Glioblastoma constitutes a major subset of brain cancers and is characterized by a high recurrence rate and a low five-year survival rate. Ginsenoside compound K (GCK), a bioactive component derived from traditional Chinese medicine, exhibits anti-allergic, anti-aging, and notable anti-tumor properties. Although previous studies have shown that GCK can inhibit glioblastoma, its precise role and underlying mechanisms remain unclear. In this study, we demonstrated the effects of GCK on glioma initiation and progression, as well as its associated mechanisms. In vitro experiments revealed that GCK markedly inhibited the proliferation and migration of glioblastoma cells and significantly disrupted their cell cycle. In vivo, intragastric administration of GCK substantially reduced the growth rate of transplanted glioblastoma and prolonged the survival of nude mice. Furthermore, RNA sequencing and Western blot analyses showed that GCK suppresses glioblastoma progression by dephosphorylating p-ERK1/2 via upregulation of DUSP5 expression. These findings highlight the critical role of GCK in glioblastoma inhibition and suggest its potential as a promising therapeutic agent for clinical treatment, underscoring the value of traditional Chinese medicine in modern oncology.

Glioblastoma (GBM) is the most common type of primary malignant brain tumor, characterized by a poor prognosis, high recurrence rate, and elevated mortality. In recent years, gene-targeted therapies leveraging small molecule compounds have gained momentum as a promising avenue for GBM intervention. Myoferlin (MYOF), a type II membrane protein of the Ferlin family, has emerged as a key regulator of membrane dynamics-governing processes such as vesicular trafficking, endocytosis, and membrane repair. In this study, we explore the previously uncharted role of MYOF in GBM progression and its potential as a diagnostic and therapeutic target. Our data reveal that silencing MYOF markedly suppresses glioma growth both in vitro and in vivo. Mechanistically, MYOF knockdown disrupts the nuclear translocation of phosphorylated STAT3 (P-STAT3), a critical oncogenic signaling event. Notably, we identified Entacapone (ENT), a small molecule capable of targeting MYOF, which significantly impedes glioma development across experimental models. These findings position MYOF as a novel molecular lever in GBM pathogenesis and highlight ENT as a potential therapeutic agent that exerts anti-glioma effects by blocking MYOF-mediated P-STAT3 nuclear import.The diagram illustrates a novel regulatory mechanism of IL-6/STAT3 signaling involving MYOF. Upon IL-6 stimulation, STAT3 undergoes phosphorylation. MYOF then binds to phosphorylated STAT3 and facilitates its translocation into the nucleus to regulate target gene expression. The compound ENT acts as a targeted inhibitor of this process by binding to MYOF, thereby blocking the nuclear transport of phosphorylated STAT3 and suppressing downstream signaling.

Glioblastoma multiforme (GBM) remains one of the most aggressive primary brain tumors with limited therapeutic options. The efficacy of standard temozolomide chemotherapy is critically influenced by O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation status. While monoclonal antibody (mAb)-based biologics represent a promising therapeutic approach, current clinical trials have failed to demonstrate significant improvement in overall patient survival. In this study, systematic screening identified histamine H1 receptor (HRH1) as a potential therapeutic target. Genetic silencing of HRH1 significantly inhibited GBM cell proliferation, migration, and invasion both in vitro and in vivo. Pharmacological validation using the HRH1-specific antagonist terfenadine confirmed the anti-tumor effects of HRH1 targeting. Based on these findings, we developed an HRH1-targeting mAb that demonstrated potent anti-tumor activity in GBM xenograft models. Mechanistic investigations revealed that the therapeutic effect was mediated through protein kinase C (PKC)-dependent regulation of the RAF/MEK/ERK signaling pathway. In conclusion, we provided a new target, HRH1, for treating GBM and constructed an effective therapeutic mAb.

