[Retracted] miR­218 inhibits the migration and invasion of glioma U87 cells through the Slit2­Robo1 pathway.

[This retracts the article DOI: 10.3892/ol.2015.2904.].

Constructing a CdS QDs/silica gel composite with high photosensitivity and prolonged recyclable operability for enhanced visible-light-driven NADH regeneration.

Visible-light-driven nicotinamide adenine dinucleotide (NADH) regeneration is one of the most effective measures, and cadmium sulfide (CdS) materials are typically used as low-cost photocatalysts. The CdS photocatalysts, however, still suffer from low regeneration efficiency and poor cycle stability. In this work, the CdS quantum dots (QDs) less than 10 nm embedded onto silica gel (CdS QDs/Silica gel) were constructed for visible-light-driven NADH regeneration by a successive ionic layer adsorption reaction and ball milling method. Results demonstrate that the photosensitivity of the CdS QDs/Silica gel composite was 31 times higher than that of the bulk CdS. Moreover, the conduction band (CB) edge of the CdS QDs/Silica gel composite is -1.34 eV, which is more negative 0.5 eV than that of the bulk CdS. The obtained CdS QDs/Silica gel composites showed the highest NADH regeneration yields of 68.8% under visible-light (LED, 420 nm) illumination and can be reused for over 40 cycles. Finally, the bioactivity of NADH toward enzyme catalysis is further confirmed by the hydrogenation of benzaldehyde to benzyl alcohol catalyzed with an alcohol dehydrogenase as enzyme catalysis.

Robust Superhydrophobic Brass Mesh with Electrodeposited Hydroxyapatite Coating for Versatile Applications.

A robust superhydrophobic brass mesh was fabricated based on a low-energy surface and a roughness on the nano/micro-meter scale. It was carried out by the forming of hydroxyapatite (HP) coatings on its surface through a constant current electro-deposition process, followed by immersion in fluoroalkylsilane solution. Surface morphology, composition and wetting behavior were investigated by field-emission scanning electron microscopy (SEM), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), high speed camera, and contact angle goniometer. Under optimal conditions, the resulting brass mesh exhibited superhydrophobicity, excellent anti-corrosion (η = 91.2%), and anti-scaling properties. While the surfactant liquid droplets of tetradecyl trimethyl ammonium bromide (TTAB) with different concentration were dropped on the superhydrophobic surface, maximum droplet rebounding heights and different contact angles (CAs) were observed and measured from side-view imaging. The plots of surfactant-concentration-maximum bounding height/CA were constructed to determine its critical-micelle-concentration (CMC) value. Close CMC results of 1.91 and 2.32 mM based on the determination of maximum rebounding height and CAs were obtained. Compared with its theoretical value of 2.1 mM, the relative errors are 9% and 10%, respectively. This indicated that the novel application based on the maximum rebounding height could be an alternative approach for the CMC determination of other surfactants.

Prognostic value of EGFR and KRAS in resected non-small cell lung cancer: a systematic review and meta-analysis.

BACKGROUND: The prognostic value of EGFR and KRAS mutations in resected non-small cell lung cancer (NSCLC) has been reported. However, conflicting results were reported in these studies. The effect of mutations in these two genes in resected NSCLC remains controversial. METHODS: We searched Internet databases for studies reporting disease-free survival (DFS) and overall survival (OS) in resected NSCLC patients with EGFR or KRAS mutations. A meta-analysis calculating the pooled hazard ratio (HR) for DFS and OS was used to measure the association of EGFR or KRAS mutations with the prognosis of patients after surgery. RESULTS: A total of 9,635 patients from 32 studies were included in this analysis. The combined HR for EGFR mutations on DFS was 0.77 (95% CI 0.66-0.90, p=0.001) and on OS was 0.72 (95% CI 0.66-0.80, p<0.00001). In addition, the combined HR for KRAS mutations on DFS was 1.5 (95% CI 1.15-1.96, p=0.002) and on OS was 1.49 (95% CI 1.28-1.73, p<0.00001). Sensitivity analysis, subgroup analysis, and bias analysis proved the stability of the results. CONCLUSION: The analysis showed that EGFR mutations were significantly associated with DFS and OS. These findings indicated that surgically treated NSCLC patients with EGFR mutations were inclined to exhibit a prolonged DFS and OS. In addition, the results indicated that KRAS mutations predicted worse DFS and OS in patients with resected NSCLC.

