The value of CT-based radiomics in predicting hemorrhagic transformation in acute ischemic stroke patients without recanalization therapy.

Objective: The aim of this study is to investigate the clinical value of radiomics based on non-enhanced head CT in the prediction of hemorrhage transformation in acute ischemic stroke (AIS). Materials and methods: A total of 140 patients diagnosed with AIS from January 2015 to August 2022 were enrolled. Radiomic features from infarcted areas on non-enhanced CT images were extracted using ITK-SNAP. The max-relevance and min-redundancy (mRMR) and the least absolute shrinkage and selection operator (LASSO) were used to select features. The radiomics signature was then constructed by multiple logistic regressions. The clinicoradiomics nomogram was constructed by combining radiomics signature and clinical characteristics. All predictive models were constructed in the training group, and these were verified in the validation group. All models were evaluated with the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA). Results: Of the 140 patients, 59 experienced hemorrhagic transformation, while 81 remained stable. The radiomics signature was constructed by 10 radiomics features. The clinicoradiomics nomogram was constructed by combining radiomics signature and atrial fibrillation. The area under the ROC curve (AUCs) of the clinical model, radiomics signature, and clinicoradiomics nomogram for predicting hemorrhagic transformation in the training group were 0.64, 0.86, and 0.86, respectively. The AUCs of the clinical model, radiomics signature, and clinicoradiomics nomogram for predicting hemorrhagic transformation in the validation group were 0.63, 0.90, and 0.90, respectively. The DCA curves showed that the radiomics signature performed well as well as the clinicoradiomics nomogram. The DCA curve showed that the clinical application value of the radiomics signature is similar to that of the clinicoradiomics nomogram. Conclusion: The radiomics signature, constructed without incorporating clinical characteristics, can independently and effectively predict hemorrhagic transformation in AIS patients.

Genome-wide association study for stalk lodging resistance related traits in maize (Zea mays L.).

BACKGROUND: The stalk traits stalk diameter, stalk length, rind penetrometer resistance and dry matter content are important indicators for measuring lodging resistance. RESULTS: In this study, 377 inbred lines were used as the basic materials, and four stalk-related traits including stalk diameter, stalk length, rind penetrometer resistance and dry matter content of the third segment of maize, were investigated at the tasseling, grain filling, and maturity stages. 461,053 high-quality SNPs which were obtained by whole genome resequencing were used for genome-wide association study. As a result of mixed linear model analysis (P < 9.77 × 10-6), 29 significant SNPs related to traits were detected, accounting for 7.19% -15.03% of phenotypic variation, among which 4, 1, 4 and 20 SNPs were found related to rind penetrometer resistance, stalk diameter, stalk length, and dry matter content respectively. Most candidate genes are related to plant element structure, signal transduction mechanisms, inorganic ion transport and metabolism, nucleotide transport and metabolism, and transporter enzyme families. Comparing mixed linear model with generalized linear model, a total of 12 candidate genes were detected repeatedly, during which the candidate gene Zm00001d014449 were detected 5 times, with a phenotypic variation interpretation rate of 9.95% -10.84%. This gene is mainly expressed in cells with active cell division and tissue differentiation, and is involved in the formation of stalk vascular bundles and the synthesis of cell walls. Another candidate gene, Zm00001d005300, encodes the transcription factor MYB44, which regulates the dependence of salt stress signal phosphorylation, can effectively inhibit the accumulation of destructive reactive oxygen species, and has a certain resistance to non-biotic stress. In addition, this study also found that 10 unknown functional genes can be further Functional verification. CONCLUSIONS: This study helps to deepen the understanding of the genetic basis of traits related to maize stalk lodging resistance, and provides theoretical guidance for future maize lodging resistance breeding.

Contrast-medium injury of spinal cord after cerebral angiography using nonionic contrast agents: A case report and literature review.