BACKGROUND:Gliomas are the most aggressive primary malignancies of the central nervous system (CNS) and exhibit marked heterogeneity that is closely associated with metabolic reprogramming. Emerging evidence underscores the pivotal role of lactylation modifications in shaping the tumor microenvironment (TME) and facilitating glioma progression. This study aimed to systematically identify key lactylation-related genes (LRGs), elucidate their functional roles and associated pathways, and explore their potential as novel therapeutic targets using multi-omics data. METHODS:We combined various datasets from the TCGA, GEO, and CGGA databases, including RNA-seq, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics. Key LRGs were identified through a multi-step analytical pipeline that involved processing scRNA-seq data using (Seurat, scoring), cell-type-specific lactylation scoring (AUCell), high-dimensional weighted gene co-expression network analysis (hdWGCNA) and applying rigorous machine learning-based feature selection utilizing 10 algorithms and 101 combinatorial strategies. We comprehensively assessed the prognostic value associated with the immune microenvironment, and spatiotemporal heterogeneity of the prioritized RAN. Functional validation was executed using shRNA-mediated knockdown in glioma cell lines, including LN229, U87, and U251, while evaluating proliferation (CCK-8, colony formation, EdU), migration (wound healing), invasion (Transwell), and pathway activity (using western blot). RESULTS:scRNA-seq analysis revealed distinct lactylation enrichment patterns across glioma cell types, with malignant cells exhibiting the highest scores. hdWGCNA identified a gene module (royal blue) strongly correlated with lactylation activity (correlation = 0.75). The intersection of this module with a curated set of LRGs yielded 22 candidate genes. Subsequent machine learning analysis using (ENet, α = 0.4) prioritized six core LRGs (PDAP1, ALYREF, CBX3, MAGOH, RAN, TMSB4X). RAN, an understudied gene in glioma, was selected for further investigation. High RAN expression correlated significantly with poor patient prognosis, reduced immune cell infiltration (assessed by ESTIMATE, CIBERSORT, xCell, ssGSEA), and distinct spatiotemporal heterogeneity within tumors (analyzed using spatial transcriptomics, Monocle2). Glioma cell invasion, migration, colony formation, and proliferation were all markedly inhibited by RAN knockdown. Mechanistically, reduced p-AKT levels following knockdown and functional rescue with a PI3K/AKT activator (SC79) indicate that RAN increased these malignant traits by activating the PI3K/AKT signaling pathway. CONCLUSION:Our study established lactylation modifications as a crucial regulator of the TME and glioma progression. Through integrative multi-omics analysis and robust machine learning techniques, we determined that RAN was a novel lactylation-associated gene. RAN is a potent, independent prognostic biomarker that promotes glioma malignancy via the PI3K/AKT pathway. Our results demonstrate RAN as a prospective therapeutic target and establish a novel framework for individualized therapy for glioma.

Glioma, one of the most common types of primary brain tumors, presents considerable challenges due to its poor prognosis. Emerging research has demonstrated a strong connection between Centromere Protein M(CENPM) and tumor progression. However, the precise role of CENPM in glioma remains poorly understood. This study delves into the involvement of CENPM in glioma progression. Data analysis revealed that heightened CENPM expression correlates with worse patient outcomes and is highly expressed in glioma. In vitro experiments showed that reducing CENPM expression inhibits glioma cell proliferation and induces G0/G1 phase cell cycle arrest. Furthermore, RNA-seq and Western Blot analyses demonstrated that CENPM activates the PI3K/AKT signaling pathway in glioma cells. In vivo experiments confirmed that knocking down CENPM leads to reduced tumor growth in glioma models and improves the prognosis of tumor-bearing mice. This study underscores the critical role of CENPM in glioma and sheds light on potential therapeutic strategies.

