Discriminant and Concurrent Validity of a Simplified DSM-Based Structured Diagnostic Instrument for the Assessment of Autism Spectrum Disorders in Youth and Young Adults

Background: To evaluate the concurrent and discriminant validity of a brief DSM-based structured diagnostic interview for referred individuals with autism spectrum disorders (ASDs). Methods: To test concurrent validity, we assessed the structured interview's agreement in 123 youth with the expert clinician assessment and the Social Responsiveness Scale (SRS). Discriminant validity was examined using 1563 clinic-referred youth. Results: The structured diagnostic interview and SRS were highly sensitive indicators of the expert clinician assessment. Equally strong was the agreement between the structured interview and SRS. We found evidence for high specificity for the structured interview. Conclusions: A simplified DSM-based ASD structured diagnostic interview could serve as a useful diagnostic aid in the assessment of subjects with ASDs in clinical and research settings

Transitional objects of grief

CITATION: Goldstein, Richard D. et al. 2020. Transitional objects of grief. Comprensive Psychiatry, 98:152161, doi:10.1016/j.comppsych.2020.152161.The original publication is available at: https://www.ncbi.nlm.nih.govBackground: Transitional objects provide security and symbolic connection with valued others when separated from them. Bereaved parents often keep, cherish and visit saved objects of their deceased child. This research examined the hypothesis that these objects behave as transitional objects of grief in bereaved mothers during three years following their infants' deaths from Sudden Infant Death Syndrome. Methods: Questionnaires were administered asking about the presence of kept objects and momentos from their deceased infant, and the frequency, location and emotions experienced during visits to them. Diagnostic criteria for Prolonged Grief Disorder (PGD) were assessed using the Parental Bereavement Questionnaire. Results: 98.6% of the mothers reported having transitional objects of grief, and most visited them more frequently than once per week regardless of PGD status. Mothers with PGD reported significantly more distress when visiting the objects, especially those visiting them privately. Mothers with PGD who felt comforted by the objects had lower risk for finding life meaningless or finding discussion about the infant intolerable. Conclusions: Transitional objects of grief are common and associated with key aspects of grief. There is a need to understand the potential therapeutic uses of transitional objects in promoting bereavement adjustment.Publisher's versio

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Using social and behavioural science to support COVID-19 pandemic response

The COVID-19 pandemic represents a massive global health crisis. Because the crisis requires large-scale behaviour change and places significant psychological burdens on individuals, insights from the social and behavioural sciences can be used to help align human behavior with the recommendations of epidemiologists and public health experts. Here we discuss evidence from a selection of research topics relevant to pandemics, including work on navigating threats, social and cultural influences on behaviour, science communication, moral decision-making, leadership, and stress and coping. In each section, we note the nature and quality of prior research, including uncertainty and unsettled issues. We identify several insights for effective response to the COVID-19 pandemic, and also highlight important gaps researchers should move quickly to fill in the coming weeks and months

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

hyperactivity disorder 10-year study of individuals with and without attention-deficit Cigarette smoking as a risk factor for other substance misuse: References Cigarette smoking as a risk factor for other substance misuse: 10-year study of individuals wi

Numerous studies have documented that attention-deficit hyperactivity disorder (ADHD) increases the risk for nicotine use across the life cycle. Milberger et al 1,2 found significant associations between ADHD and cigarette smoking in both referred and non-referred paediatric samples. Those studies documented that ADHD increased the risk for cigarette smoking in early adolescence twofold and was associated with a 2-year earlier age at onset than controls. Likewise, Tercyak et al 3 found that adolescents with ADHD were three times more likely to smoke than adolescents without ADHD. Pomerleau et al 4 documented that adult ADHD is associated with, and an increased risk for, tobacco addiction and, among smokers, increased difficulty quitting. Glass & Flory 5 summarised several possible mechanisms for this relationship, including the self-medication hypothesis and other social, cognitive and psychopathological factors. The extant literature also supports an association between ADHD and other substance use disorders (alcohol or drug misuse or dependence) that establishes itself by mid to late adolescence. Milberger et al 6 showed that although non-nicotine substance use disorders were not associated with ADHD in early to midadolescence, they were significantly and robustly associated with ADHD by late adolescence. Using two 10-year follow-up studies of ADHD, Wilens and colleagues 7 found that ADHD was a significant risk factor for the development of substance use disorders and cigarette smoking in both genders. These findings bear remarkable congruence to results from retrospective studies of adults with and without ADHD that show that ADHD is associated with an increased risk for drug and alcohol misuse and dependence substance use disorders that tend to emerge in late adolescence and young adulthood. 207 Cigarette smoking as a risk factor for other substance misuse: 10-year study of individuals with and without attention-deficit hyperactivity disorder Joseph Biederman, Carter R. Petty, Paul Hammerness, Holly Batchelder and Stephen V. Faraone Background We previously documented that cigarette smoking is a risk factor for subsequent alcohol and drug misuse and dependence in adolescent girls with attention-deficit hyperactivity disorder (ADHD)