[Show abstract][Hide abstract] ABSTRACT: A 61-year-old male presented with a rare case of glioblastoma mimicking a cerebral contusion subsequent to collapsing. The patient had been medicated for hypertension for seven years and diabetes for eight years prior to hospitalization. Brain computed tomography (CT) revealed a cerebral contusion and intracerebral hemorrhage (ICH) in the left temporal region. The patient was initially administered intravenous drugs to reduce the intracranial pressure following the diagnosis of a cerebral contusion. Serial CT revealed ICH resorption. However, the patient was again admitted due to a headache and vomiting two months later. Magnetic resonance imaging (MRI) demonstrated an enhanced ring-shaped mass around the cyst cavity within the left temporal region, with surrounding edema. The patient underwent cyst puncture drainage in the temporal region. No tumor cells were identified in the cyst fluid and the culture was also negative. The patient was admitted for a headache and vomiting for the third time one month after being discharged. A cyst, tumor and meningoencephalitis were suspected following an MRI scan. The patient was treated with a left temporal craniotomy for a mass resection and biopsy. The histological diagnosis of the biopsy specimen was that of a glioblastoma. Two months later, MRI revealed a recurrence of the glioblastoma. In the present case, a brain tumor should have initially been suspected as the cause of the ICH, despite the history of craniocerebral trauma and hypertension. Early awareness of this potential cause of ICH may facilitate a more prompt diagnosis and treatment.
[Show abstract][Hide abstract] ABSTRACT: In the current study, we aimed to understand the potential role of leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) in TMZ-resistance of U251 glioma cells. We established TMZ-resistant U251 clones (U251/TMZ cells), which expressed low level of LRIG1, but high levels of epidermal growth factor receptor (EGFR), topoisomerase-2 (Topo-2) and Bcl-2. Depletion of LRIG1 by the targeted RNA interference (RNAi) upregulated EGFR/Topo-2/Bcl-2 in U251 cells, and the cells were resistant to TMZ. Reversely, over-expression of LRIG1 in U251 cells downregulated EGFR/Topo-2/Bcl-2 expressions, and cells were hyper-sensitive to TMZ. Our data suggested EGFR-dependent mammalian target of rapamycin (mTOR) activation was important for Topo-2 and Bcl-2 expressions in U251/TMZ cells. The EGFR inhibitor and the mTOR inhibitor downregulated Topo-2/Bcl-2 expressions, both inhibitors also restored TMZ sensitivity in U251/TMZ cells. Finally, inhibition of Topo-2 or Bcl-2 by targeted RNAi(s) knockdown or by the corresponding inhibitor re-sensitized U251/TMZ cells to TMZ, indicating that both Topo-2 and Bcl-2 were important for TMZ resistance in the resistant U251 cells. Based on these results, we concluded that LRIG1 inhibits EGFR expression and the downstream signaling activation, interferes with Bcl-2/Topo-2 expressions and eventually sensitizes glioma cells to TMZ.
Biochemical and Biophysical Research Communications 07/2013; 437(4). DOI:10.1016/j.bbrc.2013.06.116 · 2.30 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Depressed skull fractures (DSF) with operation indications should be paid with enough attention because they have several complications and can influence esthetics. The optimal surgical method for DSF remains unclear. We explored the merits of dissociate bone flap cranioplasty.
From July 2006 to August 2012, we performed 30 craniotomies on patients with DSF, which were divided into 2 groups: 1 group, which consisted of 18 patients, underwent dissociate bone cranioplasty; the other 12 patients underwent lever-up cranioplasty. A helical computed tomographic scan was routinely obtained after the operation and a 3-dimensional technique was performed on some patients to evaluate the postoperative condition of the flap.
Dissociate bone flap cranioplasty was performed on the 18 patients [11 men, 7 women: age, 26-70 (41) y]. No complications were observed in these patients. Lever-up cranioplasty was applied in the 12 patients [8 men, 4 women: age, 19-60 (41.8) y]; 2 patients had wound infection and 2 emerged with epidural hematoma. Obvious statistical significance of stability (P = 0.013) and position (P = 0.015) was found between the 2 methods.
Dissociate bone flap cranioplasty is safer, more flexible, has less complications, and has better plasticity. We advocate the use of bone flap cranioplasty in dealing with DSF.
