Repetitive transcranial magnetic stimulation (rTMS) is a therapeutic strategy that shows promise in ameliorating the clinical sequelae following traumatic brain injury (TBI). These improvements are associated with neuroplastic changes in neurons and their synaptic connections. However, it has been hypothesized that rTMS may also modulate microglia and astrocytes, potentially potentiating their neuroprotective capabilities. This study aims to investigate the effects of high-frequency rTMS on microglia and astrocytes that may contribute to its neuroprotective effects. Feeney\'s weight-dropping method was used to establish rat models of moderate TBI. To evaluate the neuroprotective effect of high frequency rTMS on rats by observing the synaptic ultrastructure and the level of neuron apoptosis. The levels of several important inflammation-related proteins within microglia and astrocytes were assessed through immunofluorescence staining and western blot. Our findings demonstrate that injured neurons can be rescued through the modulation of microglia and astrocytes by rTMS. This modulation plays a key role in preserving the synaptic ultrastructure and inhibiting neuronal apoptosis. Among microglia, we observed that rTMS inhibited the levels of proinflammatory factors (CD16, IL-6 and TNF-α) and promoted the levels of anti-inflammatory factors (CD206, IL-10 and TNF-β). rTMS also reduced the levels of pyroptosis within microglia and pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD, IL-1β and IL-18). Moreover, rTMS downregulated P75NTR expression and up-regulated IL33 expression in astrocytes. These findings suggest that regulation of microglia and astrocytes is the mechanism through which rTMS attenuates neuronal inflammatory damage after moderate TBI.

Desmoid tumours of the brachial plexus are rare locally infiltrative aggressive, monoclonal, fibroblastic proliferations characterized by a variable and often unpredictable clinical course. Only 21 patients have been reported in the literature. We add another one, and report function-preserving surgery in a 34-year-old man with a desmoid tumour of the brachial plexus. The patient presented with paraesthesia and gradually progressive distal muscle weakness in the left upper limb. Electrodiagnostic studies revealed preganglionic changes in segments C8-D1. Contrast-enhanced magnetic resonance imaging showed an enhancing mass with irregular margins in the left paravertebral region encasing the subclavian artery, pre- and post-ganglionic C6-D1 nerve roots and trunks of the brachial plexus. Using an anterior transclavicular approach the tumour was decompressed, which led to a major improvement in paraesthesia and partial motor recovery. He was doing well at 6 months of follow-up. Histopathological examination showed findings consistent with desmoid tumour. A tailored multidisciplinary surgical approach, with the aim to preserve function over radiological clearance, is an acceptable treatment strategy in preserving patient\'s quality of life for such infiltrating desmoid tumours encasing the brachial plexus. Following surgery, observation and close radiological surveillance offer an optimal strategy without jeopardizing the quality of life.

Clinical outcome after traumatic brain injury (TBI) is closely associated conditions of other organs, especially lungs as well as degree of brain injury. Even if there is no direct lung damage, severe brain injury can enhance sympathetic tones on blood vessels and vascular resistance, resulting in neurogenic pulmonary edema. Conversely, lung damage can worsen brain damage by dysregulating immunity. These findings suggest the importance of brain-lung axis interactions in TBI. However, little research has been conducted on the topic. An advanced disease model using stem cell technology may be an alternative for investigating the brain and lungs simultaneously but separately, as they can be potential candidates for improving the clinical outcomes of TBI.In this review, we describe the importance of brain-lung axis interactions in TBI by focusing on the concepts and reproducibility of brain and lung organoids in vitro. We also summarize recent research using pluripotent stem cell-derived brain organoids and their preclinical applications in various brain disease conditions and explore how they mimic the brain-lung axis. Reviewing the current status and discussing the limitations and potential perspectives in organoid research may offer a better understanding of pathophysiological interactions between the brain and lung after TBI.

