bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diagnosis of human parvovirus B19 infections by detection of epitope‐type‐specific VP2 IgG
Authors: Kaikkonen Leena , Söderlund‐Venermo Maria , Brunstein John , Schou Ole , Jensen Inge Panum , Rousseau Steve , Caul E. Owen , Cohen Bernard , Valle Martti , Hedman Lea , Hedman Klaus 
Published: August 2002

AbstractIn the B19 VP2 molecule an immunodominant heptapeptide epitope has been detected, recently for which IgG antibodies are synthesized exclusively in the acute phase of B19 infection. Using this acute‐phase‐specific epitope (KYVTGIN) a 2nd‐generation epitope‐type EIA was developed, which compares serum IgG activity for native VP2 capsids exhibiting conformational VP2 epitopes with IgG activity for the KYVTGIN epitope. In this study the diagnostic performance (clinical sensitivity and specificity) of the 1st and 2nd‐generation epitope‐type EIAs and of a peptide‐based EIA utilising as antigen the KYVTGIN epitope alone was assessed in comparison with various high‐quality IgM‐ and IgG‐ based B19 assays. Serum samples from 489 patients with B19‐related symptoms and asymptomatic controls from three countries were studied. Among 323 patients with B19‐IgG, 20% were diagnosed as acute infection, 73% had past immunity and 7% were not classified due to contradictory results among the different assays. The unclassified samples were explored for viral strain diversity by PCR and DNA sequencing but all sequences obtained were B19‐like with variance of only a few per cent. The 2nd‐generation epitope‐type EIA had a diagnostic sensitivity of 98% and a diagnostic specificity of 94%. In combination with conventional approaches, the epitope‐type assays increase greatly the accuracy of B19 serodiagnosis. J. Med. Virol. 64:360–365, 2001. © 2001 Wiley‐Liss, Inc.
Genetic heterogeneity of hepatitis E virus*
Authors: Schlauder George G. , Mushahwar Isa K. 
Published: August 2002

AbstractHepatitis E virus (HEV) infection has been considered a disease associated with developing regions and attributed to oral‐fecal transmission due to inadequate sanitation. Several recent findings, however, have led to a new understanding of this virus. A number of novel isolates have been identified in patients with acute hepatitis from regions not considered endemic for HEV, and these individuals reported no recent travel to HEV endemic areas. In addition, a number of HEV‐like sequences have also been isolated from swine worldwide, suggesting the potential of an animal reservoir. Although full‐length sequence is available for some strains, the majority of HEV isolates have only been sequenced partially. Sequence comparisons and phylogenetic analyses were performed to determine the genotypic distribution of HEV isolates, based on the partial sequence data available. It has been suggested that HEV isolates segregate into four major genotypes based on full‐length comparisons. These analyses, however, indicate that HEV may be distributed into at least nine different groups. J. Med. Virol. 65:282–292, 2001. © 2001 Wiley‐Liss, Inc.
Advanced model for simulation of surface‐emitting quantum‐well lasers
Authors: Ivanov P. S. , Lysak V. V. , Sukhoivanov I. A. 
Published: August 2002

AbstractThe radial heterogeneity of the vertical‐cavity surface‐emitting lasers (VCSEL) structure leads to both heterogeneity of the pumping current radial distributions and propagation conditions of the optical wave. Hence in research, it is necessary to make a more complete account of the carrier transport and photon generation processes of the devices mentioned.In the given work we investigate a detailed mathematical model of the oxide‐confinement VCSEL with the advanced formulation of the material gain. It is possible to research thermal and speed characteristics of the device and to optimize the geometrical parameters of the laser structure. We consider that it is necessary to have identical radiuses both the oxide window and the quantum well for reduction of the delay time. Moreover, it is proved that the reducing oxide window radius leads to Gaussian distribution of radial photon distribution.The carried out researches have shown the efficiency of the application of the given model for the analysis of the effects connected with the influence of the non‐linear carrier distribution on the VCSEL behaviour. This method can be useful for VCSEL structure optimization. Copyright © 2001 John Wiley & Sons, Ltd.
Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons
Authors: Chen W.Q. , Jin H. , Nguyen M. , Carr J. , Lee Y.J. , Hsu C.C. , Faiman M.D. , Schloss J.V. , Wu J.Y. 
Published: August 2002