The Journal of craniofacial surgery 03/2013; 24(2):589-91. DOI:10.1097/SCS.0b013e3182801bae · 0.68 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background
Nemo-like kinase (NLK) is an evolutionarily conserved protein kinase involved in Wnt/beta-catenin signaling, which has been reported to be associated with gliomagenesis. In the present study, we aimed to identify a concrete mechanism of Wnt/beta-catenin pathway regulation by microRNAs (miRNAs) in glioma.Methods
Quantitative reverse-transcription polymerase chain reaction and in situ hybridization were conducted to detect the expression of miR-92b. The cell proliferation rate and cell cycle kinetics were detected using 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay and flow cytometry, cell invasion and migration were evaluated using Transwell assay and wound healing assay, and cell apoptosis was detected using annexin V staining. Furthermore, the relevant molecules regulating proliferation and invasion were examined using Western blot analysis, immunohistochemistry, and immunofluorescence staining. Luciferase reporter assay was used to identify the direct regulation of NLK by miR-92b and beta-catenin/TCF4 activity.ResultsWe first showed that the expression of miR-92b was elevated in both glioma samples and glioma cells. Furthermore, down-regulation of miR-92b triggered growth inhibition, induced apoptosis, and suppressed invasion of glioma in vitro and in vivo. Luciferase assay and Western blot analysis revealed that NLK is a direct target of miR-92b. Restoring expression of NLK inhibited glioma proliferation and invasion. Mechanistic investigation revealed that miR-92b deletion suppressed beta-catenin/TCF-4 transcription activity by targeting NLK. Moreover, expression of NLK was inversely correlated with miR-92b in glioma samples and was predictive of patient survival in a retrospective analysis.Conclusions
Our findings identify a role for miR-92b in glioma proliferation and invasion after activation of Wnt/beta-catenin signaling via NLK.
[Show abstract][Hide abstract] ABSTRACT: Calcified chronic subdural hematoma (CCSDH) is a rare pathologic entity and, until recently, has been only published as case reports. We first present a patient with a double-loculated CCSDH who obtained good reexpansion after craniotomy to remove the thick calcified inner membrane and hematoma. In addition, we reviewed 46 cases in literature and conducted a summary about the incidence, clinical characteristics, radiologic findings, and therapeutic strategies of CCSDH. Surgical treatment for CCDSH with a sudden neurological deterioration is feasible and often results in neurological improvement; however, a crucial consideration was required in asymptomatic CCSDH. It is expected that CCSDH will be rarer in the future.
[Show abstract][Hide abstract] ABSTRACT: Recent studies have revealed that miR-92a is overexpressed in several types of malignancies and provides a protumorigenic effect. Our findings demonstrate that the high expression of miR-92a in human glioma specimens is significantly correlated with low levels of BCL2L11 (Bim) protein and high-grade glioma. Here, we present the first evidence that miR-92a antisense oligonucleotide (AS-miR-92a) provides a tumor suppressive effect via induction of apoptosis in human glioma cells. In addition, we show that Bim is a direct functional target of miR-92a. Introducing Bim cDNA without 3'UTR abrogates miR-92a-induced cell survival. Further investigations will focus on the therapeutic use of AS-miR‑92a-mediated antitumor effects in glioma.
[Show abstract][Hide abstract] ABSTRACT: The dysregulation of physiological microRNA (miRNA) activity has been shown to play an important role in gliomagenesis. In a previous study, using microRNA arrays and glioma tissues found that miR-27a was upregulated, which was also identified in the glioma cell lines and samples by quantitative real-time polymerase chain reaction (qRT-PCR). In this study, in order to explore the potential roles of miR-27a in the progression of glioma, we first utilized text-mining of PubMed abstracts with natural language processing (NLP) to identify 1,168 glioma-related molecules. In addition, miR-27a targets predicted by computational methods were integrated with the results from NLP analysis, followed by Gene Ontology (GO), pathway and network analysis. We identified 33 hub genes by overlap calculation and demonstrated that miR-27a may be involved in the progression of glioma through adherens junction, focal adhesion, the neurotrophin signaling pathway, the MAPK signaling pathway, the transforming growth factor-β (TGF-β) signaling pathway, cytokine-cytokine receptor interactions, the p53 signaling pathway, the apoptotic signaling pathway, as well as others. Our data may provide researchers with a better understanding of the mechanisms of the miR-27a-target network in glioma initiation and progression.
[Show abstract][Hide abstract] ABSTRACT: To investigate neuron regeneration of aged rats after intracerebral hemorrhage(ICH).
ICH model was induced by intracerebral infusion of 100microL autologous blood in adult and aged (3 and 18 m of age, respectively) male Sprague-Dawley (SD) rats. Doublecortin(DCX), polysialylated neural cell adhesion protein(PSA-NCAM) and Bromodeoxyuridine (Brdu) in brain tissue were detected by Western blot analysis and immunohistochemical examination.
In aged rats, DCX levels in the ipsilateral basal ganglia and subventricular zone started to increase at 7d after ICH, peaked at 14 d [(670+/-145)% of controls, P<0.01]. Most DCX positive cells in ipsilateral striatum were BrdU positive. Though DCX content in ipsilateral basal ganglia [(2560+/-758) pixels]of ICH aged rats was much higher than that of aged rat controls [(450+/-97)pixels, P<0.01], it was still lower than that in adult rats.
The results demonstrate that neuron regeneration occurs in subventricular zone in the aged rats following intracerebral hemorrhage(ICH).
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 07/2008; 37(4):386-92.