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Background: Uric acid is a natural antioxidant and it has been shown that low levels of uric acid may be a risk factor for the development of Parkinson's disease. We aimed to investigate the relationship between uric acid and improvement of motor symptoms in patients with Parkinson's disease after subthalamic nucleus deep brain stimulation. Methods: We analyzed the correlation between serum uric acid levels in 64 patients with Parkinson's disease and the rate of improvement of motor symptoms 2 years after subthalamic nucleus deep brain stimulation. Results: A non-linear correlation was observed between uric acid levels and the rate of motor symptom improvement after subthalamic nucleus deep brain stimulation, during both the drug-off and drug-on periods. Conclusions: Uric acid is positively associated with the rate of motor symptom improvement in subthalamic nucleus deep brain stimulation within a certain range. [ABSTRACT FROM AUTHOR]

Understanding tumor heterogeneity and immune infiltrates within the tumor-immune microenvironment (TIME) is essential for the innovation of immunotherapies. Here, combining single-cell transcriptomics and chromatin accessibility sequencing, we profile the intratumor heterogeneity of malignant cells and immune properties of the TIME in primary central nervous system diffuse large B-cell lymphoma (PCNS DLBCL) patients. We demonstrate diverse malignant programs related to tumor-promoting pathways, cell cycle and B-cell immune response. By integrating data from independent systemic DLBCL and follicular lymphoma cohorts, we reveal a prosurvival program with aberrantly elevated RNA splicing activity that is uniquely associated with PCNS DLBCL. Moreover, a plasmablast-like program that recurs across PCNS/activated B-cell DLBCL predicts a worse prognosis. In addition, clonally expanded CD8 T cells in PCNS DLBCL undergo a transition from a pre-exhaustion-like state to exhaustion, and exhibit higher exhaustion signature scores than systemic DLBCL. Thus, our study sheds light on potential reasons for the poor prognosis of PCNS DLBCL patients, which will facilitate the development of targeted therapy. [ABSTRACT FROM AUTHOR]

Background: Uric acid is a natural antioxidant, and low levels of uric acid have been reported to be a potential risk factor in the development of nervous system diseases. Herein, we investigated whether uric acid levels play a role in trigeminal neuralgia (TN).Methods: We conducted a cohort study to compare the serum uric acid levels of patients with TN and healthy controls. We also analyzed the impact of uric acid levels on the risk of TN and symptom severity.Results: In comparison to control participants (n = 133), uric acid levels were remarkably decreased in patients with TN (n = 181). Uric acid (OR = 0.989; 95% CI 0.986-0.993; P < 0.001) was also determined as a protective factor against TN based on multivariate logistic regression models. Furthermore, nonlinear relationships between serum uric acid levels and TN incidence rate and between that and the Barrow Neurological Institute (BNI) grading were observed.Conclusions: Our study is the first to show a relationship between serum uric acid levels and TN. Specifically, low serum uric acid levels were associated with an increased risk of TN and more severe clinical symptoms. We expect that these findings will provide new insights into the prevention and treatment of TN. [ABSTRACT FROM AUTHOR]

The roles of some long non-coding RNAs (lncRNAs) in intracranial aneurysm (IA) have been investigated in many studies. The aim of this study is to elucidate the mechanism of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-143 (miR-143)/vascular endothelial growth factor-A (VEGFA) signal axis in vascular endothelial injury-induced IA. MALAT1, miR-143, and VEGFA expression in IA tissues and normal arterial tissues were detected. Matrix metalloproteinase 9 (MMP-9) in tissues, von Willebrand factor (vWF) in serum and tissues, and endothelin-1 (ET-1) in serum were detected. The modeled IA rats were injected with silenced or overexpressed MALAT1 for detecting vascular endothelial injury. Vascular endothelial cells from patients with IA were abstracted and transfected with silenced or overexpressed MALAT1 to verify the impacts of MALAT1 on cell viability and apoptosis. The connections among MALAT1, miR-143, and VEGFA were verified by online prediction, luciferase activity, and RNA-pull down assays. Overexpression of MALAT1 and VEGFA and poor expression of miR-143 were found in IA tissues. Downregulation of MALAT1 inhibited blood pressure, the expression of ET-1, vWF, and MMP-9, as well as the apoptotic index of vascular endothelial cells of rats with IA. Downregulated MALAT1 inhibited apoptosis and promoted viability of vascular endothelial cells in IA. MALAT1 bound to miR-143 and miR-143 targeted VEGFA. This study suggests that MALAT1 elevates VEGFA expression through competitive binding to miR-143, thereby boosting apoptosis and attenuating viability of vascular endothelial cells in IA. [ABSTRACT FROM AUTHOR]

A correction is presented to the article "Long Non‑coding RNA MALAT1/microRNA‑143/VEGFA Signal Axis Modulates Vascular Endothelial Injury‑Induced Intracranial Aneurysm.

