bluuebunny/crossref_metadata_2025_split huggingface dataset:
Case report: Isolation of a European bat lyssavirus type 2a from a fatal human case of rabies encephalitis
Authors: Fooks Anthony R. , McElhinney Lorraine M. , Pounder Derrick J. , Finnegan Christopher J. , Mansfield Karen , Johnson Nicholas , Brookes Sharon M. , Parsons Graham , White Kathleen , McIntyre Paul G. , Nathwani Dilip 
Published: August 2003

AbstractA 55‐year‐old bat conservationist was admitted to Ninewells Hospital, Dundee, Scotland, on November 11, 2002, with an acute haematemesis. He gave a 5‐day history of pain and paraesthesia in the left arm, followed by increasing weakness of his limbs with evidence of an evolving encephalitis with cerebellar involvement. The patient had never been vaccinated against rabies and did not receive postexposure treatment. Using a hemi‐nested reverse transcriptase‐polymerase chain reaction (RT‐PCR), saliva samples taken intravitam from different dates proved positive for rabies. A 400‐bp region of the nucleoprotein gene was sequenced for confirmation and identified a strain of European bat lyssavirus (EBLV) type 2a. The diagnosis was confirmed using the fluorescent antibody test (FAT) and by RT‐PCR on three brain samples (cerebellum, medulla, and hippocampus) taken at autopsy. In addition, a mouse inoculation test (MIT) was performed. Between 13 and 17 days postinfection, clinical signs of a rabies‐like illness had developed in all five inoculated mice. Brain smears from each infected animal were positive by the FAT and viable virus was isolated. This fatal incident is only the second confirmed case of an EBLV type‐2 infection in a human after exposure to bats. J. Med. Virol. 71:281–289, 2003. Copyright © Crown Copyright 2003. Recorded with the permission of the controller of the Majesty's Stationery Office. Published by Wiley‐Liss, Inc.
RSV‐induced bronchiolitis but not upper respiratory tract infection is accompanied by an increased nasal IL‐18 response
Authors: van Benten Inesz J. , van Drunen Cornelis M. , Koopman Laurens P. , KleinJan Alex , van Middelkoop Barbara C. , de Waal Leon , Osterhaus Albert D.M.E. , Neijens Herman J. , Fokkens Wytske J. 
Published: August 2003

AbstractThe aim of this study was to investigate potential differences in the local nasal immune response between bronchiolitis and upper respiratory tract infection induced by respiratory syncytial virus (RSV). Nasal brush samples were obtained from 14 infants with RSV bronchiolitis and from 8 infants with RSV upper respiratory tract infection. The samples were taken during infection (acute phase) and 2–4 weeks later (convalescent phase). Cytospin preparations were stained immunohistochemically for T cells, macrophages, and eosinophils. Staining also took place for intercellular adhesion molecule‐1 (ICAM‐1), T‐helper 1 (Th1)‐like (interleukin‐12 [IL‐12], interferon‐γ [IFN‐γ]), Th2‐like (IL‐4, IL‐10), and proinflammatory cytokines (IL‐6, IL‐8, IL‐18). During both RSV‐induced bronchiolitis and upper respiratory tract infection, cellular inflammation was observed. This was characterised by an increase in the numbers of nasal macrophages, which tended to be higher in bronchiolitis than in upper respiratory tract infection. Numbers of T lymphocytes and ICAM‐1 positive cells increased during both bronchiolitis and upper respiratory tract infection. There were no differences between numbers in the groups. Interestingly, a distinct nasal proinflammatory cytokine response was observed in RSV‐induced bronchiolitis. This is characterised by an increase in the number of IL‐18 positive cells. This increase is specific for bronchiolitis, as a similar increase could not be detected in RSV‐induced upper respiratory tract infection. Numbers of IL‐6 and IL‐12 positive cells were higher in both bronchiolitis and upper respiratory tract infection, and there were no differences between the groups. By contrast, the number of IL‐8, IFN‐γ, IL‐4, and IL‐10‐positive cells remained constant. In conclusion, clear differences were found in nasal immune responses of children with RSV‐induced upper respiratory tract infection or bronchiolitis. The induction of a strong IL‐18 response was typical for bronchiolitis, as this could not be observed in RSV‐induced upper respiratory tract infection, and could explain the eosinophilia that is observed frequently during bronchiolitis. J. Med. Virol. 71:290–297, 2003. © 2003 Wiley‐Liss, Inc.
Prevalence of anti‐human respiratory syncytial virus antibodies over three consecutive years in a healthy adult population
Authors: Chala Silvia R. , García‐Barreno Blanca , Melero José A. , Palomo Concepción 
Published: August 2003

