The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
William A Baumgartner - One of the best experts on this subject based on the ideXlab platform.
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Monosialoganglioside gm1 inhibits neurotoxicity after hypothermic circulatory arrest
Surgery, 1998Co-Authors: Elaine E Tseng, Mary E Blue, Juan C Troncoso, Michael V Johnston, Malcolm V Brock, Mary S Lange, Charles J Lowenstein, William A BaumgartnerAbstract:Abstract Background: Prolonged hypothermic circulatory arrest (HCA) causes clinical neurologic injury. This injury involves neuronal apoptosis, or programmed cell death. We have previously demonstrated that HCA causes glutamate excitotoxicity, increased nitric oxide (NO) production, and NO-mediated apoptosis. We hypothesized that Monosialoganglioside GM 1 inhibits NO synthase. The purpose of this study was to determine whether GM 1 inhibits NO production and neuronal apoptosis after HCA. Methods: Fourteen dogs underwent intracerebral microdialysis to measure excitatory amino acids, glutamate, aspartate, and citrulline, an equal coproduct of NO. They underwent 2 hours of HCA at 18° C and were sacrificed 8 hours after HCA. Group 1 ( n = 6) was pretreated with GM 1 , 30 mg/kg intravenously every day for 3 days, as well as before and after HCA. Group 2 control dogs ( n = 8) received vehicle only. Apoptosis was scored from 0 (normal) to 100 (severe injury). Results: Excitatory amino acids, aspartate and glutamate, coagonist glycine, and citrulline levels increased significantly over baseline during HCA and after HCA. GM 1 pretreatment did not appreciably alter levels of glutamate, aspartate, and glycine; however, it substantially decreased citrulline and therefore NO production throughout the experiment. GM 1 significantly inhibited apoptosis (group 1 vs group 2: 15.56 ± 13.60 vs 62.92 ± 6.17; P Conclusions: Our results provide the first direct evidence that GM 1 inhibits NO synthase to reduce NO production and HCA-induced neuronal apoptosis. GM 1 did not affect excitatory glutamate or aspartate levels. GM 1 has been used in clinical trials of spinal cord injury and may be efficacious in reducing neurologic injury after HCA. (Surgery 1998;124:298-306.)
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the Monosialoganglioside gm1 reduces neurologic injury associated with hypothermic circulatory arrest
Surgery, 1993Co-Authors: J M Redmond, A M Gillinov, Mary E Blue, Kenton J Zehr, Juan C Troncoso, Duke E Cameron, Michael V Johnston, William A BaumgartnerAbstract:Background. Neurologic injury associated with prolonged hypothermic circulatory arrest (HCA) may be mediated by calcium-dependent glutamate excitotoxicity (GE). The Monosialoganglioside GM 1 has been shown in vitro to limit GE in conditions of metabolic stress. To test the hypothesis that gangliosides can prevent HCA-induced brain injury, GM 1 was used in a canine model of HCA. Methods. Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 hours of HCA at 18 o C, and rewarmed to 36 o to 37 o C on closed-chest cardiopulmonary bypass. All were mechanically ventilated and monitored for 20 hours before extubation and survived for 3 days
Zhang Jian - One of the best experts on this subject based on the ideXlab platform.
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Experimental study on effect of minimally invasive hematoma aspiration combined with Monosialoganglioside on cerebral edema
Chinese Journal of Hospital Pharmacy, 2020Co-Authors: Zhang JianAbstract:OBJECTIVE To study the effect of minimally invasive hematoma aspiration combined with Monosialoganglioside(GM1) injected into peritoneal and hematoma intracavity on cerebral edema of acute stage originated by intracerebral hemorrhage.METHODS Intracerebral hemorrhage was induced by injecting Ⅳ collagenase into caudate nucleus of SD rats,and after ten hours urokinase was injected into hematoma intracavity to dissolve clot.Hematoma was removed from intracavity by use of minimally invasive hematoma aspiration.The effect of minimally invasive hematoma aspiration combined with Monosialoganglioside(GM1) on cerebral edema was evaluated by determination of brain water and immunohistochemical of AQP4 in brain tissue during different time,among aspiration group,aspiration combined with GM1 peritoneal injection group and aspiration combined with GM1 hematoma cavity injection.RESULTS Brain water of aspiration combined with GM1 peritoneal injection group and aspiration combined with GM1 hematoma cavity injection.were less than that of aspiration group(P0.05) and the number of cells and integrated optical density expressed AQP4 around hematoma on third day were smaller(P0.05),there was significant decrease in the number of cells and integrated optical density on fifth and seventh day(P0.01).CONCLUSION Minimally invasive hematoma aspiration combined with GM1 helps to reduce cerebral edema of acute stage originated by intracerebral hemorrhage in rats;AQP4 participates formation of cerebral edema;furthermore,AQP4 might be potential target that GM1 reduces cerebral edema.Medication dosage of minimal invasive hematoma aspiration combined with GM1 hematoma cavity injection.was less and more economical in treatment of intracerebral hemorrhage.
