Translational Neuroscience最新文献

Objective: To analyze the effect of gradient thrombectomy stent in vitro.

Methods: The cerebrovascular fluid circulation model was made and fixed on the test table. About 0.9% sodium chloride injection was injected to the vascular model through a miniature water pump to circulate it. Four kinds of thrombus products containing different red blood cell (RBC) volumes of 0, 5, 40, and 80% were placed at the target location as thrombus. Each type of thrombus was removed five times using SOLITAIRE stent and gradient thrombectomy stent. The thrombectomy effects were observed by comparison of the two types of stents.

Results: Thrombus containing 80% volume of RBC escaped thrombus fragments during thrombectomy with both stents. Thrombus containing 0% volume of RBC (rich in fibrin) had poor chimerism with stents. In the thrombus containing 0% RBC volume, there was no statistically significant difference between the two stents (p = 1). Thrombus removal was successful in all cases.

Conclusion: The gradient thrombectomy stent is as effective as the currently used thrombectomy stent in vitro studies, and there is much room for improvement.

The limitation of artificial intelligence (AI) large language models to diagnose diseases from the perspective of patient safety remains underexplored and potential challenges, such as diagnostic errors and legal challenges, need to be addressed. To demonstrate the limitations of AI, we used ChatGPT-3.5 developed by OpenAI, as a tool for medical diagnosis using text-based case reports of multiple sclerosis (MS), which was selected as a prototypic disease. We analyzed 98 peer-reviewed case reports selected based on free-full text availability and published within the past decade (2014-2024), excluding any mention of an MS diagnosis to avoid bias. ChatGPT-3.5 was used to interpret clinical presentations and laboratory data from these reports. The model correctly diagnosed MS in 77 cases, achieving an accuracy rate of 78.6%. However, the remaining 21 cases were misdiagnosed, highlighting the model's limitations. Factors contributing to the errors include variability in data presentation and the inherent complexity of MS diagnosis, which requires imaging modalities in addition to clinical presentations and laboratory data. While these findings suggest that AI can support disease diagnosis and healthcare providers in decision-making, inadequate training with large datasets may lead to significant inaccuracies. Integrating AI into clinical practice necessitates rigorous validation and robust regulatory frameworks to ensure responsible use.

[This corrects the article DOI: 10.1515/tnsci-2020-0127.].

Functional magnetic resonance imaging (fMRI) stands as a pivotal tool in advancing our comprehension of Schizophrenia, offering insights into functional segregations and integrations. Previous investigations employing either task-based or resting-state fMRI primarily focused on large main regions of interest (ROI), revealing the thalamus and superior temporal gyrus (STG) as prominently affected areas. Recent studies, however, unveiled the cytoarchitectural intricacies within these regions, prompting a more nuanced exploration. In this study, resting-state fMRI was conducted on 72 schizophrenic patients and 74 healthy controls to discern whether distinct thalamic nuclei and STG sub-regions exhibit varied functional integrational connectivity to main networks and to identify the most affected sub-regions in Schizophrenia. Employing seed-based analysis, six sub-ROIs - four in the thalamus and two in the STG - were selected. Our findings unveiled heightened positive functional connectivity in Schizophrenic patients, particularly toward the anterior STG (aSTG) and posterior STG (pSTG). Notably, positive connectivity emerged between the medial division of mediodorsal thalamic nuclei (MDm) and the visual network, while increased functional connectivity linked the ventral lateral nucleus of the thalamus with aSTG. This accentuated functional connectivity potentially influences these sub-regions, contributing to dysfunctions and manifesting symptoms such as language and learning difficulties alongside hallucinations. This study underscores the importance of delineating sub-regional dynamics to enhance our understanding of the nuanced neural alterations in Schizophrenia, paving the way for more targeted interventions and therapeutic approaches.

Humans live under constant threat from pathogenic microorganisms and minimizing such threat has been a major evolutionary selective force in shaping human behavior and health. A particular adaptive mechanism against the harm caused by parasites and their infectiousness is disgust sensitivity, which has evolved to detect and avoid poisonous foods as well as bodily secretions harboring virulent microorganisms. This ubiquitous and reflexive behavior requires the integration of several internal and external sensory signals between the brain, the autonomic nervous system (ANS), and the gastrointestinal tract. Although the emotional expression of disgust is experienced by almost all individuals, the neural mechanisms of sensory signals underlying disgust sensitivity may differ in certain psychiatric conditions. Psychopathy, for instance, is a personality disorder in which disgust sensitivity to contagious bodily secretions is apparently absent or downregulated from its atypical personality temperament. In this review, we provide convergent behavioral, anatomical, and cellular evidence to suggest that a fractured experience of disgust sensitivity might be an additional feature of psychopathic behavior. First, we discuss the neural networks of certain brain regions mediating the emotional states of disgust and then discuss the intersection of the ANS and gastrointestinal tract in the processing of disgust and its relevance to aberrant antisocial behavior. Together, this work highlights the interconnections between the brain and the bilateral body plan as an integrated cell network that is relevant for understanding common principles underlying function and dysfunction of disgust levels in psychiatric domains.

Background: The objective of this study (registered under number 2020 006) was to assess the internal consistency of the revised Mental Health Professional Culture Inventory (MHPCI) scale, which comprises 15 items, among mental health service workers in Romania. Methods: To examine the psychometric properties of the MHPCI questionnaire within the Romanian population, we employed two main methods: The partial credit model (PCM) and Exploratory factor analysis (EFA). Results: A total of 94 individuals were interviewed, and among them, 71 provided complete responses to the questionnaire. All 15 items demonstrate a strong fit with the PCM, as indicated by mean-square (MSQ) outfit and MSQ infit values falling within the range of 0.5 to 1.5. But items 3 and 11 exhibit MSQ values greater than 1.5, suggesting that it may be challenging to predict individuals' responses to these items. The KMO index stands at 0.7, surpassing the recommended threshold of 0.6, signifying an acceptable level of suitability. Nevertheless, only 59.3% of the total variance is accounted for by the first four factors, and these factors do not align with the dimensions identified in the original article. Conclusion: The internal structure of the Romanian version of the MHPCI demonstrates satisfactory psychometric properties. These properties will need to be further validated through additional studies conducted in diverse socio-cultural contexts.

