Mobile Behavioral Health Coaching as a Preventive Intervention for Occupational Public Health: Retrospective Longitudinal Study.

Background: Researchers have recently proposed that behavioral health coaching (BHC) is effective in promoting proactive care among employees. However, to qualify as a preventive workplace intervention, more research is needed to evaluate whether BHC can further elevate well-being among moderately mentally healthy employees.

Objective: Using real-world data, this study evaluates the preliminary effectiveness of app-based BHC against a nonrandomized control group with open access to self-help tools in improving well-being (ie, mood levels and perceived stress).

Trends in socioeconomic inequalities in incidence of severe mental illness - A population-based linkage study using primary and secondary care routinely collected data between 2000 and 2017.

Objective: In 2008, the UK entered a period of economic recession followed by sustained austerity measures. We investigate changes in inequalities by area deprivation and urbanicity in incidence of severe mental illness (SMI, including schizophrenia-related disorders and bipolar disorder) between 2000 and 2017.

Methods: We analysed 4.

Preliminary effectiveness of an evidence-based mobile application to promote resilience among working adults in Singapore and Hong Kong: Intensive longitudinal study.

Evidence-based mobile health (mHealth) applications on smartphones are a cost-effective way for employees to take proactive steps to improve well-being and performance. However, little is known about what sustains engagement on these applications and whether they could dynamically improve occupational outcomes such as resilience and mood. Using real-world data, this intensive longitudinal study examines (a) which employees would continually engage with a cognitive behavioural therapy-informed mHealth application ('Intellect'); and (b) if daily engagement of 'Intellect' would relate to better occupational outcomes on the following day.

Widening Excess Mortality During the COVID-19 Pandemic in Individuals Who Self-Harmed.

Studies on COVID-19 pandemic-associated changes in mortality following self-harm remain scarce and inconclusive. To compare mortality risks in individuals who had self-harmed to those for individuals who had not, before and during the COVID-19 pandemic (Waves 1 and 2) in Wales, the United Kingdom, using population-based routinely collected data. We linked whole population health data to all-cause mortality following an episode of self-harm between April 2016 and March 2021.

Self-harm, in-person bullying and cyberbullying in secondary school-aged children: A data linkage study in Wales.

Introduction: Although the evidence base on bullying victimization and self-harm in young people has been growing, most studies were cross-sectional, relied on self-reported non-validated measures of self-harm, and did not separate effects of in-person and cyberbullying. This study aimed to assess associations of self-harm following in-person bullying at school and cyberbullying victimization controlling for covariates.

Methods: School survey data from 11 to 16 years pupils collected in 2017 from 39 Welsh secondary schools were linked to routinely collected data.

Changes in daily mental health service use and mortality at the commencement and lifting of COVID-19 'lockdown' policy in 10 UK sites: a regression discontinuity in time design.

Objectives: To investigate changes in daily mental health (MH) service use and mortality in response to the introduction and the lifting of the COVID-19 'lockdown' policy in Spring 2020.

Design: A regression discontinuity in time (RDiT) analysis of daily service-level activity.

Setting And Participants: Mental healthcare data were extracted from 10 UK providers.

Impact of schizophrenia genetic liability on the association between schizophrenia and physical illness: data-linkage study.

Background: Individuals with schizophrenia are at higher risk of physical illnesses, which are a major contributor to their 20-year reduced life expectancy. It is currently unknown what causes the increased risk of physical illness in schizophrenia.

Aims: To link genetic data from a clinically ascertained sample of individuals with schizophrenia to anonymised National Health Service (NHS) records.

Area deprivation, urbanicity, severe mental illness and social drift - A population-based linkage study using routinely collected primary and secondary care data.

We investigated whether associations between area deprivation, urbanicity and elevated risk of severe mental illnesses (SMIs, including schizophrenia and bipolar disorder) is accounted for by social drift or social causation. We extracted primary and secondary care electronic health records from 2004 to 2015 from a population of 3.9 million.

Developing a standardised approach to the aggregation of inpatient episodes into person-based spells in all specialties and psychiatric specialties.

Background: Electronic health record (EHR) data are available for research in all UK nations and cross-nation comparative studies are becoming more common. All UK inpatient EHRs are based around episodes, but episode-based analysis may not sufficiently capture the patient journey. There is no UK-wide method for aggregating episodes into standardised person-based spells.

Gαi Proteins are Indispensable for Hearing.

Background/aims: From invertebrates to mammals, Gαi proteins act together with their common binding partner Gpsm2 to govern cell polarization and planar organization in virtually any polarized cell. Recently, we demonstrated that Gαi3-deficiency in pre-hearing murine cochleae pointed to a role of Gαi3 for asymmetric migration of the kinocilium as well as the orientation and shape of the stereociliary ("hair") bundle, a requirement for the progression of mature hearing. We found that the lack of Gαi3 impairs stereociliary elongation and hair bundle shape in high-frequency cochlear regions, linked to elevated hearing thresholds for high-frequency sound.

