bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential Reorganization of Episodic and Semantic Memory Systems in Epilepsy-Related Mesiotemporal Pathology
Authors: Cabalo Donna Gift , DeKraker Jordan , Royer Jessica , Xie Ke , Tavakol Shahin , Rodríguez-Cruces Raúl , Bernasconi Andrea , Bernasconi Neda , Weil Alexander , Pana Raluca , Frauscher Birgit , Caciagli Lorenzo , Jefferies Elizabeth , Smallwood Jonathan , Bernhardt Boris C. 
Published: September 2023

AbstractDeclarative memory encompasses episodic and semantic divisions. Episodic memory captures singular events with specific spatiotemporal relationships, while semantic memory houses context-independent knowledge. Behavioral and functional neuroimaging studies have revealed common and distinct neural substrates of both memory systems, implicating mesiotemporal lobe (MTL) regions and distributed neocortices. Here, we studied a population of patients with unilateral temporal lobe epilepsy (TLE) and variable degrees of MTL pathology as a human disease model to explore declarative memory system reorganization, and to examine neurocognitive associations. Our cohort included 20 patients with TLE as well as 60 age and sex-matched healthy controls, who underwent episodic and semantic retrieval tasks during a functional MRI session. Tasks were closely matched in terms of stimuli and trial design. Capitalizing on connectome gradient mapping techniques, we derived task-based functional topographies during episodic and semantic memory states, both in the MTL and in neocortical networks. Comparing neocortical and hippocampal functional gradients between TLE patients and healthy controls, we observed topographic reorganization during episodic but not semantic memory states, characterized by marked gradient compression in lateral temporal and midline parietal cortices in both hemispheres, cooccurring with an expansion of anterior-posterior hippocampal differentiation ipsilateral to the MTL pathology. These findings suggest that episodic processes are supported by a distributed network, implicating both hippocampus and neocortex, and such alterations can provide a compact signature of state-dependent reorganization in conditions associated with MTL damage such as TLE. Leveraging microstructural and morphological MRI proxies of MTL pathology, we furthermore observed that pathological markers selective to the hippocampus are associated with TLE-related functional reorganization. Moreover, correlation analysis and statistical mediation models revealed that these functional alterations contributed to behavioral deficits in episodic memory in patients. Altogether, our findings point to a selective mesiotemporal and neocortical functional reorganization of episodic memory systems in patients with TLE, which consistently affects behavioral memory deficits. These findings point to consistent structure-function relationships in declarative memory and reaffirm the critical role of the MTL in episodic memory systems.
REM disruption and REM Vagal Activity Predict Extinction Recall in Trauma-Exposed Individuals
Authors: Yuksel Cagri , Watford Lauren , Muranaka Monami , McCoy Emma , Lax Hannah , Mendelsohn Augustus Kram , Oliver Katelyn I. , Daffre Carolina , Acosta Alexis , Vidrin Abegail , Martinez Uriel , Lasko Natasha , Orr Scott , Pace-Schott Edward F. 
Published: September 2023

ABSTRACTAccumulating evidence suggests that rapid eye movement sleep (REM) supports the consolidation of extinction memory. REM is disrupted in PTSD, and REM abnormalities after traumatic events increase the risk of developing PTSD. Therefore, it was hypothesized that abnormal REM in trauma-exposed individuals may pave the way for PTSD by interfering with the processing of extinction memory. In addition, PTSD patients display reduced vagal activity. Vagal activity contributes to the strengthening of memories, including fear extinction memory, and recent studies show that the role of vagus in memory processing extends to memory consolidation during sleep. Therefore, it is plausible that reduced vagal activity during sleep in trauma-exposed individuals may be an additional mechanism that impairs extinction memory consolidation. However, to date, the contribution of sleep vagal activity to the consolidation of extinction memory or any emotional memory has not been investigated. To test these hypotheses, we examined the association of extinction memory with REM characteristics and REM vagal activity (indexed as heart rate variability) in a large sample of trauma-exposed individuals (n=113). Consistent with our hypotheses, REM disruption was associated with poorer physiological and explicit extinction memory. Furthermore, higher vagal activity during REM was associated with better explicit extinction memory, and physiological extinction memory in males. These findings support the notion that abnormal REM may contribute to PTSD by impairing the consolidation of extinction memory and indicate the potential utility of interventions that target REM sleep characteristics and REM vagal activity in fear-related disorders.
Cannabidiol prevents the locomotor sensitization induced by cocaine and caffeine and upregulates genes of extracellular matrix and anti-inflammatory pathways in the nucleus accumbens: a transcriptome-wide analysis
Authors: Prieto José Pedro , Fort Rafael , Eastman Guillermo , Kaminski Oliver , Ferreiro-Vera Carlos , de Medina Verónica Sanchez , Scorza Cecilia , Sotelo-Silveira José Roberto 
Published: September 2023

