Although sensitizing processes occur earlier, schizophrenia is diagnosed in young adulthood, which suggests that it might involve a pathological transition during late brain development in predisposed individuals. Parvalbumin (PV) interneuron alterations have been noticed, but their role in the disease is unclear. Here we demonstrate that adult LgDel +/À mice, a genetic model of schizophrenia, exhibit PV neuron hypo-recruitment and associated chronic PV neuron plasticity together with network and cognitive deficits. All these deficits can be permanently rescued by chemogenetic activation of PV neurons or D2R antagonist treatments, specifically in the ventral hippocampus (vH) or medial-prefrontal cortex during a late-adolescence-sensitive time window. PV neuron alterations were initially restricted to the hippocampal CA1/subiculum, where they became responsive to treatment in late adolescence. Therefore, progression to disease in schizophrenia-model mice can be prevented by treatments supporting vH-mPFC PV network function during a sensitive time window late in adolescence, suggesting therapeutic strategies to prevent the outbreak of schizophrenia.
The health issues that attract our attention when analyzing the truck driver population are the high prevalence of sedentary habits, inadequate diet, obesity, and proportion of hypertensive. All these are either considered risk factors for or a consequence of Obstructive Sleep Apnea (OSA). The objective of this study was to investigate the risk for OSA among 10,101 truck drivers and to correlate it with potentially related factors, such as serum glucose and cholesterol levels, smoking habits, alcohol and drug consumption, and self-reported physical activity. The drivers were invited to participate in the campaign "Saúde na Boléia" (Health Behind the Wheel) promoted by a Brazilian company responsible for the maintenance of approximately 360km of roads in the country. Drivers who spontaneously stopped at the campaign booths placed along the roads were invited to answer a questionnaire covering sociodemographic data such as age, alcohol, and drug consumption. All participants completed a Berlin Questionnaire and were classified as low- or high-risk subjects for OSA based on questions about snoring, tiredness during the day, and the presence of hypertension or obesity. Blood collection was accomplished at the same site by nurses and/or nursing students collaborating with the campaign for subsequent laboratory studies. Approximately 26% of the truck drivers were found to be at high-risk group for OSA. An adjusted multiple logistic model found the independent risk factors of smoking (OR=1.16; p=0.014) and drug use (OR= 1.32; p < 0.0001) were associated with high risk for OSA. The presence of self-reported occasional (OR=0.62; p<0.0001) and regular (OR=0.53; p < 0.0001) physical activity was found to be an independent factor protective of OSA. Educational programs, including ones aimed at improving one's health habits, such as engagement in physical exercise, should be considered in the development of initiatives to reduce the risk for OSA among the truck driver population.
In this paper we extend the color dipole formalism to the study of leading neutron production in $e + p \rightarrow e + n + X$ collisions at high energies and estimate the related observables, which were measured at HERA and may be analysed in future electron-proton ($ep$) colliders. In particular, we calculate the Feynman $x_F$ distribution of leading neutrons, which is expressed in terms of the pion flux and the photon-pion total cross section. In the color dipole formalism, the photon-pion cross section is described in terms of the dipole-pion scattering amplitude, which contains information about the QCD dynamics at high energies and gluon saturation effects. We consider different models for the scattering amplitude, which have been used to describe the inclusive and diffractive $ep$ HERA data. Moreover, the model dependence of our predictions with the description of the pion flux is analysed in detail. We show that the recently released H1 leading neutron spectra can be reproduced using the color dipole formalism and that these spectra could help us to observe more clearly gluon saturation effects in future $ep$ colliders.Comment: 10 pages, 5 figure
We expect to observe parton saturation in a future electron -ion collider. In this letter we discuss this expectation in more detail considering two different models which are in good agreement with the existing experimental data on nuclear structure functions. In particular, we study the predictions of saturation effects in electron -ion collisions at high energies, using a generalization for nuclear targets of the b-CGC model, which describes the ep HERA quite well. We estimate the total, longitudinal and charm structure functions in the dipole picture and compare them with the predictions obtained using collinear factorization and modern sets of nuclear parton distributions. Our results show that inclusive observables are not very useful in the search for saturation effects. In the small x region they are very difficult to disentangle from the predictions of the collinear approaches . This happens mainly because of the large uncertainties in the latter. On the other hand, our results indicate that the contribution of diffractive processes to the total cross section is about 20 % at large A and small Q 2 , allowing for a detailed study of diffractive observables. The study of diffractive processes becomes essential to observe parton saturation.
We develop a model to study tetraquark production in hadronic collisions. We focus on double parton scattering and formulate a version of the color evaporation model for the production of the X(3872) and of the T 4c tetraquark, a state composed by the cccc quarks.We find that the production cross section grows rapidly with the collision energy √ s and make predictions for the forthcoming higher energy data of the LHC.
Early life environmental exposure, particularly during perinatal period, can have a life-long impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptations to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitary-adrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.
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