LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 212

Search options

  1. Article ; Online: Approach to the Patient: Diagnosis of Primary Adrenal Insufficiency in Adults.

    Øksnes, Marianne / Husebye, Eystein S

    The Journal of clinical endocrinology and metabolism

    2023  Volume 109, Issue 1, Page(s) 269–278

    MeSH term(s) Adult ; Humans ; Addison Disease/complications ; Addison Disease/diagnosis ; Adrenal Cortex ; Autoantibodies ; Steroid 21-Hydroxylase
    Chemical Substances Autoantibodies ; Steroid 21-Hydroxylase (EC 1.14.14.16)
    Language English
    Publishing date 2023-07-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/clinem/dgad402
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.134: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article: Editorial: Glucocorticoids and cognition: recent advances in understanding their interaction, with a particular focus on clinical applicability for the treating endocrinologist.

    Ross, Ian Louis / Husebye, Eystein S / Henry, Michelle

    Frontiers in endocrinology

    2023  Volume 14, Page(s) 1339165

    MeSH term(s) Humans ; Glucocorticoids/therapeutic use ; Endocrinologists ; Addison Disease ; Hydrocortisone ; Cognition
    Chemical Substances Glucocorticoids ; Hydrocortisone (WI4X0X7BPJ)
    Language English
    Publishing date 2023-12-12
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2023.1339165
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: The genetics of autoimmune Addison disease: past, present and future.

    Røyrvik, Ellen C / Husebye, Eystein S

    Nature reviews. Endocrinology

    2022  Volume 18, Issue 7, Page(s) 399–412

    Abstract: Autoimmune Addison disease is an endocrinopathy that is fatal if not diagnosed and treated in a timely manner. Its rarity has hampered unbiased studies of the predisposing genetic factors. A 2021 genome-wide association study, explaining up to 40% of the ...

    Abstract Autoimmune Addison disease is an endocrinopathy that is fatal if not diagnosed and treated in a timely manner. Its rarity has hampered unbiased studies of the predisposing genetic factors. A 2021 genome-wide association study, explaining up to 40% of the genetic susceptibility, has revealed new disease loci and reproduced some of the previously reported associations, while failing to reproduce others. Credible risk loci from both candidate gene and genome-wide studies indicate that, like one of its most common comorbidities, type 1 diabetes mellitus, Addison disease is primarily caused by aberrant T cell behaviour. Here, we review the current understanding of the genetics of autoimmune Addison disease and its position in the wider field of autoimmune disorders. The mechanisms that could underlie the effects on the adrenal cortex are also discussed.
    MeSH term(s) Addison Disease/genetics ; Autoimmune Diseases/epidemiology ; Autoimmune Diseases/genetics ; Diabetes Mellitus, Type 1/genetics ; Endocrine System Diseases ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Humans
    Language English
    Publishing date 2022-04-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2489381-X
    ISSN 1759-5037 ; 1759-5029
    ISSN (online) 1759-5037
    ISSN 1759-5029
    DOI 10.1038/s41574-022-00653-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6336: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 93: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: [No title information]

    Ødegaard, Cecilie Smith / Samersaw-Lund, May Brit / Fric, Radek / Kirschner, Rolf S / Husebye, Eystein Sverre / Olsson, Svein-Jørund / Kahn, Pia

    Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke

    2024  Volume 144, Issue 2

    Title translation Etisk ryggrad i møte med politisk konflikt.
    Language Norwegian
    Publishing date 2024-01-26
    Publishing country Norway
    Document type Journal Article
    ZDB-ID 603504-8
    ISSN 0807-7096 ; 0029-2001
    ISSN (online) 0807-7096
    ISSN 0029-2001
    DOI 10.4045/tidsskr.24.0034
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.B 422: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 546: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Systemic interferon type I and B cell responses are impaired in autoimmune polyendocrine syndrome type 1.

    Oftedal, Bergithe E / Delaleu, Nicolas / Dolan, David / Meager, Anthony / Husebye, Eystein S / Wolff, Anette S B

    FEBS letters

    2023  Volume 597, Issue 9, Page(s) 1261–1274

    Abstract: Autoimmune polyendocrine syndrome type I (APS-1) is caused by mutations in the autoimmune regulator (AIRE) gene and characterised clinically by multiple autoimmune manifestations and serologically by autoantibodies against tissue proteins and cytokines. ... ...

