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Prior differences in previous trauma exposure primarily drive the observed racial/ethnic differences in posttrauma depression and anxiety following a recent trauma
- N. G. Harnett, N. M. Dumornay, M. Delity, L. D. Sanchez, K. Mohiuddin, P. I. Musey, Jr., M. J. Seamon, S. A. McLean, R. C. Kessler, K. C. Koenen, F. L. Beaudoin, L. A. M. Lebois, S. J. H. van Rooij, N. A. Sampson, V. Michopoulos, J. L. Maples-Keller, J. P. Haran, A. B. Storrow, C. Lewandowski, P. L. Hendry, S. Sheikh, C. W. Jones, B. E. Punches, M. C. Kurz, R. A. Swor, M. E. McGrath, L. A. Hudak, J. L. Pascual, S. L. House, X. An, J. S. Stevens, T. C. Neylan, T. Jovanovic, S. D. Linnstaedt, L. T. Germine, E. M. Datner, A. M. Chang, C. Pearson, D. A. Peak, R. C. Merchant, R. M. Domeier, N. K. Rathlev, B. J. O'Neil, P. Sergot, S. E. Bruce, M. W. Miller, R. H. Pietrzak, J. Joormann, D. M. Barch, D. A. Pizzagalli, J. F. Sheridan, J. W. Smoller, B. Luna, S. E. Harte, J. M. Elliott, K. J. Ressler
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- Journal:
- Psychological Medicine / Volume 53 / Issue 6 / April 2023
- Published online by Cambridge University Press:
- 31 January 2022, pp. 2553-2562
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Background
Racial and ethnic groups in the USA differ in the prevalence of posttraumatic stress disorder (PTSD). Recent research however has not observed consistent racial/ethnic differences in posttraumatic stress in the early aftermath of trauma, suggesting that such differences in chronic PTSD rates may be related to differences in recovery over time.
MethodsAs part of the multisite, longitudinal AURORA study, we investigated racial/ethnic differences in PTSD and related outcomes within 3 months after trauma. Participants (n = 930) were recruited from emergency departments across the USA and provided periodic (2 weeks, 8 weeks, and 3 months after trauma) self-report assessments of PTSD, depression, dissociation, anxiety, and resilience. Linear models were completed to investigate racial/ethnic differences in posttraumatic dysfunction with subsequent follow-up models assessing potential effects of prior life stressors.
ResultsRacial/ethnic groups did not differ in symptoms over time; however, Black participants showed reduced posttraumatic depression and anxiety symptoms overall compared to Hispanic participants and White participants. Racial/ethnic differences were not attenuated after accounting for differences in sociodemographic factors. However, racial/ethnic differences in depression and anxiety were no longer significant after accounting for greater prior trauma exposure and childhood emotional abuse in White participants.
ConclusionsThe present findings suggest prior differences in previous trauma exposure partially mediate the observed racial/ethnic differences in posttraumatic depression and anxiety symptoms following a recent trauma. Our findings further demonstrate that racial/ethnic groups show similar rates of symptom recovery over time. Future work utilizing longer time-scale data is needed to elucidate potential racial/ethnic differences in long-term symptom trajectories.
Socio-demographic and trauma-related predictors of depression within eight weeks of motor vehicle collision in the AURORA study
- Jutta Joormann, Samuel A. McLean, Francesca L. Beaudoin, Xinming An, Jennifer S. Stevens, Donglin Zeng, Thomas C. Neylan, Gari Clifford, Sarah D. Linnstaedt, Laura T. Germine, Scott L. Rauch, Paul I. Musey, Phyllis L. Hendry, Sophia Sheikh, Christopher W. Jones, Brittany E. Punches, Gregory Fermann, Lauren A. Hudak, Kamran Mohiuddin, Vishnu Murty, Meghan E. McGrath, John P. Haran, Jose Pascual, Mark Seamon, David A. Peak, Claire Pearson, Robert M. Domeier, Paulina Sergot, Roland Merchant, Leon D. Sanchez, Niels K. Rathlev, William F. Peacock, Steven E. Bruce, Deanna Barch, Diego A. Pizzagalli, Beatriz Luna, Steven E. Harte, Irving Hwang, Sue Lee, Nancy Sampson, Karestan C. Koenen, Kerry J. Ressler, Ronald C. Kessler
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- Journal:
- Psychological Medicine / Volume 52 / Issue 10 / July 2022
- Published online by Cambridge University Press:
- 29 October 2020, pp. 1934-1947
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Background
This is the first report on the association between trauma exposure and depression from the Advancing Understanding of RecOvery afteR traumA(AURORA) multisite longitudinal study of adverse post-traumatic neuropsychiatric sequelae (APNS) among participants seeking emergency department (ED) treatment in the aftermath of a traumatic life experience.
MethodsWe focus on participants presenting at EDs after a motor vehicle collision (MVC), which characterizes most AURORA participants, and examine associations of participant socio-demographics and MVC characteristics with 8-week depression as mediated through peritraumatic symptoms and 2-week depression.
ResultsEight-week depression prevalence was relatively high (27.8%) and associated with several MVC characteristics (being passenger v. driver; injuries to other people). Peritraumatic distress was associated with 2-week but not 8-week depression. Most of these associations held when controlling for peritraumatic symptoms and, to a lesser degree, depressive symptoms at 2-weeks post-trauma.
ConclusionsThese observations, coupled with substantial variation in the relative strength of the mediating pathways across predictors, raises the possibility of diverse and potentially complex underlying biological and psychological processes that remain to be elucidated in more in-depth analyses of the rich and evolving AURORA database to find new targets for intervention and new tools for risk-based stratification following trauma exposure.