AbstractThe titers of anti‐human respiratory syncytial virus (HRSV) antibodies have been measured by enzyme‐linked immunosorbent assay (ELISA) in a cohort of healthy adult volunteers over 3 consecutive years. Significant increases in the level of these antibodies were detected in a small percentage of individuals (3–3.3%), when paired serum samples taken from two consecutive seasons were compared. In these cases, a significant increase was generally noted in the level of antibodies directed against either the F or the G glycoproteins, and in the level of neutralizing antibodies. However, no correlation was found between the level of binding and neutralizing antibodies, when samples representative of the population under study were analyzed. These results indicate some level of infection by HRSV in the adult population. The implications of these results for the epidemiology of HRSV are discussed. J. Med. Virol. 71:298–304, 2003. © 2003 Wiley‐Liss, Inc.
Antigenic and genetic variability of human respiratory syncytial viruses (group A) isolated in Uruguay and Argentina: 1993–2001
Authors: Frabasile Sandra , Delfraro Adriana , Facal Luján , Videla Cristina , Galiano Mónica , de Sierra María José , Ruchansky Dora , Vitureira Nathalia , Berois Mabel , Carballal Guadalupe , Russi José , Arbiza Juan 
Published: August 2003

AbstractThe antigenic and genetic diversity of G glycoprotein from 25 human respiratory viruses (group A) isolated during nine consecutive epidemics (1993–2001) in Montevideo, Uruguay, and 7 strains isolated in Buenos Aires, Argentina, in the same period were analyzed. Genetic variability was evaluated by partial sequence of the G protein gene. Phylogenetic analysis indicated that most Uruguayan and Argentinean group A isolates clustered into three genotypes: GA5, GA2, and GA1. Some strains clustered into the GA3 genotype characterized previously. The antigenic analysis was carried out with a panel of anti‐G monoclonal antibodies that recognized conserved and strain‐specific epitopes. A close correlation between the antigenic and genetic relatedness of the strains analyzed was observed. J. Med. Virol. 71:305–312, 2003. © 2003 Wiley‐Liss, Inc.
Molecular characterisation of varicella‐zoster virus strains in Germany and differentiation from the Oka vaccine strain
Authors: Sauerbrei A. , Eichhorn U. , Gawellek S. , Egerer R. , Schacke M. , Wutzler P. 
Published: August 2003

AbstractWith the introduction of varicella vaccination, surveillance of varicella‐zoster virus (VZV) strains occurring in cases of chickenpox or zoster should be considered. Differentiating Oka vaccine strain from wild‐type VZV can be achieved only using molecular genotyping. In the present study, the VZV genotype was examined in 53 VZV strains isolated from patients with varicella or zoster and in 73 samples from skin eruptions, cerebrospinal fluid, and throat swabs obtained from patients with VZV infections in Germany. The polymerase chain reaction and restriction fragment length polymorphisms analysis using DNA fragments of the open reading frames 38, 54, 62, and the R5 repeat region were used. Whereas all VZV isolates could be typed, direct genotyping of viral DNA in patients' samples was achieved in 63 of 73 cases (86.3%). The dominant genotype of VZV found in 88.8% of 116 patients had the wild‐type pattern PstI+ BglI− R5A followed by the wild‐genotype PstI+ BglI+ R5A in 6.0%, the wild‐genotype PstI+ BglI− R5B in 3.4%, the wild‐genotype PstI+ BglI− R5C and the Oka vaccine genotype PstI− BglI+ R5B in 0.9% of patients each. BglI− wild‐types were found in 90.7% of patients with zoster and in 9.3% of patients with varicella. By contrast, the BglI+ wild‐type was diagnosed in five patients with varicella and in two patients with zoster. In conclusion, VZV strains found in Germany are similar to strains circulating in the United States and the United Kingdom. VZV wild‐type strains containing a BglI restriction site in ORF 54 as well as Oka vaccine strains can rarely be detected. J. Med. Virol. 71:313–319, 2003. © 2003 Wiley‐Liss, Inc.
Early NFκB activation is inhibited during focal cerebral ischemia in interleukin‐1β‐converting enzyme deficient mice
Authors: Huang Feng‐Peng , Wang Zhi‐Qiu , Wu Du‐Chu , Schielke Gerald P. , Sun Yi , Yang Guo‐Yuan 
Published: August 2003

