Suppressing Unwanted Autobiographical Memories Reduces Their Automatic Influences: Evidence from Electrophysiology and an Implicit Autobiographical Memory Test

The present study investigated the extent to which people can suppress unwanted autobiographical memories in a mock crime memory detection context. Participants encoded sensorimotor-rich memories by enacting a lab crime (stealing a ring) and received direct suppression instructions so as to evade guilt detection in a brainwave-based concealed information test. Aftereffects of suppression on automatic memory processes were measured in an autobiographical implicit association test (aIAT). Results showed that suppression attenuated brainwave activity (P300) that is associated with crime-relevant memory retrieval, rendering innocent and guilty/suppression participants indistinguishable. However, guilty/suppression and innocent participants could nevertheless be discriminated via the late posterior negative slow wave, which may reflect the need to monitor response conflict arising between voluntary suppression and automatic recognition processes. Lastly, extending recent findings that suppression can impair implicit memory processes; we provide novel evidence that suppression reduces automatic cognitive biases that are otherwise associated with actual autobiographical memories

Equivariant KK-theory of GKM bundles

Given a fiber bundle of GKM spaces, $\pi\colon M\to B$, we analyze the structure of the equivariant $K$-ring of $M$ as a module over the equivariant $K$-ring of $B$ by translating the fiber bundle, $\pi$, into a fiber bundle of GKM graphs and constructing, by combinatorial techniques, a basis of this module consisting of $K$-classes which are invariant under the natural holonomy action on the $K$-ring of $M$ of the fundamental group of the GKM graph of $B$. We also discuss the implications of this result for fiber bundles $\pi\colon M\to B$ where $M$ and $B$ are generalized partial flag varieties and show how our GKM description of the equivariant $K$-ring of a homogeneous GKM space is related to the Kostant-Kumar description of this ring.Comment: 15 page

Effect of starvation on the activity of the mitochondrial tricarboxylate carrier

AbstractThe effect of starvation on the activity of the tricarboxylate carrier has been investigated in intact rat liver mitochondria and in a reconstituted system. In both experimental conditions, the rate of citrate transport, when compared to control, is greatly reduced (35–40%) in starved rats. Similar behaviour is shown by the cytosolic lipogenic enzymes. Kinetic analysis of the carrier activity in intact mitochondria and in the proteoliposomal system has showed that during starvation only the Vmax of this process decreases while there is no change in the Km. No difference in the Arrhenius plot and in the lipid composition has been detected, which indicates that the reduced transport activity in fasted animals is not due to a change in the carrier lipid microenvironment. In starved rats, a reduction of the carrier activity has occurred even after the addition of increasing cardiolipin concentrations to proteoliposomes. These findings thus suggest that starvation-induced decrease of citrate carrier activity could be due to a change of the intrinsic properties of the transport protein

Manifolds associated with (Z2)n(Z_2)^n-colored regular graphs

In this article we describe a canonical way to expand a certain kind of $(\mathbb Z_2)^{n+1}$-colored regular graphs into closed $n$-manifolds by adding cells determined by the edge-colorings inductively. We show that every closed combinatorial $n$-manifold can be obtained in this way. When $n\leq 3$, we give simple equivalent conditions for a colored graph to admit an expansion. In addition, we show that if a $(\mathbb Z_2)^{n+1}$-colored regular graph admits an $n$-skeletal expansion, then it is realizable as the moment graph of an $(n+1)$-dimensional closed $(\mathbb Z_2)^{n+1}$-manifold.Comment: 20 pages with 9 figures, in AMS-LaTex, v4 added a new section on reconstructing a space with a $(Z_2)^n$-action for which its moment graph is a given colored grap

Brain Organoids as Model Systems for Genetic Neurodevelopmental Disorders

Neurodevelopmental disorders (NDDs) are a group of disorders in which the development of the central nervous system (CNS) is disturbed, resulting in different neurological and neuropsychiatric features, such as impaired motor function, learning, language or non-verbal communication. Frequent comorbidities include epilepsy and movement disorders. Advances in DNA sequencing technologies revealed identifiable genetic causes in an increasingly large proportion of NDDs, highlighting the need of experimental approaches to investigate the defective genes and the molecular pathways implicated in abnormal brain development. However, targeted approaches to investigate specific molecular defects and their implications in human brain dysfunction are prevented by limited access to patient-derived brain tissues. In this context, advances of both stem cell technologies and genome editing strategies during the last decade led to the generation of three-dimensional (3D) in vitro-models of cerebral organoids, holding the potential to recapitulate precise stages of human brain development with the aim of personalized diagnostic and therapeutic approaches. Recent progresses allowed to generate 3D-structures of both neuronal and non-neuronal cell types and develop either whole-brain or region-specific cerebral organoids in order to investigate in vitro key brain developmental processes, such as neuronal cell morphogenesis, migration and connectivity. In this review, we summarized emerging methodological approaches in the field of brain organoid technologies and their application to dissect disease mechanisms underlying an array of pediatric brain developmental disorders, with a particular focus on autism spectrum disorders (ASDs) and epileptic encephalopathies