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Experimental study on the effect of minimally invasive hematoma aspiration combining with the administration of Monosialoganglioside on nervous function in rats
Chinese Journal of Hospital Pharmacy, 2020Co-Authors: Zhang JianAbstract:OBJECTIVE To discuss the effect of minimally invasive hematoma aspiration combining with the administration of Monosialoganglioside(GM1)injected into peritoneal and hematoma intracavity on nervous function of acute stage originated by intracerebral hemorrhage.METHODS Intracerebral hemorrhage was induced by injecting Ⅳ collagenase into caudate nucleus of SD rats,and after ten hours urokinase was injected into hematoma intracavity to dissolve clot.Hematoma was removed from intracavity by use of minimally invasive hematoma aspiration.The effect of minimally invasive hematoma aspiration combining with the administration of Monosialoganglioside(GM1) on nervous function was evaluated by determination of defect of the nervous function and immunohistochemistry of caspase-3,GFAP in brain tissue during different time,among aspiration group,aspiration combining with GM1 peritoneal injection group and aspiration combining with GM1 hematoma cavity injection.RESULTS Positive cells and protein express of caspase-3、 GFAP of hematoma cavity group、abdominal cavity group were significantly decreased compared with aspiration group at 3 d(P0.05)、5 d、7 d,especially at 5 d、7 d(P0.01).Hematoma cavity group and abdominal cavity group were compared,positive cells and protein express of caspase-3、 GFAP of the former were significantly decreased at 3 d(P0.05)、5 d、7 d,especially at 5 d、7 d(P0.01);Neurologic functional recovery of hematoma cavity group、abdominal cavity group was more significant compared with aspiration group at 3 d(P0.05)、5 d、7 d,especially at 5 d、7 d(P0.01).Hematoma cavity group and abdominal cavity group were compared,neurologic functional recovery of the former was significantly better significant at 3 d(P0.05)、5 d、7 d,especially at 5 d、7 d(P0.01).CONCLUSION Defect of the nervous function of ICH possibly relates apoptosis and accrementition of horizontal cell.GM1 has effect of suppressing apoptosis and accrementition of horizontal cell,which possibly is one of the mechanisms of promoting neurologic functional recovery.Medication dosage of minimal invasive hematoma aspiration combining with GM1 hematoma cavity injection was effective and more economical in the treatment of intra-cerebral hemorrhage.
A C Cuello - One of the best experts on this subject based on the ideXlab platform.
