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Article ; Online: Microglia and astrocyte activation in the frontal cortex of rats with experimental autoimmune encephalomyelitis.

Chanaday, N L / Roth, G A

2016 Volume 314, Page(s) 160–169

Abstract: Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for the human disease multiple sclerosis (MS), a demyelinating and neurodegenerative pathology of the central nervous system. Both diseases share physiopathological and ... ...

Abstract	Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for the human disease multiple sclerosis (MS), a demyelinating and neurodegenerative pathology of the central nervous system. Both diseases share physiopathological and clinical characteristics, mainly associated with a neuroinflammatory process that leads to a set of motor, sensory, and cognitive symptoms. In MS, gray matter atrophy is related to the emergence of cognitive deficits and contributes to clinical progression. In particular, injury and dysfunction in certain areas of the frontal cortex (FrCx) have been related to the development of cognitive impairments with high incidence, like central fatigue and executive dysfunction. In the present work we show the presence of region-specific microglia and astrocyte activation in the FrCx, during the first hours of acute EAE onset. It is accompanied by the production of the pro-inflammatory cytokines IL-6 and TNF-α, in the absence of detectable leukocyte infiltration. These findings expand previous studies showing presynaptic neural dysfunction occurring at the FrCx and might contribute to the understanding of the mechanisms involved in the genesis and prevalence of common MS symptoms.
MeSH term(s)	Animals ; Astrocytes/physiology ; Disease Models, Animal ; Encephalitis/metabolism ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Frontal Lobe/metabolism ; Frontal Lobe/physiopathology ; Inflammation Mediators/metabolism ; Interleukin-6/metabolism ; Microglia/physiology ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Inflammation Mediators ; Interleukin-6 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2016-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2015.11.060
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Article ; Online: Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017

Roth, G.A. / GBD 2017 Causes of Death Collaborators

392 ; 10159 ; 1736 ; 1788 ; Lancet (London, England) ; United States ; United Kingdom ; England

a systematic analysis for the Global Burden of Disease Study 2017.

2018

Abstract: Background: Global development goals increasingly rely on country-specific estimates for benchmarking a nation's progress. To meet this need, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 estimated global, regional, national, ...

