Intracerebral hemorrhage (ICH) has a high rate of death and disability. LncRNA-TUG1 is essential for the pathological changes secondary to ICH. The purpose of this work was to investigate the possible mechanism by which TUG1 inhibits neural repair subsequent to ICH through adjusting miR-381-3p/brain-derived neurotrophic factor (BDNF). After the ICH model was created, miR-381-3p agomir and pcDNA-TUG1 were injected. The neural function of rats was estimated using the modified neurological severity score. To quantify the expression of genes and proteins, western blotting, immunohistochemistry, and qRT-PCR were used. To confirm the interaction between TUG1 and miR-381-3p and between miR-381-3p and BDNF mRNA, a luciferase reporter assay was employed. In rats treated with miR-381-3p agomir, a trend of improvement in neurological dysfunction was observed, while the pcDNA-TUG1-treated ones showed deterioration. Furthermore, miR-381-3p agomir increased, while pcDNA-TUG1 reduced the expression level of BDNF in ICH rats. TUG1 and BDNF mRNA were validated to attach directly to miR-381-3p. Overexpressing TUG1 inhibited the level of BDNF by sponging miR-381-3p and antagonized its protective effect on neural repair in ICH rats. Our study suggests that TUG1 can sponge miR-381-3p to downregulate BDNF expression and inhibit neural repair following ICH, demonstrating a potential signaling pathway that is conducive to a better understanding of the pathological mechanisms of ICH.
INTRODUCTION:The study aimed to determine whether apocynin (APO) can protect neurons in rats with traumatic brain injury (TBI) by activating the PI3K/Akt/Nrf2 pathway, acting as an antioxidant, and suppressing autophagy. MATERIAL AND METHODS:Ninety male Sprague-Dawley rats (220-260 g) were randomly assigned to three groups: a control group with a sham operation, a group with TBI, and a group that received APO following TBI. Saline and APO were intraperitoneally administered for three consecutive days based on the aforementioned groups. Ten rats from each group underwent behavioral assessment, and neuronal morphology was evaluated using HE staining. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) were measured using the xanthine oxidase method, barbiturate sulfate method, and dithiobenzoic acid condensation method, respectively. Rat hippocampal tissue was extracted, and Western blotting was performed to assess the expression of autophagy-related proteins as well as signaling pathway-related proteins. RESULTS:Compared to the TBI group, those treated with APO showed reduced cognitive deficits and neural damage resulting from TBI. The degree of neuronal damage in the treatment group was statistically significantly reduced. Treatment with APO in rats with TBI significantly elevated the hippocampal levels of GSH and SOD and significantly reduced the production of MDA and reactive oxygen species (ROS). Additionally, APO alleviated hippocampal neuronal autophagy by reducing LC3II and Beclin-1 expression levels. Regarding of the signaling pathway, APO elevated the expression of p-PI3K, p-Akt, Nrf2, and HO-1 in the hippocampus of TBI rats. CONCLUSIONS:In conclusion, APO represents a potential treatment for TBI due to its antioxidative and autophagy-reducing properties via the PI3K/Akt/Nrf2 pathway, thereby preventing hippocampal injury after brain trauma.
INTRODUCTION:The study aimed to observe the effects of different doses of dexmedetomidine (Dex) on pain threshold, memory, and neurological ability in rats with sleep deprivation. MATERIAL AND METHODS:Forty-eight SD rats were divided into a control group (n = 12), model group (n = 12), sleep deprivation + Dex low dose injection group (DEX low dose group), and sleep deprivation + Dex high dose injection group (high dose DEX group). The rats in the model group, DEX low dose group, and DEX high dose group were subjected to sleep deprivation for 3 hours, and the DEX low dose group and DEX high dose group were injected with Dex (6 µg/kg, 60 µg/kg, 10 min, respectively). The neurological function scores of rats in each group were compared, and the contents of PSD95 and PI3K/AKT protein were detected. RESULTS:The food intake of rats in groups B, C, and D was lower than in group A (p < 0.05), and the food intake in group D was higher than in groups B and C (p < 0.05). The escape latency of the Morris water maze test in all groups decreased gradually from day 1 to day 3 (p < 0.05). On days 2 and 3, the escape latency of group B was longer than that of group A (p < 0.05), while the escape latency of groups C and D was shorter than that of group B (p < 0.05). The target quadrant residence time of group B was shorter than that of group A (p < 0.05), while the target quadrant residence time of group C and D was longer than that of group B (p < 0.05). The neurological function score of the group B was increased (p < 0.05), while the neurological function score of groups C and D was lower than that of group B in a dose-dependent manner (p < 0.05). The PSD95 protein content and PI3K/AKT phosphorylation level in group B were lower (p < 0.05), while these values in groups C and D were higher than in group B in a dose-dependent manner (p < 0.05). CONCLUSIONS:Different doses of Dex can effectively reduce the pain threshold, enhance memory ability, and improve neurological function in sleep-deprived rats. The mechanism may be mediated by regulation of PSD95 expression and phosphorylation of the PI3K/AKT pathway.
