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Language comprehension is compositional individual words are combined structurally to form larger meaning representations. The neural basis for compositionality is at the center of a growing body of recent research. Previous work has largely used univariate analysis to investigate the question, a technique that could potentially lead to the loss of fined-grained information due to the procedure of averaging over neural responses. In a functional magnetic resonance imaging experiment, the present study examined different types of composition relations in Chinese phrases, using a 1-back composition relation probe (CRP) task and a 1-back word probe (WP) task. We first analyzed the data using the multivariate representation similarity analysis, which better captures the fine-grained representational differences in the stimuli. The results showed that the left angular gyrus (AG) represents different types of composition relations in the CRP task, but no brain areas were identified in the WP task. We also conducted a traditional univariate analysis and found greater activations in the bilateral inferior frontal gyrus in the CRP task relative to the WP task. We discuss the methodological and theoretical implications of our findings in the context of the larger language neural network identified in previous studies. Our findings highlight the role of left AG in representing and distinguishing fine-grained linguistic composition relations.
The previous results from cross-sectional studies indicate that there could be alterations across time in handgrip strength (HGS) asymmetry. One way to investigate this is to test the same children multiple times. Therefore, we aimed to evaluate the laterality of HGS in healthy young children at two different time points separated by a year.

A total of 165 preschool children (79 males and 87 females) between the ages of 4.5 and 5.6 years participated and performed maximal voluntary HGS in both hands using a Smedley handgrip dynamometer. We ran a paired sample t-test on the difference scores (right - left vs. right - left) to determine if HGS (right vs. left) differed across time.

The difference between hands (t = -4.804, p <.0001) did differ between time points. At the initial test, the mean value of the HGS in the right hand was approximately 15% higher than that of the left hand. This difference between hands was reduced following a year. The mean bias between tests (second test - initial test) and the 95% limits of agreement was -0.84 (-5.27, 3.58) kg.

Contrary to our hypothesis, HGS asymmetry during the initial test (at age 5) was not observed in the second test completed a year later (at age 6). These results suggest that HGS asymmetry is uncertain in children between 5 and 6 years. In this short-term study, it was impossible to ascertain when HGS asymmetry first appeared. Longer term studies are required to better determine when these changes occur.
Contrary to our hypothesis, HGS asymmetry during the initial test (at age 5) was not observed in the second test completed a year later (at age 6). These results suggest that HGS asymmetry is uncertain in children between 5 and 6 years. In this short-term study, it was impossible to ascertain when HGS asymmetry first appeared. Longer term studies are required to better determine when these changes occur.Tissue-resident memory γδT cells at mucosal and epithelial sites play an important role for pathogen clearance, immunosurveillance, and participating in physiological processes. Different from other barrier sites, the immune cells in uterus face the protection against infections and tolerate an allogeneic fetus during a successful pregnancy. In the previous study, we found that tissue-resident memory γδT cells were enriched both in human and murine uterus and highly expressed IL-17 that promoted the invasion of trophocytes in vitro. In the current study, we found that γδT cells in uterus but not in blood or spleens expressed higher levels of estrogen receptors. CID-1067700 manufacturer The injection of estrogen into mice increased the proportion of γδT cells in uterus but not in spleens in vivo via CXCR3-CXCL10 chemokine axis. In addition, we found that estrogen enhanced the production of IL-17 but not IFN-γ in vivo and in vitro via interferon regulatory factor 4 but not RORγt and pSTAT3 at mRNA and protein levels. The analysis of cell transcriptome sequence further identified multiple differentially expressed genes between estrogen and control γδT cells. Our study demonstrated that estrogen directly act on γδT cells in uterus to enhance the production of IL-17 that might promote the invasion of trophocytes. Furthermore, our study might provide a new idea that estrogen increased the prevalence of autoimmune diseases in women by enhancing γδT cell-derived IL-17 production in uterus and uncover the critical pathological roles for estrogen in the development of autoimmune diseases.Real protein interaction network (PIN) is dynamic. Researchers created dynamic PIN by combining static PIN with gene expression data to explain the dynamicity evolution of protein interactions. However, all available approaches failed to recognize low- or high-expression proteins as active proteins. Therefore, determining an adequate threshold is one of the system's biological challenges. In this study, a quartile one (q-one) method is proposed to determine the active time points for each protein according to its expression value's features and construct dynamic protein interaction networks (DPINs) in which a protein is added to the network if it is active in two successive time points. This leads to reduce the number of DPINs to half. The efficiency of the q-one approach and three-sigma (3-sigma) method in detecting protein complexes is evaluated using Markov cluster method, clique percolation method, and ClusterONE algorithms. In most cases, q-one outperforms the 3-sigma method in recall, precision and F-measure. This is in addition to its ability to reveal the dynamicity within the protein-protein interaction network and identify essential proteins.
Inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) regulates immunity and inflammation, but its clinical role in rheumatoid arthritis (RA) patients remains unclear. Hence, this study was conducted to explore the association of circulating ITIH4 with disease risk, clinical features, inflammatory cytokines, and treatment outcomes of RA.