ObjectiveSeveral studies have explored the relationship between intracranial aneurysms and psychiatric disorders; nevertheless, the causal connection remains ambiguous. This study aimed to evaluate the causal link between intracranial aneurysms and specific psychiatric disorders.MethodsA two-sample Mendelian randomization (MR) analysis was conducted utilizing aggregated genome-wide association study (GWAS) data from the International Stroke Genetics Association for Intracranial Aneurysms (IAs), unruptured Intracranial Aneurysm (uIA), and aneurysmal Subarachnoid Hemorrhage (aSAH). Psychiatric disorder data, encompassing Schizophrenia (SCZ), Bipolar Disorder (BD), and Panic Disorder (PD), were sourced from the Psychiatric Genomics Consortium (PGC), while Cognitive Impairment (CI) data, comprising Cognitive Function (CF) and Cognitive Performance (CP), were obtained from IEU OpenGWAS publications. Causal effects were evaluated using inverse variance weighted (IVW), MR-Egger, and weighted median methods, with the robustness of findings assessed via sensitivity analyses employing diverse methodological approaches.ResultsOur MR analysis indicated no discernible causal link between intracranial aneurysm (IA) and an elevated susceptibility to psychiatric disorders. However, among individuals with genetically predisposed unruptured intracranial aneurysms (uIA), there was a modest reduction in the risk of SCZ (IVW odds ratio [OR] = 0.95, 95% confidence interval [CI] 0.92–0.98, p = 0.0002). Similarly, IAs also exhibited a moderate reduction in SCZ risk (OR = 0.92, 95% CI 0.86–0.99, p = 0.02). Nevertheless, limited evidence was found to support a causal association between intracranial aneurysms and the risk of the other three psychiatric disorders.ConclusionOur findings furnish compelling evidence suggesting a causal influence of intracranial aneurysms on psychiatric disorders, specifically, both IAs and uIA exhibit a negative causal association with SCZ.

Introduction This study aims to investigate prognostic indicators and assess surgical interventions' impact on Primary central nervous system lymphoma-diffuse large B-cell lymphoma (PCNS-DLBCL) patients.Methods A comprehensive examination was performed on a group of 3,962 cases in the Surveillance, Epidemiology, and End Results (SEER) database, as well as 27 cases of PCNS-DLBCL from the First Affiliated Hospital of Wenzhou Medical University. The application of both univariate and multivariate Cox regression analyses facilitated the identification of significant risk factors associated with PCNS-DLBCL. Developing and verifying nomograms, the reliability of the nomogram was evaluated by C-index, ROC curve, calibration curve and decision curve analysis. Finally, by using Kaplan-Meier (KM) curves to assess the survival rates for PCNS-DLBCL patients.Results Age, gender, marital status, tumor location, HIV infection status, chemotherapy, and surgical scopes emerged as independent prognostic factors for overall survival (OS) in multivariate Cox regression analysis, whereas gender did not demonstrate significance as a factor for cancer-specific survival (CSS). The C-index, calibration curves, ROC curves, and DCA curves demonstrating strong reliability and practicality. KM analysis revealed significantly improved OS and CSS in patients who underwent surgical resection compared to those who received no surgery/biopsy, especially receiving subtotal resection (STR). In addition, among patients receiving chemotherapy, both STR and gross total resection (GTR) improved survival time compared to chemotherapy alone, particularly with STR. In the non-chemotherapy group, GTR potentially improved CSS, there was no notable disparity in OS between patients who underwent surgery and those who did not or received biopsy.Conclusion This study analyzed prognostic factors in PCNS-DLBCL patients, resulting in nomograms predicting 1-, 3-, and 5-year OS and CSS, which showed preferable performance. Combining different resection scopes with chemotherapy improved survival compared to chemotherapy alone, advocating for integrated treatment strategies. Surgery alone is not recommended based on our findings.

BACKGROUND:Glioblastoma represents the most frequently diagnosed malignant neoplasm within the central nervous system. Human glioblastoma cells can be phenotypically reprogrammed into neuron-like cells through the forced expression of NEUROG2 and SOXC factors. NEUROG2 serves as a pioneer factor, establishing an initial framework for this transformation. However, the specific role of SOXC factors has not been fully elucidated. METHODS:In this study, we used ChIP-seq to determine the potential target gene of NGN2. RNA-seq has been used to evaluate the transcriptional change during NGN2-SOX11-mediated neuron reprogramming. Immunofluorescence was used to determine the neuron reprogramming efficacy and cell proliferation ability. ChIP-qPCR, Co-IP, and Western Blot were performed to investigate the mechanism. RESULTS:Our findings reveal that SOXC factors, in contrast to their previously identified function as transcriptional activators, act as transcriptional repressors. They achieve this by recruiting TRIM28 to suppress the expression of ECT2, a RhoGEF. This suppression results in the differential regulation of RhoA, RAC1, and CDC42 activities throughout the reprogramming process. We further establish that small molecules targeting RhoA and its effectors can substitute for SOXC factors in facilitating the neuronal reprogramming of glioblastoma cells. CONCLUSION:These results underscore the pivotal role of SOXC factors' transcriptional repression and illuminate one of their specific downstream targets.