Comorbidity within mental disorders: a comprehensive analysis based on 145 990 survey respondents from 27 countries
- J. J. McGrath, C. C. W. Lim, O. Plana-Ripoll, Y. Holtz, E. Agerbo, N. C. Momen, P. B. Mortensen, C. B. Pedersen, J. Abdulmalik, S. Aguilar-Gaxiola, A. Al-Hamzawi, J. Alonso, E. J. Bromet, R. Bruffaerts, B. Bunting, J. M. C. de Almeida, G. de Girolamo, Y. A. De Vries, S. Florescu, O. Gureje, J. M. Haro, M. G. Harris, C. Hu, E. G. Karam, N. Kawakami, A. Kiejna, V. Kovess-Masfety, S. Lee, Z. Mneimneh, F. Navarro-Mateu, R. Orozco, J. Posada-Villa, A. M. Roest, S. Saha, K. M. Scott, J. C. Stagnaro, D. J. Stein, Y. Torres, M. C. Viana, Y. Ziv, R. C. Kessler, P. de Jonge
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- Journal:
- Epidemiology and Psychiatric Sciences / Volume 29 / 2020
- Published online by Cambridge University Press:
- 12 August 2020, e153
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Aims
Epidemiological studies indicate that individuals with one type of mental disorder have an increased risk of subsequently developing other types of mental disorders. This study aimed to undertake a comprehensive analysis of pair-wise lifetime comorbidity across a range of common mental disorders based on a diverse range of population-based surveys.
MethodsThe WHO World Mental Health (WMH) surveys assessed 145 990 adult respondents from 27 countries. Based on retrospectively-reported age-of-onset for 24 DSM-IV mental disorders, associations were examined between all 548 logically possible temporally-ordered disorder pairs. Overall and time-dependent hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards models. Absolute risks were estimated using the product-limit method. Estimates were generated separately for men and women.
ResultsEach prior lifetime mental disorder was associated with an increased risk of subsequent first onset of each other disorder. The median HR was 12.1 (mean = 14.4; range 5.2–110.8, interquartile range = 6.0–19.4). The HRs were most prominent between closely-related mental disorder types and in the first 1–2 years after the onset of the prior disorder. Although HRs declined with time since prior disorder, significantly elevated risk of subsequent comorbidity persisted for at least 15 years. Appreciable absolute risks of secondary disorders were found over time for many pairs.
ConclusionsSurvey data from a range of sites confirms that comorbidity between mental disorders is common. Understanding the risks of temporally secondary disorders may help design practical programs for primary prevention of secondary disorders.
Intermittent explosive disorder subtypes in the general population: association with comorbidity, impairment and suicidality
- K. M. Scott, Y. A. de Vries, S. Aguilar-Gaxiola, A. Al-Hamzawi, J. Alonso, E. J. Bromet, B. Bunting, J. M. Caldas-de-Almeida, A. Cía, S. Florescu, O. Gureje, C-Y. Hu, E. G. Karam, A. Karam, N. Kawakami, R. C. Kessler, S. Lee, J. McGrath, B. Oladeji, J. Posada-Villa, D. J. Stein, Z. Zarkov, P. de Jonge
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- Journal:
- Epidemiology and Psychiatric Sciences / Volume 29 / 2020
- Published online by Cambridge University Press:
- 23 June 2020, e138
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Aims
Intermittent explosive disorder (IED) is characterised by impulsive anger attacks that vary greatly across individuals in severity and consequence. Understanding IED subtypes has been limited by lack of large, general population datasets including assessment of IED. Using the 17-country World Mental Health surveys dataset, this study examined whether behavioural subtypes of IED are associated with differing patterns of comorbidity, suicidality and functional impairment.
MethodsIED was assessed using the Composite International Diagnostic Interview in the World Mental Health surveys (n = 45 266). Five behavioural subtypes were created based on type of anger attack. Logistic regression assessed association of these subtypes with lifetime comorbidity, lifetime suicidality and 12-month functional impairment.
ResultsThe lifetime prevalence of IED in all countries was 0.8% (s.e.: 0.0). The two subtypes involving anger attacks that harmed people (‘hurt people only’ and ‘destroy property and hurt people’), collectively comprising 73% of those with IED, were characterised by high rates of externalising comorbid disorders. The remaining three subtypes involving anger attacks that destroyed property only, destroyed property and threatened people, and threatened people only, were characterised by higher rates of internalising than externalising comorbid disorders. Suicidal behaviour did not vary across the five behavioural subtypes but was higher among those with (v. those without) comorbid disorders, and among those who perpetrated more violent assaults.
ConclusionsThe most common IED behavioural subtypes in these general population samples are associated with high rates of externalising disorders. This contrasts with the findings from clinical studies of IED, which observe a preponderance of internalising disorder comorbidity. This disparity in findings across population and clinical studies, together with the marked heterogeneity that characterises the diagnostic entity of IED, suggests that it is a disorder that requires much greater research.
Outcome and its predictors in schizophrenia - The northern Finland 1966 birth cohort
- E. Lauronen, J. Miettunen, J. Veijola, G. Murray, P. Jones, J. McGrath, M. Isohanni
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- Journal:
- European Psychiatry / Volume 22 / Issue S1 / March 2007
- Published online by Cambridge University Press:
- 16 April 2020, p. S84
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Background and aims
Follow-up studies of schizophrenia have reported divergent rates of outcomes. In addition to definition and measurement challenges, one reason for divergence may be due to sampling biases. Our aim was to report clinical and social outcomes of schizophrenia in the longitudinal, unselected, population-based Northern Finland 1966 Birth Cohort, and describe associated factors.
MethodsSubjects with DSM-III-R schizophrenia (N=109) were followed prospectively from mid-pregnancy up to age 35 years. Used outcome measures were positive and negative symptoms, global clinical impression, use of antipsychotics, psychiatric hospitalisations, social and occupational functioning. Several definitions of good and poor outcomes were explored, and predictors of outcomes were analysed.
ResultsIn a subsample of 59 cases with complete information of outcomes, good clinical outcome varied from 10% to 59%, and good social outcome 15-46%, depending on definition of outcomes. Poor clinical outcome varied 41-77% and poor social 37-54%. Two subjects recovered fully using the most stringent definition of outcome. Lack of friends in childhood, father's high social class, lower school performance and earlier age of illness onset predicted poor outcomes. When the whole sample was considered, early infant development around the age of 1 year was associated with worse course of illness.
ConclusionsOutcomes were heterogeneous and relatively poor in this sample of relatively young schizophrenia subjects. The results were influenced by the definitions and measurements of outcomes. Persons having a sub-optimal developmental trajectory with poor social contacts, poor school performance, and early age of illness onset seem to have the worst outcome.
