資訊中心 >產品文獻集>Neuroscience (17)    相關產品:

  ✔本篇論文使用華聯產品:Mouse OneArray  
 PLoS One. 2015, 10(3):e0118832. doi: 10.1371/journal.pone.0118832. eCollection 2015.
 Behavior Training Reverses Asymmetry in Hippocampal Transcriptome of the Cav3.2 Knockout Mice 
 Ni-Chun Chung, Ying-Hsueh Huang, Chuan-Hsiung Chang, James C. Liao, Chih-Hsien Yang, Chien-Chang Chen, Ingrid Y. Liu
  Abstract
.Homozygous Cav3.2 knockout mice, which are defective in the pore-forming subunit of a low voltage activated T-type calcium channel, have been documented to show impaired maintenance of late-phase long-term potentiation (L-LTP) and defective retrieval of context-associated fear memory. To investigate the role of Cav3.2 in global gene expression, we performed a microarray transcriptome study on the hippocampi of the Cav3.2-/- mice and their wild-type littermates, either naïve (untrained) or trace fear conditioned. We found a significant left-right asymmetric effect on the hippocampal transcriptome caused by the Cav3.2 knockout. Between the naive Cav3.2-/- and the naive wild-type mice, 3522 differentially expressed genes (DEGs) were found in the left hippocampus, but only 4 DEGs were found in the right hippocampus. Remarkably, the effect of Cav3.2 knockout was partially reversed by trace fear conditioning. The number of DEGs in the left hippocampus was reduced to 6 in the Cav3.2 knockout mice after trace fear conditioning, compared with the wild-type naïve mice. To our knowledge, these results demonstrate for the first time the asymmetric effects of the Cav3.2 and its partial reversal by behavior training on the hippocampal transcriptome.
   

  ✔本篇論文使用華聯產品:Mouse OneArray  
 International forum of allergy & rhinology. 2015 Jul 3. doi: 10.1002/alr.21586.
 Dexamethasone affects mouse olfactory mucosa gene expression and attenuates genes related to neurite outgrowth
 
 
 Jun Tian, Jayant M. Pinto, Yi Xin, Henghui Zhang, Li Li, Zhifu Sun, Yongxiang Wei
  Abstract
BACKGROUND: Olfaction is one of the important senses for humans. Systemic glucocorticoids are the most commonly used medications for olfactory loss because of their strong anti-inflammatory effects. However, their effect on olfactory function is still controversial and the precise mechanism is not clear. To gain a global view of the effect of systematic glucocorticoid treatment on gene expression in the olfactory mucosa (OM), we profiled these changes in a murine model of olfaction in order to identify underlying molecular mechanisms. METHODS: C57BL/6 mice were injected daily for 2 weeks (WK2) with dexamethasone (DEX, intraperitoneally, 1 mg/kg body weight) vs 1 day of DEX (D1) vs controls, which received saline (Ctrl) (n = 9/group). Total RNA from the OM was used to analyze global gene expression. Genes showing changes in expression were compared using the Database for Annotation, Visualization and Integrated Discovery (DAVID, v6.7) and the General Olfactory Sensitivity Database (GOSdb; http://genome.weizmann.ac.il/GOSdb). RESULTS: Between the WK2 and Ctrl groups, 3351 genes were differentially expressed, of which 236 genes were related to olfactory function. Genes involved in axon guidance, cell projection, and inflammation were enriched and overlapped significantly with those in the GOSdb. CONCLUSION: Systemic glucocorticoids exert effects on transcription of a notable number of genes in the OM and appear to orchestrate changes related to axon guidance, cell projection, and inflammation. Further examination may allow targeted therapies that lack the side effects of this category of medication.
   

