Showing Publication Results for :

OGD
Full Name of the Resource : Oomycete Genomics Database: ESTs and annotation
Resource Category : Databases -> Genomic Databases (Non-Human) -> Other fungi

  1. Title of the Paper : 1, 5-Dicaffeoylquinic acid-mediated glutathione synthesis through activation of Nrf2 protects against OGD/reperfusion-induced oxidative stress in astrocytes (View at PubMed)
    Contributors : Cao, X.; Xiao, H.; Zhang, Y.; Zou, L.; Chu, Y.; Chu, X.
    Address : Department of Neurology, Second Clinical College, Jinan University, Shenzhen, 518020, People\'s Republic of China.
    Publication Name : Brain Res
    Volume : 1347
    Pages : 142-8
    ISSN : 1872-6240 (Electronic) 0006-8993 (Linking)
    Language : English
    Abstract : Oxidative stress plays an important role in pathological processes of cerebral ischemia followed by reperfusion. The effect of 1, 5-dicaffeoylquinic acid (1, 5-diCQA) on primary culture rat cortical astrocytes induced by oxygen and glucose deprivation (OGD)/reperfusion was evaluated in this study. Appropriate concentration of 1, 5-diCQA pretreatment significantly suppressed cell death, reduced the production of reactive oxygen species, prevented glutathione (GSH) depletion, increased the activity of glutamate-cysteine ligase (GCL), and triggered Nrf2 nuclear translocation in astrocytes induced by 4h of OGD and 20 h of reperfusion. Interestingly, these protective effects were greatly attenuated in Nrf2 siRNA-transfected cells. We conclude that 1, 5-diCQA has antioxidant signaling properties that upregulate GSH synthesis by stimulating the Nrf2 pathway in astrocytes and protects them from cell death in an in vitro model of ischemia/reperfusion.



  2. Title of the Paper : Changes in membrane potential and the intracellular calcium concentration during CSD and OGD in layer V and layer II/III mouse cortical neurons (View at PubMed)
    Contributors : Gniel, H. M.; Martin, R. L.
    Address : School of Biochemistry and Molecular Biology, The Australian National Univ., Canberra, Australia. helen.gniel@anu.edu.au
    Publication Name : J Neurophysiol
    Volume : 104
    Issue : 6
    Pages : 3203-12
    ISSN : 1522-1598 (Electronic) 0022-3077 (Linking)
    Language : English
    Abstract : Cortical spreading depression (CSD) is an episode of electrical silence following intense neuronal activity that propagates across the cortex at approximately 3-6 mm/min and is associated with transient neuronal depolarization. CSD is benign in normally perfused brain tissue, but there is evidence suggesting that repetitive CSD contributes to infarct growth following focal ischemia. Studies to date have assumed that the cellular responses to CSD are uniform across neuronal types because there are no data to the contrary. In this study, we investigated the effect of CSD on membrane potential and the intracellular calcium concentration ([Ca(2+)](i)) of mouse layer V and layer II/III pyramidal neurons in brain slices. To place the data in context, we made similar measurements during anoxic depolarization induced by oxygen and glucose deprivation (OGD). The [Ca(2+)](i) was quantified using the low-affinity ratiometric indicator Fura-4F. During both CSD- and OGD-induced depolarization, the membrane potential approached 0 mV in all neurons. In layer V pyramids OGD resulted in an increase in [Ca(2+)](i) to a maximum of 3.69 +/- 0.73 (SD) muM (n = 12), significantly greater than the increase to 1.81 +/- 0.70 muM in CSD (n = 34; P < 0.0001). Membrane potential and [Ca(2+)](i) returned to nearly basal levels following CSD but not OGD. Layer II/III neurons responded to CSD with a greater peak increase in [Ca(2+)](i) than layer V neurons (2.88 +/- 0.6 muM; n = 9; P < 0.01). We conclude there is a laminar difference in the response of pyramidal neurons to CSD; possible explanations are discussed.