AbstractCannabidiol (CBD), a non-psychotomimetic phytocannabinoid found in theCannabisplant, has emerged as a potential therapeutic agent for psychostimulant use disorders. In recent work, we demonstrated that CBD is able to attenuate the expression of locomotor sensitization and the enhanced metabolic activity in the nucleus accumbens (NAc) generated by the combination of cocaine and caffeine. CDB interacts directly or indirectly with several molecular targets, so the underlying mechanisms of its beneficial effects are hard to determine. Here we used high-throughput RNA-sequencing in mice’s NAc after a sensitization protocol with combined cocaine plus caffeine and a CBD pre-treatment, to identify the major pathways and genes involved in CBD attenuating behavioral effects. Results indicated that CBD pretreatment consistently reduced both the acquisition and expression of cocaine and caffeine locomotor sensitization. The transcriptome analysis revealed that CBD pre-treatment enriched genes and functional association between proteins mainly related to extracellular matrix (ECM) organization and cell interactions in the NAc. Moreover, the neuroinflammation and BDNF signaling pathways were also influenced by CBD. Some specially enriched genes such as Tnc were identified as interesting specific candidates for follow-up studies. These findings provide valuable and novel insights into molecular mechanisms of CBD putatively associated with a protective effect on psychostimulant actions. A better understanding of the therapeutic targets of CBD can open new avenues for psychostimulant use disorder treatment strategies.
SoxB1 transcription factors are essential for initiating and maintaining the neural plate border gene expression
Authors: Schock Elizabeth N. , York Joshua R. , Li Austin P. , Tu Ashlyn Y. , LaBonne Carole 
Published: September 2023

AbstractSoxB1 transcription factors (Sox2/3) are well known for their role in early neural fate specification in the embryo, but little is known about functional roles for SoxB1 factors in non-neural ectodermal cell types, such as the neural plate border (NPB). UsingXenopus laevis, we set out to determine if SoxB1 transcription factors have a regulatory function in NPB formation. Herein, we show that SoxB1 factors are necessary for NPB formation, and that prolonged SoxB1 factor activity blocks the transition from a NPB to a neural crest state. Using ChIP-seq we demonstrate that Sox3 is enriched upstream of NPB genes in early NPB cells and, surprisingly, in blastula stem cells. Depletion of SoxB1 factors in blastula stem cells results in downregulation of NPB genes. Finally, we identify Pou5f3 factors as a potential SoxB1 partners in regulating the formation of the NPB and show their combined activity is needed to maintain NPB gene expression. Together, these data identify a novel role for SoxB1 factors in the establishment and maintenance of the NPB, in part through partnership with Pou5f3 factors.
Activity-dependent synapse clustering underlies eye-specific competition in the developing retinogeniculate system
Authors: Zhang Chenghang , Vatan Tarlan , Speer Colenso M. 
Published: September 2023

AbstractCo-active synaptic connections are often spatially clustered to facilitate local dendritic computations underlying learning, memory, and basic sensory processing. In the mammalian visual system, retinal ganglion cell (RGC) axons converge to form clustered synaptic inputs that enable local signal integration in the dorsal lateral geniculate nucleus (dLGN) of the thalamus. While visual experience promotes retinogeniculate synapse clustering after eye-opening, the earliest events in cluster formation prior to visual experience are unknown. Here, using volumetric super-resolution single-molecule localization microscopy and eye-specific labeling of developing retinogeniculate synapses in mice, we show that synaptic clustering is eye-specific and activity-dependent during retinogeniculate refinement in the first postnatal week. We identified a subset of retinogeniculate synapses with multiple active zones that are surrounded by like-eye synapses and depleted of synapse clustering from the opposite eye. In mutant mice with disrupted spontaneous retinal wave activity, synapses with multiple active zones still form, but do not exhibit the synaptic clustering seen in controls. These results highlight a role for spontaneous retinal activity in regulating eye-specific synaptic clustering in circuits essential for visual perception and behavior.
Cyclic nucleotide-induced bidirectional long-term synaptic plasticity inDrosophilamushroom body
Authors: Yamada Daichi , Davidson Andrew M. , Hige Toshihide 
Published: September 2023

