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Impaired theory of mind in patients reduced the latter, but not the former, group difference to non-significance. No significant correlations emerged between symptom severity and task performance. Together, these findings suggest that the understanding of others' minds partly contributes to the appreciation of social rules and norms in patients with severe chronic courses of schizophrenia.
Early-stage visual processing deficits are evident in chronic schizophrenia. Consistent with a cascade model of information processing, whereby early perceptual processes have downstream effects on higher-order cognition, impaired visual processing is associated with deficits in social cognition in this clinical population. However, the nature of this relationship in the early phase of illness is unknown. Here, we present data from a study of early visual processing and social cognitive performance in recent-onset schizophrenia (ROSz).
Thirty-two people with ROSz and 20 healthy controls (HC) completed a visual backward masking task using stimuli of real world objects (Object Masking) to assess early-stage (i.e., 0-125 ms post-stimulus onset) visual processing. Subjects also completed two tasks of social cognition, one assessing relatively low-level processes of emotion identification (Emotion Biological Motion, EmoBio), and another assessing more complex, higher-order theory of mind abilities (The Awarenetage visual processing, low-level social cognition, and high-level social cognition were all significantly impaired in ROSz. Early-stage visual processing was associated with performance on the social cognitive tasks in ROSz, consistent with a cascade model of information processing. However, significant cascading effects within social cognition were not supported. These data suggest that interventions directed at early visual processing may yield downstream effects on social cognitive processes.
Early-stage visual processing, low-level social cognition, and high-level social cognition were all significantly impaired in ROSz. Early-stage visual processing was associated with performance on the social cognitive tasks in ROSz, consistent with a cascade model of information processing. However, significant cascading effects within social cognition were not supported. These data suggest that interventions directed at early visual processing may yield downstream effects on social cognitive processes.Much has been written about the placebo effects in functional gastrointestinal disorders (FGD), especially in irritable bowel syndrome (IBS), driven by the early hypothesis that in randomized controlled trials (RCTs) of IBS, the placebo effect might be specifically high and thus, corrupts the efficacy of novel drugs developed for this condition. This narrative review is based on a specific search method, a database (www.jips.online) developed since 2004 containing more than 4,500 papers (data papers, meta-analyses, systematic reviews, reviews) pertinent to the topic placebo effects/placebo response. Three central questions-deducted from the body of current literature-are addressed to explore the evidence behind this hypothesis What is the size placebo effect in FGD, especially in IBS, and is it different from the placebo effect seen in other gastrointestinal disorders? Is the placebo effect in FGD different from other functional, non-intestinal disorders, e.g. in other pain syndromes? Is the placebo effect in FGD related to placebo effects seen in psychiatry, e.g. in depression, anxiety disorders, and alike? Following this discussion, a fourth question is raised as the result of the three What are the consequences of this for future drug trials in FGD? In summary it is concluded that, contrary to common belief and discussion, the placebo effect seen in RCT in FGD is not specifically high and extraordinary as compared to other comparable (i.e. functional) disorders. It shares less than expected commonalities with the placebo effect in psychiatry, and very few predictors have yet been identified that determine its effect size, especially some that are driven by design features of the studies. Current practice of RCT in IBS seems to limit and control the placebo effect quite well, and future trial practice, e.g. head-to-head trial, still offers options to maintain this control, even in the absence of placebos used.Schizophrenia is a type of neurodevelopmental psychiatric disorder. However, to date, scientists have not discovered the etiology and effective treatment of this condition. We injected the early growth response gene (EGR3) into the bilateral hippocampus to build a schizophrenia rat model. Behavioral phenotyping and resting-state functional magnetic resonance imaging (rs-fMRI) were used to analyze the behavioral and cerebral alterations in the schizophrenia rat model. The efficacy of risperidone therapy was also evaluated. We divided 34 rats into four groups schizophrenia model group (E group), sham-operation group (FE group), healthy control group (H group), and risperidone therapy group (T group). Open field test and Morris water maze were conducted as behavioral experiments. Next, we performed rs-fMRI after four weeks of EGR3 transfection and risperidone treatment and analyzed imaging data using regional homogeneity (ReHo), the amplitude of low-frequency fluctuations (ALFF), and functional connectivity (FC). We examined the difference in behavioral and neural activation among the four groups and considered the correlations between behavior and imaging results. EGR3 gene transfection decreased the total moved distance in the open field test and the duration in the Q5 zone of the Morris water maze. Risperidone treatment reversed the trend and improved the performance of rats in these behavioral tests. Schizophrenia induced several neural alterations in ALFF and ReHo metrics of the rat brain, and risperidone could partly reverse these alterations. The results suggest that similar research is required for schizophrenia and that risperidone may be a novel treatment for dysregulated neural activation in schizophrenia.
The clinical characteristics of bipolar disorder (current major depressive episode) (BD) overlap with unipolar depressive disorder (UD), which makes it difficult to perform an accurate diagnosis. We identified plasma microRNAs (miRNAs) that distinguished BD from UD and explored the relationship between miRNA expression levels and clinical characteristics.