Parkinson's disease (PD) is a neurodegenerative disorder that predominantly affects dopaminergic neurons in the substantia nigra and ventral tegmental area, resulting in symptoms such as tremors, muscle rigidity, bradykinesia, and potential cognitive and affective disturbances. The effective delivery of pharmacological agents to the central nervous system is hindered by various factors, including the restrictive properties of the blood‒brain barrier and blood‒spinal cord barrier, as well as the physicochemical characteristics of the drugs. Traditional drug delivery methods may not provide the therapeutic concentrations necessary for functional restoration in PD patients. However, lipid-based nanoparticles (NPs) offer new possibilities for enhancing the bioavailability of established treatment regimens and developing innovative therapies that can modify the course of the disease. This review provides a concise overview of recent advances in lipid-based NP strategies aimed at mitigating specific pathological mechanisms relevant to PD progression. This study also explores the potential applications of nanotechnological innovations in the development of advanced treatment modalities for individuals with PD.

Introduction: Depression, the leading cause of disability worldwide, is known to be exacerbated by severe acute respiratory syndrome coronavirus 2 infection, worsening coronavirus disease 2019 (COVID-19) outcomes. However, the mechanisms and treatments for this comorbidity are not well understood.

Methods: This study utilized Gene Expression Omnibus datasets for COVID-19 and depression, combined with protein-protein interaction networks, to identify key genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed to understand gene functions. The CIBERSORT algorithm and NetworkAnalyst were used to examine the relationship of immune cell infiltration with gene expression and to predict transcription factors (TFs) and microRNAs (miRNAs) interactions. The Connectivity Map database was used to predict drug interactions with these genes.

Results: TRUB1, PLEKHA7, and FABP6 were identified as key genes enriched in pathways related to immune cell function and signaling. Seven TFs and nineteen miRNAs were found to interact with these genes. Nineteen drugs, including atorvastatin and paroxetine, were predicted to be significantly associated with these genes and potential therapeutic agents for COVID-19 and depression.

Conclusions: This research provides new insights into the molecular mechanisms of post-COVID-19 depression and suggests potential therapeutic strategies, marking a step forward in understanding and treating this complex comorbidity.

Background: Neuropathic pain is a common symptom of Guillain-Barré syndrome (GBS). The infiltration of macrophages in the dorsal root ganglion (DRG) contributed to neuropathic pain in nerve injury. The underlying mechanisms of neuropathic pain in patients with GBS remain unknown. Experimental autoimmune neuritis (EAN) is a useful mice model of GBS. Our study aimed to explore whether the infiltration of macrophages in DRG is associated with neuropathic pain of EAN.

Methods: Male C57BL/6 mice were randomly divided into two groups, the EAN group (n = 12) and the control group (n = 12). Six mice in each group were sacrificed after anesthetization in the attack and remission phase, respectively. The 50% paw withdrawal threshold and clinical score were measured, and macrophages with its subtypes were detected in the spleen and DRG tissue.

Results: More macrophages infiltrated the DRG of the EAN group in the attack phase and mostly surrounded neurons in the DRG. The proportion of macrophages and pro-inflammatory macrophages in the spleen of mice with EAN was significantly higher than the control group in the attack phase.

Conclusion: The infiltration of macrophages in DRG might be associated with neuropathic pain of EAN and pro-inflammatory macrophages may involve in neuropathic pain of EAN.

There is an urgent need to identify effective drugs for the treatment of nerve injury caused by unconjugated bilirubin (UCB). Our previous research found that cystatin C (CST3) alleviates UCB-induced neurotoxicity by promoting autophagy in nerve cells, but that autophagy inhibitors did not completely inhibit the effects of CST3. This study investigated whether CST3 could alleviate the neurotoxicity of UCB by promoting the secretion and transport of exosomes containing UCB to the liver for metabolism. It demonstrated that hyperbilirubinemia mice treated with CST3 had a higher number of serum exosomes than those in hyperbilirubinemia mice treated with phosphate-buffered saline. CST3-mediated protection against UCB-induced damage was abolished when autophagy and extracellular vesicle inhibitors were used in combination. The number of exosomes in the CST3 overexpression group was higher than that in the control group. Molecular docking experiments showed that UCB and CST3 had high docking score (-8.2). These results suggest that UCB may be excreted from cells by exosomes, and CST3 may promote this process by binding to UCB and entering the exosomes. We demonstrated that the effect of CST3 relied on liver cells with normal UDP-glucuronyl transferase1A1 (UGT1A1) activity in a coculture system of HT22 and L02 cells. CST3 levels were lower in exosomes secreted by L02 cells than in those secreted by human umbilical vein endothelial cells (HUVECs), whereas CST3 levels were higher in the culture supernatants of L02 cells than in the culture supernatants of HUVECs. This suggests that UCB exosomes in L02 cells may be released and internalized by CST3 and that UCB is then processed by UGT1A1 to conjugate UCB, thus reducing its toxicity. These results suggest that CST3 might alleviate UCB-induced neurotoxicity by promoting the clearance of UCB from cells via exosomes and that these effects are dependent on UGT1A1 activity in liver cells.