Abstract	Background: Global development goals increasingly rely on country-specific estimates for benchmarking a nation's progress. To meet this need, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 estimated global, regional, national, and, for selected locations, subnational cause-specific mortality beginning in the year 1980. Here we report an update to that study, making use of newly available data and improved methods. GBD 2017 provides a comprehensive assessment of cause-specific mortality for 282 causes in 195 countries and territories from 1980 to 2017. Methods: The causes of death database is composed of vital registration (VR), verbal autopsy (VA), registry, survey, police, and surveillance data. GBD 2017 added ten VA studies, 127 country-years of VR data, 502 cancer-registry country-years, and an additional surveillance country-year. Expansions of the GBD cause of death hierarchy resulted in 18 additional causes estimated for GBD 2017. Newly available data led to subnational estimates for five additional countries-Ethiopia, Iran, New Zealand, Norway, and Russia. Deaths assigned International Classification of Diseases (ICD) codes for non-specific, implausible, or intermediate causes of death were reassigned to underlying causes by redistribution algorithms that were incorporated into uncertainty estimation. We used statistical modelling tools developed for GBD, including the Cause of Death Ensemble model (CODEm), to generate cause fractions and cause-specific death rates for each location, year, age, and sex. Instead of using UN estimates as in previous versions, GBD 2017 independently estimated population size and fertility rate for all locations. Years of life lost (YLLs) were then calculated as the sum of each death multiplied by the standard life expectancy at each age. All rates reported here are age-standardised. Findings: At the broadest grouping of causes of death (Level 1), non-communicable diseases (NCDs) comprised the greatest fraction of deaths, contributing to 73·4% (95% uncertainty interval [UI] 72·5-74·1) of total deaths in 2017, while communicable, maternal, neonatal, and nutritional (CMNN) causes accounted for 18·6% (17·9-19·6), and injuries 8·0% (7·7-8·2). Total numbers of deaths from NCD causes increased from 2007 to 2017 by 22·7% (21·5-23·9), representing an additional 7·61 million (7·20-8·01) deaths estimated in 2017 versus 2007. The death rate from NCDs decreased globally by 7·9% (7·0-8·8). The number of deaths for CMNN causes decreased by 22·2% (20·0-24·0) and the death rate by 31·8% (30·1-33·3). Total deaths from injuries increased by 2·3% (0·5-4·0) between 2007 and 2017, and the death rate from injuries decreased by 13·7% (12·2-15·1) to 57·9 deaths (55·9-59·2) per 100 000 in 2017. Deaths from substance use disorders also increased, rising from 284 000 deaths (268 000-289 000) globally in 2007 to 352 000 (334 000-363 000) in 2017. Between 2007 and 2017, total deaths from conflict and terrorism increased by 118·0% (88·8-148·6). A greater reduction in total deaths and death rates was observed for some CMNN causes among children younger than 5 years than for older adults, such as a 36·4% (32·2-40·6) reduction in deaths from lower respiratory infections for children younger than 5 years compared with a 33·6% (31·2-36·1) increase in adults older than 70 years. Globally, the number of deaths was greater for men than for women at most ages in 2017, except at ages older than 85 years. Trends in global YLLs reflect an epidemiological transition, with decreases in total YLLs from enteric infections, respiratory infections and tuberculosis, and maternal and neonatal disorders between 1990 and 2017; these were generally greater in magnitude at the lowest levels of the Socio-demographic Index (SDI). At the same time, there were large increases in YLLs from neoplasms and cardiovascular diseases. YLL rates decreased across the five leading Level 2 causes in all SDI quintiles. The leading causes of YLLs in 1990-neonatal disorders, lower respiratory infections, and diarrhoeal diseases-were ranked second, fourth, and fifth, in 2017. Meanwhile, estimated YLLs increased for ischaemic heart disease (ranked first in 2017) and stroke (ranked third), even though YLL rates decreased. Population growth contributed to increased total deaths across the 20 leading Level 2 causes of mortality between 2007 and 2017. Decreases in the cause-specific mortality rate reduced the effect of population growth for all but three causes: substance use disorders, neurological disorders, and skin and subcutaneous diseases. Interpretation: Improvements in global health have been unevenly distributed among populations. Deaths due to injuries, substance use disorders, armed conflict and terrorism, neoplasms, and cardiovascular disease are expanding threats to global health. For causes of death such as lower respiratory and enteric infections, more rapid progress occurred for children than for the oldest adults, and there is continuing disparity in mortality rates by sex across age groups. Reductions in the death rate of some common diseases are themselves slowing or have ceased, primarily for NCDs, and the death rate for selected causes has increased in the past decade. Bill & Melinda Gates Foundation.
Subject code	610
Language	English
Publishing date	2018-11-08
Publisher	Elsevier
Publishing country	de
Document type	Article ; Online
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Article ; Online: Treatment with a hybrid between the synapsin ABC domains and the B subunit of E. coli heat-labile toxin reduces frequency of proinflammatory cells and cytokines in the central nervous system of rats with EAE.

Bibolini, M J / Scerbo, M J / Roth, G A / Monferran, C G

Neuroscience

2014 Volume 277, Page(s) 217–228

Abstract: Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are crucially dependent on the invasion of activated autoreactive lymphocytes and blood macrophages into the central nervous system (CNS). Proinflammatory ... ...