INTRODUCTION: Contrast-induced spinal cord injury (CIS) is an uncommon yet severe neurological complication following cerebral angiography. It can lead to dire consequences, including limb paralysis, respiratory distress, and even death. PATIENT CONCERNS: After undergoing cerebral angiography, a 41-year-old male initially displayed symptoms of dizziness and blurred vision, which advanced into dysphoria and limb weakness within 3 hours. These initial symptoms diminished by the 12th hour. Yet, 18 hours following the procedure, the patient developed quadriplegia and paresthesia below the T5 level, even though his deep sensory functions persisted unaffected. DIAGNOSIS: The magnetic resonance imaging and diffusion weighted imaging scans excluded the presence of cerebrovascular ischemia or subarachnoid hemorrhage. However, the magnetic resonance angiography displayed arterial vasospasms in both posterior cerebral arteries and the V4 segment of the right vertebral artery. The encephalopathy symptoms faded within 12 hours, suggesting a probable contrast-induced encephalopathy diagnosis. An magnetic resonance imaging on day 4 revealed an intensified signal in the spinal cord from C1 to T1. This finding supported the diagnosis of CIS. INTERVENTIONS: Following treatment with mannitol, methylprednisolone, and nimodipine, the patient's contrast-induced encephalopathy symptoms resolved completely within 12 hours. With a 2-week regimen of aspirin, methylprednisolone, and rehabilitative training, the neurological symptoms from CIS showed steady improvement. OUTCOMES: The symptoms and signs of CIS gradually improved after 2 weeks' treatment and rehabilitation program. CONCLUSION: Given the grave outcomes of CIS, like limb paralysis, breathing difficulties, and even fatality, it is imperative to remain cautious about this complication, even with the use of modern, less harmful contrast agents.

Enriched Environment Enhances Sociability Through the Promotion of ESyt1-Related Synaptic Formation in the Medial Prefrontal Cortex.

Sociability stands as a crucial factor in the evolutionary success of all mammalian species. Notably, enriched environment (EE) housing has been shown to enhance sociability in mice. However, the precise underlying molecular mechanism remains elusive. In this study, we established an EE paradigm, housing mice for a 14-day period. Both enhanced sociability and an increased spine density in the medial prefrontal cortex (mPFC) of mice subjected to EE were detected. To elucidate the potential molecular pathway, we conducted high-performance liquid chromatography tandem mass spectrometry (HPLC-MS) analysis of the entire mPFC from both EE and home-caged (HC) housed mice. Our analysis identified 16 upregulated and 20 downregulated proteins in the EE group. Among them, Extended Synaptotagmin 1 (ESyt1), an activity-dependent endoplasmic reticulum (ER)-plasma membrane (PM) tethering protein associated with synaptic function and growth, emerged as a potentially key player in the increased synapse formation and enhanced sociability observed in EE-housed mice. Further investigation, involving the knockdown of ESyt1 expression via sh ESyt1 lentivirus in the mPFC, revealed that ESyt1 is crucial for increased spine density of mPFC and enhanced sociability of mice in an enriched environment but not in normal condition. Overall, our findings uncover a novel mechanistic insight into the positive influence of environmental enrichment on social behavior via ESyt1-mediated pathways.

Effects of dietary inflammatory index, blood lead levels, and flavonoid intake on stroke risk in older Americans: A cross-sectional study.

OBJECTIVES: We aimed to investigate the relationship between dietary flavonoids, the dietary inflammatory index (DII), blood lead levels, and stroke and evaluate how these factors interact with one another in relation to stroke. MATERIALS AND METHODS: We analyzed data from 3675 older American adults aged ≥60 years, obtained from the National Health and Nutrition Examination Survey. Since this database does not specifically differentiate between hemorrhagic and ischemic strokes, our data include both types. We utilized the DII to assess the inflammatory potential of the diet, calculated using 24 h dietary recalls. To determine the association between dietary flavonoids, blood lead levels, DII, and stroke, we performed multivariate logistic regression, subgroup analysis, and restricted cubic splines. We modeled additive interactions to assess the relationship between blood lead levels and DII. RESULTS: A high intake of flavonols, flavan-3-ols, and total flavonoids correlated negatively with stroke risk, whereas blood lead levels had a positive association. After adjusting for confounders, stroke risk was found to increase with higher DII. Restricted cubic splines analysis revealed that flavan-3-ols, total flavonoids, blood lead levels, and DII were linearly related to stroke, while the relationships with flavonoids and flavonols were nonlinear. Additionally, a significant interaction was detected between high DII and elevated blood lead levels in relation to stroke risk. CONCLUSIONS: Intake of flavan-3-ol, flavanols, and total flavonoids is negatively associated with stroke risk, while higher blood lead levels and DII are positively related to it. High DII and elevated blood lead levels interact synergistically to influence stroke risk.