ObjectiveChronic subdural hematoma (CSDH) is a neurological condition with high recurrence rates, primarily observed in the elderly population. Although several risk factors have been identified, predicting CSDH recurrence remains a challenge. Given the potential of machine learning (ML) to extract meaningful insights from complex data sets, our study aims to develop and validate ML models capable of accurately predicting postoperative CSDH recurrence.MethodsData from 447 CSDH patients treated with consecutive burr-hole irrigations at Wenzhou Medical University’s First Affiliated Hospital (December 2014-April 2019) were studied. 312 patients formed the development cohort, while 135 comprised the test cohort. The Least Absolute Shrinkage and Selection Operator (LASSO) method was employed to select crucial features associated with recurrence. Eight machine learning algorithms were used to construct prediction models for hematoma recurrence, using demographic, laboratory, and radiological features. The Border-line Synthetic Minority Over-sampling Technique (SMOTE) was applied to address data imbalance, and Shapley Additive Explanation (SHAP) analysis was utilized to improve model visualization and interpretability. Model performance was assessed using metrics such as AUROC, sensitivity, specificity, F1 score, calibration plots, and decision curve analysis (DCA).ResultsOur optimized ML models exhibited prediction accuracies ranging from 61.0% to 86.2% for hematoma recurrence in the validation set. Notably, the Random Forest (RF) model surpassed other algorithms, achieving an accuracy of 86.2%. SHAP analysis confirmed these results, highlighting key clinical predictors for CSDH recurrence risk, including age, alanine aminotransferase level, fibrinogen level, thrombin time, and maximum hematoma diameter. The RF model yielded an accuracy of 92.6% with an AUC value of 0.834 in the test dataset.ConclusionOur findings underscore the efficacy of machine learning algorithms, notably the integration of the RF model with SMOTE, in forecasting the recurrence of postoperative chronic subdural hematoma. Leveraging the RF model, we devised an online calculator that may serve as a pivotal instrument in tailoring therapeutic strategies and implementing timely preventive interventions for high-risk patients.

Cell fate and proliferation ability can be transformed through reprogramming technology. Reprogramming glioblastoma cells into neuron-like cells holds great promise for glioblastoma treatment, as it induces their terminal differentiation. NeuroD4 (Neuronal Differentiation 4) is a crucial transcription factor in neuronal development and has the potential to convert astrocytes into functional neurons. In this study, we exclusively employed NeuroD4 to reprogram glioblastoma cells into neuron-like cells. In vivo, the reprogrammed glioblastoma cells demonstrated terminal differentiation, inhibited proliferation, and exited the cell cycle. Additionally, NeuroD4 virus-infected xenografts exhibited smaller sizes compared to the GFP group, and tumor-bearing mice in the GFP+NeuroD4 group experienced prolonged survival. Mechanistically, NeuroD4 overexpression significantly reduced the expression of SLC7A11 and Glutathione peroxidase 4 (GPX4). The ferroptosis inhibitor ferrostatin-1 effectively blocked the NeuroD4-mediated process of neuron reprogramming in glioblastoma. To summarize, our study demonstrates that NeuroD4 overexpression can reprogram glioblastoma cells into neuron-like cells through the SLC7A11-GSH-GPX4 signaling pathway, thus offering a potential novel therapeutic approach for glioblastoma.

