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  1. Article ; Online: Psychedelics and ketamine are a symptom of psychiatry's woes, not a cure.

    Miller, Andrew H / Raison, Charles L

    Molecular psychiatry

    2023  Volume 28, Issue 8, Page(s) 3167–3168

    MeSH term(s) Humans ; Hallucinogens/therapeutic use ; Ketamine/pharmacology ; Ketamine/therapeutic use ; Mental Disorders/drug therapy ; Mental Disorders/diagnosis ; Psychiatry
    Chemical Substances Hallucinogens ; Ketamine (690G0D6V8H)
    Language English
    Publishing date 2023-06-23
    Publishing country England
    Document type Letter
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-023-02132-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4812: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  2. Article ; Online: Guilt by Association: Inflammation and Shared Genetic Risk Between Stress-Related and Immune Disorders.

    Miller, Andrew H / Binder, Elisabeth B

    The American journal of psychiatry

    2023  Volume 180, Issue 4, Page(s) 259–261

    MeSH term(s) Humans ; Guilt ; Veterans ; Risk Factors ; Inflammation/genetics ; Immune System Diseases ; Stress Disorders, Post-Traumatic
    Language English
    Publishing date 2023-04-12
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 280045-7
    ISSN 1535-7228 ; 0002-953X
    ISSN (online) 1535-7228
    ISSN 0002-953X
    DOI 10.1176/appi.ajp.20230078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Beyond depression: the expanding role of inflammation in psychiatric disorders.

    Miller, Andrew H

    World psychiatry : official journal of the World Psychiatric Association (WPA)

    2020  Volume 19, Issue 1, Page(s) 108–109

    Language English
    Publishing date 2020-01-10
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2236130-3
    ISSN 2051-5545 ; 1723-8617
    ISSN (online) 2051-5545
    ISSN 1723-8617
    DOI 10.1002/wps.20723
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  4. Book: Biological mechanisms of psychosocial effects on disease: implications for cancer control

    Miller, Andrew H.

    [on February 28 - March 1, 2002 ... a multidisciplinary scientific meeting]

    (Brain, behavior, and immunity ; 17, Suppl. 1)

    2003  

    Author's details guest ed.: Andrew H. Miller
    Series title Brain, behavior, and immunity ; 17, Suppl. 1
    Brain, behavior and immunity
    Collection Brain, behavior and immunity
    Language English
    Size S134 S.
    Publisher Elsevier
    Publishing place Amsterdam
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT013729377
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Zs A 2276 -17,Suppl.1- not available for loan Zeitschriften-Lesesaal

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  5. Article ; Online: Mechanistic insights from animal models of neurofibromatosis type 1 cognitive impairment.

    Miller, Andrew H / Halloran, Mary C

    Disease models & mechanisms

    2022  Volume 15, Issue 8

    Abstract: Neurofibromatosis type 1 (NF1) is an autosomal-dominant neurogenetic disorder caused by mutations in the gene neurofibromin 1 (NF1). NF1 predisposes individuals to a variety of symptoms, including peripheral nerve tumors, brain tumors and cognitive ... ...

    Abstract Neurofibromatosis type 1 (NF1) is an autosomal-dominant neurogenetic disorder caused by mutations in the gene neurofibromin 1 (NF1). NF1 predisposes individuals to a variety of symptoms, including peripheral nerve tumors, brain tumors and cognitive dysfunction. Cognitive deficits can negatively impact patient quality of life, especially the social and academic development of children. The neurofibromin protein influences neural circuits via diverse cellular signaling pathways, including through RAS, cAMP and dopamine signaling. Although animal models have been useful in identifying cellular and molecular mechanisms that regulate NF1-dependent behaviors, translating these discoveries into effective treatments has proven difficult. Clinical trials measuring cognitive outcomes in patients with NF1 have mainly targeted RAS signaling but, unfortunately, resulted in limited success. In this Review, we provide an overview of the structure and function of neurofibromin, and evaluate several cellular and molecular mechanisms underlying neurofibromin-dependent cognitive function, which have recently been delineated in animal models. A better understanding of neurofibromin roles in the development and function of the nervous system will be crucial for identifying new therapeutic targets for the various cognitive domains affected by NF1.
    MeSH term(s) Animals ; Cognitive Dysfunction ; Genes, Neurofibromatosis 1 ; Models, Animal ; Neurofibromatosis 1/complications ; Neurofibromatosis 1/genetics ; Neurofibromin 1/genetics ; Quality of Life
    Chemical Substances Neurofibromin 1
    Language English
    Publishing date 2022-08-29
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049422
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  6. Article ; Online: Burning down the house: reinventing drug discovery in psychiatry for the development of targeted therapies.

    Miller, Andrew H / Raison, Charles L

    Molecular psychiatry

    2022  Volume 28, Issue 1, Page(s) 68–75

    Abstract: Despite advances in neuroscience, limited progress has been made in developing new and better medications for psychiatric disorders. Available treatments in psychiatry rely on a few classes of drugs that have a broad spectrum of activity across disorders ...