Identifying key regulating miRNAs in hepatocellular carcinomas by an omics' method.

The miRNAs play important regulating roles in the pathogenesis of hepatocellular carcinoma (HCC). To uncover key regulating miRNAs in HCC that were neglected by traditional analyzing methods of transcriptomics data, we proposed a novel molecular-network-based omics' (MNBO) method. With this method, we predicted HCC-regulating miRNAs, and confirmed the role of a novel miR-590-3P/EED axis by a clinical study and in vitro, in vivo wet-experiments. The miR-590-3P is significantly down-regulated in HCC patients. And low level of miR-590-3P in HCC is associated with poor prognosis of patients. In HCC cell lines, the miR-590-3P suppressed cell proliferation by inhibiting the transformation G1 phase to S phases of the cell cycle. Moreover, the miR-590-3P inhibited migration and invasion of HCC cells. Further investigations indicated that miR-590-3P play its roles by inhibiting polycomb protein EED. The experiments in animal model implied miR-590-3P could be a potential therapeutic agent for HCC in the future. In conclusion, the discovery of miR-590-3P revealed the MNBO would be a useful strategy to uncover key regulating miRNAs in HCC.

Driver genes in non-small cell lung cancer: Characteristics, detection methods, and targeted therapies.

Lung cancer is one of the most common causes of cancer-related death in the world. The large number of lung cancer cases is non-small cell lung cancer (NSCLC), which approximately accounting for 75% of lung cancer. Over the past years, our comprehensive knowledge about the molecular biology of NSCLC has been rapidly enriching, which has promoted the discovery of driver genes in NSCLC and directed FDA-approved targeted therapies. Of course, the targeted therapies based on driver genes provide a more exact option for advanced non-small cell lung cancer, improving the survival rate of patients. Now, we will review the landscape of driver genes in NSCLC including the characteristics, detection methods, the application of target therapy and challenges.

Precision medicine for hepatocellular carcinoma: driver mutations and targeted therapy.

Hepatocellular carcinoma (HCC) is the third most frequent cause of tumor-related mortality and there are an estimated approximately 850,000 new cases annually. Most HCC patients are diagnosed at middle or advanced stage, losing the opportunity of surgery. The development of HCC is promoted by accumulated diverse genetic mutations, which confer selective growth advantages to tumor cells and are called "driver mutations". The discovery of driver mutations provides a novel precision medicine strategy for late stage HCC, called targeted therapy. In this review, we summarized currently discovered driver mutations and corresponding signaling pathways, made an overview of identification methods of driver mutations and genes, and classified targeted drugs for HCC. The knowledge of mutational landscape deepen our understanding of carcinogenesis and promise future precision medicine for HCC patients.

The impact of methods to handle missing data on the estimated prevalence of dementia and mild cognitive impairment in a cross-sectional study including non-responders.