Improvement of the Stability and Optical Properties of CsPbBr3 QDs.

All-inorganic perovskite quantum dots (CsPbX3 QDs) (X = Cl, Br, I) have the advantages of adjustable emission position, narrow emission spectrum, high fluorescence quantum efficiency (PLQY), easy preparation, and elevated defect tolerance; therefore, they are widely used in optoelectronic devices, such as solar cells, light-emitting diodes, and lasers. However, their stability still constrains their development due to their intrinsic crystal structure, ionic exchange of surface ligands, and exceptional sensitivity to environmental factors, such as light, water, oxygen, and heat. Therefore, in this paper, we investigate the stability improvement of CsPbX3 QDs and apply fabricated high-efficiency, stable perovskite QDs to solar cells to improve the performance of the cells further. In this paper, we focus on CsPbBr3 QDs with intrinsic extreme stability and optimize CsPbBr3 QDs using strategies, such as Mn+ doping, ligand regulation, and polymer encapsulation, which can improve optical properties while ensuring their stability. The test results show that the above five methods can improve the strength and luminescence performance of QDs, with the best stability achieved when PMMA encapsulates QDs with a ratio of PMMA = 2:1 and PLQY increases from 60.2% to 90.1%.

Mettl3 Mediated m6A Methylation Involved in Epithelial-Mesenchymal Transition by Targeting SOCS3/STAT3/SNAI1 in Cigarette Smoking-Induced COPD.

Purpose: Persistent inflammation and epithelial-mesenchymal transition are essential pathophysiological processes in chronic obstructive pulmonary disease (COPD) and involve airway remodeling. m6A methylation modification was discovered to play an important role in various diseases. Nevertheless, the regulatory role of m6A methylation has not yet been investigated in cigarette smoking-induced COPD. The study aims to explore the regulatory role of m6A methylation in cigarette smoking-induced COPD. Patients and Methods: In this study, two Gene Expression Omnibus (GEO) datasets were first utilized to analyze the expression profiles of m6A RNA methylation regulators in COPD. We then established a cell model of COPD by exposing human bronchial epithelial cells (HBECs) to cigarette smoke extract (CSE) in vitro and detected the expression of m6A writer Mettl3 and EMT phenotype markers. RNA interference, cycloleucine, RT-qPCR, western blot, MeRIP-sequencing, and cell migration assay were performed to investigate the potential effect of Mettl3 on the EMT process in CSE-induced HBECs. Results: Our results showed that Mettl3 expression was significantly elevated in cigarette smoking-induced COPD patients and in a cellular model of COPD. Furthermore, Mettl3 silence and cycloleucine treatment inhibited the EMT process of HBECs caused by CSE. Mechanically, Mettl3 silence weakens the m6A methylation of SOCS3 mRNA to enhance the protein expression of SOCS3, inhibiting CSE-induced SOCS3/STAT3/SNAI1 signaling and EMT processes in HBECs. Conclusion: Our study inferred that Mettl3-mediated m6A RNA methylation modification modulates CSE-induced EMT by targeting SOCS3 mRNA and ultimately serves as a crucial regulator in the emergence of COPD. This conclusion reinforces the regulatory role of m6A methylation in COPD.

Combined analysis of single-cell and bulk RNA sequencing reveals the expression patterns of circadian rhythm disruption in the immune microenvironment of Alzheimer's disease.