    Abstract Autoimmune polyendocrine syndrome type I (APS-1) is caused by mutations in the autoimmune regulator (AIRE) gene and characterised clinically by multiple autoimmune manifestations and serologically by autoantibodies against tissue proteins and cytokines. We here hypothesised that lack of AIRE expression in thymus affects blood immune cells and performed whole-blood microarray analysis (N = 16 APS-I patients vs 16 controls), qPCR verification, and bioinformatic deconvolution of cell subsets. We identified B cell responses as being downregulated in APS-1 patients, which was confirmed by qPCR; these results call for further studies on B cells in this disorder. The type I interferon (IFN-I) pathway was also downregulated in APS-1, and the presence of IFN antibodies is the likely reason for this mild overall downregulation of the IFN-I genes in most APS-1 patients.
    MeSH term(s) Humans ; Polyendocrinopathies, Autoimmune/genetics ; Interferon Type I/genetics ; Autoantibodies/genetics ; Cytokines/genetics ; Mutation
    Chemical Substances Interferon Type I ; Autoantibodies ; Cytokines
    Language English
    Publishing date 2023-04-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1002/1873-3468.14625
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.B 282: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Regulatory T cells in autoimmune primary adrenal insufficiency.

    Sjøgren, Thea / Bjune, Jan-Inge / Husebye, Eystein S / Oftedal, Bergithe E / Wolff, Anette S B

    Clinical and experimental immunology

    2023  Volume 215, Issue 1, Page(s) 47–57

    Abstract: Primary adrenal insufficiency (PAI) is most often caused by an autoimmune destruction of the adrenal cortex resulting in failure to produce cortisol and aldosterone. The aetiology is thought to be a combination of genetic and environmental risk factors, ... ...

    Abstract Primary adrenal insufficiency (PAI) is most often caused by an autoimmune destruction of the adrenal cortex resulting in failure to produce cortisol and aldosterone. The aetiology is thought to be a combination of genetic and environmental risk factors, leading to breakdown of immunological tolerance. Regulatory T cells (Tregs) are deficient in many autoimmune disorders, but it is not known whether they contribute to development of PAI. We aimed to investigate the frequency and function of naive and expanded Tregs in patients with PAI and polyendocrine syndromes compared to age- and gender-matched healthy controls. Flow cytometry was used to assess the frequency and characterize functional markers of blood Tregs in PAI (N = 15). Expanded Treg suppressive abilities were assessed with a flow cytometry based suppression assay (N = 20), while bulk RNA-sequencing was used to examine transcriptomic differences (N = 16) and oxygen consumption rate was measured by a Seahorse cell metabolic assay (N = 11). Our results showed that Treg frequency and suppressive capacity were similar between patients and controls. An increased expression of killer-cell leptin-like receptors and mitochondrial genes was revealed in PAI patients, but their expanded Tregs did not display signs of mitochondrial dysfunction. Our findings do not support a clear role for Tregs in the contribution of PAI development.
    MeSH term(s) Humans ; T-Lymphocytes, Regulatory ; Addison Disease/genetics ; Immune Tolerance ; Hydrocortisone/metabolism ; Flow Cytometry ; Forkhead Transcription Factors/metabolism
    Chemical Substances Hydrocortisone (WI4X0X7BPJ) ; Forkhead Transcription Factors
    Language English
    Publishing date 2023-08-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad087
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.B 337: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article ; Online: Single cell characterization of blood and expanded regulatory T cells in autoimmune polyendocrine syndrome type 1.

    Sjøgren, Thea / Islam, Shahinul / Filippov, Igor / Jebrzycka, Adrianna / Sulen, André / Breivik, Lars E / Hellesen, Alexander / Jørgensen, Anders P / Lima, Kari / Tserel, Liina / Kisand, Kai / Peterson, Pärt / Ranki, Annamari / Husebye, Eystein S / Oftedal, Bergithe E / Wolff, Anette S B

    iScience

    2024  Volume 27, Issue 4, Page(s) 109610

    Abstract: Immune tolerance fails in autoimmune polyendocrine syndrome type 1 (APS-1) because ... ...

    Abstract Immune tolerance fails in autoimmune polyendocrine syndrome type 1 (APS-1) because of
    Language English
    Publishing date 2024-03-27
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2024.109610
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  8. Article: B Cells and Autoantibodies in AIRE Deficiency.

    Wolff, Anette S B / Braun, Sarah / Husebye, Eystein S / Oftedal, Bergithe E

    Biomedicines

    2021  Volume 9, Issue 9

    Abstract: Autoimmune polyendocrine syndrome type 1 (APS-1) is a rare but severe monogenetic autoimmune endocrine disease caused by failure of the Autoimmune Regulator (AIRE). AIRE regulates the negative selection of T cells in the thymus, and the main pathogenic ... ...