  ✔本篇論文使用華聯產品:Human miRNA OneArray  
 Tumor Biology. 2014 Jul 16.
 MiR-7-5p is frequently downregulated in glioblastoma microvasculature and inhibits vascular endothelial cell proliferation by targeting RAF1
 
 
 Zhiguo Liu, Yuguang Liu, Lianling Li, Zhenkuan Xu, Baibin Bi, Jian Yi Li, Yunyan Wang
  Abstract
The aberrant expression of microRNAs (miRNAs) is always associated with tumor development and progression. Microvascular proliferation is one of the unique pathologic features of glioblastoma (GBM) . In this study, the microvasculature from GBM or normal brain tissue derived from neurosurgeries was purified and total RNA was isolated from purified microvasculature. The difference of miRNA expression profiles betweenglioblastoma microvasculature and normal brain capillaries was investigated. It was found that miR-7-5p in GBM microvessels was significantly reduced compared with that in normal brain capillaries. In the in vitro experiments, overexpression of miR-7-5p significantly inhibited human umbilical vein endothelial cell proliferation. Forced expression of miR-7-5p in human umbilical vein endothelial cells in vitro significantly reduced the protein level of RAF1 and repressed the activity of the luciferase, a reporter vector carrying the 3'-untranslated region of RAF1. These findings indicate that RAF1 is one of the miR-7-5p target genes. Furthermore, a significant inverse correlation between miR-7-5p expression and RAF1 protein level in GBMmicrovasculature was found. These data suggest that miR-7-5p functions as a tumor suppressor gene to regulate GBM microvascular endothelial cellproliferation potentially by targeting the RAF1 oncogene, implicating an important role for miR-7-5p in the pathogenesis of GBM. It may serve as a guide for the antitumor angiogenesis drug development.
   

  ✔本篇論文使用華聯產品:Rat OneArray  
 Journal of Neurosurgery Spine. 2014 Jul 25.
 Nerve growth factor promotes expression of novel genes in intervertebral disc cells that regulate tissue degradation
 
 
 Ting-Hsien Kao, Yi-Jen Peng, Hsi-Kai Tsou, Donald M. Salter, Herng-Sheng Lee
  Abstract
Object: Increased neurotrophin activity in degenerative intervertebral discs (IVDs) is one potential cause of chronic low-back pain (LBP). The aim of the study was to assess if nerve growth factor (NGF) might alter gene expression of IVD cells and contribute to disc degeneration by enhancingexpression or activity of factors that cause breakdown of IVD matrix. Methods: Rat-tail IVD cells were stimulated by NGF and subjected to microarray analysis. Real-time polymerase chain reaction, Western blotting, and immunocytochemistry of rat and human IVD cells and tissues treated with NGF in vitro in the absence or presence of the NGF inhibitor Ro 08-2750 were used to confirm findings of the microarray studies. Phosphorylation of mitogen-activated protein kinase (MAPK) was used to identify cell signaling pathways involved in NGF stimulation in the absence or presence of Ro 08-2750. Results: Microarray analysis demonstrated increased expression of chitinase 3-like 1 (Chi3l1), lipocalin 2 (Lcn2), and matrix metalloproteinase-3 (Mmp3) following NGF stimulation of rat IVD cells in vitro. Increased gene expression was confirmed by real-time polymerase chain reaction with a relative increase in the Mmp/Timp ratio. Increased expression of Chi3l1, Lcn2, and Mmp3 following NGF stimulation was also demonstrated in rat cells and human tissue in vitro. Effects of NGF on protein expression were blocked by an NGF inhibitor and appear to function through the extracellular-regulation kinase 1/2 (ERK1/2) MAPK pathway. Conclusions Nerve growth factor has potential effects on matrix turnover activity and influences the catabolic/anabolic balance of IVD cells in an adverse way that may potentiate IVD degeneration. Anti-NGF treatment might be beneficial to ameliorate progressive tissue breakdown in IVD degeneration and may lead to pain relief.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 Oncology Reports. 2014 Jul 17. doi: 10.3892/or.2014.3335.
 WWOX modulates the gene expression profile in the T98G glioblastoma cell line rendering its phenotype less malignant
 
 
 KATARZYNA KOŚLA, MAGDALENA NOWAKOWSKA, KAROLINA POSPIECH, ANDRZEJ K. BEDNAREK
  Abstract
The aim of the present study was to assess the influence of WWOX gene upregulation on the transcriptome and phenotype of the T98G glioblastomacell line. The cells with high WWOX expression demonstrated a significantly different transcription profile for approximately 3,000 genes. The main cellular pathways affected were Wnt, TGF£], Notch and Hedgehog. Moreover, the WWOX-transfected cells proliferated at less than half the rate, exhibited greatly lowered adhesion to ECM, increased apoptosis and impaired 3D culture formation. They also demonstrated an increased ability for crossing the basement membrane. Our results indicate that WWOX, apart from its tumor-suppressor function, appears to be a key regulator of the main cellular functions of the cell cycle and apoptosis. Furthermore, our results showed that WWOX may be involved in controlling metabolism, cytoskeletal structure and differentiation.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 European Journal of Neuroscience. 2014 Jun 5. doi: 10.1111/ejn.12602.
 Human cellular differences in cAMP-CREB signaling correlate with light-dependent melatonin suppression and bipolar disorder
 