The role of genetic liability in the association of urbanicity at birth and during upbringing with schizophrenia in Denmark
- D. Paksarian, B. B. Trabjerg, K. R. Merikangas, O. Mors, A. D. Børglum, D. M. Hougaard, J. J. McGrath, C. B. Pedersen, P. B. Mortensen, E. Agerbo
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- Journal:
- Psychological Medicine / Volume 48 / Issue 2 / January 2018
- Published online by Cambridge University Press:
- 29 June 2017, pp. 305-314
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Background
Studies have indicated that the association of urbanicity at birth and during upbringing with schizophrenia may be driven by familial factors such as genetic liability. We used a population-based nested case–control study to assess whether polygenic risk score (PRS) for schizophrenia was associated with urbanicity at birth and at age 15, and to assess whether PRS and parental history of mental disorder together explained the association between urbanicity and schizophrenia.
MethodsData were drawn from Danish population registries. Cases born since 1981 and diagnosed with schizophrenia between 1994 and 2009 were matched to controls with the same sex and birthdate (1549 pairs). Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of a separate, large meta-analysis.
ResultsThose with higher PRS were more likely reside in the capital compared with rural areas at age 15 [odds ratio (OR) 1.19, 95% confidence interval (CI) 1.01–1.40], but not at birth (OR 1.09, 95% CI 0.95–1.26). Adjustment for PRS produced almost no change in relative risks of schizophrenia associated with urbanicity at birth, but slightly attenuated those for urban residence at age 15. Additional adjustment for parental history led to slight attenuation of relative risks for urbanicity at birth [incidence rate ratio (IRR) for birth in capital = 1.54, 95% CI 1.18–2.02; overall p = 0.016] and further attenuation of relative risks for urbanicity at age 15 (IRR for residence in capital = 1.32, 95% CI 0.97–1.78; overall p = 0.148).
ConclusionsWhile results regarding urbanicity during upbringing were somewhat equivocal, genetic liability as measured here does not appear to explain the association between urbanicity at birth and schizophrenia.
Genetic and phenotypic overlap of specific obsessive-compulsive and attention-deficit/hyperactive subtypes with Tourette syndrome
- M. E. Hirschtritt, S. M. Darrow, C. Illmann, L. Osiecki, M. Grados, P. Sandor, Y. Dion, R. A. King, D. Pauls, C. L. Budman, D. C. Cath, E. Greenberg, G. J. Lyon, D. Yu, L. M. McGrath, W. M. McMahon, P. C. Lee, K. L. Delucchi, J. M. Scharf, C. A. Mathews
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- Journal:
- Psychological Medicine / Volume 48 / Issue 2 / January 2018
- Published online by Cambridge University Press:
- 27 June 2017, pp. 279-293
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Background
The unique phenotypic and genetic aspects of obsessive-compulsive (OCD) and attention-deficit/hyperactivity disorder (ADHD) among individuals with Tourette syndrome (TS) are not well characterized. Here, we examine symptom patterns and heritability of OCD and ADHD in TS families.
MethodOCD and ADHD symptom patterns were examined in TS patients and their family members (N = 3494) using exploratory factor analyses (EFA) for OCD and ADHD symptoms separately, followed by latent class analyses (LCA) of the resulting OCD and ADHD factor sum scores jointly; heritability and clinical relevance of the resulting factors and classes were assessed.
ResultsEFA yielded a 2-factor model for ADHD and an 8-factor model for OCD. Both ADHD factors (inattentive and hyperactive/impulsive symptoms) were genetically related to TS, ADHD, and OCD. The doubts, contamination, need for sameness, and superstitions factors were genetically related to OCD, but not ADHD or TS; symmetry/exactness and fear-of-harm were associated with TS and OCD while hoarding was associated with ADHD and OCD. In contrast, aggressive urges were genetically associated with TS, OCD, and ADHD. LCA revealed a three-class solution: few OCD/ADHD symptoms (LC1), OCD & ADHD symptoms (LC2), and symmetry/exactness, hoarding, and ADHD symptoms (LC3). LC2 had the highest psychiatric comorbidity rates (⩾50% for all disorders).
ConclusionsSymmetry/exactness, aggressive urges, fear-of-harm, and hoarding show complex genetic relationships with TS, OCD, and ADHD, and, rather than being specific subtypes of OCD, transcend traditional diagnostic boundaries, perhaps representing an underlying vulnerability (e.g. failure of top-down cognitive control) common to all three disorders.
Mental disorders among college students in the World Health Organization World Mental Health Surveys – CORRIGENDUM
- R. P. Auerbach, J. Alonso, W. G. Axinn, P. Cuijpers, D. D. Ebert, J. G. Green, I. Hwang, R. C. Kessler, H. Liu, P. Mortier, M. K. Nock, S. Pinder-Amaker, N. A. Sampson, S. Aguilar-Gaxiola, A. Al-Hamzawi, L. H. Andrade, C. Benjet, J. M. Caldas-de-Almeida, K. Demyttenaere, S. Florescu, G. de Girolamo, O. Gureje, J. M. Haro, E. G. Karam, A. Kiejna, V. Kovess-Masfety, S. Lee, J. J. McGrath, S. O’Neill, B.-E. Pennell, K. Scott, M. ten Have, Y. Torres, A. M. Zaslavsky, Z. Zarkov, R. Bruffaerts
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- Journal:
- Psychological Medicine / Volume 47 / Issue 15 / November 2017
- Published online by Cambridge University Press:
- 02 May 2017, p. 2737
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The quality of mental health literacy measurement tools evaluating the stigma of mental illness: a systematic review
- Y. Wei, P. McGrath, J. Hayden, S. Kutcher
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- Journal:
- Epidemiology and Psychiatric Sciences / Volume 27 / Issue 5 / October 2018
- Published online by Cambridge University Press:
- 02 May 2017, pp. 433-462
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Aims.
Stigma of mental illness is a significant barrier to receiving mental health care. However, measurement tools evaluating stigma of mental illness have not been systematically assessed for their quality. We conducted a systematic review to critically appraise the methodological quality of studies assessing psychometrics of stigma measurement tools and determined the level of evidence of overall quality of psychometric properties of included tools.
