Explore the vast range of titles available.

3,4-Methylenedioxymethamphetamine (MDMA, ‘ecstasy’) releases serotonin and norepinephrine. MDMA is reported to produce empathogenic and prosocial feelings. It is unknown whether MDMA in fact alters empathic concern and prosocial behavior. We investigated the acute effects of MDMA using the Multifaceted Empathy Test (MET), dynamic Face Emotion Recognition Task (FERT) and Social Value Orientation (SVO) test. We also assessed effects of MDMA on plasma levels of hormones involved in social behavior using a placebo-controlled, double-blind, random-order, cross-over design in 32 healthy volunteers (16 women). MDMA enhanced explicit and implicit emotional empathy in the MET and increased prosocial behavior in the SVO test in men. MDMA did not alter cognitive empathy in the MET but impaired the identification of negative emotions, including fearful, angry and sad faces, in the FERT, particularly in women. MDMA increased plasma levels of cortisol and prolactin, which are markers of serotonergic and noradrenergic activity, and of oxytocin, which has been associated with prosocial behavior. In summary, MDMA sex-specifically altered the recognition of emotions, emotional empathy and prosociality. These effects likely enhance sociability when MDMA is used recreationally and may be useful when MDMA is administered in conjunction with psychotherapy in patients with social dysfunction or post-traumatic stress disorder.

•Celecoxib-tramadol co-crystal (CTC) is a first-in-class API-API co-crystal.•Celecoxib absorption is inhibited when co-administered with tramadol.•Celecoxib absorption interference is minimized with CTC.•CTC do not result in higher systemic exposure compared to tramadol or celecoxib.•This study validates the dosing regimen for a subsequent factorial Phase 3 study. Celecoxib-tramadol co-crystal (CTC) is a first-in-class co-crystal of celecoxib and racemic tramadol. This Phase 1 bioavailability study compared single-dose pharmacokinetic (PK) parameters of CTC with those of the individual reference products from the United States, immediate-release celecoxib and tramadol, taken alone and simultaneously to determine their systemic exposure. This was a single-center, randomized, single-dose, open-label, 4-period, 4-sequence, crossover study conducted in healthy subjects between October and December 2016. Study treatments included 200-mg CTC (equivalent to 112-mg celecoxib and 88-mg tramadol; Treatment-1); 100-mg tramadol (Treatment-2); 100-mg celecoxib (Treatment-3); and 100-mg celecoxib plus 100-mg tramadol (Treatment-4). The PK parameters of interest were Cmax, AUC0–T, and AUC0–∞, which were also calculated normalized to the dose. Tmax was only considered as supportive. The statistical analysis was based on a parametric analysis of variance model of the PK parameters; the two-sided 90% CI of the ratio of geometric mean values for the Cmax, AUC0–T, and AUC0–∞ was based on ln-transformed data, and Tmax was rank-transformed. Thirty-six subjects aged 18 to 55 years (21 male subjects, 15 female subjects; mean age, 35 years) participated in the study. Celecoxib from CTC presented a lower Cmax, reduced AUCs, and a faster Tmax. The interference in celecoxib absorption when celecoxib and tramadol are administered together was minimized with the CTC. For Treatment-1, -3, and -4, celecoxib PK parameters were 259, 318, and 165 ng/mL (Cmax), respectively; 1930, 2348, and 1929 ng • h/mL (AUC0–T); and 1.5, 3.0, and 2.5 hours (Tmax). Tramadol and its active metabolite O-desmethyl tramadol from CTC presented lower Cmax and AUCs as well as a longer Tmax. Tramadol/O-desmethyl tramadol PK parameters for Treatment-1, -2, and -4 were 214/55, 305/78, and 312/78 ng/mL for Cmax; 2507/846, 2709/965, and 2888/1010 ng • h/mL for AUC0–T; and 3.0/4.0, 2.0/2.5, and 1.9/2.5 hours for Tmax. Reported adverse events (none unexpected) occurred more frequently with Treatment-2 and Treatment-4. The aim of this study was to compare the PK profile of the US-marketed tramadol and celecoxib products with CTC to determine their systemic exposure and to validate the dosing regimen for a subsequent pivotal factorial Phase 3study. PK parameters of each active component in CTC were favorably modified by co-crystallization and did not result in higher systemic exposure compared with US-marketed celecoxib, tramadol, and their concomitant administration. © 2021 Elsevier HS Journals, Inc.

Brain-derived neurotrophic factor (BDNF) has been shown to increase in an intensity dependent manner in response to aerobic exercise. However, previous research investigating the use of resistance exercise to increase BDNF levels has been less conclusive, likely due to the low intensity nature of traditional resistance exercise programs. This study examined the influence of acute resistance exercise to-fatigue on serum BDNF levels and blood lactate. Acute crossover study. Eleven untrained to intermediately trained males (age: 25.0±1.3 year) and five untrained females (age: 23.2±1.1 year) were recruited to undertake two bouts of resistance exercise. Strength (five sets of five repetitions, 180s recovery) and hypertrophy (three sets of ten repetitions, 60s recovery) based resistance exercise was implemented to-fatigue to examine the effect on serum BDNF and blood lactate levels immediately post-, and 30min post-exercise. An interaction (p<0.01; ES=0.52) was observed between conditions immediately post-exercise, with hypertrophy resulting in significantly greater BDNF levels when compared with strength exercise. Changes in lactate and BDNF from baseline to post- exercise were positively correlated following hypertrophy exercise (r=0.70; p<0.01), but not correlated following strength exercise (r=0.18; p=0.56). The use of a to-fatigue hypertrophy based resistance exercise protocol provides the necessary stimulus to increase peripheral serum BDNF. Mechanistically, the presence of lactate does not appear to drive the BDNF response during resistance exercise.

Self-determination is on the agenda of Indigenous peoples all over the world. This analysis by an Indigenous feminist scholar challenges the United Nations-based human rights agendas and colonial theory that until now have shaped Indigenous models of self-determination. Gender inequality and gender violence, Dian Million argues, are critically important elements in the process of self-determination.Million contends that nation-state relations are influenced by a theory of trauma ascendant with the rise of neoliberalism. Such use of trauma theory regarding human rights corresponds to a therapeutic narrative by Western governments negotiating with Indigenous nations as they seek self-determination.Focusing on Canada and drawing comparisons with the United States and Australia, Million brings a genealogical understanding of trauma against a historical filter. Illustrating how Indigenous people are positioned differently in Canada, Australia, and the United States in their articulation of trauma, the author particularly addresses the violence against women as a language within a greater politic. The book introduces an Indigenous feminist critique of this violence against the medicalized framework of addressing trauma and looks to the larger goals of decolonization. Noting the influence of humanitarian psychiatry, Million goes on to confront the implications of simply dismissing Indigenous healing and storytelling traditions.Therapeutic Nationsis the first book to demonstrate affect and trauma's wide-ranging historical origins in an Indigenous setting, offering insights into community healing programs. The author's theoretical sophistication and original research make the book relevant across a range of disciplines as it challenges key concepts of American Indian and Indigenous studies.