pPKCα mediated-HIF-1α activation related to the morphological modifications occurring in neonatal myocardial tissue in response to severe and mild hyperoxia

In premature babies birth an high oxygen level exposure can occur and newborn hyperoxia exposure can be associated with free radical oxygen release with impairment of myocardial function, while in adult animal models short exposure to hyperoxia seems to protect heart against ischemic injury. Thus, the mechanisms and consequences which take place after hyperoxia exposure are different and related to animals age. The aim of our work has been to analyze the role played by HIF-1α in the occurrence of the morphological modifications upon hyperoxia exposure in neonatal rat heart. Hyperoxia exposure induces connective compartment increase which seems to allow enhanced blood vessels growth. An increased hypoxia inducible factor-1α (HIF-1α) translocation and vascular endothelial growth factor (VEGF) expression has been found upon 95% oxygen exposure to induce morphological modifications. Upstream pPKC-α expression increase in newborn rats exposed to 95% oxygen can suggest PKC involvement in HIF-1α activation. Since nitric oxide synthase (NOS) are involved in heart vascular regulation, endothelial NOS (e-NOS) and inducible NOS (i-NOS) expression has been investigated: a lower eNOS and an higher iNOS expression has been found in newborn rats exposed to 95% oxygen related to the evidence that hyperoxia provokes a systemic vasoconstriction and to the iNOS pro-apoptotic action, respectively. The occurrence of apoptotic events, evaluated by TUNEL and Bax expression analyses, seems more evident in sample exposed to severe hyperoxia. All in all such results suggest that in newborn rats hyperoxia can trigger oxygen free radical mediated membrane injury through a pPKCα mediated HIF-1α signalling system, even though specificity of such response could be obtained by in vivo administration to the rats of specific inhibitors of PKCα. This intracellular signalling can switch molecular events leading to blood vessels development in parallel to pro-apoptotic events due to an immature anti-oxidant defensive system in newborn rat hearts

p53 and telomerase control rat myocardial tissue response to hypoxia and ageing

Cellular senescence implies loss of proliferative and tissue regenerative capability. Also hypoxia, producing Reactive Oxygen Species (ROS), can damage cellular components through the oxidation of DNA, proteins and lipids, thus influencing the shortening of telomeres

pinus koraiensis seed oil pinno thin tm supplementation reduces body weight gain and lipid concentartion in liver and plasma of mice

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Chitlac-coated Thermosets Enhance Osteogenesis and Angiogenesis in a Co-culture of Dental Pulp Stem Cells and Endothelial Cells

Dental pulp stem cells (DPSCs) represent a population of stem cells which could be useful in oral and maxillofacial reconstruction. They are part of the periendothelial niche, where their crosstalk with endothelial cells is crucial in the cellular response to biomaterials used for dental restorations. DPSCs and the endothelial cell line EA.hy926 were co-cultured in the presence of Chitlac-coated thermosets in culture conditions inducing, in turn, osteogenic or angiogenic differentiation. Cell proliferation was evaluated by 3\u2013[4,5\u2013dimethyl\u2013thiazol\u20132\u2013yl\u2013]\u20132,5\u2013diphenyl tetrazolium bromide (MTT) assay. DPSC differentiation was assessed by measuring Alkaline Phosphtase (ALP) activity and Alizarin Red S staining, while the formation of new vessels was monitored by optical microscopy. The IL-6 and PGE2 production was evaluated as well. When cultured together, the proliferation is increased, as is the DPSC osteogenic differentiation and EA.hy926 vessel formation. The presence of thermosets appears either not to disturb the system balance or even to improve the osteogenic and angiogenic differentiation. Chitlac-coated thermosets confirm their biocompatibility in the present co-culture model, being capable of improving the differentiation of both cell types. Furthermore, the assessed co-culture appears to be a useful tool to investigate cell response toward newly synthesized or commercially available biomaterials, as well as to evaluate their engraftment potential in restorative dentistry