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To date, there is insufficient evidence to explain the role of adenosinergic receptors in the reconsolidation of long-term spatial memory. In this work, the role of the adenosinergic receptor family (A1, A2A, A2B, and A3) in this process has been elucidated. It was demonstrated that when infused bilaterally into the hippocampal CA1 region immediately after an early nonreinforced test session performed 24 h posttraining in the Morris water maze task, adenosine can cause anterograde amnesia for recent and late long-term spatial memory. This effect on spatial memory reconsolidation was blocked by A1 or A3 receptor antagonists and mimicked by A1 plus A3 receptor agonists, showing that this effect occurs through A1 and A3 receptors simultaneously. The A3 receptor alone participates only in the reconsolidation of late long-term spatial memory. When the memory to be reconsolidated was delayed (reactivation 5 d posttraining), the amnesic effect of adenosine became transient and did not occur in a test performed 5 d after the reactivation of the mnemonic trace. Finally, it has been shown that the amnesic effect of adenosine on spatial memory reconsolidation depends on the occurrence of protein degradation and that the amnesic effect of inhibition of protein synthesis on spatial memory reconsolidation is dependent on the activation of A3 receptors., (© 2023 Bosetto Fiebrantz et al.; Published by Cold Spring Harbor Laboratory Press.)

Conventional approaches for lattice dynamics based on static interatomic forces do not fully account for the effects of time-reversal-symmetry breaking in magnetic systems. Recent approaches to rectify this involve incorporating the first-order change in forces with atomic velocities under the assumption of adiabatic separation of electronic and nuclear degrees of freedom. In this Letter, we develop a first-principles method to calculate this velocity-force coupling in extended solids and show via the example of ferromagnetic CrI_{3} that, due to the slow dynamics of the spins in the system, the assumption of adiabatic separation can result in large errors for splittings of zone-center chiral modes. We demonstrate that an accurate description of the lattice dynamics requires treating magnons and phonons on the same footing.

It has already been shown that both consolidation and reconsolidation of long-term memories require protein synthesis and de novo gene transcription immediately after training or mnemonic trace reactivation sessions. A few studies have also shown that consolidation of long-term memories also requires a late second wave of de novo gene transcription. Does such a requirement also occur for reconsolidation? By using two different mRNA synthesis inhibitors, we show that blockade of hippocampal late gene expression during a restricted post-training or postretrieval time window hinders the retention of long-term spatial memory for the Morris water maze task without affecting the functionality of the hippocampus. Our results indicate that spatial memory consolidation induces the activation of the late hippocampal genes transcriptional machinery and suggests a late gene expression-dependent reconsolidation process that operates in the dorsal hippocampus to stabilize the reactivated mnemonic trace., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Introduction: We aimed to estimate the prevalence and incidence of specific symptoms and predictors of post-acute COVID-19 syndrome using data collected from an anonymous online survey., Methods: We included adult participants with symptoms ≥60 days (D60+), fulfilling the World Health Organization COVID-19 cases definition, and/or hospitalized for COVID-19 at the time of infection (D0). Self-reported symptoms were collected at D0 and D60+. Logistic regression was performed to identify factors associated with self-reported cutaneous signs prevalence and self-reported tachycardia and/ or HBP incidence on D60+., Results: From April to June 2020, 956 members of a Twitter long-term COVID-19 community were included in the study population: 81% were women, 81% were aged <50 year, 22% were smokers, and 95% have never been hospitalized. At D60+, the 956 participants reported a broad spectrum of symptoms which were also present at D0+. At D60+, 16% and 39% of participants reported cutaneous signs and tachycardia and/or hypertension, respectively. The incidence of self-reported tachycardia and/or hypertension at D60+ was 12%. Female gender (AOR=2.56; 95% CI: 1.22-6.1) and smoking (AOR=2.34; 95% CI: 1.39-3.92) were associated with prevalence of cutaneous signs at D60+. Smoking (AOR=2.05; 95% CI: 1.2- 3.47) was the main correlate of tachycardia and/or HBP incidence at D60+., Conclusions: The incidence of self-reported tachycardia and/or hypertension is not negligible and suggests an interaction between COVID-19 and smoking. Reinforcing symptoms monitoring of people after acute COVID-19, mainly women and smokers, and expanding the promotion of smoking cessation strategies are novel priorities in this COVID-19 era., Competing Interests: The authors have each completed and submitted an ICMJE form for disclosure of potential conflicts of interest. The authors declare that they have no competing interests, financial or otherwise, related to the current work. J. Bonini and F. Péretz report that since the initial planning of the work, their institution received a payment from Centre Hospitalier d’Auxerre, Auxerre, France. P. Carrieri reports that in the past 36 months received an INTERCEPT grant unrelated to this work., (© 2022 Barthélémy H. et al.)