  3. Title of the Paper : Comparison of neuroprotective effects of erythropoietin (EPO) and carbamylerythropoietin (CEPO) against ischemia-like oxygen-glucose deprivation (OGD) and NMDA excitotoxicity in mouse hippocampal slice cultures (View at PubMed)
    Contributors : Montero, M.; Poulsen, F. R.; Noraberg, J.; Kirkeby, A.; van Beek, J.; Leist, M.; Zimmer, J.
    Address : Department of Anatomy and Neurobiology, Institute of Medical Biology, University of Southern Denmark, Winslowparken 21 st, DK-5000 Odense C, Denmark. mmontero@health.sdu.dk
    Publication Name : Exp Neurol
    Volume : 204
    Issue : 1
    Pages : 106-17
    Publication Year : 2007
    ISSN : 0014-4886 (Print) 0014-4886 (Linking)
    Language : English
    Abstract : In addition to its well-known hematopoietic effects, erythropoietin (EPO) also has neuroprotective properties. However, hematopoietic side effects are unwanted for neuroprotection, underlining the need for EPO-like compounds with selective neuroprotective actions. One such compound, devoid of hematopoietic bioactivity, is the chemically modified, EPO-derivative carbamylerythropoietin (CEPO). For comparison of the neuroprotective effects of CEPO and EPO, we subjected organotypic hippocampal slice cultures to oxygen-glucose deprivation (OGD) or N-methyl-d-aspartate (NMDA) excitotoxicity. Hippocampal slice cultures were pretreated for 24 h with 100 IU/ml EPO (=26 nM) or 26 nM CEPO before OGD or NMDA lesioning. Exposure to EPO and CEPO continued during OGD and for the next 24 h until histology, as well as during the 24 h exposure to NMDA. Neuronal cell death was quantified by cellular uptake of propidium iodide (PI), recorded before the start of OGD and NMDA exposure and 24 h after. In cultures exposed to OGD or NMDA, CEPO reduced PI uptake by 49+/-3 or 35+/-8%, respectively, compared to lesion-only controls. EPO reduced PI uptake by 33+/-5 and 15+/-8%, respectively, in the OGD and NMDA exposed cultures. To elucidate a possible mechanism involved in EPO and CEPO neuroprotection against OGD, the integrity of alpha-II-spectrin cytoskeletal protein was studied. Both EPO and CEPO significantly reduced formation of spectrin cleavage products in the OGD model. We conclude that CEPO is at least as efficient neuroprotectant as EPO when excitotoxicity is modeled in mouse hippocampal slice cultures.



  4. Title of the Paper : Marine compound Xyloketal B protects PC12 cells against OGD-induced cell damage (View at PubMed)
    Contributors : Zhao, J.; Li, L.; Ling, C.; Li, J.; Pang, J. Y.; Lin, Y. C.; Liu, J.; Huang, R.; Wang, G. L.; Pei, Z.; Zeng, J.
    Address : Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, PR China.
    Publication Name : Brain Res
    Volume : 1302
    Pages : 240-7
    Publication Year : 2009
    ISSN : 1872-6240 (Electronic) 0006-8993 (Linking)
    Language : English
    Abstract : Xyloketal B is a novel marine compound with unique chemical structure isolated from mangrove fungus Xylaria sp. (no. 2508). Recently, we have demonstrated that Xyloketal B is an antioxidant and can protect against oxidized low density lipoprotein (LDL)-induced cell injury. In the present study, we investigated whether Xyloketal B can protect against ischemia-induced cell injury in an in vitro oxygen glucose deprivation (OGD) model of ischemic stroke in PC12 cells. We found that Xyloketal B could directly scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical and protect PC12 cells against OGD insult. Furthermore, Xyloketal B alleviated OGD-induced mitochondria superoxide, mitochondria fragmentation and GTPase dynamin-related protein 1 (Drp1) overexpression as well as reduction of mitochondrial membrane potential. All together, the present study demonstrates that Xyloketal B protects PC12 cells against OGD-induced cell injury and that the anti-oxidative property and protective action on mitochondria may account for its neuroprotective actions.