OBJECTIVE: Although several statistical methods for adjusting for missing data have been developed and are widely applied in research, few studies have investigated these methods in adjusting for missingness in datasets that aim to estimate the prevalence of dementia. We attempted to develop a more feasible approach for handling missingness in a cross-sectional study among elderly. METHODS: Five methods of estimating prevalence, including stratified weighting (SW), inverse-probability weighting (IPW), hot deck imputation (HDI), ordinal logistic regression (OLR) and multiple imputation (MI), were applied to handle the missing data yielded by a dataset that include 2231 non-responders. RESULTS: Compared with the results of the complete case analysis, the differences in the prevalence rates of dementia and mild cognitive impairment (MCI) calculated by the prevalence-estimating methods after adjusting for non-responders were less than 7% and 6%, respectively. In contrast to the results of other methods, the estimated prevalence of dementia and MCI calculated by MI increased when more predictive factors were included, and the lowest rate of missing data was achieved using MI. Using the participants' ages, the cognitive screening sores and activity of daily life sores as predictive variables when correcting for missingness induced relatively larger effects on the estimated dementia prevalence. CONCLUSIONS: When adjusting for missingness while estimating the prevalence of dementia in cross-sectional studies, a simple method, such as SW, is recommended when limited information is available, whereas MI is the preferred method when additional information is available. Further simulation studies are needed to determine the optimal approach.

MiR-218 inhibits the tumorgenesis and proliferation of glioma cells by targeting Robo1.

BACKGROUND: Malignant glioma is the most common primary brain tumors directly correlated with the high mortality and poor prognosis in clinical practice. MicroRNAs (miRNAs or miRs) influence numerous cancer-relevant processes including cell proliferation, differentiation and metabolism. However, the role of microRNA in malignant glioma is largely unknown. This study aimed to study the role of miR-218, a tumor-suppressive microRNA, in glioma development both in vivo and in vitro. METHODS: The expression level of miR-218, Slit2 and Robo1 was examined by either quantitative (polymerase chain reaction) or western-blotting from both human glioma tissue and glioma cell lines. U87 cells were transfected with miR-218 and then the expression levels of Slit2 and Robo1 were quantified. Cell proliferation was measured both by the in vitro proliferation assay and in vivo graft studies. The luciferase reporter assay was employed to validate the downstream target of miR-218. RESULTS: The expression of miR-218 was lower in glioma cell lines and glioma tissues from the patients with decreased Slit2 and increased Robo1 protein levels. The over-expression of miR-218 inhibited the tumorgenesis and proliferation of glioma cells remarkably. Furthermore, the over-expressing miR-218 in glioma cells results in the downregulation of Robo1 and upregulation of Slit2. Using luciferase reporter assays, we found that Robo1 was a direct downstream target of miR-218. CONCLUSION: Over-expression of miR-218 in glioma cells may inhibit the proliferation and tumorigenicity through targeting Robo1, suggesting that miR-218 could be a potential target for developing therapies in treating glioma.

ROS-p53-cyclophilin-D signaling mediates salinomycin-induced glioma cell necrosis.

BACKGROUND: The primary glioblastoma multiforme (GBM) is the most malignant form of astrocytic tumor with an average survival of approximately 12-14 months. The search for novel and more efficient chemo-agents against this disease is urgent. Salinomycin induces broad anti-cancer effects; however, its role in GBM and the underlying mechanism are not clear. RESULTS: Here we found that salinomycin induced both apoptosis and necrosis in cultured glioma cells, and necrosis played a major role in contributing salinomycin's cytotoxicity. Salinomycin induced p53 translocation to mitochondria, where it formed a complex with cyclophilin-D (CyPD). This complexation was required for mitochondrial permeability transition pore (mPTP) opening and subsequent programmed necrosis. Blockade of Cyp-D by siRNA-mediated depletion or pharmacological inhibitors (cyclosporin A and sanglifehrin A) significantly suppressed salinomycin-induced glioma cell necrosis. Meanwhile, p53 stable knockdown alleviated salinomycin-induced necrosis in glioma cells. Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death. CONCLUSIONS: Thus, salinomycin mainly induces programmed necrosis in cultured glioma cells.

miR-218 inhibits the migration and invasion of glioma U87 cells through the Slit2-Robo1 pathway.

