bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influenza vaccination of HIV‐1‐positive and hiv‐1‐negative former intravenous drug users
Authors: Amendola Antonella , Boschini Antonio , Colzani Daniela , Anselmi Giovanni , Oltolina Arianna , Zucconi Roberta , Begnini Marco , Besana Silvia , Tanzi Elisabetta , Zanetti Alessandro Remo 
Published: August 2002

AbstractThe immunogenicity of an anti‐influenza vaccine was assessed in 409 former intravenous drug user volunteers and its effect on the levels of HIV‐1 RNA, proviral DNA and on CD4+ lymphocyte counts in a subset HIV‐1‐positive subjects was measured. HIV‐1‐positive individuals (n = 72) were divided into three groups on the basis of their CD4+ lymphocyte counts, while the 337 HIV‐1‐negative participants were allocated into group four. Haemagglutination inhibiting (HI) responses varied from 45.8 to 70% in the HIV‐1‐positive subjects and were significantly higher in group four (80.7% responses to the H1N1 strain, 81.6% to the H3N2 strain, and 83% to the B strain). The percentage of subjects with HI protective antibody titres (≥ 1:40) increased significantly after vaccination, especially in HIV‐1 uninfected subjects. Immunization caused no significant changes in CD4+ counts and in neither plasma HIV‐1 RNA nor proviral DNA levels. Therefore, vaccination against influenza may benefit persons infected by HIV‐1. J. Med. Virol. 65:644–648, 2001. © 2001 Wiley‐Liss, Inc.
Primary human herpesvirus‐6 associated with an afebrile seizure in a 3‐week‐old infant
Authors: Zerr Danielle M. , Yeung Laurence C. , Obrigewitch Rose Mary , Huang Meei‐Li , Frenkel Lisa M. , Corey Lawrence 
Published: August 2002

AbstractWe describe a 3‐week‐old male infant with an afebrile seizure in whom serologic and polymerase chain reaction (PCR) findings support concomitant primary human herpesvirus 6 (HHV‐6) infection. Although HHV‐6 infection has been associated with first‐time febrile seizures and encephalitis in both immunocompetent and immunocompromised hosts, it has not been associated previously with afebrile seizures in healthy infants. This report provides additional evidence of the neuropathogenic potential of HHV‐6. J. Med. Virol. 66:384‐387, 2002. © 2002 Wiley‐Liss, Inc.
Inhalation anesthetic‐induced neuroinvasion by an attenuated strain of West Nile virus in mice
Authors: Katz Yeshayahu , Lustig Shlomo , Ben‐Shlomo Izhar , Kobiler David , Ben‐Nathan David 
Published: August 2002

AbstractThere are contradictory reports regarding the effects of inhalation anesthetics on the immune system. Measurable immune responses have been studied in vitro, but little is known about the in vivo effects in the intact organism. We used an attenuated, non‐neuroinvasive, nonlethal strain of the encephalitic West Nile virus, termed WN‐25, which can become lethal in combination with environmental stressors, to study possible modulatory immune effects of inhalation anesthetics in mice. Both single short‐term exposure and repeated exposure to halothane and nitrous oxide were studied. Exposure to 30% CO2 served as a positive control. Mortality, brain invasion, spleen weight, and antiviral antibodies served as the experimental endpoints. Halothane and nitrous oxide led to viral brain invasion, increased mortality, and suppressed immune response in a concentration‐ and time‐dependent manner. Repeated exposures had a cumulative effect. Assessment of the stability of the viral attenuation did not demonstrate any alteration in the character of the virus, suggesting an increased access to the brain by inhalation anesthetics that led to the fatal encephalitis. These findings may be of special concern to populations at risk, such as operating room staff and patients undergoing general anesthesia in endemic areas of encephalitic virus species, in which subclinical infection may develop into an overt disease. J. Med. Virol. 66:576–580, 2002. © 2002 Wiley‐Liss, Inc.
Kinetics and localization of brain phosphate activated glutaminase
Authors: Kvamme Elling , Torgner Ingeborg Aa. , Roberg Bjørg 
Published: August 2002

