bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transmission of SEN virus from mothers to their babies
Authors: Pirovano Silvia , Bellinzoni Marco , Ballerini Cristina , Cariani Elisabetta , Duse Marzia , Albertini Alberto , Imberti Luisa 
Published: August 2002

AbstractSera from 30 women at high risk for infection, one half of which were SEN virus positive (SENV+), were collected at delivery to study SENV mother‐to child transmission. Thirteen of their babies were positive for at least one SENV strain: one baby was SENV+ at birth, eight became positive within 6 months from delivery, and four became positive in the following months. Our data indicate that vertical transmission of SENV does occur, presumably, at delivery, but it may not induce persistent viremia. This is supported by the fact that, generally, SENV is not detected at birth, by the high SENV homology in the sequences found in the mothers and in their children, by a lack of other risk factors for infection of the babies, and by the irregular detection of SENV in the follow‐up. No clinical events surely linked to SENV infection were found, but transient elevations of alanine aminotransferase were observed in babies followed for a long period of time. J. Med. Virol. 66:421‐427, 2002. © 2002 Wiley‐Liss, Inc.
Detection of varicella‐zoster virus DNA in throat swabs of patients with herpes zoster and on air purifier filters
Authors: Suzuki Kayoko , Yoshikawa Tetsushi , Tomitaka Akiko , Suzuki Kyoko , Matsunaga Kayoko , Asano Yoshizo 
Published: August 2002

AbstractZoster patients are considered to be less contagious than those with varicella because their infectious lesions are localized. However, it is not known when the spread of varicella‐zoster virus (VZV) from zoster patients begins, how long it continues, and how far the virus spreads from the zoster patients. Twelve cases of hospitalized zoster patients were studied. The polymerase chain reaction (PCR) was used to detect VZV DNA in samples taken from the surface of their eruptions, throats, and the air purifier filters in their rooms. In all patients, VZV DNA was detected in the samples from eruptions. VZV DNA was detected in 8 of 12 patients from the throats. VZV DNA was detected for 9 of 12 patients from the filter samples. This study shows the possibility of a wide distribution of VZV DNA to the environment from infected patients. VZV may be excreted from cutaneous eruptions or from the throats of patients. J. Med. Virol. 66:567–570, 2002. © 2002 Wiley‐Liss, Inc.
Space–time wavelet expansion iterative solution of non‐uniform transmission lines with arbitrary loads
Authors: Barmada S. , Raugi M. 
Published: August 2002

AbstractIn this paper a method based on the double expansion by wavelet on the interval in space and time of non‐uniform transmission line equations with arbitrary loads is presented. The differential time domain equations are transformed into a Lyapunov equation which is adaptively solved. Hence, a Fourier‐like approach for the time‐domain solution of transient electromagnetics problems is obtained avoiding the typical problems of time‐stepping techniques. The accuracy of the solution can be selected by choosing an adequate number of components of the wavelet basis. Different cases have been studied to show the effectiveness of the method. Copyright © 2001 John Wiley & Sons, Ltd.
An extended Huygens' principle for modelling scattering from general discontinuities within hollow waveguides
Authors: Ferrari Ronald L. 
Published: August 2002

AbstractThe modal fields, generalized scattering matrix (GSM) theory and dyadic Green's functions relating to a general uniform hollow waveguide are briefly reviewed in a mutually consistent normalization. By means of an analysis linking these three concepts, an extended version of the mathematical expression of Huygens' principle is derived, applying to scattering from an arbitrary object within a hollow waveguide. The integral‐equation result expresses the total field in terms of the incident waveguide modal fields, the dyadic Green's functions and the tangential electromagnetic field on the surface of the object. It is shown how the extended principle may be applied in turn to perfect conductor, uniform material and inhomogeneous material objects using a quasi method of moments (MM) approach, coupled in the last case with the finite element method. The work reported, which indicates how the GSM of the object may be recovered, is entirely theoretical but displays a close similarity with established MM procedures. Copyright © 2001 John Wiley & Sons, Ltd.
Influence of antioxidants on the blood‐brain barrier permeability during epileptic seizures
Authors: Öztaş Baria , Kılıç Şehri , Dural Esen , İspir Turgay 
Published: August 2002