AbstractOur previous study demonstrated that the inhibition of interleukin‐1β (IL‐1β) reduces ischemic brain injury; however, the molecular mechanism of the action of IL‐1 in cerebral ischemia is unclear. We are investigating currently the role of NFκB during focal cerebral ischemia, using mutant mice deficient in the interleukin‐1 converting enzyme gene (ICE KO) in a middle cerebral artery occlusion (MCAO) model. Adult male ICE KO and wild‐type mice (n = 120) underwent up to 24 hr of permanent MCAO. Cytoplasmic phospho‐NFκB/p65 expression in ischemic brain was examined using Western blot analysis and immunohistochemistry. NFκB DNA‐binding activity was detected using electrophoretic mobility shift assay (EMSA). Furthermore, ICAM‐1 expression was examined in both the ICE KO and wild‐type mice (WT). Western blot analysis and immunostaining showed that the level of cytosolic phosphorylated NFκB/p65 increased after 2 and 4 hr of MCAO in WT mice; however, NFκB/p65 was significantly reduced after MCAO in the ICE KO mice (P < 0.05). EMSA showed that NFκB DNA‐binding activity increased after MCAO in WT mice; but this effect was reduced in the ICE KO mice. The number of ICAM‐1‐positive vessels in the ischemic hemisphere was greatly attenuated in the ICE KO mice (P < 0.05), which paralleled the results of immunohistochemistry. Our results demonstrate that NFκB phosphorylation is reduced in ICE KO mice, suggesting that ICE or IL‐1 are involved in early NFκB phosphorylation. Because cerebral ischemia induced infarction is significantly reduced in ICE KO mice, we conclude that early NFκB phosphorylation plays a disruptive role in the ischemic process. © 2003 Wiley‐Liss, Inc.
Characterization of the mouse olfactory glutathione S‐transferases during the acute phase response
Authors: Weech Michelle , Quash Michelle , Walters Eric 
Published: August 2003

AbstractThe acute phase response (APR) has been shown to alter expression and activity of biotransformation enzymes, such as the phase I cytochromes P450 and phase II glutathione S‐transferases (GSTs). The cytochromes P450 and GSTs are expressed abundantly and colocalized to non‐neuronal cells of the olfactory mucosa. Previous studies indicate that olfactory cytochromes P450 expression and activity is altered during periods of localized inflammation and infection. Little is understood, however, about the influence of the APR on olfactory GST enzymes. This study investigated effects of the APR on olfactory GST isozymes expression and activity in mouse olfactory mucosa after 24‐hr treatment with the acute phase inducer, polyinosinic: polycytidylic acid (polyIC). Western blot analysis using antibodies directed against specific GST isoforms α (A1‐1), μ (M1‐1), and π (P1‐1) demonstrated that their expression was unaltered by polyIC treatment. In contrast, olfactory P450 2E1 expression was significantly decreased. Enzymatic activity of the olfactory GSTs toward the general substrate, 1‐chloro‐2,4‐dinitrobenzene (CDNB) was unchanged during the APR. Analysis of olfactory glutathione content during the APR showed that it was also unaffected by polyIC. The insensitivity of these olfactory GST isoforms during the APR may play a significant role toward limiting the impact of infection and inflammation on the olfactory system. © 2003 Wiley‐Liss, Inc.
Chronic nicotine administration increases NGF‐like immunoreactivity in frontoparietal cerebral cortex
Authors: Martínez‐Rodríguez R. , Toledano A. , Álvarez M.I. , Turégano L. , Colman O. , Rosés P. , Gómez de Segura I. , De Miguel E. 
Published: August 2003

AbstractNicotine/nicotine agonists, which have been proposed as therapeutic agents for the treatment of Alzheimer's disease and other neurodegenerative disorders, produce a wide variety of effects on the nervous system. Some mechanisms involved remain poorly understood. In this work, immunohistochemical techniques were used to determine the effect of nicotine on nerve growth factor (NGF) in the frontoparietal (motor, somatosensory) brain cortex of the albino rat. Nicotine was chronically administered intraperitoneally using osmotic pumps (0.35 mg nicotine base/kg body weight/day for 14 days). An increase in the number and the immunoreaction intensity of NGF‐like positive pyramidal and nonpyramidal neurons of these cortical areas was observed after treatment. Immunopositive astroglial cells were always seen in sections of treated animals but not in controls. The neuropil of control animals was, in general, devoid of reaction, but in treated animals, immunopositive prolongations were located randomly, some in close association with capillaries. At the electron microscopic level, these prolongations were demonstrated as belonging to neurons (dendrites and axons) and astroglial cells. Nicotinic activation of selected neurons and glial cells seems to trigger NGF/neurotrophic mechanisms, suggesting their use may be of benefit in prevention and treatment of neurodegenerative diseases. © 2003 Wiley‐Liss, Inc.
CNS gene expression pattern associated with spontaneous experimental autoimmune encephalomyelitis
Authors: Matejuk Agata , Hopke Corwyn , Dwyer Jami , Subramanian Sandhya , Jones Richard E. , Bourdette Dennis N. , Vandenbark Arthur A. , Offner Halina 
Published: August 2003