Intracerebral hemorrhage (ICH) is an acute cerebrovascular disease with high mortality and long-term disability rates. Stem cell transplantation and neurotrophic factor therapy have shown great potential in ICH. It has been established that mutated NT3 (NT3P75 - 2) can enhance the positive biological functions of NT3 by decreasing its affinity to the P75-2 receptor. The present study aimed to explore whether NT3P75-2 could further improve neurological recovery after ICH. First, we constructed three stable BMSC cell lines (GFP, GFP-NT3 overexpressed and GFP-NT3P75 - 2 overexpressed) by lentivirus infection. Next, rats were injected with fresh supernatants of these three cell lines on days 1 (24 h) and 3 (72 h) post-ICH induction. Behavioral evaluations were conducted to assess the neurological recovery of ICH rats. We further evaluated changes in microglia activation, neuron survival and proliferation of neural stem cells. Compared with the GFP group and the GFP-NT3 group, animals in the GFP-NT3P75 - 2 group exhibited better motor function improvements and milder neuroinflammation response. Meanwhile, overexpression of NT3P75 - 2 significantly decreased neuronal apoptosis and increased number of SOX2 - positive cells. Taken together, our study demonstrated that early administration of NT3P75 - 2 enriched BMMSC supernatants significantly enhanced neuro-functional recovery after ICH by regulating neuroinflammation response, neuronal survival and increasing neural stem cell number, providing a new therapeutic strategy and direction for early treatment of ICH.

A nonhuman primate model of ischemic stroke is considered as an ideal preclinical model to replicate various aspects of human stroke because of their similarity to humans in genetics, neuroanatomy, physiology, and immunology. However, it remains challenging to produce a reliable and reproducible stroke model in nonhuman primates due to high mortality and variable outcomes. Here, we developed a focal cerebral ischemic model induced by topical application of 50% ferric chloride (FeCl3) onto the MCA-M1 segment through a cranial window in the cynomolgus monkeys. We found that FeCl3 rapidly produced a stable intraarterial thrombus that caused complete occlusion of the MCA, leading to the quick decrease of the regional cerebral blood flow in 10 min. A typical cortical infarct was detected 24 hours by magnetic resonance imaging (MRI) and was stable at least for 1 month after surgery. The sensorimotor deficit assessed by nonhuman primate stroke scale was observed at 1 day and up to 3 months after ischemic stroke. No spontaneous revascularization or autolysis of thrombus was observed, and vital signs were not affected. All operated cynomolgus monkeys survived. Our data suggested that FeCl3-induced stroke in nonhuman primates was a replicable and reliable model that is necessary for the correct prediction of the relevance of experimental therapeutic approaches in human beings.

Tumor metabolism characterized by aerobic glycolysis makes the Warburg effect a unique target for tumor therapy. Recent studies have found that glycogen branching enzyme 1 (GBE1) is involved in cancer progression. However, the study of GBE1 in gliomas is limited. We determined by bioinformatics analysis that GBE1 expression is elevated in gliomas and correlates with poor prognoses. In vitro experiments showed that GBE1 knockdown slows glioma cell proliferation, inhibits multiple biological behaviors, and alters glioma cell glycolytic capacity. Furthermore, GBE1 knockdown resulted in the inhibition of the NF-κB pathway as well as elevated expression of fructose-bisphosphatase 1 (FBP1). Further knockdown of elevated FBP1 reversed the inhibitory effect of GBE1 knockdown, restoring glycolytic reserve capacity. Furthermore, GBE1 knockdown suppressed xenograft tumor formation in vivo and conferred a significant survival benefit. Collectively, GBE1 reduces FBP1 expression through the NF-κB pathway, shifting the glucose metabolism pattern of glioma cells to glycolysis and enhancing the Warburg effect to drive glioma progression. These results suggest that GBE1 can be a novel target for glioma in metabolic therapy.

