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Respiratory syncytial virus (RSV) infection in airway epithelial cells is the main cause of bronchiolitis in children. Excessive mucus secretion is one of the primary symbols in RSV related lower respiratory tract infections (RSV‐related LRTI). However, the pathological processes of mucus hypersecretion in RSV‐infected airway epithelial cells remains unclear. The current study explores the involvement of miR‐34b/miR‐34c in mucus hypersecretion in RSV‐infected airway epithelial cells by targeting FGFR1. First, miR‐34b/miR‐34c and FGFR1 mRNA were quantified by qPCR in throat swab samples and cell lines, respectively. Then, the luciferase reporters’ assay was designed to verify the direct binding between FGFR1 and miR‐34b/miR‐34c. Finally, the involvement of AP‐1 signalling was assessed by western blot. This study identified that miR‐34b/miR‐34c was involved in c‐Jun‐regulated MUC5AC production by targeting FGFR1 in RSV‐infected airway epithelial cells. These results provide some useful insights into the molecular mechanisms of mucus hypersecretion which may also bring new potential strategies to improve mucus hypersecretion in RSV disease.

Gliomas, originating from the glial cells, are the most lethal type of primary tumors in the central nervous system. Standard treatments like surgery have not significantly improved the prognosis of glioblastoma patients. Recently, immune therapy has become a novel and effective option. As a conserved group of transcriptional regulators, the Sry-type HMG box (SOX) family has been proved to have a correlation with numerous diseases. Based on the large-scale machine learning, we found that the SOX family, with significant immune characteristics and genomic profiles, can be divided into two distinct clusters in gliomas, among which SOX10 was identified as an excellent immune regulator of macrophage in gliomas. The high expression of SOX10 is related to a shorter OS in LGG, HGG, and pan-cancer groups but benefited from the immunotherapy. It turned out in single-cell sequencing that SOX10 is high in neurons, M1 macrophages, and neural stem cells. Also, macrophages are found to be elevated in the SOX10 high-expression group. SOX10 has a positive correlation with macrophage cytokine production and negative regulation of macrophages’ chemotaxis and migration. In conclusion, our study demonstrates the outstanding cluster ability of the SOX family, indicating that SOX10 is an immune regulator of macrophage in gliomas, which can be an effective target for glioma immunotherapy.

Traditional glioblastoma (GBM) cell lines do not maintain the heterogeneity of the original tumor, cell interactions, and therapy response, thus limiting their investigation in GBM theranostics. Herein, a kind of GBM tumor-targeting nanoparticles (NPs) TCFNP@iRGD are designed and constructed, which are generated by photoacoustic (PA) contrast agent 2-(3-cyano-4,5,5-trimethylfuran-2(5H)-ylidene) malononitrile (TCF)-OH through facile nanoprecipitation and decorated with an active targeting ligand iRGD. Their potential in GBM detection via PA imaging on glioma patient-derived cells intracranial xenograft models is evaluated for the first time. Excellent tumor-specific PA mapping performance of GBM is realized by TCFNP@iRGD, demonstrating its promising potential in the clinical diagnosis of GBM.

Aging has a significant role in the proliferation and development of cancers. This study explored the expression profiles, prognostic value, and potential roles of aging-related genes in gliomas. We designed risk score and cluster models based on aging-related genes and glioma cases using LASSO Cox regression analysis, consensus clustering analysis and univariate cox regression analyses. High risk score was related to malignant clinical features and poor prognosis based on 10 datasets, 2953 cases altogether. Genetic alterations analysis revealed that high risk scores were associated with genomic aberrations of aging-related oncogenes. GSVA analysis exhibited the potential function of the aging-related genes. More immune cell infiltration was found in high-risk group cases, and glioma patients in high-risk group may be more responsive to immunotherapy. Knock-down of CTSC, an aging-related gene, can inhibit cell cycle progression, colony formation, cell proliferation and increase cell senescence in glioma cell lines in vitro. Indeed, high expression of CTSC was associated with poor prognosis in glioma cases. In conclusion, this study revealed that aging-related genes have prognostic potential for glioma patients and further identified potential mechanisms for aging-related genes in tumorigenesis and progression in gliomas.

