bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epstein‐Barr virus specific salivary antibodies as related to stress caused by examinations
Authors: Sarid O. , Anson O. , Yaari A. , Margalith M. 
Published: August 2002

AbstractEpstein‐Barr virus (EBV) is prevalent in 90% of the population. After primary infection it remains in a latent state and the majority of the virus carriers are asymptomatic during their life. Among the immunocompromized patients such as organ and bone marrow transplant recipients, individuals lacking T cell immunity, and patients treated with corticosteroid, cancer, and AIDS patients EBV primary infection and reactivation can cause life threatening diseases. Immunosupression may occur also during stressful events, which induce corticosteroid release and thus activate EBV. The effect of examination stress on EBV reactivation among female students was studied by detecting the values of EBV specific IgG and IgA salivary antibodies. Sequential saliva samples were obtained from first year female students before, during, and after two important examinations. EBV specific IgG and IgA salivary antibodies were tested by enzyme‐linked immunosorbent assay (ELISA). Hepatitis A virus (HAV) salivary antibodies served as a non‐latent virus control. A statistically significant increase in the values of EBV specific IgG and IgA antibodies was detected in samples collected during the examinations, as compared to the samples collected two months before and one month after the exams (P < 0.05). HAV antibody levels did not change significantly between the four time points. The menstrual cycle had no significant effect on the results. No significant symptoms were reported during the whole study. These results indicate that among female students who endure stress during academic examinations, a significant increase in EBV specific IgG and IgA salivary antibody values could be detected. EBV reactivation should be confirmed by measuring salivary EBV DNA or infectious virus. J. Med. Virol. 64:149–156, 2001. © 2001 Wiley‐Liss, Inc.
Nucleotide sequence analysis and development of consensus primers of RT‐PCR for detection of norwalk‐like viruses prevailing in Japan
Authors: Kawamoto Hiroyoshi , Yamazaki Kenji , Utagawa Etsuko , Ohyama Tohru 
Published: August 2002

AbstractA total of 177 different nucleotide sequences of the RNA polymerase region of Norwalk‐like viruses (NLVs) genomes, collected via a nation‐wide survey project in Japan between 1989 and 1998, were examined by reverse transcription‐polymerase chain reaction (RT‐PCR) employing various primer pairs. The nucleotide sequences of different strains showed great diversity, with a range of 57 to 100% identities among strains. The strains could be classified into five clusters: Norwalk (NV), Snow Mountain agent/Bristol virus (SMA/BV), Toronto virus/Mexico virus (TV/MX), and Japan specific cluster 1 and 2 (JP‐1 and JP‐2). Within each cluster there is greater than 85% identity of amino acid sequence (more than 75% identity of nucleotide sequences), based on sequence homology analysis. We believe that two of the five clusters, JP‐1and JP‐2, define new specific clusters found in Japan according to phylogenetic and pair‐wise comparison studies. An RT‐PCR procedure was designed using new consensus primer pairs, P1/P2, P1/P3, and Y1/Y2 based on multiple alignment of collected nucleotide sequences, that are expected to detect nearly all NLVs prevailing in Japan. The usefulness of the primers was tested by ten different laboratories in Japan using a panel of ten fecal samples containing different virus strains. The identification of these primer pairs will facilitate routine diagnosis of NLV infection by RT‐PCR and offers the potential for their direct detection in food and environmental samples. J. Med. Virol. 64:569–576, 2001. © 2001 Wiley‐Liss, Inc.
Epidemiological survey of neonatal non‐polio enterovirus infection in the Netherlands
Authors: Verboon‐Maciolek M.A. , Krediet T.G. , van Loon A.M. , Kaan J. , Galama J.M.D. , Gerards L.J. , Fleer A. 
Published: August 2002

AbstractThe epidemiological, virological, and clinical data of 119 infants less than 30 days of age with enteroviral infection collected from January 1993 to November 1995 by the diagnostic virology laboratories were analyzed retrospectively. Ninety‐eight isolates (83%) were obtained in the period of May 1 to December 1 with a peak in the summer months. Sixty‐five percent (n = 78) of neonates became ill within the first 2 weeks of life. Echoviruses and Coxsackie virus type B were isolated most frequently, in 77 (65%) and 29 (24%) infants, respectively. Diagnosis was made by viral isolation from stool, nasopharyngeal swab, cerebrospinal fluid, and blood. One hundred four (87%) infants developed fever and 25 (21%) infants had diarrhea. A clinical diagnosis of sepsis was made in 42 (35%) infants and meningitis was diagnosed in 28 (24%) cases. The great majority of sepsis cases (36/86%) occurred in infants less than 15 days of age. In conclusion, non‐polio enteroviruses (especially echoviruses) are a common and underreported cause of neonatal infection in the Netherlands in the summer months and are associated with a clinical diagnosis of sepsis or meningitis cases in the first 2 weeks of life in a high proportion of cases. J. Med. Virol. 66:241–245, 2002. © 2002 Wiley‐Liss, Inc.
Local treatment of HPV‐induced skin lesions by Cidofovir
Authors: Stragier Ilse , Snoeck Robert , De Clercq Erik , Van den Oord Joost J. , Van Ranst Marc , De Greef Hugo 
Published: August 2002

