Increased intracranial pressure is common in patients with cerebral hydatid disease. CT and MRI are the first-line diagnostic procedures. Surgery is the treatment of choice for the majority of intracranial hydatid cysts. Multiple and deep seated lesions should receive medical treatment postoperatively.

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IntroductionCerebral vasospasm (CVS) is the most common neurological complication after aneurysmal subarachnoid hemorrhage (aSAH) and associated with poor functional outcome and mortality. Reports on incidence and predictors of CVS in Chinese patients with aSAH were scarce. We aimed to estimate the incidence and predictors of angiographic vasospasm (AV), symptomatic vasospasm (SV), and cerebral infarction in Chinese patients with aSAH.MethodsWe retrospectively reviewed the medical records of 542 consecutive aSAH patients admitted to neurosurgery department of the First Affiliated Hospital of Xinjiang Medical University in Urumqi city of China between January 1, 2011 and December 31, 2015. AV, SV and cerebral infarction were defined based on clinical data and neuroimaging findings. Univariate and multivariate analyses were performed to identify predictors of AV, SV or cerebral infarction.Results343 (63.3%) patients fulfilled the inclusion and exclusion criteria. Of them, 182(53.1%) developed AV, 99 (28.9%) developed SV, and 87 (25.4%) developed cerebral infarction. A history of hypertension, poor modified Fisher grade (3–4) and poor Hunt-Hess grade (4–5) on admission were common risk factors for AV, SV and cerebral infarction. Patients from Uyghur ethnic group or other minorities were less likely to develop AV, SV or cerebral infarction, compared to those from Han ethic group after adjustment of other potential confounders. Additionally, age ≥53 years, leukocyte count ≥11× 109/L on admission and being current or former smokers were independent risk factors of cerebral infarction. Leukocyte count ≥11× 109/L on admission and aneurysm size ≥ 10 mm were independent risk factors of SV. Serum glucose level ≥7.0 mmol/L on admission was an independent risk factor of AV.ConclusionRisk factors of different definitions of CVS were diverse in Chinese patients with aSAH; however, risk factors of SV and cerebral infarction seem to be similar. We recommend early and aggressive therapy in these patients at-risk of CVS.

The aim of this study was to investigate the changes in serum pituitary hormone levels and the mechanism of hyponatremia in aneurysmal subarachnoid hemorrhage (SAH). Nuclear medical tests and serum electrolyte monitoring were performed in 49 aneurysmal SAH cases and 10 healthy volunteers. The levels of serum pituitary hormones were significantly higher in the SAH patients compared with the control group on days 1–3 and 7–9 after SAH onset (P<0.05). The peak value occurred on days 7–9. The rate of hyponatremia was 49.0% in the 49 SAH patients. The incidence of severe hyponatremia was significantly higher in Fisher grades III–IV and Hunt-Hess grades III–IV compared with Fisher grades I–II and Hunt-Hess grades I–II, respectively (P<0.05). There was no correlation between the site of aneurysm and the rate of hyponatremia. The incidence of symptomatic cerebral vasospasm was significantly higher in the hyponatremia group and Fisher grades III–IV compared with the normal serum sodium group and Fisher grades I–II, respectively. Serum pituitary hormone levels were positively correlated with blood loss and disease severity in patients with aneurysmal SAH. Hyponatremia may be considered an important indicator of SAH. SAH patients are likely to benefit from intense monitoring and regulation of serum sodium.

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Background Lethal genes in low-grade gliomas (LGGs) may have an essential prognostic significance and therefore need to be systematically analyzed. The purpose of this study is to analyze essential genes correlated with cell survival by evaluating CRISPR-cas9 screening data, leading to the identification of novel treatment targets for patients. Methods In this study, genes related to cell viability from the Depmap CRISPR-cas9 screen were intersected to differentially expressed genes (DEGs) between tumor and GTEx normal tissues from TCGA. The LASSO regression method was used to construct a signature that used to anticipate overall survival in patients with LGG. An evaluation of the signature was carried out using both multivariate and univariate Cox regression. Then, we determined which key pathways were modulated by this signature by comparing DEGs between low- and high-risk patients. WGCNA was conducted to identify modules associated with high-risk. In this study, we also performed enrichment analysis to identify pathways mediated by DEGs, overlapping genes, and genes shared in the WGCNA. Finally, we used to western blot, qRT-PCR and IHC to detect the expression of hub genes. Results Using the TCGA database, 145 oncogenes were identified as overexpressed. These genes were intersected with lethal genes identified in the Depmap database, which are enriched in Hippo pathways. A total of 19 genes were used to construct the gene signature by means of LASSO regression. The median risk score (0.752324) was employed to distinguish between low- and high-risk patients. The patients with high-risk characteristics showed a shorter OS duration in the internal training, the internal validation, and the external validation datasets. Ultimately, the Hippo signaling pathway was the predominantly enriched pathway in 145 genes, DEGs, and 3 modular genes in WGCNA. Finally, we found differences of hub genes expression in different clinical samples. Importantly, protein and mRNA expression of REP65 was significantly up-regulated in tumor cells both in the public cohort and our cohort. Conclusion The hippo signaling pathway detected based on CRISPR-cas9 screening is a critical regulator of viability and tumor proliferation and therefore is an innovative new target for treating cancerous brain tumors, including LGG.