Idiopathic normal pressure hydrocephalus (iNPH) is a rare neurological disorder with no clear prevalence factors and is a significant danger to the elderly. The intracranial glymphatic system is the internal environment that maintains brain survival and metabolism, and thus fluid exchange changes in the glymphatic system under various pathological conditions can provide important insights into the pathogenesis and differential diagnosis of many neurodegenerative diseases such as iNPH. iNPH can be diagnosed using a combination of clinical symptoms, imaging findings and history, and cerebrospinal fluid biomarkers due to the glymphatic system disorder. However, only few researchers have linked the two. Shunt surgery can improve the glymphatic system disorders in iNPH patients, and the surgical approach is determined using a combination of clinical diagnosis and trials. Therefore, we have composed this review to provide a future opportunity for elucidating the pathogenesis of iNPH based on the glymphatic system, and link the glymphatic system to the diagnosis and treatment of iNPH. The review will provide new insights into the medical research of iNPH.

Severe RSV infection is the main cause of hospitalization to children under the age of five. The regulation of miRNAs on the severity of RSV infection is unclear. The aim of the study was to identify the critical differential expression miRNAs (DE miRNAs) that can regulate the pathological response in RSV‐infected airway epithelial cells. In this study, miRNA and mRNA chips of RSV‐infected airway epithelia from Gene Expression Omnibus (GEO) were screened and analysed, separately. DE miRNAs‐targeted genes were performed for further pathway and process enrichment analysis. DE miRNA‐targeted gene functional network was constructed on the basis of miRNA‐mRNA interaction. The screened critical miRNA was also investigated by bioinformatics analysis. Then, RSV‐infected human bronchial epithelial cells (HBECs) were constructed to verify the expression of the DE miRNAs. Finally, specific synthetic DE miRNAs mimics were used to confirm the effect of DE miRNAs on the RSV‐infected HBECs. 45 DE miRNAs were identified from GEO62306 dataset. Our results showed that hsa‐mir‐34b‐5p and hsa‐mir‐34c‐5p decreased significantly in HBECs after RSV infection. Consistent with the biometric analysis, hsa‐mir‐34b/c‐5p is involved in the regulation of mucin expression gene MUC5AC. In RSV‐infected HBECs, the inducement of MUC5AC production by decreased hsa‐mir‐34b/c‐5p was partly mediated through activation of c‐Jun. These findings provide new insights into the mechanism of mucus obstruction after RSV infection and represent valuable targets for RSV infection and airway obstruction treatment.

Airway epithelial cells (AECs) play a key role in asthma susceptibility and severity. Integrin β4 (ITGB4) is a structural adhesion molecule that is down-regulated in the airway epithelium of asthma patients. Although a few studies hint toward the role of ITGB4 in asthmatic inflammation pathogenesis, their specific resultant effects remain unexplored. In the present study, we determined the role of ITGB4 of AECs in the regulation of Th2 response and identified the underpinning molecular mechanisms. We found that ITGB4 deficiency led to exaggerated lung inflammation and AHR with higher production of CCL17 in house dust mite (HDM)-treated mice. ITGB4 regulated CCL17 production in AECs through EGFR, ERK and NF-κB pathways. EFGR-antagonist treatment or the neutralization of CCL17 both inhibited exaggerated pathological marks in HDM-challenged ITGB4-deficient mice. Together, these results demonstrated the involvement of ITGB4 deficiency in the development of Th2 responses of allergic asthma by down-regulation of EGFR and CCL17 pathway in AECs.