AbstractHuman papillomavirus (HPV) induced epithelial cell proliferation is responsible for a broad range of lesions. Treatment of such lesions is characterized by a high relapse rate. Four patients are described who were treated locally with cidofovir (cream 1% or injection of 2.5 mg/ml solution) for multi‐treated relapsing HPV‐associated lesions. Three of the four patients had a complete response. The fourth patient showed a clinical response in the first cycle of treatment, but new lesions appeared during four successive cycles of cidofovir. J. Med. Virol. 67:241–245, 2002. © 2002 Wiley‐Liss, Inc.
Metabolic substrates other than glucose support axon function in central white matter
Authors: Brown Angus M. , Wender Regina , Ransom Bruce R. 
Published: August 2002

AbstractWe tested the hypothesis that non‐glucose energy sources can support axon function in the rat optic nerve. Axon function was assessed by monitoring the stimulus‐evoked compound action potential (CAP). CAP was maintained at full amplitude for 2 hr in 10 mM glucose. 20 mM lactate, 20 mM pyruvate, 10 mM fructose, or 10 mM mannose supported axon function as effectively as did glucose, and 10 mM glutamine provided partial support, but β‐hydroxybutyrate, octanoate, sorbitol, alanine, aspartate, and glutamate failed to support axon function. Our results indicated that a variety of compounds can sustain function in CNS myelinated axons. Axons probably use lactate, pyruvate, and glutamine directly as energy substrates, whereas mannose and fructose could be shuttled through astrocytes to lactate, which is then exported to axons. © 2001 Wiley‐Liss, Inc.
Brain armadillo protein δ‐catenin interacts with Abl tyrosine kinase and modulates cellular morphogenesis in response to growth factors
Authors: Lu Q. , Mukhopadhyay N.K. , Griffin J.D. , Paredes M. , Medina M. , Kosik K.S. 
Published: August 2002

Abstractδ‐Catenin associates with adhesive junctions and facilitates cellular morphogenesis (Lu et al., ). Here we show that δ‐catenin colocalizes with actin filaments and Abl tyrosine kinase in the growth cones of cultured hippocampal neurons. PC12 cells induced to express δ‐catenin show accelerated neurite extension upon nerve growth factor (NGF) stimulation. STI571, an Abl family kinase inhibitor, further accentuates these stimulatory effects. δ‐Catenin is a potent substrate for Abl in vitro using an immunocomplex assay and most of the Abl‐induced tyrosine phosphorylation within cells is present in the N‐terminus of δ‐catenin. When δ‐catenin‐expressing epithelial cells are induced to scatter in response to hepatocyte growth factor (HGF), STI571 leads to the rapid redistribution of δ‐catenin and changes in cellular morphology. We suggest that δ‐catenin is a possible Abl substrate and acts downstream of Abl to orchestrate actin‐based cellular morphogenesis. © 2002 Wiley‐Liss, Inc.
Peptidyl α‐keto amide inhibitor of calpain blocks excitotoxic damage without affecting signal transduction events
Authors: Caba Ebru , Brown Queenie B. , Kawasaki Brian , Bahr Ben A. 
Published: August 2002

AbstractThe cysteine protease calpain is activated by calcium and has a wide range of substrates. Calpain‐mediated cellular damage is associated with many neuropathologies, and calpain also plays a role in signal transduction events that are essential for cell maintenance, including the activation of important kinases and transcription factors. In the present study, the hippocampal slice culture was used as a model of excitotoxicity to test whether the neuroprotection elicited by selective calpain inhibition is associated with changes in cell signaling. Peptidyl α‐keto amide and α‐keto acid inhibitors reduced both calpain‐mediated cytoskeletal damage and the concomitant synaptic deterioration resulting from an N‐methyl‐D‐aspartate exposure. The α‐keto amide CX295 was protective when infused into slice cultures before or after the excitotoxic episode. The slices protected with CX295 exhibited normal activation levels of mitogen‐activated protein kinase and the transcription factor nuclear factor‐κB. Thus, selective inhibition of calpain provides neuroprotection without influencing critical signaling pathways. © 2002 Wiley‐Liss, Inc.
Baclofen is neuroprotective and prevents loss of calcium/calmodulin‐dependent protein kinase II immunoreactivity in the ischemic gerbil hippocampus
Authors: Babcock Alex M. , Everingham Andi , Paden Charles M. , Kimura Maki 
Published: August 2002