AbstractThe cellular concentration of phosphate, the main activator of phosphate activated glutaminase (PAG) is rather constant in brain and kidney. The enzyme activity, however, is modulated by a variety of compounds affecting the binding of phosphate, such as glutamate, calcium, certain long chain fatty acids, fatty acyl CoA derivatives, members of the tricarboxylic acid cycle and protons (Kvamme et al. [2000] Neurochem. Res. 25:1407–1419). Therefore, the kinetic and allosteric properties of the enzyme are essential for regulating the enzyme activity in situ, especially because the enzymically active pool of PAG is assumed to have an external localization in the inner mitochondrial membrane, being exposed to cytosolic variation in the content of effectors. This has largely been overlooked. A hypothetical model for the allosteric interactions based on the sequential induced fit allosteric model by Koshland et al. ([1966] Biochemistry 5:365–385) is presented. Furthermore, it has been generally accepted that there exist only two isoforms of PAG, the kidney PAG that is similar to brain PAG, and the liver PAG. Therefore, the immunoreactivity of brain cells against kidney PAG antibodies has been considered a measure of PAG protein. Gomez‐Fabre et al. ([2000] Biochem. J. 345:365–375) recently found, however, that a PAG mRNA from human breast cancer ZR75 cells is present in human brain and liver, but not in the kidney. We observed only traces of PAG immunoreactivity in cultured astrocytes and cultured neuroblastoma cells, regardless whether antibodies against the C‐ and N‐termini of kidney PAG or antibodies against liver PAG were used, but considerable enzyme activity, demonstrating hitherto unknown isoforms of PAG (Torgner et al. [2001] FEBS Lett. 268(Suppl 1):PS2–031). © 2001 Wiley‐Liss, Inc.
Alterations in expression of genes coding for key astrocytic proteins in acute liver failure
Authors: Desjardins Paul , Bélanger Mireille , Butterworth Roger F. 
Published: August 2002

AbstractCerebral edema and hepatic encephalopathy are major complications of acute liver failure. Brain herniation caused by increased intracranial pressure as a result of cell swelling is the major cause of death in this condition. Evidence available currently suggests that the rapid accumulation of ammonia by the brain is the major cause of the central nervous system complications of acute liver failure. Increased brain ammonia may cause cell swelling via the osmotic effects of an increase in astrocytic glutamine concentrations or by inhibition of glutamate removal from brain extracellular space. Acute liver failure results in altered expression of several genes in brain, some of which code for important proteins involved in CNS function such as the glucose (GLUT‐1) and glutamate (GLT‐1) transporters, the astrocytic structural protein glial fibrillary acidic protein (GFAP) the “peripheral‐type” benzodiazepine receptor (PTBR) and the water channel protein, aquaporin IV. Loss of expression of GLT‐1 results in increased extracellular brain glutamate in acute liver failure. Experimental acute liver failure also results in post‐translational modifications of the serotonin and noradrenaline transporters resulting in increased extracellular concentrations of these monoamines. Therapeutic measures currently used to prevent and treat brain edema and encephalopathy in patients with acute liver failure include mild hypothermia and the ammonia‐lowering agent L‐ornithine‐L‐aspartate. © 2001 Wiley‐Liss, Inc.
Measurement of human tricarboxylic acid cycle rates during visual activation by 13C magnetic resonance spectroscopy
Authors: Chhina Navjeet , Kuestermann Ekkehard , Halliday Jane , Simpson Liz J. , Macdonald Ian A. , Bachelard Herman S. , Morris Peter G. 
Published: August 2002

AbstractMeasurement by 13C magnetic resonance spectroscopy (MRS) of the incorporation of label from [1‐13C] glucose, initially into C4 of glutamate, allows the regional tricarboxylic acid (TCA) cycle flux (FTCA) to be determined in the human brain. In this study, a direct 13C MRS approach was used at 3T, with NOE enhancement and 1H decoupling with WALTZ16, to determine basal FTCA in six volunteers. The values found in the visual cortex are similar to those reported in previous 13C MRS studies, and consistent with PET measurements of the cerebral metabolic rate for glucose, CMRglc. In two preliminary activation studies using light emitting diode (LED) goggles flashing at 8 Hz, compared to darkness as control, increases in FTCA were found from 0.60 ± 0.10 to 0.94 ± 0.03 μmol/min/g (56%) and from 0.34 ± 0.14 to 0.56 ± 0.07 μmol/min/g (65%). These are upper estimates, but they are similar to the increases in CMRglc reported in PET studies, and strongly suggest, in contrast to these PET studies, that cerebral glucose is metabolized oxidatively, even during intense visual stimulation. This is supported by the observation that very little 13C label is incorporated into C3 lactate, as would be expected if glucose were metabolized anaerobically. There is evidence for incorporation of glucose into cerebral glycogen, but this is a relatively minor component of cerebral glucose metabolism. © 2001 Wiley‐Liss, Inc.
Local uptake of 14C‐labeled acetate and butyrate in rat brain in vivo during spreading cortical depression
Authors: Dienel Gerald A. , Liu Kenian , Cruz Nancy F. 
Published: August 2002