After the enrollment of 93 active RA patients and 50health controls (HCs), their serum ITIH4level was analyzed by enzyme-linked immunosorbent assay (ELISA). For RA patients only, serum ITIH4level at week (W) 6 and W12 after treatment was also analyzed. Besides, serum tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-17A at baseline of RA patients were also detected by ELISA.

ITIH4 was downregulated in RA patients (151.1 (interquartile range (IQR) 106.2-213.5) ng/mL) than in HCs (306.8 (IQR 238.9-435.1) ng/mL) (p<0.001). Furthermore, ITIH4 was negatively related to C-reactive protein (CRP) (r
=-0.358, p<0.001) and 28-joint disease activity score using erythrocyte sedimentation rate (DAS28-ESR) (r
=-0.253, p=0.014) in RA patients, but not correlated with other clinical features (all p>0.05). Besides, ITIH4 was negatively linked with TNF-α (r
=-0.337, p=0.001), IL-6 (r
=-0.221, p=0.033), and IL-17A (r
=-0.368, p<0.001) in RA patients, but not correlated with IL-1β (r
=-0.195, p=0.061). Moreover, ITIH4 was gradually elevated in RA patients from baseline to W12 after treatment (p<0.001). Additionally, the increment of ITIH4 at W6 and W12 was linked with treatment response and remission in RA patients (all p<0.05).

Circulating ITIH4 possesses clinical utility in monitoring disease risk, inflammation, disease activity, and treatment outcomes of RA.
Circulating ITIH4 possesses clinical utility in monitoring disease risk, inflammation, disease activity, and treatment outcomes of RA.The disruption of the blood-brain barrier (BBB) plays a critical role in the pathology of ischemic stroke. p75 neurotrophin receptor (p75NTR ) contributes to the disruption of the blood-retinal barrier in retinal ischemia. However, whether p75NTR influences the BBB permeability after acute cerebral ischemia remains unknown. The present study investigated the role and underlying mechanism of p75NTR on BBB integrity in an ischemic stroke mouse model, middle cerebral artery occlusion (MCAO). After 24 h of MCAO, astrocytes and endothelial cells in the infarct-affected brain area up-regulated p75NTR . Genetic p75NTR knockdown (p75NTR+/- ) or pharmacological inhibition of p75NTR using LM11A-31, a selective inhibitor of p75NTR , both attenuated brain damage and BBB leakage in MCAO mice. Astrocyte-specific conditional knockdown of p75NTR mediated with an adeno-associated virus significantly ameliorated BBB disruption and brain tissue damage, as well as the neurological functions after stroke. Further molecular biological examinations indicated that astrocytic p75NTR activated NF-κB and HIF-1α signals, which upregulated the expression of MMP-9 and vascular endothelial growth factor (VEGF), subsequently leading to tight junction degradation after ischemia. As a result, increased leukocyte infiltration and microglia activation exacerbated brain injury after stroke. Overall, our results provide novel insight into the role of astrocytic p75NTR in BBB disruption after acute cerebral ischemia. The p75NTR may therefore be a potential therapeutic target for the treatment of ischemic stroke.Dopamine in the prefrontal cortex is essential for the regulation of social behavior. However, stress-causing social withdrawal also promotes dopamine release in the prefrontal cortex. Thus, this evidence suggests opposite functions of dopamine in the prefrontal cortex. However, the influence of dopamine on prefrontal functions is yet to be fully understood. Here, we show that dopamine differentially modulated the neuronal activity triggered by social stimuli in the prefrontal cortex, depending on the duration of the dopamine activation (transient or sustained activation). Using chemogenetic techniques, we have found that social behavior was negatively regulated by a sustained increase in dopamine neuronal activity in the ventral tegmental area, while it was positively regulated by an acute increase. The duration of social interactions was positively correlated with the transient dopamine release triggered by social stimuli in the prefrontal cortex and negatively correlated with the sustained increase in prefrontal dopamine levels. Furthermore, the elevation of neural calcium signal, triggered by social stimuli, in the prefrontal cortex was attenuated by the persistent elevation of prefrontal dopamine levels, whereas an acute increase in dopamine levels enhanced it. Additionally, the chronic excess of dopamine suppressed c-Fos induction triggered by social stimuli in prefrontal neurons expressing dopamine D1 receptors, but not D2 receptors. These results suggest that sustained activation of prefrontal dopamine, at the opposite of its transient activation, can reduce prefrontal activity associated with social behavior, even for identical dopamine concentrations. Thus, dopamine plays opposite roles in modulating prefrontal activity depending on the duration of its action.
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