Abstract：
:There is evidence to suggest that, in acute liver failure (ALF), brain ammonia and proinflammatory cytokines may act synergistically to cause brain edema and its complications (intracranial hypertension, brain herniation). However, the molecular mechanisms involved remain to be established. In order to address this issue, semi-quantitative RT-PCR was used to measure the expression of genes coding for astrocytic proteins with an established role in cell volume regulation in cerebral cortical astrocytes exposed to toxic agents previously identified in experimental and clinical ALF. Such agents include ammonia, the proinflammatory cytokine interleukin-1beta (IL-1beta) and combinations of the two. Exposure of cultured astrocytes to recombinant IL-1beta (but not ammonia) resulted in increased expression of aquaporin-4 (AQP-4). Both ammonia and proinflammatory mediators led to decreased expression of glial fibrillary acidic protein (GFAP), a cytoskeletal protein, but these effects were not additive. On the other hand, heme oxygenase-1 (HO-1) and inducible nitric oxide synthase (iNOS) expression were significantly increased by exposure to both ammonia and proinflammatory mediators and although modest, these effects were additive suggestive of a synergistic mechanism. These findings suggest that worsening of brain edema and its complications in ALF due to proinflammatory mechanisms may result from exacerbation of oxidative stress-related mechanisms rather than upregulation of AQP-4 or decreases in expression of the astrocytic structural protein GFAP.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Chastre A,Jiang W,Desjardins P,Butterworth RFdoi
10.1007/s11011-010-9185-ysubject
Has Abstractpub_date
2010-03-01 00:00:00pages
17-21issue
1eissn
0885-7490issn
1573-7365journal_volume
25pub_type
杂志文章abstract：:Cyclic AMP is part of an endogenous mechanism that downregulates inflammatory response, and its intracellular concentration is regulated chiefly by cyclic nucleotide phosphodiesterases type 4. The goal of the present study was to determine whether phosphodiesterases 4 are involved in the inflammatory response of astro...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-009-9150-9
更新日期：2009-09-01 00:00:00
abstract：:The role of oxidative stress in the pathogenesis of phenylketonuria (PKU)-associated disorders has been implicated. Ischemia modified albumin (IMA) is a modified form of serum albumin, which is produced under the conditions of oxidative stress. The aim of this study was to measure the serum level of IMA in the PKU pat...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-017-0165-3
更新日期：2018-06-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
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更新日期：2015-04-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-018-0342-z
更新日期：2019-02-01 00:00:00
abstract：:Maple syrup urine disease (MSUD) or branched-chain alpha-keto aciduria (BCKA) is an inherited disorder caused by a deficiency of the branched-chain alpha-keto acid dehydrogenase complex (BCKAD) activity. The blockage of this pathway leads to tissue accumulation of the branched-chain amino acids (BCAA) leucine, isoleuc...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-006-9030-5
更新日期：2006-12-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-020-00615-1
更新日期：2020-12-01 00:00:00
abstract：:The effect of factors released from N2A neuroblastoma cells on the expression of myelin protein genes in glioma C6 cells, i.e., proteolipid protein (PLP) and myelin-associated glycoprotein (MAG), was studied. Both cells lines were propagated in serum-free DMEM-F10 (1:1) medium. The addition of 50% N2A conditioned medi...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/BF01000160
更新日期：1992-09-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-019-00430-3
更新日期：2019-08-01 00:00:00
abstract：:Mutations in the HTT gene, consisting of expansion of CAG triplets, cause the Huntington's disease (HD), one of the major neurodegenerative disorders. Formation of aggregates of mutant huntingtin (mHTT, the product of the mutant HTT gene) leads to cellular dysfunctions, and subsequent neurodegeneration which manifest ...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-019-00405-4
更新日期：2019-06-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章,meta分析
doi：10.1007/s11011-017-0128-8
更新日期：2018-02-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/BF01000159
更新日期：1992-09-01 00:00:00
abstract：:Due to the high ability of cadmium to cross the blood-brain barrier, cadmium (Cd) causes severe neurological damages. Hence, the purpose of this study was to investigate the possible protective effect of Mangifera indica leaf extract (MLE) against Cd-induced neurotoxicity. Rats were divided into eight groups. Group 1 ...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-018-0222-6
更新日期：2018-08-01 00:00:00
abstract：:Heart failure patients often manifest white matter hyperintensites on brain magnetic resonance imaging (MRI). White matter hyperintnsities have also been linked with cognitive problems in patients with heart failure. Sleep disordered breathing may contribute to structural brain changes in heart failure. The purpose of...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-018-0309-0