Rationale: Cell reprogramming technology is utilized to prevent cancer progression by transforming cells into terminally differentiated, non-proliferating states. Polypyrimidine tract binding protein 1 (PTBP1) is an RNA binding protein required for the growth of neurons and may directly transform multiple normal human cells into functioning neurons in vitro and in vivo when expressed at low levels. As a result, we identified it as a key to inhibiting cancer cell proliferation by boosting glioblastoma cell neural differentiation. Methods: Immunocytofluorescence (ICF) targeting TUJ1, MAP2, KI67, and EdU were utilized to evaluate glioblastoma cell reprogramming under PTBP1 knockdown or other conditions. PTBP1 and other target genes were detected using Western blotting and qRT-PCR. Activating protein phosphatase 2A (PP2A) and RhoA were detected using specific kits. CCK8 assays were employed to detect cell viability. Bioluminescence, immunohistofluorescence (IHF), and Kaplan-Meier survival analyses were utilized to demonstrate the in vivo reprogramming efficiency of PTBP1 knockdown in U87 murine glioblastoma model. In this study, RNA-seq technology was used to examine the intrinsic pathway. Results: The expression of TUJ1 and MAP2 neural markers, as well as the absence of KI67 and EdU proliferative markers in U251, U87, and KNS89 cells, indicated that glioblastoma cell reprogramming was successful. In vivo, U87 growth generated xenografts was substantially shrank due to PTBP1 knockdown induced neural differentiation, and these tumor-bearing mice had a prolonged survival time. Following RNA-seq, ten potential downstream genes were eliminated. Lentiviral interference and inhibitors blocking tests demonstrated that UNC5B receptor and its downstream signaling were essential in the neural differentiation process mediated by PTBP1 knockdown in glioblastoma cells. Conclusions: Our results indicate that PTBP1 knockdown promotes neural differentiation of glioblastoma cells via UNC5B receptor, consequently suppressing cancer cell proliferation in vitro and in vivo, providing a promising and feasible approach for glioblastoma treatment.

Background The treatment for spontaneous intracerebral hemorrhage (ICH) is still controversial, especially for hematomas in the basal ganglia. A retrospective case-control study with propensity score matching was performed to compare the outcomes of conventional craniotomy and conservative treatment for patients with minor ICH in the basal ganglia. Methods We retrospectively collected the data of consecutive patients with minor basal ganglia hemorrhage from January 2018 to August 2019. We compared clinical outcomes of two groups using propensity score matching. The extended Glasgow outcome scale obtained by phone interviews based on questionnaires at a 12-month follow-up was used as the primary outcome measure. According to a previous prognosis algorithm, patients were divided into good and poor prognosis groups to obtain a dichotomized (favorable or unfavorable) outcome as the primary outcome. Secondary outcomes included hospitalized complications, mortality, and modified Rankin score at 12 months. Results A total of 54 patients were analyzed, and the baseline characteristics of patients in the surgery and conservative treatment groups were well matched. The primary favorable outcome at 12 months was significantly higher in the conservative treatment group than in the surgery group (81% vs 44%; OR 1.833, 95% CI 1.159–2.900; P =0.005). The incidence of pneumonia in the surgery group was significantly higher than that in the conservative treatment group ( P =0.005). Conclusions It is not recommended to undertake conventional craniotomy for patients with a minor hematoma (25–40 ml) in the basal ganglia. An open craniotomy might induce worse long-term functional outcomes than the conservative treatment.

Bone marrow mesenchymal stem cells (BMMSCs)-based therapy has emerged as a promising novel therapy for Traumatic Brain Injury (TBI). However, the therapeutic quantity of viable implanted BMMSCs necessary to initiate efficacy is still undetermined. Increased oxidative stress following TBI, which leads to the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase signaling pathway, has been implicated in accounting for the diminished graft survival and therapeutic effect. To prove this assertion, we silenced the expression of NADPH subunits (p22-phox, p47-phox, and p67-phox) and small GTPase Rac1 in BMMSCs using shRNA. Our results showed that silencing these proteins significantly reduced oxidative stress and cell death/apoptosis, and promoted implanted BMMSCs proliferation after TBI. The most significant result was however seen with Rac1 silencing, which demonstrated decreased expression of apoptotic proteins, enhanced in vitro survival ratio, reduction in TBI lesional volume and significant improvement in neurological function post shRac1-BMMSCs transplantation. Additionally, two RNA-seq hub genes (VEGFA and MMP-2) were identified to play critical roles in shRac1-mediated cell survival. In summary, we propose that knockdown of Rac1 gene could significantly boost cell survival and promote the recovery of neurological functions after BMMSCs transplantation in TBI mice.

