GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Effects of urban living environments on mental health in adults
    Springer Science and Business Media LLC ; 2023
    In:  Nature Medicine Vol. 29, No. 6 ( 2023-06), p. 1456-1467
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 29, No. 6 ( 2023-06), p. 1456-1467
    Abstract: Urban-living individuals are exposed to many environmental factors that may combine and interact to influence mental health. While individual factors of an urban environment have been investigated in isolation, no attempt has been made to model how complex, real-life exposure to living in the city relates to brain and mental health, and how this is moderated by genetic factors. Using the data of 156,075 participants from the UK Biobank, we carried out sparse canonical correlation analyses to investigate the relationships between urban environments and psychiatric symptoms. We found an environmental profile of social deprivation, air pollution, street network and urban land-use density that was positively correlated with an affective symptom group ( r  = 0.22, P perm   〈  0.001), mediated by brain volume differences consistent with reward processing, and moderated by genes enriched for stress response, including CRHR1 , explaining 2.01% of the variance in brain volume differences. Protective factors such as greenness and generous destination accessibility were negatively correlated with an anxiety symptom group ( r  = 0.10, P perm   〈  0.001), mediated by brain regions necessary for emotion regulation and moderated by EXD3 , explaining 1.65% of the variance. The third urban environmental profile was correlated with an emotional instability symptom group ( r  = 0.03, P perm   〈  0.001). Our findings suggest that different environmental profiles of urban living may influence specific psychiatric symptom groups through distinct neurobiological pathways.
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/s41591-023-02365-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 1484517-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Validation of a new emotion regulation self-report questionnaire for children
    Springer Science and Business Media LLC ; 2022
    In:  BMC Psychiatry Vol. 22, No. 1 ( 2022-12-22)
    Details
    In: BMC Psychiatry, Springer Science and Business Media LLC, Vol. 22, No. 1 ( 2022-12-22)
    Abstract: To examine and validate the self-report Questionnaire on the Regulation of Unpleasant Moods in Children (FRUST), which is a modified and shortened version of the Questionnaire for the Assessment of Emotion Regulation in Children and Adolescents (FEEL-KJ). Methods The data comprised child and parent ratings of a community-screened sample with differing levels of affective dysregulation (AD) ( N  = 391, age: M  = 10.64, SD  = 1.33, 56% male). We conducted latent factor analyses to establish a factor structure. Subsequently, we assessed measurement invariance (MI) regarding age, gender, and AD level and evaluated the internal consistencies of the scales. Finally, we examined the convergent and divergent validity of the instrument by calculating differential correlations between the emotion regulation strategy (ERS) scales and self- and parent-report measures of psychopathology. Results A four-factor model, with one factor representing Dysfunctional Strategies and the three factors Distraction , Problem-Solving and Social Support representing functional strategies provided the best fit to our data and was straightforward to interpret. We found strong MI for age and gender and weak MI for AD level. Differential correlations with child and parent ratings of measures of psychopathology supported the construct validity of the factors. Conclusions We established a reliable and valid self-report measure for the assessment of ERS in children. Due to the reduced number of items and the inclusion of highly specific regulatory behaviors, the FRUST might be a valuable contribution to the assessment of ER strategies for diagnostic, therapeutic, and research purposes.
