Development and Technical Adequacy of the District Capacity Assessment

The purpose of this article is to describe the methods and results used to establish the district capacity assessment’s (DCA) content validity, response process validity, construct validity, internal consistency, and test–retest reliability. The DCA measures a district’s ability to support school-level implementation of evidence-based practices (EBPs). Assessment results are then used to guide action planning. The DCA is grounded in the understanding that districts must develop knowledge and skills in the use of implementation science methods if they are to support successful use of an innovation. Specifically, three studies were conducted. The first study established the DCA’s content validity, that is, the extent to which the DCA represents constructs comprising district-level implementation capacity. The second study established the DCA’s internal structure, or the relationships among the items compared to the constructs being measured and how well the items measured the same construct. The third and final study assessed how the results of the DCA varied over time, thus establishing the instrument’s test–retest reliability. District Implementation Teams, researchers, or facilitators who use the DCA can be confident that the assessment is founded on research drawing from implementation science practices and methods

Human genetics and neuropathology suggest a link between miR-218 and amyotrophic lateral sclerosis pathophysiology

Motor neuron–specific microRNA-218 (miR-218) has recently received attention because of its roles in mouse development. However, miR-218 relevance to human motor neuron disease was not yet explored. Here, we demonstrate by neuropathology that miR-218 is abundant in healthy human motor neurons. However, in amyotrophic lateral sclerosis (ALS) motor neurons, miR-218 is down-regulated and its mRNA targets are reciprocally up-regulated (derepressed). We further identify the potassium channel Kv10.1 as a new miR-218 direct target that controls neuronal activity. In addition, we screened thousands of ALS genomes and identified six rare variants in the human miR-218-2 sequence. miR-218 gene variants fail to regulate neuron activity, suggesting the importance of this small endogenous RNA for neuronal robustness. The underlying mechanisms involve inhibition of miR-218 biogenesis and reduced processing by DICER. Therefore, miR-218 activity in motor neurons may be susceptible to failure in human ALS, suggesting that miR-218 may be a potential therapeutic target in motor neuron disease