AbstractGlutamate‐induced excitotoxicity has been implicated as an important mechanism underlying a variety of brain injuries and neurodegenerative diseases. Previously we have shown that taurine has protective effects against glutamate‐induced neuronal injury in cultured neurons. Here we propose that the primary underlying mechanism of the neuroprotective function of taurine is due to its action in preventing or reducing glutamate‐induced elevation of intracellular free calcium, [Ca2+]i. This hypothesis is supported by the following findings. First, taurine transport inhibitors, e.g., guanidinoethyl sulfonate and β‐alanine, have no effect on taurine's neuroprotective function, suggesting that taurine protects against glutamate‐induced neuronal damage through its action on the extracellular membranes. Second, glutamate‐induced elevation of [Ca2+]i is reduced to the basal level upon addition of taurine. Third, pretreatment of cultured neurons with taurine prevents or greatly suppresses the elevation of [Ca2+]i induced by glutamate. Furthermore, taurine was found to inhibit the influx but not the efflux of 45Ca2+ in cultured neurons. Taurine has little effect on the binding of [3H]glutamate to the agonist binding site and of [3H]MDL 105,519 to the glycine binding site of the N‐methyl‐D‐aspartic acid receptors, suggesting that taurine inhibits 45Ca2+ influx through other mechanisms, including its inhibitory effect on the reverse mode of the Na+/Ca2+ exchangers (Wu et al. [2000] In: Taurine 4: taurine and excitable tissues. New York: Kluwer Academic/Plenum Publishers. p 35–44) rather than serving as an antagonist to the N‐methyl‐D‐aspartic acid receptors. J. Neurosci. Res. 66:612–619, 2001. © 2001 Wiley‐Liss, Inc.
Lactate reduces glutamate‐induced neurotoxicity in rat cortex
Authors: Ros Jacqueline , Pecinska Nadja , Alessandri Beat , Landolt Hans , Fillenz Marianne 
Published: August 2002

AbstractExperiments were carried out to test the hypothesis that lactate reduces the neurotoxicity of glutamate in vivo. MAP2 immunohistochemistry was used to measure lesion size, and microdialysis to measure the changes in glucose and lactate in the extracellular compartment. After implantation of a microdialysis probe 100 mM glutamate with or without 6 mM lactate was added to the perfusion medium and infused into the cortex of unanesthetized rats. Infusion of 100 mM glutamate for a period of 30 min produced a lesion of 6.05 ± 0.64 mm3, an increase in lactate of 124 ± 19% above basal and a 21 ± 9% reduction of glucose below basal level. When 6mM L‐lactate was perfused together with 100 mM glutamate there was a significant reduction in the size of the lesion and there was no reduction in dialysate glucose. When L‐lactate was replaced with D‐lactate the lesion size and the increase in dialysate lactate were greater than after glutamate alone. The neuroprotective role of L‐lactate is attributed to its ability to meet the increased energy demands of neurones exposed to high concentrations of glutamate. © 2001 Wiley‐Liss, Inc.
Quantitative imaging of glutathione in hippocampal neurons and glia in culture using monochlorobimane
Authors: Keelan Julie , Allen Nicola J. , Antcliffe David , Pal Shoubik , Duchen Michael R. 
Published: August 2002

AbstractGlutathione (GSH) is a major antioxidant system in the mammalian central nervous system (CNS). Abnormalities of GSH metabolism have been associated with many disorders of the CNS, including Parkinson's, Alzheimer's, and Huntingdon's diseases and ischaemic/reperfusion injury. Investigation of GSH levels in the CNS generally relies on biochemical assays from cultures enriched for different cell types. Because glia influence neuronal metabolism, we have studied cultures in which neurons and glia are cocultured. This approach demands fluorescence imaging to differentiate between the different cell types in the culture, permitted by the use of monochlorobimane (MCB), which reacts with GSH to produce a fluorescent product. We have defined the conditions required to ensure steady‐state MCB loading and show the specificity of MCB for GSH through a reaction catalysed by glutathione‐S‐transferase (GST). [GSH] was consistently higher in glia than in neurons, and [GSH] in both cell types decreased with time in culture. Inhibition of GSH synthesis by buthionine sulfoximine (BSO) caused a greater proportional depletion of GSH in glia than in neurons. The depletion of GSH induced by BSO was significantly greater in cells cultured for >10 days. Furthermore, release of GSH from glia and its breakdown by the ectoenzyme γ‐glutamyltranspeptidase (γGT) maintains [GSH] in neurons. In older cultures, inhibition of γGT by acivicin caused significant depletion of neuronal GSH. After inhibition of GSH synthesis by BSO, inhibition of the glia‐neuron trafficking pathway by acivicin caused widespread neuronal death. Such neurotoxicity was independent of the endogenous glutamate and nitric oxide synthase, suggesting that it is not due to secondary excitotoxicity. © 2001 Wiley‐Liss, Inc.
Proliferation of Schwann cells and regulation of cyclin D1 expression in an animal model of Charcot‐Marie‐Tooth disease type 1A
Authors: Atanasoski Suzana , Scherer Steven S. , Nave Klaus‐Armin , Suter Ueli 
Published: August 2002

