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Abstract We describe the decoherence instability of Schrödinger Cat states in the two-site Bose-Hubbard model with an attractive on-site interaction between particles. For N particles with onsite attractive energy U and hopping amplitude between sites t, Cat states exist for $$u\equiv \frac{UN}{2t}

Autism spectrum disorder (ASD) is a developmental disorder characterised by deficits in social interactions and communication, with stereotypical and repetitive behaviours. Recent evidence suggests that maternal immune dysregulation may predispose offspring to ASD. Independent samples t-tests revealed downregulation of IL-17A concentrations in cases, when compared to controls, at both 15 weeks (p = 0.02), and 20 weeks (p = 0.02), which persisted at 20 weeks following adjustment for confounding variables. This adds to the growing body of evidence that maternal immune regulation may play a role in foetal neurodevelopment. [This article was written on behalf of the SCOPE Consortium.]

Abstract We describe the trapping and absorption of audible sound in centimeter-scale claddings of two-dimensional, locally resonant phononic crystals. In a square lattice of local resonators consisting of steel cores and cellulose shells, embedded in a viscous foam, dual acoustic-range band gaps extending from about 200 to $$2850 \text { Hz}$$ 2850 Hz are achieved. The spectral range consists of a low-frequency, local resonance gap, separated from a higher frequency Bragg resonance gap, by narrow bands of slow-sound modes. We demonstrate that thin claddings of such phononic crystal, of only three unit cells in thickness, can effectively prevent sound transmission, by a combination of reflection and absorption, over much of the audible spectrum. Moreover, frequency-selective sound transmission can be enabled by engineering waveguide channels that transmit sound through the local resonance gap, the Bragg gap, or both. This offers a path to sound-sculpting claddings that can surround a noise-generating source. The viscoelastic foam in our cladding is treated using a fractional Voigt model, capable of describing experimentally observed responses.

Abstract Ketamine has rapid and sustained antidepressant effects in patients with treatment-resistant depression (TRD). However, the underlying mechanisms of action are not well understood. There is increasing evidence that TRD is associated with a pro-inflammatory state and that ketamine may inhibit inflammatory processes. We thus investigated whole blood transcriptional profiles related to TRD and gene expression changes associated with treatment response to ketamine. Whole blood was collected at baseline (21 healthy controls [HC], 26 patients with TRD) and then again in patients with TRD 24 hours following a single intravenous infusion of ketamine (0.5 mg/kg). We performed RNA-sequencing and analyzed (a) baseline transcriptional profiles between patients with TRD and HC, (b) responders vs. non-responders before ketamine treatment, and (c) gene expression signatures associated with clinical improvement. At baseline, patients with TRD compared to HC showed a gene expression signature indicative of interferon signaling pathway activation. Prior to ketamine administration, the metabotropic glutamate receptor gene GRM2 and the ionotropic glutamate receptor gene GRIN2D were upregulated in responders compared to non-responders. Response to ketamine was associated with a distinct transcriptional signature, however, we did not observe gene expression changes indicative of an anti-inflammatory effect. Future studies are needed to determine the role of the peripheral immune system in the antidepressant effect of ketamine.

Recent advances in next-generation sequencing (NGS) technologies have opened the door to a wellspring of information regarding the composition of the gut microbiota. Leveraging NGS technology, early metagenomic studies revealed that several diseases, such as Alzheimer’s disease, Parkinson’s disease, autism, and myalgic encephalomyelitis, are characterized by alterations in the diversity of gut-associated microbes. More recently, interest has shifted toward understanding how these microbes impact their host, with a special emphasis on their interactions with the brain. Such interactions typically occur either systemically, through the production of small molecules in the gut that are released into circulation, or through signaling via the vagus nerves which directly connect the enteric nervous system to the central nervous system. Collectively, this system of communication is now commonly referred to as the gut-microbiota-brain axis. While equally important, little attention has focused on the causes of the alterations in the composition of gut microbiota. Although several factors can contribute, mucosal immunity plays a significant role in shaping the microbiota in both healthy individuals and in association with several diseases. The purpose of this review is to provide a brief overview of the components of mucosal immunity that impact the gut microbiota and then discuss how altered immunological conditions may shape the gut microbiota and consequently affect neuroimmune diseases, using a select group of common neuroimmune diseases as examples.

BackgroundHuman monkeypox is a zoonotic disease endemic to parts of Africa. Similar to other orthopoxviruses, virus and host have considerable interactions through immunomodulation. These interactions likely drive the establishment of a productive infection and disease progression, resulting in the range of disease presentations and case fatality rates observed for members of the Orthopoxvirus genus.ObjectivesMuch of our understanding about the immune response to orthopoxvirus infection comes from either in vitro or in vivo studies performed in small animals or non-human primates. Here, we conducted a detailed assessment of cytokine responses to monkeypox virus using serum from acutely ill humans collected during monkeypox active disease surveillance (2005-2007) in the Democratic Republic of the Congo.Study designNineteen serum samples that were from patients with confirmed monkeypox virus infections were selected for cytokine profiling. Cytokine profiling was performed on the Bio-Rad Bioplex 100 system using a 30-plex human cytokine panel.ResultsCytokine profiling revealed elevated cytokine concentrations in all samples. Overproduction of certain cytokines (interleukin [IL]-2R, IL-10, and granulocyte macrophage-colony stimulating factor were observed in patients with serious disease (defined as >250 lesions based on the World Health Organization scoring system).ConclusionsThe data suggest that cytokine modulation affects monkeypox disease severity in humans.