Abstract	Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are crucially dependent on the invasion of activated autoreactive lymphocytes and blood macrophages into the central nervous system (CNS). Proinflammatory mononuclear cells and activated local microglia mediate inflammation, demyelination and axonal damage at the target organ. Previously, we observed that the administration of a hybrid between the synapsin ABC domains and the B subunit of Escherichia coli heat labile-enterotoxin (LTBABC) to rats with EAE ameliorated disease by modulating the peripheral Th1 response to myelin basic protein (MBP). In the present study, we investigated the effect of LTBABC administration on proinflammatory cell frequency in the CNS of rats with EAE. Treatment with the hybrid in the inductive phase of EAE attenuated disease severity and diminished histological inflammatory infiltrates and demyelination in the spinal cord of rats with acute EAE. Lower frequencies of infiltrating and local macrophages as well as CD4+ T cells that produce the proinflammatory cytokines interferon-gamma (IFN-γ) and interleukin (IL)-17 were found at the target organ. Concomitantly, low levels of INF-γ and IL-17 and increased levels of IL-10 were measured in cultures of CNS infiltrating cells and spinal cord tissue. An increased frequency of CD4+CD25+Foxp3 cells was observed at the disease peak and at the beginning of the recovery stage. These results provide further evidence for the immunomodulatory properties of the fusion protein LTBABC in autoimmune demyelinating disease affecting the central nervous system.
MeSH term(s)	Animals ; Bacterial Toxins/administration & dosage ; Bacterial Toxins/genetics ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/physiology ; Cattle ; Cells, Cultured ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Enterotoxins/administration & dosage ; Enterotoxins/genetics ; Escherichia coli ; Escherichia coli Proteins/administration & dosage ; Escherichia coli Proteins/genetics ; Female ; Interferon-gamma/metabolism ; Interleukin-10/metabolism ; Interleukin-17/metabolism ; Macrophages/drug effects ; Macrophages/physiology ; Male ; Neuroprotective Agents/administration & dosage ; Rats, Wistar ; Recombinant Fusion Proteins/administration & dosage ; Spinal Cord/drug effects ; Spinal Cord/pathology ; Spinal Cord/physiopathology ; Synapsins/administration & dosage ; Synapsins/genetics
Chemical Substances	Bacterial Toxins ; Enterotoxins ; Escherichia coli Proteins ; Interleukin-17 ; Neuroprotective Agents ; Recombinant Fusion Proteins ; Synapsins ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6) ; heat-labile enterotoxin, E coli (D9K3SN2LNY)
Language	English
Publishing date	2014-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2014.06.070
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Article: Small mammal herbivory: Feedbacks that help maintain desertified ecosystems

Roth, G.A / Whitford, W.G / Steinberger, Y

Journal of arid environments. 2009 Jan., v. 73, issue 1

2009

Abstract: We tested the hypothesis that herbivores contribute to feedbacks maintaining arid ecosystems in a degraded state. We studied small mammal herbivory on a subshrub, broom snakeweed (Gutierrezia sarothrae), and perennial grasses at three sites: (1) ungrazed ...

Abstract	We tested the hypothesis that herbivores contribute to feedbacks maintaining arid ecosystems in a degraded state. We studied small mammal herbivory on a subshrub, broom snakeweed (Gutierrezia sarothrae), and perennial grasses at three sites: (1) ungrazed black grama (Bouteloua eriopoda) grassland; (2) grassland degraded by intense short-duration grazing; and (3) mesquite (Prosopis glandulosa) coppice dunes. Snakeweed was browsed by herbivores primarily during dry winter months. The average percent of G. sarothrae standing crop biomass removed by browsing was 9.2 in ungrazed grassland, 7.4 in intensely grazed grassland, and 4.1 in the dunes. In ungrazed grassland, an average of 12% of grass cover was harvested by herbivores; in the intensely grazed plots - 80%. Herbivore exclusion plots showed that jackrabbits (Lepus californicus) were the primary browsers on snakeweed and rodents on grasses and G. sarothrae inflorescences. Rodent removal of G. sarothrae inflorescences allows wind dispersal of seeds in disturbed and desertified areas, thereby increasing abundance of this poisonous shrub. Grass-tiller cutting by rodents provides a strong feedback that may be responsible for keeping the grass cover low on the intensely grazed areas. Jackrabbit pruning has little effect on G. sarothrae abundance at any stage of desertification.
Keywords	grasslands ; ecosystems ; small mammals ; rodents ; herbivores ; grazing ; browsing ; Gutierrezia sarothrae ; Bouteloua eriopoda ; Prosopis glandulosa ; desertification ; New Mexico
Language	English
Dates of publication	2009-01
Size	p. 62-65.
Document type	Article
ZDB-ID	428507-4
ISSN	1095-922X ; 0140-1963
ISSN (online)	1095-922X
ISSN	0140-1963
DOI	10.1016/j.jaridenv.2008.09.003
Database	NAL-Catalogue (AGRICOLA)

