The classic concept of the absence of lymphatic vessels in the central nervous system (CNS), suggesting the immune privilege of the brain in spite of its high metabolic rate, was predominant until recent times. On the other hand, this idea left questioned how cerebral interstitial fluid is cleared of waste products. It was generally thought that clearance depends on cerebrospinal fluid (CSF). Not long ago, an anatomically and functionally discrete paravascular space was revised to provide a pathway for the clearance of molecules drained within the interstitial space. According to this model, CSF enters the brain parenchyma along arterial paravascular spaces. Once mixed with interstitial fluid and solutes in a process mediated by aquaporin-4, CSF exits through the extracellular space along venous paravascular spaces, thus being removed from the brain. This process includes the participation of perivascular glial cells due to a sieving effect of their end-feet. Such draining space resembles the peripheral lymphatic system, therefore, the term „glymphatic” (glial-lymphatic) pathway has been coined. Specific studies focused on the potential role of the glymphatic pathway in healthy and pathological conditions, including neurodegenerative diseases. This mainly concerns Alzheimer’s disease (AD), as well as hemorrhagic and ischemic neurovascular disorders; other acute degenerative processes, such as normal pressure hydrocephalus or traumatic brain injury are involved as well. Novel morphological and functional investigations also suggested alternative models to drain molecules through perivascular pathways, which enriched our insight of homeostatic processes within neural microenvironment. Under the light of these considerations, the present article aims to discuss recent findings and concepts on nervous lymphatic drainage and blood-brain barrier (BBB) in an attempt to understand how peripheral pathological conditions may be detrimental to the CNS, paving the way to neurodegeneration.Ovonic threshold switch (OTS) has received great attention in neuromorphic computing due to its support for high-density synapse array as a selector and leaky-integration-firing functions Hodgkin-Huxley neurons. However, there is no simple and complete model for device simulation and integrated circuit design, which hindered application until now. In this work, we developed a compact physical model of OTS based on the Poole-Frenkel effect accompanied by the thermal dissipation effect for the first time. The thermal dissipation effect describes the energy flow between the device and the environment so that the model is more practical. Compared with previous experiments, the numerical results fairly fitted the electrical characteristics, demonstrating the model validity. In addition, the relation of the device performance with material and structure was deduced, which can facilitate optimizing the OTS device. The model will be useful for device design and implemented with high speed for simplicity.Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders characterized by impaired skills in social interaction and communication in addition to restricted and repetitive behaviors. Many different factors may contribute to ASD development; in particular, oxytocin receptor (OXTR) deficiency has been reported to be associated with ASD, although the detailed mechanism has remained largely unknown. Epidemiological study has shown that maternal diabetes is associated with ASD development. In this study, we aim to investigate the potential role of OXTR on maternal diabetes-mediated social deficits in offspring. Our in vitro study of human neuron progenitor cells showed that hyperglycemia induces OXTR suppression and that this suppression remains during subsequent normoglycemia. Further investigation showed that OXTR suppression is due to hyperglycemia-induced persistent oxidative stress and epigenetic methylation in addition to the subsequent dissociation of estrogen receptor β (ERβ) from the OXTR promoter. Furthermore, our in vivo mouse study showed that maternal diabetes induces OXTR suppression; prenatal OXTR deficiency mimics and potentiates maternal diabetes-mediated anxiety-like behaviors, while there is less of an effect on autism-like behaviors. Additionally, postnatal infusion of OXTR partly, while infusion of ERβ completely, reverses maternal diabetes-induced social deficits. We conclude that OXTR may be an important factor for ASD development and that maternal diabetes-induced suppression of oxytocin receptor contributes to social deficits in offspring.Contradictory results have been obtained in the studies that compare contour integration abilities in Autism Spectrum Disorders (ASDs) and typically developing individuals. The present study aimed to explore the limiting factors of contour integration ability in ASD and verify the role of the external visual noise by a combination of psychophysical and eye-tracking approaches. To this aim, 24 children and adolescents with ASD and 32 age-matched participants with typical development had to detect the presence of contour embedded among similar Gabor elements in a Yes/No procedure. The results obtained showed that the responses in the group with ASD were not only less accurate but also were significantly slower compared to the control group at all noise levels. The detection performance depended on the group differences in addition to the effect of the intellectual functioning of the participants from both groups. The comparison of the agreement and accuracy of the responses in the double-pass experiment showed that the results of the participants with ASD are more affected by the increase of the external noise. It turned out that the internal noise depends on the level of the added external noise the difference between the two groups was non-significant at the low external noise and significant at the high external noise. In accordance with the psychophysical results, the eye-tracking data indicated a larger gaze allocation area in the group with autism. These findings may imply higher positional uncertainty in ASD due to the inability to maintain the information of the contour location from previous presentations and interference from noise elements in the contour vicinity. Psychophysical and eye-tracking data suggest lower efficiency in using stimulus information in the ASD group that could be caused by fixation instability and noisy and unstable perceptual template that affects noise filtering.Neuroinflammation driven by type-I interferons in the CNS is well established to exacerbate the progression of many CNS pathologies both acute and chronic. The role of adaptor protein Stimulator of Interferon Genes (STING) is increasingly appreciated to instigate type-I IFN-mediated neuroinflammation. As an upstream regulator of type-I IFNs, STING modulation presents a novel therapeutic opportunity to mediate inflammation in the CNS. This review will detail the current knowledge of protective and detrimental STING activity in acute and chronic CNS pathologies and the current therapeutic avenues being explored.