AbstractActivation of the cAMP pathway is one of the common mechanisms underlying long-term potentiation (LTP). In theDrosophilamushroom body, simultaneous activation of odor-coding Kenyon cells (KCs) and reinforcement-coding dopaminergic neurons activates adenylyl cyclase in KC presynaptic terminals, which is believed to trigger synaptic plasticity underlying olfactory associative learning. However, learning induces long-term depression (LTD) at these synapses, contradicting the universal role of cAMP as a facilitator of transmission. Here, we develop a system to electrophysiologically monitor both short-term and long-term synaptic plasticity at KC output synapses and demonstrate that they are indeed an exception where activation of the cAMP/protein kinase A pathway induces LTD. Contrary to the prevailing model, our cAMP imaging finds no evidence for synergistic action of dopamine and KC activity on cAMP synthesis. Furthermore, we find that forskolin-induced cAMP increase alone is insufficient for plasticity induction; it additionally requires simultaneous KC activation to replicate the presynaptic LTD induced by pairing with dopamine. On the other hand, activation of the cGMP pathway paired with KC activation induces slowly developing LTP, proving antagonistic actions of the two second-messenger pathways predicted by behavioral study. Finally, KC subtype-specific interrogation of synapses reveals that different KC subtypes exhibit distinct plasticity duration even among synapses on the same postsynaptic neuron. Thus, our work not only revises the role of cAMP in synaptic plasticity by uncovering the unexpected convergence point of the cAMP pathway and neuronal activity, but also establishes the methods to address physiological mechanisms of synaptic plasticity in this important model.Abstract FigureMushroom body (MB) is the olfactory learning center of theDrosophilabrain (left). Dopamine input activates the cAMP/Protein kinase A pathway in Kenyon cells (KCs), the principal neurons of the MB. When it coincides with KC activity, it induces presynaptic long-term depression at the synapses on the MB output neuron (Top right). A subset of dopaminergic neurons is also known to release nitric oxide, which activates the cGMP pathway. When it coincides with KC activity, it induces long-term potentiation (Bottom right). Created withBioRender.com.
Curcumin and turmeric extract inhibit SARS-CoV-2 pseudovirus cell entry and spike-mediated cell fusion
Authors: Septisetyani Endah Puji , Lestari Dinda , Paramitasari Komang Alit , Prasetyaningrum Pekik Wiji , Kastian Ria Fajarwati , Anam Khairul , Santoso Adi , Eriani Kartini 
Published: September 2023

AbstractTurmeric extract (TE) with curcumin as its main active ingredient has been studied as a potential COVID-19 therapeutic. Curcumin has been studied in silico and in vitro against a naive SARS-CoV-2 virus, yet little is known about TE’s impact on SARS-CoV-2 infection. Moreover, no study reveals the potential of both curcumin and TE on the inhibition of SARS-CoV-2 cell-to-cell transmission. Here, we investigated the effects of both curcumin and TE on inhibiting SARS-CoV-2 entry and cell-to-cell transmission using pseudovirus (PSV) and syncytia models. We performed a PSV entry assay in 293T or 293 cells expressing hACE2. The cells were pretreated with curcumin or TE and then treated with PSV with or without the test samples. Next, we carried out syncytia assay by co-transfecting 293T cells with plasmids encoding spike, hACE2, and TMPRSS2 to be treated with the test samples. The results showed that in PSV entry assay on 293T/hACE/TMPRSS2 cells, both curcumin and TE inhibited PSV entry at concentrations of 1 µM and 10 µM for curcumin and 1 µg/ml and 10 µg/ml for TE. Moreover, both curcumin and TE reduced syncytia formation compared to control cells. Our study shows that TE and curcumin are potential inhibitors of SARS-CoV-2 infection at entry points, either by direct or indirect infection models.GRAPHICAL ABSTRACT
Acute and chronic psychosocial stress by the brain-derived neurotrophic factor in male humans: a highly standardized and controlled study
Authors: Herhaus Benedict , Heni Martin , Bloch Wilhelm , Petrowski Katja 
Published: September 2023

