Background: PYD and CARD domain-containing (PYCARD) was upregulated in TMZ-resistant cell lines and glioma tissue and was correlated with poor prognosis, its role in glioma is unclear known. The aim of this study was to elucidate the relationship between PYCARD and glioma based on Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and Chinese Glioma Genome Atlas (CGGA) databases.Methods: Glioma-resistant cells were compared with parental cells based on the GSE53014 and GSE113510 data sets. The relationship between PYCARD, tumor microenvironment, and long noncoding RNAs (lncRNAs) was assessed using logistic regression. Moreover, Kaplan-Meier and Cox regression were used to analyze the relationship between PYCARD expression and survival rate. Gene set enrichment analysis (GSEA) was also used to determine the biological function of PYCARD and lncRNAs. Cell viability and cell migration assays were used to evaluate the ability of cells to migrate and proliferate. Finally, we analyzed the expression patterns of PYCARD genes in a wide range of cancers.Results: Elevated expression of PYCARD promoted glioma cell proliferation and migration. PYCARD expression was significantly positively associated with gamma delta T cells but negatively correlated with M2 macrophages in glioblastoma multiforme (GBM). Likewise, PYCARD expression was significantly positively associated with monocytes but negatively associated with activated mast cells in low grade glioma (LGG).We also found that 3 PYCARD-related lncRNAs in GBM and 4 PYCARD-related lncRNAs in LGG had a predictive value for glioma patients. The pan-cancer analysis showed that PYCARD expression was higher in most cancer groups.Conclusions: High expression of PYCARD is an independent predictor of unfavorable prognosis and chemotherapy resistance in glioma.

Cerebellar glioblastoma multiforme (cGBM) is rare in adults, accounting for <1% of all patients with glioblastoma multiforme (GBM). The accurate diagnosis of cGBM is important for establishing a suitable therapeutic schedule. However, the diagnosis of cerebellar GBM is not usually suspected preoperatively because of its rarity. Generally, patients with cGBMs typically presented with symptoms of raised intracranial pressure, and infrequently cerebellar symptoms such as gait ataxia and disequilibrium. Nevertheless, the authors reported a cGMB patient, with his clinical presentations and imaging characteristics mimicking a vestibular schwannoma. To the best of our knowledge, this is the first reported patient with cGBM mimicking a vestibular schwannoma. Furthermore, the diagnosis, treatment, and prognosis for cGBM were broadly investigated.

Brain abscess is a rare but potentially lethal infection of brain parenchyma, requiring prompt surgical intervention and high-dose antibiotic therapy. Brain abscess is a known complication of surgically treated intracerebral hemorrhage (ICH), but it is exceptionally rare that it occurs at the same site of a nonoperated ICH. Such cases may result from hematogenous spread from distant foci (pneumonia, infectious endocarditis) or contiguous sites. Herein, the authors report a case of 75-year-old woman presenting with a brain abscess 6 weeks after a nonoperated ICH. As the patient suffered from pneumonia during the course of ICH, the authors suspected that the brain abscess might originate from the pneumonia via hematogenous spread. The awareness of brain abscess formation at the site of ICH is of great importance for early diagnosis and prompt treatment.

ObjectiveWe previously demonstrated that spinal cord injury (SCI) induced hippocampus injury and depression in rodents. Ginsenoside Rg1 effectively prevents neurodegenerative disorders. Here, we investigated the effects of ginsenoside Rg1 on the hippocampus after SCI. MethodsWe used a rat compression SCI model. Western blotting and morphologic assays were used to investigate the protective effects of ginsenoside Rg1 in the hippocampus. ResultsBrain-derived neurotrophic factor/extracellular signal-regulated kinases (BDNF/ERK) signaling was altered in the hippocampus at 5 weeks after SCI. SCI attenuated neurogenesis and enhanced the expression of cleaved caspase-3 in the hippocampus; however, ginsenoside Rg1 attenuated cleaved caspase-3 expression and improved neurogenesis and BDNF/ERK signaling in the rat hippocampus. The results suggest that SCI affects BDNF/ERK signaling, and ginsenoside Rg1 can attenuate hippocampal damage after SCI. ConclusionWe speculate that the protective effects of ginsenoside Rg1 in hippocampal pathophysiology after SCI may involve BDNF/ERK signaling. Ginsenoside Rg1 shows promise as a therapeutic pharmaceutical product when seeking to counter SCI-induced hippocampal damage.

