Serving Justice-Involved Youth with Disabilities

Disability is an important intersectional identity in juvenile justice trends. Youth with intellectual disabilities, developmental disabilities, and mental health disabilities are more likely to be involved in the juvenile justice system or multiple systems, and intersecting identities can increase the risk of justice involvement, particularly when disability overlaps with other identities associated with higher rates of discipline or justice involvement, such as race and lower socioeconomic status. This points to the importance of practitioners being aware of personal and systemic barriers that may influence youths’ experiences and outcomes related to key transition points. Youth with disabilities often require more intense and individualized services during and after justice involvement, and overall have poor post-release education and employment outcomes. Many youth experience challenges in obtaining resources and navigating multiple systems, necessitating additional transition support as they pursue life outcomes. Locating and reaching out to justice-involved youth with disabilities served by multiple systems is a known challenge. Success in this area requires strong collaborations between state and local government agencies, and the community partners and stakeholders who support youth upon release. In this policy brief, the authors discuss barriers and evidence-based practices in locating, serving, and supporting justice-involved youth with disabilities, focusing on efforts to re-engage youth with their former setting (school, home, and community), while also preparing them for future education, employment, independent living, and reducing the risk of recidivism through appropriate resources, services, and supports

Effect of New Zealand Blackcurrant Extract on Performance During the Running Based Anaerobic Sprint Test in Trained Youth and Recreationally Active Male Football Players

It was observed previously that New Zealand blackcurrant (NZBC) extract reduced slowing of the maximal 15 m sprint speed during the Loughborough Intermittent Shuttle Test. We examined the effect of NZBC extract on the performance of the Running Based Anaerobic Sprint Test (RAST, 6 × 35-m sprints with 10 seconds passive recovery) in trained youth and recreationally active football players. Fifteen recreationally active (University team) (age: 20 ± 1 years, height: 174 ± 19 cm, body mass: 80 ± 13 kg) and nine trained youth players (English professional club) (age: 17 ± 0 years, height: 178 ± 8 cm, body mass: 69 ± 9 kg, mean ± SD) participated in three testing sessions. Prior to the RASTs, participants consumed two capsules of NZBC extract (600 mg?day?1 CurraNZ®) or placebo (P) for 7 days (double blind, randomised, cross-over design, wash-out at least 14 days). Ability difference between groups was shown by sprint 1 time. In the placebo condition, trained youth players had faster times for sprint 1 (5.00 ± 0.05 s) than recreationally active players (5.42 ± 0.08 s) (p < 0.01). In trained youth players, there was a trend for an effect of NZBC extract (p = 0.10) on the slowing of the sprint 1 time. NZBC extract reduced slowing of the sprint 5 time (P: 0.56 ± 0.22 s; NZBC: 0.35 ± 0.25, p = 0.02) and this was not observed in recreationally active players (P: 0.57 ± 0.48 s; NZBC: 0.56 ± 0.33, p = 0.90). For fatigue index, expressed as a % change in fastest sprint time, there was a strong trend to be lower in both trained youth and recreationally active players combined by NZBC extract (P: ?13 ± 7%; NZBC: ?11 ± 6%, p = 0.06) with 12 participants (five trained youth) experiencing less fatigue. New Zealand blackcurrant extract seems to benefit repeated sprint performance only in trained football players

Skin manifestations of inborn errors of NF-κB

More than 400 single gene defects have been identified as inborn errors of immunity, including many arising from genes encoding proteins that affect NF-κB activity. We summarise the skin phenotypes in this subset of disorders and provide an overview of pathogenic mechanisms. NF-κB acts cell-intrinsically in basal epithelial cells during differentiation of skin appendages, influences keratinocyte proliferation and survival, and both responses to and amplification of inflammation, particularly TNF. Skin phenotypes include ectodermal dysplasia, reduction and hyperproliferation of keratinocytes, and aberrant recruitment of inflammatory cells, which often occur in combination. Phenotypes conferred by these rare monogenic syndromes often resemble those observed with more common defects. This includes oral and perineal ulceration and pustular skin disease as occurs with Behcet's disease, hyperkeratosis with microabscess formation similar to psoriasis, and atopic dermatitis. Thus, these genotype-phenotype relations provide diagnostic clues for this subset of IEIs, and also provide insights into mechanisms of more common forms of skin disease