Total miRNAs from blood plasma from seven UD patients, seven BD patients, and six controls were analyzed. The identified miRNAs were validated in a separate population group. Depression severity and early life adversities were assessed. Bioinformatic analysis was conducted to investigate the target genes that were identified and the pathways associated with the altered miRNAs.
Compared to controls, 42 miRNAs were differentially expressed in patients. miR-19b-3p, miR-3921, and miR-1180-3p were selected to validate the microarray results. Only miR-19b-3p was validated as down-regulated in patients. The primary predicted genes associated with miR-19b-3p were MAPK1, PTEN, and PRKAA1. The most relevant KEGG pathways included mTOR, FoxO, and the PI3-K/Akt signaling pathway. XCT790 order BD patients were more likely to have higher expression levels of miR-19b-3p and more severe childhood trauma experience compared to UD patients.
Plasma miR-19b-3p is a potential non-invasive biomarker that might be useful in distinguishing UD from BD. miR-19b3p was predicted to be involved in the pathway of inflammatory dysregulation associated with experiencing early childhood trauma.
Plasma miR-19b-3p is a potential non-invasive biomarker that might be useful in distinguishing UD from BD. miR-19b3p was predicted to be involved in the pathway of inflammatory dysregulation associated with experiencing early childhood trauma.[This corrects the article DOI 10.3389/fphys.2020.00298.].During embryonic development, symmetric ectodermal thickenings [olfactory placodes (OP)] give rise to several cell types that comprise the olfactory system, such as those that form the terminal nerve ganglion (TN), gonadotropin releasing hormone-1 neurons (GnRH-1ns), and other migratory neurons in rodents. Even though the genetic heterogeneity among these cell types is documented, unidentified cell populations arising from the OP remain. One candidate to identify placodal derived neurons in the developing nasal area is the transcription factor Isl1, which was recently identified in GnRH-3 neurons of the terminal nerve in fish, as well as expression in neurons of the nasal migratory mass (MM). Here, we analyzed the Isl1 genetic lineage in chemosensory neuronal populations in the nasal area and migratory GnRH-1ns in mice using in situ hybridization, immunolabeling a Tamoxifen inducible Isl1CreERT and a constitutive Isl1Cre knock-in mouse lines. In addition, we also performed conditional Isl1 ablation in developing GnRH neurons. We found Isl1 lineage across non-sensory cells of the respiratory epithelium and sustentacular cells of OE and VNO. We identified a population of transient embryonic Isl1 + neurons in the olfactory epithelium and sparse Isl1 + neurons in postnatal VNO. Isl1 is expressed in almost all GnRH neurons and in approximately half of the other neuron populations in the MM. However, Isl1 conditional ablation alone does not significantly compromise GnRH-1 neuronal migration or GnRH-1 expression, suggesting compensatory mechanisms. Further studies will elucidate the functional and mechanistic role of Isl1 in development of migratory endocrine neurons.Patients with chronic pulmonary conditions such as chronic obstructive pulmonary disease (COPD) often develop skeletal muscle dysfunction, which is strongly and independently associated with poor outcomes including higher mortality. Some of these patients also develop chronic CO2 retention, or hypercapnia, which is also associated with worse prognosis. While muscle dysfunction in these settings involve reduction of muscle mass and disrupted fibers' metabolism leading to suboptimal muscle work, mechanistic research in the field has been limited by the lack of adequate animal models. Over the last years, we have established a rodent model of COPD-induced skeletal muscle dysfunction that allowed a disaggregated interrogation of the cellular and physiological effects driven by COPD from the ones unique to hypercapnia. We found that while COPD and hypercapnia synergistically contribute to muscle atrophy, they are antagonistic processes regarding fibers respiratory capacity. We propose that AMP-activated protein kinase (AMPK) is a crucial regulator of CO2 signaling in hypercapnic muscles, which leads to both net protein catabolism and improved mitochondrial respiration to support a transition into a substrate-rich, fuel-efficient metabolic mode that allows muscle cells cope with the CO2 toxicity.We tested the hypothesis that older adults would not likely experience deficits in maximal and explosive plantar flexion strength and standing balance performance induced by prolonged Achilles tendon vibration compared with young adults. Fifteen older men (OM, 73 ± 5 years) and 15 young men (YM, 24 ± 4 years) participated in two interventions on different days lying in a quiet supine position for 30 min with or without prolonged vibration to the Achilles tendon. Before and after the interventions, maximal voluntary contraction (MVC) torque during plantar flexion, rate of torque development (RTD), and center of pressure (COP) speed during single-leg standing were measured. The root mean square of the electromyogram (RMS-EMG) during performance and V-wave and voluntary activation during MVC were assessed. The MVC torque (7 ± 7%) and RTD (16 ± 15%) of YM but not OM significantly decreased after vibration. In addition, the relative changes observed in YM positively correlated with changes in RMS-EMG of the medial gastrocnemius (MG) (MVC torque and RTD) and in MG V-wave and voluntary activation (MVC torque).
Homepage: https://www.selleckchem.com/products/xct-790.html
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