Methods.We searched PubMed, PsycINFO, EMBASE, CINAHL, the Cochrane Library and ERIC databases for eligible studies. We conducted risk-of-bias analysis with the Consensus-based Standards for the Selection of Health Measurement Instruments checklist, rating studies as excellent, good, fair or poor. We further rated the level of evidence of the overall quality of psychometric properties, combining the study quality and quality of each psychometric property, as: strong, moderate, limited, conflicting or unknown.
Results.We identified 117 studies evaluating psychometric properties of 101 tools. The quality of specific studies varied, with ratings of: excellent (n = 5); good (mostly on internal consistency (n = 67)); fair (mostly on structural validity, n = 89 and construct validity, n = 85); and poor (mostly on internal consistency, n = 36). The overall quality of psychometric properties also varied from: strong (mostly content validity, n = 3), moderate (mostly internal consistency, n = 55), limited (mostly structural validity, n = 55 and construct validity, n = 46), conflicting (mostly test–retest reliability, n = 9) and unknown (mostly internal consistency, n = 36).
Conclusions.We identified 12 tools demonstrating limited evidence or above for (+, ++, +++) all their properties, 69 tools reaching these levels of evidence for some of their properties, and 20 tools that did not meet the minimum level of evidence for all of their properties. We note that further research on stigma tool development is needed to ensure appropriate application.
The association between childhood adversities and subsequent first onset of psychotic experiences: a cross-national analysis of 23 998 respondents from 17 countries
- J. J. McGrath, K. A. McLaughlin, S. Saha, S. Aguilar-Gaxiola, A. Al-Hamzawi, J. Alonso, R. Bruffaerts, G. de Girolamo, P. de Jonge, O. Esan, S. Florescu, O. Gureje, J. M. Haro, C. Hu, E. G. Karam, V. Kovess-Masfety, S. Lee, J. P. Lepine, C. C. W. Lim, M. E. Medina-Mora, Z. Mneimneh, B. E. Pennell, M. Piazza, J. Posada-Villa, N. Sampson, M. C. Viana, M. Xavier, E. J. Bromet, K. S. Kendler, R. C. Kessler,
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- Journal:
- Psychological Medicine / Volume 47 / Issue 7 / May 2017
- Published online by Cambridge University Press:
- 09 January 2017, pp. 1230-1245
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Background
Although there is robust evidence linking childhood adversities (CAs) and an increased risk for psychotic experiences (PEs), little is known about whether these associations vary across the life-course and whether mental disorders that emerge prior to PEs explain these associations.
MethodWe assessed CAs, PEs and DSM-IV mental disorders in 23 998 adults in the WHO World Mental Health Surveys. Discrete-time survival analysis was used to investigate the associations between CAs and PEs, and the influence of mental disorders on these associations using multivariate logistic models.
ResultsExposure to CAs was common, and those who experienced any CAs had increased odds of later PEs [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.9–2.6]. CAs reflecting maladaptive family functioning (MFF), including abuse, neglect, and parent maladjustment, exhibited the strongest associations with PE onset in all life-course stages. Sexual abuse exhibited a strong association with PE onset during childhood (OR 8.5, 95% CI 3.6–20.2), whereas Other CA types were associated with PE onset in adolescence. Associations of other CAs with PEs disappeared in adolescence after adjustment for prior-onset mental disorders. The population attributable risk proportion (PARP) for PEs associated with all CAs was 31% (24% for MFF).
ConclusionsExposure to CAs is associated with PE onset throughout the life-course, although sexual abuse is most strongly associated with childhood-onset PEs. The presence of mental disorders prior to the onset of PEs does not fully explain these associations. The large PARPs suggest that preventing CAs could lead to a meaningful reduction in PEs in the population.
Mental disorders among college students in the World Health Organization World Mental Health Surveys
- R. P. Auerbach, J. Alonso, W. G. Axinn, P. Cuijpers, D. D. Ebert, J. G. Green, I. Hwang, R. C. Kessler, H. Liu, P. Mortier, M. K. Nock, S. Pinder-Amaker, N. A. Sampson, S. Aguilar-Gaxiola, A. Al-Hamzawi, L. H. Andrade, C. Benjet, J. M. Caldas-de-Almeida, K. Demyttenaere, S. Florescu, G. de Girolamo, O. Gureje, J. M. Haro, E. G. Karam, A. Kiejna, V. Kovess-Masfety, S. Lee, J. J. McGrath, S. O'Neill, B.-E. Pennell, K. Scott, M. ten Have, Y. Torres, A. M. Zaslavsky, Z. Zarkov, R. Bruffaerts
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- Journal:
- Psychological Medicine / Volume 46 / Issue 14 / October 2016
- Published online by Cambridge University Press:
- 03 August 2016, pp. 2955-2970
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Background
Although mental disorders are significant predictors of educational attainment throughout the entire educational career, most research on mental disorders among students has focused on the primary and secondary school years.
MethodThe World Health Organization World Mental Health Surveys were used to examine the associations of mental disorders with college entry and attrition by comparing college students (n = 1572) and non-students in the same age range (18–22 years; n = 4178), including non-students who recently left college without graduating (n = 702) based on surveys in 21 countries (four low/lower-middle income, five upper-middle-income, one lower-middle or upper-middle at the times of two different surveys, and 11 high income). Lifetime and 12-month prevalence and age-of-onset of DSM-IV anxiety, mood, behavioral and substance disorders were assessed with the Composite International Diagnostic Interview (CIDI).
ResultsOne-fifth (20.3%) of college students had 12-month DSM-IV/CIDI disorders; 83.1% of these cases had pre-matriculation onsets. Disorders with pre-matriculation onsets were more important than those with post-matriculation onsets in predicting subsequent college attrition, with substance disorders and, among women, major depression the most important such disorders. Only 16.4% of students with 12-month disorders received any 12-month healthcare treatment for their mental disorders.