Recent years have seen significant developments in the study of strong light-matter coupling including the control of chemical reactions by altering the vibrational normal modes of molecules. In the vibrational strong coupling regime, the normal modes of the system become hybrid modes which mix nuclear, electronic, and photonic degrees of freedom. First-principles methods capable of treating light and matter degrees of freedom on the same level of theory are an important tool in understanding such systems. In this work, we develop and apply a generalized force constant matrix approach to the study of mixed vibration-photon (vibro-polariton) states of molecules based on the cavity Born-Oppenheimer approximation and quantum-electrodynamical density-functional theory. With this method, vibro-polariton modes and infrared spectra can be computed via linear-response techniques analogous to those widely used for conventional vibrations and phonons. We also develop an accurate model that highlights the consistent treatment of cavity-coupled electrons in the vibrational strong coupling regime. These electronic effects appear as new terms previously disregarded by simpler models. This effective model also allows for an accurate extrapolation of single and two molecule calculations to the collective strong coupling limit of hundreds of molecules. We benchmark these approaches for single and many CO 2 molecules coupled to a single photon mode and the iron pentacarbonyl Fe(CO) 5 molecule coupled to a few photon modes. Our results are the first ab initio results for collective vibrational strong coupling effects. This framework for efficient computations of vibro-polaritons paves the way to a systematic description and improved understanding of the behavior of chemical systems in vibrational strong coupling.

Cystic fibrosis (CF), a genetic disorder, is characterized by chronic lung disease. Small non-coding RNAs are key regulators of gene expression and participate in various processes, which are dysregulated in CF; however, they remain poorly studied. Here, we determined the complete microRNAs (miRNAs) expression pattern in three CF ex vivo models. The miRNA profiles of air-liquid interface cultures of airway epithelia (bronchi, nasal cells, and nasal polyps) samples from patients with CF and non-CF controls were obtained by deep sequencing. Compared with non-CF controls, several miRNAs were deregulated in CF samples; for instance, miR-181a-5p and the miR-449 family were upregulated. Moreover, mature miRNAs often showed variations (i.e. isomiRs) relative to their reference sequence, such as miR-101, suggesting that miRNAs consist of heterogeneous repertoires of multiple isoforms with different effects on gene expression. Analysis of miR-181a-5p and miR-101-3p roles indicated that they regulate the expression of WISP1, a key component of cell proliferation/migration programs. We showed that miR-101 and miR-181a-5p participated in aberrant recapitulation of wound healing programs by controlling WISP1 mRNA and protein level. Our miRNA expression data bring new insights into CF physiopathology and define new potential therapeutic targets in CF. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd., (© 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.)

Nonequilibrium atomic structures can host exotic and technologically relevant properties in otherwise conventional materials. Oxygen octahedral rotation forms a fundamental atomic distortion in perovskite oxides, but only a few patterns are predominantly present at equilibrium. This has restricted the range of possible properties and functions of perovskite oxides, necessitating the utilization of nonequilibrium patterns of octahedral rotation. Here, we report that a designed metastable pattern of octahedral rotation leads to robust room-temperature ferroelectricity in CaTiO 3 , which is otherwise nonpolar down to 0 K. Guided by density-functional theory, we selectively stabilize the metastable pattern, distinct from the equilibrium pattern and cooperative with ferroelectricity, in heteroepitaxial films of CaTiO 3 . Atomic-scale imaging combined with deep neural network analysis confirms a close correlation between the metastable pattern and ferroelectricity. This work reveals a hidden but functional pattern of oxygen octahedral rotation and opens avenues for designing multifunctional materials.

