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Background: Produce prescription programs are gaining traction in the U.S.; however, data on the impact of such approaches in pediatric populations are limited. The purpose of our clinic-based comparative effectiveness randomized controlled trial (CE RCT) is to evaluate the preliminary effectiveness of two produce prescription strategies (at-home delivery and grocery store vouchers) implemented by the Brighter Bites non-profit organization in improving obesity-related health outcomes and dietary behaviors among low-income 5-12-year-olds in Houston, Texas. This paper presents the study design, intervention components, and the study measures., Methods: Participants (n = 150) are being recruited from two pediatric clinics in Houston, Texas. Child eligibility criteria are aged 5-12 years, Medicaid recipients, body-mass index (BMI) percentile ≥85 and living within 10 miles of a Brighter Bites distribution site. Following consent and baseline measures, children are randomized into one of three arms: (1) Bi-weekly $25 vouchers redeemable for produce at stores (n = 50), (2) Bi-weekly produce delivery to participants' homes through DoorDash (n = 50), and (3) wait-list usual care controls (n = 50). Intervention participants also receive Brighter Bites nutrition education materials. Main child outcome measures are BMI z-scores, blood pressure, hemoglobin A1c, liver panels, and lipid panels. Other outcomes including household food insecurity, child diet quality, and home nutrition environment will be collected through parent surveys. Outcome measures are collected at baseline and post-intervention. Process evaluation will measure program dosage, reach, acceptability, and feasibility., Conclusions: Our paper presents the design and next steps to ensure the successful implementation of a produce prescription program in a pediatric clinic setting., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dr. Shreela Sharma serves on the board of directors of Brighter Bites 501c3 non-profit organization. This is an unpaid board position. No other authors report any conflicts of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: The microtubule-associated protein tau accumulates into toxic aggregates in multiple neurodegenerative diseases. We found previously that loss of D 2 -family dopamine receptors ameliorated tauopathy in multiple models including a Caenorhabditis elegans model of tauopathy., Methods: To better understand how loss of D 2 -family dopamine receptors can ameliorate tau toxicity, we screened a collection of C. elegans mutations in dopamine-related genes (n = 45) for changes in tau transgene-induced behavioral defects. These included many genes responsible for dopamine synthesis, metabolism, and signaling downstream of the D 2 receptors., Results: We identified one dopamine synthesis gene, DOPA decarboxylase (DDC), as a suppressor of tau toxicity in tau transgenic worms. Loss of the C. elegans DDC gene, bas-1, ameliorated the behavioral deficits of tau transgenic worms, reduced phosphorylated and detergent-insoluble tau accumulation, and reduced tau-mediated neuron loss. Loss of function in other genes in the dopamine and serotonin synthesis pathways did not alter tau-induced toxicity; however, their function is required for the suppression of tau toxicity by bas-1. Additional loss of D 2 -family dopamine receptors did not synergize with bas-1 suppression of tauopathy phenotypes., Conclusions: Loss of the DDC bas-1 reduced tau-induced toxicity in a C. elegans model of tauopathy, while loss of no other dopamine or serotonin synthesis genes tested had this effect. Because loss of activity upstream of DDC could reduce suppression of tau by DDC, this suggests the possibility that loss of DDC suppresses tau via the combined accumulation of dopamine precursor levodopa and serotonin precursor 5-hydroxytryptophan., (Published by Elsevier Inc.)