ConclusionsMental disorders are common among college students, have onsets that mostly occur prior to college entry, in the case of pre-matriculation disorders are associated with college attrition, and are typically untreated. Detection and effective treatment of these disorders early in the college career might reduce attrition and improve educational and psychosocial functioning.
2-Photon Characterization of Optical Proteolytic Beacons for Imaging Changes in Matrix-Metalloprotease Activity in a Mouse Model of Aneurysm
- Darren G. Haskett, David Maestas, Stephen J. Howerton, Tyler Smith, D. Catalina Ardila, Tom Doetschman, Urs Utzinger, Dominic McGrath, J. Oliver McIntyre, Jonathan P. Vande Geest
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- Journal:
- Microscopy and Microanalysis / Volume 22 / Issue 2 / April 2016
- Published online by Cambridge University Press:
- 23 February 2016, pp. 349-360
- Print publication:
- April 2016
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Abdominal aortic aneurysm is a multifactorial disease that is a leading cause of death in developed countries. Matrix-metalloproteases (MMPs) are part of the disease process, however, assessing their role in disease initiation and progression has been difficult and animal models have become essential. Combining Förster resonance energy transfer (FRET) proteolytic beacons activated in the presence of MMPs with 2-photon microscopy allows for a novel method of evaluating MMP activity within the extracellular matrix (ECM). Single and 2-photon spectra for proteolytic beacons were determined in vitro. Ex vivo experiments using the apolipoprotein E knockout angiotensin II-infused mouse model of aneurysm imaged ECM architecture simultaneously with the MMP-activated FRET beacons. 2-photon spectra of the two-color proteolytic beacons showed peaks for the individual fluorophores that enable imaging of MMP activity through proteolytic cleavage. Ex vivo imaging of the beacons within the ECM revealed both microstructure and MMP activity. 2-photon imaging of the beacons in aneurysmal tissue showed an increase in proteolytic cleavage within the ECM (p<0.001), thus indicating an increase in MMP activity. Our data suggest that FRET-based proteolytic beacons show promise in assessing MMP activity within the ECM and will therefore allow future studies to identify the heterogeneous distribution of simultaneous ECM remodeling and protease activity in aneurysmal disease.
Contributors
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- By Mitchell Aboulafia, Frederick Adams, Marilyn McCord Adams, Robert M. Adams, Laird Addis, James W. Allard, David Allison, William P. Alston, Karl Ameriks, C. Anthony Anderson, David Leech Anderson, Lanier Anderson, Roger Ariew, David Armstrong, Denis G. Arnold, E. J. Ashworth, Margaret Atherton, Robin Attfield, Bruce Aune, Edward Wilson Averill, Jody Azzouni, Kent Bach, Andrew Bailey, Lynne Rudder Baker, Thomas R. Baldwin, Jon Barwise, George Bealer, William Bechtel, Lawrence C. Becker, Mark A. Bedau, Ernst Behler, José A. Benardete, Ermanno Bencivenga, Jan Berg, Michael Bergmann, Robert L. Bernasconi, Sven Bernecker, Bernard Berofsky, Rod Bertolet, Charles J. Beyer, Christian Beyer, Joseph Bien, Joseph Bien, Peg Birmingham, Ivan Boh, James Bohman, Daniel Bonevac, Laurence BonJour, William J. Bouwsma, Raymond D. Bradley, Myles Brand, Richard B. Brandt, Michael E. Bratman, Stephen E. Braude, Daniel Breazeale, Angela Breitenbach, Jason Bridges, David O. Brink, Gordon G. Brittan, Justin Broackes, Dan W. Brock, Aaron Bronfman, Jeffrey E. Brower, Bartosz Brozek, Anthony Brueckner, Jeffrey Bub, Lara Buchak, Otavio Bueno, Ann E. Bumpus, Robert W. Burch, John Burgess, Arthur W. Burks, Panayot Butchvarov, Robert E. Butts, Marina Bykova, Patrick Byrne, David Carr, Noël Carroll, Edward S. Casey, Victor Caston, Victor Caston, Albert Casullo, Robert L. Causey, Alan K. L. Chan, Ruth Chang, Deen K. Chatterjee, Andrew Chignell, Roderick M. Chisholm, Kelly J. Clark, E. J. Coffman, Robin Collins, Brian P. Copenhaver, John Corcoran, John Cottingham, Roger Crisp, Frederick J. Crosson, Antonio S. Cua, Phillip D. Cummins, Martin Curd, Adam Cureton, Andrew Cutrofello, Stephen Darwall, Paul Sheldon Davies, Wayne A. Davis, Timothy Joseph Day, Claudio de Almeida, Mario De Caro, Mario De Caro, John Deigh, C. F. Delaney, Daniel C. Dennett, Michael R. DePaul, Michael Detlefsen, Daniel Trent Devereux, Philip E. Devine, John M. Dillon, Martin C. Dillon, Robert DiSalle, Mary Domski, Alan Donagan, Paul Draper, Fred Dretske, Mircea Dumitru, Wilhelm Dupré, Gerald Dworkin, John Earman, Ellery Eells, Catherine Z. Elgin, Berent Enç, Ronald P. Endicott, Edward Erwin, John Etchemendy, C. Stephen Evans, Susan L. Feagin, Solomon Feferman, Richard Feldman, Arthur Fine, Maurice A. Finocchiaro, William FitzPatrick, Richard E. Flathman, Gvozden Flego, Richard Foley, Graeme Forbes, Rainer Forst, Malcolm R. Forster, Daniel Fouke, Patrick Francken, Samuel Freeman, Elizabeth Fricker, Miranda Fricker, Michael Friedman, Michael Fuerstein, Richard