    Type of Medium: Online Resource
    ISSN: 1471-244X
    URL: Article
    DOI: 10.1186/s12888-022-04440-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2050438-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    The Mitochondrial Disruptor Devimistat (CPI-613) Synergizes with Genotoxic Anticancer Drugs in Colorectal Cancer Therapy in a Bim-Dependent Manner
    American Association for Cancer Research (AACR) ; 2022
    In:  Molecular Cancer Therapeutics Vol. 21, No. 1 ( 2022-01-01), p. 100-112
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 21, No. 1 ( 2022-01-01), p. 100-112
    Abstract: Colorectal cancer is one of the most frequent tumor entities, with an increasing incidence and mortality in younger adults in Europe and the United States. Five-year survival rates for advanced colorectal cancer are still low, highlighting the need for novel targets in colorectal cancer therapy. Here, we investigated the therapeutic potential of the compound devimistat (CPI-613) that targets altered mitochondrial cancer cell metabolism and its synergism with the antineoplastic drugs 5-fluorouracil (5-FU) and irinotecan (IT) in colorectal cancer. Devimistat exerted a comparable cytotoxicity in a panel of established colorectal cancer cell lines and patient-derived short-term cultures independent of their genetic and epigenetic status, whereas human colonic epithelial cells were more resistant, indicating tumor selectivity. These findings were corroborated in intestinal organoid and tumoroid models. Mechanistically, devimistat disrupted mitochondrial membrane potential and severely impaired mitochondrial respiration, resulting in colorectal cancer cell death induction independent of p53. Combination treatment of devimistat with 5-FU or IT demonstrated synergistic cell killing in colorectal cancer cells as shown by Combenefit modeling and Chou–Talalay analysis. Increased cell death induction was revealed as a major mechanism involving downregulation of antiapoptotic genes and accumulation of proapoptotic Bim, which was confirmed by its genetic knockdown. In human colorectal cancer xenograft mouse models, devimistat showed antitumor activity and synergized with IT, resulting in prolonged survival and enhanced therapeutic efficacy. In human tumor xenografts, devimistat prevented IT-triggered p53 stabilization and caused synergistic Bim induction. Taken together, our study revealed devimistat as a promising candidate in colorectal cancer therapy by synergizing with established antineoplastic drugs in vitro and in vivo.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-21-0393
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2062135-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Presentation_1.pdf
    Frontiers Media SA ; 2022
    In:  Frontiers in Behavioral Neuroscience Vol. 16 ( 2022-7-6)
    Details
    In: Frontiers in Behavioral Neuroscience, Frontiers Media SA, Vol. 16 ( 2022-7-6)
    Abstract: Attention-Deficit Hyperactivity Disorder (ADHD) is a complex and heterogeneous neurodevelopmental condition for which curative treatments are lacking. Whilst pharmacological treatments are generally effective and safe, there is considerable inter-individual variability among patients regarding treatment response, required dose, and tolerability. Many of the non-pharmacological treatments, which are preferred to drug-treatment by some patients, either lack efficacy for core symptoms or are associated with small effect sizes. No evidence-based decision tools are currently available to allocate pharmacological or psychosocial treatments based on the patient's clinical, environmental, cognitive, genetic, or biological characteristics. We systematically reviewed potential biomarkers that may help in diagnosing ADHD and/or stratifying ADHD into more homogeneous subgroups and/or predict clinical course, treatment response, and long-term outcome across the lifespan. Most work involved exploratory studies with cognitive, actigraphic and EEG diagnostic markers to predict ADHD, along with relatively few studies exploring markers to subtype ADHD and predict response to treatment. There is a critical need for multisite prospective carefully designed experimentally controlled or observational studies to identify biomarkers that index inter-individual variability and/or predict treatment response.
    Type of Medium: Online Resource
    ISSN: 1662-5153
    URL: Article
    URL: Article
    DOI: 10.3389/fnbeh.2022.900981
    DOI: 10.3389/fnbeh.2022.900981.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2452960-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Leistungen von Kindern mit einer Störung der Aufmerksamkeit im HAWIK-IV
    Hogrefe Publishing Group ; 2012
    In:  Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie Vol. 40, No. 3 ( 2012-05), p. 191-199
    Details
    In: Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, Hogrefe Publishing Group, Vol. 40, No. 3 ( 2012-05), p. 191-199
    Abstract: Gegenstand der vorliegenden Arbeit waren die Leistungen im HAWIK-IV von N = 433 Kindern und Jugendlichen mit AD(H)S. Untersucht wurden zudem die Abhängigkeit der Testergebnisse von komorbiden Störungen und die Spezifität gegenüber anderen Psychopathologien anhand von Teilgruppen (n = 212, n = 262, n = 117). Diese wurden durch Ausschluss von Personen mit Komorbiditäten auf (a) der ersten, (b) der zweiten und (c) der ersten und/oder der zweiten Achse des Multiaxialen Klassifikationsschemas für psychische Störungen des Kindes- und Jugendalters gebildet. Zur Prüfung der Spezifität des AD(H)S-Profils gegenüber dem Profil anderer psychischer Störungen wurde die komorbiditätsfreie Teilgruppe (n = 117) zudem mit einer Gruppe von Kindern mit einer Angst- oder emotionalen Störung (N = 41) verglichen. Wie erwartet zeigte sich eine signifikante Schwäche in der Arbeitsgeschwindigkeit sowohl in der Gesamtstichprobe aller AD(H)S-Kinder als auch in den um komorbide Störungen bereinigten Teilstichproben. Auch im Bereich des Arbeitsgedächtnisses lag ein Defizit vor, das jedoch in der Teilgruppe ohne Komorbiditäten nicht mehr nachweisbar war. Das Profil dieser Gruppe unterschied sich nicht signifikant von dem Profil der klinischen Kontrollgruppe. Die Ergebnisse unterstützen die Annahme, dass AD(H)S mit Defiziten in der Verarbeitungsgeschwindigkeit assoziiert ist. Das Arbeitsgedächtnis scheint nur bei Vorliegen komorbider Störungen ein signifikantes Defizit darzustellen.