Prioritising biosecurity investment between protecting agricultural and environmental systems

This paper is motivated by the observation that there is a difference between the time paths of damage valuations for invasions which affect agricultural compared with environmental systems. In particular, unlike agricultural systems, studies have shown that the social valuation of an environmental system is likely to be exponentially positively related to the extent of its deterioration. This paper explores the implications of this difference in determining biosecurity investment priorities. It is concluded that because of this difference an environmental system will often not be prioritised for such protection over an agricultural system even though its ultimate social value exceeds that of the agricultural system

\u3ci\u3eVarroa destructor\u3c/i\u3e Mites Vector and Transmit Pathogenic Honey Bee Viruses Acquired From an Artificial Diet

The ectoparasitic mite Varroa destructoris one of the most destructive pests of the honey bee (Apis mellifera) and the primary biotic cause of colony collapse in many regions of the world. These mites inflict physical injury on their honey bee hosts from feeding on host hemolymph and fat body cells/cellular components, and serve as the vector for deadly honey bee viruses, including Deformed wing virus (DWV) and the related Varroa destructor virus-1 (VDV-1) (i.e., DWV-like viruses). Studies focused on elucidating the dynamics of Varroa-mediated vectoring and transmission of DWV-like viruses may be confounded by viruses present in ingested host tissues or the mites themselves. Here we describe a system that includes an artificial diet free of insect tissue-derived components for maintaining Varroa mites for in vitro experimentation. Using this system, together with the novel engineered cDNA clone-derived genetically tagged VDV-1 and wild-type DWV, we demonstrated for the first time that Varroa mites provided an artificial diet supplemented with engineered viruses for 36 hours could acquire and transmit sufficient numbers of virus particles to establish an infection in virus-naïve hosts. While the in vitro system described herein provides for only up to five days of mite survival, precluding study of the long-term impacts of viruses on mite health, the system allows for extensive insights into the dynamics of Varroa-mediated vectoring and transmission of honey bee viruses

Recurrent miscalling of missense variation from short-read genome sequence data

Background: Short-read resequencing of genomes produces abundant information of the genetic variation of individuals. Due to their numerous nature, these variants are rarely exhaustively validated. Furthermore, low levels of undetected variant miscalling will have a systematic and disproportionate impact on the interpretation of individual genome sequence information, especially should these also be carried through into in reference databases ofgenomic variation. Results: We find that sequence variation from short-read sequence data is subject to recurrent-yet-intermittent miscalling that occurs in a sequence intrinsic manner and is very sensitive to sequence read length. The miscalls arise from difficulties aligning short reads to redundant genomic regions, where the rate of sequencing error approaches the sequence diversity between redundant regions. We find the resultant miscalled variants to be sensitive to small sequence variations between genomes, and thereby are often intrinsic to an individual, pedigree, strain or human ethnic group. In human exome sequences, we identify 2–300 recurrent false positive variants per individual, almost all of which are present in public databases of human genomic variation. From the exomes of non-reference strains of inbred mice, we identify 3–5000 recurrent false positive variants per mouse – the number of which increasing with greater distance between an individual mouse strain and the reference C57BL6 mouse genome. We show that recurrently miscalled variants may be reproduced for a given genome from repeated simulation rounds of read resampling, realignment and recalling. As such, it is possible to identify more than two-thirds of false positive variation from only ten rounds of simulation. Conclusion: Identification and removal of recurrent false positive variants from specific individual variant sets will improve overall data quality. Variant miscalls arising are highly sequence intrinsic and are often specific to an individual, pedigree or ethnicity. Further, read length is a strong determinant of whether given false variants will be called for any given genome – which has profound significance for cohort studies that pool datasets collected and sequenced at different points in time