A. Fumerton, Alan Gabbey, Pieranna Garavaso, Daniel Garber, Jorge L. A. Garcia, Robert K. Garcia, Don Garrett, Philip Gasper, Gerald Gaus, Berys Gaut, Bernard Gert, Roger F. Gibson, Cody Gilmore, Carl Ginet, Alan H. Goldman, Alvin I. Goldman, Alfonso Gömez-Lobo, Lenn E. Goodman, Robert M. Gordon, Stefan Gosepath, Jorge J. E. Gracia, Daniel W. Graham, George A. Graham, Peter J. Graham, Richard E. Grandy, I. Grattan-Guinness, John Greco, Philip T. Grier, Nicholas Griffin, Nicholas Griffin, David A. Griffiths, Paul J. Griffiths, Stephen R. Grimm, Charles L. Griswold, Charles B. Guignon, Pete A. Y. Gunter, Dimitri Gutas, Gary Gutting, Paul Guyer, Kwame Gyekye, Oscar A. Haac, Raul Hakli, Raul Hakli, Michael Hallett, Edward C. Halper, Jean Hampton, R. James Hankinson, K. R. Hanley, Russell Hardin, Robert M. Harnish, William Harper, David Harrah, Kevin Hart, Ali Hasan, William Hasker, John Haugeland, Roger Hausheer, William Heald, Peter Heath, Richard Heck, John F. Heil, Vincent F. Hendricks, Stephen Hetherington, Francis Heylighen, Kathleen Marie Higgins, Risto Hilpinen, Harold T. Hodes, Joshua Hoffman, Alan Holland, Robert L. Holmes, Richard Holton, Brad W. Hooker, Terence E. Horgan, Tamara Horowitz, Paul Horwich, Vittorio Hösle, Paul Hoβfeld, Daniel Howard-Snyder, Frances Howard-Snyder, Anne Hudson, Deal W. Hudson, Carl A. Huffman, David L. Hull, Patricia Huntington, Thomas Hurka, Paul Hurley, Rosalind Hursthouse, Guillermo Hurtado, Ronald E. Hustwit, Sarah Hutton, Jonathan Jenkins Ichikawa, Harry A. Ide, David Ingram, Philip J. Ivanhoe, Alfred L. Ivry, Frank Jackson, Dale Jacquette, Joseph Jedwab, Richard Jeffrey, David Alan Johnson, Edward Johnson, Mark D. Jordan, Richard Joyce, Hwa Yol Jung, Robert Hillary Kane, Tomis Kapitan, Jacquelyn Ann K. Kegley, James A. Keller, Ralph Kennedy, Sergei Khoruzhii, Jaegwon Kim, Yersu Kim, Nathan L. King, Patricia Kitcher, Peter D. Klein, E. D. Klemke, Virginia Klenk, George L. Kline, Christian Klotz, Simo Knuuttila, Joseph J. Kockelmans, Konstantin Kolenda, Sebastian Tomasz Kołodziejczyk, Isaac Kramnick, Richard Kraut, Fred Kroon, Manfred Kuehn, Steven T. Kuhn, Henry E. Kyburg, John Lachs, Jennifer Lackey, Stephen E. Lahey, Andrea Lavazza, Thomas H. Leahey, Joo Heung Lee, Keith Lehrer, Dorothy Leland, Noah M. Lemos, Ernest LePore, Sarah-Jane Leslie, Isaac Levi, Andrew Levine, Alan E. Lewis, Daniel E. Little, Shu-hsien Liu, Shu-hsien Liu, Alan K. L. Chan, Brian Loar, Lawrence B. Lombard, John Longeway, Dominic McIver Lopes, Michael J. Loux, E. J. Lowe, Steven Luper, Eugene C. Luschei, William G. Lycan, David Lyons, David Macarthur, Danielle Macbeth, Scott MacDonald, Jacob L. Mackey, Louis H. Mackey, Penelope Mackie, Edward H. Madden, Penelope Maddy, G. B. Madison, Bernd Magnus, Pekka Mäkelä, Rudolf A. Makkreel, David Manley, William E. Mann (W.E.M.), Vladimir Marchenkov, Peter Markie, Jean-Pierre Marquis, Ausonio Marras, Mike W. Martin, A. P. Martinich, William L. McBride, David McCabe, Storrs McCall, Hugh J. McCann, Robert N. McCauley, John J. McDermott, Sarah McGrath, Ralph McInerny, Daniel J. McKaughan, Thomas McKay, Michael McKinsey, Brian P. McLaughlin, Ernan McMullin, Anthonie Meijers, Jack W. Meiland, William Jason Melanson, Alfred R. Mele, Joseph R. Mendola, Christopher Menzel, Michael J. Meyer, Christian B. Miller, David W. Miller, Peter Millican, Robert N. Minor, Phillip Mitsis, James A. Montmarquet, Michael S. Moore, Tim Moore, Benjamin Morison, Donald R. Morrison, Stephen J. Morse, Paul K. Moser, Alexander P. D. Mourelatos, Ian Mueller, James Bernard Murphy, Mark C. Murphy, Steven Nadler, Jan Narveson, Alan Nelson, Jerome Neu, Samuel Newlands, Kai Nielsen, Ilkka Niiniluoto, Carlos G. Noreña, Calvin G. Normore, David Fate Norton, Nikolaj Nottelmann, Donald Nute, David S. Oderberg, Steve Odin, Michael O’Rourke, Willard G. Oxtoby, Heinz Paetzold, George S. Pappas, Anthony J. Parel, Lydia Patton, R. P. Peerenboom, Francis Jeffry Pelletier, Adriaan T. Peperzak, Derk Pereboom, Jaroslav Peregrin, Glen Pettigrove, Philip Pettit, Edmund L. Pincoffs, Andrew Pinsent, Robert B. Pippin, Alvin Plantinga, Louis P. Pojman, Richard H. Popkin, John F. Post, Carl J. Posy, William J. Prior, Richard Purtill, Michael Quante, Philip L. Quinn, Philip L. Quinn, Elizabeth S. Radcliffe, Diana Raffman, Gerard Raulet, Stephen L. Read, Andrews Reath, Andrew Reisner, Nicholas Rescher, Henry S. Richardson, Robert C. Richardson, Thomas Ricketts, Wayne D. Riggs, Mark Roberts, Robert C. Roberts, Luke Robinson, Alexander Rosenberg, Gary Rosenkranz, Bernice Glatzer Rosenthal, Adina L. Roskies, William L. Rowe, T. M. Rudavsky, Michael Ruse, Bruce Russell, Lilly-Marlene Russow, Dan Ryder, R. M. Sainsbury, Joseph Salerno, Nathan Salmon, Wesley C. Salmon, Constantine Sandis, David H. Sanford, Marco Santambrogio, David Sapire, Ruth A. Saunders, Geoffrey Sayre-McCord, Charles Sayward, James P. Scanlan, Richard Schacht, Tamar Schapiro, Frederick F. Schmitt, Jerome B. Schneewind, Calvin O. Schrag, Alan D. Schrift, George F. Schumm, Jean-Loup Seban, David N. Sedley, Kenneth Seeskin, Krister