目的 分析神经重症监护室仪器设备管理现状,探讨改进对策.方法 2020年8月—2020年10月医院仪器设备采用传统纸质管理,2020年11月—2021年1月医院仪器设备应用二维码管理.比较应用二维码管理前后仪器管理情况(包括仪器规范登记、及时维护、时钟准确、性能完好、有效使用率)、护理人员满意度及护士仪器相关理论、操作、应急处置考核成绩.结果 应用二维码管理后,仪器规范登记、及时维护、时钟准确、性能完好、有效使用率均高于应用前(p<0.05);护理人员满意度明显提升(p<0.05);护士仪器相关理论知识、操作、仪器故障应急处置考核成绩均高于应用前(p<0.05).结论 应用二维码管理仪器设备,不仅能规范仪器设备的使用,而且能够提高护士仪器相关理论知识、操作、仪器故障应急处置水平,提高工作效率.

目的 观察改良吸痰法对非人工气道患者减少肺部感染的应用效果.方法 2020年1—11月该院收治的脑出血、脑梗死、蛛网膜下腔出血且未建立人工气道的患者77例,随机分为观察组39例与对照组38例.观察组采用改良的吸痰手法,对照组参照基础护理学采用普通吸痰手法.比较两组吸痰前与吸痰后两小时动脉血气分析中PaO2、PaCO2水平,气道黏膜损伤及肺部感染发生情况.结果 两组吸痰后两小时PaO2水平较吸痰前上升,PaCO2水平较吸痰前下降,且观察组PaO2水平明显高于对照组;观察组每日吸痰次数少于对照组,气道黏膜损伤率(15.4％)和肺部感染发生率(20.5％)低于对照组(36.8％、44.7％),差异均有统计学意义(P<0.05).结论 改良吸痰手法能有效帮助未建立人工气道患者排出痰液,降低肺部感染发生率,改善患者预后.

Adult neurogenesis plays critical roles in maintaining brain homeostasis and responding to neurogenic insults. However, the adult mammalian spinal cord lacks an intrinsic capacity for neurogenesis. Here we show that spinal cord injury (SCI) unveils a latent neurogenic potential of NG2+ glial cells, which can be exploited to produce new neurons and promote functional recovery after SCI. Although endogenous SOX2 is required for SCI-induced transient reprogramming, ectopic SOX2 expression is necessary and sufficient to unleash the full neurogenic potential of NG2 glia. Ectopic SOX2-induced neurogenesis proceeds through an expandable ASCL1+ progenitor stage and generates excitatory and inhibitory propriospinal neurons, which make synaptic connections with ascending and descending spinal pathways. Importantly, SOX2-mediated reprogramming of NG2 glia reduces glial scarring and promotes functional recovery after SCI. These results reveal a latent neurogenic potential of somatic glial cells, which can be leveraged for regenerative medicine.

We aim to evaluate the tumor metabolic suppressive activity of Oridonin (extract of Rabdosia rubescens) in glioma and elucidate its potential mechanism. Effects of Oridonin on U251/U87 cells were determined by CCK8, RTCA, colony formation, flow cytometry, wound healing, and Transwell assay. Xenograft tumor model to evaluate the effect of Oridonin on glioma cells in vivo. Cellular bioenergetics were measured by Seahorse. RNA-seq was performed to screen potential biological pathways in Oridonin treated cells. Bioinformatics analysis of PCK2 in glioma was performed based on TCGA/CGGA. Endogenous PCK2 was knocked-down by lentivirus packaged shRNA. We found Oridonin significantly inhibited cell growth in U251/U87 in vitro and in vivo. Both oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were decreased in Oridonin-treated U251/U87 cells. Oridonin treatment led to PCK2 down-regulation. Additionally, PCK2 was up-regulated in higher grade glioma and correlated with poor outcomes. Furthermore, PCK2 depletion significantly inhibited cell growth and decreased OCR/ECAR in U251/U87 which coincided with the effects of Oridonin. Therefore, we evaluated the potent anti-tumor property of Oridonin in glioma. Importantly, we demonstrated that PCK2 might be a novel target of Oridonin on glioma by inducing energy crisis and increasing oxidative stress.