This study aimed to identify potential therapeutic targets for spinal cord ependymoma (SCE) and key signaling pathways associated with the transforming growth factor b (TGF-b) signaling pathway through bioinformatics analysis, molecular biology validation, and clinical characteristics. Differentially expressed genes (DEGs) in SCE were identified using the limma package in R, and a Venn diagram was created to obtain the intersection of TGF-b signaling pathway-related genes and DEGs. Next, the clusterProfiler package was employed for enrichment analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Also, a protein-protein interaction network of DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins website, and Cytoscape was used to visualize and screen the top 20 key genes. Additionally, quantitative real-time polymerase chain reaction and western blot were used to validate the mRNA and protein expression levels, respectively, of SMAD4, TGFB1, and TGFB receptor 1 (TGFBR1) in clinical samples. A total of 61 differentially expressed TGF-b signaling pathway-related genes were associated with 1) biological processes, such as the transmembrane receptor protein serine/threonine kinase signaling pathway, TGF-b receptor signaling pathway, and pathway-restricted SMAD protein phosphorylation; 2) cell components, such as the plasma membrane signaling receptor complex and collagen-containing extracellular matrix; and 3) molecular function, such as SMAD binding, growth factor binding, and cytokine binding. The protein-protein interaction network consisted of 57 nodes and 339 edges, and three key genes (SMAD4, TGFB1, and TGFBR1) were screened. The TGF-b and Hippo signaling pathways may have potential roles in SCE progression, and SMAD4, TGFB1, and TGFBR1 are potential key genes.

In this study, we investigated whether changes in the expression of the a-synuclein gene occur and participate in post-ischemic brain neurodegeneration of Alzheimer's disease phenotype. The current study assessed the expression of the a-synuclein gene by RT-PCR after 10-minute brain ischemia in rats in CA3 area with survival at 2, 7, and 30 days and 6, 12, 18, and 24 months. Reduced gene expression was observed at 2 days, 6, and 24 months after ischemia. In the remaining observation periods, i.e., 7 and 30 days and 12 and 18 months, its expression was significantly above control values. In post-ischemic brain, where survival times ranged from 2 days to 2 years, we noted biphasic changes in overexpression of the a-synuclein gene in the CA3 area of the hippocampus. The presented data correlate very well with previous studies, which found an increase in protein levels in the brain and strong immunostaining for a-synuclein after ischemia. Finally, the results clearly indicate that changes in the expression of the a-synuclein gene play an important role in acute and secondary brain injury and the development of brain neurodegeneration after ischemia of Alzheimer's disease phenotype. Overall, studies show that a-synuclein is an attractive target for the development of new therapies to minimize ischemic brain damage and neurological dysfunction.

The aim of the study was to investigate the clinical efficacy of Buyang Huanwu Decoction (BHD) in the treatment of patients who had an acute ischemic stroke (AIS).

Alzheimer's disease (AD) is classified as a neurodegenerative disorder without efficacious therapeutic interventions. Accumulating evidence has demonstrated the deposition of b-amyloid peptide (Ab) in the spinal cord in several mouse AD models. Neuregulin 2 (Nrg2), structurally homologous to neuregulin 1 (Nrg1), exerts a regulatory influence over various biological processes within the nervous system. However, the neuroprotective role of Nrg2 in the spinal cord in AD remains unclear.

The nucleotide-binding domain leucine-rich repeat-containing family pyrin domain-containing 3 (NLRP3) inflammasome has been implicated in numerous neurological disorders, including epilepsy, through its role in inflammation and pyroptosis. Dihydromyricetin (DHM) has neuroprotective effects in patients with neurological disorders. However, the impact of DHM on the NLRP3 inflammasome pathway in epilepsy and related cognitive impairment is yet to be fully understood. Herein, we evaluated whether DHM can alleviate pilocarpine-induced neuronal injury and learning and memory disorders in the hippocampal body of rats by regulating the NLRP3 inflammasome.

