Attention-deficit/hyperactivity disorder (ADHD) is the most common mental disorder in childhood, and primary care clinicians provide a major component of the care for children with ADHD. However, because of limited available evidence, the American Academy of Pediatrics guidelines did not include adolescents and young adults. Contrary to previous beliefs, it has become clear that, in most cases, ADHD does not resolve once children enter puberty. This article reviews the current evidence about the diagnosis and treatment of adolescents and young adults with ADHD and describes how the information informs practice. It describes some of the unique characteristics observed among adolescents, as well as how the core symptoms change with maturity. The diagnostic process is discussed, as well as approaches to the care of adolescents to improve adherences. Both psychosocial and pharmacologic interventions are reviewed, and there is a discussion of these patients' transition into young adulthood. The article also indicates that research is needed to identify the unique adolescent characteristics of ADHD and effective psychosocial and pharmacologic treatments.

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In this challenging, high-needs client group, early-programme stage of change, therapists' perceptions of motivation, therapeutic alliance and psychopathy did not predict how much change prisoners made. Regardless of initial levels, prisoners whose alliance increased the most over the course of treatment made the most change.

The insulinotropic actions of glucagon-like peptide 1 receptor (GLP-1R) in b-cells have made it a useful target to manage type 2 diabetes. Metabolic stress reduces b-cell sensitivity to GLP-1, yet the underlying mechanisms are unknown. We hypothesized that Glp1r expression is heterogeneous among b-cells and that metabolic stress decreases the number of GLP-1R positive b-cells. Here, analyses of publicly-available single-cell RNA-Seq sequencing (scRNASeq) data from mouse and human β-cells indicated that significant populations of b-cells do not express the Glp1r gene, supporting heterogeneous GLP-1R expression. To check these results, we used complementary approaches employing FACS coupled with quantitative RT-PCR, a validated GLP-1R antibody, and flow cytometry to quantify GLP-1R promoter activity, gene expression, and protein expression in mouse α-, β-, and δ-cells. Experiments with Glp1r reporter mice and a validated GLP-1R antibody indicated that >90% of the b-cells are GLP-1R positive, contradicting the findings with the scRNASeq data. α-cells did not express Glp1r mRNA and δ-cells expressed Glp1r mRNA but not protein. We also examined the expression patterns of GLP-1R in mouse models of metabolic stress. Multiparous female mice had significantly decreased β-cell Glp1r expression, but no reduction in GLP-1R protein levels or GLP-1R-mediated insulin secretion. These findings suggest caution in interpreting the results of scRNASeq for low abundance transcripts such as the incretin receptors and indicate that GLP-1R is widely expressed in β-cells, absent in α-cells, and expressed at the mRNA, but not protein, level in δ-cells.

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