AbstractTransgenic mice with T‐cell receptor (TCR) specific for myelin basic protein (MBP)‐Ac1‐11 peptide and homozygous for the RAG‐1 mutation (T/R− mice) spontaneously develop acute progressive experimental autoimmune encephalomyelitis (Sp‐EAE) mediated by CD4+ T cells. Microarray analysis of spinal cord tissue obtained from symptomatic versus non‐symptomatic T/R− mice revealed strongly upregulated transcripts for genes involved in antigen presentation and processing, signal transduction, transcription regulation, metabolism, development, cell cycle, and many other processes involved in the induction of clinical and pathological signs of Sp‐EAE. Several highly expressed genes were related directly to inflammation, including cytokines/receptors, chemokines/receptors, acute phase, complement molecules, and others. Many CNS‐specific genes were also upregulated in sick mice. Abundance of message for the Tg TCR BV8S2 gene as well as several monocyte/macrophage‐associated genes would suggest that both components play a crucial role in the pathogenesis of Sp‐EAE. The profile of transcriptional changes found during the development of Sp‐EAE provides the first description of the encephalitogenic process in the absence of purposeful immunization with myelin peptides and immune‐enhancing adjuvants. This unique approach is the first to implicate molecules and pathways that contribute naturally to onset of paralysis and demyelination, and thus may provide unique insights and novel treatment strategies for human diseases such as multiple sclerosis. © 2003 Wiley‐Liss, Inc.
Is the soluble KDI domain of γ1 laminin a regeneration factor for the mammalian central nervous system?
Authors: Liebkind Ron , Laatikainen Timo , Liesi Päivi 
Published: August 2003

AbstractRegeneration of adult mammalian CNS is poor as a result of environmental factors that prevent axon growth. The major factors hampering regeneration of central axons include proteins released from the damaged myelin sheets of the injured neuronal pathways and formation of the glial scar. By using an experimental model of human CNS injury, we show that survival and neurite outgrowth of human central neurons are significantly enhanced by the soluble KDI domain of γ1 laminin. Our results indicate that the KDI domain appears to neutralize both glia‐derived inhibitory signals and inhibitory molecules released from the myelin of the adult human spinal cord. We propose that the KDI domain may enhance regeneration of injuries in the adult mammalian CNS. © 2003 Wiley‐Liss, Inc.
Brain‐derived neurotrophic factor mitigates chronic ethanol‐induced attenuation of γ‐aminobutyric acid responses in cultured cerebellar granule cells
Authors: Ericson Mia , Haythornthwaite Alison R. , Yeh Pamela W.L. , Yeh Hermes H. 
Published: August 2003

AbstractThis study examined the effect of chronic exposure to ethanol and brain‐derived neurotrophic factor (BDNF) on the responsiveness of cerebellar granule cells to γ‐aminobutyric acid (GABA). Cerebellar granule cell cultures were chronically exposed to ethanol (100 mM), BDNF (20 ng/ml), or the combination of ethanol and BDNF. Whole‐cell current responses of granule cells to exogenously applied GABA were monitored following at least 5 days of chronic exposure. In the ethanol‐treated cultures, granule cell responsiveness to GABA was attenuated. Concomitant exposure of cultures to ethanol and BDNF mitigated the ethanol‐induced attenuation of GABA response, although BDNF, by itself, did not affect responsiveness to GABA. BDNF increased the expression of the GABAA receptor α6 subunit, whereas ethanol had no effect, in chronically treated granule cell cultures. In addition, concomitant treatment with BDNF and ethanol did not increase the expression of the GABAA receptor α6 subunit, so the subunit expression alone could not account for the mitigating effect of BDNF. We propose that different mechanisms regulating responsiveness to GABA underlie the effects induced by ethanol and BDNF, with the former influencing the expression of functional GABAA receptors and the latter involving the activation of the TrkB receptor and its downstream signaling pathways. © 2003 Wiley‐Liss, Inc.
Activation of the mitogen‐activated protein kinase pathway through p75NTR: A common mechanism for the neurotrophin family
Authors: Lad Shivanand P. , Neet Kenneth E. 
Published: August 2003