Author Correction: Defective Gpsm2/Gα signalling disrupts stereocilia development and growth cone actin dynamics in Chudley-McCullough syndrome.

This corrects the article DOI: 10.1038/ncomms14907.

Premature mortality among people with severe mental illness - New evidence from linked primary care data.

Studies assessing premature mortality in people with severe mental illness (SMI) are usually based in one setting, hospital (secondary care inpatients and/or outpatients) or community (primary care). This may lead to ascertainment bias. This study aimed to estimate standardised mortality ratios (SMRs) for all-cause and cause-specific mortality in people with SMI drawn from linked primary and secondary care populations compared to the general population.

Defective Gpsm2/Gα signalling disrupts stereocilia development and growth cone actin dynamics in Chudley-McCullough syndrome.

Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gα, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits.

Salience network connectivity in the insula is associated with individual differences in interoceptive accuracy.

The insula and the anterior cingulate cortex are core brain regions that anchor the salience network, one of several large-scale intrinsic functional connectivity networks that have been derived consistently using resting-state functional magnetic resonance imaging (fMRI). While several studies have shown that the insula and anterior cingulate cortex play important roles in interoceptive awareness, no study to date has examined the association between intrinsic salience network connectivity and interoceptive awareness. In this study, we sought to test this idea in 26 healthy young participants who underwent a resting-state fMRI scan and a heartbeat counting task outside the scanner in the same session.

Loss of auditory sensitivity from inner hair cell synaptopathy can be centrally compensated in the young but not old brain.

A dramatic shift in societal demographics will lead to rapid growth in the number of older people with hearing deficits. Poorer performance in suprathreshold speech understanding and temporal processing with age has been previously linked with progressing inner hair cell (IHC) synaptopathy that precedes age-dependent elevation of auditory thresholds. We compared central sound responsiveness after acoustic trauma in young, middle-aged, and older rats.

BDNF in Lower Brain Parts Modifies Auditory Fiber Activity to Gain Fidelity but Increases the Risk for Generation of Central Noise After Injury.

For all sensory organs, the establishment of spatial and temporal cortical resolution is assumed to be initiated by the first sensory experience and a BDNF-dependent increase in intracortical inhibition. To address the potential of cortical BDNF for sound processing, we used mice with a conditional deletion of BDNF in which Cre expression was under the control of the Pax2 or TrkC promoter. BDNF deletion profiles between these mice differ in the organ of Corti (BDNF (Pax2) -KO) versus the auditory cortex and hippocampus (BDNF (TrkC) -KO).

Cochlear NMDA receptors as a therapeutic target of noise-induced tinnitus.

Background: Accumulating evidence suggests that tinnitus may occur despite normal auditory sensitivity, probably linked to partial degeneration of the cochlear nerve and damage of the inner hair cell (IHC) synapse. Damage to the IHC synapses and deafferentation may occur even after moderate noise exposure. For both salicylate- and noise-induced tinnitus, aberrant N-methyl-d-aspartate (NMDA) receptor activation and related auditory nerve excitation have been suggested as origin of cochlear tinnitus.

L-type CaV1.2 deletion in the cochlea but not in the brainstem reduces noise vulnerability: implication for CaV1.2-mediated control of cochlear BDNF expression.

Voltage-gated L-type Ca(2+) channels (L-VGCCs) like CaV1.2 are assumed to play a crucial role for controlling release of trophic peptides including brain-derived neurotrophic factor (BDNF). In the inner ear of the adult mouse, besides the well-described L-VGCC CaV1.

The reduced cochlear output and the failure to adapt the central auditory response causes tinnitus in noise exposed rats.

Tinnitus is proposed to be caused by decreased central input from the cochlea, followed by increased spontaneous and evoked subcortical activity that is interpreted as compensation for increased responsiveness of central auditory circuits. We compared equally noise exposed rats separated into groups with and without tinnitus for differences in brain responsiveness relative to the degree of deafferentation in the periphery. We analyzed (1) the number of CtBP2/RIBEYE-positive particles in ribbon synapses of the inner hair cell (IHC) as a measure for deafferentation; (2) the fine structure of the amplitudes of auditory brainstem responses (ABR) reflecting differences in sound responses following decreased auditory nerve activity and (3) the expression of the activity-regulated gene Arc in the auditory cortex (AC) to identify long-lasting central activity following sensory deprivation.

Noise-induced inner hair cell ribbon loss disturbs central arc mobilization: a novel molecular paradigm for understanding tinnitus.

Increasing evidence shows that hearing loss is a risk factor for tinnitus and hyperacusis. Although both often coincide, a causal relationship between tinnitus and hyperacusis has not been shown. Currently, tinnitus and hyperacusis are assumed to be caused by elevated responsiveness in subcortical circuits.