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Article: Jackrabbit (Lepus californicus) herbivory changes dominance in desertified Chihuahuan Desert ecosystems

Roth, G.A / Whitford, W.G / Steinberger, Y

Journal of arid environments. 2007 Aug., v. 70, issue 3

2007

Keywords	Larrea tridentata ; Flourensia ; shrubs ; desertification ; plant ecology ; ecosystems ; hares ; Lepus californicus ; wild animals ; herbivores ; browsing ; canopy ; mortality ; compensatory growth ; spatial distribution ; feeding preferences ; New Mexico
Language	English
Dates of publication	2007-08
Size	p. 418-426.
Document type	Article
ZDB-ID	428507-4
ISSN	1095-922X ; 0140-1963
ISSN (online)	1095-922X
ISSN	0140-1963
DOI	10.1016/j.jaridenv.2007.01.009
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Article: Passive transfer of experimental autoimmune encephalomyelitis in Wistar rats: dissociation of clinical symptoms and biochemical alterations.

Degano, A L / Roth, G A

Journal of neuroscience research

2000 Volume 59, Issue 2, Page(s) 283–290

Abstract: We have used passive transfer of myelin-reactive lymphocytes in the Wistar rat model of experimental autoimmune encephalomyelitis (EAE) to investigate the nature of the central nervous system immunopathological alterations induced by these cells. ... ...

Abstract	We have used passive transfer of myelin-reactive lymphocytes in the Wistar rat model of experimental autoimmune encephalomyelitis (EAE) to investigate the nature of the central nervous system immunopathological alterations induced by these cells. Mononuclear cells from lymph nodes or spleen from sick myelin/complete Freund's adjuvant-immunized donors did not transfer clinical disease. However, depending on the previous treatment of the transferred cells, recipients develop central nervous system biochemical and histological alterations. Fresh cells from lymph nodes immediately transferred after procurement from the sick EAE donor rat were capable of inducing the most significant diminution in the content of myelin basic protein, sulfatides, and 2',3'-cyclic nucleotide-3'-phosphohydrolase activity, with concomitant inflammatory infiltrations of white matter, principally in spinal cord and cerebellar lobules. Similar alterations were observed when animals were injected with spleen mononuclear cells activated in the presence of a nonspecific mitogen as concanavalin A. However, antigen-specific activated spleen cells generated by culturing in the presence of bovine myelin induced alterations to a lesser degree. Results point to a dissociation of the clinical disease from the central nervous system biochemical and histopathological lesions occurring in the EAE-transferred Wistar rats and indicate that these alterations in EAE are induced principally by T cells activated in vivo rather than by cells activated in vitro by myelin antigens. Therefore, these findings suggest a possible participation of lymphocytes unlike the encephalitogenic T cells in the induction of the described alterations and provide a useful model to explore further the subclinical responses to this experimental disease.
MeSH term(s)	2',3'-Cyclic-Nucleotide Phosphodiesterases/analysis ; Animals ; Autoantibodies/blood ; Cattle ; Cells, Cultured ; Central Nervous System/chemistry ; Central Nervous System/immunology ; Concanavalin A ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Female ; Male ; Myelin Basic Protein/immunology ; Myelin Basic Protein/pharmacology ; Myelin Sheath/enzymology ; Myelin Sheath/immunology ; Rats ; Rats, Wistar ; T-Lymphocytes/cytology ; T-Lymphocytes/enzymology ; T-Lymphocytes/transplantation
Chemical Substances	Autoantibodies ; Myelin Basic Protein ; Concanavalin A (11028-71-0) ; 2',3'-Cyclic-Nucleotide Phosphodiesterases (EC 3.1.4.-)
Language	English
Publishing date	2000-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/(sici)1097-4547(20000115)59:2<283::aid-jnr15>3.0.co;2-s
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Article ; Online: Ventilation during cardiopulmonary bypass: impact on heat shock protein release.