AbstractNeurotrophins interact with two distinct classes of cell‐surface receptors, the Trk receptor tyrosine kinase family and the common neurotrophin receptor p75NTR. For many years, the biological role of p75NTR remained obscure, being relegated to modulating Trk binding of neurotrophins. Recently, the importance of p75NTR as a signaling receptor in itself has become increasingly clear. The signals initiated by p75NTR are likely to be as complex as those for the Trk family and probably depend on the cell system in which such signaling is being studied. In this study, all members of the neurotrophin family were demonstrated to be capable of stimulating p75NTR‐mediated activation of the mitogen‐activated protein kinase (MAPK) family (ERK1,2). This activation is rapid and transient, peaking at 5–15 min, depending on the cell system. The classical MAPK cascade consists of the reaction series Ras‐Raf‐MEK‐MAPK. The p75NTR‐induced MAPK activation is MEK dependent but Raf independent. This result implies that neurotrophin activation of p75NTR results in some cascade (as yet unknown) that bypasses Raf and converges on MEK to result in activation of MAPK. This activated MAPK is then able to translocate to the nucleus. The effect of this MAPK activation on cell survival is dependent on cell type. These results support the concept that signaling from the p75NTR receptor is more diverse and extensive than previously believed. © 2003 Wiley‐Liss, Inc.
Complementary DNA cloning and characterization of RANDAM‐2, a type I membrane molecule specifically expressed on glutamatergic neuronal cells in the mouse cerebrum
Authors: Kotani Masaharu , Tajima Youichi , Osanai Taka , Irie Atsushi , Iwatsuki Ken , Kanai‐Azuma Masami , Imada Masato , Kato Hiroko , Shitara Hiroshi , Kubo Hideo , Sakuraba Hitoshi 
Published: August 2003

AbstractA membrane‐surface glycoprotein, RANDAM‐2, is one of the neuronal cell lineage‐specific antigens involved in the neuronal differentiation of P19 embryonic carcinoma (EC) cells and the mouse central nervous system (CNS). Complementary DNA cloning of RANDAM‐2 indicated that its nucleotide sequence completely matched that of PA2.26 antigen, a sialomucin‐like transmembrane glycoprotein previously found on tumorigenic keratinocytes. RANDAM‐2 transcripts were detectable from the embryonic stage of 6.5 days, and then the expression continued throughout the remaining embryonic stages and adulthood, with a localization restricted to the CNS. In growth factor‐induced neurospheres and adult cerebrum, RANDAM‐2‐expressing cells coincided well not only with nestin‐positive cells but also with glutamate‐positive neurons, but not with γ‐aminobutyric acid‐positive ones. These results indicate that RANDAM‐2 is one of the type I membrane surface antigens constitutively expressed on undifferentiated neuronal cells and the glutamatergic neuronal cells during mouse neurogenesis. © 2003 Wiley‐Liss, Inc.
Exogenous glutamate and taurine exert differential actions on light‐induced release of two endogenous amino acids in isolated rat retina
Authors: Barabás Péter , Kovács Ilona , Kardos Julianna , Schousboe Arne 
Published: August 2003

AbstractA dark‐adapted isolated rat retina, preloaded with [14C]glutamate ([14C]Glu) and [3H]taurine ([3H]Tau), was superfused with artificial cerebrospinal fluid (ACSF) in the absence and presence of Glu (1 mM) or Tau (1 mM), as well as the Glu uptake inhibitors dihydrokainic acid (DHK, 0.04 mM) and trans‐L‐pyrrolidine‐2,4‐dicarboxylate (t‐PDC, 0.004 mM). After 10 min of light stimulation, the extracellular level of [14C]Glu and [3H]Tau was reduced to 82 ± 2% and 65 ± 4% of the control, respectively. Basal release was enhanced when Tau and t‐PDC were applied together, although none of the compounds had any effect when applied individually. Glu and DHK had no effect. The decrease of [14C]Glu efflux evoked by light stimuli was enhanced by t‐PDC and Tau, either added separately or together, whereas Glu and DHK were without effect. In contrast, [3H]Tau efflux variations induced by light stimuli were reduced markedly by both Tau and Glu. These findings suggest distinctly different roles of Tau and Glu in light‐induced responses in mammalian retina, including a possible role for Tau in light adaptation processes. © 2003 Wiley‐Liss, Inc.