 
 Ludmila Gaspar, Maan van de Werken, Anne-Sophie Johansson, Ermanno Moriggi, Bjorn Owe-Larsson, Janwillem W. H. Kocks, Gabriella B. Lundkvist, Marijke C. M. Gordijn, Steven A. Brown
  Abstract
Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter-individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter-individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome-wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP-mediated signaling in a human neuroendocrine response to light - the light-dependent suppression of the circadian hormonemelatonin - that shows wide inter-individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREBsignaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral-based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility.
   

  ✔本篇論文使用華聯產品:Human miRNA OneArray  
 European Journal of Neuroscience. 2013 Dec 5. doi: 10.1111/ejn.12444.
 Widespread microRNA dysregulation in multiple system atrophy ¡V disease-related alteration in miR-96
 
 
 Kiren Ubhi, Edward Rockenstein, Christine Kragh, Chandra Inglis, Brian Spencer, Sarah Michael, Michael Mante, Anthony Adame, Douglas Galasko, Eliezer Masliah
  Abstract
MicroRNA (miRNA) are short sequences of RNA that function as post-transcriptional regulators by binding to target mRNA transcripts resulting in translational repression. A number of recent studies have identified miRNA as being involved in neurodegenerative disorders including Alzheimer's disease, Parkinson's disease and Huntington's disease. However, the role of miRNA in multiple system atrophy (MSA), a progressive neurodegenerative disorder characterized by oligodendroglial accumulation of alpha-synuclein remains unexamined. In this context, this study examined miRNA profiles in MSA cases compared with controls and in transgenic (tg) models of MSA compared with non-tg mice. The results demonstrate a widespread dysregulation of miRNA in MSA cases, which is recapitulated in the murine models. The study employed a cross-disease, cross-species approach to identify miRNA that were either specifically dysregulated in MSA or were commonly dysregulated in neurodegenerative conditions such as Alzheimer's disease, dementia with Lewy bodies, progressive supranuclear palsy and corticobasal degeneration or the tg mouse model equivalents of these disorders. Using this approach we identified a number of miRNA that were commonly dysregulated between disorders and those that were disease-specific. Moreover, we identified miR-96 as being up-regulated in MSA. Consistent with the up-regulation of miR-96, mRNA and protein levels of members of the solute carrier protein family SLC1A1 and SLC6A6, miR-96 target genes, were down-regulated in MSA cases and a tg model of MSA. These results suggest that miR-96 dysregulation may play a role in MSA and its target genes may be involved in the pathogenesis of MSA.
   

  ✔本篇論文使用華聯產品:Mouse OneArray  
 PLOS ONE. 2013, 8(10): e76265. doi:10.1371/journal.pone.0076265.
 Modeling the Neurovascular Niche: Unbiased Transcriptome Analysis of the Murine Subventricular Zone in Response to Hypoxic Insult
 
 
 Qi Li, Sandra Canosa, Kelly Flynn, Michael Michaud, Michael Krauthammer, Joseph A. Madri
  Abstract
Premature infants often experience chronic hypoxia, resulting in cognitive & motor neurodevelopmental handicaps. These sometimes devastating handicaps are thought to be caused by compromised neural precursor cell (NPC) repair/recovery resulting in variable central nervous system (CNS) repair/recovery. We have identified differential responses of two mouse strains (C57BL/6 & CD1) to chronic hypoxia that span the range of responsiveness noted in the premature human population. We previously correlated several CNS tissue and cellular behaviors with the different behavioral parameters manifested by these two strains. In this report, we use unbiased array technology to interrogate the transcriptome of the subventricular zone (SVZ) in these strains. Our results illustrate differences in mRNA expression in the SVZ of both C57BL/6 and CD1 mice following hypoxia as well as differences between C57BL/6 and CD1 SVZ under both normoxic and hypoxic conditions. Differences in expression were found in gene sets associated with Sox10-mediated neural functions that explain, in part, the differential cognitive and motor responsiveness to hypoxic insult. This may shed additional light on our understanding of the variable responses noted in the human premature infant population and facilitate early intervention approaches. Further interrogation of the differentially expressed gene sets will provide a more complete understanding of the differential responses to, and recovery from, hypoxic insult allowing for more informed modeling of the ranges of disease severity observed in the very premature human population.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 EMBO Molecular Medicine. 2013, 5(4):531-47. doi: 10.1002/emmm.201201783.
 Smurf2-mediated degradation of EZH2 enhances neuron differentiation and improves functional recovery after ischaemic stroke
 