Beer, L / Szerafin, T / Mitterbauer, A / Kasiri, M M / Debreceni T Palotás, L / Dworschak, M / Roth, G A / Ankersmit, H J

The Journal of cardiovascular surgery

2014 Volume 55, Issue 6, Page(s) 849–856

Abstract: Aim: Cardiopulmonary bypass (CPB), utilized in on-pump coronary artery bypass graft procedures (CABG) induces generalized immune suppression, release of heat shock proteins (HSP), inflammatory markers and apoptosis-specific proteins. We hypothesized ... ...

Abstract	Aim: Cardiopulmonary bypass (CPB), utilized in on-pump coronary artery bypass graft procedures (CABG) induces generalized immune suppression, release of heat shock proteins (HSP), inflammatory markers and apoptosis-specific proteins. We hypothesized that continued mechanical ventilation during cardiopulmonary bypass attenuates immune response and HSP liberation. Methods: Thirty patients undergoing conventional coronary artery bypass graft (CABG) operation were randomized into a ventilated on CPB (VG; N.=15) and a non-ventilated CPB group (NVG; N.=15). Blood samples were drawn at the beginning and end of surgery, as well as on the five consecutive postoperative days (POD). Molecular markers were measured by ELISA. Data are given as mean ± (SD). Mann-Whitney-U-test was used for statistical analysis. Results: Serum concentrations of HSP70 were significantly lower in VG compared to NVG on POD-1 (VG: 1629±608 vs. NVG: 5203±2128.6 pg/mL, P<0.001). HSP27 and HSP60 depicted a minor increase in both study groups at the end of surgery without any intergroup differences (HSP27: VG 6207.9±1252.5 vs. NVG 7424.1±2632.5; HSP60: VG 1046.2±478.8 vs. NVG 1223.5±510.1). IL-8 and CK-18 M30 evidenced the highest serum concentrations at the end of surgery (IL-8: VG 119.5±77.9 vs. NVG 148.0±184.55; CK-18 M30: VG 62.1±39.2 vs. NVG 67.5±33.9) with no differences between groups. Decreased ICAM-1 serum concentrations were detected postoperatively, however ICAM-1 concentrations on POD-1 to POD-5 showed slightly elevated concentrations in both study groups with no intergroup differences. Conclusion: Significantly less HSP70 was detectable in patients receiving uninterrupted mechanical lung ventilation on CPB, indicating either different inflammatory response, cellular stress or cell damage between the ventilated and non-ventilated group. These data suggest that continued mechanical ventilation has a modulatory effect on the immune response in patients after CABG surgery.
MeSH term(s)	Aged ; Aged, 80 and over ; Austria ; Biomarkers/blood ; Cardiopulmonary Bypass/adverse effects ; Chaperonin 60/blood ; Coronary Artery Bypass/methods ; Female ; HSP27 Heat-Shock Proteins/blood ; HSP70 Heat-Shock Proteins/blood ; Heat-Shock Proteins/blood ; Humans ; Inflammation/blood ; Inflammation/etiology ; Inflammation/immunology ; Inflammation/prevention & control ; Inflammation Mediators/blood ; Male ; Middle Aged ; Mitochondrial Proteins/blood ; Respiration, Artificial ; Time Factors ; Treatment Outcome
Chemical Substances	Biomarkers ; Chaperonin 60 ; HSP27 Heat-Shock Proteins ; HSP70 Heat-Shock Proteins ; HSPB1 protein, human ; HSPD1 protein, human ; Heat-Shock Proteins ; Inflammation Mediators ; Mitochondrial Proteins
Language	English
Publishing date	2014-12
Publishing country	Italy
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	80143-4
ISSN	1827-191X ; 0021-9509
ISSN (online)	1827-191X
ISSN	0021-9509
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Article ; Online: Participation of the GABAergic system on the glutamate release of frontal cortex synaptosomes from Wistar rats with experimental autoimmune encephalomyelitis.

Cid, M P / Vilcaes, A A / Rupil, L L / Salvatierra, N A / Roth, G A

Neuroscience

2011 Volume 189, Page(s) 337–344

Abstract: We previously found that the glutamate release was decreased in synaptosomes from rat cerebral cortex during the development of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis. Various other reports have shown a ... ...