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potentiation of nerve growth factor induced alterations in cholinergic fibre length and presynaptic terminal size in cortex of lesioned rats by the Monosialoganglioside gm1
Neuroscience, 1993Co-Authors: L Garofalo, Alfredo Ribeirodasilva, A C CuelloAbstract:Abstract The effect of Monosialoganglioside GM1 and/or nerve growth factor treatment on the cholinergic innervation of the rat cortex was studied using both light- and electron-microscopic techniques assisted by image analysis. Adult male Wistar rats were unilaterally decorticated and received continuous infusions, via minipump, of vehicle, GM1 (1.5 mg/day) and/or nerve growth factor (12 μg/day) into the cerebroventricular space. Treatments were initiated immediately post-lesion and ended after seven days. Thirty days post-lesion (i.e. 23 days after the end of drug administration) brains were processed for choline acetyltransferase immunocytochemistry for either light- or electron-microscopic analysis. At this timepoint choline acetyltransferase-immunoreactive neurons in the ipsilateral nucleus basalis magnocellularis were significantly reduced in size especially in the mid portion of this nucleus, in lesion vehicle-treated rats. Moreover, decreases in choline acetyltransferase immunoreactive fibre length (ranging from 31 to 50%) and varicosity number (ranging from 26 to 39%) occurred in all cortical layers within a portion of the remaining cortex of these animals. Monosialoganglioside GM1 or nerve growth factor treatment equally attenuated deficits in nucleus basalis magnocellularis cell size and cortical choline acetyltransferase immunoreactive fibre length. However, nerve growth factor, but not Monosialoganglioside GM1 treatment also increased choline acetyltransferase-immunoreactive varicosity number above control levels. In lesioned rats which received both nerve growth factor and the Monosialoganglioside GM1, the mean cross-sectional area of nucleus basalis magnocellularis cholinergic neurons did not differ significantly from control values. By contrast, cortical choline acetyltransferase-immunoreactive fibre length and varicosity number were significantly increased above control values and that induced by nerve growth factor treatment alone. Quantitative electron-microscopic analysis showed that cholinergic boutons in cortical layer V were considerably shrunken in lesioned vehicle-treated rats and that GM1 treatment failed to significantly attenuate this deficit. However, exogenous nerve growth factor provoked a significant increase (35% above control values) in cortical cholinergic presynaptic terminal size which was even further augmented by concurrent GM1 treatment (69% above control values). This trophic factor-induced increase in bouton size was confirmed using serial electron microscopy and computer-assisted three-dimen-sional reconstruction of the cholinergic varicosities. The number of synaptic contacts in cortical layer V was also found to be significantly reduced (45% of control values) in lesioned vehicle-treated rats but was maintained at control levels by exogenous GM1 treatment. In addition, a significant increase (95% above control levels) in the number of choline acetyltransferase-immunoreactive boutons with synaptic differentiations was noted in lesioned nerve growth factor-treated rats. Concurrent GM1 and nerve growth factor treatment did not cause a further increase in synaptic number. Cortical cholinergic innervation and the size of choline acetyltransferase-immunoreactive nucleus basalis magnocellularis neurons were not altered in unlesioned rats by GM1, nerve growth factor or nerve growth factor and GM1 treatment. These results demonstrate that GM1 can attenuate deficits in cortical cholinergic innervation following injury and can further augment nerve growth factor induced synaptic remodelling in the injured adult rat brain.
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long term protective effects of human recombinant nerve growth factor and Monosialoganglioside gm1 treatment on primate nucleus basalis cholinergic neurons after neocortical infarction
Neuroscience, 1993Co-Authors: Paolo Liberini, Erik P Pioro, Dusica Maysinger, F R Ervin, A C CuelloAbstract:Abstract Infarction induces biochemical and morphological retrograde degenerative changes in cholinergic neurons of the rat nucleus basalis magnocellularis [Sofroniew et al . (1983) Brain Res . 289 , 370–374]. In the present study, this lesion model has been reproduced in the non-human primate ( Cercopithecus aethiops ) to investigate whether degenerative changes affecting the cortex surrounding the lesioned area and the ipsilateral basal forebrain are prevented by the early administration of recombinant human nerve growth factor alone or in combination with the Monosialoganglioside GM1. Six months after surgery and treatment, the monkeys were processed either for biochemistry (choline acetyltransferase assay) or immunocytochemistry. In lesioned vehicle-treated animals, choline acetyltransferase activity significantly decreased by 28% in the cortex surrounding the injured area and by 31% in the ipsilateral nucleus basalis of Meynert when compared with values of sham-operated monkeys. These biochemical changes were fully prevented with the administration of nerve growth factor alone or in combination with the Monosialoganglioside GM1. The morphometrical analysis revealed a significant shrinkage of cholinergic neurons (61 ± 1.4% of sham-operated cell size) and loss of neuritic processes (59 ± 10% of sham-operated values) within the intermediate nucleus basalis region of lesioned vehicle-treated animals. Although a protection of the cholinergic cell bodies within the nucleus basalis was found with both treatments, a significant recovery of the neuritic processes (84 ± 7.2% of sham-operated values) was assessed only in the double-treated monkeys. These results indicate that the early administration of nerve growth factor alone or in combination with the Monosialoganglioside GM1 induces a long-term protective effect on the nucleus basalis cholinergic neurons in cortical injured non-human primates.