Malignant gliomas are the most common primary brain tumors in adults and are associated with the highest mortality rate. Glioma invasion is one of the most notable causes of the poor prognosis of this cancer. Preventing the invasive behavior of malignant glioma cells by altering effector molecules can significantly improve the prognosis of a patient. microRNAs (miRNAs) are small noncoding RNAs, ~22 nucleotides in length, that are able to function as oncogenes or tumor suppressors in human cancer. In the present study, the expression level of miRNA 218 (miR-218) was found to be markedly downregulated in glioma cell lines and human primary glioma tissues. miR-218 upregulation was found to dramatically reduce the migratory speed and invasive ability of glioma cells. Furthermore, it was demonstrated that ectopic expression of miR-218 in glioma cells resulted in the downregulation of roundabout, axon guidance receptor, homolog 1 (Robo1), upregulation of Slit homolog 2 (Slit2) and the expression of associated proteins following Robo1 knockdown by small interfering RNA. In addition, it was demonstrated that miR-218 inactivated the Slit2-Robo1 pathway through downregulating Robo1 expression by directly targeting the 3'-untranslated region (3'-UTR) of Robo1. The present results indicate that miR-218 plays important roles in preventing the invasiveness of glioma cells, and reveals a novel mechanism of miRNA-mediated direct suppression of the Slit2-Robo1 pathway in glioma.

Alterations in enterocyte mitochondrial respiratory function and enzyme activities in gastrointestinal dysfunction following brain injury.

AIM: To determine the alterations in rat enterocyte mitochondrial respiratory function and enzyme activities following traumatic brain injury (TBI). METHODS: Fifty-six male SD rats were randomly divided into seven groups (8 rats in each group): a control group (rats with sham operation) and traumatic brain injury groups at 6, 12, 24 h, days 2, 3, and 7 after operation. TBI models were induced by Feendy's free-falling method. Mitochondrial respiratory function (respiratory control ratio and ADP/O ratio) was measured with a Clark oxygen electrode. The activities of respiratory chain complex I-IV and related enzymes were determined by spectrophotometry. RESULTS: Compared with the control group, the mitochondrial respiratory control ratio (RCR) declined at 6 h and remained at a low level until day 7 after TBI (control, 5.42 ± 0.46; 6 h, 5.20 ± 0.18; 12 h, 4.55 ± 0.35; 24 h, 3.75 ± 0.22; 2 d, 4.12 ± 0.53; 3 d, 3.45 ± 0.41; 7 d, 5.23 ± 0.24, P < 0.01). The value of phosphate-to-oxygen (P/O) significantly decreased at 12, 24 h, day 2 and day 3, respectively (12 h, 3.30 ± 0.10; 24 h, 2.61 ± 0.21; 2 d, 2.95 ± 0.18; 3 d, 2.76 ± 0.09, P < 0.01) compared with the control group (3.46 ± 0.12). Two troughs of mitochondrial respiratory function were seen at 24 h and day 3 after TBI. The activities of mitochondrial complex I (6 h: 110 ± 10, 12 h: 115 ± 12, 24 h: 85 ± 9, day 2: 80 ± 15, day 3: 65 ± 16, P < 0.01) and complex II (6 h: 105 ± 8, 12 h: 110 ± 92, 24 h: 80 ± 10, day 2: 76 ± 8, day 3: 68 ± 12, P < 0.01) were increased at 6 h and 12 h following TBI, and then significantly decreased at 24 h, day 2 and day 3, respectively. However, there were no differences in complex I and II activities between the control and TBI groups. Furthermore, pyruvate dehydrogenase (PDH) activity was significantly decreased at 6 h and continued up to 7 d after TBI compared with the control group (6 h: 90 ± 8, 12 h: 85 ± 10, 24 h: 65 ± 12, day 2: 60 ± 9, day 3: 55 ± 6, day 7: 88 ± 11, P < 0.01). The changes in α-ketoglutaric dehydrogenase (KGDH) activity were similar to PDH, except that the decrease in KGDH activity began at 12 h after TBI (12 h: 90 ± 12, 24 h: 80 ± 9, day 2: 76 ± 15, day 3: 68 ± 7, day 7: 90 ± 13, P < 0.01). No significant change in malate dehydrogenase (MDH) activity was observed. CONCLUSION: Rat enterocyte mitochondrial respiratory function and enzyme activities are inhibited following TBI. Mitochondrial dysfunction may play an important role in TBI-induced gastrointestinal dysfunction.