Anterior nucleus of the thalamus deep brain stimulation (ANT DBS) offers a treatment option for patients with drug-resistant epilepsy (DRE). This treatment modality is particularly useful in cases of multifocal DRE originating from the frontal and temporal lobes. Here we present a 36-year-old epileptic patient who underwent ANT DBS implantation. The incidence of seizures dropped significantly after surgery, though the patient still experienced occasional seizure episodes. After 9 months, the patient sustained a head injury due to bilateral tonic-clonic seizures (BTCS), leading to the development of a chronic subdural hematoma (cSDH) and subsequent displacement of the ANT DBS electrodes. Following the evacuation of the left cSDH, MRI revealed properly positioned DBS electrodes, with no need for additional adjustments. The follow-up period was uncomplicated, showing a 68% reduction in focal impaired awareness seizures (FIAS) and an 80% reduction in BTCS at 24 months. To our knowledge, this is the first report of a patient who developed a cSDH with subsequent displacement of both DBS leads implanted in the ANT.

This study assessed the effect of batatasin-III on cerebral microvascular endothelial cell (EC) injury. Endothelial cell injury was induced in isolated cells by oxygenglucose deprivation/reperfusion (OGD/R) conditions. During 4 h of OGD insult, cells were treated with batatasin-III at different concentrations, and an MTT assay was performed to estimate cellular viability. Nitric oxide, mitochondrial membrane potential (MMP), and release of lactate dehydrogenase (LDH) were determined in ECs exposed to OGD/R. Cerebral ischemia was performed to induce brain injury to assesses the effect of batatasin-III. There was improvement in the viability of cell and reduction of release of LDH in batatasin-III-treated, OGD/R-induced EC injury. Treatment with batatasin-III ameliorates the altered integrity of mitochondrial membrane and expression of apoptotic proteins in OGD/R injured ECs. Apoptosis of neuronal cells and infarct size were reduced in batatasin-III-treated middle cerebral artery occlusion (MCAO) rats, and pathological changes were reversed. Based on study data, we concluded that cerebral injury was attenuated by batatasin-III treatment by reducing oxidative stress and cellular apoptosis.

Glioma is a highly aggressive malignant tumor with high mortality, which is prone to metastasis and recurrence. This study investigated the biological function and related mechanism of action of the long non-coding RNA SNHG22 (lncRNA SNHG22; SNHG22) on glioma cells and its prognostic value.

Neuropathic pain (NP), a severe nervous system ailment, is affected by microRNA's role in microglial polarization. MiR-182 helps ease this pain, particularly from spared nerve injury, but its regulatory mechanism remains poorly understood. In this study, we first observed that lipopolysaccharide (LPS) triggered M1 polarization, leading to an increase in CD86, iNOS, p-PI3K and p-AKT and a decrease in CD206, Arg-1 and miR-182 expression levels. Following that, BV-2 cells underwent transfection with miR-182 mimics or inhibitors to examine the influence of miR-182 on the polarization states and PI3K/AKT signaling. The inflammatory cytokines were determined using ELISA assay. Overexpression of miR-182 decreased pro-inflammatory cytokines, upregulated the expression of CD206 and Arg-1, while downregulating CD86, p-PI3K and p-AKT in LPS-induced BV-2 cells, which were abolished by the PI3K/AKT activator 740Y-P. The in vivo data demonstrated that the pain level in an NP rat model, triggered by chronic constriction injury (CCI) surgery, was markedly decreased by the intrathecal administration of lentiviral (LV)-mediated miR-182, as measured by paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL). Additionally, miR-182 reduced the levels of pro-inflammatory cytokines (TNF-a, IL-1b, and IL-6) and the number of M1-polarized microglia in the NP rat. However, the neuroprotective benefits of miR-182 were negated when 740Y-P was administered. In conclusion, these data suggest that miR-182 can alleviate NP and neuroinflammation by promoting the shift from M1 to M2 phenotype polarization via suppressing the PI3K/AKT signaling pathway.

