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Objective: Training programs exist that prepare college students, faculty, and staff to identify and support students potentially at risk for suicide. Kognito is an online program that trains users through simulated interactions with virtual humans. This study evaluated Kognito's effectiveness in preparing users to intervene with at-risk students. Participants: Training was completed by 2,727 university students, faculty, and staff from April, 2014 through September, 2015. Methods: Voluntary and mandatory participants at a land-grant university completed Kognito modules designed for higher education, along with pre- and post-assessments. Results: All modules produced significant gains in reported Preparedness, Likelihood, and Self-Efficacy in intervening with troubled students. Despite initial disparities in reported abilities, after training participants reported being similarly capable of assisting at-risk students, including LGBTQ and veteran students. Conclusions: Kognito training appears to be effective, on a large scale, in educating users to act in a facilitative role for at-risk college students.

Microdeletion of the human 16p11.2 gene locus has been linked to autism spectrum disorder (ASD) and intellectual disability and confers risk for a number of other neurodevelopmental deficits. Transgenic mice carrying 16p11.2 deletion (16p11+/-) display phenotypes reminiscent of those in human patients with 16p11.2 deletion syndrome, but the molecular mechanisms and treatment strategies for these phenotypes remain unknown. In this study, we have found that both male and female 16p11+/- mice exhibit deficient NMDA receptor (NMDAR) function in the medial prefrontal cortex (mPFC), a brain region critical for high-level "executive" functions. Elevating the activity of mPFC pyramidal neurons with a CaMKII-driven Gq-DREADD (Gq-coupled designer receptors exclusively activated by designer drugs) led to the significant increase of NR2B subunit phosphorylation and the restoration of NMDAR function, as well as the amelioration of cognitive and social impairments in 16p11+/- mice. These results suggest that NMDAR hypofunction in PFC may contribute to the pathophysiology of 16p11.2 deletion syndrome and that restoring PFC activity is sufficient to rescue the behavioral deficits. [ABSTRACT FROM AUTHOR]

One of the core symptoms of autism spectrum disorder (ASD) is impaired social interaction. Currently, no pharmacotherapies exist for this symptom due to complex biological underpinnings and distinct genetic models which fail to represent the broad disease spectrum. One convincing hypothesis explaining social deficits in human ASD patients is amotivation, however it is unknown whether mouse models of ASD represent this condition. Here we used two highly trusted ASD mouse models (male Shank3‐deficient [Shank3+/ΔC] mice modeling the monogenic etiology of ASD, and inbred BTBR mice [both male and female] modeling the idiopathic and highly polygenic pathology for ASD) to evaluate the level of motivation to engage in a social interaction. In the behavioral paradigms utilized, a social stimulus was placed in the open arm of the elevated plus maze (EPM), or the light compartment of the light‐dark box (LDB). To engage in a social interaction, mice were thus required to endure innately aversive conditions (open areas, height, and/or light). In the modified EPM paradigm, both Shank3+/ΔC and BTBR mice demonstrated decreased open‐arm engagement with a social stimulus but not a novel object, suggesting reduced incentive to engage in a social interaction in these models. However, these deficits were not expressed under the less severe aversive pressures of the LDB. Collectively, we show that ASD mouse models exhibit diminished social interaction incentive, and provide a new investigation strategy facilitating the study of the neurobiological mechanisms underlying social reward and motivation deficits in neuropsychiatric disorders. [ABSTRACT FROM AUTHOR]

We report on a solid-state-based laser system at 1028 nm. The light is generated by a diode laser seeded ytterbium fiber amplifier. In two build-up cavities, its frequency is doubled and quadrupled to 514 nm and 257 nm, respectively. At 514 nm, the system delivers up to 4.7 W of optical power. In the fourth harmonic, up to 173 mW are available limited by the nonlinear crystal. The frequency of the laser is mode-hop-free tunable by 16 GHz in 10 ms in the UV. Therefore, the system is suitable as a low maintenance, efficient, and tunable narrowband replacement for frequency doubled Ar + laser systems.