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Resume L’eczema de contact palpebral aux antibiotiques en collyre est de plus en plus rapporte, mais la famille des fluoroquinolones est exceptionnellement en cause. Les patch tests sont utilises afin de confirmer la nature de l’allergene ; cependant, les faux-negatifs sont de plus en plus retrouves. Des tests alternatifs, comme le ROAT (Repeated Open Application Test), peuvent s’averer utiles. Nous rapportons le cas d’un enfant de 6 ans, presentant un eczema palpebral a la norfloxacine avec patch tests negatifs, ou le ROAT avait tout son interet.

Summary Memories formed during infancy are forgotten in adulthood, a phenomenon called ‘infantile amnesia’. New research suggests that these memories can be artificially recovered in adulthood, suggesting that they were never completely lost in the first place.

Emerging evidence indicates that distinct hippocampal domains differentially drive cognition and emotion [1, 2]; dorsal regions encode spatial, temporal, and contextual information [3-5], whereas ventral regions regulate stress responses [6], anxiety-related behaviors [7, 8], and emotional states [8-10]. Although previous studies demonstrate that optically manipulating cells in the dorsal hippocampus can drive the behavioral expression of positive and negative memories, it is unknown whether changes in cellular activity in the ventral hippocampus can drive such behaviors [11-14]. Investigating the extent to which distinct hippocampal memories across the longitudinal axis modulate behavior could aid in the understanding of stress-related psychiatric disorders known to affect emotion, memory, and cognition [15]. Here, we asked whether tagging and stimulating cells along the dorsoventral axis of the hippocampus could acutely, chronically, and differentially promote context-specific behaviors. Acute reactivation of both dorsal and ventral hippocampus cells that were previously active during memory formation drove freezing behavior, place avoidance, and place preference. Moreover, chronic stimulation of dorsal or ventral hippocampal fear memories produced a context-specific reduction or enhancement of fear responses, respectively, thus demonstrating bi-directional and context-specific modulation of memories along the longitudinal axis of the hippocampus. Fear memory suppression was associated with a reduction in hippocampal cells active during retrieval, while fear memory enhancement was associated with an increase in basolateral amygdala activity. Together, our data demonstrate that discrete sets of cells throughout the hippocampus provide key nodes sufficient to bi-directionally reprogram both the neural and behavioral expression of memory.

A growing body of evidence suggests that meditation training may have a range of salubrious effects, including improved telomere regulation. Telomeres and the enzyme telomerase interact with a variety of molecular components to regulate cell-cycle signaling cascades, and are implicated in pathways linking psychological stress to disease. We investigated the effects of intensive meditation practice on these biomarkers by measuring changes in telomere length (TL), telomerase activity (TA), and telomere-related gene (TRG) expression during a 1-month residential Insight meditation retreat. Multilevel analyses revealed an apparent TL increase in the retreat group, compared to a group of experienced meditators, similarly comprised in age and gender, who were not on retreat. Moreover, personality traits predicted changes in TL, such that retreat participants highest in neuroticism and lowest in agreeableness demonstrated the greatest increases in TL. Changes observed in TRGs further suggest retreat-related improvements in telomere maintenance, including increases in Gar1 and HnRNPA1, which encode proteins that bind telomerase RNA and telomeric DNA. Although no group-level changes were observed in TA, retreat participants’ TA levels at post-assessment were inversely related to several indices of retreat engagement and prior meditation experience. Neuroticism also predicted variation in TA across retreat. These findings suggest that meditation training in a retreat setting may have positive effects on telomere regulation, which are moderated by individual differences in personality and meditation experience. (ClinicalTrials.gov #NCT03056105).

