Methods: The 12-month prevalence of specific psychopathological syndromes among 1772 adults from the general population was estimated by a structured interview.

Additionally, participants underwent spirometry and were asked about obstructive lung disease in the year prior to the study.

Logistic and linear regression models were used to relate obstructive lung disease and spirometrically defined airway obstruction to mental health problems.

Results: Mental health problems were found in 35.7% of the participants. After adjusted for sociodemographic, clinical and life-style factors, asthma and chronic bronchitis were associated with almost all domains of mental health problems. In contrast, independent of its definition, spirometric airflow limitation was only related to generalized anxiety (odds ratios ranging from 2.3 to 2.7).

A reduced ratio of forced expiratory volume in one second to forced vital capacity was associated with mental health problems in general and panic and general anxiety in particular.

Conclusion: Our findings suggest an association of objective measure of airflow limitation to generalized anxiety and panic.

While the causal relationship between obstructive lung disease, airflow limitation and anxiety remains to be determined, clinicians should pay diagnostic attention to the significant overlap of these conditions.

Abstract

This article describes the history of the diagnostic class of neurodevelopmental disorders (NDDs) up to DSM-5.

We further analyze how the development of genetics will transform the classification and diagnosis of NDDs. In DSM-5, NDDs include intellectual disability (ID), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD).

Physicians in German-, French- and English-speaking countries (eg, Weikard, Georget, Esquirol, Down, Asperger, and Kanner) contributed to the phenomenological definitions of these disorders throughout the 18th and 20th centuries.

These diagnostic categories show considerable comorbidity and phenotypic overlap. NDDs are one of the chapters of psychiatric nosology most likely to benefit from the approach advocated by the National Institute of Mental Health’s Research Domain Criteria project.

Genetic research supports the hypothesis that ID, ASD, ADHD, schizophrenia, and bipolar disorder lie on a neurodevelopmental continuum.

The identification of recurrently observed copy number variants and disruptive gene variants in ASD (eg, CDH8, 16p11.2, SCN2A) led to the adoption of the genotype-first approach to characterize individuals at the etiological level.


Reams of relevant research (including our own) proves Jobs right. Innovators excel at connecting the unconnected. They engage in associational thinking.

At Apple (or at any innovative company), they take a little bit of this, sprinkle in a little bit of that and that and that to churn out market-busting ideas such as iTunes, and the iPod, iPhone, and iPad (along with a few market disasters like the G4 Cube computer).

Abstractin English, Spanish, French

This article describes the history of the diagnostic class of neurodevelopmental disorders (NDDs) up to DSM-5.

We further analyze how the development of genetics will transform the classification and diagnosis of NDDs. In DSM-5, NDDs include intellectual disability (ID), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD).

Physicians in German-, French- and English-speaking countries (eg, Weikard, Georget, Esquirol, Down, Asperger, and Kanner) contributed to the phenomenological definitions of these disorders throughout the 18th and 20th centuries.

These diagnostic categories show considerable comorbidity and phenotypic overlap.

NDDs are one of the chapters of psychiatric nosology most likely to benefit from the approach advocated by the National Institute of Mental Health's Research Domain Criteria project.

Genetic research supports the hypothesis that ID, ASD, ADHD, schizophrenia, and bipolar disorder lie on a neurodevelopmental continuum.

The identification of recurrently observed copy number variants and disruptive gene variants in ASD (eg, CDH8, 16p11.2, SCN2A) led to the adoption of the genotype-first approach to characterize individuals at the etiological level. .

Abstract

Events in fetal life impact long-term health outcomes. The placenta is the first organ to form and is the site of juxtaposition between the maternal and fetal circulations.

Most diseases of pregnancy are caused by, impact, or are reflected in the placenta.

The purpose of this review is to describe the main inflammatory processes in the placenta, discuss their immunology, and relate their short- and long-term disease associations.

Acute placental inflammation (API), including maternal and fetal inflammatory responses corresponds to the clinical diagnosis of chorioamnionitis and is associated with respiratory and neurodevelopmental diseases.

The chronic placental inflammatory pathologies (CPI), include chronic villitis of unknown etiology, chronic deciduitis, chronic chorionitis, eosinophilic T-cell vasculitis, and chronic histiocytic intervillositis.

These diseases are less-well studied, but have complex immunology and show mechanistic impacts on the fetal immune system.

Overall, much work remains to be done in describing the long-term impacts of placental inflammation on offspring health.

Abstract

Maternal infection and inflammation during pregnancy are associated with neurodevelopmental disorders in offspring, but little is understood about the molecular mechanisms underlying this epidemiologic phenomenon.

Here, we leveraged single-cell RNA sequencing to profile transcriptional changes in the mouse fetal brain in response to maternal immune activation (MIA) and identified perturbations in cellular pathways associated with mRNA translation, ribosome biogenesis and stress signaling.

We found that MIA activates the integrated stress response (ISR) in male, but not female, MIA offspring in an interleukin-17a-dependent manner, which reduced global mRNA translation and altered nascent proteome synthesis.

Moreover, blockade of ISR activation prevented the behavioral abnormalities as well as increased cortical neural activity in MIA male offspring.

Our data suggest that sex-specific activation of the ISR leads to maternal inflammation-associated neurodevelopmental disorders.

New insights into the detection, pathophysiology and treatment of inflammation-induced injury in the immature brain

The immature brain is especially vulnerable to inflammatory factors, before, during and after birth. This publication presents new insights into the detection, pathophysiology and treatment of inflammation-induced injury in the developing brain from both clinical and basic science perspectives.

Cellular mechanisms that lead to perinatal brain injury are presented, with specific emphasis on inflammation, brain development and potential treatment strategies. In particular, studies report on inflammatory pathways involved in perinatal brain injury, including caspases, STAT3, toll-like receptors and oxidative stress. Some data demonstrate how different inflammatory cell types may contribute to the injury, such as microglia and mast cells, and how peripheral organs can influence the cerebral inflammatory response.

Further, new developments in neuroprotective therapies using human amnion epithelial cells to reduce inflammation-induced brain damage in the fetus are described.

This publication is recommended to both clinicians and basic scientists who are interested in the developing nervous system, its vulnerability to inflammation and the short- and long-term consequences for neurologic development.