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acetylcholine release in vivo effects of chronic treatment with Monosialoganglioside gm1
Neuropharmacology, 1990Co-Authors: Dusica Maysinger, Mario Herreramarschitz, Urban Ungerstedt, A C CuelloAbstract:Rats with unilateral cortical devascularizing lesions were treated with the Monosialoganglioside GM1 in two different ways. One group of animals received GM1 (5 mg/kg/day, for 7 days), through a permanent cannula implanted intracerebroventricularly (i.c.v.) and connected to an osmotic minipump. The other group was treated with microencapsulated GM1 placed directly onto the surface of the lesioned cortex. The effect of GM1, administered into the lateral ventricle and supracortically, on the release of ACh in vivo was studied, using a microdialysis system combined with sensitive high performance liquid chromatography (HPLC). The release of acetylcholine and choline was studied in the cortex and striatum of the rat under nonstimulated (basal) and KCl (100 mM)-stimulating conditions. The non-stimulated release of acetylcholine was only measurable in the presence of neostigmine and was found to be about 30 μ M in the cortex and approximately 10 times greater in the striatum. A large concentration of KCl led to a remarkable increase of acetylcholine in the control (C) and vehicle-treated lesioned groups (V i.c.v., V cap: 11–13 fold), but was greater in the GM1-treated groups (GM1 i.c.v., GM1 cap: 20–25 fold). In contrast, KCl-stimulated release of ACh in striata from GM1-treated lesioned groups was significantly less (5–10 fold), compared to the unlesioned controls (C: 16 fold) and lesioned vehicle-treated rats (V i.c.v. and V cap: 16–18 fold). The release of choline was not increased significantly by large concentrations of KCl present in the perfusion medium. In all experimental groups, and in both structures of the brain, ratios between stimulated and non-stimulated release of choline was between 0.7–1.2. Results from this study support the idea that GM1, applied either intracerebroventricularly or locally, at the site of the cortical lesion (in a microencapsulated form), leads to a “functional recovery” of cholinergic neurons in the remaining cortex, adjacent to the devascularizing injury.
Akemi Suzuki - One of the best experts on this subject based on the ideXlab platform.
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A micro method involving micro high-performance liquid chromatography-mass spectrometry for the structural characterization of neutral glycosphingolipids and Monosialogangliosides
Journal of Biochemistry, 1991Co-Authors: Minoru Suzuki, Tamio Yamakawa, Akemi SuzukiAbstract:: A micro method involving high-performance liquid chromatography-fast atom bombardment mass spectrometry (HPLC/FAB/MS) has been developed for the sensitive structural characterization of neutral glycosphingolipids and Monosialogangliosides. The method involves a micro silica gel column (0.3 mm i.d. x 100 mm) and a micro HPLC apparatus working at a flow rate of 6 microliters/min. All injected materials can be structurally characterized by mass spectrometry without the splitting or wasting of materials, which was not possible with our previous method [M. Suzuki et al. (1990) J. Biochem. 108, 92-98]. A mixture containing 160 ng each of five neutral glycosphingolipids (GlcCer, LacCer, Gb3Cer, Gb4Cer, and IV3 alpha GalNAc-Gb4Cer) and a mixture containing 160 ng each of three Monosialogangliosides [GM3(NeuAc), GM2(NeuAc), and GM1(NeuAc)] were injected into the micro HPLC with programmed elution with isopropanol-n-hexane-water with or without ammonium hydroxide. Each glycosphingolipid was separated by mass chromatography and the obtained mass spectra were suitable for structural characterization. Thus, the characterization of glycosphingolipids was achieved with small amounts of materials, 160 ng each, and in mixtures.
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High-performance liquid chromatography-mass spectrometry of glycosphingolipids: II. Application to neutral glycolipids and Monosialogangliosides.