[Guiding value of brain tissue oxygenation plus intracranial pressure monitoring in severe traumatic brain injury patients].

OBJECTIVE: To elucidate the effectiveness of brain tissue oxygenation (PbtO2) plus intracranial pressure (ICP) monitoring and targeted therapy in patients of severe traumatic brain injury (TBI). METHODS: A total of 46 patients with severe TBI (Glasgow coma scale, GCS scale ≤ 8) admitted at Jiangyin People's Hospital from June 2009 to June 2012 were divided randomly into 2 groups and evaluated prospectively.Patients undergoing ICP plus PbtO2 monitoring were compared with controls with ICP monitoring alone.Therapies of both patient groups were attempted to maintain an ICP < 20 mm Hg and a cerebral perfusion pressure (CPP) ≥ 60 mm Hg.Among those with PbtO2 monitoring, oxygenation was maintained at a level of ≥ 20 mm Hg.The scores of Glasgow outcome scale (GOS) were compared between two groups at Month 6 post-injury. RESULTS: The mean daily ICP and CPP levels were similar in each group.The mortality rate was 21.7% in patients with ICP monitoring alone and the favorable outcome rate was 47.8%.However, those receiving combined management had a significantly reduced mortality rate of 8.7% and good outcome rate of 65.2% (P < 0.05). CONCLUSION: The combined use of both ICP and PbtO2 may be associated with reduced mortality and improved outcome in patients with severe TBI.

The short chain cell-permeable ceramide (C6) restores cell apoptosis and perifosine sensitivity in cultured glioblastoma cells.

Primary glioblastoma multiforme is the most malignant form of astrocytic tumor with an average survival of approximately 12-14 months. The combination of novel Akt inhibitors with anti-cancer therapeutics has achieved improved anti-tumor efficiency. In the current study, we examined the synergistic anti-cancer ability of Akt inhibitor perifosine in combination with short-chain ceramide (C6) against glioblastoma cells (U87MG and U251MG), and studied the underlying mechanisms. We found that perifosine, which blocked Akt/mammalian target of rapamycin activation, only induced moderate cell death and few cell apoptosis in cultured glioblastoma cells. On the other hand, perifosine administration induced significant protective autophagy, which inhibited cell apoptosis induction. Inhibition of autophagy by 3-methyaldenine or by autophagy-related gene-5 RNA interference significantly enhanced perifosine-induced apoptosis and cytotoxicity. We found that the short chain cell-permeable ceramide (C6) significantly enhanced cytotoxic effects of perifosine in cultured glioblastoma cells. For mechanism study, we observed that ceramide (C6) inhibited autophagy induction to restore cell apoptosis and perifosine sensitivity. In conclusion, our study suggests that autophagy inhibition by ceramide (C6) restores perifosine-induced apoptosis and cytotoxicity in glioblastoma cells.

Intraoperative microvascular Doppler monitoring in intracranial aneurysm surgery.