BACKGROUND: After spinal cord injury (SCI), a large number of survivors suffer from severe motor dysfunction (MD). Although the injury site is in the spinal cord, excitability significantly decreases in the primary motor cortex (M1), especially in the lower extremity (LE) area. Unfortunately, M1 LE area-targeted repetitive transcranial magnetic stimulation (rTMS) has not achieved significant motor improvement in individuals with SCI. A recent study reported that the M1 hand area in individuals with SCl contains a compositional code (the movement-coding component of neural activity) that links matching movements from the upper extremities (UE) and the LE. However, the correlation between bilateral M1 hand area excitability and overall functional recovery is unknown.
OBJECTIVE: To clarify the changes in the excitability of the bilateral M1 hand area after SCI and its correlation with motor recovery, we aim to specify the therapeutic parameters of rTMS for SCI motor rehabilitation.
METHODS: This study is a 12-month prospective cohort study. The neurophysiological and overall functional status of the participants will be assessed. The primary outcomes included single-pulse and paired-pulse TMS. The second outcome included functional near-infrared spectroscopy (fNIRS) measurements. Overall functional status included total motor score, modified Ashworth scale score, ASIA Impairment Scale grade, spinal cord independence measure and modified Barthel index. The data will be recorded for individuals with SCI at disease durations of 1 month, 2 months, 4 months, 6 months and 12 months. The matched healthy controls will be measured during the same period of time after recruitment.
CONCLUSIONS: The present study is the first to analyze the role of bilateral M1 hand area excitability changes in the evaluation and prediction of overall functional recovery (including motor function and activities of daily living) after SCI, which will further expand the traditional theory of the predominant role of M1, optimize the current rTMS treatment, and explore the brain-computer interface design for individuals with SCI.
BACKGROUND: ChiCTR2300068831.

BACKGROUND: Glioblastoma (GBM) is a high-grade and heterogeneous subtype of glioma that presents a substantial challenge to human health, characterized by a poor prognosis and low survival rates. Despite its known involvement in regulating leukemia and melanoma, the function and mechanism of DNAJC1 in GBM remain poorly understood.
METHODS: Utilizing data from the TCGA, CGGA, and GEO databases, we investigated the expression pattern of DNAJC1 and its correlation with clinical characteristics in GBM specimens. Loss-of-function experiments were conducted to explore the impact of DNAJC1 on GBM cell lines, with co-culture experiments assessing macrophage infiltration and functional marker expression.
RESULTS: Our analysis demonstrated frequent overexpression of DNAJC1 in GBM, significantly associated with various clinical characteristics including WHO grade, IDH status, chromosome 1p/19q codeletion, and histological type. Moreover, Kaplan‒Meier and ROC analyses revealed DNAJC1 as a negative prognostic predictor and a promising diagnostic biomarker for GBM patients. Functional studies indicated that silencing DNAJC1 impeded cell proliferation and migration, induced cell cycle arrest, and enhanced apoptosis. Mechanistically, DNAJC1 was implicated in stimulating extracellular matrix reorganization, triggering the epithelial-mesenchymal transition (EMT) process, and initiating immunosuppressive macrophage infiltration.
CONCLUSIONS: Our findings underscore the pivotal role of DNAJC1 in GBM pathogenesis, suggesting its potential as a diagnostic and therapeutic target for this challenging disease.

The transmembrane death receptor Fas transduces apoptotic signals upon binding its ligand, FasL. Although Fas is highly expressed in cancer cells, insufficient cell surface Fas expression desensitizes cancer cells to Fas-induced apoptosis. Here, we show that the increase in Fas microaggregate formation on the plasma membrane in response to the inhibition of endocytosis sensitizes cancer cells to Fas-induced apoptosis. We used a clinically accessible Rho-kinase inhibitor, fasudil, that reduces endocytosis dynamics by increasing plasma membrane tension. In combination with exogenous soluble FasL (sFasL), fasudil promoted cancer cell apoptosis, but this collaborative effect was substantially weaker in nonmalignant cells. The combination of sFasL and fasudil prevented glioblastoma cell growth in embryonic stem cell-derived brain organoids and induced tumor regression in a xenograft mouse model. Our results demonstrate that sFasL has strong potential for apoptosis-directed cancer therapy when Fas microaggregate formation is augmented by mechano-inhibition of endocytosis.

