Translating evidence-based treatment for digital health delivery: a protocol for family-based treatment for anorexia nervosa using telemedicine.

BACKGROUND: Family-based treatment (FBT) is an efficacious outpatient intervention for young people diagnosed with Anorexia Nervosa (AN). To date, treatment to protocol has relied on standard face-to-face delivery. Face-to-face therapy is subject to geographic, temporal and human factors, rendering it particularly susceptible to inequities and disruption. This has resulted in poorer service provision for rural and regional families, and recently a significant challenge to providing face-to-face services during the COVID-19 global pandemic. The present study examines whether FBT for AN can be successfully translated to a digital delivery platform to address these access issues. METHOD: Forty young people aged 12 to 18 years who meet DSM-5 diagnostic criteria for AN, and live in a rural or regional setting, will along with their family be recruited to the study. Trained therapists will provide 18 sessions of FBT over 9 months via telemedicine to the home of the young person and their family. The analysis will examine treatment effectiveness, feasibility, acceptability, and cost-effectiveness. DISCUSSION: The study addresses the treatment needs of families not able to attend face-to-face clinical services for evidence-based treatment for eating disorders. This might be due to several barriers, including a lack of local services or long travel distances to services. There has been a recent and unprecedented demand for telemedicine to facilitate the continuity of care during COVID-19 despite geographical circumstances. If delivering treatment in this modality is clinically and economically effective and feasible, it will facilitate access to potentially lifesaving, evidence-based treatments for families formerly unable to access such care and provide evidence for the continuity of services when and where face-to-face treatment is not feasible.

Dihydroorotate dehydrogenase is a high affinity binding protein for A77 1726 and mediator of a range of biological effects of the immunomodulatory compound.

A protein with high affinity (Kd 12 nM) for the immunomodulatory compound A77 1726 has been isolated from mouse spleen and identified as the mitochondrial enzyme dihydroorotate dehydrogenase (EC 1.3.3.1). The purified protein had a pI 9.6-9.8 and a subunit Mr of 43,000. Peptides derived from the mouse protein displayed high microsequence similarity to human and rat dihydroorotate dehydrogenase with, respectively, 35 and 39 out of 43 identified amino acids identical. Dihydroorotate dehydrogenase catalyzes the fourth step in de novo pyrimidine biosynthesis. The in vitro antiproliferative effects of A77 1726 are mediated by enzyme inhibition and can be overcome by addition of exogenous uridine. The rank order of potency of A77 1726 and its analogues in binding or enzyme inhibition was similar to that for inhibition of the mouse delayed type hypersensitivity response. It is proposed that inhibition of dihydroorotate dehydrogenase is an in vivo mechanism of action of the A77 1726 class of compounds. This was confirmed using uridine to counteract inhibition of the murine acute graft versus host response.

Actions of the novel bronchodilator, trimetaquinol, on bovine pulmonary vein.

The actions of the beta-sympathomimetic bronchodilator trimetaquinol (TMQ) were examined on bovine pulmonary vein smooth muscle in vitro. TMQ partially and reversibly inhibited 5-hydroxytryptamine (5HT) induced contractions of the vein strips. The relaxant activity was neither blocked by propranolol (10(-7) M) nor enhanced by phentolamine (10(-7) M). Isoproterenol, alone or in the presence of phentolamine (10(-7) M), was much less effective than TMQ in relaxing 5HT-induced contractions. From these results it is suggested that TMQ functions via a "non-beta-adrenergic" mechanism to relax bovine pulmonary vein smooth muscle.