Brain metastasis (BM), a devastating complication of advanced malignancy, has a high incidence in non-small cell lung cancer (NSCLC). As novel systemic treatment drugs and improved, more sensitive imaging investigations are performed, more patients will be diagnosed with BM. However, the main treatment methods face a high risk of complications at present. Therefore, based on immunotherapy of tumor immune microenvironment has been proposed. The development of NSCLC and its BM is closely related to the tumor microenvironment, the surrounding microenvironment where tumor cells live. In the event of BM, the metastatic tumor microenvironment in BM is composed of extracellular matrix, tissue-resident cells that change with tumor colonization and blood-derived immune cells. Immune-related cells and chemicals in the NSCLC brain metastasis microenvironment are targeted by BM immunotherapy, with immune checkpoint inhibition therapy being the most important. Blocking cancer immunosuppression by targeting immune checkpoints provides a suitable strategy for immunotherapy in patients with advanced cancers. In the past few years, several therapeutic advances in immunotherapy have changed the outlook for the treatment of BM from NSCLC. According to emerging evidence, immunotherapy plays an essential role in treating BM, with a more significant safety profile than others. This article discusses recent advances in the biology of BM from NSCLC, reviews novel mechanisms in diverse tumor metastatic stages, and emphasizes the role of the tumor immune microenvironment in metastasis. In addition, clinical advances in immunotherapy for this disease are mentioned.

The choroid plexus is a tissue located in the lateral ventricles of the brain and is composed mainly of choroid plexus epithelium cells. The main function is currently thought to be the secretion of cerebrospinal fluid and the regulation of its pH, and more functions are gradually being demonstrated. Assistance in the removal of metabolic waste and participation in the apoptotic pathway are also the functions of choroid plexus. Besides, it helps to repair the brain by regulating the secretion of neuropeptides and the delivery of drugs. It is involved in the immune response to assist in the clearance of infections in the central nervous system. It is now believed that the choroid plexus is in an inflammatory state after damage to the brain. This state, along with changes in the cilia, is thought to be an abnormal physiological state of the choroid plexus, which in turn leads to abnormal conditions in cerebrospinal fluid and triggers hydrocephalus. This review describes the pathophysiological mechanism of hydrocephalus following choroid plexus epithelium cell abnormalities based on the normal physiological functions of choroid plexus epithelium cells, and analyzes the attempts and future developments of using choroid plexus epithelium cells as a therapeutic target for hydrocephalus.

Linear scleroderma is the most common type of localized scleroderma in children. Lesions rarely involve areas other than the skin, and nervous system involvement is even rare. We reported a case of a 6-year-old girl who was admitted to the hospital with recurrent seizures for 4 weeks. Before that, she had left frontal plaques for more than 1 year. Radiological imaging of the brain showed multiple abnormal lesions and skin biopsy of the plaques indicated scleroderma. After drug therapy, the girl had no recurrence of epilepsy, and no obvious abnormalities were found in the reexamination of neuroimaging. We performed further radiological examination on this patient and reviewed the literatures for this rare case.

The pentraxin is a superfamily of proteins with the same domain known as the pentraxin domain at C-terminal. This family has two subgroups, namely; short pentraxins (C-reactive protein and serum amyloid P component) and long pentraxins (neuronal pentraxin 1, neuronal pentraxin 2, neuronal pentraxin receptor, pentraxin 3 and pentraxin 4). Each group shares a similar structure with the pentameric complexes arranged in a discoid shape. Previous studies revealed the functions of different pentraxin family members. Most of them are associated with human innate immunity. Inflammation has commonly been associated with tumor progression, implying that the pentraxin family might also participate in tumor progression. Therefore, we reviewed the basic characteristics and functions of the pentraxin family and their role in tumor progression.

Asthma and bronchiectasis are known to be two distinct diseases with different etiology, pathophysiology, management, and prognosis. However, a high prevalence of bronchiectasis has been reported in patients with severe asthma. Thus, it is of great importance to identify the impact of bronchiectasis on asthmatic patients.Databases including PubMed, Embase, Cochrane, Web of Science were searched comprehensively to identify relevant human clinical studies published until February 2020.Two investigators (Gelei Lan and Guochao Shi) independently obtained the potentially eligible articles based on their titles and abstracts. When opinions differed between the investigators, discussions were made to reach an agreement. The authors of the included studies were contacted for inquiry when necessary.Six observational studies with 1004 patients were included in the meta-analysis. The mean prevalence of bronchiectasis in patients with asthma was 35.2% (ranging from 2.2% to 47%). Asthmatic patients with bronchiectasis were older, had a longer disease duration, exhibited greater severity, and showed more frequent exacerbations and hospitalization, and poorer lung function, compared with the patients without bronchiectasis.Despite of the heterogeneity between included studies and detectable publication bias, this meta-analysis demonstrated the impact of comorbid bronchiectasis on asthmatic patients. Thus, coexistence of bronchiectasis should be considered a clinical phenotype of asthma, which may have associations with exacerbation and hospitalization.