Recent studies have provided evidence that there are two possible systems for empathy: affective empathy (AE) and cognitive empathy (CE). Neuroimaging paradigms have proven that the insular cortex is involved in empathy processing, particularly in AE. However, these observations do not provide causal evidence for the role of the insula in empathy. Although impairments in empathy have been described following insular damage in a few case studies, it is not clear whether insular cortex is involved in CE and whether these two systems are impaired independently or laterally in patients with insular gliomas. In this study, we assessed 17 patients with an insular glioma, 17 patients with a noninsular glioma, and 30 healthy controls using a method that combined a self-report empathy questionnaire with the emotion recognition task, assessment of empathy for others' pain, and the emotional perspective-taking paradigm. We found that patients with an insular glioma had lower scores for empathic concern and perspective taking than did either healthy controls or lesion controls. The patients' abilities to recognize facial emotions, perceive others' pain, and understand the emotional perspectives of others were also significantly impaired. Furthermore, we did not observe a laterality effect on either AE or CE among those with insular lesions. These findings revealed that both AE and CE are impaired in patients with an insular glioma and that the insular cortex may be a central neuroanatomical structure in both the AE and CE systems. [ABSTRACT FROM AUTHOR]

The potential value of cerebral dopamine neurotrophic factor (CDNF) in treating Parkinson's disease (PD) remains controversial. To evaluate the therapeutic effects of CDNF-expressing bone marrow derived mesenchymal stem cell (CDNF-MSCs) injections in a rat model of Parkinson's disease, we chose three different routes of CDNF-MSC administration, including intra-striatal, intra-ventricular, and intravenous pathways. Parkinsonism was induced by intra-striatal unilateral injection of 6-OHDA and then rats were subsequently randomized into three groups for either intra-striatal, intra-ventricular or intravenous injection for CDNF-MSC grafting. Therapeutic effects were evaluated by observing dopaminergic (DA) neurons both in the substantia nigra compacta (SNc) and within the striatum and by monitoring apomorphine-induced rotational behavior (circling). Data show that one intra-venous administration of CDNF-MSCs was ineffective for treating Parkinson's disease-like neurodegeneration. Conversely, intra-striatal grafts can reduce loss of DA neurons both in the SNc and striatum with improvement of Parkinson's-related behaviors, compared to intra-ventricular injections. Thus, intra-striatal grafts composed of CDNF-MSCs may provide a strategy for therapeutic delivery to treat PD. [ABSTRACT FROM AUTHOR]

Purpose: Previous researches have reported gray and white matter microalterations in primary trigeminal neuralgia (TN) with neurovascular compression (NVC). The central mechanism underlying TN without NVC are unknown but may include changes in specific brain regions or circuitries. This study aimed to investigate abnormalities in the gray matter (GM) and white matter (WM) of the whole brain and the possible pathogenetic mechanism underlying this disease. Methods: We analyzed brain morphologic images of TN patients, 23 with NVC (TN wNVC) and 22 without NVC (TN wNVC) compared with 45 healthy controls (HC). All subjects underwent 3T-magnetic resonance imaging and pain scale evaluation. Voxel-based morphometry (VBM) and surface-based morphometry (SBM) were used to investigate whole brain grey matter quantitatively; graph theory was applied to obtain network measures based on extracted DTI data based on DTI data of the whole brains. Sensory and affective pain rating indices were assessed using the visual analog scale (VAS) and short-form McGill Pain Questionnaire (SF-MPQ). Results: The VBM and SBM analyses revealed widespread decreases in GM volume and cortical thickness in TN wNVC compared to TN woNVC, and diffusion metrics measures and topology organization changes revealed DTI showed extensive WM integrity alterations. However, above structural changes differed between TN wNVC and TN woNVC, and were related to specific chronic pain modulation mechanism. Conclusion: Abnormalities in characteristic regions of GM and WM structural network were found in TN woNVC compared with TN wNVC group, suggesting differences in pathophysiology of two types of TN. [ABSTRACT FROM AUTHOR]