    Type of Medium: Online Resource
    ISSN: 1422-4917 , 1664-2880
    URL: Article
    DOI: 10.1024/1422-4917/a000169
    Language: German
    Publisher: Hogrefe Publishing Group
    Publication Date: 2012
    detail.hit.zdb_id: 2083294-1
    SSG: 2,1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Repair of O 6-carboxymethylguanine adducts by O 6-methylguanine-DNA methyltransferase in human colon epithelial cells
    Oxford University Press (OUP) ; 2021
    In:  Carcinogenesis Vol. 42, No. 8 ( 2021-08-19), p. 1110-1118
    Details
    In: Carcinogenesis, Oxford University Press (OUP), Vol. 42, No. 8 ( 2021-08-19), p. 1110-1118
    Abstract: The protein O6-methylguanine-DNA methyltransferase (MGMT) is able to repair the mutagenic O6-methylguanine (O6-MeG) adduct back to guanine. In this context, it may protect against colorectal cancer formation associated with N-nitroso compounds. Such compounds may be endogenously formed by nitrosylation of amino acids, which can give rise to mutagenic O6-MeG and O6-carboxymethylguanine (O6-CMG) adducts. It is well established that O6-MeG is repaired by MGMT. However, up to now, whether O6-CMG is repaired by this enzyme remains unresolved. Therefore, the aim of the present study was to analyze the fate of both types of O6-guanine adducts in the presence and absence of MGMT activity. To this end, MGMT activity was efficiently blocked by its chemical inhibitor O6-benzylguanine in human colon epithelial cells (HCECs). Exposure of cells to azaserine (AZA) caused significantly higher levels of both O6-MeG and O6-CMG adducts in MGMT-inhibited cells, with O6-CMG as the more abundant DNA lesion. Interestingly, MGMT inhibition did not result in higher levels of AZA-induced DNA strand breaks in spite of elevated DNA adduct levels. In contrast, MGMT inhibition significantly increased DNA strand break formation after exposure to temozolomide (TMZ), a drug that exclusively generates O6-MeG adducts. In line with this finding, the viability of the cells was moderately reduced by TMZ upon MGMT inhibition, whereas no clear effect was observed in cells treated with AZA. In conclusion, our study clearly shows that O6-CMG is repaired by MGMT in HCEC, thereby suggesting that MGMT might play an important role as a tumor suppressor in diet-mediated colorectal cancer.
    Type of Medium: Online Resource
    ISSN: 0143-3334 , 1460-2180
    URL: Article
    DOI: 10.1093/carcin/bgab049
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1474206-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Addressing Global Environmental Challenges to Mental Health Using Population Neuroscience : A Review
    American Medical Association (AMA) ; 2023
    In:  JAMA Psychiatry Vol. 80, No. 10 ( 2023-10-01), p. 1066-
    Details
    In: JAMA Psychiatry, American Medical Association (AMA), Vol. 80, No. 10 ( 2023-10-01), p. 1066-
    Abstract: Climate change, pollution, urbanization, socioeconomic inequality, and psychosocial effects of the COVID-19 pandemic have caused massive changes in environmental conditions that affect brain health during the life span, both on a population level as well as on the level of the individual. How these environmental factors influence the brain, behavior, and mental illness is not well known. Observations A research strategy enabling population neuroscience to contribute to identify brain mechanisms underlying environment-related mental illness by leveraging innovative enrichment tools for data federation, geospatial observation, climate and pollution measures, digital health, and novel data integration techniques is described. This strategy can inform innovative treatments that target causal cognitive and molecular mechanisms of mental illness related to the environment. An example is presented of the environMENTAL Project that is leveraging federated cohort data of over 1.5 million European citizens and patients enriched with deep phenotyping data from large-scale behavioral neuroimaging cohorts to identify brain mechanisms related to environmental adversity underlying symptoms of depression, anxiety, stress, and substance misuse. Conclusions and Relevance This research will lead to the development of objective biomarkers and evidence-based interventions that will significantly improve outcomes of environment-related mental illness.