AbstractExcessive release of glutamate during transient cerebral ischemia initiates a cascade of events that leads to the delayed and selective death of neurons located in the hippocampus. Activity of calcium calmodulin kinase II (CaM kinase), a protein kinase critical to neuronal functioning, disappears following ischemia. The in vivo link between glutamate excitoxicity and alterations in CaM kinase activity has not been extensively studied. Baclofen, a selective γ‐aminobutyric acid (GABA)B receptor agonist, has been shown to inhibit glutamate release. The present study evaluated the neuroprotective efficacy of this compound and assessed early changes in hippocampal‐dependent behaviors and CaM kinase immunoreactivity following transient cerebral ischemia. Baclofen (50 mg/kg) prevented both the loss of hippocampal CA1 pyramidal cells and the reduction in hippocampal CaM kinase immunoreactivity observed in control animals following ischemic insult. Cerebral ischemia produced a significant increase in working memory errors; however, baclofen failed to attenuate this memory deficit. Results confirm that baclofen is neuroprotective and support a link between glutamate excitotoxicity and reductions in CaM kinase immunoreactivity. © 2002 Wiley‐Liss, Inc.
Ethanol exposure enhances cell death in the developing cerebral cortex: Role of brain‐derived neurotrophic factor and its signaling pathways
Authors: Climent E. , Pascual M. , Renau‐Piqueras J. , Guerri C. 
Published: August 2002

AbstractExposure to ethanol during fetal development induces brain damage, causing cell loss in several brain areas and affecting synaptic connections. Because neurotrophin signaling plays an important role in neuronal survival and differentiation, we have investigated the effect of ethanol exposure on cell death in the developing cerebral cortex and whether this effect correlates with alterations in brain‐derived neurotrophic factor (BDNF) levels, expression of its receptors, TrkB, and its signaling. We report that chronic ethanol intake during gestation and lactation enhances natural cell death and induces cell necrosis, decreases BDNF levels, and increases the ratio of the truncated to full‐length TrkB mRNA receptors during postnatal developing cerebral cortex. Furthermore, we provide evidence that during brain development BDNF activates the extracellular signal‐regulated kinases (ERK1 and ERK2) and the phosphoinoside‐3‐kinase (PI‐3‐K/Akt) pathways. However, BDNF‐induced cell signaling throughout the above‐mentioned survival pathways is significantly reduced by ethanol exposure. These findings suggest that ethanol‐induced alterations in BDNF availability and in its receptor function might impair intracellular signaling pathways involved in cell survival, growth, and differentiation, leading to enhanced natural cell death during cerebral cortex development. © 2002 Wiley‐Liss, Inc.
Impairment of adenylyl cyclase and of spatial memory function after microsphere embolism in rats
Authors: Nagakura Akira , Miyake‐Takagi Keiko , Takagi Norio , Fukui Masato , Takeo Satoshi 
Published: August 2002

AbstractThe purpose of the present study was to characterize alterations in the adenylyl cyclase (AC), cyclic adenosine 3′,5′‐monophosphate (cAMP), and spatial memory function after sustained cerebral ischemia. Sustained cerebral ischemia was induced by injection of 900 microspheres (48 μm in diameter) into the right (ipsilateral) hemisphere of rats. Alterations in the AC and cAMP in the cerebral cortex and hippocampus were examined up to 7 days after the embolism. A decrease in the cAMP content was seen in the ipsilateral hemisphere throughout the experiment. Microsphere embolism (ME) decreased the activity of Ca2+/calmodulin (CaM)‐sensitive AC in the ipsilateral hemisphere throughout the experiment, whereas the basal and 5′‐guanylyl imidodiphosphate (Gpp(NH)p)‐sensitive AC activities were not altered. Immunoblotting analysis of AC subtypes with specific antibodies showed a decrease in the immunoreactivity of AC‐I in the ipsilateral hemisphere during these periods. No significant differences in the immunoreactivity of AC‐V/VI and AC‐VIII were observed after ME. The levels of GTP‐binding proteins Gαs, Gαi, and Gβwere unchanged. Furthermore, microsphere‐embolized rats showed prolongation of the escape latency in the water maze task determined on the seveth to ninth day after the operation. These results suggest that sustained cerebral ischemia may induce the impairment of the AC, particularly a selective reduction in the AC‐I level and activity, coupled with the decrease in cAMP content. This reduction may play an appreciable role in the disturbance in cAMP‐mediated signal transduction system, possibly leading to learning and memory dysfunction. © 2002 Wiley‐Liss, Inc.
Interferon‐β treatment of experimental autoimmune encephalomyelitis leads to rapid nonapoptotic termination of T cell infiltration
Authors: Schmidt Jens , Stürzebecher Steffen , Toyka Klaus Viktor , Gold Ralf 
Published: August 2002