BACKGROUND: Surgical treatment of intracranial aneurysms is often compromised by incomplete exclusion of the aneurysm or stenosis of parent vessels. Intraoperative microvascular Doppler (IMD) is an attractive, noninvasive, and inexpensive tool. The present study aimed to evaluate the usefulness and reliability of IMD for guiding clip placement in aneurysm surgery. METHODS: A total of 92 patients with 101 intracranial aneurysms were included in the study. IMD with a 1.5-mm diameter, 20-MHz microprobe was used before and after clip application to confirm aneurysm obliteration and patency of parent vessels and branching arteries. IMD findings were verified postoperatively with digital subtraction angiography (DSA) or dual energy computed tomography angiography (DE-CTA). Ninety consecutive patients, harboring 108 aneurysms, who underwent surgery without IMD was considered as the control group. RESULTS: The microprobe detected all vessels of the Circle of Willis and their major branches. Clips were repositioned in 24 (23.8%) aneurysms on the basis of the IMD findings consistent with incomplete exclusion and/or stenosis. IMD identified persistent weak blood flow through the aneurismal sac of 11 of the 101 (10.9%) aneurysms requiring clip adjustment. Stenosis or occlusion of the parent or branching arteries as indicated by IMD necessitated immediate clip adjustment in 19 aneurysms (18.8%). The mean duration of the IMD procedure was 4.8 minutes. The frequency of clip adjustment (mean: 1.8 times per case) was associated with the size and location of the aneurysm. There were no complications related to the use of IMD, and postoperative angiograms confirmed complete aneurysm exclusion and parent vessel patency. About 8.3% (9/108) aneurysms were unexpectedly incompletely occluded, and 10.2% (11/108) aneurysms and parent vessel stenosis without IMD were detected by postoperative DSA or DE-CTA. IMD could reduce the rate of residual aneurysm and unanticipated vessel stenosis which demonstrated statistically significant advantages compared with aneurysm surgery without IMD. CONCLUSION: IMD is a safe, easily performed, reliable, and valuable tool that is suitable for routine use in intracranial surgery, especially in complicated, large, and giant aneurysms with wide neck or without neck.

A c.464T>a mutation in VHL gene in a Chinese family with VHL syndrome.

Von Hippel-Lindau (VHL) is a tumor suppressor that negatively regulates the production of angiogenic factors. Mutations in the VHL gene cause VHL syndrome, which is characterized by highly vascularized tumors. Here we report a c.464T>A mutation of the VHL gene in three patients with hemangioblastoma from a Chinese family. This mutation was not reported previously and was absent in the unaffected family members. The mutation is predicted to cause Val to Glu substitution at VHL protein residue 155 in a conserved region. Previous biochemical studies demonstrated that residue Val-155 was critical for VHL protein binding to chaperonin TRiC/CCT, an essential step for proper VHL protein folding. Our finding of naturally occurring VHL V155E mutation in patients with VHL syndrome supports the functional importance of Val-155 residue in VHL protein and illustrates the diversity of VHL gene defects underlying VHL syndrome.

Epidemiologic characterization of human papillomavirus infection in rural Chaozhou, eastern Guangdong Province of China.

BACKGROUND: Human papilloma virus (HPV) infection was the main cause of cervical cancer. There were only a few reports and detailed data about epidemiological research of HPV infection in rural population of China. MATERIALS AND METHODS: The cervical cells of rural Chaozhou women were collected, and multiplex real time PCR was firstly performed to detect high-risk HPV (HR-HPV) infection, which could detect 13 types of HR-HPV (types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68). Then, HPV-positive samples were typed by HPV GenoArray test. RESULTS: HR-HPV DNA was detected by multiplex real time-PCR in 3830 of 48559 cases (7.89%). There was a peak incidence in age of 55-60 years group, and a lower incidence in who lived in plain group compared with suburban, mountain and seashore group. 3380 cases of HPV positive sample were genotyped, 11.01% (372/3380) cases could not be classified, among the typed 3008 cases, 101 cases were identified without HR-HPV type infection, 2907 cases were infected with one HR-HPV type at least, the 6 most common HR-HPV types in descending order of infection, were type 52 (33.4%, 16 (20.95%), 58 (15.93%), 33 (9.94%), 68 (9.22%) and 18 (8.36%). The combined prevalence of HPV types 16 and 18 accounted for 28.52% of total infection. However, type 52 plus 58 presented 48.23% of total infection. 2209/2907 cases were infected with a single HPV type and 698/2907 cases were infected with multiple types, and multiple infection constituent ratio increased with age, with a peak incidence in age 55-60 years group. CONCLUSIONS: Our findings showed low prevalence of HPV vaccine types (16 and 18) and relatively high prevalence of HPV-52 and -58, support the hypothesis that the second-generation HPV vaccines including HPV-52 and -58 may offer higher protection for women in rural Guangdong Province.