 
 Chou RH, Shyu WC, Hsieh SC, Wu CS, Chiang SY, Chang WJ, Chen JN, Tseng YJ, Lin YH, Lee W, Yeh SP, Hsu JL, Yang CC, Hung SC, Yu YL, Hung MC
  Abstract
EZH2 plays an important role in stem cell renewal and maintenance by inducing gene silencing via its histone methyltransferase activity. Previously, we showed that EZH2 downregulation enhances neuron differentiation of human mesenchymal stem cells (hMSCs); however, the underlying mechanisms of EZH2- regulated neuron differentiation are still unclear. Here, we identify Smurf2 as the E3 ubiquitin ligase responsible for the polyubiquitination and proteasomemediated degradation of EZH2, which is required for neuron differentiation. A ChIP-on-chip screen combined with gene microarray analysis revealed that PPARg was the only gene involved in neuron differentiation with significant changes in both its modification and expression status during differentiation. Moreover, knocking down PPARg prevented cells from undergoing efficient neuron differentiation. In animal model, rats implanted with intracerebral EZH2-knocked-down hMSCs or hMSCs plus treatment with PPARg agonist (rosiglitazone) showed better improvement than those without EZH2 knockdown or rosiglitazone treatment after a stroke. Together, our results support Smurf2 as a regulator of EZH2 turnover to facilitate PPARg expression, which is specifically required for neuron differentiation, providing a molecular mechanism for clinical applications in the neurodegenerative diseases.
   

  ✔本篇論文使用華聯產品:Experimental Accessories  
 PLOS ONE. 2012, 7(8):e43304. doi: 10.1371/journal.pone.0043304.
 Luteolin Induces microRNA-132 Expression and Modulates Neurite Outgrowth in PC12 Cells
 
 
 Lian-Fang Lin, Szu-Ping Chiu, Ming-Jiuan Wu, Pei-Yi Chen, Jui-Hung Yen
  Abstract
Luteolin, a food-derived flavonoid, has been reported to exert neurotrophic properties that are associated with its capacity to promote neuronal survival and neurite outgrowth. In this study, we report for the first time that luteolin induces the persistent expression of microRNA-132 (miR-132) in PC12 cells. The correlation between miR- 132 knockdown and a decrease in luteolin-mediated neurite outgrowth may indicate a mechanistic link by which miR-132 functions as a mediator for neuritogenesis. Furthermore, we find that luteolin led to the phosphorylation and activation of cAMP response element binding protein (CREB), which is associated with the up-regulation of miR-132 and neurite outgrowth. Moreover, luteolin-induced CREB activation, miR-132 expression and neurite outgrowth were inhibited by adenylate cyclase, protein kinase A (PKA) and MAPK/ERK kinase 1/2 (MEK1/2) inhibitors but not by protein kinase C (PKC) or calcium/calmodulin-dependent protein kinase II (CaMK II) inhibitors. Consistently, we find that luteolin treatment increases ERK phosphorylation and PKA activity in PC12 cells. These results show that luteolin induces the up-regulation of miR-132, which serves as an important regulator for neurotrophic actions, mainly acting through the activation of cAMP/PKA- and ERK-dependent CREB signaling pathways in PC12 cells.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 BioChip Journal. 2012, 6(3):254-261. doi: 10.1007/s13206-012-6308-z.
 Gene expression profile analysis in cultured human neuronal cells after static magnetic stimulation
 