Background: Circadian rhythm disruption (CRD) represents a critical contributor to the pathogenesis of Alzheimer's disease (AD). Nonetheless, how CRD functions within the AD immune microenvironment remains to be illustrated. Methods: Circadian rhythm score (CRscore) was utilized to quantify the microenvironment status of circadian disruption in a single-cell RNA sequencing dataset derived from AD. Bulk transcriptome datasets from public repository were employed to validate the effectiveness and robustness of CRscore. A machine learning-based integrative model was applied for constructing a characteristic CRD signature, and RT-PCR analysis was employed to validate their expression levels. Results: We depicted the heterogeneity in B cells, CD4+ T cells, and CD8+ T cells based on the CRscore. Furthermore, we discovered that CRD might be strongly linked to the immunological and biological features of AD, as well as the pseudotime trajectories of major immune cell subtypes. Additionally, cell-cell interactions revealed that CRD was critical in the alternation of ligand-receptor pairs. Bulk sequencing analysis indicated that the CRscore was found to be a reliable predictive biomarker in AD patients. The characteristic CRD signature, which included 9 circadian-related genes (CRGs), was an independent risk factor that accurately predicted the onset of AD. Meanwhile, abnormal expression of several characteristic CRGs, including GLRX, MEF2C, PSMA5, NR4A1, SEC61G, RGS1, and CEBPB, was detected in neurons treated with Aß1-42 oligomer. Conclusion: Our study revealed CRD-based cell subtypes in the AD microenvironment at single-cell level and proposed a robust and promising CRD signature for AD diagnosis. A deeper knowledge of these mechanisms may provide novel possibilities for incorporating "circadian rhythm-based anti-dementia therapies" into the treatment protocols of individualized medicine.

Stroke risk study based on deep learning-based magnetic resonance imaging carotid plaque automatic segmentation algorithm.

Introduction: The primary factor for cardiovascular disease and upcoming cardiovascular events is atherosclerosis. Recently, carotid plaque texture, as observed on ultrasonography, is varied and difficult to classify with the human eye due to substantial inter-observer variability. High-resolution magnetic resonance (MR) plaque imaging offers naturally superior soft tissue contrasts to computed tomography (CT) and ultrasonography, and combining different contrast weightings may provide more useful information. Radiation freeness and operator independence are two additional benefits of M RI. However, other than preliminary research on MR texture analysis of basilar artery plaque, there is currently no information addressing MR radiomics on the carotid plaque. Methods: For the automatic segmentation of MRI scans to detect carotid plaque for stroke risk assessment, there is a need for a computer-aided autonomous framework to classify MRI scans automatically. We used to detect carotid plaque from MRI scans for stroke risk assessment pre-trained models, fine-tuned them, and adjusted hyperparameters according to our problem. Results: Our trained YOLO V3 model achieved 94.81% accuracy, RCNN achieved 92.53% accuracy, and MobileNet achieved 90.23% in identifying carotid plaque from MRI scans for stroke risk assessment. Our approach will prevent incorrect diagnoses brought on by poor image quality and personal experience. Conclusion: The evaluations in this work have demonstrated that this methodology produces acceptable results for classifying magnetic resonance imaging (MRI) data.

Structurally diverse diterpenoids from the roots of Euphorbia fischeriana Steud.

Four new diterpenoids (1-4), and 18 known ones were isolated from the roots of Euphorbia fischeriana Steud (Euphorbiaceae). These diterpenoids shared six skeleton types, including ent-atisane, kaurane, 3,4-secokaurane, lathyrane, 4,5-secoatisane and ingenane diterpenoids. The structures of the new diterpenoids were characterized by a combination of spectroscopic techniques and X-ray crystallography. Moreover, biological evaluation revealed that compounds (16S*)-atisan-3ß,16,17-triol (7), (16S*)-3ß,16,17,18-tetrahydroxykaurane (12) and (16S*)-3α-hydroxykauran-16,17-acetonide (15) showed inhibitory activity against the interferon regulatory factors (IRFs) involved pathway.

Acrocalyenes A and B, Two New Diterpenoids from Sinomenium acutum Associated Fungus Acrocalymma sp.