Segerberg, Charlene Haddock Seigfried, Dennis M. Senchuk, James F. Sennett, William Lad Sessions, Stewart Shapiro, Tommie Shelby, Donald W. Sherburne, Christopher Shields, Roger A. Shiner, Sydney Shoemaker, Robert K. Shope, Kwong-loi Shun, Wilfried Sieg, A. John Simmons, Robert L. Simon, Marcus G. Singer, Georgette Sinkler, Walter Sinnott-Armstrong, Matti T. Sintonen, Lawrence Sklar, Brian Skyrms, Robert C. Sleigh, Michael Anthony Slote, Hans Sluga, Barry Smith, Michael Smith, Robin Smith, Robert Sokolowski, Robert C. Solomon, Marta Soniewicka, Philip Soper, Ernest Sosa, Nicholas Southwood, Paul Vincent Spade, T. L. S. Sprigge, Eric O. Springsted, George J. Stack, Rebecca Stangl, Jason Stanley, Florian Steinberger, Sören Stenlund, Christopher Stephens, James P. Sterba, Josef Stern, Matthias Steup, M. A. Stewart, Leopold Stubenberg, Edith Dudley Sulla, Frederick Suppe, Jere Paul Surber, David George Sussman, Sigrún Svavarsdóttir, Zeno G. Swijtink, Richard Swinburne, Charles C. Taliaferro, Robert B. Talisse, John Tasioulas, Paul Teller, Larry S. Temkin, Mark Textor, H. S. Thayer, Peter Thielke, Alan Thomas, Amie L. Thomasson, Katherine Thomson-Jones, Joshua C. Thurow, Vzalerie Tiberius, Terrence N. Tice, Paul Tidman, Mark C. Timmons, William Tolhurst, James E. Tomberlin, Rosemarie Tong, Lawrence Torcello, Kelly Trogdon, J. D. Trout, Robert E. Tully, Raimo Tuomela, John Turri, Martin M. Tweedale, Thomas Uebel, Jennifer Uleman, James Van Cleve, Harry van der Linden, Peter van Inwagen, Bryan W. Van Norden, René van Woudenberg, Donald Phillip Verene, Samantha Vice, Thomas Vinci, Donald Wayne Viney, Barbara Von Eckardt, Peter B. M. Vranas, Steven J. Wagner, William J. Wainwright, Paul E. Walker, Robert E. Wall, Craig Walton, Douglas Walton, Eric Watkins, Richard A. Watson, Michael V. Wedin, Rudolph H. Weingartner, Paul Weirich, Paul J. Weithman, Carl Wellman, Howard Wettstein, Samuel C. Wheeler, Stephen A. White, Jennifer Whiting, Edward R. Wierenga, Michael Williams, Fred Wilson, W. Kent Wilson, Kenneth P. Winkler, John F. Wippel, Jan Woleński, Allan B. Wolter, Nicholas P. Wolterstorff, Rega Wood, W. Jay Wood, Paul Woodruff, Alison Wylie, Gideon Yaffe, Takashi Yagisawa, Yutaka Yamamoto, Keith E. Yandell, Xiaomei Yang, Dean Zimmerman, Günter Zoller, Catherine Zuckert, Michael Zuckert, Jack A. Zupko (J.A.Z.)
- Edited by Robert Audi, University of Notre Dame, Indiana
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- The Cambridge Dictionary of Philosophy
- Published online:
- 05 August 2015
- Print publication:
- 27 April 2015, pp ix-xxx
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A computational analysis of flanker interference in depression
- D. G. Dillon, T. Wiecki, P. Pechtel, C. Webb, F. Goer, L. Murray, M. Trivedi, M. Fava, P. J. McGrath, M. Weissman, R. Parsey, B. Kurian, P. Adams, T. Carmody, S. Weyandt, K. Shores-Wilson, M. Toups, M. McInnis, M. A. Oquendo, C. Cusin, P. Deldin, G. Bruder, D. A. Pizzagalli
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- Journal:
- Psychological Medicine / Volume 45 / Issue 11 / August 2015
- Published online by Cambridge University Press:
- 02 March 2015, pp. 2333-2344
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Background
Depression is characterized by poor executive function, but – counterintuitively – in some studies, it has been associated with highly accurate performance on certain cognitively demanding tasks. The psychological mechanisms responsible for this paradoxical finding are unclear. To address this issue, we applied a drift diffusion model (DDM) to flanker task data from depressed and healthy adults participating in the multi-site Establishing Moderators and Biosignatures of Antidepressant Response for Clinical Care for Depression (EMBARC) study.
MethodOne hundred unmedicated, depressed adults and 40 healthy controls completed a flanker task. We investigated the effect of flanker interference on accuracy and response time, and used the DDM to examine group differences in three cognitive processes: prepotent response bias (tendency to respond to the distracting flankers), response inhibition (necessary to resist prepotency), and executive control (required for execution of correct response on incongruent trials).
ResultsConsistent with prior reports, depressed participants responded more slowly and accurately than controls on incongruent trials. The DDM indicated that although executive control was sluggish in depressed participants, this was more than offset by decreased prepotent response bias. Among the depressed participants, anhedonia was negatively correlated with a parameter indexing the speed of executive control (r = −0.28, p = 0.007).
ConclusionsExecutive control was delayed in depression but this was counterbalanced by reduced prepotent response bias, demonstrating how participants with executive function deficits can nevertheless perform accurately in a cognitive control task. Drawing on data from neural network simulations, we speculate that these results may reflect tonically reduced striatal dopamine in depression.