INTRODUCTION:Spinal cord injury (SCI) is one of the major causes of paralysis and physical inability, and its management remains a challenge. The present study evaluated the effect of MK-2206 dihydrochloride in rats with SCI. MATERIAL AND METHODS:An impactor device was used to induce SCI, which was treated with MK-2206 12 mg/kg, s.c., daily for 10 days. The effect of MK-2206 on SCI was determined by estimating the locomotor function, inflammatory mediators, and oxidative stress parameters in all groups of rats. Western blot assay was performed to estimate the expression of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt) protein in the spinal tissue of SCI rats. Moreover, the effect of MK-2206 on the apoptosis of spinal tissue of SCI rats was assessed. RESULTS:Study data suggest that treatment with MK-2206 reverses the alteration in the neuronal function in SCI rats. Cytokines and oxidative stress were observed to be ameliorated in the MK-2206-treated group compared to the SCI group. Moreover, treatment with MK-2206 attenuated PI3K and Akt protein expression in the spinal tissue of SCI rats. Treatment with MK-2206 significantly reduced the apoptosis of spinal tissue in SCI rats. CONCLUSIONS:The data suggest that treatment with MK-2206 prevents injury to the neuronal tissue in SCI rats by modulating the PI3k/Akt pathway.
Mucin 1 (MUC1), a transmembrane glycoprotein, is aberrantly expressed in multiple cancers and implicated in tumor progression. This study investigated MUC1 expression in glioma tissues and cell lines, its correlation with tumor malignancy, and the effect of differential expression on patient prognosis. Bioinformatics analysis using the GEPIA database evaluated MUC1 expression in pan-cancer and its effect on the prognosis of glioma patients. Clinical samples from 9 glioma patients with WHO grades II-IV and 2 normal brain tissues with traumatic brain injury controls were analyzed via immunohistochemistry. RT-qPCR and Western blot were used to analyze MUC1 expression in glioblastoma (GBM) cell lines (U251, U87, A172, LN229) and normal human astrocytes (NHA). MUC1 was significantly overexpressed in glioma tissues compared to normal brain tissue (p < 0.05), with higher expression correlating with advanced tumor grade. High MUC1 levels predicted poor patient survival (p < 0.01). GBM cell lines exhibited elevated MUC1 mRNA and protein levels vs. NHA (p < 0.001). MUC1 correlation with glioma malignancy and patient outcomes represents a prognostic biomarker and potential therapeutic target, underscoring its relevance in neuropathology practice.
INTRODUCTION:Interleukin 12 (IL-12) is a driver of type 1 immunity. Interleukin 12 reduces inflammation in an autoimmune condition in the spinal cord. The aim of this study was to investigate the therapeutic effect of IL-12 in the experimental autoimmune encephalomyelitis model. MATERIAL AND METHODS:Interleukin 12 expression was mapped in neurons, oligodendrocytes, natural killer cells, and T lymphocyte cells in the spinal cord of experimental autoimmune encephalomyelitis mice. RESULTS:Interleukin 12 ablation in neurons, oligodendrocytes, natural killer, and T lymphocyte cells in mice and their susceptibility to experimental autoimmune encephalomyelitis showed that the neuroprotective role of IL-12 is mediated by neuroectoderm-derived cells - neurons. CONCLUSIONS:Single-nucleus RNA sequencing revealed an IL-12 receptor-induced neuroprotective effect that prevents neurodegeneration, sustains trophic factor release in neuroinflammation, and maintains spinal cord integrity.