AbstractOverexpression of PMP22 is responsible for the most common form of inherited neuropathy, Charcot‐Marie‐Tooth disease (CMT) type 1A. The PMP22‐transgenic rat (CMT rat) is an animal model of CMT1A, and its peripheral nerves show the characteristic features of ongoing demyelination and remyelination that is also seen in CMT1A patients. Since Schwann cell proliferation is a prominent feature of peripheral nerves in inherited peripheral neuropathies, we examined proliferation and the expression of cyclin D1 in CMT rats. D‐type cyclins are required for the initial steps in cell division and nuclear import is crucial for the function of cyclin D1 in promoting cell proliferation. Like normal myelinating Schwann cells in wild‐type rats, remyelinating Schwann cells in CMT rats show perinuclear cyclin D1 expression. Schwann cells with nuclear cyclin D1 expression, as well as proliferating Schwann cells, were both associated with demyelinated axonal segments. Supernumerary onion bulb Schwann cells, however, do not express cyclin D1 and were not proliferating. Thus, cyclin D1 expression and its subcellular localization correlate directly with distinct physiological states of Schwann cells in this animal model of CMT1A. © 2002 Wiley‐Liss, Inc.
Role of CB1 and CB2 receptors in the inhibitory effects of cannabinoids on lipopolysaccharide‐induced nitric oxide release in astrocyte cultures
Authors: Molina‐Holgado Francisco , Molina‐Holgado Eduardo , Guaza Carmen , Rothwell Nancy J. 
Published: August 2002

AbstractThe purpose of this study was to investigate the role of the central cannabinoid receptor (CB1) in mediating the actions of the endogenous cannabinoid agonist anandamide and the synthetic cannabinoid CP‐55940. Activation of primary mouse astrocyte cultures by exposure to bacterial lipopolysaccharide (LPS) caused a marked (approximately tenfold) increase in nitric oxide (NO) release. Coincubation with the cannabinoid agonists anandamide or CP‐55940 markedly inhibited release of NO (–12% to –55%). This effect was abolished by SR‐141716A (1 μM), a CB1 receptor antagonist. SR‐141716A alone also significantly increased NO release in response to LPS, suggesting that endogenous cannabinoids modify inflammatory responses. In contrast, coincubation with the CB2 receptor antagonist SR‐144528 (1 μM) abolished the inhibitory effects of the endogenous cannabinoid anandamide on LPS‐induced NO release, although this may reflect nonspecific effects of this ligand or cannabinoid actions through atypical receptors of anandamide. We also showed that endogenous or synthetic cannabinoids inhibit LPS‐induced inducible NO synthase expression (mRNA and protein) in astrocyte cultures. These results indicate that CB1 receptors may promote antiinflammatory responses in astrocytes. © 2002 Wiley‐Liss, Inc.
Myelin protein zero exists as dimers and tetramers in native membranes of Xenopus laevis peripheral nerve
Authors: Thompson Amanda J. , Cronin Maureen S. , Kirschner Daniel A. 
Published: August 2002

AbstractProtein zero (P0) glycoprotein is the major integral membrane protein of the peripheral nervous system myelin in higher vertebrates. Previous findings indicate the formation of tetrameric assemblies from studies on isolated P0. To determine whether in intact myelin the P0 exists as oligomers, we isolated myelin from sciatic nerve of Xenopus laevis and analyzed it using sodium dodecyl sulfate and urea gel electrophoresis. P0 oligomerization was confirmed using Western blotting, which showed monomeric P0 at ∼30 kDa and oligomeric P0 at ∼60 kDa and ∼120 kDa. A variety of denaturing conditions failed to convert any appreciable amount of oligomer to monomer. Instead, the addition of these denaturants further increased the amount of dimer and tetramer while decreasing the amount of monomer. Native gels showed dimeric P0 without the appearance of monomer or tetramer, suggesting that dimeric P0, the most prominent form of the protein, is the most stable and likely occurs in the native myelin membrane array. © 2002 Wiley‐Liss, Inc.
Suppression of BDNF‐induced expression of neuropeptide Y (NPY) in cortical cultures by oxygen‐glucose deprivation: A model system to study ischemic mechanisms in the perinatal brain
Authors: Barnea Ayalla , Roberts Jodie 
Published: August 2002