Malignant gliomas remain significant challenges in clinic and pose dismal prognosis on patients. In this study, we focused on growth arrest-specific 5 (GAS5), a tumor suppressive long non-coding RNA in glioma, explored its crosstalk with miR-424, and examined their biological functions in glioma. Expressions of GAS5 and miR-424 were measured using qRT-PCR. The regulation of GAS5 on miR-424 expression was examined in GAS5-overexpressing glioma cells by combining methylation-specific PCR, western blotting, and RNA immunoprecipitation. Functional significance of GAS5 and miR-424 on in vitro cell proliferation, apoptosis, migration, invasion, and in vivo tumor growth was examined using colony formation, flow cytometry, wound healing, transwell assay, and the xenograft model, respectively. The potential targeting of AKT3 by miR-424 was investigated using luciferase reporter assay. GAS5 and miR-424 were significantly down-regulated in glioma cells. GAS5 directly interacted with enhancer of zeste homolog 2 (EZH2), stimulated the formation of polycomb repressive complex 2 (PRC2), reduced the levels of DNA methyltransferases (Dnmts), alleviated promoter methylation of miR-424, and promoted miR-424 expression. Functionally, GAS5, by up-regulating miR-424, inhibited cell proliferation, migration, and invasion, while increased apoptosis of glioma cells in vitro, and suppressed xenograft growth in vivo. miR-424 directly inhibited AKT3 and altered the expressions of AKT3 targets, cyclinD1, c-Myc, Bax, and Bcl-2, which might contribute to its tumor suppressive activities. GAS5, by inhibiting methylation and boosting expression of miR-424, inhibits AKT3 signaling and suppresses multiple malignant phenotypes. Therefore, stimulating GAS5/miR-424 signaling may benefit the treatment of glioma.

Hydrocephalus is a common neurological disease with complex etiology. It is characterized by the accumulation and continuous growth of cerebrospinal fluid in the ventricular system and subarachnoid space. Hydrocephalus can be caused by congenital genetic factors, brain trauma and cerebral hemorrhage. Through the efforts of many researchers, the pathogenesis of hydrocephalus is being completed, but it has not been fully explained. The imbalance of cerebrospinal fluid production and absorption into the sinus, and disorder of the cerebrospinal fluid circulation pathway or the osmotic pressure maintenance in the ventricle can lead to increased cerebrospinal fluid and ventricular dilatation.脑积水是一种常见但病因复杂的神经系统疾病，以脑脊液在脑室系统及蛛网膜下腔内聚积并不断增长为特征，既可由先天性遗传因素导致，也可由后天脑外伤、脑出血等疾病诱发。脑脊液的产生与被吸收进入静脉窦的不平衡、脑脊液循环通路受阻或者脑室内渗透压维持功能紊乱均能导致脑脊液增多、脑室扩张。.

To explore the clinical characters, treatment and prognosis for pediatric optic pathway gliomas (OPGs). Methods: A total of 26 patients with OPGs, who were diagnosed and treated at Neurosurgery of Xiangya Hospital of Central South University between June 2010 and November 2017, were retrospectively reviewed, and their average age was 5.5 years old. The influential factors for patients' progression-free survival (PFS) and overall survival (OS) were analyzed. Results: All patients were classified into Type II and Type III based on Dodge classification and received surgery treatment. Vision was improved after surgery in 20 patients. Twenty-four patients (92.3%) were continually followed up, and 14 patients (58.3%) received post-radiation treatment. Twenty-one patients were still alive and 15 patients' symptoms were not progressed. The PFS and OS in patients received radiation therapy were better than those without radiation therapy (PFS: P0.01; OS: P0.05). The postoperative visual prognosis might be related to the choice of surgical approach. Conclusion: Treatment of children with OPGs should include surgery and postoperative radiotherapy. The eyesight protection in surgery is as important as tumor resection.目的：探讨儿童视路胶质瘤(optic pathway gliomas，OPGs)的临床特点、治疗方法及预后情况。方法：回顾性分析湘雅医院神经外科自2010年6月至2017年11月收治的26例OPGs患儿的临床及随访资料，平均年龄为5岁6个月，分析视力、总生存及无进展生存的影响因素。结果：本组患儿均为DodgeII型和III型，且接受肿瘤切除手术，术后患儿视力好转20例。随访了24例(92.3%)患儿，14例接受放射治疗，总生存21例，无进展生存15例。接受放射治疗患儿无进展生存及总生存均优于未接受放射治疗患儿，差异均具有统计学意义(无进展生存：P0.01；总生存：P0.05)；患儿术后视力预后与手术入路的选择相关。结论：儿童视路胶质瘤的治疗应包括手术与术后放射治疗。为保证患儿术后生活质量，保护视力与切除肿瘤同样重要。.