Psychosis prevalence and physical, metabolic and cognitive co-morbidity: data from the second Australian national survey of psychosis
- V. A. Morgan, J. J. McGrath, A. Jablensky, J. C. Badcock, A. Waterreus, R. Bush, V. Carr, D. Castle, M. Cohen, C. Galletly, C. Harvey, B. Hocking, P. McGorry, A. L. Neil, S. Saw, S. Shah, H. J. Stain, A. Mackinnon
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- Journal:
- Psychological Medicine / Volume 44 / Issue 10 / July 2014
- Published online by Cambridge University Press:
- 02 January 2014, pp. 2163-2176
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Background
There are insufficient data from nationwide surveys on the prevalence of specific psychotic disorders and associated co-morbidities.
MethodThe 2010 Australian national psychosis survey used a two-phase design to draw a representative sample of adults aged 18–64 years with psychotic disorders in contact with public treatment services from an estimated resident population of 1 464 923 adults. This paper is based on data from 1642 participants with an International Classification of Diseases (ICD)-10 psychotic disorder. Its aim is to present estimates of treated prevalence and lifetime morbid risk of psychosis, and to describe the cognitive, physical health and substance use profiles of participants.
ResultsThe 1-month treated prevalence of psychotic disorders was 3.10 cases per 1000 population aged 18–64 years, not accounting for people solely accessing primary care services; lifetime morbid risk was 3.45 per 1000. Mean premorbid intelligence quotient was approximately 0.5 s.d.s below the population mean; current cognitive ability (measured with a digit symbol coding task) was 1.6 s.d.s below the population mean. For both cognitive tests, higher scores were significantly associated with better independent functioning. The prevalence of the metabolic syndrome was high, affecting 60.8% of participants, and pervasive across diagnostic groups. Of the participants, two-thirds (65.9%) were current smokers, 47.4% were obese and 32.4% were sedentary. Of the participants, half (49.8%) had a lifetime history of alcohol abuse/dependence and 50.8% lifetime cannabis abuse/dependence.
ConclusionsOur findings highlight the need for comprehensive, integrative models of recovery to maximize the potential for good health and quality of life for people with psychotic illness.
31 - Prospects for the future of mood disorder therapeutics
- from Section 6 - Future directions
- Edited by J. John Mann, Columbia University, New York
- Edited in association with Patrick J. McGrath, Columbia University, New York, Steven P. Roose, Columbia University, New York
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- Clinical Handbook for the Management of Mood Disorders
- Published online:
- 05 May 2013
- Print publication:
- 09 May 2013, pp 394-399
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Summary
Dialectical behavior therapy (DBT) is a form of cognitive behavior therapy (CBT) for mood disorders. There are three categories of core strategies employed in DBT: change strategies, acceptance and validation strategies, and dialectical strategies. Change strategies in DBT, for the most part, are based on learning principles. One rationale for using DBT to treat mood disorders is the significant co-morbidity between borderline personality disorder (BPD) and mood disorders. Adapting DBT is different from adopting DBT. In the latter, DBT, e.g. the modes of treatment delivery, may be changed to meet the needs of the setting or target population. Programs which adopt comprehensive DBT benefit from the existing evidence base. DBT is an efficacious treatment proven to reduce suicidal behavior and nonsuicidal self-injury. DBT has been adapted for both bipolar adolescents and geriatric patients with treatment-resistant depression or depression co-morbid with BPD.
Contents
- Edited by J. John Mann, Columbia University, New York
- Edited in association with Patrick J. McGrath, Columbia University, New York, Steven P. Roose, Columbia University, New York
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- Clinical Handbook for the Management of Mood Disorders
- Published online:
- 05 May 2013
- Print publication:
- 09 May 2013, pp v-vi
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Section 5 - The promise of biomarkers and response prediction
- Edited by J. John Mann, Columbia University, New York
- Edited in association with Patrick J. McGrath, Columbia University, New York, Steven P. Roose, Columbia University, New York
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- Clinical Handbook for the Management of Mood Disorders
- Published online:
- 05 May 2013
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- 09 May 2013, pp 358-393
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Summary
This chapter deals with brain imaging techniques. MRI and computer tomography (CT) scans have been used to identify changes in brain morphology in major depressive disorder (MDD). Functional MRI (fMRI), positron emission tomography (PET), and single photon emission computer tomography (SPECT) have all been utilized to identify regions of the brain that are differentially activated in MDD when compared to healthy control subjects. Altered correlation of activity between the frontal lobe and the amygdale has been reported during fMRI studies of patients with MDD. Both bipolar disorder and MDD are likely heterogeneous conditions with different molecular, cellular, genetic, or environmental causes that produce the same clinical phenotype of the disorder. Technical advances in neuroimaging techniques may allow for new questions to be asked into the biological underpinnings of mood disorders and may be used to predict responses to treatments.
Section 6 - Future directions
- Edited by J. John Mann, Columbia University, New York
- Edited in association with Patrick J. McGrath, Columbia University, New York, Steven P. Roose, Columbia University, New York
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- Clinical Handbook for the Management of Mood Disorders
- Published online:
- 05 May 2013
- Print publication:
- 09 May 2013, pp 394-399
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Summary
There has been considerable controversy over the correct diagnosis for patients with mood disorder associated with the lifetime occurrence of hypomanic symptoms which are sub-threshold for the diagnosis of bipolar disorder. Extrapolating from the accelerating accumulation of knowledge of the biology of psychiatric disorders over the last several decades, it is easy to anticipate that this trend will continue and that such knowledge will define the molecular pathways whereby genes and environment affect the risk for mood disorders. There are early efforts to apply proteomic methods to mood disorders. Electrophysiology, primarily in the form of electroencephalographic recording, has shown significant promise in application to mood disorder therapeutics. An important intellectual trend is that the rapidly advancing technologies of quantitative neuroscience and molecular genetics appear to be making enormous progress toward demonstrating a neurobiological substrate of mood disorder.
Clinical Handbook for the Management of Mood Disorders - Half title page
- Edited by J. John Mann, Columbia University, New York
- Edited in association with Patrick J. McGrath, Columbia University, New York, Steven P. Roose, Columbia University, New York
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- Book:
- Clinical Handbook for the Management of Mood Disorders
- Published online:
- 05 May 2013
- Print publication:
- 09 May 2013, pp i-ii
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