AbstractObjectiveThe neurotrophic protein brain-derived neurotrophic factor (BDNF) plays a pivotal role in brain function and is affected by acute and chronic stress. We here investigate the patterns of BDNF and cortisol stress reactivity and recovery under the standardized stress protocol of the TSST and the effect of perceived chronic stress on the basal BDNF levels in healthy young men.MethodsTwenty-nine lean young men underwent the Trier Social Stress Test (TSST) and a resting condition. Serum BDNF and cortisol were measured before and repeatedly after both conditions. The perception of chronic stress was assessed by the Trier Inventory for Chronic Stress (TICS).ResultsAfter the TSST, there was a significant increase over time for BDNF and cortisol. Stronger increase in cortisol in response to stress was linked to an accelerated BDNF decline after stress. Basal resting levels of BDNF was significantly predicted by chronic stress perception.ConclusionsThe increased BDNF level following psychosocial stress suggest a stress-induced neuroprotective mechanism. The presumed interplay between BDNF and the HPA-axis indicates an antagonistic relationship of cortisol on BDNF recovery post-stress. Chronically elevated high cortisol levels, as present in chronic stress, could thereby contribute to reduced neurogenesis, and an increased risk of neurodegenerative conditions in persons suffering from chronic stress.HighlightsAcute psychosocial stress increases serum BDNF and cortisolStress-induced cortisol secretion may accelerate the decline of BDNF after stress.Chronic stress is linked to lower basal serum BDNF levels
AsymptomaticPlasmodium falciparumCarriage at the End of the Dry Season is Associated with Subsequent Infection and Clinical Malaria in Eastern Gambia
Authors: Fogang Balotin , Lellouche Lionel , Ceesay Sukai , Drammeh Sainabou , Jaiteh Fatou K. , Guery Marc-Antoine , Landier Jordi , Haanappel Cynthia , Froberg Janeri , Conway David , D’Alessandro Umberto , Bousema Teun , Claessens Antoine 
Published: September 2023

AbstractBackgroundChronic carriage of asymptomatic low-densityPlasmodium falciparumparasitaemia in the dry season may support maintenance of acquired immunity that protects against clinical malaria. However, the relationship between chronic low-density infections and subsequent risk of clinical malaria episodes remains unclear.MethodsIn a 2-years study (December 2014 to December 2016) in eastern Gambia, nine cross-sectional surveys using molecular parasite detection were performed in the dry and wet season. During the 2016 malaria transmission season, passive case detection identified episodes of clinical malaria.ResultsAmong the 5,256 samples collected, 444 (8.4%) were positive forP. falciparum. A multivariate model identified village of residence, male sex, age ≥5 years old, anaemia, and fever as independent factors associated withP. falciparumparasite carriage. Infections did not cluster over time within the same households or recurred among neighbouring households. Asymptomatic parasite carriage at the end of dry season was associated with a higher risk of infection (Hazard Ratio, HR= 3.0, p< 0.0001) and clinical malaria (HR= 1.561, p= 0.057) during the following transmission season. Age and village of residence were additional predictors of infection and clinical malaria during the transmission season.ConclusionChronic parasite carriage during the dry season is associated with an increased risk of malaria infection and clinical malaria. It is unclear whether this is due to environmental exposure or to other factors.
Goal-Oriented Attentional Self-Regulation Training in Chronic Mild Traumatic Brain Injury Leads to Microstructural Plasticity in Prefrontal White Matter
Authors: Karbasforoushan Haleh , Wren-Jarvis Jamie , Hwang Anna , Santiago Rachel , Raptentsetsang Sky , Cai Lanya T. , Xiao Jaclyn , Maruyama Brian A. , Abrams Gary M. , Novakovic-Agopian Tatjana , Mukherjee Pratik 
Published: September 2023