Journal of Biochemistry, 1990Co-Authors: Minoru Suzuki, Tamio Yamakawa, Akemi SuzukiAbstract:: We previously reported a method of high-performance liquid chromatography-fast atom bombardment mass spectrometry (HPLC/FAB/MS) for the structural characterization of molecular species of GlcCer and IV3 beta Gal-Gb4Cer [M. Suzuki et al. (1989) J. Biochem. 105, 829-833]. In this paper, we report a modification of this HPLC/FAB/MS method, which was used for the separation and characterization of neutral glycosphingolipids (GlcCer, LacCer, Gb3Cer, Gb4Cer, and IV3 alpha GalNAc-Gb4Cer) and Monosialogangliosides [GM3(NeuAc or NeuGc), GM2 (NeuAc or NeuGc), and GM1 (NeuAc or NeuGc)]. Mixtures of the purified neutral glycolipids and Monosialogangliosides were subjected to HPLC on a silica gel column, with programmed elution with isopropanol-n-hexane-water, with or without ammonium hydroxide. In order to obtain mass spectra and mass chromatograms of individual components, effluent from the HPLC column was mixed with a methanol solution of triethanolamine, which was used as the matrix for the FAB ionization, and one-thirtieth of the effluent mixture was introduced into a mass spectrometer through a frit interface. A mixture of the five neutral glycolipids, 5 micrograms of each, gave five peaks on a mass chromatogram obtained by monitoring of the corresponding major pseudo-molecular ions. A mixture of the six Monosialogangliosides, 5 micrograms of each, gave six peaks on a mass chromatogram obtained by monitoring of the major pseudo-molecular ions, indicating that GM3, GM2, and GM1 were clearly separated, and that separation due to differences in sialic acid species was also achieved. In the mass spectra of the neutral glycolipids and Monosialogangliosides, pseudo-molecular ions and fragment ions due to the elimination of sugar moieties were clearly detected.(ABSTRACT TRUNCATED AT 250 WORDS)
Juan C Troncoso - One of the best experts on this subject based on the ideXlab platform.
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Monosialoganglioside gm1 inhibits neurotoxicity after hypothermic circulatory arrest
Surgery, 1998Co-Authors: Elaine E Tseng, Mary E Blue, Juan C Troncoso, Michael V Johnston, Malcolm V Brock, Mary S Lange, Charles J Lowenstein, William A BaumgartnerAbstract:Abstract Background: Prolonged hypothermic circulatory arrest (HCA) causes clinical neurologic injury. This injury involves neuronal apoptosis, or programmed cell death. We have previously demonstrated that HCA causes glutamate excitotoxicity, increased nitric oxide (NO) production, and NO-mediated apoptosis. We hypothesized that Monosialoganglioside GM 1 inhibits NO synthase. The purpose of this study was to determine whether GM 1 inhibits NO production and neuronal apoptosis after HCA. Methods: Fourteen dogs underwent intracerebral microdialysis to measure excitatory amino acids, glutamate, aspartate, and citrulline, an equal coproduct of NO. They underwent 2 hours of HCA at 18° C and were sacrificed 8 hours after HCA. Group 1 ( n = 6) was pretreated with GM 1 , 30 mg/kg intravenously every day for 3 days, as well as before and after HCA. Group 2 control dogs ( n = 8) received vehicle only. Apoptosis was scored from 0 (normal) to 100 (severe injury). Results: Excitatory amino acids, aspartate and glutamate, coagonist glycine, and citrulline levels increased significantly over baseline during HCA and after HCA. GM 1 pretreatment did not appreciably alter levels of glutamate, aspartate, and glycine; however, it substantially decreased citrulline and therefore NO production throughout the experiment. GM 1 significantly inhibited apoptosis (group 1 vs group 2: 15.56 ± 13.60 vs 62.92 ± 6.17; P Conclusions: Our results provide the first direct evidence that GM 1 inhibits NO synthase to reduce NO production and HCA-induced neuronal apoptosis. GM 1 did not affect excitatory glutamate or aspartate levels. GM 1 has been used in clinical trials of spinal cord injury and may be efficacious in reducing neurologic injury after HCA. (Surgery 1998;124:298-306.)
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the Monosialoganglioside gm1 reduces neurologic injury associated with hypothermic circulatory arrest
Surgery, 1993Co-Authors: J M Redmond, A M Gillinov, Mary E Blue, Kenton J Zehr, Juan C Troncoso, Duke E Cameron, Michael V Johnston, William A BaumgartnerAbstract:Background. Neurologic injury associated with prolonged hypothermic circulatory arrest (HCA) may be mediated by calcium-dependent glutamate excitotoxicity (GE). The Monosialoganglioside GM 1 has been shown in vitro to limit GE in conditions of metabolic stress. To test the hypothesis that gangliosides can prevent HCA-induced brain injury, GM 1 was used in a canine model of HCA. Methods. Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 hours of HCA at 18 o C, and rewarmed to 36 o to 37 o C on closed-chest cardiopulmonary bypass. All were mechanically ventilated and monitored for 20 hours before extubation and survived for 3 days