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Objective::Based on gene array technology, gene set enrichment analysis (GSEA) and immune infiltration analysis were performed on chip data of intracranial aneurysm (IA) mRNA expression profile, in order to provide theoretical basis for understanding the formation mechanism of IA. Method::The GSE75436 raw data were obtained from the gene expression omnibus (GEO). GSEA of biological process (BP) in gene ontology (GO) and Kyoto gene and genome encyclopedia (KEGG) signaling pathways were analyzed for gene expression profile by R software. The CIBERSORT deconvolution method was used to analyze the infiltration ratio of 22 types of immune cells in the expression profile. And COREMINE database was used to predict traditional Chinese medicines (TCMs), which were significant correlation with the enrichment result. Result::The GSEA results showed that the changes in gene expression of IA samples mainly involved in the regulation of cytokines, activation and differentiation of leukocyte, inflammatory immune response and other processes. The infiltration matrix analysis of immune cells showed that mast cells resting and neutrophils were significantly reduced in IA samples. The comparison of paired samples showed that mast cells and natural killer cells (NK cells) were significantly activated in the IA samples of the same individual, while neutrophils and T cells CD4 naive were significantly reduced. Through COREMINE prediction, it was found that Stephaniae Tetrandrae Radix was correlated with the activation of granulocytes, Sapindi Mukorossi Semen and Pistaciae Chinensis Cortex were correlated with the activation of neutrophils, Trichosanthis Semen, Paeoniae Radix Alba and Ligustri Lucidi Fructus were correlated with the cytotoxicity mediated by NK cells. Conclusion::Activation of mast cells and NK cells are closely associated with the occurrence and development of IA. The inflammatory immune processes and pathways such as nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) signaling pathway and cytotoxicity mediated by NK cells may be important factors in the pathogenesis of IA, and TCMs such as Stephaniae Tetrandrae Radix may be the potential molecular drug sources.
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Glioma is the most common intracranial malignant tumor of the nervous system. It is highly invasive, resistant to conventional treatment, and easy to relapse. The main treatment strategy is surgery plus radiotherapy, but the prognosis is still poor. Glioma stem cells (GSCs) are a group of cells with neural stem cell-like properties in glioma. As the starting cells of glioma, they are considered to be the key factors for tumorigenesis and recurrence. CD133 is considered to be a biomarker for glioblastoma and is used as a marker for GSCs. Although its biological significance is currently controversial, more and more studies have shown that CD133 is involved in GSCs-mediated tumor formation and recurrence. This article mainly reviews the GSCs surface marker CD133 and its related targeted therapies.
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Objective Mild hypothermia (MHT) can effectively protect the brain in traumatic brain injury (TBI). This study was to investigate the effects of MHT on the calmodulin (CAM) expression and brain edema in the rat model of TBI. Methods Ninety adult SD rats were randomly divided into a sham operation, a normal temperature and an MHT group of equal number. Immediately after TBI, the rats of the MHT group maintained at a rectal temperature of (32 ± 0.5) °C for 6 hours. Modified neurological severity scores (mNSS) were obtained from 6 rats in each group at 1, 3, 5 and 7 days after modeling, and the rest of the animals subjected to brain MRI at 6, 12, 24 and 48 hours and then killed for determination of the CAM gene transcription and protein expression in the brain tissue by real-time PCR, immunohistochemistry and Western blot. Results The mNSSs were significantly higher in the MHT and normal temperature groups than in the sham operation control (P < 0.05) at all time points, neurological severity markedly decreased in the MHT group compared with the normal temperature group (P < 0.05). At 6, 12, 24 and 48 hours, the expression of CAM mRNA was remarkably down-regulated in the MHT group (1.83 ± 0.19, 1.72 ± 0.12, 1.59 ± 0.06 and 1.60 ± 0.07) in comparison with the normal temperature group (2.76 ± 0.25, 2.49 ± 0.18, 2.04 ± 0.14 and 1.65 ± 0.09) (P < 0.05), even lower in the MHT than in the normal temperature group (P < 0.05), but higher in both of the two groups than in the sham operation group (P < 0.05). At 6, 12, 24 and 48 hours, the volume of brain edema was significantly reduced in the MHT group ([32.14 ± 4.52], [36.52 ± 4.10], [42.10 ± 4.38] and [46.25 ± 5.02] mm3) as compared with the normal temperature group ([48.56 ± 5.35], [53.13 ± 6.31], [59.23 ± 6.82] and [62.35 ± 7.25] mm3) (P < 0.05). Conclusion Mild hypothermia can improve the neurological function and reduce the CAM expression and brain edema in the brain tissue of rats with traumatic brain injury, which may be related to the neuroprotective effect of mild hypothermia.