La pancreatite aigue est une presentation exceptionnelle de la tuberculose pancreatique. Elle est particulierement exceptionnelle chez l’immunocompetent. Nous rapportons le cas d’une patiente de 20 ans sans antecedents medicaux. Elle consultait pour des epigastralgies atypiques calmees par la position anteflechie qui evoluaient depuis 15 jours dans un contexte de fievre non chiffree. L’examen trouvait une fievre a 39°C, une sensibilite epigastrique et une ascite. La biologie notait une hyperleucytose a 12.000 elements/mm3 a predominance polynucleaire, les hemocultures, les prelevements urinaires et la radiographie thoracique etaient normaux. La lipasemie etait a 423 ui/l. Le scanner abdominal trouvait l’aspect de pancreatite aigue classee stade C selon la classification de Balthazard et l’echoendoscopie ne trouvait pas d’obstacle sur la voie biliaire principale. Le liquide d’ascite etait riche en lymphocyte (89%), en protide a 58g/l, en lipase: 325 UI/l et en adenosine desaminase a 65g/l. L’origine tuberculeuse a ete evoquee et l’intradermoreaction a la tuberculine etait positive a 17 mm. La recherche d’autre localisation de tuberculose etait negative. La patiente a recu le traitement antibacillaire pendant 9 mois et l’evolution clinique et radiologique etait bonne. Le diagnostic de tuberculose pancreatique etait retenu a posteriori sur la bonne evolution sous traitement medical. Nous allons faire le point sur cette pathologie exceptionnelle chez l’adulte immunocompetent.

Research suggests that dysfunctional glutamatergic signalling may contribute to depression, a debilitating mood disorder affecting millions of individuals worldwide. Ketamine, a N-methyl-D-aspartate (NMDA) receptor antagonist, exerts rapid antidepressant effects in approximately 70% of patients. Glutamate evokes the release of D-serine from astrocytes and neurons, which then acts as a co-agonist and binds at the glycine site on the NR1 subunit of NMDA receptors. Several studies have implicated glial deficits as one of the underlying facets of the neurobiology of depression. The present study tested the hypothesis that D-serine modulates behaviours related to depression. The behavioural effects of a single, acute D-serine administration were examined in several rodent tests of antidepressant-like effects, including the forced swim test (FST), the female urine sniffing test (FUST) following serotonin depletion, and the learned helplessness (LH) paradigm. D-serine significantly reduced immobility in the FST without affecting general motor function. Both D-serine and ketamine significantly rescued sexual reward-seeking deficits caused by serotonin depletion in the FUST. Finally, D-serine reversed LH behaviour, as measured by escape latency, number of escapes, and percentage of mice developing LH. Mice lacking NR1 expression in forebrain excitatory neurons exhibited a depression-like phenotype in the same behavioural tests, and did not respond to D-serine treatment. These findings suggest that D-serine produces antidepressant-like effects and support the notion of complex glutamatergic dysfunction in depression. It is unclear whether D-serine has a convergent influence on downstream synaptic plasticity cascades that may yield a similar therapeutic profile to NMDA antagonists like ketamine.

Buckypaper is a thin sheet fabricated from the aggregation of carbon nanotubes. The generally accepted method for forming such carbon nanotube (CNT) films involves the use of stable suspension of carbon nanotubes in water. These suspensions can then be membrane-filtered under pressure to yield uniform films. After preparation of a stable solution, it should be membrane-filtrated on the surface of a filter. Usually, the quality of a buckypaper depends on sonication time and power, surfactant type and concentration, filter type, and concentration of carbon nanotube. In order to investigate the surface quality of buckypapers, low-magnification images could give rather useful information about the roughness of surface. Analysis of the 100 × images clearly shows that with increasing the suspension concentration, the smoothness of buckypaper surface will decrease. Therefore, from this viewpoint, decreasing the concentration can enhance the quality of the buckypaper. Surface of the filter also affects on the buckypaper quality. Therefore, for filtration of the suspension, a filter with suitable material, pore sizes, and surface should be used. As the pore sizes of the filter are usually small, the filtration process may be very time-consuming. Since the process is carring out under pressure and also due to the brittle nature of the buckypaper, removal of the buckypaper from the surface of the filter is a very serious and important stage and depends on the filter type, concentration, and type of CNTs. The buckypaper usually can be removed from the filter mechanically. The type of CNTs (MWNT or SWNT) may change the above-mentioned factors.