  5. Title of the Paper : Minocycline attenuates both OGD-induced HMGB1 release and HMGB1-induced cell death in ischemic neuronal injury in PC12 cells (View at PubMed)
    Contributors : Kikuchi, K.; Kawahara, K.; Biswas, K. K.; Ito, T.; Tancharoen, S.; Morimoto, Y.; Matsuda, F.; Oyama, Y.; Takenouchi, K.; Miura, N.; Arimura, N.; Nawa, Y.; Meng, X.; Shrestha, B.; Arimura, S.; Iwata, M.; Mera, K.; Sameshima, H.; Ohno, Y.; Maenosono, R.; Yoshida, Y.; Tajima, Y.; Uchikado, H.; Kuramoto, T.; Nakayama, K.; Shigemori, M.; Hashiguchi, T.; Maruyama, I.
    Address : Department of Advanced Therapeutics, Division of Laboratory and Vascular Medicine, Field of Cardiovascular and Respiratory Disorders, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
    Publication Name : Biochem Biophys Res Commun
    Volume : 385
    Issue : 2
    Pages : 132-6
    Publication Year : 2009
    ISSN : 1090-2104 (Electronic) 0006-291X (Linking)
    Language : English
    Abstract : High mobility group box-1 (HMGB1), a non-histone DNA-binding protein, is massively released into the extracellular space from neuronal cells after ischemic insult and exacerbates brain tissue damage in rats. Minocycline is a semisynthetic second-generation tetracycline antibiotic which has recently been shown to be a promising neuroprotective agent. In this study, we found that minocycline inhibited HMGB1 release in oxygen-glucose deprivation (OGD)-treated PC12 cells and triggered the activation of p38mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK1/2). The ERK kinase (MEK)1/2 inhibitor U-0126 and p38MAPK inhibitor SB203580 blocked HMGB1 release in response to OGD. Furthermore, HMGB1 triggered cell death in a dose-dependent fashion. Minocycline significantly rescued HMGB1-induced cell death in a dose-dependent manner. In light of recent observations as well as the good safety profile of minocycline in humans, we propose that minocycline might play a potent neuroprotective role through the inhibition of HMGB1-induced neuronal cell death in cerebral infarction.



  6. Title of the Paper : Neuroprotection by NGF in the PC12 in vitro OGD model: involvement of mitogen-activated protein kinases and gene expression (View at PubMed)
    Contributors : Tabakman, R.; Jiang, H.; Shahar, I.; Arien-Zakay, H.; Levine, R. A.; Lazarovici, P.
    Address : Department of Pharmacology and Experimental Therapeutics, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel.
    Publication Name : Ann N Y Acad Sci
    Volume : 1053
    Pages : 84-96
    Publication Year : 2005
    ISSN : 0077-8923 (Print) 0077-8923 (Linking)
    Language : English
    Abstract : Neurodegenerative disorders and chronic disability due to stroke in the brain or spinal cord afflict a large sector of the population. To investigate the mechanism involved in ischemic stroke and to develop neuroprotective drugs/therapies, in vivo and in vitro, pharmacological models are needed. To investigate the cellular and molecular neuroprotective mechanisms of nerve growth factor (NGF), a member of the nervous system neurotrophin family of growth factors, under ischemia, we used an oxygen-glucose-deprivation (OGD) device and pheochromocytoma PC12 cells exposed to a paradigm of ischemic insult. Pretreatment of the cultures with 50 ng/mL of NGF, 18 h prior to OGD insult, conferred 30% of neuroprotection. Time-course experiments showed marked activation of the ERK, JNK, and p-38 MAPK isoforms during the OGD phase, but not during OGD reperfusion. Pretreatment of the cultures with 50 ng/mL of NGF, 18 h prior to OGD insult, resulted in 50% attenuation of OGD-induced activation of JNK 1, and 20% and 50% attenuation of OGD-induced activation of p-38 alpha and beta, respectively. The effect of NGF on gene expression in the PC12 ischemic model using Affymatrix Rat DNA-Microarray technology indicates that only 6% of the genes are differentially regulated (induced/suppressed) by OGD insult and/or NGF. These findings support the notion that pretreatment with NGF confers neuroprotection from OGD insult, a phenomenon coincidentally related to differential inhibition of MAPK stress kinase isoforms and differential gene expression. This ischemic model may be useful to investigate molecular mechanisms of OGD-induced neurotoxicity and NGF-induced neuroprotection, and to generate novel therapeutic concepts for stroke treatment.



