The influence of hatha yoga on stress, anxiety, and suppression: A randomized controlled trial.

Engaging in yoga may mitigate stress and anxiety in individuals while potentially enhancing one's capacity to manage distractions. Our research aimed to explore the relation between these two outcomes: Can an eight-week yoga program foster distraction suppression, thereby reducing stress and discomfort? To answer this question, we used Hatha Yoga, the most commonly practiced form of yoga. We tested if the intervention improved participants' ability to suppress distractions and selectively decrease self-reported stress and stress reactivity. In Addition, we investigated whether such an intervention would increase participants' mindfulness. Our study included 98 healthy yoga novices between 18 and 40 years who were randomly assigned to either an experimental or a waitlist condition, with each participant completing pre- and post-intervention assessments, including questionnaires, as well as electrophysiological and behavioral measures. After eight weeks of yoga practice, significant reductions in self-reported stress and stress reactivity levels, as well as increased mindfulness, were observed among those participating in the intervention relative to those in the waitlist control group. There were, however, no significant changes in state or trait anxiety due to the intervention. Changes in stress measures could not be explained by changes in participants' ability to suppress distractors, which was not affected by the intervention. Overall, our findings suggest that regular participation in Hatha Yoga can improve mental health outcomes without impacting cognitive functioning directly related to distractor suppression. CLINICAL TRIAL REGISTRATION NUMBER: NCT05232422.

Novel tests of capture by irrelevant abrupt onsets: No evidence for a mediating role of search task difficulty during color search.

According to the attentional dwelling hypothesis, task-irrelevant abrupt-onset cues capture attention in a stimulus-driven way by eliciting spatial shifts and further dwelling at cue position until target onset. Consequently, search can be facilitated for targets at cued locations relative to uncued locations. Critically, effects of stimulus-driven capture can go undetected in mean reaction times and error rates when search is too easy. In contrast, according to the priority accumulation framework (PAF), cueing effects for task-irrelevant cues differ from cueing effects by task-relevant cues. Most critically, cueing effects by irrelevant cues do not necessarily index spatial shifts and more dwelling but rather retrieval of cueing information. We used both behavioral measures (i.e., cueing effects and distractor compatibility effects) and event-related potentials on direct visual orienting activity elicited by the cue (Experiment 2) as well as consequences on target processing (Experiment 1) to investigate whether task-irrelevant abrupt onsets elicited attention shifts and led to further dwelling. We found behavioral support for attentional effects of task-irrelevant cues, surprisingly, however, only when search displays remained on-screen until response. We found no support for the attentional dwelling hypothesis or for PAF in the size of cueing effects as a function of search difficulty. Critically, lateralized ERPs revealed that salience of abrupt onsets per se is not sufficient to elicit spatial shifts during color search. Finally, neurophysiological evidence demonstrates that choices toward the implementation of experimental protocols can dramatically alter behavioral results on attentional effects of salient, but task-irrelevant abrupt onsets and conclusions drawn from them.

Cyclic reactivation of distinct feature dimensions in human visual working memory.

Several recent behavioral studies have observed 4-10 Hz rhythmic fluctuations in attention-related performance over time. So far, this rhythmic attentional sampling has predominantly been demonstrated with regards to external visual attention, directed toward one single feature dimension. Whether and how attention might sample from concurrent internal representations of different feature dimensions held in working memory (WM) is currently largely unknown. To elucidate this issue, we conducted a human behavioral dense-sampling experiment, in which participants had to hold representations of two distinct feature dimensions (color and orientation) in WM. By querying the contents of WM at 72 time-points after encoding, we estimated the activity time course of the individual feature representations. Our results demonstrate an oscillatory component at 9.4 Hz in the joint time courses of both representations, presumably reflecting a common early perceptual sampling process in the alpha-frequency range. Furthermore, we observed an oscillatory component at 3.5 Hz in the time course difference between the two representations. This likely corresponds to a later attentional sampling process and indicates that internal representations of distinct features are activated in alteration. In summary, we demonstrate the cyclic reactivation of internal WM representations of distinct feature dimensions, as well as the co-occurrence of behavioral fluctuations at distinct frequencies, presumably associated to internal perceptual- and attentional rhythms. In addition, our findings also challenge a model of strict parallel processing in visual search, thus, providing novel input to the ongoing debate on whether search for more than one target feature constitutes a parallel- or a sequential mechanism.