INTRODUCTION:The purpose of this study was to explore the effect of ubiquitin-specific protease (USP) 22 overexpression on spinal cord injury (SCI) in rats and its potential mechanism, to assess its role in the recovery of neurological function. MATERIAL AND METHODS:A rat model of SCI was established. The rats were divided into four groups: the Sham group, the SCI group, the SCI + USP22Ad-USP22 group, and the SCI + vector group. The Basso Mouse Scale for locomotion was used for motor function scores. Real-time quantitative polymerase chain reaction and western blot were applied to detect the expression levels of USP22, inducible nitric oxide synthase, cluster of differentiation (CD) 86, arginase 1, and CD206. Additionally, the expression of inflammatory markers and microglial activation were assessed using immunofluorescence and enzyme-linked immunosorbent assay. Furthermore, western blot was employed to measure the expression levels of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome pathway-related proteins. RESULTS:USP22 overexpression significantly improved the motor function of SCI rats, reduced the levels of microglial activation, and inhibited the activation of the nuclear factor-kB pathway. Additionally, USP22 overexpression not only reduced the expression levels of pro-inflammatory mediators (inducible nitric oxide synthase, CD86, tumor necrosis factor a, interleukin (IL)-1b, and IL-6) but also increased the expression levels of anti-inflammatory markers (arginase 1 and CD206). Furthermore, USP22 overexpression inhibited the expression of NLRP3 inflammasome-related proteins, alleviated neuro- inflammatory responses and promoted neurological function recovery. CONCLUSIONS:USP22 overexpression can improve neuroinflammation and motor function in SCI model rats, which may be related to the inhibition of NLRP3 inflammasome pathway activation.
INTRODUCTION:Ischemic stroke (IS) is a disease caused by blood circulation disorders in the brain, ischemia, and hypoxia, resulting in ischemic necrosis or softening of localized brain tissue. Lipoic acid (ALA) is effective in resisting oxidative stress and alleviating the inflammatory response. This study evaluated the mechanism and effects of ALA on neurovascular unit remodeling after cerebral infarction. MATERIAL AND METHODS:In male C57BL/6 mice, cerebral infarction was induced using distal middle cerebral artery occlusion (dMCAO). In an in vitro model, cells were allocated to control, model, low dose, medium dose, and high dose groups. Infarct volume analysis, Evans blue extravasation, and enzyme-linked immunosorbent assay (ELISA) kits were used to evaluate the effects of ALA on IS. Cell Counting Kit-8 (CCK-8), 5-ethynyl 2'-deoxyuridine staining (EDU) staining, Western blot and immunohistochemistry were used to evaluate the mechanism of ALA in IS. RESULTS:This study found that the cerebral infarct volume of the ALA treatment group was similar to dMCAO mice. Treatment with ALA reduced the area of Evans blue compared with dMCAO mice at 7 days, and promoted astrocyte and pericyte proliferation in the peri-infarct area at 28 days. Meanwhile, treatment with ALA also increased vascular endothelial growth factor (VEGF), angiopoietin (Ang)-1 and claudin-5 protein expression levels, suppressed Ang-2 and matrix metalloproteinase-9 (MMP-9) protein expression levels, reduced neuronal apoptosis inhibitory protein (NAIP), leucine-rich repeat (LRR), and PYD domain-containing protein 3 (NLRP3) expression levels, and induced phosphorylated-adenosine monophosphate-activated protein kinase (p-AMPK) protein expression levels in cerebral infarction mice (all p < 0.05). On the other hand, ALA restored cell growth and the number of EDU cells, promoted cell migration, elevated superoxide dismutase (SOD) activity, reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and inhibited inflammation levels in the in vitro model (all p < 0.05). Treatment with ALA also suppressed NLRP3 and Ang-2 protein expression, reduced MMP-9 protein expression, and induced VEGF, Ang-1, claudin-5, and p-AMPK protein expression levels in the in vitro model (all p < 0.05). CONCLUSIONS:ALA improved neurovascular unit remodeling after cerebral infarction through anti-inflammation effects via the AMPK/NLRP3 signaling pathway.