We identified two new diterpenoidal acrocalyenes A (1) and B (2) through chemical investigation on Acrocalymma sp., a plant-associated fungus from the tender stem isolates of Sinomenium acutum collected from the Qinling Mountains, along with seven already-recognized compounds (3-9). The HR-ESI-TOF-MS and 1D/2D NMR data were utilized for structural elucidation of these compounds, and the single-crystal X-ray diffraction was employed for absolute configuration clarification of the novel acrocalyenes 1 and 2. Bioassays revealed that the cytotoxicities of compounds 2, 4, 6, 7, and 8 against three human carcinoma cells (RKO, HeLa and HCC-1806) were moderate to strong, with IC50 between 6.70-38.82 µM. These isolates were also evaluated for their fungal resistant potentials against Botrytis cinerea, Fusarium culmorum and Fusarium solani, in which 3 displayed significant inhibitory effects on all three phytopathogenic fungi, showing respective MIC of 50, 25 and 25 µM.

Tectorigenin attenuates the OGD/R-induced HT-22 cell damage through regulation of the PI3K/AKT and the PPARγ/NF-κB pathways.

Tectorigenin (TEC) is an effective compound that derived from many plants, such as Iris unguicularis, Belamcanda chinensis and Pueraria thunbergiana Benth. Evidence suggested that TEC has anti-tumor, anti-oxidant activity, anti-bacterial and anti-inflammatory effects. In addition, there has some evidence indicated that TEC is a potential anti-stroke compound; however, its specific roles and associated mechanism have not yet been elucidated. In the present study, we aimed to investigate the anti-inflammatory, anti-oxidant activity and anti-apoptosis effects of TEC on oxygen-glucose deprivation/reperfusion (OGD/R)-induced HT-22 cells, and clarified the relevant mechanisms. Here, we observed that TEC significantly promoted cell survival, impeded cell apoptosis, inhibited ROS and inflammatory cytokines IL-1ß, IL-6, TNF-α production in OGD/R-induced HT-22 cells. Moreover, TEC activated PI3K/AKT signal pathway, increased PPARγ expression and inhibited NF-κB pathway activation in OGD/R-induced HT-22 cells. Further studies indicated that PPARγ inhibitor GW9662 activated NF-κB pathway after TEC treatment in OGD/R-induced HT-22 cells. Also, PI3K/AKT inhibitor LY294002, PPARγ inhibitor GW9662 and NF-κB activator LPS both reversed the effects of TEC on OGD/R-induced HT-22 cell biology. Taken together, this research confirmed that TEC benefit to HT-22 cell survival and against OGD/R damage through the PI3K/AKT and PPARγ/NF-κB pathways. These results indicated that TEC might be an effective compound in the treatment for ischemic brain injury.

lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR­106a­5p­mediated P38 MAPK signaling.

Glioma is diagnosed as the most common intracranial malignant tumor. Cancer stem cells determine stemness and radioresistance, and may facilitate glioma recurrence. The present study aimed to investigate whether the long non­coding RNA (lncRNA) transmembrane phosphatase with tensin homology pseudogene 1 (TPTEP1) regulated cell stemness and radioresistance of glioma, and determine the underlying molecular mechanism of TPTEP1 in the modulation of glioma progression. Cell and molecular biology techniques were applied for investigating the role of TPTEP1 in glioma cell lines, animal model, and clinical samples. The results demonstrated that TPTEP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo. In addition, TPTEP1 augmented MAPK14 expression by competitively interacting with microRNA (miR)­106a­5p, thus activating the P38 MAPK signaling pathway, and suppressing glioma stemness and radioresistance. TPTEP1 functionally bound to miR­106a­5p, which formed a reciprocal regulatory loop to stimulate the P38 MAPK signaling pathway. Low TPTEP1 expression levels were detected in high­grade glioma tissues compared with low­grade glioma tissues, and were positively associated with poor prognosis of patients with glioma. Furthermore, analysis using data from The Cancer Genome Atlas database confirmed the molecular mechanism and biological significance of dysregulation of TPTEP1 in glioma progression. Taken together, the results of the present study suggest that TPTEP1 may be applied as a diagnostic and prognostic indicator for glioma, and may be an alternative target for the treatment of glioma.

Effect of matrine on JAK2/STAT3 signaling pathway and brain protection in rats with cerebral ischemia-reperfusion.