AbstractImpaired attention is one of the most common, debilitating, and persistent consequence of traumatic brain injury (TBI), which impacts overall cognitive and executive functions in these patients. Previous neuroimaging studies, trying to understand the neural mechanism underlying attention impairment post TBI, have highlighted the role of prefrontal white matter tracts in attentional functioning in mild TBI. Goal-Oriented Attentional Self-Regulation (GOALS) is a cognitive rehabilitation training program that targets executive control functions in participants by applying mindfulness-based attention regulation and goal management strategies. GOALS training has been demonstrated to improve attention and executive functioning in patients with chronic TBI. However, its impact on microstructural integrity of attention-associated prefrontal white matter tracts is still unclear. Here, using diffusion MRI in a pilot randomized controlled trial, we investigated the effect of GOALS training on prefrontal white matter microstructure in US military veterans with chronic mild TBI (mTBI), compared to a matched control group of veterans with chronic mTBI who received standard of care brain health education. We also tested for an association between microstructural white matter changes and sustained attention ability in these patients pre- and post-GOALS training. Our results show significantly better white matter microstructural integrity in left and right anterior corona radiata in the GOALS group compared to the control group post-training. Moreover, we found a significant correlation between sustained attention ability of GOALS training participants and white matter integrity of their right anterior corona radiata pre- and post-training. Finally, our findings indicated that the improved white matter integrity of the anterior corona radiata in GOALS training participants was the result of increased neurite density and decreased fiber orientation dispersion within this tract.
Influenza virus circulation and vaccine effectiveness during June 2021–May 2023 in Thailand
Authors: Prasert Kriengkrai , Praphasiri Prabda , Nakphook Sutthichai , Ditsungnoen Darunee , Sapchookul Patranuch , Sornwong Kanlaya , Naosri Suriya , Okada Pilailuk Akkapaiboon , Suntarattiwong Piyarat , Chotpitayasunondh Tawee , Montgomery Martha P. , Davis William W. , Pittayawonganon Chakrarat 
Published: September 2023

AbstractWe evaluated 2023 Southern Hemisphere influenza vaccine effectiveness against medically attended illness using surveillance data from nine Thai hospitals and a test-negative design. During June 2022–May 2023, influenza vaccine provided protection against seeking care for influenza illness (adjusted vaccine effectiveness 43%; 95% confidence interval 15–61).
Single-cell multimodal profiling of atherosclerosis identifies CD200 as a cell surface lineage marker of vascular smooth muscle cells and their derived cells
Authors: Bashore Alexander C. , Chung Allen , Ibikunle Chinyere , Yan Hanying , Xue Chenyi , Li Mingyao , Bauer Robert C. , Reilly Muredach P. 
Published: September 2023

AbstractVascular smooth muscle cells (VSMCs) play a central role in the development of atherosclerosis due in part to their capability to phenotypically transition into either a protective or harmful state. However, the ability to identify and trace VSMCs and their progeny in vivo is limited due to the lack of well-defined VSMC cell surface markers. Therefore, investigations into VSMC fate must utilize lineage-tracing mouse models, which are time-consuming and challenging to generate and not feasible in humans. Here, we employed CITE-seq to characterize the phenotypic expression of 119 cell surface proteins in mouse atherosclerosis. We found that CD200 is a highly expressed and specific marker of VSMCs, which persists even with phenotypic modulation. We validated our findings using a combination of flow cytometry, qPCR, and immunohistochemistry, all confirming that CD200 can identify and mark VSMCs and their derived cells in early to advanced mouse atherosclerotic lesions. Additionally, we describe a similar expression pattern of CD200 in human coronary and carotid atherosclerosis. Thus, our data support the use of CD200 as a lineage marker for VSMCs and VSMC-derived cells in mouse and human atherosclerosis.
Folate depletion alters mouse trophoblast stem cell regulationin vitro
Authors: Rakoczy Joanna , Watson Erica D. 
Published: September 2023

AbstractMaternal folate deficiency increases risk of congenital malformations, yet its effect on placenta development is unclear. Here, we investigated how folate-depleted culture medium affects the developmental potential of mouse trophoblast stem cells (TSCs). When cultured in stem cell conditions, TSC viability was unaffected by folate depletion, but ectopic differentiation of several trophoblast cell subtypes occurred. When cultured in conditions that promote differentiation, folate-depleted TSCs were driven towards a syncytiotrophoblast cell fate potentially at the expense of other lineages. Additionally, trophoblast giant cell nuclei were small implicating folate in the regulation of endoreduplication. Therefore, dietary folate intake likely promotes placenta development.