    Type of Medium: Online Resource
    ISSN: 2168-622X
    URL: Article
    DOI: 10.1001/jamapsychiatry.2023.2996
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2023
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Natural Merosesquiterpenes Activate the DNA Damage Response via DNA Strand Break Formation and Trigger Apoptotic Cell Death in p53-Wild-Type and Mutant Colorectal Cancer
    MDPI AG ; 2021
    In:  Cancers Vol. 13, No. 13 ( 2021-06-30), p. 3282-
    Details
    In: Cancers, MDPI AG, Vol. 13, No. 13 ( 2021-06-30), p. 3282-
    Abstract: Colorectal cancer (CRC) is a frequently occurring malignant disease with still low survival rates, highlighting the need for novel therapeutics. Merosesquiterpenes are secondary metabolites from marine sponges, which might be useful as antitumor agents. To address this issue, we made use of a compound library comprising 11 isolated merosesquiterpenes. The most cytotoxic compounds were smenospongine 〉 ilimaquinone ≈ dactylospontriol, as shown in different human CRC cell lines. Alkaline Comet assays and γH2AX immunofluorescence microscopy demonstrated DNA strand break formation in CRC cells. Western blot analysis revealed an activation of the DNA damage response with CHK1 phosphorylation, stabilization of p53 and p21, which occurred both in CRC cells with p53 knockout and in p53-mutated CRC cells. This resulted in cell cycle arrest followed by a strong increase in the subG1 population, indicative of apoptosis, and typical morphological alterations. In consistency, cell death measurements showed apoptosis following exposure to merosesquiterpenes. Gene expression studies and analysis of caspase cleavage revealed mitochondrial apoptosis via BAX, BIM, and caspase-9 as the main cell death pathway. Interestingly, the compounds were equally effective in p53-wild-type and p53-mutant CRC cells. Finally, the cytotoxic activity of the merosesquiterpenes was corroborated in intestinal tumor organoids, emphasizing their potential for CRC chemotherapy.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers13133282
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2527080-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Global perspective of familial hypercholesterolaemia: a cross-sectional study from the EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC)
    Elsevier BV ; 2021
    In:  The Lancet Vol. 398, No. 10312 ( 2021-11), p. 1713-1725
    Details
    In: The Lancet, Elsevier BV, Vol. 398, No. 10312 ( 2021-11), p. 1713-1725
    Type of Medium: Online Resource
    ISSN: 0140-6736
    URL: Article
    DOI: 10.1016/S0140-6736(21)01122-3
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2067452-1
    detail.hit.zdb_id: 3306-6
    detail.hit.zdb_id: 1476593-7
    SSG: 5,21
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Lipoic Acid Synergizes with Antineoplastic Drugs in Colorectal Cancer by Targeting p53 for Proteasomal Degradation
    MDPI AG ; 2019
    In:  Cells Vol. 8, No. 8 ( 2019-07-30), p. 794-
    Details
    In: Cells, MDPI AG, Vol. 8, No. 8 ( 2019-07-30), p. 794-
    Abstract: Lipoic acid (LA) is a redox-active disulphide compound, which functions as a pivotal co-factor for mitochondrial oxidative decarboxylation. LA and chemical derivatives were shown to target mitochondria in cancer cells with altered energy metabolism, thereby inducing cell death. In this study, the impact of LA on the tumor suppressor protein p53 was analyzed in various colorectal cancer (CRC) cell lines, with a focus on the mechanisms driving p53 degradation. First, LA was demonstrated to trigger the depletion of both wildtype and mutant p53 protein in all CRC cells tested without influencing its gene expression and preceded LA-triggered cytotoxicity. Depletion of p53 coincided with a moderate, LA-dependent ROS production, but was not rescued by antioxidant treatment. LA induced the autophagy receptor p62 and differentially modulated autophagosome formation in CRC cells. However, p53 degradation was not mediated via autophagy as shown by chemical inhibition and genetic abrogation of autophagy. LA treatment also stabilized and activated the transcription factor Nrf2 in CRC cells, which was however dispensable for p53 degradation. Mechanistically, p53 was found to be readily ubiquitinylated and degraded by the proteasomal machinery following LA treatment, which did not involve the E3 ubiquitin ligase MDM2. Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells8080794
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2661518-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...