Intracranial Rosai-Dorfman disease (RDD) is a rare clinical histiocytosis proliferative disease. A 12-year-old boy with dizziness and headache for 1 month was admitted into Pediatric Neurosurgery of Xiangya Hospital, Central South University. The patient underwent total tumor resection and postoperative application of hormones and chemotherapy. During follow-up of 8 months, patient's condition was stable and no tumor recurrence was observed. For patient with a trend of tumor progression, stereotactic biopsy can help to confirm the diagnosis and determine the surgical strategy such as disposal of bone flaps. The treatment is mainly based on surgical intervention, supplemented by radiotherapy, chemotherapy and hormone therapy. Without affecting the nerve function, the surgeon should try to completely resect the tumor.颅内Rosai-Dorfman病(Rosai-Dorfman disease，RDD)是一类临床罕见的组织细胞增生性疾病。中南大学湘雅医院收治1例12岁颅内RDD患儿，主诉为头痛、头晕1个月，行肿瘤全切除手术，术后应用激素及化学药物治疗。随访8个月，病情稳定，未见肿瘤复发。对于此类肿瘤且有进展趋势者，应用立体定向活检术有助于明确诊断及手术方案的选择(如骨瓣取舍等)。本病以手术干预为主，辅以放射治疗、化学药物治疗及激素治疗等方案，且手术应在不影响神经功能的情况下力求全切肿瘤。.

In this study, our findings indicated that FOXO1 expression frequently decreased in glioma tissues and cells. FOXO1 expression decrease correlated with glioma progression and predicted a worse overall survival of glioma patients. Restored FOXO1 expression inhibited glioma cells invasion and suppressed glioma cells proliferation in vitro and growth in vivo. Additionally, we found that KLF4 expression frequently increased in glioma tissues and negatively correlated with FOXO1 expression. Bioinformatics analysis and experimental results indicated that KLF4 transcriptionally repressed FOXO1 expression in glioma cells. Moreover, KLF4 expression increase correlated with glioma progression and predicted a poorer overall survival of glioma patients. KLF4 knockdown attenuated glioma cells invasion and growth. These data provide a rationale for targeted intervention on KLF4-FOXO1 signaling pathway to suppress glioma progression.

Objective To evaluate the outcomes of 177 cases of craniopharyngioma (CP) treated via a unilateral subfrontal approach. Methods A total of 177 continuous microscopic surgeries were performed by the senior author (Y.X.). The tumors were divided into 6 groups using the diaphragm sellae and the third ventricle floor as the anatomic references. The preoperative, postoperative, and long-term follow-up data were analyzed to evaluate the extent of tumor resection, recurrence, and functional status. Results The subfrontal-basal approach was used in 169 (91.4%) cases. Total resection was achieved in 167 (94.4%) cases. A total of 158 patients were followed from 6 to 130 months. There were 3 perioperative and 23 delayed deaths. Twenty-two patients had tumor recurrence (12.7%). The progression-free survival was 80% at 5 years and 72% at 10 years. The overall survival was 84.0% at 2.5 years and 83.2% at 10 years. There was a significant increase of pituitary dysfunction after total resection. Neurologic function was stable in most patients. Rate of hypothalamic dysfunction and mortality were higher in patients with intraventricular CPs. Of the surviving patients, 91.8% were living independently with acceptable morbidities at the end of the study. Conclusions Most CPs extend along the intrasellar-suprasellar-third ventricle axis. A subfrontal-basal approach is a simple, safe, and effective approach to resecting CPs extending along the vertical axis. A translamina terminalis approach is an ideal corridor to resect intraventricular CP. The benefit of radical resection remains controversial, especially for CPs involving the infundibulotuberal region.

