An evaluation of a digital pain management programme: clinical effectiveness and cost savings.

Introduction: Chronic pain is one of the most prevalent causes of disability worldwide, and digital interventions may be one of the ways to meet this need. Randomised controlled trials have demonstrated that digital interventions can be effective in treating chronic pain. This study aimed to establish the clinical effectiveness of a web-based pain management programme (PMP), specifically whether it would lead to improved clinical outcomes and reduced health care costs in a real-world clinical setting.

Synthesis, biochemical evaluation and rationalisation of the inhibitory activity of a range of 4-hydroxyphenyl ketones as potent and specific inhibitors of the type 3 of 17beta-hydroxysteroid dehydrogenase (17beta-HSD3).

We report the synthesis and biochemical evaluation of a number of 4-hydroxyphenyl ketones as potential inhibitors of the enzyme 17beta-hydroxysteroid dehydrogenase (17beta-HSD). In particular, we evaluated compounds against the catalysis of the conversion of androstenedione (AD) to testosterone (T) [17beta-HSD type 3 (17beta-HSD3)], furthermore, in an effort to determine the specificity of our compounds, we evaluated the ability of the compounds to inhibit the catalysis of the conversion of estrone (E1) to estradiol (E2) [17beta-HSD type 1 (17beta-HSD1)] as well as the conversion of dehydroepiandrosterone (DHEA) to AD [by 3beta-hydroxysteroid dehydrogenase (3beta-HSD)]. The results of our study suggest that the synthesised compounds are, in general, able to inhibit 17beta-HSD3 whilst being weak inhibitors of 17beta-HSD1.

Synthesis, biochemical evaluation and rationalisation of the inhibitory activity of a series of 4-hydroxyphenyl ketones as potential inhibitors of 17beta-hydroxysteroid dehydrogenase type 3 (17beta-HSD3).

We report the preliminary results of the synthesis and biochemical evaluation of a number of 4-hydroxyphenyl ketones as inhibitors of the isozyme of the enzyme 17beta-hydroxysteroid dehydrogenase (17beta-HSD) responsible for the conversion of androstenedione (AD) to testosterone (T), more specifically type 3 (17beta-HSD3). The results of our study suggest that we have synthesised compounds which are, in general, potent inhibitors of 17beta-HSD3, in particular, we discovered that 1-(4-hydroxy-phenyl)-nonan-1-one (8) was the most potent (IC(50) = 2.86 +/- 0.