Safety and efficacy of a digital therapeutic for substance use disorder: Secondary analysis of data from a NIDA clinical trials network study.

: Traditional treatments for substance use disorders (SUDs) rely heavily on face-to-face interactions, which pose substantial limitations for patients. A clinical trial of a digital therapeutic (DT), delivering behavioral therapy demonstrated safety and efficacy in a population including patients with opioid use disorder (OUD) not treated with buprenorphine, which is not a guideline-recommended approach. This study re-analyzed the data excluding patients with OUD to more closely approximate real-world patient populations.

Real-world evidence from users of a behavioral digital therapeutic for chronic insomnia.

Background: There have been many research trials of various digital therapeutics, but few real world evaluations of their efficacy. This type of data, however, can provide a more rounded understanding of their impact, utility, reach, and adoption. Findings presented here focus on outcome and patient engagement data of SHUTi (Sleep Health Using the Internet), a digital therapeutic delivering Cognitive Behavioral Therapy for insomnia (CBT-I), in a large real-world dataset of adults with insomnia.

Engagement patterns with a digital therapeutic for substance use disorders: Correlations with abstinence outcomes.

Introduction: Patient engagement may play a key role in the success or failure of treatments for substance use disorder (SUD). This exploratory analysis of data from a large, multisite effectiveness trial (NCT01104805) sought to determine how patient engagement with a digital therapeutic for SUD delivered at clinics was associated with abstinence outcomes.

Methods: The study evaluated engagement for 206 participants enrolled in a treatment program for SUDs related to cocaine, alcohol, cannabis, or other stimulants who were randomized to receive treatment as usual (TAU) or reduced TAU plus the digital Therapeutic Education System (TES) for 12 weeks.

Evaluation of the cost-utility of a prescription digital therapeutic for the treatment of opioid use disorder.

The opioid epidemic continues to generate a significant mental and physical health burden on patients, and claims the life of almost 150 Americans daily. Making matters worse, an increase in relapses and/or opioid-related deaths has been reported in more than 40 U.S.

Safety and efficacy of a prescription digital therapeutic as an adjunct to buprenorphine for treatment of opioid use disorder.

Objectives: To evaluate the safety and efficacy of a digital therapeutic in treatment-seeking individuals with opioid use disorder (OUD) in an analysis of randomized clinical trial (RCT) data (ClinicalTrials.gov identifier: NCT00929253).

Methods: Secondary analysis of an RCT including 170 adults meeting DSM-IV criteria for OUD.

Real-world evidence for a prescription digital therapeutic to treat opioid use disorder.

Objectives: To evaluate patient engagement and usage of a prescription digital therapeutic (PDT) and associated outcomes of opioid use and treatment retention in a large real-world dataset of patients with opioid use disorder (OUD) treated with buprenorphine medication for opioid use disorder (MOUD). PDTs are software-based disease treatments evaluated for safety and effectiveness in randomized clinical trials (RCTs), and authorized by the U.S.

The Vitamin D Receptor Regulates Tissue Resident Macrophage Response to Injury.

Ligand-dependent actions of the vitamin D receptor (VDR) play a pleiotropic role in the regulation of innate and adaptive immunity. The liganded VDR is required for recruitment of macrophages during the inflammatory phase of cutaneous wound healing. Although the number of macrophages in the granulation tissue 2 days after wounding is markedly reduced in VDR knockout (KO) compared with wild-type mice, VDR ablation does not alter macrophage polarization.

The vitamin D receptor is required for activation of cWnt and hedgehog signaling in keratinocytes.

Alopecia (hair loss) in vitamin D receptor (VDR)-null mice is due to absence of ligand-independent actions of the VDR that are required for initiation of postmorphogenic hair cycles. Investigations were undertaken to determine whether the VDR is required for the induction of signaling pathways that play an important role in this process. The induction of cWnt and hedgehog target genes that characterizes early anagen was found to be dramatically attenuated in VDR(-/-) mice, relative to wild-type (WT) mice.

Ligand-dependent actions of the vitamin D receptor are required for activation of TGF-β signaling during the inflammatory response to cutaneous injury.

The vitamin D receptor (VDR) has both 1,25-dihydroxyvitamin D-dependent and -independent actions in the epidermis. Ligand-dependent actions of the VDR have been shown to promote keratinocyte differentiation and to regulate formation of the epidermal barrier. In contrast, the actions of the VDR that regulate postmorphogenic hair cycling do not require 1,25-dihydroxyvitamin D.

Lymphoid enhancer-binding factor-1 (LEF1) interacts with the DNA-binding domain of the vitamin D receptor.

Ligand-independent actions of the vitamin D receptor (VDR) are required for normal post-morphogenic hair cycles; however, the molecular mechanisms by which the VDR exerts these actions are not clear. Previous studies demonstrated impaired regulation of the canonical Wnt signaling pathway in primary keratinocytes lacking the VDR. To identify the key effector of canonical Wnt signaling that interacts with the VDR, GST pulldown studies were performed.

The vitamin D receptor, the skin and stem cells.

The active metabolite of vitamin D, 1,25-dihydroxyvitamin D, has been shown to have pro-differentiation and antiproliferative effects on keratinocytes that are mediated by interactions with its nuclear receptor. Other cutaneous actions of the vitamin D receptor have been brought to light by the cutaneous phenotype of humans and mice with non-functional vitamin D receptors. Although mice lacking functional vitamin D receptors develop a normal first coat of hair, they exhibit impaired cyclic regeneration of hair follicles that leads to the development of alopecia.

Vitamin D and human health: lessons from vitamin D receptor null mice.

The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)(2)D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1alpha-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency.

The LIM protein LIMD1 influences osteoblast differentiation and function.

The balance between bone resorption and bone formation involves the coordinated activities of osteoblasts and osteoclasts. Communication between these two cell types is essential for maintenance of normal bone homeostasis; however, the mechanisms regulating this cross talk are not completely understood. Many factors that mediate differentiation and function of both osteoblasts and osteoclasts have been identified.

The LIM protein, Limd1, regulates AP-1 activation through an interaction with Traf6 to influence osteoclast development.

Increasingly a number of proteins important in the regulation of bone osteoclast development have been shown primarily influence osteoclastogenesis under conditions of physiologic or pathologic stress. Why basal osteoclastogenesis is normal and how these proteins regulate stress osteoclastogenic responses, as opposed to basal osteoclastogenesis, is unclear. LIM proteins of the Ajuba/Zyxin family localize to cellular sites of cell adhesion where they contribute to the regulation of cell adhesion and migration, translocate into the nucleus where they can affect cell fate, but are also found in the cytoplasm where their function is largely unknown.

Canine PKD1 is a single-copy gene: genomic organization and comparative analysis.

Most cases of autosomal dominant polycystic kidney disease are caused by mutations in the gene PKD1, encoding polycystin-1. To gain insight into the role of polycystin-1 in tubulogenesis and cystogenesis using the well-characterized canine kidney epithelial cell line MDCK, we have now cloned and characterized the exon/intron structure of the canine gene PKD1. FISH analysis showed that the dog genome lacks the multiple PKD1 homologs present in human.