INTRODUCTION:Triggering receptor expressed on myeloid cells 2 (TREM2), part of the immunoglobulin superfamily, is implicated in various malignancies. However, its role in glioma formation remains unclear. Our study uncovered a potential mechanism involving TREM2. MATERIAL AND METHODS:The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) datasets were utilized to assess the expression levels of TREM2 and DNAX-activating protein of 12 kDa (DAP12), explore their relationship, and evaluate their impact on patient prognosis. Western blotting was used to measure TREM2 expression in different glioma grades. Co-immunoprecipitation (Co-IP) was used to examine TREM2 and DAP12 interaction. Cell proliferation, invasion, and apoptosis were assessed via the cell proliferation test, cell invasion assay, and flow cytometry. An intracranial xenograft model was created by injecting tumor cells into nude mice. Mice injected with si-DAP12-transfected or non-transfected glioma cells were treated with 740Y-P, followed by survival analysis and immunohistochemistry. RESULTS:TREM2 and DAP12 were overexpressed in gliomas, with high levels associated with lower overall survival (p < 0.05 and p < 0.01). There was a strong positive correlation between TREM2 and DAP12 expression (p < 0.0001). TREM2 positively regulated DAP12, forming a complex that influenced glioma cell proliferation, apoptosis, and invasion (p < 0.05, p < 0.01, and p < 0.001). DAP12 knockdown significantly inhibited proliferation and invasion while promoting apoptosis of glioma cells, linked to the PI3K/AKT signaling pathway (p < 0.05 and p < 0.01). 740Y-P treatment counteracted the effects of DAP12 knockdown (p < 0.05, p < 0.01, p < 0.001, and p < 0.0001). In vivo, DAP12 knockdown inhibited glioma tumorigenicity (p < 0.001). CONCLUSIONS:TREM2 positively regulates DAP12 and forms a complex that impacts glioma development via the PI3K/AKT pathway. Targeting the TREM2/DAP12 complex presents a potential therapeutic approach for gliomas.
Brainstem gliomas in adults are a rare and heterogeneous group of brain tumours, which account for less than 2% of all adult gliomas and usually involve the pons (60-63%). The medulla oblongata and the midbrain are the least common locations of brainstem gliomas (25% and 12-15%, respectively). Survival and overall prognosis depend on the underlying pathology and pathological tumour grade. The authors present a female patient with medulla oblongata rapidly growing brainstem glioma (documented in a series of brain MRI examinations), which resulted in quick progression of neurological symptoms with cardiopulmonary insufficiency and death. The rapid growth of this lethal lesion and clinical deterioration made it impossible to perform stereotactic biopsy and implement optimal oncological treatment. Neuropathological brain and spinal cord postmortem examination revealed glioblastoma IDH-wildtype CNS WHO G4.
INTRODUCTION:Gliomas are among the most aggressive brain tumors, with limited treatment options and poor patient outcomes. Recent studies suggest that miRNAs play a crucial role in tumor development and progression. This study aimed to leverage transcriptomics data to identify critical miRNAs involved in glioma, which may serve as potential therapeutic targets. MATERIAL AND METHODS:GO and KEGG analyses were used to investigate target genes. Protein-protein interaction analysis identified CCND1 as a key gene, and miR-129-5p was selected for its interaction with CCND1. The expression levels of miR-129-5p and CCND1 in glioma samples and cells were measured. Dual-luciferase assays confirmed their targeting relationship. Functional assays (CCK-8, wound healing, Transwell) were conducted in U87 cells, and the impact on the PI3K/AKT pathway was analyzed by western blot. In vivo studies were performed in nude mice. RESULTS:miR-129-5p expression was significantly reduced in glioma tissues and U87 cells compared to normal tissues or cells, while CCND1 was markedly increased. Dual-luciferase reporter assays confirmed that miR-129-5p directly targets CCND1. Overexpression of miR-129-5p reduced U87 cell proliferation, migration, and invasion, and inhibited the PI3K/AKT pathway. In vivo, miR-129-5p suppressed tumor growth and improved mouse survival. CONCLUSIONS:miR-129-5p may exert a tumor-suppressive effect in glioma by targeting CCND1 and suppressing the PI3K/AKT signaling pathway.
INTRODUCTION:A molecular sequencing and phenotyping study was conducted on chemokines CCL2, CCL5, and CXCL10 to assess the relation to multiple sclerosis (MS). MATERIAL AND METHODS:The molecular detection study included extractions of DNA from the blood of cases and a control group, as well as amplification and confirmation of all extracted DNA. The 490-bp primer-size PCR product corresponded to CCL2, the 481-bp primer-size PCR product corresponded to CCL5, and the 310-bp primer-size PCR product corresponded to CXCL10. RESULTS:DNA sequencing of CCL2, CCL5, and CXCL10 showed that there was convergence between the obtained results and data from the GenBank database (NCBI) with 99% identity (439/445) in the forward CCL2 sequence, which had a single transition mutation, GGT to GGG. In addition, the reverse CCL2 showed 99% identity (426/427) when compared with the GenBank database (NCBI), which found a single deletion mutation, TGA to GGG. There was convergence between the studied CCL5 isolated and that of the GenBank database (NCBI) with 99% identity (443/447) in the forward CCL5. Four mutations were recorded: three transversions - TTT to TTA, AAA to AAT, and GCC to GCA - and one deletion, TGA to TGG. On the other hand, the reverse CCL2 showed 99% identity (436/439) when compared with the GenBank database (NCBI), with three mutations: two deletions - TGA to TG-, and CCA to CC- - and one transversion, ATT to ATA. Also, there was convergence between the studied CXCL10 isolated and that of the GenBank database (NCBI), with 98% identity 64/65 in the forward CXCL10 and one transversion mutation, GGT to GGG. CONCLUSIONS:New genes for the chemokines CCL2, CCL5 and CXCL10 have been recorded. The results were registered in the NCBI database under accession numbers LC727557, LC727558, and LC727558, respectively. The study revealed the important roles of chemokines in the pathogenesis of MS, suggesting their potential as targets for future therapy.