BACKGROUND: Ischemic encephalopathy is a common clinical disease. The main treatment goal is to achieve vascular recanalization. However, after vascular recanalization, the reperfusion of fresh blood can change local cell metabolism, thus adversely affecting cell structure and function, which can result in reperfusion injury. OBJECTIVES: To explore the effect of matrine intervention of different concentrations on JAK2/STAT3 signaling pathway and brain protection in rats with cerebral ischemia-reperfusion. MATERIAL AND METHODS: Healthy male Sprague Dawley rats were divided into a blank control group (20 rats), a model group (80 rats) and a sham group (20 rats). In the model group, the middle cerebral artery was occluded with suture method to establish cerebral ischemia-reperfusion model rats, which were subdivided into cerebral ischemia-reperfusion group, and 5, 10 and 20 mg/kg matrine groups, with 20 rats in each group. Indicators including neurological function score, brain infarct size, brain water content, lactic dehydrogenase activity, protein expressions of p-JAK2 and p-STAT3, as well as superoxide dismutase activity and malondialdehyde content were evaluated. RESULTS: Compared with cerebral ischemia-reperfusion group, all the indicators were significantly improved in the 3 matrine treatment groups in a dose-dependent manner, and protein expressions of p-JAK2 and p-STAT3 in the brain tissue and brain cell apoptosis rate were decreased with the increase of matrine concentration (all p < 0.05). CONCLUSIONS: Matrine can significantly ameliorate the neurological function and brain edema of rats with cerebral ischemia-reperfusion, and improve superoxide dismutase, malondialdehyde and lactic dehydrogenase levels in the brain tissue and brain cell apoptosis rate. The mechanism of matrine may be related to the inhibition of abnormal JAK2/STAT3 signaling pathway activation.

[Effects of butylphthalide on microglia activation in frontal lobe of rats after chronic sleep deprivation].

Objective: To evaluate the effects of butylphthalide on microglia activation and inflammatory factors in frontal lobe of rats after chronic sleep deprivation. Methods: Rats were divided into four groups(n＝8): control group, platform group, chronic sleep deprivation group and butylphthalide intervention group. Chronic sleep deprivation was performed in rats of chronic sleep deprivation group and butylphthalide intervention group for 18 h per day using the multiple platforms method, and sleep deprivation lasted for 28 days. At the same time, rats in platform group were put in platform, while rats in control group were in normal sleep. After 28 days of sleep deprivation, rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/kg for 14 days, meanwhile rats in other groups were intraperitoneally injected with saline. Then brains were collected and ionized calcium binding adaptor molecule-1 (Iba-1) positive cells in cortex in frontal lobe were studied and counted. The expressions of inducible nitric oxide synthase (iNOS) and arginase1 (Arg1) in frontal lobe were detected by Western blot, and the mRNA levels of interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α) were determined by real-time PCR. Results: Compared with control or platform group, the Iba-1 positive cells in chronic sleep deprivation group were large with long process, and increased cell counts were also found in the chronic sleep deprivation group (all P＜0. 05). Moreover, the mRNA expression levels of iNOS, IL-1, IL-6, TNF-α were increased, while the expression of Arg1 was decreased in frontal lobe in rats of the chronic sleep deprivation group compared with the control or platform group (all P＜0. 05). The Iba-1 positive cells in butylphthalide intervention group were reduced compared with chronic sleep deprivation group (P＜0. 05). And the mRNA expression levels of iNOS, IL-1, IL-6 and TNF-α were decreased, while the expression of Arg1 did not chang in rats of the butylphthalide intervention group compared with the chronic sleep deprivation group (all P＜0. 05). Conclusion: Butylphthalide might inhibit the activation and decrease the inflammatory factors in frontal lobe of rats after chronic sleep deprivation.

[The effects of prenatal radiation of mobile phones on white matter in cerebellum of rat offspring].