  7. Title of the Paper : Protein aggregation in neurons following OGD: a role for Na+ and Ca2+ ionic dysregulation (View at PubMed)
    Contributors : Chen, X.; Kintner, D. B.; Baba, A.; Matsuda, T.; Shull, G. E.; Sun, D.
    Address : Neuroscience Training Program, University of Wisconsin School of Medicine and Public Health, Waisman Center, Madison, Wisconsin, USA.
    Publication Name : J Neurochem
    Volume : 112
    Issue : 1
    Pages : 173-82
    ISSN : 1471-4159 (Electronic) 0022-3042 (Linking)
    Language : English
    Abstract : In this study, we investigated whether disruption of Na(+) and Ca(2+) homeostasis via activation of Na(+)-K(+)-Cl(-) cotransporter isoform 1 (NKCC1) and reversal of Na(+)/Ca(2+) exchange (NCX(rev)) affects protein aggregation and degradation following oxygen-glucose deprivation (OGD). Cultured cortical neurons were subjected to 2 h OGD and 1-24 h reoxygenation (REOX). Redistribution of ubiquitin and formation of ubiquitin-conjugated protein aggregates occurred in neurons as early as 2 h REOX. The protein aggregation progressed further by 8 h REOX. There was no significant recovery at 24 h REOX. Moreover, the proteasome activity in neurons was inhibited by 80-90% during 2-8 h REOX and recovered partially at 24 h REOX. Interestingly, pharmacological inhibition or genetic ablation of NKCC1 activity significantly decreased accumulation of ubiquitin-conjugated protein aggregates and improved proteasome activity. A similar protective effect was obtained by blocking NCX(rev) activity. Inhibition of NKCC1 activity also preserved intracellular ATP and Na(+) homeostasis during 0-24 h REOX. In a positive control study, disruption of endoplasmic reticulum Ca(2+) with thapsigargin triggered redistribution of free ubiquitin and protein aggregation. We conclude that overstimulation of NKCC1 and NCX(rev) following OGD/REOX partially contributes to protein aggregation and proteasome dysfunction as a result of ionic dysregulation.



  8. Title of the Paper : Surgical OGD--a dying art? (View at PubMed)
    Contributors : Bell, R. E.; Griffiths, N. J.; Bates, T.
    Address : Department of Surgery, William Harvey Hospital, Ashford, Kent, UK. rach_bell@hotmail.com
    Publication Name : Ann R Coll Surg Engl
    Volume : 85
    Issue : 1
    Pages : 14-7
    Publication Year : 2003
    ISSN : 0035-8843 (Print) 0035-8843 (Linking)
    Language : English
    Abstract : INTRODUCTION: Reductions in surgical training and the increases in medical gastroenterology have raised concerns that surgeons may not be adequately trained in upper gastrointestinal (GI) endoscopy. METHOD: To evaluate this problem, a questionnaire was sent to all current surgical specialist registrars (SpRs) in the South Thames East Region. RESULTS: There was an 82% (52/63) response rate. Only 50% (26/52) of trainees had received more than 6 months\' training in upper GI endoscopy. 83% (43/52) were in posts which did not provide adequate elective exposure for training. 50% (26/52) were required to provide an emergency service, despite a paucity of experience and less than 50% were able to perform therapeutic injection. In the main, emergency endoscopy is performed with substandard equipment, poor facilities, and untrained staff. CONCLUSIONS: Surgical trainees are poorly trained and do not have the necessary skills to provide an emergency service for upper GI haemorrhage. Emergency endoscopy facilities are severely under resourced.