Heart rate variability (HRV) and heart rate (HR) dynamics are used to predict the survival probability of patients after acute myocardial infarction (AMI), but the association has been established in patients with mixed levels of left ventricular ejection fraction (LVEF).

We investigated whether the survival predictors of HRV and HR dynamics depend on LVEF after AMI.

We studied 687 post-AMI patients including 147 with LVEF ≤35% and 540 with LVEF >35%, of which 23 (16%) and 22 (4%) died during the 25 month follow-up period, respectively. None had an implanted cardioverter-defibrillator. From baseline 24 h ECG, the standard deviation (SDNN), root mean square of successive difference (rMSSD), percentage of successive difference >50 ms (pNN50) of normal-to-normal R-R interval, ultra-low (ULF), very-low (VLF), low (LF), and high (HF) frequency power, deceleration capacity (DC), short-term scaling exponent (α

), non-Gaussianity index (λ

), and the amplitude of cyclic variation of HR (Acv) were calccted by indices reflecting decreased HRV or HR responsiveness and cardiac parasympathetic dysfunction, whereas in patients without low LVEF, the risk is predicted by a combination of indices that reflect decreased HRV or HR responsiveness and indicator that reflects abrupt large HR changes suggesting sympathetic involvement.There is a long-standing debate regarding the cognitive nature of (dis)honesty Is honesty an automatic response or does it require willpower in the form of cognitive control in order to override an automatic dishonest response. In a recent study (Speer et al., 2020), we proposed a reconciliation of these opposing views by showing that activity in areas associated with cognitive control, particularly the inferior frontal gyrus (IFG), helped dishonest participants to be honest, whereas it enabled cheating for honest participants. These findings suggest that cognitive control is not needed to be honest or dishonest per se but that it depends on an individual’s moral default. However, while our findings provided insights into the role of cognitive control in overriding a moral default, they did not reveal whether overriding honest default behavior (non-habitual dishonesty) is the same as overriding dishonest default behavior (non-habitual honesty) at the neural level. This speaks to the question as to whether cognitive control mechanisms are domain-general or may be context specific. To address this, we applied multivariate pattern analysis to compare neural patterns of non-habitual honesty to non-habitual dishonesty. We found that these choices are differently encoded in the IFG, suggesting that engaging cognitive control to follow the norm (that cheating is wrong) fundamentally differs from applying control to violate this norm.Background Low-intensity transcranial ultrasound (LITUS) may have a therapeutic effect on Parkinson’s disease (PD) patients to some extent. Fractional anisotropy (FA) and relaxation time T2∗ that indicate the integrity of fiber tracts and iron concentrations in brain tissue have been used to evaluate the therapeutic effects of LITUS. Purpose This study aims to use FA and T2∗ values to evaluate the therapeutic effects of LITUS in a PD rat model. Materials and Methods Twenty Sprague-Dawley rats were randomly divided into a hemi-PD group (n = 10) and a LITUS group (n = 10). Single-shot spin echo echo-planar imaging and fast low-angle shot T2WI sequences at 3.0 T were used. The FA and T2∗ values on the right side of the substantia nigra (SN) pars compacta were measured to evaluate the therapeutic effect of LITUS in the rats. Results One week after PD-like signs were induced in the rats, the FA value in the LITUS group was significantly larger compared with the PD group (0.214 ± 0.027 vs. 0.340 ± 0.032, t = 2.864, P = 0.011). At the 5th and 6th weeks, the FA values in the LITUS group were significantly smaller compared with the PD group (5th week 0.290 ± 0.037 vs. 0.405 ± 0.027, t = 2.385, P = 0.030; 6th week 0.299 ± 0.021 vs. 0.525 ± 0.028, t = 6.620, P less then 0.0001). In the 5th and 6th weeks, the T2∗ values in the injected right SN of the LITUS group were significantly higher compared with the PD group (5th week, 12.169 ± 0.826 in the LITUS group vs. 7.550 ± 0.824 in the PD group; 6th week, 11.749 ± 0.615 in the LITUS group vs. 7.550 ± 0.849 in the PD group). Conclusion LITUS had neuroprotective effects and can reduce the damage of 6-OHDA-induced neurotoxicity in hemi-PD rats. The combination of FA and T2∗ assessments can potentially serve as a new and effective method to evaluate the therapeutic effects of LITUS.