Age-dependent oxidative stress is considered to be involved in degenerative processes in age-related neurodegenerative disorders. The L1 cell adhesion molecule (L1CAM or L1) plays an essential role in the regeneration process following neural lesions in the adult nervous system. Protein kinase D1 (PKD1) is increasingly implicated in neuroprotection. Hence, the present study aimed to investigate the possible functional association between L1 and phosphorylated PKD1 (pPKD1) in oxidative stress-induced senescence. The study revealed that recombinant L1 (rL1) upregulated PKD1 phosphorylation, the pErk1/2 level and the Bcl2/Bax ratio in SK-N-SH cells in a concentration-dependent manner, with a peak level observed at 5 nM. L1 also increased the pPKD1 level in human pluripotent stem cells. In the 20 µM H2O2-induced senescence SK-N-SH cell model, L1 also increased the pPKD1 level and decreased the number of SA-b-gal-positive cells. On the whole, the results of the present study suggest that L1 is capable of modulating PKD1 phosphorylation to inhibit oxidative stress-induced senescence.
Progressive multifocal leukoencephalopathy (PML) is a demyelination disease of the central nervous system (CNS) caused by viral infection with John Cunningham polyomavirus (JC virus, JCV). PML affects mainly patients with immunodeficiency. Since the diagnosis is often challenging, it requires the close cooperation of clinicians. Due to the lack of specific treatment of JCV infection leading to PML, the current treatment is based on reversing the immunosuppression. Here we present a case of a 58-year-old woman who was ultimately diagnosed with PML based on neuropathological analysis of stereotactic biopsy specimens
INTRODUCTION:The aim was to explore the factors influencing hemorrhagic transformation (HT) after mechanical thrombectomy (MT) in acute anterior circulation large vessel occlusion stroke (ALVOS) and establish a corresponding prediction model. MATERIAL AND METHODS:A retrospective study was conducted on 180 ALVOS patients who underwent MT in our hospital between May 2022 and December 2023. The patients were divided into a bleeding group (134 cases) and a non-bleeding group (46 cases) based on whether there was intracranial hemorrhage in the immediate follow-up head CT after surgery. Logistic regression analysis was performed to explore the factors influencing HT after MT in ALVOS patients. A logistic regression prediction model based on risk factors was constructed. The predictive ability of the model was validated using receiver operating characteristic (ROC) curves. RESULTS:Significant differences were detected between the bleeding group and the non-bleeding group in terms of age, diabetes, NIHSS score on admission, time from onset to admission, time from onset to vascular recanalization, number of embolectomy attempts, and application of tirofiban (p < 0.05). Diabetes, NIHSS score on admission, time from onset to admission, time from onset to vascular recanalization, number of embolectomy attempts, and application of tirofiban were all significant factors influencing HT in ALVOS patients who underwent MT (p < 0.05). The logistic risk prediction model was constructed using the following model: Logit (P) = 0.625 × combined diabetes + 0.071 × NIHSS score + 0.035 × onset to hospital time + 2.321 × onset to vascular recanalization time + 1.461 × number of embolectomy attempts + 0.993 × application of tirofiban. The model had the likelihood ratio chi square (c2) = 196.85, DF = 6, p 2.03, the AUC was 0.882, 95% CI was 0.792-0.175, Z = 20.331, p < 0.001, with the predictive sensitivity of 85.35% and the specificity of 85.74%. CONCLUSIONS:Age, diabetes, NIHSS score on admission, time from onset to admission, time from onset to vascular recanalization, number of thrombectomy attempts, and use of tirofiban were independent risk factors for HT after MT in ALVOS patients. A logistic risk prediction model incorporating independent risk factors had some predictive value for HT after thrombolysis.