To evaluate the value of shunting surgery in the treatment for patients with meningeal carcinomatosis. Methods: The therapeutic process of shunting surgery was analyzed in 5 meningeal carcinomatosis patients. Results: The intracranial pressure could effectively be controlled, and the associated symptoms could be relieved. No complications associated with shunting surgery were found during the hospitalization and follow-up. One patient, who did not receive the surgery, died in 2 months later. Conclusion: Shunting surgery can effectively relieve the intracranial pressure caused by meningeal carcinomatosis, decrease the mortality and morbidity caused by intractable intracranial hypertension in these patients, and improve their live quality.目的：评估分流手术在癌性脑膜病患者治疗中的价值。方法：回顾性分析5例采取分流手术治疗的癌性脑膜病患者的治疗经过。结果：5例患者颅内压得到了有效的控制，相关症状明显缓解。住院期间及随访期间未发现与分流手术相关的并发症。1例患者未实施分流手术，2月后死亡。结论：分流手术可有效缓解癌性脑膜病所致的颅内压增高，可减少因顽固性颅高压所致的死亡与残障，可提高癌症患者的生活质量。.

Altres ajuts: This work was supported by Celyad, SA (Mont-Saint-Guibert, Belgium). Celyad has received research grants from the Walloon Region (Belgium, DG06 funding). Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort. This multinational, randomized, double-blind, sham-controlled study was conducted in 39 hospitals. Patients with symptomatic ischaemic heart failure on guideline-directed therapy (n = 484) were screened; n = 348 underwent bone marrow harvest and mesenchymal stem cell expansion. Those achieving > 24 million mesenchymal stem cells (n = 315) were randomized to cardiopoietic cells delivered endomyocardially with a retention-enhanced catheter (n = 157) or sham procedure (n = 158). Procedures were performed as randomized in 271 patients (n = 120 cardiopoietic cells, n = 151 sham). The primary efficacy endpoint was a Finkelstein–Schoenfeld hierarchical composite (all-cause mortality, worsening heart failure, Minnesota Living with Heart Failure Questionnaire score, 6-min walk distance, left ventricular end-systolic volume, and ejection fraction) at 39 weeks. The primary outcome was neutral (Mann–Whitney estimator 0.54, 95% confidence interval [CI] 0.47–0.61 [value > 0.5 favours cell treatment], P = 0.27). Exploratory analyses suggested a benefit of cell treatment on the primary composite in patients with baseline left ventricular end-diastolic volume 200–370 mL (60% of patients) (Mann–Whitney estimator 0.61, 95% CI 0.52–0.70, P = 0.015). No difference was observed in serious adverse events. One (0.9%) cardiopoietic cell patient and 9 (5.4%) sham patients experienced aborted or sudden cardiac death. The primary endpoint was neutral, with safety demonstrated across the cohort. Further evaluation of cardiopoietic cell therapy in patients with elevated end-diastolic volume is warranted.

A number of microRNAs have been identified to be important regulators of tumorigenesis. Previous research has shown that miR-124 is abundantly expressed in normal brain tissue; however, only a few reports have focused on the biological impact of miR-124 on glioma cells, and the underlying mechanisms need to be elucidated. Therefore, we investigated the effect of miR-124a on glioma cell proliferation and invasion; furthermore, the underlying molecular mechanism was examined. The present study demonstrated that miR-124a expression was downregulated in human glioma tissues, and its expression level was negatively correlated with the pathological grade of the glioma. Restoration of miR-124a inhibited glioma cell proliferation and invasion in vitro. Furthermore, we found that miR-124a directly targeted and suppressed IQ motif containing GTPase activating protein 1 (IQGAP1), a well-known regulator of actin dynamics and cell motility. RNA interference assay showed that IQGAP1 knockdown led to downregulation of β-catenin and downstream cyclin D1. Taken together, our study revealed that miR-124a could inhibit glioma cell proliferation and invasion by blocking the expression of the IQGAP1 gene and downstream β-catenin and cyclin D1. This research may provide a useful molecular therapy for gliomas.