Abstract	We previously found that the glutamate release was decreased in synaptosomes from rat cerebral cortex during the development of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis. Various other reports have shown a deficit in the expression of proteins associated with GABAergic neurotransmission in the neocortex of patients with multiple sclerosis and it was also demonstrated that the activation of GABAA receptors leads to an inhibition of glutamate release. Now, in order to evaluate the events that may affect the neuronal function in EAE synaptosomes, we analyzed the participation of the GABAergic system in glutamate release and in the flunitrazepam-sensitive GABAA receptor density. This revealed alterations in the GABAergic system of the frontal cortex synaptosomes from EAE animals. GABA induced a decrease in the 4-aminopyridine-evoked glutamate release in control synaptosomes which was abolished by picrotoxin, a GABAA receptor antagonist. In contrast, synaptosomes from EAE rats showed a loss in the inhibition of glutamate release mediated by GABA. Furthermore, the flunitrazepam-sensitive GABAA receptor density was decreased during the acute stage of the disease in synaptosomes from EAE rats. We also observed a loss of inhibition in the Ca2+-dependent phosphorylation of synapsin I mediated by GABA in nerve terminals from EAE animals, which could explain the loss of GABAergic regulation on evoked glutamate release. The changes observed in the GABAA receptor density as well as the loss of GABAergic inhibition of glutamate release were partially reverted in cortical synaptosomes from recovered EAE animals. These results suggest that the decrease in the flunitrazepam-sensitive GABAA receptor density may explain the observed failure of GABAergic regulation in the glutamate release of synaptosomes from EAE rats, which might contribute to the appearance of clinical symptoms and disease progression.
MeSH term(s)	4-Aminopyridine/pharmacology ; Animals ; Calcium/metabolism ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Flunitrazepam/pharmacology ; Frontal Lobe/drug effects ; Frontal Lobe/metabolism ; GABA Antagonists/pharmacology ; GABA Modulators/pharmacology ; Glutamic Acid/metabolism ; Nerve Endings/metabolism ; Phosphorylation ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; Synapsins/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	GABA Antagonists ; GABA Modulators ; Receptors, GABA-A ; Synapsins ; Glutamic Acid (3KX376GY7L) ; gamma-Aminobutyric Acid (56-12-2) ; Flunitrazepam (620X0222FQ) ; 4-Aminopyridine (BH3B64OKL9) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-08-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2011.05.005
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Article ; Online: Lipocalin-2 serum levels are increased in acute hepatic failure.

Roth, G A / Nickl, S / Lebherz-Eichinger, D / Schmidt, E M / Ankersmit, H J / Faybik, P / Hetz, H / Krenn, C G

Transplantation proceedings

2013 Volume 45, Issue 1, Page(s) 241–244

Abstract: Lipocalin-2 (LCN-2), which is expressed in immunocytes as well as hepatocytes, is upregulated in cells under stress from infection or inflammation with increase in serum levels. We sought to investigate the relevance of LCN-2 in the setting of acute ... ...