Despite the long-established therapeutic efficacy of lithium in the treatment of bipolar disorder (BPD), its molecular mechanism of action remains elusive. Newly developed stable isotope-resolved metabolomics (SIRM) is a powerful approach that can be used to elucidate systematically how lithium impacts glial and neuronal metabolic pathways and activities, leading ultimately to deciphering its molecular mechanism of action. The effect of lithium on the metabolism of three different (13)C-labeled precursors ([U-(13)C]-glucose, (13)C-3-lactate or (13)C-2,3-alanine) was analyzed in cultured rat astrocytes and neurons by nuclear magnetic resonance (NMR) spectroscopy and gas chromatography mass spectrometry (GC-MS). Using [U-(13)C]-glucose, lithium was shown to enhance glycolytic activity and part of the Krebs cycle activity in both astrocytes and neurons, particularly the anaplerotic pyruvate carboxylation (PC). The PC pathway was previously thought to be active in astrocytes but absent in neurons. Lithium also stimulated the extracellular release of (13)C labeled-lactate, -alanine (Ala), -citrate, and -glutamine (Gln) by astrocytes. Interrogation of neuronal pathways using (13)C-3-lactate or (13)C-2,3-Ala as tracers indicated a high capacity of neurons to utilize lactate and Ala in the Krebs cycle, particularly in the production of labeled Asp and Glu via PC and normal cycle activity. Prolonged lithium treatment enhanced lactate metabolism via PC but inhibited lactate oxidation via the normal Krebs cycle in neurons. Such lithium modulation of glycolytic, PC and Krebs cycle activity in astrocytes and neurons as well as release of fuel substrates by astrocytes should help replenish Krebs cycle substrates for Glu synthesis while meeting neuronal demands for energy. Further investigations into the molecular regulation of these metabolic traits should provide new insights into the pathophysiology of mood disorders and early diagnostic markers, as well as new target(s) for effective therapies.

In this paper, damage mechanisms in the composite bounded skin/stiffener constructions under monotonic tension loading are investigated. The approach uses experiments to detect the failure mechanisms, two and three-dimensional stress analysis to determine the location of first matrix cracking and computational fracture mechanics to investigate the potential for cracks and delamination growth. The laminates strength and damage mechanisms obtained from both experimental and finite elements analysis are presented for several laminates lay-up configurations. Observations on the performed experiments show matrix crack initiation and propagation in the skin and near the flange tip, causing the flange to almost fully debounded from the skin in some cases, interlaminar debounding and fiber breakage up to the failure of the components. The finite elements analysis is also show that the matrix cracks are initiated in the first skin layer for most of the cases. With increasing the applied load the matrix cracks are propagated through the thickness to reach the next layer and causes delamination between the two layers. With increasing the applied load this delamination is propagated up to the occurrence of unstable delamination growth or the first fiber breakage known as the final failure of the component. The obtained experimental failure loads are compared with those calculated by the finite elements analysis.

Objectives: Several intracellular signaling cascades, such as the extracellular signal-regulated kinase (ERK), Wnt-signaling/GSK-3, PLC/PKC, and PI3K pathways, have been shown to be affected directly or indirectly by mood stabilizers. Clinical imaging studies reveal that mood disorders are associated with structural and/or metabolic changes in specific brain regions such as the anterior cingulate cortex (ACC). Here we investigated the extent to which perturbation of one of the affected pathways, the ERK pathway, in the ACC influences affective-related behavior. Methods: The regional perturbation was induced by two means: local continuous infusion of PD98059, an ERK pathway inhibitor, and microinjection of a lentiviral-mediated gene delivery system encoding functional negative ERK1. The outcomes were monitored with a battery of affective-related tests similar to those used in several previous studies. Results: Compared to their respective controls, rats infused with PD98059 or injected with the lentiviral negative ERK1 construct displayed hyperactivities in multiple tests, exhibited preferentially more open-arm activity in the elevated-plus-maze test, consumed more sweetened liquid in a saccharin preference test, and showed heightened response to amphetamine. Conclusions: These data support a role for the ACC ERK pathway in the regulation of affective-related behaviors. However, the medial prefrontal cortex (mPFC) comprises at least three other regions that will need to be similarly examined before specific roles of the ACC ERK pathway can be definitively attributed to affective behaviors. Additionally, responses of other signaling pathways to mood stabilizers in these mPFC regions, as well as the limbic regions to which they project, will be important to examine.