Neuroinflammation plays a significant role in the pathological progression of traumatic brain injury (TBI) and represents a promising therapeutic target. The present study focused on exploring the mechanism of long noncoding RNA rhabdomyosarcoma 2 associated transcripts (RMST) in TBI-induced neuroinflammation.

Intervertebral discs are generally known as the body's largest avascular structures. In the human body, there is not yet a collective resource characterizing intervertebral vascularization. When an intervertebral disc herniation occurs, new blood vessels proliferate in the capsule of the herniated tissue. In this study, we aimed to investigate intervertebral disc degeneration, neovascularization, and histopathological findings in patients who underwent surgical treatment.

The aim was to develop an artificial intelligence (AI)-based identification system using a deep learning method based on convolutional neural networks to analyze pathological kidney images. We constructed a rat chronic kidney disease (CKD) model and used different drug interventions to study the pathological changes in the kidneys, which is convenient for machine in-depth learning and the construction of a recognition system. The reliability and credibility of the system were assessed by a blind comparative analysis. Microscopic image recognition and classification: Five pathological groups were subjected to three types of staining to obtain 15 image groups. Fifty jpg images were captured from each image group, so that 750 images were captured for training. The average hard disk space per image was 354 kb. Because the input image was 1000 pixels wide with a large resolution, multiple sampling was required to extract feature information. This implies that the level of span multiplication greatly affected the performance of the network during sampling. First, the ResPool samples with the same number of channels, followed by the output of a convolution layer, were assembled as the incremental channel. Thus, the feature extraction network of this work successfully implemented the idea of residual learning and did not introduce errors in the deep network to achieve the expected effect. The neural network model of this study designed a ResPool sampling structure based on the idea of residual learning, completed glomerular instance segmentation and damage analysis, and improved the accuracy of image recognition tasks.

Spinal cord stimulation (SCS) is considered an efficient and safe method of treating intractable chronic pain from various origins such as persistent spinal pain syndrome (PSPS) or complex regional pain syndrome (CRPS). The complications related to SCS therapy are usually classified as mechanical or biological. Myelopathy related to dense scar tissue formation around epidural paddle electrodes implanted for SCS therapy is extremely rarely reported. We have studied all reported cases of surgical management of this complication and we sought to find predisposing factors responsible for development of this rare but dangerous complication.

Paclitaxel (PTX) is a potent chemotherapy drug commonly used to treat various solid tumours, including breast and ovarian cancers. However, its effectiveness in treating IDH-wildtype glioblastoma has been limited due to challenges crossing the blood-brain barrier (BBB). Glioblastoma remains one of the most difficult cancers to treat, with a median survival of 15 months from diagnosis. Recent advancements in nanotechnology have led to innovative PTX delivery systems that enhance its bioavailability and enable targeted brain therapy. These include nanoparticles composed of biocompatible materials that enhance drug solubility and targeting while addressing BBB permeability. Examples include albumin-bound PTX (Abraxane), self-assembled nanoparticles from natural bioactive molecules, poly(lactic-co-glycolic acid) (PLGA)-based nanoparticles, and hydrophilic nano-prodrugs, each showing promise in enhancing the therapeutic impact of PTX. These systems utilize biocompatible nanoparticles that enhance drug solubility, targeting, and BBB permeability. Numerous ongoing clinical trials and preclinical studies are exploring the efficacy of these nanocarrier systems in overcoming drug resistance and improving patient outcomes. The latest advancements in PTX-based nanotherapeutics for glioblastoma focus on overcoming the BBB, developing nanoparticle delivery systems, and evaluating the clinical significance of these developments.