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Objective The expressions of inflammatory factors and brain edema after traumatic brain injury (TBI) are the main factors for deterioration of the condition.TBI after drunkenness is even more difficult to be managed than simple TBI.This study was to discuss the effects of drunkenness on the inflammatory factors TNF-o and IL-6 and the aquaporin-4 (AQP-4) protein in rats after TBI.Methods Forty-eight male adult SD rats were randomly divided into a TBI and an ethanol (ETH) pretreatment group.TBI was induced using the Feeney's method after intraperitoneal injection of 3％ chloral hydrate at 30 mg/kg (the TBI group) or following gavage of ETH (the ETH group).At 1,3 and 5 days after modeling,modified neurological function scores (mNSS) were obtained,the expressions of TNF-α,IL-6 and AQP-4 protein determined by Western blot,and the levels of TNF-α.IL-6 and AOP-4 mRNA measured by RT-PCR at 6,24 and 72 hours.Results Compared with the TBI group,the ETH group showed significantly decreased mNSS at 1 day (9.00±0.63 vs 7.17±1.72,P＜0.05),3 days (7.00±1.10 vs 4.83±1.47,P＜0.05) and 5 days after modeling (5.50±1.05 vs 3.83± 0.75,P＜ 0.05),but remarkably up-regulated expressions of TNF-α (0.068± 0.008 vs 0.257 ± 0.008,P＜ 0.01),IL-6 (0.102 ±0.013 vs 0.320±0.016,P＜0.01) and APQ4 (0.054±0.007 vs 0.212±0.015,P＜0.01) at 6 hours,as well as at 24 and 72 hours (P＜0.01).Conclusion Drunkenness may increase the expressions of inflammatory factors and brain edema after traumatic brain injury and consequently aggravate secondary brain injury.
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<p><b>OBJECTIVE</b>To investigate the correlation between dynamic change of IL-32 level and disease development in the patients with acute leukemia(AL) and to explore its clinical significance.</p><p><b>METHODS</b>The serum IL-32 levels and IL-32 mRNA expression in 82 cases of AL and 30 healthy persons were measured by ELISA and real-time PCR.</p><p><b>RESULTS</b>Compared with healthy persons, the serum IL-32 protein level and IL-32 mRNA expression in AL, acute lymphoblastic leukemia(ALL) and acute non-lymphocytic leukemia(ANLL) groups all were significantly higher(P<0.05). The serum level of IL-32 protein and mRNA expression in newly diagnosed, PR and relapsed ALL and ANLL groups were all higher than those in the control group(P<0.05), and the serum protein level of IL-32 in relapsed ALL and ANLL groups were higher than that in other stage group(P<0.05). The serum levels of IL-32 protein and mRNA were not significantly different between CR and control group(P>0.05).</p><p><b>CONCLUSION</b>The IL-32 in the peripheral blood of patients with AL has been found to be closely related with the occurrence and development of disease, therefore, monitoring the dynamic changes of serum IL-32 level would contribute to the clinical judgment of the severity, the IL-32 levels can be used as indicators for the therapeutic efficacy for AL.</p>
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BACKGROUND: Acute poisoning (AP) may cause failure of the liver and kidney, and even death. This study aimed to investigate the efficacy of artificial liver support system (ALSS) on the treatment of liver failure after acute poisoning. METHODS: A total of 31 patients with liver failure caused by AP were admitted to emergency ICU, central ICU, and Department of Gastroenterology from 2005 to 2009 in Zhongshan Hospital Affiliated to Xiamen University, China. Among them, 13 patients served as a treatment group, and used ALSS in addition to detoxification treatment and protective treatment of liver function, and the other 18 patients served as a control group receiving detoxification treatment and protective treatment of liver function. RESULTS: In the treatment group, 10 patients (76.9％) were cured or improved, 2 died, and 1 was discharged against advice. In the 18 patients in the control group, 7 (38.9％) were cured or improved, 3 died, and 8 were discharged against advice. There was a significant difference in the rates of improvement between the two groups (P<0.05). CONCLUSION: ALSS is a safe and effective clinical method for the treatment of acute toxic liver failure.