AbstractWe investigated the possible mechanisms how interferon (IFN)‐β may control T cell infiltration in the CNS in experimental autoimmune encephalomyelitis (EAE). Adoptive transfer (AT) EAE was induced in groups of six female Lewis rats. Animals were treated with 3 × 105 units of recombinant rat IFN‐β s.c. once at 18 hr, or with 10 mg/kg methylprednisolone (MP) i.v. twice at 18 and 6 hr prior to dissection, or with a combination of both. T cell apoptosis was detected by immunohistochemistry on paraffin sections of spinal cord, using morphological criteria and TUNEL staining. Double labeling of immune cells was done for tumor necrosis factor (TNF)‐α and metalloproteinase (MMP) 2. Disruption of the blood–brain barrier (BBB) was visualized by staining for albumin. In severe EAE, an increase of T cell apoptosis was seen after IFN‐β alone (all data presented as mean ± SD: 24.5% ± 2.2%, P < 0.05, vs. 19.4% ± 3.1% in controls), and in combination with MP (29.4% ± 7.3%, P < 0.05 vs. controls). Only the combination therapy decreased T cell infiltration (53.9 ± 17.7 cells/mm2, P < 0.05, vs. 99.5 ± 35.2 cells/mm2 in controls). In moderate EAE, the rate of T cell apoptosis was slightly increased after IFN‐β (21.2% ± 5.2% vs. 17.4% ± 5.0% in controls), whereas MP alone (25.5% ± 3.5%, P < 0.01 vs. controls) and the combination therapy (22.4% ± 4.8%, P < 0.05 vs. controls) had a clear augmenting effect. IFN‐β tended to decrease T cell infiltration (46.1 ± 12.7 cells/mm2) compared to controls (59.2 ± 18.5 cells/mm2). The rate of TNF‐α‐expressing T cells was significantly decreased by IFN‐β and in combination with MP. Also, TNF‐α expression in macrophages was significantly reduced by IFN‐β and by the combination therapy. The rate of MMP2‐expressing macrophages was lower after IFN‐β but clearly decreased only in combination with MP. BBB disruption was ameliorated after IFN‐β but significantly only in combination with MP. Our study indicates that IFN‐β affects the immunopathological process in EAE in several ways, but apoptosis appears as a minor component. In view of treatment of MS relapses, the synergistic effects in this study corroborate the use of a combination therapy with high‐dose MP and IFN‐β. J. Neurosci. Res. 65:59–67, 2001. © 2001 Wiley‐Liss, Inc.
Axon‐Schwann cell interactions regulate the expression of fibroblast growth factor‐5 (FGF‐5)
Authors: Scarlato Marina , Xu Theodore , Bannerman Peter , Beesley Jacqueline , Reddy Usha R. , Rostami Abdolmohammad , Scherer Steven S. , Pleasure David 
Published: August 2002

AbstractWe screened for genes whose expression is significantly up‐ or downregulated during Wallerian degeneration in adult rat sciatic nerve with cDNA arrays. Fibroblast growth factor‐5 (FGF‐5) mRNA seemed to be induced. This was confirmed by northern blotting and in situ hybridization, as well as Western blotting for FGF‐5 in axotomized nerve. Axon‐Schwann cell interactions decreased the steady‐state level of FGF‐5 mRNA in regenerating sciatic nerves, and forskolin diminished its expression in cultured Schwann cells. We conclude that denervated Schwann cells synthesize FGF‐5, which is a secreted, neuronotrophic member of the FGF family. J. Neurosci. Res. 66:16–22, 2001. © 2001 Wiley‐Liss, Inc.
Selective effect of hypothyroidism on expression of myelin markers during development
Authors: Barradas Penha C. , Vieira Rafael S. , De Freitas Marta S. 
Published: August 2002