Clinical experiences of ruptured posteroinferior cerebellar artery aneurysms and anatomical analysis in the cadaver in a single center of China.

OBJECTIVE: Posteroinferior cerebellar artery (PICA) aneurysms are uncommon and have not been well investigated previously. We report our series of 29 ruptured PICA aneurysms with surgical treatment along with the description of the surgical anatomy of the PICA to the lower cranial nerves in cadaveric specimen. METHODS: All patients with ruptured PICA aneurysms who were surgically treated at the First Affiliated Hospital of Soochow University during the period from January 1995 to December 2008 were reviewed retrospectively. Data relating to clinical, radiological, and intraoperative findings were analyzed. Forty formalin-fixed cerebellar hemispheres provided the material for the study of describing the detailed surgical anatomic relationship of the PICA to the lower cranial nerves. RESULTS: In our series, ruptured PICA aneurysms reached an incidence of 2.35% of all ruptured intracranial aneurysms. There were 13 aneurysms (44.8%) located in the proximal segment, and 16 (55.2%) located in the distal segment. Of these, 89.7% were saccular, 6.9% fusiform, and 3.4% dissecting aneurysms. Usually, the surgical outcome was influenced by Poor admission grade, the presence of obstructive hydrocephalus and associated distal AVM. In cadaveric specimen, 17.5% of PICAs passed between the glossopharyngeal and vagus nerves, 7.5% between the vagus and accessory nerves, and 62.5% through the rootlets of the accessory nerve. CONCLUSION: This report summarizes the presentation and outcome of a large series of 29 patients with ruptured PICA aneurysms, and we conclude that ruptured PICA with surgical treatment usually gets well recovered. The study does, however, also demonstrate that the anatomic relationship of the PICA and lower cranial nerves is somehow variable and irregular. Recognition of the findings in cadaveric dissection is essential in treating lesions of this region.

Development of clinically relevant orthotopic xenograft mouse model of metastatic lung cancer and glioblastoma through surgical tumor tissues injection with trocar.

OBJECTIVE: Orthotopic models are important in cancer research. Here we developed orthotopic xenograft mouse model of metastatic lung cancer and glioblastoma with a specially designed system. METHODS: Tiny fragments of surgical tumors were implanted into the mice brain with a trocar system. Immunohistochemistry was performed to detect brain tumor stem cells among glioblastoma tissues, including both the original and resulting ones with monoclonal antibody against CD133. RESULTS: Besides the constant high take rates in both models; brain transplants perfectly resembled their original tumors in biological behaviors. The brain tumor stem cells, positively stained with CD133 were found, though not frequently, in both original and resulting glioblastoma tissues. CONCLUSIONS: Orthotopic model established with a trocar system is effective and injection of tumor tissues containing stem cells promise the forming of new tumor mass when grafted.

[Microsurgical anatomy and clinic significance of posterior inferior cerebellar artery].

OBJECTIVE: To study the microsurgical anatomy of the posterior inferior cerebellar artery (PICA) for neurosurgery. METHODS: Twenty Chinese adult brain samples (40 sides) were measured with microscope for the diameters, lengths, origins, courses, and the branches of the PICA. The relationship between the PICA and cranial nerves was also checked. RESULTS: There were 35 PICAs in 20 brain samples. The mean diameter of the PICAs was (1.6 +/- 0.6) mm, the mean length from PICAs' origin of vertebral artery to the vertebrobasilar junction was (16 +/- 5) mm. In 35 PICAs, 28 PICAs go through the rootlets of XII cranial nerves, 7 PICAs go through inferior XII cranial nerves, and 32 PICAs go through the rootlets of XI cranial nerves. CONCLUSIONS: PICA is an important branch artery with more variation and complex relationship to the cranial nerves trend in the vertebral artery system. It is necessary to master the microsurgical anatomy of PICA and to be careful protection during the neurosurgical operations.