Glioma is the most prevalent primary brain tumor, causing significant mortality and morbidity. lncRNAs have great potential in tumor-targeted therapy, including for glioma via sponging microRNAs. Previous studies have shown that LINC00900 and miR-186-5p likely play a significant role in glioma progression. However, the relationship between them has not been elucidated. The purpose of this study was to explore the role of LINC00900 in the prognosis of gliomas and its underlying molecular mechanisms.

Stathmin, recognised as the protein associated with the disassembly of microtubules, plays a vital role in the modulation of human fear as well as anxiety responses. However, it is unclear whether stathmin regulates the specific mechanism of disruption of fear-associated memory resulting from posttraumatic stress disorder (PTSD). This study aims to observe the impact of stathmin on deficit in fear-based memory during PTSD and investigate the underlying mechanisms involved, in order to establish an empirical foundation for elucidating the molecular mechanisms underlying the pathogenesis of PTSD.

Anatomical studies of the brain and successive analyses of this organ were performed in ancient times. Indeed, notes found in the Edwin Smith Papyrus mention that the Egyptians identified the meninges and gyri millennia ago. Their successors examined the content of the skull, examined it and illustrated it in greater detail. Alexandrians (Herophilus and Erasistratus) described the cerebral ventricles and blood circulation and supply to the brain. More accurate depictions emerged during the Renaissance with Leonardo da Vinci (1452-1519), Charles Estienne (1504-1564) and Andreas Vesalius (1514-1564), followed by Thomas Bartholin (1616-1680), Franciscus Sylvius (1614-1672) and later scholars. The present study focuses on neuroanatomy and is devoted to the study of nervous system structures by the eminent pathologist Rudolph Virchow. When reorganizing the procedure and reporting of the post-mortem examination, including a meticulous autopsy of the brain, neuropathology was a discipline yet to be developed. He pioneered a new approach to the autopsy and analysis of its results, aiming to benefit not only the patients but also clinicians and pathologists.

This study aimed to investigate the effect of sequential treatment with butylphthalide on neurological and cognitive functions and collateral circulation in patients with acute cerebral infarction (ACI).

Burkitt lymphoma (BL) is a specific, rare (1-2% of all cases of lymphoma) and aggressive type of B-cell non-Hodgkin lymphoma. If BL recurs during treatment, it usually becomes drug-resistant to subsequent treatment regimens and the prognosis is very poor. We present an extremely rare case of recurrent BL infiltrating the central nervous system (CNS) in a 27-year-old HIV-infected patient who had completed GMALL-B-ALL/NHL2002 protocol treatment 4 months earlier. Radiological and neuropathological examinations of cerebral recurrence of BL, followed by specialized oncological treatment, were discussed. Currently, with antiretroviral therapy and intensive immunochemotherapy for the immunodeficiency-associated BL variant, disease recurrence in the CNS is extremely rare. The magnetic resonance imaging (MRI) findings and laboratory tests are unspecific, as shown in the present case. The final diagnosis can be established properly by performing image-guided stereotactic biopsy or flow cytometry with cytology examination of cerebrospinal fluid. After confirmation of isolated cerebral recurrence of BL, the patient received intensive treatment according to the R-MIV protocol and achieved a second complete remission.

Glioma, as the deadliest malignant tumor, is one of the most difficult problems in medicine. This study aims to further elucidate the molecular mechanism of glioma development and explore possible miRNAs as targets for glioma prognosis and molecular therapy.

Vitamin B 12 deficiency can cause subacute combined degeneration of the spinal cord and cerebellar lesions. The patient, a 78-year-old woman, presented with an unstable gait, speech impairment and memory decline for one month. The neurological examination revealed ataxia, cerebellar speech disorder and mild cognitive impairment. Head and cervical vertebra magnetic resonance imaging (MRI) showed spinal cord and cerebellar lesions. The patient's symptoms improved after supplementation with vitamin B 12 . We found few reports of such cases in the literature. In this case report, we describe the entire diagnostic and treatment process of vitamin B 12 deficiency involving cerebellar lesions and briefly discuss the related pathogenesis, research progress and treatment.