The 2021 World Health Organization classification of CNS tumours was greeted with enthusiasm as well as an initial potential overwhelm. However, with time and experience, our understanding of its key aspects has notably improved. Using our collective expertise gained in neuro-oncology units in hospitals in different countries, we have compiled a practical guide for radiologists that clarifies the classification criteria for diffuse gliomas in adults. Its format is clear and concise to facilitate its incorporation into everyday clinical practice. The document includes a historical overview of the classifications and highlights the most important recent additions. It describes the main types in detail with an emphasis on their appearance on imaging. The authors also address the most debated issues in recent years. It will better prepare radiologists to conduct accurate presurgical diagnoses and collaborate effectively in clinical decision making, thus impacting decisions on treatment, prognosis, and overall patient care.

BACKGROUND: Transfontanellar brain ultrasound is an essential tool for monitoring the size of the ventricles in preterm neonates and has many advantages over other alternative diagnostic techniques, including its accessibility and non-use of ionizing radiation. When considering the normal ventricular size, it is essential to have reference measurements based on age-matched populations. The objective of this article is to present our reference measures, based on a sample of preterm infants that we have studied.
METHODS: A retrospective observational study was conducted. Measurements of the Levene index, frontal horn thickness, and Evans index were obtained in preterm neonates from 25 to 45 weeks, over a period of 5 years, between January 2016 and December 2020. After applying the exclusion criteria, a sample of 199 patients and 350 ultrasound scans were obtained. The independent samples t-test and the Mann-Whitney test were used for the comparison of samples.
RESULTS: The distribution of the right and left Levene indices was normal (Shapiro-Wilk test with p = 0.16 and 0.05, respectively), unlike the thickness distribution of the frontal horns (p < 0.05 on both sides). No significant differences were detected between the sexes (p = 0.08). A linear correlation was found between the biparietal diameter and the Levene index.
CONCLUSIONS: From the results obtained in our study, we present reference tables for ventricular size, with the 3rd, 25th, 50th, 75th, and 97th, being the first ones made in our country.

OBJECTIVE: To determine the effect of mild chronic traumatic brain injury (cTBI) on cerebral blood flow and metabolism.
METHODS: 62 cTBI and 40 healthy controls (HCs) with no prior history of cTBI underwent both pulsed arterial spin labeling functional magnetic resonance imaging (PASL-fMRI) and fluorodeoxyglucose positron emission tomography (FDG-PET) scanning via a Siemens mMR (simultaneous PET/MRI) scanner. 30 participants also took part in a series of neuropsychological clinical measures (NCMs). Images were processed using statistical parametric mapping software relevant to each modality to generate relative cerebral blood flow (rCBF) and glucose metabolic standardized uptake value ratio (gSUVR) grey matter maps. A voxel-wise two-sample T-test and two-tailed gaussian random field correction for multiple comparisons was performed.
RESULTS: cTBI patients showed a significant increase in rCBF and gSUVR in the right thalamus as well as a decrease in bilateral occipital lobes and calcarine sulci. An inverse relationship between rCBF and gSUVR was found in the left frontal lobe, the left precuneus and regions in the right temporal lobe. Within those regions rCBF values correlated with 9 distinct NCMs and gSUVR with 3.
CONCLUSIONS: Simultaneous PASL-fMRI and FDG-PET can identify functional changes in a mild cTBI population. Within this population FDG-PET identified more regions of functional disturbance than ASL fMRI and NCMs are shown to correlate with rCBF and glucose metabolism (gSUVR) in various brain regions. As a result, both imaging modalities contribute to understanding the underlying pathophysiology and clinical course of mild chronic traumatic brain injury.

Over the past two decades, research into the genetic susceptibility behind pheochromocytoma and paraganglioma (PPGL) has surged, ranking them among the most heritable tumors. Massive sequencing combined with careful patient selection has so far identified more than twenty susceptibility genes, leading to an over-detection of variants of unknown significance (VUS) that require precise molecular markers to determine their pathogenic role. Moreover, some PPGL patients remain undiagnosed, possibly due to mutations in regulatory regions of already known genes or mutations in undiscovered genes. Accurate classification of VUS and identification of new genes require well-defined clinical and molecular markers that allow effective genetic diagnosis of most PPGLs.