A preliminary inquiry, conducted on Martinique Island, sought to determine kite-surfers' sun-protection knowledge and behaviours. Results revealed good levels of knowledge and behaviours, but very frequent sunburns (74% had at least one sunburn during the last 6 months), with particularly severe sunburns exclusively among vacationers. These results argue for the double need to focus sunburn-prevention programs on vacationers and technically adapt sun-protection means to a tropical maritime environment., (© International Society of Travel Medicine, 2017. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Impaired airway homeostasis in chronic obstructive pulmonary disease (COPD) could be partly related to club cell secretory protein (CCSP) deficiency. We hypothesize that CCSP G38A polymorphism is involved and aim to examine the influence of the CCSP G38A polymorphism on CCSP transcription levels and its regulatory mechanisms. CCSP genotype and CCSP levels in serum and sputum were assessed in 66 subjects with stable COPD included in a 1-yr observational study. Forty-nine of them had an exacerbation. In an in vitro study, the impact on the CCSP promoter of 38G wild-type or 38A variant was assessed. BEAS-2B cells were transfected by either the 38G or 38A construct, in the presence/absence of cigarette smoke extract (CSE) or lipopolysaccharides (LPS). Cotransfections with modulating transcription factors, p53 and Nkx2.1, identified by in silico analysis by using ConSite and TFSEARCH were conducted. A allele carrier COPD patients had lower serum and sputum CCSP levels, especially among active smokers, and a decreased body mass index, airflow obstruction, dyspnea, and exercise capacity (BODE) score. In vitro, baseline CCSP transcription levels were similar between the wild and variant constructs. CSE decreased more profoundly the CCSP transcription level of 38A transfected cells. The opposite effect was observed with p53 cotransfection. LPS stimulation induced CCSP repression in 38A promoter transfected cells. Cotransfection with Nkx2.1 significantly activated the CCSP promoters irrespective of the polymorphism. Circulating CCSP levels are associated with smoking and the CCSP G38A polymorphism. CSE, LPS, and the Nkx2.1 and p53 transcription factors modulated the CCSP promoter efficiency. The 38A polymorphism exaggerated the CCSP repression in response to p53 and CSE., (Copyright © 2016 the American Physiological Society.)

Purpose: Although 97-99% of CFTR mutations have been identified, great efforts must be made to detect yet-unidentified mutations., Methods: We developed a small-scale next-generation sequencing approach for reliably and quickly scanning the entire gene, including noncoding regions, to identify new mutations. We applied this approach to 18 samples from patients suffering from cystic fibrosis (CF) in whom only one mutation had hitherto been identified., Results: Using an in-house bioinformatics pipeline, we could rapidly identify a second disease-causing CFTR mutation for 16 of 18 samples. Of them, c.1680-883A>G was found in three unrelated CF patients. Analysis of minigenes and patients' transcripts showed that this mutation results in aberrantly spliced transcripts because of the inclusion of a pseudoexon. It is located only three base pairs from the c.1680-886A>G mutation (1811+1.6kbA>G), the fourth most frequent mutation in southwestern Europe. We next tested the effect of antisense oligonucleotides targeting splice sites on these two mutations on pseudoexon skipping. Oligonucleotide transfection resulted in the restoration of the full-length, in-frame CFTR transcript, demonstrating the effect of antisense oligonucleotide-induced pseudoexon skipping in CF., Conclusion: Our data confirm the importance of analyzing noncoding regions to find unidentified mutations, which is essential to designing targeted therapeutic approaches.

The CFTR gene displays a tightly regulated tissue-specific and temporal expression. Mutations in this gene cause cystic fibrosis (CF). In this study we wanted to identify trans-regulatory elements responsible for CFTR differential expression in fetal and adult lung, and to determine the importance of inhibitory motifs in the CFTR-3'UTR with the aim of developing new tools for the correction of disease-causing mutations within CFTR. We show that lung development-specific transcription factors (FOXA, C/EBP) and microRNAs (miR-101, miR-145, miR-384) regulate the switch from strong fetal to very low CFTR expression after birth. By using miRNome profiling and gene reporter assays, we found that miR-101 and miR-145 are specifically upregulated in adult lung and that miR-101 directly acts on its cognate site in the CFTR-3'UTR in combination with an overlapping AU-rich element. We then designed miRNA-binding blocker oligonucleotides (MBBOs) to prevent binding of several miRNAs to the CFTR-3'UTR and tested them in primary human nasal epithelial cells from healthy individuals and CF patients carrying the p.Phe508del CFTR mutation. These MBBOs rescued CFTR channel activity by increasing CFTR mRNA and protein levels. Our data offer new understanding of the control of the CFTR gene regulation and new putative correctors for cystic fibrosis., (Copyright ©ERS 2015.)