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The purpose of this study was to evaluate the impact of weighted vests on the amount of time 3 elementary-age students with autism, intellectual disabilities, and sensory processing abnormalities engaged in appropriate in-seat behavior. An alternating treatments design was used to examine the duration of appropriate in-seat behavior under three conditions: baseline or no vests (A), vests with no weights (B), and weighted vests (BC). Because weighted vests did not have an effect on appropriate in-seat behavior for any participant, a second experiment was conducted. Noncontingent reinforcement (NCR) was assessed within the context of a withdrawal design. NCR had an optimal effect on the participants' in-seat behavior. (Contains 2 tables and 6 figures.)

In a phase 2 trial of once‐weekly tirzepatide (1, 5, 10, or 15 mg), dulaglutide (1.5 mg), or placebo, the dual glucose‐dependent insulinotropic polypeptide and glucagon‐like peptide‐1 receptor agonist tirzepatide dose‐dependently reduced HbA1c and body weight in patients with type 2 diabetes. In this post hoc analysis, inflammation, endothelial dysfunction, and cellular stress biomarkers were measured at baseline, 4, 12, and 26 weeks to evaluate the additional effects of tirzepatide on cardiovascular risk factors. At 26 weeks, tirzepatide 10 and 15 mg decreased YKL‐40 (also known as chitinase‐3 like‐protein‐1), intercellular adhesion molecule 1 (ICAM‐1), leptin, and growth differentiation factor 15 levels versus baseline, and YKL‐40 and leptin levels versus placebo and dulaglutide. Tirzepatide 15 mg also decreased ICAM‐1 levels versus placebo and dulaglutide, and high‐sensitivity C‐reactive protein (hsCRP) levels versus baseline and placebo, but not dulaglutide. GlycA, interleukin 6, vascular cell adhesion molecule 1, and N‐terminal‐pro hormone B‐type natriuretic peptide levels were not significantly changed in any group. YKL‐40, hsCRP, and ICAM‐1 levels rapidly decreased within 4 weeks of treatment with tirzepatide 10 and 15 mg, whereas the decrease in leptin levels was more gradual and did not plateau by 26 weeks. In this hypothesis‐generating exploratory analysis, tirzepatide decreased several biomarkers that have been associated with cardiovascular risk. [ABSTRACT FROM AUTHOR]

New chemistry students have trouble with the idea that loss of electrons leads to a more positive oxidation number and with recognizing oxidative and reductive processes. Determining oxidation-reduction on a number line, using the ROLR (Right-Oxidation-Left-Reduction or 'roller') scheme can be helpful. The line can be used for a clearer link between loss or gain of electrons and change in oxidation number. Other mnemonic devices are discussed.

Explores the potential for native American tribe to bring a suit against a state for its refusal to negotiate a tribal-state compact in good faith. Indian tribes' gaming operations investment; Impact of the Indian Gaming Regulatory Act; Evolution of regulatory takings jurisprudence; Function of a regulatory taking analysis in tribal gaming; Similar situations that produced fifth amendment challenges.

The farnesoid X receptor (FXR, NR1H4) is a bile acid-responsive nuclear receptor that plays critical roles in the transcriptional regulation genes involved in cholesterol, bile acid, triglyceride, and carbohydrate metabolism. By microarray analysis of hepatic genes from female Zucker diabetic fatty (ZDF) rats treated with the FXR agonist GW4064, we have identified dimethylarginine dimethylaminohydrolase-1 (DDAH1) as an FXR target gene. DDAH1 is a key catabolic enzyme of asymmetric dimethylarginine (ADMA), a major endogenous nitric-oxide synthase inhibitor. Sequence analysis of the DDAH1 gene reveals the presence of an FXR response element (FXRE) located 90 kb downstream of the transcription initiation site and within the first intron. Functional analysis of the putative FXRE demonstrated GW4064 dose-dependent transcriptional activation from the element, and we have demonstrated that the FXRE sequence binds the FXR-RXR heterodimer. In vivo administration of GW4064 to female ZDF rats promoted a dose-dependent and >6-fold increase in hepatic DDAH1 gene expression. The level of serum ADMA was reduced concomitantly. These findings provide a mechanism by which FXR may increase endothelium-derived nitric oxide levels through modulation of serum ADMA levels via direct regulation of hepatic DDAH1 gene expression. Thus, beneficial clinical outcomes of FXR agonist therapy may include prevention of atherosclerosis and improvement of the metabolic syndrome. [ABSTRACT FROM AUTHOR]