There is lacking research on risk factors and prediction models associated with Post-hemorrhagic hydrocephalus (PHH). Thus, this present study aimed to analyze the risk factors of PHH and establish a risk-scoring system through a large-scale study. A retrospective study of 382 patients with intracranial hemorrhage assessed age, history and diagnosis, Glasgow coma score (GCS), and fever time. After univariate and logistic regression analysis, a risk scoring system was established according to independent risk factors and evaluated using the area under the curve (AUC). Of the 382 patients, 133 (34.8%) had PHH, 43 (11.3%) received surgical treatment. Factor classification showed that age > 60 years old [odds ratio (OR): 0.347, II = 5 points], GCS < 5 (OR: 0.09, IV = 10 points), GCS 6‒8 (OR = 0.232, III = 6 points), fever time > 9 (OR: 0.202, III = 7 points), fever time 5–9 (OR: 0.341, II = 5 points), CSF-TP x time > 14,4000 group (OR: 0.267, IV = 6 points), and CSF-TP x time 9,601‒14,400 group (OR: 0.502, III = 3 points) were independent risk factors. The result of the receiver operating characteristic (ROC) prediction showed that AUC = 0.790 (0.744‒0.836). Low-risk (IV-VII), moderate (VIII-X), and high-risk group (XI-XIII) incidence of PHH were 11.76%, 50.55%, and 70.00% (p < 0.001), respectively. The coincidence rates in the validation cohort were 26.00%, 74.07%, and 100.0% (p < 0.001), respectively. AUC value was 0.860 (0.780‒0.941). The predictive model was conducive to determining the occurrence of PHH and facilitating early intervention.

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Objective: Our previous results have demonstrated that spinal cord injury(SCI) can induce hippocampus injury and depression in rodents. Ginsenoside Rg1 is efficient to prevent neurodegenerative disorders. This study aim to investigate the effects of ginsenoside Rg1 in hippocampus after SCI. Method:We used a rat compression SCI model. Western blotting and morphological assays were used to investigate protective effects of Ginsenoside Rg1 in the hippocampus. Results: The results demonstrated that BDNF/ERK signaling is altered in the hippocampus at 5 weeks after SCI. SCI attenuates neurogenesis and enhances the expression of cleaved caspase-3 in the hippocampus. Moreover, ginsenoside Rg1 can attenuate the expression of cleaved caspase-3 and improve the number of neurogenesis and the expression of BDNF/ERK signaling in the rat hippocampus. The results thus suggest that SCI affects BDNF/ERK signaling, and ginsenoside Rg1 can attenuate the damage of hippocampus after SCI. Conclusion:We speculate that the protective effects of ginsenoside Rg1 in hippocampal pathophysiological after SCI may involve BDNF/ERK signaling. Ginsenoside Rg1 may serve as a therapeutic pharmaceutical product in the futurewhen seeking to counter SCI-induced hippocampal damage.

Background: Post-hemorrhagic hydrocephalus (PHH) is a common complication of cerebral, ventricular, and subarachnoid hemorrhage, and craniocerebral injury. There is lacking research on risk factors and prediction models associated with PHH. This present study aimed to analyze the risk factors of PHH and establish a risk-scoring system through a large-scale study. Methods: A retrospective study of 382 patients with intracranial hemorrhage assessed age, history and diagnosis, Glasgow coma score (GCS), and fever duration. After univariate and logistic regression analysis, risk scoring system was established according to independent risk factors. Area under curve (AUC) was used to evaluate the scoring system and validate the accuracy of the dataResults: Of the 382 patients, 133 (34.8%) had PHH, 43 (11.3%) received surgical treatment. We determined the age, GCS, days (total fever time when body temperature ≥ 38.5◦C), and cerebrospinal fluid total protein (CSF-TP) x time (from the onset of the disease to the obtainment of CSF-TP after lumbar puncture) as the important risk factors for PHH. Factor classification showed that age > 60 years old [odds ratio (OR): 0.347, II = 5 points], GCS < 5 (OR: 0.09, IV = 10 points), GCS 6-8 (OR = 0.232, III = 6 points), fever days > 9 (OR: 0.202, III = 7 points), fever days 5-9 (OR: 0.341, II = 5 points), CSF-TP x time > 14,4000 group (OR: 0.267, IV = 6 points), and CSF-TP x time 9,601-14,400 group (OR: 0.502, III = 3 points) were independent risk factors. The result of the receiver operating characteristic (ROC) prediction showed that AUC = 0.790 (0.744-0.836). Low-risk (IV-VII), moderate (VIII-X), and high-risk group (XI-XIII) incidence of PHH, respectively: 11.76%, 50.55%, and 70.00% (p < 0.001). The coincidence rates in the validation cohort were 26.00%, 74.07%, and 100.0% (p < 0.001), respectively. AUC value was 0.860 (0.780 - 0.941).Conclusion: The predictive model was conducive in determining the occurrence of PHH and facilitating early intervention.