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Background: Extracellular peroxiredoxin 1 (Prdx1) has been implicated to play a pivotal role in regulating inflammation; however, its function in tissue hypoxia-induced inflammation, such as severe cardiogenic shock patients, has not yet been defined. Thus, the objective of this study was to test the hypothesis that Prdx1 possesses prognostic value and instigates systemic inflammatory response syndrome in cardiogenic shock patients undergoing extracorporeal membrane oxygenation (ECMO) support.Methods: We documented the early time course evolution of circulatory Prdx1, hypoxic marker carbonic anhydrase IX, inflammatory cytokines including IL-6, IL-8, IL-10, MCP-1, TNF-α, IL-1β, and danger signaling receptors (TLR4 and CD14) in a cohort of cardiogenic shock patients within 1 day after ECMO support. In vitro investigations employing cultured murine macrophage cell lines and human monocytes were applied to clarify the relationship between Prdx1 and inflammatory response.Results: Prdx1 not only peaked earlier than all the other cytokines we studied during the initial course, but also predicted a worse outcome in patients who had higher initial Prdx1 plasma levels. The Prdx1 levels in patients positively correlated with hypoxic markers carbonic anhydrase IX and lactate, and inflammatory cytokines. In vitro study demonstrated that hypoxia/reoxygenation induced Prdx1 release from human monocytes and enhanced the responsiveness of the monocytes in Prdx1-induced cytokine secretions. Furthermore, functional inhibition by Prdx1 antibody implicated a crucial role of Prdx1 in hypoxia/reoxygenation-induced IL-6 secretion.Conclusions: Prdx1 release during the early phase of ECMO support in cardiogenic shock patients is associated with the development of systemic inflammatory response syndrome and poor clinical outcomes. Thus, circulating Prdx1 provides not only prognostic information but may be a promising target against ischemia/reperfusion injury. [ABSTRACT FROM AUTHOR]

Purpose: Accurate segmentation of the cisternal segment of the trigeminal nerve plays a critical role in identifying and treating different trigeminal nerve-related disorders, including trigeminal neuralgia (TN). However, the current manual segmentation process is prone to interobserver variability and consumes a significant amount of time. To overcome this challenge, we propose a deep learning-based approach, U-Net, that automatically segments the cisternal segment of the trigeminal nerve. Methods: To evaluate the efficacy of our proposed approach, the U-Net model was trained and validated on healthy control images and tested in on a separate dataset of TN patients. The methods such as Dice, Jaccard, positive predictive value (PPV), sensitivity (SEN), center-of-mass distance (CMD), and Hausdorff distance were used to assess segmentation performance. Results: Our approach achieved high accuracy in segmenting the cisternal segment of the trigeminal nerve, demonstrating robust performance and comparable results to those obtained by participating radiologists. Conclusion: The proposed deep learning-based approach, U-Net, shows promise in improving the accuracy and efficiency of segmenting the cisternal segment of the trigeminal nerve. To the best of our knowledge, this is the first fully automated segmentation method for the trigeminal nerve in anatomic MRI, and it has the potential to aid in the diagnosis and treatment of various trigeminal nerve-related disorders, such as TN., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2025 Li-Ming Hsu et al. International Journal of Biomedical Imaging published by John Wiley & Sons Ltd.)

The integration of functional magnetic resonance imaging (fMRI) with advanced neuroscience technologies in experimental small animal models offers a unique path to interrogate the causal relationships between regional brain activity and brain-wide network measures-a goal challenging to accomplish in human subjects. This review traces the historical development of the neuromodulation techniques commonly used in rodents, such as electrical deep brain stimulation, optogenetics, and chemogenetics, and focuses on their application with fMRI. We discuss their advantageousness roles in uncovering the signaling architecture within the brain and the methodological considerations necessary when conducting these experiments. By presenting several rodent-based case studies, we aim to demonstrate the potential of the multimodal neuromodulation approach in shedding light on neurovascular coupling, the neural basis of brain network functions, and their connections to behaviors. Key findings highlight the cell-type and circuit-specific modulation of brain-wide activity patterns and their behavioral correlates. We also discuss several future directions and feature the use of mediation and moderation analytical models beyond the intuitive evoked response mapping, to better leverage the rich information available in fMRI data with neuromodulation. Using fMRI alongside neuromodulation techniques provide insights into the mesoscopic (relating to the intermediate scale between single neurons and large-scale brain networks) and macroscopic fMRI measures that correlate with specific neuronal events. This integration bridges the gap between different scales of neuroscience research, facilitating the exploration and testing of novel therapeutic strategies aimed at altering network-mediated behaviors. In conclusion, the combination of fMRI with neuromodulation techniques provides crucial insights into mesoscopic and macroscopic brain dynamics, advancing our understanding of brain function in health and disease. EVIDENCE LEVEL: 1 TECHNICAL EFFICACY: Stage 1., (© 2024 International Society for Magnetic Resonance in Medicine.)