AbstractSpreading depression severely disrupts ion homeostasis, causes sensory neglect and motor impairment, and is associated with stroke and migraine. Glucose utilization (CMRglc) and lactate production rise during spreading depression, but the metabolic changes in different brain cell types are unknown. Uptake of 14C‐labeled compounds known to be preferentially metabolized by the glial tricarboxylic acid cycle was, therefore, examined during unilateral KCl‐induced spreading cortical depression in conscious, normoxic rats. [14C]Metabolites derived from [14C]butyrate in K+‐treated tissue rose 21% compared to that of untreated contralateral control cortex, whereas incorporation of H14CO3 into metabolites in K+‐treated tissue was reduced to 86% of control. Autoradiographic analysis showed that laminar labeling of cerebral cortex by both 14C‐labeled acetate and butyrate was elevated heterogeneously throughout cortex by an average of 23%; the increase was greatest (∼40%) in tissue adjacent to the K+ application site. Local uptake of acetate, butyrate, and deoxyglucose showed similar patterns, and monocarboxylic acid uptake was highest in the structures in which apparent loss of labeled metabolites of [6‐14C]glucose was greatest. Enhancement of net uptake of acetate and butyrate in cerebral cortex during spreading depression is tentatively ascribed to increased astrocyte metabolism. © 2001 Wiley‐Liss, Inc.
In vitro evidence that 5‐hydroxytryptamine increases efflux of glial glutamate via 5‐HT2A receptor activation
Authors: Meller R. , Harrison P.J. , Elliott J.M. , Sharp T. 
Published: August 2002

AbstractRecent studies have established the presence of 5‐hydroxytryptamine (5‐HT)2A receptors on glial cells in culture and in the brain in situ. Here we used cultured C6 glioma cells to investigate the possibility that 5‐HT2A receptors on glia regulate glutamate release from the cell. The efflux of endogenous glutamate from cultured C6 glioma cells was increased by addition of 5‐HT in a concentration‐dependent manner (maximal effect +200%). The efflux of serine and aspartate was not altered. The effect of 5‐HT was mimicked by both the nonselective 5‐HT receptor agonist quipazine and the selective 5‐HT2 receptor agonist 4‐iodo‐2,5‐dimethoxyamphetamine (DOI; both 0.01–100 μM). The 5‐HT2A receptor antagonists ketanserin (1 μM) and spiperone (1 μM) inhibited the glutamate response to 5‐HT, quipazine, and DOI, whereas the effect of 5‐HT was not inhibited by the 5‐HT2B/C receptor antagonist SB200646 (1 μM). The effect of 5‐HT on glutamate was specific in that it was reduced in low‐calcium medium but was not prevented by furosemide (5 mM), which prevents cell swelling‐induced glutamate release. Finally, the glutamate uptake inhibitor 2,4,trans‐pyrollidine dicarboxylic acid (50 μM) did not block the 5‐HT‐induced efflux of glutamate, making involvement of glutamate transport unlikely. In conclusion, 5‐HT stimulates the efflux of glutamate from C6 glioma cells following 5‐HT2A receptor activation and involves a calcium‐dependent mechanism. © 2002 Wiley‐Liss, Inc.
Study of expression of myelin basic proteins (MBPs) in developing rat brain using a novel antibody reacting with four major isoforms of MBP
Authors: Akiyama Kyoichi , Ichinose Sachiyo , Omori Akira , Sakurai Yoko , Asou Hiroaki 
Published: August 2002

