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Background There is extensive evidence for volumetric reductions in the hippocampus in patients with anorexia nervosa (AN), however the impact on function is unclear. Pattern separation and recognition are hippocampus-dependent forms of learning thought to underlie stimulus discrimination. Methods The present study used the Mnemonic Similarity Task to investigate pattern separation and recognition for the first time in patients with AN (N = 46) and healthy controls (N = 56). An Analysis of Covariance examined between-group differences, controlling for age, antidepressant use and method of task delivery (remote vs. in person). Results When controlling for covariates, pattern recognition memory scores were lower in the AN group with a medium effect size (d = 0.51). In contrast, there was a small effect whereby patients with AN had a greater pattern separation score than controls (d = 0.34), albeit this difference was not significant at the p = 0.05 threshold (p = 0.133). Furthermore, pattern separation and recognition memory abilities were not related to age, body mass index, eating disorder psychopathology or trait anxiety levels. Conclusions This preliminary study provides initial evidence for an imbalance in pattern separation and recognition abilities in AN, a hippocampus-dependent cognitive ability. Further studies should endeavour to investigate pattern separation and recognition performance further in AN, as well as investigate other hippocampus-dependent functions. Supplementary Information The online version contains supplementary material available at 10.1186/s40337-021-00406-8., Plain English summary The hippocampus is an area of the brain that is vital for memory and learning, and it is not understood the extent to which its function is impaired in anorexia nervosa (AN). This paper used the Mnemonic Similarity Task to assess pattern separation, a hippocampus-dependent form of memory, in AN. This task involves showing participants a sequence of objects, who then categorise them as “indoor” or “outdoor” objects. Participants are later shown a sequence of objects, although some of the images are replaced by a similar but slightly different image. The task involves recognising whether an image has previously been seen (pattern recognition) and also whether it is similar to, but distinct, from a previous image (i.e. pattern separation). In this study, individuals with AN showed reduced performance in pattern recognition, when statistically controlling for their age, how the task was delivered and their use of antidepressant medication. However, their performance in pattern separation was intact. This may indicate an imbalance in this hippocampus-dependent form of memory in AN. Supplementary Information The online version contains supplementary material available at 10.1186/s40337-021-00406-8.

Objectives: To investigate the effect of weight stigma in news media on (a) intentions to increase physical activity (PA), improve diet quality and lose weight, and (b) changes in PA, diet quality and body mass index (BMI) over one month, in (i) women of all weight categories and (ii) a subsample of women living with obesity. Methods: UK-based women (N = 172; subgroup with obesity N = 81) were assigned to read an experimental (weight stigma; N = 75) or control (smoking stigma; N = 97) news article. Questionnaires were administered immediately after, and one month subsequently to collect information on BMI, PA, diet quality, intentions, past stigma, and diet and PA self-efficacy. Logistic and linear regression analyses were used to assess the effect of weight stigma on all outcome variables. Results: In the whole sample, there was no significant effect of weight stigma on any primary or secondary outcome. In women with obesity, there was no significant effect of weight stigma on diet quality (0.26 units, 95% CI: −0.36 to 0.87) or PA (−1.83 units, 95% CI: −11.11 to 7.44) at follow up, but exposure to weight stigma was associated with a significant increase in BMI at 1-month follow-up (1.15 kg/m2, 95% CI: 0.38 to 1.92) compared with the control group. Conclusions: In people with obesity, exposure to weight-stigmatising media may contribute to increased BMI over time. Larger trials with longer follow-up are needed to confirm these findings.

Purpose of review: In recent years, the food addiction hypothesis of loss-of-control eating has gained traction in the field of eating disorders. In particular, the neural process of food addiction plays a dominant role in the recently formulated “addictive appetite” model of bulimia nervosa and binge eating disorder. Nonetheless, several components of the food addiction hypothesis, including the presence of withdrawal and tolerance effects, as well as the proposition that some foods possess “addicting” properties, remain highly controversial. In response, the current review synthesises existing evidence for withdrawal and tolerance effects in people with bulimia nervosa. Recent findings: The recent development of a validated tool to measure withdrawal from highly processed foods will aid in measuring withdrawal symptoms and testing hypotheses related to withdrawal in the context of food addiction. We subsequently describe preclinical and human evidence for a central insulin- and dopamine-mediated pathway by which recurrent loss-of-control binge eating is maintained in bulimia nervosa. Summary: Evidence in populations with bulimia nervosa and loss-of-control eating provides preliminary support for the role of food addiction in the maintenance of bulimia nervosa. Future longitudinal research is needed to develop a clearer profile of illness progression and to clarify the extent to which dysregulation in glucose metabolism contributes to food craving and symptom maintenance in bulimia nervosa.

Maesa perlarius is a medicinal plant that produces maesabalides, which possess selective and strong anti-leishmania activity. In this study, M. perlarius plants were regenerated from leaf-derived calli. Shoots were induced in Murashige and Skoog medium in the presence of thidiazuron in combination with alpha-naphthalene acetic acid. In contrast to seed-derived plants, callus-derived regenerants were tetraploid showing typical characteristics of higher ploidy phenotypes. We assessed the impact of indirect plant regeneration and associated increase in ploidy on the production of saponin by means of LC-MS analysis. Tetraploid M. perlarius produce a saponin profile, which was not significantly different from seed grown plants. Based on this study, we concluded that saponin production in M. perlarius is not qualitatively changed by a genome-doubling event.

International audience; Nemaline myopathy is a neuromuscular disorder, characterized by muscle weakness and hypotonia and is, in 20% of the cases, caused by mutations in the gene encoding alpha-skeletal muscle actin, ACTA1. It is a heterogeneous disease with various clinical phenotypes and severities. In patients the ultrastructure of muscle cells is often disturbed by nemaline rods and it is thought this is the cause for muscle weakness. To search for possible defects during muscle cell differentiation we expressed alpha-actin mutants in myoblasts and allowed these cells to differentiate into myotubes. Surprisingly, we observed two striking new phenotypes in differentiating myoblasts: rounding up of cells and bleb formation, two features reminiscent of apoptosis. Indeed expression of these mutants induced cell death with apoptotic features in muscle cell culture, using AIF and endonuclease G, in a caspase-independent but calpain-dependent pathway. This is the first report on a common cellular defect induced by NM causing actin mutants, independent of their biochemical phenotypes or rod and aggregate formation capacity. These data suggest that lack of type II fibers or atrophy observed in nemaline myopathy patients may be also due to an increased number of dying muscle cells.

Background Nemaline myopathy is a neuromuscular disorder characterized by the presence of nemaline bodies in patient muscles. 20% of the cases are associated with α-skeletal muscle actin mutations. We previously showed that actin mutations can cause four different biochemical phenotypes and that expression of NM associated actin mutants in fibroblasts, myoblasts and myotubes induces a range of cellular defects. Findings We conducted the same biochemical experiments for twelve new actin mutants associated with nemaline myopathy. We observed folding and polymerization defects. Immunostainings of these and eight other mutants in transfected cells revealed typical cellular defects such as nemaline rods or aggregates, decreased incorporation in F-actin structures, membrane blebbing, the formation of thickened actin fibres and cell membrane blebbing in myotubes. Conclusion Our results confirm that NM associated α-actin mutations induce a range of defects at the biochemical level as well as in cultured fibroblasts and muscle cells.