Social hierarchy formation is strongly evolutionarily conserved. Across species, rank within social hierarchy has large effects on health and behavior. To investigate the relationship between social rank and stress susceptibility, we exposed ranked male and female mice to social and non-social stressors and manipulated social hierarchy position. We found that rank predicts same sex social stress outcomes: dominance in males and females confers resilience while subordination confers susceptibility. Pre-existing rank does not predict non-social stress outcomes in females and weakly does so in males, but rank emerging under stress conditions reveals social interaction deficits in male and female subordinates. Both history of winning and rank of cage mates affect stress susceptibility in males: rising to the top rank through high mobility confers resilience and mice that lose dominance lose stress resilience, although gaining dominance over a subordinate animal does not confer resilience. Overall, we have demonstrated a relationship between social status and stress susceptibility, particularly when taking into account individual history of winning and the overall hierarchy landscape in male and female mice.

There is a debate about the ability to improve cognitive abilities such as fluid intelligence through training on tasks of working memory capacity. The question addressed in the research presented here is who benefits the most from training: people with low cognitive ability or people with high cognitive ability? Subjects with high and low working memory capacity completed a 23-session study that included 3 assessment sessions, and 20 sessions of training on 1 of 3 training regiments: complex span training, running span training, or an active-control task. Consistent with other research, the authors found that training on 1 executive function did not transfer to ability on a different cognitive ability. High working memory subjects showed the largest gains on the training tasks themselves relative to the low working memory subjects--a finding that suggests high spans benefit more than low spans from training with executive function tasks.

Abstract Background Myalgic encephalomyelitis (ME) is a complex and debilitating disease that often initially presents with flu-like symptoms, accompanied by incapacitating fatigue. Currently, there are no objective biomarkers or laboratory tests that can be used to unequivocally diagnosis ME; therefore, a diagnosis is made when a patient meets series of a costly and subjective inclusion and exclusion criteria. The purpose of the present study was to evaluate the utility of four clinical parameters in diagnosing ME. Methods In the present study, we utilized logistic regression and classification and regression tree analysis to conduct a retrospective investigation of four clinical laboratory in 140 ME cases and 140 healthy controls. Results Correlations between the covariates ranged between [− 0.26, 0.61]. The best model included the serum levels of the soluble form of CD14 (sCD14), serum levels of prostaglandin E2 (PGE2), and serum levels of interleukin 8, with coefficients 0.002, 0.249, and 0.005, respectively, and p-values of 3 × 10−7, 1 × 10−5, and 3 × 10−3, respectively. Conclusions Our findings show that these parameters may help physicians in their diagnosis of ME and may additionally shed light on the pathophysiology of this disease.

Autism spectrum disorders (ASD) are severe heterogeneous neurodevelopmental disorders characterized by dysfunctions in social interaction and communication skills, repetitive and stereotypic verbal and nonverbal behaviors. Published findings have identified widespread changes in the immune systems of children with autism, at the systemic and cellular levels, suggesting that autism may, in fact, be a systemic disorder with connections to abnormal immune responses. Evaluating autism is hindered by a lack of specific biomarkers, making these pathologies difficult to diagnose. A critical priority for the future of ASD management is the identification of potential targets for the development of diagnostic and therapeutic strategies. The purpose of this brief report is to raise awareness regarding the involvement of different inflammatory processes in ASD and the need to assess them as a part of a biomedical evaluation. An extensive analysis of biomarkers relating to inflammation, immune dysfunctions, intestinal dysfunctions and infections will assist in the management of the autistic patient through a more personalized therapy.

Insulin resistance is a chronic inflammatory condition accompanying obesity or high fat diets that leads to type 2 diabetes. It is hypothesized that lipids and gut bacterial compounds in particular contribute to metabolic inflammation by activating the immune system; however, the receptors detecting these “instigators” of inflammation remain largely undefined. Here, we show that circulating activators of NOD1, a receptor for bacterial peptidoglycan, increase with high fat feeding in mice, suggesting that NOD1 could be a critical sensor leading to metabolic inflammation. Hematopoietic depletion of NOD1 did not prevent weight gain but protected chimeric mice against diet-induced glucose and insulin intolerance. Mechanistically, while macrophage infiltration of adipose tissue persisted, notably these cells were less pro-inflammatory, had lower CXCL1 production, and consequently, lower neutrophil chemoattraction into the tissue. These findings reveal macrophage NOD1 as a cell-specific target to combat diet-induced inflammation past the step of macrophage infiltration, leading to insulin resistance.