AbstractMyelin basic proteins (MBPs) are the major protein components of myelin. MBP isoforms are known to have different expression patterns. In order to distinguish the different expression patterns on myelination, we have developed a novel antibody reacting with the four major isoforms of MBPs with molecular masses of 21.5 kDa, 18.5 kDa, 17.0 kDa, and 14.0 kDa. These MBPs were initially separated by acid urea gel and sodium dodecyl sulfate polyacrylamide gel electrophoreses and detected with the luminol reaction. Then the antibody developed was used to determine the relative amounts of MBP isoforms. The MBPs of oligodendrocytes were detected by the enhanced luminol reaction using Renaissance (Dupont NEN, Boston, MA). From the immunological aspect, the MBP monoclonal antibody (Sires et al. [1981] Science 214:87–89) was revealed to recognize MBPs with molecular masses of 21.5 kDa and 18.5 kDa. Furthermore, we found that Ile‐166 in the rat 18.5‐kDa MBP isomers was replaced by methionine. The 14.0‐kDa and 18.5‐kDa isoforms of MBP are the most abundant MBP species and comprise more than 70% of the total MBPs in 3.5‐and 24‐month‐old rats. MBPs are expressed during development and the compositions of MBPs in mature (3.5 months old) and aged (24 months old) rats were almost the same. The expression of the 14.0‐kDa and 18.5‐kDa MBPs occurred earlier in the cerebellum and the spinal cord than in the cerebrum by approximately 1 week. MBPs are also expressed upon oligodendrocyte maturation by interacting with astrocytes. The above results suggest that the regulation of MBP isoforms during development and oligodendrocyte differentiation may indicate the point of occurrence of both the unique patterns of isoform expression and the shift in intracellular localization of MBPs with the maturation of oligodendrocytes. © 2002 Wiley‐Liss, Inc.
Glial transporters for glutamate, glycine, and GABA: II. GABA transporters
Authors: Gadea Ana , López‐Colomé Ana María 
Published: August 2002

AbstractThe termination of chemical neurotransmission in the central nervous system (CNS) involves the rapid removal of neurotransmitter from synapses. This is fulfilled by specific transport systems in neurons and glia, including those for γ‐aminobutyric acid (GABA), the main inhibitory neurotransmitter in the brain. Glial cells express the cloned Na+/Cl−‐dependent, high‐affinity GABA transporters (GATs) GAT1, GAT2, and GAT3, as well as the low‐affinity transporter BGT1. In situ hybridization and immunocytochemistry have revealed that each transporter shows distinct regional distribution in the brain and the retina. The neuronal vs. glial localization of the different transporters is not clear‐cut, and variations according to species, neighboring excitatory synapses, and developmental stage have been reported. The localization, stoichiometry, and regulation of glial GATs are outlined, and the participation of these structures in development, osmoregulation, and neuroprotection are discussed. A decrease in GABAergic neurotransmission has been implicated in the pathophysiology of several CNS disorders, particularly in epilepsy. Since drugs which selectively inhibit glial but not neuronal GABA uptake exert anticonvulsant activity, clearly the establishment of the molecular mechanisms controlling GATs in glial cells will be an aid in the chemical treatment of several CNS‐related diseases. J. Neurosci. Res. 63:461–468, 2001. © 2001 Wiley‐Liss, Inc.
Domoic acid‐induced neuronal damage in the rat hippocampus: Changes in apoptosis related genes (Bcl‐2, Bax, caspase‐3) and microglial response
Authors: Ananth C. , Thameem Dheen S. , Gopalakrishnakone P. , Kaur C. 
Published: August 2002

AbstractDomoic acid (DA), a potent neurotoxin, administered intravenously (0.75 mg/kg body weight) in adult rats evoked seizures accompanied by nerve cell damage in the present study. Neuronal degeneration and microglial reaction in the hippocampus were investigated, and the temporal profile of bcl‐2, bax, and caspase‐3 genes in cell death or survival was assessed following the administration of DA. Nissl staining showed darkly stained degenerating neurons in the hippocampus following the administration of DA at 1–21 days, the degeneration being most severe at 5 days. Ultrastructural study in CA1 and CA3 regions of hippocampus revealed two types of neuronal degeneration, cells that exhibited swollen morphology and shrunken electron‐dense cells. Immunoreactivity of Bcl‐2 and Bax was increased considerably at 16 hr and 24 hr in the neurons of the hippocampus following DA administration. No significant change was observed in the immunoreactivity of caspase‐3 in the controls and DA‐treated rats at any time interval. Microglial cells in the hippocampus showed intense immunoreaction with the antibodies OX‐42 and OX‐6 at 1–21 days after DA administration, indicating the up‐regulation of complement type 3 receptors and major histocompatibility complex type II antigens for increased phagocytic activity and antigen presentation, respectively. Terminal deoxynucleotidyl‐transferase‐mediated dUTP nick end labeling (TUNEL) showed occasional positive neurons in the CA1 and CA3 regions at 5 days after DA administration, with no positive cells in the controls. RT‐PCR analysis revealed that bcl‐2 and bax mRNA transcripts in the hippocampus were significantly increased at 16 hr and gradually decreased at 24 hr following the administration of DA. Although bax and bcl‐2 mRNA expression is rapidly induced at early stages, in situ hybridization analysis revealed complete loss of bcl‐2, bax, and caspase‐3 mRNA at 24 hr after DA administration in the region of neuronal degeneration in the hippocampus. These results indicate that the pattern of neuronal degeneration observed during DA‐induced excitotoxic damage is mostly necrotic. J. Neurosci. Res. 66:177–190, 2001. © 2001 Wiley‐Liss, Inc.
Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells
Authors: Guan Zhi‐Zhong , Zhang Xiao , Mousavi Malahat , Tian Jian‐Ying , Unger Christina , Nordberg Agneta 
Published: August 2002