AbstractThe aim of this study was to establish a culture system that can serve as a model to study hypoxic‐ischemic mechanisms regulating the functional expression of NPY neurons in the perinatal brain. Using an aggregate culture system derived from the rat fetal cortex, we defined the effects of oxygen and glucose deprivation on NPY expression, using BDNF‐induced production of NPY as a functional criterion. NPY neurons exhibited a differential susceptibility to oxygen and glucose deprivation. Although the neurons could withstand oxygen deprivation for 16 hr, they were dramatically damaged by 8 hr of glucose deprivation and by 1–4 hr of deprivation of both oxygen and glucose (N+Glu−). One‐hour exposure to N+Glu− led to a transient inhibition (≈50%) of NPY production manifesting within 24 hr and recovering by 5 days thereafter, a 2‐hr exposure to N+Glu− led to a sustained inhibition (50–75%) manifesting 1–5 days thereafter, and a 4‐hr exposure to N+Glu− led to a total irreversible suppression of BDNF‐induced production of NPY manifesting within 24 hr and lasting 8 days after re‐supply of oxygen and glucose. Moreover, 1‐hr exposure to N+Glu− led to a substantial and 4‐hr exposure led to a total disappearance of immunostaining for MAP‐2 and NPY but not for GFAP; indicating that neurons are the primary cell‐type damaged by oxygen‐glucose deprivation. Analysis of cell viability (LDH, MTT) indicated that progressive changes in cell integrity take place during the 4‐hr exposure to N+Glu− followed by massive cell death 24 hr thereafter. Thus, we defined a culture system that can serve as a model to study mechanisms by which ischemic insult leads to suppression and eventually death of NPY neurons. Importantly, changes in NPY neurons can be integrated into the overall scheme of ischemic injury in the perinatal brain. © 2002 Wiley‐Liss, Inc.
β‐Amyloid peptide induces ultrastructural changes in synaptosomes and potentiates mitochondrial dysfunction in the presence of ryanodine
Authors: Mungarro‐Menchaca Xavier , Ferrera Patricia , Morán Julio , Arias Clorinda 
Published: August 2002

AbstractIn Alzheimer's disease (AD), loss of synapses exceeds neuronal loss and some evidence suggests a role of β‐amyloid protein (Aβ) in synaptic degeneration through a mechanism which may involve intraneuronal Ca2+ dyshomeostasis. Emerging evidence points to the participation of the internal Ca2+ stores in the pathophysiology of neurodegeneration in AD. To test the involvement of intrasynaptic Ca2+ mobilization in Aβ toxicity, we explored the role of ryanodine receptor activation in rat cortical synaptosomes taken as a model system for the central presynapses. Evaluation of synaptosomal mitochondrial redox capacity was assessed by the MTT reduction technique, and ultrastructural changes of synaptosomes after exposure to Aβ and ryanodine were evaluated by electron microscopy. Our results show that Aβ potentiates mitochondrial dysfunction in the presence of ryanodine and induces morphological changes consisting of mitochondrial swelling and intense small synaptic vesicles depletion. These changes were accompanied by a reduction in the content of synaptophysin and actin proteins. The reduction of actin immunoreactivity was reversed in the presence of a wide range caspase inhibitors, suggesting the activation of synaptic apoptotic mechanisms. © 2002 Wiley‐Liss, Inc.
Tenascin‐R is expressed by Schwann cells in the peripheral nervous system
Authors: Probstmeier Rainer , Nellen Jörg , Gloor Sergio , Wernig Anton , Pesheva Penka 
Published: August 2002

AbstractThe extracellular matrix glycoprotein tenascin‐R (TN‐R) has been implicated in a variety of cell‐matrix interactions involved in the molecular control of axon guidance and neural cell migration during development and regeneration of the central nervous system (CNS). Whereas TN‐R is amply expressed in the early postnatal and adult mammalian CNS, the protein has so far not been detected in different compartments of the peripheral nervous system (PNS). Here we provide first evidence that TN‐R (predominantly TN‐R 160 isoform) is transiently expressed in the sciatic nerve of late embryonic (E14–18) and neonatal mice, while at later developmental stages, both protein and mRNA are downregulated. In vitro, TN‐R protein was found to be expressed by both undifferentiated and neuronally differentiated PC12 cells and by L1‐positive Schwann cells (SC), but not by other neural and non‐neural cell types in cell cultures derived from embryonic (E17/18) hindlimbs and neonatal sciatic nerves. In the developing PNS, TN‐R expression correlated with axon growth and SC migration during the period of skeletal muscle innervation. Based on different in vitro approaches, we found that the substrate‐bound glycoprotein selectively inhibits the fibronectin‐dependent: (1) neurite outgrowth from dorsal root ganglion neurons (strongly expressing α5β1 integrin and the disialoganglioside GD3) by a ganglioside‐sensitive signaling mechanism; and (2) migration of primary myoblasts and other non‐neuronal cells in a ganglioside‐independent manner. Our findings suggest the functional role of TN‐R in PNS pattern formation during distinct stages of axon pathfinding and skeletal muscle innervation. J. Neurosci. Res. 64:70–78, 2001. © 2001 Wiley‐Liss, Inc.
Nongenomic antiapoptotic signal transduction by estrogen in cultured cortical neurons
Authors: Honda Kazuhiro , Shimohama Shun , Sawada Hideyuki , Kihara Takeshi , Nakamizo Tomoki , Shibasaki Hiroshi , Akaike Akinori 
Published: August 2002