To evaluate the time and effect of shunt operation on cryptococcal meningitis. A total 7 patients received shunt operation for the therapy of cryptococcal meningitis patients and the data was retrospectively analyzed. Intracranial hypertension-caused symptoms were resolved immediately. There was no complication, no infection dissemination and no recrudescence of cryptococcal meningitis. Shunt operation is effective for intracranial hypertension caused by cryptococcal meningitis. It does not affect the antifungal treatment.目的：探讨分流手术在新型隐球菌脑膜炎患者治疗中的时机并评价其疗效。方法：回顾性分析7例采取分流手术治疗新型隐球菌脑膜炎患者的经过。结果：7例患者颅内压得到了有效的控制，相关症状明显缓解。住院及随访期间未出现与分流手术相关的并发症，未发生因分流手术造成的隐球菌播散及难治性隐球菌感染，也未发生因此导致的感染复燃。结论：分流手术可以有效缓解新型隐球菌脑膜炎所致的颅内压增高，且不对抗隐球菌的治疗产生不良影响。.

To explore the treatment and pathophysiology of extra-axil cerebrospinal fluid accumulation aft er skull surgery.The treatment of 46 cases of pineal regional tumor was retrospectively studied.The CT showed that all patients had postoperative extra-axil cerebrospinal fluid accumulation in 6 hours after operation. 5 cases displayed symptomatic accumulation of extra-axil cerebrospinal fluid. 1 died 30 days aft er discharge, 4 performed S-P shunt and 3 of them switched to V-P shunt after S-P shunt failed.Much more attention should be paid to postoperative accumulation of extra-axil cerebrospinal fluid. Both V-P and S-P are the effective strategies of therapy.

Glioblastoma (GBM) is the most lethal brain tumor due to the resistance to conventional therapies, such as radiotherapy and chemotherapy. TAZ, an important mediator of the Hippo pathway, was found to be up-regulated in diverse cancers, including in GBM, and plays important roles in tumor initiation and progression. However, little is known about the regulation of TAZ expression in tumors. In this study, we found that miR-125a-5p is an important regulator of TAZ in glioma cells by directly targeting the TAZ 3' UTR. MiR-125a-5p levels are inversely correlated with that of TAZ in normal astrocytes and a panel of glioma cell lines. MiR-125a-5p represses the expression of TAZ target genes, including CTGF and survivin, and inhibits cell proliferation and induces the differentiation of GBM cells; whereas over-expression of TAZ rescues the effects of miR-125a-5p. This study revealed a mechanism for TAZ deregulation in glioma cells, and also demonstrated a tumor suppressor role of miR-125a-5p in glioblastoma cells.

Glioma is the most common malignant and fatal primary tumor in the central nervous system in adults. Recent data has suggested a profound role for microRNAs (miRs) in cancer progression. The present study demonstrated, via quantitative polymerase chain reaction (qPCR) analysis, that miR-203 expression was markedly lower in highly invasive U87MG glioma cells and glioma tissues. Wound healing and Transwell assays demonstrated that restoration of miR-203 expression inhibited U87MG cell migration and invasion. Restoration of miR-203 expression additionally sensitized the cells to temozolomide (TMZ) as determined by MTS assay. By contrast, miR-203 inhibition in A172 cells exerted opposite effects. Bioinformatic analysis combined with experimental analysis revealed that miR-203 directly targeted E2F3 via the conserved miR-203 target site within the E2F3 3'-untranslational region. E2F3 knockdown with specific small hairpin RNA also inhibited U87MG cell migration and invasion, and sensitized them to TMZ. Importantly, miR-203 and E2F3 showed inverse expression patterns in invasive glioma tissues, as demonstrated by qPCR and luciferase assay. These results suggested that miR-203 may function as a tumor suppressor in glioma progression and that the miR-203/E2F3 axis may be a novel candidate in the development of rational therapeutic strategies for glioma.