AbstractThyroid hormones are critical for maturation of the central nervous system. In a previous study, we showed a change in the pattern of mature myelinated nerve fibers by 2′3′‐cyclic nucleotide 3′‐phosphodiesterase (CNPase) in developing hypothyroid animals, which suggests a possible role for thyroid hormones in myelin compaction. The classical myelin markers myelin basic protein (MBP) and proteolipidic protein (PLP) are expressed later in oligodendroglial development, when myelin sheath formation is in progress. A myelin constituent designated myelin‐associated/oligodendrocytic basic protein (MOBP) has been identified and related to myelin compaction. We assessed the developmental sequence of appearance of CNPase, MBP, MOPB, and PLP proteins in cerebellum (Cb) and corpus callosum (cc) in an experimental hypothyroidism model. The appearance of both MOBP isoforms occurred at postnatal day (P)25 and P30 in cc and Cb, respectively, followed by an increase with age in the control group. However, all the MOBP isoforms were weakly detectable in both regions at P30 from the hypothyroid (H) group, and the higher molecular weight isoform remains decreased in cc, even at P90. The developmental pattern of expression of CNPase, MBP, and PLP proteins was also delayed in the H group. CNPase and MBP expression was recovered in cc and Cb, whereas PLP remained below control levels at P90 in cc. Our data show that the experimental hypothyroidism affects the developmental pattern of the oligodendrocytic/myelin markers. Furthermore, thyroid hormone may modulate specific genes, as demonstrated by permanent down‐regulation of MOBP and PLP expression in adulthood. J. Neurosci. Res. 66:254–261, 2001. © 2001 Wiley‐Liss, Inc.
Transforming growth factor‐β1 enhances expression of brain‐derived neurotrophic factor and its receptor, TrkB, in neurons cultured from rat cerebral cortex
Authors: Sometani Ayako , Kataoka Hiroshige , Nitta Atsumi , Fukumitsu Hidefumi , Nomoto Hiroshi , Furukawa Shoei 
Published: August 2002

AbstractThe effects of transforming growth factor (TGF)‐β1 on expression of brain‐derived neurotrophic factor (BDNF) and its high‐affinity receptor, TrkB, in neurons cultured from the cerebral cortex of 18‐day‐old embryonic rats were examined. BDNF mRNA was significantly increased from 24–48 hr after the TGF‐β1 treatment over 20 ng/ml. Accumulation of BDNF protein in the culture medium was also potentiated by TGF‐β1, although the intracellular content of BDNF was nearly unchanged. The enhancement of BDNF mRNA expression was suppressed by the co‐presence of decorin, a small TGF‐β‐binding proteoglycan that inhibits the biological activities of TGF‐βs. mRNA expression of full‐length TrkB, the bioactive high‐affinity receptor for BDNF, was also upregulated after treatment with TGF‐β1. These observations suggest that: 1) TGF‐β1 potentiates BDNF/TrkB autocrine or local paracrine system; and 2) the neurotrophic activity of TGF‐β1 is partly responsible for the BDNF induced by TGF‐β1 itself. To test this latter possibility, we examined the neuronal survival activity of TGF‐β1 with or without K252a, a selective inhibitor of Trk family tyrosine kinases. TGF‐β1 significantly enhanced neuronal survival, but the co‐presence of K252a completely suppressed the activity, demonstrating the involvement of Trk receptor signaling in TGF‐β1‐mediated neuronal survival in cultured rat cortical neurons. These results seem to be in line with recent findings by other investigators that some neurotrophic factors including BDNF require TGF‐βs as a cofactor to exert their neurotrophic activities. J. Neurosci. Res. 66:369–376, 2001. © 2001 Wiley‐Liss, Inc.
Customer perceptions of justice in service transactions: the effects of strong and weak ties
Authors: Holbrook Robert L. , Kulik Carol T. 
Published: August 2002

AbstractThis research used a justice perspective to investigate the effects of outcome favorability, opportunity for voice, and interpersonal treatment in a service context. Results suggest that all three variables influenced customer reactions to bank loan decisions. Weak‐tie customers were more sensitive to outcome favorability than strong‐tie customers. Strong‐tie customers were more sensitive to opportunity for voice than weak‐tie customers. Implications for improving customer reactions to service transactions are discussed. Copyright © 2001 John Wiley & Sons, Ltd.