 
 Wooseok Im, Soon-Tae Lee, Seung Chan Kim
  Abstract
Although the magnetic force has been used in various human environments and medicines, their influence on the nervous system has not been fully elucidated. In this study, we investigated mRNA expressions profiles of neuronal cells after the application of static magnetic fields. Two perpetual magnets were applied to the cultured SH-SY5Y human neuronal cell, and the gene expression profiles were evaluated by using human mRNA microarray targeting 30968 genes. Results showed that the expressions of 827-known genes were altered in response to the magnetic force. Among them, 112 genes showed significant changes (>2-fold changes); 44 genes were up-regulated and 68 genes were down-regulated. Among the upregulated genes, we further confirmed the increased expressions of synapsin III and chloride channel-2 by using RT-PCR and immunocytochemistry. These results suggest that static magnetic fields influence neuronal-and biological-related gene expression profiles in human neuronal cells.
   

  ✔本篇論文使用華聯產品:Mouse&Rat miRNA OneArray  
 Environmental Science & Technology. 2012, 46(12):6822-9. doi: 10.1021/es3008547.
 Prenatal and Neonatal Exposure to Perfluorooctane Sulfonic Acid Results in Changes in miRNA Expression Profiles and Synapse Associated Proteins in Developing Rat Brains
 
 
 Faqi Wang, Wei Liu, Junsheng Ma, Mingxi Yu, Jiayin Dai, Yihe Jin
  Abstract
We previously identified a number of perfluorooctane sulfonic acid (PFOS)-responsive transcripts in developing rat brains using microarray analysis. However, the underlying mechanisms and functional consequences remain unclear. We hypothesized that microRNAs (miRNAs), which have emerged as powerful negative regulators of mRNA and protein levels, might be responsible for PFOS-induced mRNA changes and consequent neural dysfunctions. We used eight miRNA arrays to profile the expression of brain miRNAs in neonatal rats on postnatal days (PND) 1 and 7 with maternal treatment of 0 (Control) and 3.2 mg/kg of PFOS feed from gestational day 1 to PND 7, and subsequently examined six potentially altered synapse-associated proteins to evaluate presumptive PFOS-responsive functions. Twenty-four brain miRNAs on PND 1 and 17 on PND 7 were significantly altered with PFOS exposure (P < 0.05), with miR-466b, -672, and -297, which are critical in neurodevelopment and synapse transmission, showing a more than 5-fold reduction. Levels of three synapse-involved proteins, NGFR, TrkC, and VGLUT2, were significantly decreased with no protein up-regulated on PND 1 or 7. Perfluorooctane sulfonic acid might affect calcium actions during synapse transmission in the nervous system by interfering with SYNJ1, ITPR1, and CALM1 via their targeting miRNAs. Our results indicated that miRNA had little direct regulatory effect on the expression of mRNAs and synapse-associated proteins tested in the developing rat brain exposed to PFOS, and it seems that the PFOS-induced synaptic dysfunctions and changes in transcripts resulted from a combinatory action of biological controllers and processes, rather than directed by one single factor.
   

  ✔本篇論文使用華聯產品:Mouse OneArray, Mouse&Rat miRNA OneArray  
 Neuron. 2012, 73(4):774-88. doi: 10.1016/j.neuron.2012.02.003.
 EPAC Null Mutation Impairs Learning and Social Interactions via Aberrant Regulation of miR-124 and Zif268 Translation
 
 
 Ying Yang, Xiaogang Shu, Dan Liu, You Shang, Yan Wu, Lei Pei, Xin Xu, Qing Tian, Jian Zhang, Kun Qian, Ya-Xian Wang, Ronald S. Petralia, Weihong Tu, Ling-Qiang Zhu, Jian-Zhi Wang, Youming Lu
  Abstract
EPAC proteins are the guanine nucleotide exchange factors that act as the intracellular receptors for cyclic AMP. Two variants of EPAC genes including EPAC1 and EPAC2 are cloned and are widely expressed throughout the brain. But, their functions in the brain remain unknown. Here, we genetically delete EPAC1 (EPAC1(-/-)), EPAC2 (EPAC2(-/-)), or both EPAC1 and EPAC2 genes (EPAC(-/-)) in the forebrain of mice. We show that EPAC null mutation impairs long-term potentiation (LTP) and that this impairment is paralleled with the severe deficits in spatial learning and social interactions and is mediated in a direct manner by miR-124 transcription and Zif268 translation. Knockdown of miR-124 restores Zif268 and hence reverses all aspects of the EPAC(-/-) phenotypes, whereas expression of miR-124 or knockdown of Zif268 reproduces the effects of EPAC null mutation. Thus, EPAC proteins control miR-124 transcription in the brain for processing spatial learning and social interactions.
   