Abstract	Lipocalin-2 (LCN-2), which is expressed in immunocytes as well as hepatocytes, is upregulated in cells under stress from infection or inflammation with increase in serum levels. We sought to investigate the relevance of LCN-2 in the setting of acute hepatic failure, particularly when addressed with the molecular adsorbent recirculating system (MARS). We measured serum LCN-2 concentrations with enzyme-linked immunosorbent assay (ELISA) in 8 patients with acute-on-chronic-liver failure (ACLF) and acute liver failure (ALF) who were treated with MARS. The controls were 14 patients with stable chronic hepatic failure (CHF). LCN-2 was determined immediately before and after the first MARS session. Baseline LCN-2 serum concentrations were significantly increased among ACLF and ALF patients as compared with CHF (P = .004 and P = .0086, respectively). There was no significant difference between the ALF and ACLF group. Moreover, serum LCN-2 levels did not change significantly during the MARS treatment. Serum LCN-2 levels, therefore, may be useful to discern acute from chronic hepatic failure and to monitor the course as well as the severity of the disease.
MeSH term(s)	Acute-Phase Proteins ; Adolescent ; Adult ; Aged ; Critical Care ; End Stage Liver Disease/blood ; Enzyme-Linked Immunosorbent Assay ; Female ; Gene Expression Regulation ; Hepatocytes/cytology ; Humans ; Inflammation ; International Normalized Ratio ; Lipocalin-2 ; Lipocalins/blood ; Liver Failure, Acute/blood ; Male ; Middle Aged ; Molecular Weight ; Proto-Oncogene Proteins/blood ; Young Adult
Chemical Substances	Acute-Phase Proteins ; LCN2 protein, human ; Lipocalin-2 ; Lipocalins ; Proto-Oncogene Proteins
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	82046-5
ISSN	1873-2623 ; 0041-1345
ISSN (online)	1873-2623
ISSN	0041-1345
DOI	10.1016/j.transproceed.2012.02.047
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Article ; Online: Molecular mechanisms involved in interleukin 1-beta (IL-1β)-induced memory impairment. Modulation by alpha-melanocyte-stimulating hormone (α-MSH).

Gonzalez, P / Machado, I / Vilcaes, A / Caruso, C / Roth, G A / Schiöth, H / Lasaga, M / Scimonelli, T

Brain, behavior, and immunity

2013 Volume 34, Page(s) 141–150

Abstract: Pro-inflammatory cytokines can affect cognitive processes such as learning and memory. Particularly, interleukin-1β (IL-1β) influences the consolidation of hippocampus-dependent memories. We previously reported that administration of IL-1β in dorsal ... ...

Abstract	Pro-inflammatory cytokines can affect cognitive processes such as learning and memory. Particularly, interleukin-1β (IL-1β) influences the consolidation of hippocampus-dependent memories. We previously reported that administration of IL-1β in dorsal hippocampus impaired contextual fear memory consolidation. Different mechanisms have been implicated in the action of IL-1β on long-term potentiation (LTP), but the processes by which this inhibition occurs in vivo remain to be elucidated. We herein report that intrahippocampal injection of IL-1β induced a significant increase in p38 phosphorylation after contextual fear conditioning. Also, treatment with SB203580, an inhibitor of p38, reversed impairment induced by IL-1β on conditioned fear behavior, indicating that this MAPK would be involved in the effect of the cytokine. We also showed that IL-1β administration produced a decrease in glutamate release from dorsal hippocampus synaptosomes and that treatment with SB203580 partially reversed this effect. Our results indicated that IL-1β-induced impairment in memory consolidation could be mediated by a decrease in glutamate release. This hypothesis is sustained by the fact that treatment with d-cycloserine (DCS), a partial agonist of the NMDA receptor, reversed the effect of IL-1β on contextual fear memory. Furthermore, we demonstrated that IL-1β produced a temporal delay in ERK phosphorylation and that DCS administration reversed this effect. We also observed that intrahippocampal injection of IL-1β decreased BDNF expression after contextual fear conditioning. We previously demonstrated that α-MSH reversed the detrimental effect of IL-1β on memory consolidation. The present results demonstrate that α-MSH administration did not modify the decrease in glutamate release induced by IL-1β. However, intrahippocampal injection of α-MSH prevented the effect on ERK phosphorylation and BDNF expression induced by IL-1β after contextual fear conditioning. Therefore, in the present study we determine possible molecular mechanisms involved in the impairment induced by IL-1β on fear memory consolidation. We also established how this effect could be modulated by α-MSH.
MeSH term(s)	Animals ; Conditioning (Psychology)/drug effects ; Conditioning (Psychology)/physiology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fear/drug effects ; Fear/physiology ; Glutamic Acid/metabolism ; Hippocampus/drug effects ; Hippocampus/metabolism ; Interleukin-1beta/toxicity ; Male ; Memory Disorders/chemically induced ; Memory Disorders/metabolism ; Rats, Wistar ; alpha-MSH/pharmacology ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Interleukin-1beta ; Glutamic Acid (3KX376GY7L) ; alpha-MSH (581-05-5) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2013-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2013.08.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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