While deep brain stimulation (DBS) is widely employed for managing motor symptoms in Parkinson's disease (PD), its exact circuit mechanisms remain controversial. To identify the neural targets affected by therapeutic DBS in PD, we analyzed DBS-evoked whole brain activity in female hemi-parkinsonian rats using function magnetic resonance imaging (fMRI). We delivered subthalamic nucleus (STN) DBS at various stimulation pulse repetition rates using optogenetics, allowing unbiased examinations of cell-type specific STN feed-forward neural activity. Unilateral STN optogenetic stimulation elicited pulse repetition rate-dependent alterations of blood-oxygenation-level-dependent (BOLD) signals in SNr (substantia nigra pars reticulata), GP (globus pallidus), and CPu (caudate putamen). Notably, these manipulations effectively ameliorated pathological circling behavior in animals expressing the kinetically faster Chronos opsin, but not in animals expressing ChR2. Furthermore, mediation analysis revealed that the pulse repetition rate-dependent behavioral rescue was significantly mediated by optogenetically induced activity changes in GP and CPu, but not in SNr. This suggests that the activation of GP and CPu are critically involved in the therapeutic mechanisms of STN DBS.

Objectives The pathophysiology of perihaematomal oedema (PO) surrounding a primary intracerebral haemorrhage (ICH) is complicated and incompletely understood. We prospectively investigated the components of PO with voxel-based analysis of the apparent diffusion coefficient (ADC) value and assessed its predictive value for functional outcome. Design Forty-six patients with ICH who were enrolled for clinical evaluation underwent MRI scans within 24 h after ICH. Based on the ADC value of the ipsilateral voxels divided by the mean ADC value of the contralateral mirror region of interest, the voxels with oedema were classified into three categories: cytotoxic, vasogenic and undetermined. The percentages of cytotoxic and vasogenic oedema were then calculated and correlated with clinical outcome according to the modified Rankin Scale (mRS) at 6 months after ICH. The intraobserver and interobserver reliability of this method were examined using intraclass correlation coefficients. Results The intraclass correlation coefficients showed that analysis using the voxel-based method is highly reliable. Among the clinical variables tested, age and serum creatinine levels were positively correlated with percentage of cytotoxic oedema. Age, history of coronary artery disease, National Institutes of Health Stroke Scale score and percentage of cytotoxic oedema were all associated with mRS at 6 months after ICH. Conclusions The pathophysiological processes within PO are complicated. Voxel-based analysis of ADC values may help to identify the components of PO and may be beneficial for decision making and predicting outcome.

Background: T-cells play a critical role in the immunological surveillance network against cancer formation. The activation of T-cells is initiated by binding of T-cell receptors (TCR) with antigen epitopes. Polymorphisms of TCR-gamma microsatellite (short tandem repeats, STR) marker has been associated with early-onset colorectal cancer. The aim of this study was to test the relationship of TCR-gamma STR genetic polymorphisms and hepatocellular carcinoma (HCC)., Materials and Methods: A total of 225 chronic hepatitis B- or C-related HCC and liver cirrhosis patients were enrolled in this study. The other 225 sex-matched cirrhotic patients without HCC were recruited as controls. Their TCR-ygammaSTR polymorphisms at loci D7S1818 and D7S2206 were measured by polymerase chain reaction. Dietary habits and other possible risk factors for HCC were also assessed by a structured questionnaire., Results: Compared to controls, the HCC patients were older in age (64.9 +/- 10.3 vs. 53.5 +/- 10.1 years, p < 0.001) and had a higher percentage of family history of HCC (13.3% vs. 7.6%, p = 0.045) and habitual alcohol use (23.1% vs. 15.6%, p= 0.042). A total of 20 genotypes of TCR-gamma D7S1818 STR were detected. Of these, the genotype 16 (13/14 of repeat number of GA A) had a higher percentage in the HCC groups than in the controls (13.8% vs. 6.7%, p = 0.013). After adjustment for age, family history of HCC and habitual alcohol use, the TCR-gamma genotype 16 remained a significant risk factor for HCC (OR: 2.18, 95% CI: 1.02-4.65, p= 0.045)., Conclusion: The TCR-gamma STR polymorphism may be associated with HCC susceptibility.