Damage accumulation in laminated composite is a major concern in the design and use of composite structures. Accumulated damage can affect laminated response and ultimate strength, which are critical to design of load-carrying structural components. For the optimal design of composite structures, laminate response beyond the point of initial matrix cracking must be known, and subsequent damage and failure modes induced by accumulated matrix crack must be understood.

SummaryThe hippocampus is assumed to retrieve memory by reinstating patterns of cortical activity that were observed during learning. To test this idea, we monitored the activity of individual cortical neurons while simultaneously inactivating the hippocampus. Neurons that were active during context fear conditioning were tagged with the long-lasting fluorescent protein H2B-GFP and the light-activated proton pump ArchT. These proteins allowed us to identify encoding neurons several days after learning and silence them with laser stimulation. When tagged CA1 cells were silenced, we found that memory retrieval was impaired and representations in the cortex (entorhinal, retrosplenial, perirhinal) and the amygdala could not be reactivated. Importantly, hippocampal inactivation did not alter the total amount of activity in most brain regions. Instead, it selectively prevented neurons that were active during learning from being reactivated during retrieval. These data provide functional evidence that the hippocampus reactivates specific memory representations during retrieval.

Background: Electronic health records (EHR) commonly contain patient addresses that provide valuable data for geocoding and spatial analysis, enabling more comprehensive descriptions of individual patients for clinical purposes. Despite the widespread use of EHR in clinical decision support and interventions, no systematic review has examined the extent to which spatial analysis is used to characterize patient phenotypes., Objective: This study reviews advanced spatial analyses that employed individual-level health data from EHR within the US to characterize patient phenotypes., Methods: We systematically evaluated English-language peer-reviewed articles from PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar databases from inception to August 20, 2023, without imposing constraints on time, study design, or specific health domains., Results: Only 49 articles met the eligibility criteria. These articles utilized diverse spatial methods, with a predominant focus on clustering techniques, while spatiotemporal analysis (frequentist and Bayesian) and modeling were relatively underexplored. A noteworthy surge (n = 42, 85.7%) in publications was observed post-2017. The publications investigated a variety of adult and pediatric clinical areas, including infectious disease, endocrinology, and cardiology, using phenotypes defined over a range of data domains, such as demographics, diagnoses, and visits. The primary health outcomes investigated were asthma, hypertension, and diabetes. Notably, patient phenotypes involving genomics, imaging, and notes were rarely utilized., Conclusions: This review underscores the growing interest in spatial analysis of EHR-derived data and highlights knowledge gaps in clinical health, phenotype domains, and spatial methodologies. Additionally, this review proposes guidelines for harnessing the potential of spatial analysis to enhance the context of individual patients for future clinical decision support., Competing Interests: Conflicts of interest None declared. Additional Declarations: The authors declare no competing interests.

Background: Hospital-acquired infections present a major concern for healthcare systems in the U.S. and worldwide. Drug-resistant infections result in increased costs and prolonged hospital stays. Methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE) are responsible for many drug-resistant infections in the U.S. We undertook two parallel studies aimed to investigate the differences in the microbial communities of individuals colonized with MRSA (or VRE) as compared to their respective non-colonized counterparts matched for age, sex, race, ethnicity, unit of admission, and diagnostic-related group, when available., Results: The VRE study showed considerably more Enterococcus genus communities in the VRE colonized samples. Our findings for both MRSA and VRE studies suggest a strong association between 16S rRNA gene alpha diversity, beta diversity, and colonization status. When we assessed the colonized microbial communities in isolation, the differences disappeared, suggesting that the colonized microbial communities drove the change. Isolating Staphylococcus, we saw significant differences expressed across colonization in specific sequence variants., Conclusions: The differences seen in the microbial communities from MRSA (or VRE) colonized samples as compared to non-colonized match-pairs are driven by the isolated communities of the Staphylococcus (or Enterococcus) genus, the removal of which results in the disappearance of any differences in the diversity observed across the match-pairs., Competing Interests: Declarations Competing Interests The authors declare that no competing interests.