  ✔本篇論文使用華聯產品:Mouse OneArray  
 Comparative Immunology, Microbiology and Infectious Diseases. 2011, 34(6):503-12. doi: 10.1016/j.cimid.2011.09.003.
 Innate immune response gene expression profiles in central nervous system of mice infected with rabies virus
 
 
 Pingsen Zhao, Lili Zhao, Tao Zhang, Yinglin Qi, Tiecheng Wang, Kejian Liu, Hualei Wang, Hao Feng, Hongli Jin, Chuan Qin, Songtao Yang, Xianzhu Xia
  Abstract
The present study was focused on the modulation of innate immune response genes in CNS of mouse in response to rabies virus (RABV) infection. The global gene expression changes in brains of RABV- or mock-infected mice were investigated using DNA microarray analysis and quantitative real-time PCR. Then functional enrichment of the differentially expressed mRNAs was performed. Microarray analysis showed that 390 genes in brain were significantly (P<0.01) regulated in response to RABV infection, with obviously up-regulated genes like interferon (IFN) stimulated genes (ISGs), IFN inducible transcription factors, cytokines and complement, etc. The significant pathways of differentially expressed genes are mainly involved in JAK-STAT signaling pathway, antigen processing and presentation, ubiquitin mediated proteolysis and complement cascades. The results suggest that the modulated genes in infected CNS were possibly involved in pathogenesis of rabies. Conversely, they may have protective effects.
   

  ✔本篇論文使用華聯產品:Array technology and applications  
 Journal of the Chinese Medical Association. 2010, 73(3):139-143. doi: 10.1016/S1726-4901(10)70028-9.
 Good Mortality Prediction by Glasgow Coma Scale for Neurosurgical Patients
 
 
 Hsien-Wei Ting, Ming-Shung Chen, Yueh-Chun Hsieh, Chien-Lung Chan
  Abstract
Background: How to effectively use the finite resources of an intensive care unit (ICU) for neurosurgical patients is a critical decision-making process. Mortality prediction models are effective tools for allocating facilities. This study intended to distinguish the prediction power of the Acute Physiology and Chronic Health Evaluation II (APACHE II), the Simplified Acute Physiology Score II (SAPS II), and the Glasgow Coma Scale (GCS) for neurosurgical patients. Methods: According to the definitions of the APACHE II, this study recorded both APACHE II and SAPS II scores of 154 neurosurgical patients in the ICU of a 600-bed general hospital. Linear regression models of GCS (GCS-mr) were constructed. The t test, receiver operating characteristic (ROC) curve and Wilcoxon signed rank test were used as the statistical evaluation methods. Results: There were 50 (32.5%) females and 104 (67.5%) males in this study. Among them, 108 patients survived and 46 patients died. The areas under the ROC curves (AUC) of SAPS II and APACHE II were 0.872 and 0.846, respectively. The AUC of GCS-mr was 0.866, and the R2 was 0.389. The evaluation powers of SAPS II, GCS-mr and APACHE II were the same (p > 0.05). Patients with GCS ≤ 5 or motor component of GCS (GCS-M) ≤ 3 had a higher probability of mortality than patients with GCS > 5 or GCS-M > 3 (p < 0.01). Conclusion: The predictive powers of SAPS II, APACHE II and GCS-mr were the same. The GCS-mr is more convenient for predicting mortality in neurosurgical patients. Both GCS ≤ 5 and GCS-M ≤ 3 are good indicators of mortality in these patients.
   

  ✔本篇論文使用華聯產品:Mouse OneArray  
 Invest Ophthalmol Vis Sci. 2011, 25;52(1):527-40. doi: 10.1167/iovs.10-5731.
 Sigma receptor 1 modulates ER stress in retinal neurons.
 