    Abstract Autoimmune polyendocrine syndrome type 1 (APS-1) is a rare but severe monogenetic autoimmune endocrine disease caused by failure of the Autoimmune Regulator (AIRE). AIRE regulates the negative selection of T cells in the thymus, and the main pathogenic mechanisms are believed to be T cell-mediated, but little is known about the role of B cells. Here, we give an overview of the role of B cells in thymic and peripheral tolerance in APS-1 patients and different AIRE-deficient mouse models. We also look closely into which autoantibodies have been described for this disorder, and their implications. Based on what is known about B cell therapy in other autoimmune disorders, we outline the potential of B cell therapies in APS-1 and highlight the unresolved research questions to be answered.
    Language English
    Publishing date 2021-09-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines9091274
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  9. Article ; Online: Metabolic Complications in Adrenal Insufficiency.

    Ueland, Grethe A / Husebye, Eystein S

    Frontiers of hormone research

    2018  Volume 49, Page(s) 104–113

    Abstract: Pharmacological glucocorticoid treatment is associated with adverse metabolic consequences such as hypertension, overweight, reduced glucose tolerance, diabetes mellitus and ultimately increased mortality in cardiovascular disease. Here we review the ... ...

    Abstract Pharmacological glucocorticoid treatment is associated with adverse metabolic consequences such as hypertension, overweight, reduced glucose tolerance, diabetes mellitus and ultimately increased mortality in cardiovascular disease. Here we review the evidence of detrimental effects of hormone replacement therapy in adrenal insufficiency (AI). Registry studies indicate increased cardiovascular mortality, hypertension, diabetes, and dyslipidemia in both primary and secondary AI, but when cohorts with carefully characterized patients are studied the picture is less clear, and recently patients with primary AI was reported to have less hypertension and lower body mass index than controls. Whether near physiological replacement therapy increase long-term cardiovascular morbidity and mortality in AI is still unclear.
    MeSH term(s) Adrenal Insufficiency/drug therapy ; Cardiovascular Diseases/chemically induced ; Cardiovascular Diseases/etiology ; Diabetes Mellitus/chemically induced ; Diabetes Mellitus/etiology ; Dyslipidemias/chemically induced ; Dyslipidemias/etiology ; Glucocorticoids/adverse effects ; Hormone Replacement Therapy/adverse effects ; Humans ; Hypertension/chemically induced ; Hypertension/etiology
    Chemical Substances Glucocorticoids
    Language English
    Publishing date 2018-04-05
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 1662-3762 ; 0301-3073
    ISSN (online) 1662-3762
    ISSN 0301-3073
    DOI 10.1159/000486004
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  10. Article ; Online: Rare copy number variation in autoimmune Addison's disease.

    Artaza, Haydee / Eriksson, Daniel / Lavrichenko, Ksenia / Aranda-Guillén, Maribel / Bratland, Eirik / Vaudel, Marc / Knappskog, Per / Husebye, Eystein S / Bensing, Sophie / Wolff, Anette S B / Kämpe, Olle / Røyrvik, Ellen C / Johansson, Stefan

    Frontiers in immunology

    2024  Volume 15, Page(s) 1374499

    Abstract: Autoimmune Addison's disease (AAD) is a rare but life-threatening endocrine disorder caused by an autoimmune destruction of the adrenal cortex. A previous genome-wide association study (GWAS) has shown that common variants near immune-related genes, ... ...

    Abstract Autoimmune Addison's disease (AAD) is a rare but life-threatening endocrine disorder caused by an autoimmune destruction of the adrenal cortex. A previous genome-wide association study (GWAS) has shown that common variants near immune-related genes, which mostly encode proteins participating in the immune response, affect the risk of developing this condition. However, little is known about the contribution of copy number variations (CNVs) to AAD susceptibility. We used the genome-wide genotyping data from Norwegian and Swedish individuals (1,182 cases and 3,810 controls) to investigate the putative role of CNVs in the AAD aetiology. Although the frequency of rare CNVs was similar between cases and controls, we observed that larger deletions (>1,000 kb) were more common among patients (OR = 4.23, 95% CI 1.85-9.66, p = 0.0002). Despite this, none of the large case-deletions were conclusively pathogenic, and the clinical presentation and an AAD-polygenic risk score were similar between cases with and without the large CNVs. Among deletions exclusive to individuals with AAD, we highlight two ultra-rare deletions in the genes
    MeSH term(s) Humans ; Addison Disease/genetics ; Addison Disease/pathology ; DNA Copy Number Variations ; Genome-Wide Association Study ; Genetic Predisposition to Disease ; Polymorphism, Single Nucleotide ; Adaptor Proteins, Signal Transducing/genetics
    Chemical Substances LRBA protein, human (EC 2.7.10.-) ; Adaptor Proteins, Signal Transducing
    Language English
    Publishing date 2024-03-18
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1374499
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top