Sepsis-associated brain injury can lead to severe neurobehavioral and cognitive impairments due to inflammation, oxidative stress, and blood-brain barrier (BBB) dysfunction. Remimazolam (RM), a novel benzodiazepine, may have therapeutic potential for managing these complications. This study aimed to explore the therapeutic effects and potential molecular mechanisms of RM on BBB injury and brain injury in septic rats. Septic rat models were constructed using cecal ligation and puncture (CLP), with 75 rats randomly assigned to five groups (15 rats per group). RM (5 mg/kg, 10 mg/kg, and 20 mg/kg) was injected intraperitoneally to treat the rats. Neurobehavioral and cognitive functions were evaluated via neurological scores, water maze, and Y-maze tests. Brain water content was measured using the dry-wet weight method, and BBB permeability was assessed with Evans blue staining. Oxidative stress and inflammatory markers were detected using enzyme-linked immunosorbent assays and biochemical kits. Western blot analysis was performed to evaluate RM's effects on TLR4/NF-κB pathway proteins. RM treatment alleviated neurobehavioral and cognitive dysfunction while reducing inflammation and oxidative stress in septic rat brain tissue, with 10 mg/kg RM showing the greatest efficacy. RM also reduced brain water content and BBB damage, downregulating TLR4/NF-κB pathway proteins. These findings suggest that RM can effectively alleviate blood-brain barrier and brain injury in septic rats by inhibiting the TLR4/NF-κB pathway. The therapeutic effects observed may pave the way for future clinical research into RM's use for managing sepsis-associated brain injury.
Collision tumors, a rare phenomenon wherein two tumors with different histological features appear in the same anatomical region, present a challenging clinical diagnosis, particularly in the context of intraspinal collision tumors. This study reports the clinical data of a patient with an intraspinal collision tumor composed of schwannomas and ependymomas. A 47-year-old woman was admitted to the hospital with a six-month history of lumbosacral pain and numbness in both lower extremities. Lumbar magnetic resonance imaging (MRI) revealed two space-occupying lesions in the L1-2 spinal canal, which were initially diagnosed as two separate neurogenic tumors. Subsequent pathological examination revealed a collision tumor comprising a schwannoma and ependymoma. Intraspinal collision tumors, especially those combining schwannoma and ependymocytoma, are exceedingly rare. When two separate or conjoined tumors are present at the same anatomical site, the possibility of a collision tumor should be considered, despite its rarity. Interestingly, it was found that vertebral collision tumors tend to involve hemangiomas, whereas intraspinal collision tumors predominantly involve schwannomas.
INTRODUCTION:Aim of the study was to explore the association between ferroptosis genes in peripheral blood and immune infiltration in epileptic patients. MATERIAL AND METHODS:Our study investigated epilepsy-related differentially expressed genes (DEGs) and differential ferroptosis genes in the peripheral blood of epilepsy patients. Additionally, we collected serum from 45 epileptic patients and 45 healthy individuals to detect ferroptosis-related indicators and validate the expression levels of randomly selected differential ferroptosis genes. Subsequently, we screened model-related genes by least absolute shrinkage and selection operator regression and constructed a diagnostic model. Moreover, we analyzed peripheral immune infiltration through single-sample gene set enrichment analysis, and assessed the correlation between model-related genes and FerroScore with immune infiltration in epilepsy. RESULTS:Epilepsy-related DEGs were markedly enriched in the immune pathway and may be involved in ferroptosis. According to our findings, glutathione was dramatically lower in epileptic patients, whereas the expression of ATG5 was significantly elevated. Furthermore, based on 26 model-related differential ferroptosis genes, FerroScore was constructed and exhibited favorable diagnostic performance (AUC: 0.573-0.763). Herein, seven genes (FBXW7, MYB, QSOX1, PARP15, RB1, PTGS2, and TFRC) showed a significant correlation with FerroScore. Finally, notable variations in peripheral immune infiltration were observed in epileptic patients, with PRR5 and FerroScore showing close associations with them. CONCLUSIONS:Taken together, our observations suggest that in the peripheral blood of epileptic patients, FerroScore may help identify the occurrence of ferroptosis, while ferroptosis is strongly associated with immune infiltration. The study may shed novel light on the pathogenesis and treatment of epilepsy.
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.
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.