Procedural Control Versus Resources as Potential Origins of Human Hyper Selectivity.

In the current review, we argue that experimental results usually interpreted as evidence for cognitive resource limitations could also reflect functional necessities of human information processing. First, we point out that selective processing of only specific features, objects, or locations at each moment in time allows humans to monitor the success and failure of their own overt actions and covert cognitive procedures. We then proceed to show how certain instances of selectivity are at odds with commonly assumed resource limitations. Next, we discuss examples of seemingly automatic, resource-free processing that challenge the resource view but can be easily understood from the functional perspective of monitoring cognitive procedures. Finally, we suggest that neurophysiological data supporting resource limitations might actually reflect mechanisms of how procedural control is implemented in the brain.

Continuous, Lateralized Auditory Stimulation Biases Visual Spatial Processing.

Sounds in our environment can easily capture human visual attention. Previous studies have investigated the impact of spatially localized, brief sounds on concurrent visuospatial attention. However, little is known on how the presence of a continuous, lateralized auditory stimulus (e.g., a person talking next to you while driving a car) impacts visual spatial attention (e.g., detection of critical events in traffic). In two experiments, we investigated whether a continuous auditory stream presented from one side biases visual spatial attention toward that side. Participants had to either passively or actively listen to sounds of various semantic complexities (tone pips, spoken digits, and a spoken story) while performing a visual target discrimination task. During both passive and active listening, we observed faster response times to visual targets presented spatially close to the relevant auditory stream. Additionally, we found that higher levels of semantic complexity of the presented sounds led to reduced visual discrimination sensitivity, but only during active listening to the sounds. We provide important novel results by showing that the presence of a continuous, ongoing auditory stimulus can impact visual processing, even when the sounds are not endogenously attended to. Together, our findings demonstrate the implications of ongoing sounds on visual processing in everyday scenarios such as moving about in traffic.

Protein Kinase D1, Reduced in Human Pancreatic Tumors, Increases Secretion of Small Extracellular Vesicles From Cancer Cells That Promote Metastasis to Lung in Mice.

