Resisting the sirens of temptation while studying : using reappraisal to increase focus, enthusiasm and performance

One of the major obstacles in the learning process is temptation, which has the power to divert students from even their most important goals (e.g. getting a degree). In two studies, we tested the hypothesis that cognitive reappraisal could be used to successfully resist temptation. Participants had to memorize tedious material while being tempted by pictures pasted on the wall (Study 1) or by funny clips on the television (Study 2). In Study 1, compared to a control group, participants who were instructed to reappraise the task as an opportunity to improve their memory were less tempted by the pictures, maintained their enthusiasm for the task, and showed better performance in a subsequent memory test. Study 2 replicated and extended the findings from Study 1, showing that cognitive reappraisal is effective whether the target of reappraisal is the temptation itself, or the longer term goal. Taken together, our findings provide compelling evidence that cognitive reappraisal (of either the task or the temptation) may be a useful tool for increasing students' task performance and enthusiasm

Lead me not into temptation : using cognitive reappraisal to reduce goal inconsistent behavior

Temptations besiege us, and we must resist their appeal if we are to achieve our long-term goals. In two studies, we tested the hypothesis that cognitive reappraisal could be used to successfully maintain performance in a task embedded in temptation. In Study 1, 62 participants had to search for information on the Internet while resisting attractive task-irrelevant content on preselected sites. In Study 2, 58 participants had to count target words in a funny TV sequence. Compared to the no-reappraisal condition, participants who understood the situation as a test of willpower (the reappraisal condition) (1) performed better at the task (Studies 1 and 2), and (2) were less tempted by the attractive content of the TV sequence (Study 2). These findings suggest that, by making the temptation less attractive and the task more appealing, cognitive reappraisal can help us resist temptation

Mean and standard errors of the scores on performance, before and after manipulation by group (Study 1).

<p>Mean and standard errors of the scores on performance, before and after manipulation by group (Study 1).</p

Mean and standard errors of the scores on performance (Panel A) and susceptibility to temptation (Panel B) by group (Study 2).

<p>Mean and standard errors of the scores on performance (Panel A) and susceptibility to temptation (Panel B) by group (Study 2).</p

Dysregulated miRNA biogenesis downstream of cellular stress and ALS-causing mutations: a new mechanism for ALS

Interest in RNA dysfunction in amyotrophic lateral sclerosis (ALS) recently aroused upon discovering causative mutations in RNA-binding protein genes. Here, we show that extensive down-regulation of miRNA levels is a common molecular denominator for multiple forms of human ALS. We further demonstrate that pathogenic ALS-causing mutations are sufficient to inhibit miRNA biogenesis at the Dicing step. Abnormalities of the stress response are involved in the pathogenesis of neurodegeneration, including ALS. Accordingly, we describe a novel mechanism for modulating microRNA biogenesis under stress, involving stress granule formation and re-organization of DICER and AGO2 protein interactions with their partners. In line with this observation, enhancing DICER activity by a small molecule, enoxacin, is beneficial for neuromuscular function in two independent ALS mouse models. Characterizing miRNA biogenesis downstream of the stress response ties seemingly disparate pathways in neurodegeneration and further suggests that DICER and miRNAs affect neuronal integrity and are possible therapeutic targets

Biallelic DMXL2 mutations impair autophagy and cause Ohtahara syndrome with progressive course.

Ohtahara syndrome, early infantile epileptic encephalopathy with a suppression burst EEG pattern, is an aetiologically heterogeneous condition starting in the first weeks or months of life with intractable seizures and profound developmental disability. Using whole exome sequencing, we identified biallelic DMXL2 mutations in three sibling pairs with Ohtahara syndrome, belonging to three unrelated families. Siblings in Family 1 were compound heterozygous for the c.5135C4T (p.Ala1712Val) missense substitution and the c.4478C4G (p.Ser1493*) nonsense substitution; in Family 2 were homozygous for the c.4478C4A (p.Ser1493*) nonsense substitution and in Family 3 were homozygous for the c.7518-1G4A (p.Trp2507Argfs*4) substitution. The severe developmental and epileptic encephalopathy manifested from the first day of life and was associated with deafness, mild peripheral polyneuropathy and dysmorphic features. Early brain MRI investigations in the first months of life revealed thin corpus callosum with brain hypomyelination in all. Follow-up MRI scans in three patients revealed progressive moderate brain shrinkage with leukoencephalopathy. Five patients died within the first 9 years of life and none achieved developmental, communicative or motor skills following birth. These clinical findings are consistent with a developmental brain disorder that begins in the prenatal brain, prevents neural connections from reaching the expected stages at birth, and follows a progressive course. DMXL2 is highly expressed in the brain and at synaptic terminals, regulates v-ATPase assembly and activity and participates in intracellular signalling pathways; however, its functional role is far from complete elucidation. Expression analysis in patient-derived skin fibroblasts demonstrated absence of the DMXL2 protein, revealing a loss of function phenotype. Patients’ fibroblasts also exhibited an increased LysoTrackerÕ signal associated with decreased endolysosomal markers and degradative processes. Defective endolysosomal homeostasis was accompanied by impaired autophagy, revealed by lower LC3II signal, accumulation of polyubiquitinated proteins, and autophagy receptor p62, with morphological alterations of the autolysosomal structures on electron microscopy. Altered lysosomal homeostasis and defective autophagy were recapitulated in Dmxl2-silenced mouse hippocampal neurons, which exhibited impaired neurite elongation and synaptic loss. Impaired lysosomal function and autophagy caused by biallelic DMXL2 mutations affect neuronal development and synapse formation and result in Ohtahara syndrome with profound developmental impairment and reduced life expectancy