    Abstract Despite advances in neuroscience, limited progress has been made in developing new and better medications for psychiatric disorders. Available treatments in psychiatry rely on a few classes of drugs that have a broad spectrum of activity across disorders with limited understanding of mechanism of action. While the added value of more targeted therapies is apparent, a dearth of pathophysiologic mechanisms exists to support targeted treatments, and where mechanisms have been identified and drugs developed, results have been disappointing. Based on serendipity and early successes that led to the current drug armamentarium, a haunting legacy endures that new drugs should align with outdated and overinclusive diagnostic categories, consistent with the idea that "one size fits all". This legacy has fostered clinical trial designs focused on heterogenous populations of patients with a single diagnosis and non-specific outcome variables. Disturbingly, this approach likely contributed to missed opportunities for drugs targeting the hypothalamic-pituitary-adrenal axis and now inflammation. Indeed, cause-and-effect data support the role of inflammatory processes in neurotransmitter alterations that disrupt specific neurocircuits and related behaviors. This pathway to pathology occurs across disorders and warrants clinical trial designs that enrich for patients with increased inflammation and use primary outcome variables associated with specific effects of inflammation on brain and behavior. Nevertheless, such trial designs have not been routinely employed, and results of anti-inflammatory treatments have been underwhelming. Thus, to accelerate development of targeted therapeutics including in the area of inflammation, regulatory agencies and the pharmaceutical industry must embrace treatments and trials focused on pathophysiologic pathways that impact specific symptom domains in subsets of patients, agnostic to diagnosis. Moreover, closer collaboration among basic and clinical investigators is needed to apply neuroscience knowledge to reveal disease mechanisms that drive psychiatric symptoms. Together, these efforts will support targeted treatments, ultimately leading to new and better therapeutics in psychiatry.
    MeSH term(s) Humans ; Hypothalamo-Hypophyseal System ; Pituitary-Adrenal System ; Psychiatry ; Drug Discovery ; Inflammation
    Language English
    Publishing date 2022-12-02
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-022-01887-y
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    Zs.A 4812: Show issues Location:
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  7. Article ; Online: Fibroblast and myofibroblast activation in normal tissue repair and fibrosis.

    Younesi, Fereshteh Sadat / Miller, Andrew E / Barker, Thomas H / Rossi, Fabio M V / Hinz, Boris

    Nature reviews. Molecular cell biology

    2024  

    Abstract: The term 'fibroblast' often serves as a catch-all for a diverse array of mesenchymal cells, including perivascular cells, stromal progenitor cells and bona fide fibroblasts. Although phenotypically similar, these subpopulations are functionally distinct, ...

    Abstract The term 'fibroblast' often serves as a catch-all for a diverse array of mesenchymal cells, including perivascular cells, stromal progenitor cells and bona fide fibroblasts. Although phenotypically similar, these subpopulations are functionally distinct, maintaining tissue integrity and serving as local progenitor reservoirs. In response to tissue injury, these cells undergo a dynamic fibroblast-myofibroblast transition, marked by extracellular matrix secretion and contraction of actomyosin-based stress fibres. Importantly, whereas transient activation into myofibroblasts aids in tissue repair, persistent activation triggers pathological fibrosis. In this Review, we discuss the roles of mechanical cues, such as tissue stiffness and strain, alongside cell signalling pathways and extracellular matrix ligands in modulating myofibroblast activation and survival. We also highlight the role of epigenetic modifications and myofibroblast memory in physiological and pathological processes. Finally, we discuss potential strategies for therapeutically interfering with these factors and the associated signal transduction pathways to improve the outcome of dysregulated healing.
    Language English
    Publishing date 2024-04-08
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2031313-5
    ISSN 1471-0080 ; 1471-0072
    ISSN (online) 1471-0080
    ISSN 1471-0072
    DOI 10.1038/s41580-024-00716-0
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    Zs.MG 26: Show issues

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  8. Article ; Online: Identifying Immunophenotypes of Inflammation in Depression: Dismantling the Monolith.

    Felger, Jennifer C / Miller, Andrew H

    Biological psychiatry

    2020  Volume 88, Issue 2, Page(s) 136–138

    MeSH term(s) Blood Cells ; Depression ; Humans ; Inflammation
    Language English
    Publishing date 2020-07-02
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 209434-4
    ISSN 1873-2402 ; 0006-3223
    ISSN (online) 1873-2402
    ISSN 0006-3223
    DOI 10.1016/j.biopsych.2020.04.024
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    Zs.A 720: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  9. Article ; Online: Trial failures of anti-inflammatory drugs in depression.

    Miller, Andrew H / Pariante, Carmine M

    The lancet. Psychiatry

    2020  Volume 7, Issue 10, Page(s) 837

    MeSH term(s) Anti-Inflammatory Agents ; Bipolar Disorder ; Celecoxib ; Depression ; Humans ; Minocycline
    Chemical Substances Anti-Inflammatory Agents ; Minocycline (FYY3R43WGO) ; Celecoxib (JCX84Q7J1L)
    Language English
    Publishing date 2020-09-25
    Publishing country England
    Document type Letter ; Comment
    ISSN 2215-0374
    ISSN (online) 2215-0374
    DOI 10.1016/S2215-0366(20)30357-6
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  10. Article: Collagen organization and structure in

    Jennings, Christian M / Markel, Andrew C / Domingo, Mari J E / Miller, Kristin S / Bayer, Carolyn L / Parekh, Sapun H

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Pelvic organ prolapse (POP) is a gynecological disorder described by the descent of superior pelvic organs into or out of the vagina as a consequence of disrupted muscles and tissue. A thorough understanding of the etiology of POP is limited by the ... ...

    Abstract Pelvic organ prolapse (POP) is a gynecological disorder described by the descent of superior pelvic organs into or out of the vagina as a consequence of disrupted muscles and tissue. A thorough understanding of the etiology of POP is limited by the availability of clinically relevant samples, restricting longitudinal POP studies on soft-tissue biomechanics and structure to POP-induced models such as fibulin-5 knockout (
    Language English
    Publishing date 2024-02-01
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.31.578106
    Database MEDical Literature Analysis and Retrieval System OnLINE

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