AbstractEstrogen replacement therapy in menopausal women has been suggested to be beneficial in preventing the progression of cognitive impairment in Alzheimer disease. We demonstrated previously that the phosphatidylinositol 3‐kinase (PI3‐K)/Akt signal transduction pathway plays a pivotal role on the neuroprotection provided by 17β‐estradiol against acute glutamate toxicity. In the present study, we investigated the mechanism of neuroprotection against apoptosis because acute glutamate toxicity predominantly induced necrosis. 17β‐estradiol provided neuroprotection against apoptosis induced by staurosporine. This neuroprotection was inhibited by pretreatment with a PI3‐K inhibitor, LY294002. An estrogen receptor specific antagonist, ICI182780, also suppressed the neuroprotection provided by 17β‐estradiol. Western blotting analysis demonstrated that treatment with 17β‐estradiol induced the phosphorylation of Akt within 5 min, which was suppressed by pretreatment with LY294002 and ICI182780. Furthermore, 17β‐estradiol induced phosphorylation of the cAMP response element binding protein (CREB) at Ser133 within 15 min and then upregulated Bcl‐2 in a PI3‐K/Akt‐dependent manner. Because CREB is known to be a transcription factor for Bcl‐2, these results suggest that 17β‐estradiol exerts its antiapoptotic effects by CREB phosphorylation and Bcl‐2 upregulation via nongenomic activation of the PI3‐K/Akt pathway in cultured cortical neurons. J. Neurosci. Res. 64:466–475, 2001. © 2001 Wiley‐Liss, Inc.
Lipopolysaccharide‐induced switch between retinoid receptor (RXR) α and glucocorticoid attenuated response gene (GARG)‐16 messenger RNAs in cultured rat microglia
Authors: Kitamura Yoshihisa , Spleiss Olivia , Li Hongwei , Taniguchi Takashi , Kimura Hiroshi , Nomura Yasuyuki , Gebicke‐Haerter Peter J. 
Published: August 2002

AbstractGlucocorticoid‐attenuated response genes (GARG) belong to a recently described family of genes responsive to the action of dexamethasone. Full‐length cDNA of one member of this family, GARG16, has been cloned from rat microglia and regulation of its mRNA expression has been studied. Moreover, regulation of retinoid/retinoic acid activated transcription factor (RXR/RAR) mRNAs in mixed astrocyte and in purified microglia cultures has been investigated. RARβ mRNA was undetectable in microglia by RT‐PCR, whereas clearly present in the mixed cultures. RXRα, RARγ, and GARG16 mRNAs were found in both culture systems. RXRα mRNA was strongly expressed in control microglia but rapidly declined upon treatment with LPS. Conversely, GARG16 mRNA was almost untraceable in control microglia but rapidly increased by LPS. Time‐course studies revealed an oscillating behavior of expression of both mRNAs during the first 6 hr, which receded to control levels (RXRα high, GARG16 low) at 72 hr of LPS‐treatment. Additionally, p38 MAPK and SEK phosphorylations peaked at 1 hr followed by steady declines, whereas MEK and c‐Jun showed double peaks at 1+4 hr and 1+6 hr, respectively, before subsiding to control levels. This behavior was not observed in comparative studies with TNF‐α, interleukin‐10 (IL‐10), or interferon‐γ inducible protein 10 (IP‐10). Finally, inhibitors of p38 MAPK, p42/p44 ERK, and PKCα as well as the use of dexamethasone revealed major influences of the p38 MAPK‐c‐Jun‐AP‐1 signaling pathway on RXRα and GARG16 mRNA expressions. The counter regulatory control of GARG16 and RXRα mRNA expression is believed to be an example of a fine‐tuned cellular mechanism to react to inflammatory stimuli. J. Neurosci. Res. 64:553–563, 2001. © 2001 Wiley‐Liss, Inc.