  9. Title of the Paper : Transnasal OGD: practice survey and impact of a live video retransmission (View at PubMed)
    Contributors : Dumonceau, J. M.; Dumortier, J.; Deviere, J.; Kahaleh, M.; Ponchon, T.; Maffei, M.; Costamagna, G.
    Address : Division of Gastroenterology and Hepatology, Geneva University Hospital, Micheli-du-Crest Street 24, 1205 Geneva, Switzerland. jmdumonceau@hotmail.com
    Publication Name : Dig Liver Dis
    Volume : 40
    Issue : 9
    Pages : 776-83
    Publication Year : 2008
    ISSN : 1878-3562 (Electronic) 1590-8658 (Linking)
    Language : English
    Abstract : BACKGROUND: Unsedated transnasal oesogastroduodenoscopy significantly improves patient tolerance compared to unsedated conventional peroral oesogastroduodenoscopy. AIMS: To assess the adoption of transnasal oesogastroduodenoscopy among endoscopists from various European countries and its determinants. METHODS: A survey was distributed to 624 endoscopists attending a live course on digestive endoscopy; a poll was also performed immediately before and after live video retransmission of a transnasal oesogastroduodenoscopy. RESULTS: Answer rate was 48%; transnasal oesogastroduodenoscopy was practised by 31% of respondents. In multivariate analysis, practice of transnasal oesogastroduodenoscopy was associated with location in France and Netherlands (P<0.0001), availability of many gastroscopes (P<0.0001) and less frequent use of sedation (P=0.006). Endoscopists who did not practise transnasal oesogastroduodenoscopy cited doubts about its advantages over conventional oesogastroduodenoscopy and lack of training (34% each) as barriers to adoption. Seventy-four percent of endoscopists practicing transnasal oesogastroduodenoscopy did actually use it in <20% of eligible cases. Live video retransmission of a transnasal oesogastroduodenoscopy increased the proportion of endoscopists interested in this technique (P=0.006). CONCLUSIONS: Adoption of transnasal oesogastroduodenoscopy largely varies between European countries; endoscopists practicing this technique use it in a minority of eligible cases. Live case demonstration may decrease barriers to the adoption of this technique.



  10. Title of the Paper : Trichostatin A enhances OGD-astrocyte viability by inhibiting inflammatory reaction mediated by NF-kappaB (View at PubMed)
    Contributors : Niu, F.; Zhang, X.; Chang, L.; Wu, J.; Yu, Y.; Chen, J.; Xu, Y.
    Address : Department of Neurology, Drum Tower Hospital of Nanjing Medical University, PR China.
    Publication Name : Brain Res Bull
    Volume : 78
    Issue : 6
    Pages : 342-6
    Publication Year : 2009
    ISSN : 1873-2747 (Electronic) 0361-9230 (Linking)
    Language : English
    Abstract : In this study we investigate the protective effects of Trichostatin A (TSA) on astrocyte injury after oxygen-glucose deprivation (OGD) and further explore its possible protective mechanisms of inhibiting inflammatory reaction mediated by nuclear factor-kappaB (NF-kappaB). In the in vitro model of astrocyte OGD, TSA treatment was used at different doses and time points before deprivation. Astroglial viability was determined by MTT assay. Then tumor necrosis factor-alpha, interleukin-1beta (IL-1beta), and IL-6 mRNA were measured by RT-PCR. Furthermore, the expression of phosphorylated p65, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinases (ERK), MAPK/c-Jun N-terminal (JNK) and MAPK/p38 was assayed by Western blot. The results showed that TSA at the five doses (12.5, 25, 50, 100, and 200 ng/ml) significantly enhanced the astrocytes viability by 25.3%, 46.1%, 37.5%, 34.9%, and 22% of the vehicle, respectively. The level of TNF-alpha, IL-1beta and IL-6 mRNA in astrocytes was increased after OGD and down-regulated by TSA (p<0.05). In addition, the phosphorylation p65 was markedly activated in the astrocytes after OGD compared to the control (p<0.05). TSA inhibited phosphorylation of p65 but did not affect the MAPK pathway. Our results suggest that TSA protects astrocytes from damage after OGD by the inhibition of the inflammatory reaction and this protection is at least partially through the suppression of phosphorylation of NF-kappaB p65.



  11. Title of the Paper : [Welcome address by the president of the Federal Chamber of Physicians at the opening ceremony of the 56th OGD Congress 2006] (View at PubMed)
    Contributors : Hoppe, J. D.
    Address : Bundesarztekammer Berlin, Germany.
    Publication Name : Gesundheitswesen
    Volume : 68
    Issue : 11
    Pages : 659-60
    Publication Year : 2006
    ISSN : 1439-4421 (Electronic) 0941-3790 (Linking)
    Language : ger