Lower WHO grade II and III gliomas (LGGs) are characterized by widespread genetic and transcriptional heterogeneity, yet little is known about the heterogeneity of the DNA Damage Repair (DDR), its function in tumor biology, coupling with the transcriptome and tumor microenvironment (TM) and its possible impact for tumor development. In this study, the DNA damage repair (DDR) alterations among LGG have been studied via multi-omics data integration. For this, LGG patients have been grouped into distinct subtypes (DDR-activated and the DDR-suppressed subtype) based on different clinicalparameters and molecular characteristics. The differences in gene mutation, immune spectrum, and immune cell infiltration between the two DDR subtypes were compared. We generated DDR subtype features (DDR scores) to implement DDR classification in LGG and confirmed the results using a multi-layer data cohort.The DDR activation subgroup was found to be associated with poorer overall survival based on molecular subtypes, and clinicopathological features of advanced-age and higher-grade were more common in the DDR-activated subgroup. DDR-suppressed subtypes also exhibited more frequent mutations in IDH1. We also found significant upregulation of activated immune cells in the DDR-activated subgroup, which indicates significant influence posed by infiltration of immune cells on tumor progression as well as immunotherapeutic responses. In addition, six DDR genes were selected to construct a DDR signature of LGG, dividing patients into low- and high-risk groups. The QRT-PCR results showed that the expression levels of CDK1, CDK2, TYMS, SMC4, and WEE1 were found to be considerably higher for LGG samples compared to normal brain tissue samples (p < 0.05).In conclusion, our work sheds light on the DDR heterogeneity of LGG and advances our knowledge of the molecular pathways in DDR that lead to LGG.

Background: Lower WHO grade II and III gliomas (LGGs) are characterized by widespread genetic and transcriptional heterogeneity, yet little is known about the heterogeneity of the DNA Damage Repair (DDR), its function in tumor biology, coupling with the transcriptome and tumor microenvironment (TM) and its possible impact for tumor development. Methods: In this study, we analyzed gene expression profiles downloaded from TCGA, CGGA, and GEO databases. The DNA damage repair (DDR) alterations among LGG have been studied via multi-omics data integration. For this, LGG patients have been grouped into distinct subtypes (DDR-activated and the DDR-suppressed subtype) based on different clinicalparameters and molecular characteristics. The differences in gene mutation, immune spectrum, and immune cell infiltration between the two DDR subtypes were compared. We generated DDR subtype features (DDR scores) to implement DDR classification in LGG and confirmed the results using a multi-layer data cohort. In addition, the characteristics of DDR subtypes predicted by immunotherapy responses and their roles in the tumor immune microenvironment (TIM) were explored. Result: The DDR activation subgroup was found to be associated with poorer overall survival based on molecular subtypes, and clinicopathological features of advanced-age and higher-grade were more common in the DDR-activated subgroup. DDR-suppressed subtypes also exhibited more frequent mutations in IDH1. We also found significant upregulation of activated immune cells in the DDR-activated subgroup, which indicates significant influence posed by infiltration of immune cells on tumor progression as well as immunotherapeutic responses. In addition, six DDR genes were selected to construct a DDR signature of LGG, dividing patients into low- and high-risk groups. Within the IMvigor210 cohort, there were fewer CR/PR groups in the high-score patients, as well as concomitant shorter survival times. CR/PR group had higher DDR characteristics scores compared to the SD/PD group. QRT-PCR results showed that the expression levels of CDK1, CDK2, TYMS, SMC4, and WEE1 were found to be considerably higher for LGG samples compared to normal brain tissue samples (p < 0.05). Conclusion: In conclusion, our work sheds light on the DDR heterogeneity of LGG and advances our knowledge of the molecular pathways in DDR that lead to LGG.