 29–44

    Abstract: Macrophage activation syndrome (MAS), a form of secondary hemophagocytic lymphohistiocytosis, is a frequently fatal complication of a variety of pediatric inflammatory disorders. MAS has been most commonly associated with systemic juvenile idiopathic ... ...

    Abstract Macrophage activation syndrome (MAS), a form of secondary hemophagocytic lymphohistiocytosis, is a frequently fatal complication of a variety of pediatric inflammatory disorders. MAS has been most commonly associated with systemic juvenile idiopathic arthritis (sJIA), as approximately 10% of children with sJIA develop fulminant MAS, with another 30-40% exhibiting a more subclinical form of the disease. Children with other rheumatologic conditions such as systemic lupus erythematosus and Kawasaki disease are also at risk for MAS. Moreover, MAS also complicates various genetic autoinflammatory disorders such as gain of function mutations in the cytosolic inflammasome NLRC4, pediatric hematologic malignancies (e.g., T-cell lymphoma), and primary immunodeficiencies characterized by immune dysregulation. Disease-specific and broadly inclusive diagnostic criteria have been developed to facilitate the diagnosis of MAS. Recently, simple screening tools such as the serum ferritin to erythrocyte sedimentation rate ratio have been proposed. Early diagnosis and rapid initiation of immunosuppression are essential for the effective management of MAS. With a better understanding of the pathophysiology of MAS and the advent of novel therapeutics, a broad immunosuppressive approach to treatment is giving way to targeted anti-cytokine therapies. These treatments include agents that block interleukin-1 (IL-1), IL-6, IL-18, interferon-γ, as well as inhibitors of downstream targets of cytokine signaling (e.g., Janus kinases). Increased early recognition of MAS among pediatric inflammatory disorders combined with the use of effective and less toxic cytokine-targeted therapies should lower the mortality of this frequently fatal disorder.
    MeSH term(s) Child ; Humans ; Inflammation/complications ; Inflammation/pathology ; Lymphohistiocytosis, Hemophagocytic/diagnosis ; Lymphohistiocytosis, Hemophagocytic/pathology ; Lymphohistiocytosis, Hemophagocytic/therapy ; Macrophage Activation Syndrome/diagnosis ; Macrophage Activation Syndrome/pathology ; Macrophage Activation Syndrome/therapy
    Language English
    Publishing date 2019-11-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1492748-2
    ISSN 1179-2019 ; 1174-5878
    ISSN (online) 1179-2019
    ISSN 1174-5878
    DOI 10.1007/s40272-019-00367-1
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    Zs.A 5205: Show issues Location:
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  9. Article ; Online: MIS-C: early lessons from immune profiling.

    Henderson, Lauren A / Yeung, Rae S M

    Nature reviews. Rheumatology

    2020  Volume 17, Issue 2, Page(s) 75–76

    MeSH term(s) COVID-19/immunology ; Child ; Host-Pathogen Interactions/immunology ; Humans ; Mucocutaneous Lymph Node Syndrome/virology ; SARS-CoV-2/physiology ; Systemic Inflammatory Response Syndrome/immunology
    Language English
    Publishing date 2020-12-21
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2491532-4
    ISSN 1759-4804 ; 1759-4790
    ISSN (online) 1759-4804
    ISSN 1759-4790
    DOI 10.1038/s41584-020-00566-y
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  10. Article ; Online: Long-term exposure to ambient O

    Wyatt, Lauren H / Cleland, Stephanie E / Wei, Linda / Paul, Naman / Patil, Amrita / Ward-Caviness, Cavin / Henderson, Sarah B / Rappold, Ana G

    Environmental pollution (Barking, Essex : 1987)

    2023  Volume 320, Page(s) 121085

    Abstract: A growing body of evidence indicates that exposure to air pollution affects cognitive performance; however, few studies have assessed this in the context of repeated measures within a large group of individuals or in a population with a large age range. ... ...

    Abstract A growing body of evidence indicates that exposure to air pollution affects cognitive performance; however, few studies have assessed this in the context of repeated measures within a large group of individuals or in a population with a large age range. In this study, we evaluated the associations between long-term exposure to fine particulate matter (PM
    MeSH term(s) Humans ; Young Adult ; Air Pollutants/analysis ; Retrospective Studies ; Air Pollution/analysis ; Particulate Matter/analysis ; Ozone/analysis ; Cognition ; Environmental Exposure/analysis
    Chemical Substances Air Pollutants ; Particulate Matter ; Ozone (66H7ZZK23N)
    Language English
    Publishing date 2023-01-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 280652-6
    ISSN 1873-6424 ; 0013-9327 ; 0269-7491
    ISSN (online) 1873-6424
    ISSN 0013-9327 ; 0269-7491
    DOI 10.1016/j.envpol.2023.121085
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