AbstractThe mechanism for a large loss of neuronal nicotinic acetylcholine receptors (nAChRs) in brains with neurodegenerative diseases remains unclear. Based on our previous results of [3H]epibatidine binding influenced by lipid peroxidation, we suggest that nAChR deficit in neurodegenerative diseases might be related to the neurons attacked by free radicals. To further understand how free radicals influence the expression of nAChRs, we detected [125I]α‐bungarotoxin binding, nAChR subunit protein and mRNA during the early stage of damage by oxidative stress in PC12 cells in the present study. The results showed that free radical insult (FeSO4) within the concentration range (1 –100 μM) used in the study induced dose‐dependent increases in lipid peroxidation and toxicity to PC12 cells, but did not result in apoptosis or necrosis. Significant reductions in [125I]α‐bungarotoxin binding site, protein level for the α3 and α7 subunits, and mRNA level for the α7 subunit were observed in PC12 cells treated by FeSO4 at the concentrations without inducing cell death compared to control. Pretreatment of cultural cells with antioxidant such as Vitamin E and reduced glutathione prevented the inhibiting effect of free radicals on [125I]α‐bungarotoxin and [3H]epibatidine bindings. The present results further demonstrate that oxidative stress might reduce the number of [125I]α‐bungarotoxin binding site and selectively suppress the expression of the nAChR subunits at protein and mRNA levels during the early stages of damage in PC12 cells. J. Neurosci. Res. 66:551–558, 2001. © 2001 Wiley‐Liss, Inc.
PKC and PKA, but not PKG mediate LPS‐induced CGRP release and [Ca2+]i elevation in DRG neurons of neonatal rats
Authors: Hou Lingfei , Wang Xian 
Published: August 2002

AbstractCalcitonin gene‐related peptide (CGRP), is produced in dorsal root ganglia (DRG) neurons and released from primary afferent neurons to mediate hemodynamic effects and neurogenic inflammation. In this work, we determined whether lipopolysaccharide (LPS), an inflammatory stimulator, could trigger CGRP release from cultured DRG neurons and if so, which cellular signaling pathway was involved in this response. Cytoplasmic concentration of calcium ([Ca2+]i) plays a key role in neurotransmitter release, therefore [Ca2+]i was also determined in cultured DRG cells using fluo‐3/AM. The results showed that LPS (0.1–10 μg/ml) evoked CGRP release in a time‐ and concentration‐dependent manner from DRG neurons. LPS also increased [Ca2+]i in a concentration‐dependent manner. The protein kinase C (PKC) inhibitors, calphostin C 0.5 μM or RO‐31‐8220 0.1 μM, and the cAMP‐dependent protein kinase (PKA) specific inhibitor RP‐CAMPS 30 μM or nonspecific inhibitor H8 1 μM inhibited 1 μg/ml LPS‐evoked CGRP release and [Ca2+]i increase from DRG neurons. The cGMP‐dependent protein kinase (PKG) inhibitor Rp‐8‐pCPT‐cGMPS 30 μM did not block the LPS response. These data suggest that LPS may stimulate CGRP release and [Ca2+]i elevation through PKC and PKA, but not PKG signaling pathway in DRG neurons of neonatal rats. J. Neurosci. Res. 66:592–600, 2001. © 2001 Wiley‐Liss, Inc.
Social support, group consensus and stressor–strain relationships: social context matters*
Authors: Bliese Paul D. , Britt Thomas W. 
Published: August 2002

AbstractIn this study, we examined the degree to which individuals' reactions to stressors were influenced by the quality of their shared social environments. Based on social support theory, we proposed that individuals in positive social environments would show lower levels of strain when exposed to stressors than would individuals in negative social environments. The quality of the shared social environment was assessed by measuring the degree of consensus among group members about an issue of importance to the group—namely about the group leadership. Social influence theory provides compelling reasons to believe that this measure of consensus should be a strong indicator of the quality of the social environment within the groups. In multilevel analyses using a sample of 1923 soldiers who were members of 52 Companies deployed to Haiti, we found that the quality of the social environment moderated relationships between (a) work stressors and morale and (b) work stressors and depression. Copyright © 2001 John Wiley & Sons, Ltd.