Biology subjects

Newman, L. A.

Publications and source records attributed to Newman, L. A..

3 recordsLinked to original sources

bioRxiv2021

Effects of tDCS on the attentional blink revisited: A statistical evaluation of a replication attempt

The attentional blink (AB) phenomenon reveals a bottleneck of human information processing: the second of two targets is often missed when they are presented in rapid succession among distractors. In our previous work, we showed that the size of the AB can be changed by applying transcranial direct current stimulation (tDCS) over the left dorsolateral prefrontal cortex (lDLPFC) (London & Slagter, Journal of Cognitive Neuroscience, 33, 756-68, 2021). Although AB size at the group level remained unchanged, the effects of anodal and cathodal tDCS were negatively correlated: if a given individuals AB size decreased from baseline during anodal tDCS, their AB size would increase during cathodal tDCS, and vice versa. Here, we attempted to replicate this finding. We found no group effects of tDCS, as in the original study, but we no longer found a significant negative correlation. We present a series of statistical measures of replication success, all of which confirm that both studies are not in agreement. First, the correlation here is significantly smaller than a conservative estimate of the original correlation. Second, the difference between the correlations is greater than expected due to sampling error, and our data are more consistent with a zero-effect than with the original estimate. Finally, the overall effect when combining both studies is small and not significant. Our findings thus indicate that the effects of lDPLFC-tDCS on the AB are less substantial than observed in our initial study. Although this should be quite a common scenario, null findings can be difficult to interpret and are still under-represented in the brain stimulation and cognitive neuroscience literatures. An important auxiliary goal of this paper is therefore to provide a tutorial for other researchers, to maximize the evidential value from null findings.

neuroscience↗

bioRxiv2020

Gene network modeling via TopNet reveals robust epistatic interactions between functionally diverse tumor critical mediator genes

Malignant cell transformation and the underlying genomic scale reprogramming of gene expression require cooperation of multiple oncogenic mutations. Notably, this cooperation is reflected in the synergistic regulation of downstream genes, so-called cooperation response genes (CRGs). CRGs impact diverse hallmark features of cancer cells and are not known to be functionally connected. Yet, they act as critical mediators of the cancer phenotype at an unexpectedly high frequency of >50%, as indicated by genetic perturbations. Here we demonstrate that CRGs function within a network of strong genetic interdependencies that are critical to the robustness of the malignant state. Our approach, termed TopNet, utilizes attractor-based ternary network modeling that takes the novel approach of incorporating uncertainty in the underlying gene perturbation data and is capable of identifying non-linear gene interactions. TopNet reveals topological gene network architecture that effectively predicts previously unknown, functionally relevant epistatic gene interactions, and thus, among a broad range of applications, has utility for identification of non-mutant targets for cancer intervention.

cancer biology↗

bioRxiv2020

Extracellular levels of glucose in the hippocampus and striatum during maze training for food or water reward in rats.

Peripheral and central administration of glucose potently enhance cognitive functions. The present experiments examined changes in brain extracellular glucose levels while rats were trained to solve hippocampus-sensitive place or striatum-sensitive response learning tasks for food or water reward. During the first minutes of either place or response training, extracellular glucose levels declined in both the hippocampus and striatum, an effect not seen in untrained, rewarded rats. Subsequently, glucose increased in both brain areas under all training conditions, approaching asymptotic levels [~]15-25 min into training. Compared to untrained-food controls, training with food reward resulted in significant glucose increases in the hippocampus but not striatum; striatal glucose levels exhibited large increases to food intake in both trained and untrained groups. In rats trained to find water, glucose levels increased significantly above the values seen in untrained rats in both hippocampus and striatum. In contrast to results seen with lactate measurements, the magnitude of training-related increases in hippocampus and striatum glucose levels did not differ by task under either reward condition. The decreases in glucose early in training might reflect an increase in brain glucose consumption, perhaps triggering increased brain uptake of glucose from blood, as evident in the increases in glucose later in training. Together with past findings measuring lactate levels under the same conditions, the initial decreases in glucose may also stimulate increased production of lactate from astrocytes to support neural metabolism directly and/or to act as a signal to increase blood flow and glucose uptake into the brain. HighlightsO_LIGlucose levels in hippocampus and striatum decrease at the start of training. C_LIO_LIGlucose levels increase in both brain areas later in training. C_LIO_LIGlucose changes in both brain areas were similar for place and response tasks. C_LIO_LIGlucose levels responded similarly to training for either food and water rewards. C_LIO_LIEarly decreases in glucose may trigger increased production astrocytic lactate. C_LI

neuroscience↗