 
 Yonju Ha, Ying Dun, Muthusamy Thangaraju, Jennifer N Duplantier, Zheng Dong, Kebin Liu, Vadivel Ganapathy, Sylvia B Smith
  Abstract
To investigate the mechanism of £m receptor 1 (£mR1) neuroprotection in retinal neurons. Oxidative stress, which is implicated in diabetic retinopathy, was induced in mouse primary ganglion cells (GCs) and RGC-5 cells, and the effect of the £mR1 ligand (+)-pentazocine on pro- and anti-apoptotic and endoplasmic reticulum (ER) stress gene expression was examined. Binding of £mR1 to BiP, an ER chaperone protein, and £mR1 phosphorylation status were examined by immunoprecipitation. Retinas were harvested from Ins2Akita/+ diabetic mice treated with (+)-pentazocine, and the expression of ER stress genes and of the retinal transcriptome was evaluated. Oxidative stress induced the death of primary GCs and RGC-5 cells. The effect was decreased by the application of (+)-pentazocine. Stress increased £mR1 binding to BiP and enhanced £mR1 phosphorylation in RGC-5 cells. BiP binding was prevented, and £mR1 phosphorylation decreased in the presence of (+)-pentazocine. The ER stress proteins PERK, ATF4, ATF6, IRE1£, and CHOP were upregulated in RGC-5 cells during oxidative stress, but decreased in the presence of (+)-pentazocine. A similar phenomenon was observed in retinas of Ins2Akita/+ diabetic mice. Retinal transcriptome analysis of Ins2Akita/+ mice compared with wild-type revealed differential expression of the genes critically involved in oxidative stress, differentiation, and cell death. The expression profile of those genes was reversed when the Ins2Akita/+ mice were treated with (+)-pentazocine. In retinal neurons, the molecular chaperone £mR1 binds BiP under stressful conditions; (+)-pentazocine may exert its effects by dissociating £mR1 from BiP. As stress in retinal cells increases, phosphorylation of £mR1 is increased, which is attenuated when agonists bind to the receptor.
   

  ✔本篇論文使用華聯產品:Human OneArray  
 NATURE. 2010, 466(7305):503-7. doi: 10.1038/nature09261.
 Histone H4K20/H3K9 demethylase PHF8 regulates zebrafish brain and craniofacial development.
 
 
 Hank H. Qi, Madathia Sarkissian, Gang-Qing Hu, Zhibin Wang, Arindam Bhattacharjee, D. Benjamin Gordon, Michelle Gonzales, Fei Lan, Pat P. Ongusaha, Maite Huarte, Nasser K. Yaghi, Huijun Lim, Benjamin A. Garcia, Leonardo Brizuela, Keji Zhao, Thomas M. Roberts, Yang Shi.
  Abstract
X-linked mental retardation (XLMR) is a complex human disease that causes intellectual disability. Causal mutations have been found in approximately 90 X-linked genes; however, molecular and biological functions of many of these genetically defined XLMR genes remain unknown. PHF8 (PHD (plant homeo domain) finger protein 8) is a JmjC domain-containing protein and its mutations have been found in patients with XLMR and craniofacial deformities. Here we provide multiple lines of evidence establishing PHF8 as the first mono-methyl histone H4 lysine 20 (H4K20me1) demethylase, with additional activities towards histone H3K9me1 and me2. PHF8 is located around the transcription start sites (TSS) of approximately 7,000 RefSeq genes and in gene bodies and intergenic regions (non-TSS). PHF8 depletion resulted in upregulation of H4K20me1 and H3K9me1 at the TSS and H3K9me2 in the non-TSS sites, respectively, demonstrating differential substrate specificities at different target locations. PHF8 positively regulates gene expression, which is dependent on its H3K4me3-binding PHD and catalytic domains. Importantly, patient mutations significantly compromised PHF8 catalytic function. PHF8 regulates cell survival in the zebrafish brain and jaw development, thus providing a potentially relevant biological context for understanding the clinical symptoms associated with PHF8 patients. Lastly, genetic and molecular evidence supports a model whereby PHF8 regulates zebrafish neuronal cell survival and jaw development in part by directly regulating the expression of the homeodomain transcription factor MSX1/MSXB, which functions downstream of multiple signalling and developmental pathways. Our findings indicate that an imbalance of histone methylation dynamics has a critical role in XLMR.