Linking Adherence to Effectiveness in Family-Based Adolescent ADHD Academic Training and Medication Decision-Making Protocols.

Objective: Changing Academic Support in the Home for Adolescents with ADHD (CASH-AA) and Medication Integration Protocol (MIP) are two family-based behavioral protocols designed to promote family solutions to academic problems and medication decision-making. Building on a randomized control trial examining these protocols, the current study examined how protocol dose, an indicator of treatment adherence, was associated with treatment outcomes.

Method: The sample consisted of 145 adolescent clients (M age = 14.

Measurement of Λ_{b}^{0}, Λ_{c}^{+}, and Λ Decay Parameters Using Λ_{b}^{0}→Λ_{c}^{+}h^{-} Decays.

A comprehensive study of the angular distributions in the bottom-baryon decays Λ_{b}^{0}→Λ_{c}^{+}h^{-}(h=π,K), followed by Λ_{c}^{+}→Λh^{+} with Λ→pπ^{-} or Λ_{c}^{+}→pK_{S}^{0} decays, is performed using a data sample of proton-proton collisions corresponding to an integrated luminosity of 9  fb^{-1} collected by the LHCb experiment at center-of-mass energies of 7, 8, and 13 TeV. The decay parameters and the associated charge-parity (CP) asymmetries are measured, with no significant CP violation observed. For the first time, the Λ_{b}^{0}→Λ_{c}^{+}h^{-} decay parameters are measured.

Problem Adaptation Therapy for Older Adults with Chronic Pain and Negative Emotions in Primary Care (PATH-Pain): A Randomized Clinical Trial.

Objective: To test the efficacy of Problem Adaptation Therapy for Pain (PATH-Pain) versus Usual Care (UC) in reducing pain-related disability, pain intensity, and depression among older adults with chronic pain and negative emotions.

Design: RCT assessing the between-group differences during the acute (0-10 weeks) and follow-up (weeks 11-24) phase of treatment.

Setting: A geriatrics primary care site.

Complex Genetic Framework in Familial Amyotrophic Lateral Sclerosis With a C9ORF72 Mutation: A Case Report.

A significantly diverse clinical presentation of amyotrophic lateral sclerosis (ALS), even in its best-studied familial form, continues to hinder current efforts to develop effective disease-modifying drugs for the cure of this rapidly progressive, fatal neuromuscular disease. We have previously shown that clinical heterogeneity of sporadic ALS (sALS) could be explained, at least in part, by its polygenic nature as well as by the presence of mutated genes linked to non-ALS neurological diseases and genes known to mediate ALS-related pathologies. We hypothesized that a similar genetic framework could also be present in patients with familial ALS (fALS).