BACKGROUND & AIMS: Pancreatic tumor cells release small extracellular vesicles (sEVs, exosomes) that contain lipids and proteins, RNA, and DNA molecules that might promote formation of metastases. It is not clear what cargo these vesicles contain and how they are released. Protein kinase D1 (PRKD1) inhibits cell motility and is believed to be dysregulated in pancreatic ductal adenocarcinomas. We investigated whether it regulates production of sEVs in pancreatic cancer cells and their ability to form premetastatic niches for pancreatic cancer cells in mice. METHODS: We analyzed data from UALCAN and human pancreatic tissue microarrays to compare levels of PRKD1 between tumor and nontumor tissues. We studied mice with pancreas-specific disruption of Prkd1 (PRKD1KO mice), mice that express oncogenic KRAS (KC mice), and KC mice with disruption of Prkd1 (PRKD1KO-KC mice). Subcutaneous xenograft tumors were grown in NSG mice from Panc1 cells; some mice were then given injections of sEVs. Pancreata and lung tissues from mice were analyzed by histology, immunohistochemistry, and/or quantitative polymerase chain reaction; we performed nanoparticle tracking analysis of plasma sEVs. The Prkd1 gene was disrupted in Panc1 cells using CRISPR-Cas9 or knocked down with small hairpin RNAs, or PRKD1 activity was inhibited with the selective inhibitor CRT0066101. Pancreatic cancer cell lines were analyzed by gene-expression microarray, quantitative polymerase chain reaction, immunoblot, and immunofluorescence analyses. sEVs secreted by Panc1 cell lines were analyzed by flow cytometry, transmission electron microscopy, and mass spectrometry. RESULTS: Levels of PRKD1 were reduced in human pancreatic ductal adenocarcinoma tissues compared with nontumor tissues. PRKD1KO-KC mice developed more pancreatic intraepithelial neoplasia, at a faster rate, than KC mice, and had more lung metastases and significantly shorter average survival time. Serum from PRKD1KO-KC mice had increased levels of sEVs compared with KC mice. Pancreatic cancer cells with loss or inhibition of PRKD1 increased secretion of sEVs; loss of PRKD1 reduced phosphorylation of its substrate, cortactin, resulting in increased F-actin levels at the plasma membrane. sEVs from cells with loss or reduced expression of PRKD1 had altered content, and injection of these sEVs into mice increased metastasis of xenograft tumors to lung, compared with sEVs from pancreatic cells that expressed PRKD1. PRKD1-deficient pancreatic cancer cells showed increased loading of integrin α6ß4 into sEVs-a process that required CD82. CONCLUSIONS: Human pancreatic ductal adenocarcinoma has reduced levels of PRKD1 compared with nontumor pancreatic tissues. Loss of PRKD1 results in reduced phosphorylation of cortactin in pancreatic cancer cell lines, resulting in increased in F-actin at the plasma membrane and increased release of sEVs, with altered content. These sEVs promote metastasis of xenograft and pancreatic tumors to lung in mice.

Heterogeneity of Cell Surface Glutamate and GABA Receptor Expression in Shank and CNTN4 Autism Mouse Models.

Autism spectrum disorder (ASD) refers to a large set of neurodevelopmental disorders, which have in common both repetitive behavior and abnormalities in social interactions and communication. Interestingly, most forms of ASD have a strong genetic contribution. However, the molecular underpinnings of this disorder remain elusive. The SHANK3 gene (and to a lesser degree SHANK2) which encode for the postsynaptic density (PSD) proteins SHANK3/SHANK2 and the CONTACTIN 4 gene which encodes for the neuronal glycoprotein CONTACTIN4 (CNTN4) exhibit mutated variants which are associated with ASD. Like many of the other genes associated with ASD, both SHANKs and CNTN4 affect synapse formation and function and are therefore related to the proper development and signaling capability of excitatory and inhibitory neuronal networks in the adult mammal brain. In this study, we used mutant/knock-out mice of Shank2 (Shank2-/-), Shank3 (Shank3αß-/-), and Cntn4 (Cntn4-/-) as ASD-models to explore whether these mice share a molecular signature in glutamatergic and GABAergic synaptic transmission in ASD-related brain regions. Using a biotinylation assay and subsequent western blotting we focused our analysis on cell surface expression of several ionotropic glutamate and GABA receptor subunits: GluA1, GluA2, and GluN1 were analyzed for excitatory synaptic transmission, and the α1 subunit of the GABAA receptor was analyzed for inhibitory synaptic transmission. We found that both Shank2-/- and Shank3αß-/- mice exhibit reduced levels of several cell surface glutamate receptors in the analyzed brain regions-especially in the striatum and thalamus-when compared to wildtype controls. Interestingly, even though Cntn4-/- mice also show reduced levels of some cell surface glutamate receptors in the cortex and hippocampus, increased levels of cell surface glutamate receptors were found in the striatum. Moreover, Cntn4-/- mice do not only show brain region-specific alterations in cell surface glutamate receptors but also a downregulation of cell surface GABA receptors in several of the analyzed brain regions. The results of this study suggest that even though mutations in defined genes can be associated with ASD this does not necessarily result in a common molecular phenotype in surface expression of glutamatergic and GABAergic receptor subunits in defined brain regions.