OBJECTIVE: To evaluate the effects of prenatal radiation of 850～1 900 MHz mobile phone on white matter in cerebellum of adult rat offspring. METHODS: Pregnant rats were randomly divided into short term maternal radiation group, long term maternal radiation group and control group. Rats in short term and long term maternal radiation group were exposed to 6 h/d and 24 h/d mobile phone radiation during 1-17 days of pregnancy, respectively. The cerebellums of offspring rats at the age of 3 month(n＝8)were taken. Cell morphology in cerebellum was studied by hematoxylin-eosin (HE) staining. The expressions of myelin basic protein (MBP), neurofilament-L (NF-L) and glial fibrillary acidic protein (GFAP) in cerebellum of rat offspring were detected by immunohistochemistry and Western blot. RESULTS: Compared to control group, the morphological changes of purkinje cells in cerebellum were obvious in rat offspring of short term and long term maternal radiation group. Compared to control group, decreased MBP and NF-L expressions and increased GFAP expression were observed in long term maternal radiation group(all P＜0.05). Compared to short term radiation group, the expressions of MBP and NF-L were down-regulated (all P＜0.05) and the expression of GFAP was up- regulated(P＜0.05) in long term radiation group. CONCLUSION: Prenatal mobile phone radiation might lead to the damage of myelin and axon with activity of astrocytes in cerebellum of male rat offspring, which is related to the extent of radiation.

Enriched Environment Decreases Cognitive Impairment in Elderly Rats With Prenatal Mobile Phone Exposure.

Mobile phone use has rapidly increased worldwide, and pregnant women are passively or actively exposed to the associated electromagnetic radiation. Maternal cell phone exposure is related to behavioral difficulties in young offspring. However, whether prenatal mobile phone exposure can predispose the elderly offspring to cognitive impairment is unclear. The enriched environment (EE) has shown positive effects on cognition in an immature brain, but its impact on aging offspring after prenatal cell phone exposure is unknown. This study aimed to investigate whether prenatal exposure to mobile phone exerts long-term effects on cognition in elderly rat offspring and whether EE during adulthood can rescue cognitive impairment by altering the synaptic plasticity. Pregnant rats were subjected to prenatal short-term or long-term cell phone exposure and offspring rats were randomly assigned to standard or EE. Spatial learning and memory were investigated using Morris water maze (MWM) in elderly rat offspring. Hippocampal cellular morphology was assessed by hematoxylin-eosin staining and synaptic ultrastructure was evaluated with transmission electron microscopy. Expression of synaptophysin (SYN), postsynaptic density-95 (PSD-95), and brain-derived neurotrophic factor (BDNF) were detected by western blot. The results demonstrated that prenatal long-term but not short-term exposure to mobile phone lead to cognitive impairment, morphological changes in the hippocampal cells, reduced synaptic number, decreased SYN, PSD-95, and BDNF expression in elderly offspring, which were alleviated by postnatal EE housing. These findings suggest that prenatal long-term mobile phone exposure may pose life-long adverse effects on elderly offspring and impair cognition by disrupting the synaptic plasticity, which may be reversed by postnatal EE housing.

Spinal Cord Syphilitic Gumma Presenting with Brown-Séquard Syndrome: A Case Report and Literature Review.

BACKGROUND: Spinal neurosyphilis manifesting as a solitary syphilitic gumma is exceedingly rare. There are non-specific imaging findings and challenges in the diagnosis of spinal syphilitic gumma, which could be easily misdiagnosed as tumor lesions and require surgical resection or biopsy. CLINICAL PRESENTATION: We report the case of a 45-year-old female patient who was diagnosed with Spinal syphilitic gumma. Our case is the first reported case of spinal cord syphilitic gumma with intradural-extramedullary and intramedullary involvement. CONCLUSION: Spinal syphilitic gumma exhibits diverse clinical manifestations, lacks specific imaging features, accompanied by the patient's history deliberately concealed. Since clinicians do not have sufficient knowledge about such rare cases, misdiagnosis and missed diagnosis will be likely. When there is clinical suspicion for spinal syphilitic gumma, clinicians should pay close attention to relevant medical history, carry out a comprehensive physical examination and specific serological tests and cerebrospinal fluid (CSF) analysis. In summary, in cases with stable neurologic conditions, a trial administration of intravenous penicillin with follow-up imaging may be the optimal treatment option, and in cases with rapid progression or acute exacerbation, a surgical resection together with systemic antibiotic treatment for syphilis after surgery may be the best treatment strategy.