更新日期：2018-12-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-016-9831-0
更新日期：2016-08-01 00:00:00
abstract：:MRPS22 gene defect is a very rare newly discovered mitochondrial disorder. We report a 4-month-old severely affected male infant with MRPS22 mutation. Whole exome sequencing revealed a novel homozygous splicing mutation c.339 + 5 G > A in MRPS22 gene. He has mild dysmorphism, hypotonia, developmental delay but not hyp...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-017-0074-5
更新日期：2017-10-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-019-00461-w
更新日期：2019-12-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-017-0054-9
更新日期：2017-10-01 00:00:00
abstract：:Attention alterations are reported in cirrhotics. Aiming at clarifying attention functioning in cirrhotics, an inquiry on the functioning of the anterior (AAS) and the posterior (PAS) attention system was performed. Thirty-six cirrhotics without overt hepatic encephalopathy (24 with EEG or TMT-A alterations) and 16 ma...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-005-4149-3
更新日期：2005-06-01 00:00:00
abstract：:Schizophrenia (SCZ) and bipolar disorder (BD) are severe psychiatric disorders that share many genetic risk factors. This study aimed to investigate the association of phosphoinositide-3-kinase regulatory subunit1 (PIK3R1) gene rs3756668 and rs3730089 polymorphisms with SCZ and BD risks and determine the expression le...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-020-00552-z
更新日期：2020-06-01 00:00:00
abstract：:Maternal separation in non-human primates has been proposed as a model of early adversity. The symptoms of separation anxiety were studied in vervet monkeys, during the weaning period, when psychotropic medications were administered. The control group received a normal diet and treatment groups received citalopram, re...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-006-9011-8
更新日期：2006-09-01 00:00:00
abstract：:Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with severe liver disease. Although the mechanisms responsible for HE remain elusive, ammonia is generally considered to be involved in its pathogenesis, and astrocytes are thought to be the principal target of ammonia neurotoxici...
journal_title：Metabolic brain disease
pub_type： 杂志文章,评审
doi：10.1023/a:1023858902184
更新日期：2003-06-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-013-9399-x
更新日期：2013-09-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章,评审
doi：10.1007/s11011-005-7910-8
更新日期：2005-12-01 00:00:00
abstract：:Type 2 diabetes (T2D) and Alzheimer's disease (AD) are two progressive disorders with high prevalence worldwide. Polymorphisms in tumor necrosis factor-alpha (TNF-α) and apolipoprotein E (ApoE) genes might be associated with both T2D and AD, representing possible genetic markers for the development of the AD in subjec...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-012-9310-1
更新日期：2012-12-01 00:00:00
abstract：:Amyloid-beta (Aβ) interacts with the serine/threonine protein kinase AKT (also known as protein kinase B)/glycogen synthase kinase 3β (GSK3β) pathway and deactivates GSK3β signaling, which result in microtubule protein tau phosphorylation. Atorvastatin, a HMG-CoA reductase inhibitor, has been proven to improve learnin...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-016-9803-4
更新日期：2016-06-01 00:00:00
abstract：:The availability of an animal model is crucial in studying the pathophysiological mechanisms of disease and to test possible therapies. Now, there are several models for the study of liver diseases, but there still remains a lack of a satisfactory animal model of chronic liver disease with hepatic encephalopathy (HE) ...
journal_title：Metabolic brain disease
pub_type： 杂志文章,评审
doi：10.1007/s11011-005-7925-1
更新日期：2005-12-01 00:00:00
abstract：:Pipecolic acid (PA) levels are increased in severe metabolic disorders of the central nervous system such as Zellweger syndrome, infantile Refsum disease, neonatal adrenoleukodystrophy and hyperlysinemia. The affected individuals present progressive neurological dysfunction, hypotonia and growth retardation. The mecha...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-013-9466-3
更新日期：2014-03-01 00:00:00
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journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-006-9031-4
更新日期：2006-12-01 00:00:00
abstract：:D-glycerate 2 kinase (DGK) is an enzyme that mediates the conversion of D-glycerate, an intermediate metabolite of serine and fructose metabolism, to 2-phosphoglycerate. Deficiency of DGK leads to accumulation of D-glycerate in various tissues and its massive excretion in urine. D-glyceric aciduria (DGA) is an autosom...
journal_title：Metabolic brain disease
pub_type： 杂志文章,评审
doi：10.1007/s11011-019-0384-x
更新日期：2019-04-01 00:00:00
abstract：:Hepatic encephalopathy can be a life-threatening complication of fulminant hepatic failure. By understanding the pathophysiology involved in the induction of this neuropsychiatric disorder, future therapeutic and/or preventive attempts could be considered. In this study, an attempt has been made in order to shed more ...
journal_title：Metabolic brain disease
pub_type： 杂志文章
doi：10.1007/s11011-008-9091-8
更新日期：2008-09-01 00:00:00