AbstractPentylenetetrazol‐induced seizures in rats lead to the breakdown of the blood‐brain barrier. We compared the disruption of the blood‐brain barrier during epileptic seizure in untreated rats and in rats treated with vitamin E or selenium. The rats were supplemented with nontoxic doses of sodium selenite (4 pp) in drinking water for 3 months, or vitamin E (70 mg/kg) was given intraperitoneally for 30 min before the pentylenetetrazole injection. Evans‐blue was used as a blood‐brain barrier tracer and was given intravenously at a dose of 4 ml/kg of a 2% solution. The rats were divided into four experimental groups. Group I: control (n = 24); Group II: pentylenetetrazole‐induced seizure (n = 12); Group III: vitamin E injected + seizure (n = 12); Group IV: Selenium supplemented + seizure (n = 12). The rats subjected to epileptic seizures showed Evans‐blue albumin extravasations especially in the thalamic nuclei, brainstem, occipital, and frontal cortex. Mean values for Evans‐blue dye were found to be 0.28 ± 0.04 mg % brain tissue in control rats and 1.6 ± 0.2 mg % brain tissue after epileptic seizures (P < 0.01). The magnitude of distribution of the blood‐brain barrier during epileptic seizures was significantly less in rats treated with vitamin E or selenium. The mean value for Evans‐blue dye was found to be 1.2 ± 0.1 mg % brain tissue in selenium supplemented rats and 1.2 ± 0.1 mg % brain tissue in vitamin E injected rats after epileptic seizures. This difference between treated and untreated animals was found to be significant (P < 0.05). The findings of the present study suggest that free radicals contribute to disruption of the blood‐brain barrier during pentylenetetrazol‐induced seizures. J. Neurosci. Res. 66:674–678, 2001. © 2001 Wiley‐Liss, Inc.
Selective CC chemokine receptor expression by central nervous system‐infiltrating encephalitogenic T cells during experimental autoimmune encephalomyelitis
Authors: Fife Brian T. , Paniagua Mary C. , Lukacs Nicholas W. , Kunkel Steven L. , Karpus William J. 
Published: August 2002

AbstractExperimental autoimmune encephalomyelitis (EAE) is a CD4+ T cell disease of the central nervous system (CNS) characterized by mononuclear cell infiltration, demyelination, and paralysis. Recent studies describing the relationship of chemokine expression with development of clinical disease have led to the hypothesis that distinct chemokine receptors corresponding to specific ligands are expressed by CNS‐infiltrating antigen‐specific encephalitogenic T cells as well as host‐derived bystander T cells and monocytes. In an effort to study encephalitogenic T cell chemokine receptor expression, we examined CC chemokine receptor expression from resting, activated, and CNS‐isolated CD4+ T cells. CCR1, CCR2, CCR3, CCR5, CCR6, CCR7, and CCR8 mRNA is expressed by normal CD4+ T cells. In vitro activated T cells expressed CCR1, CCR2, CCR3, CCR5, CCR6, CCR7, and CCR8 mRNA as well as CCR4. After EAE induction, CCR1 mRNA was expressed by donor‐derived encephalitogenic and host‐derived CD4+ T cells isolated only from CNS and not from spleen. In vivo neutralization of the CCR1 ligand, macrophage inflammatory protein‐1α (CCL3), resulted in less encephalitogenic CD4+ T cell CNS infiltration. These results demonstrate the importance of CC chemokine receptor expression by CD4+ encephalitogenic T cells for CNS infiltration and subsequent disease development. J. Neurosci. Res. 66:705–714, 2001. © 2001 Wiley‐Liss, Inc.
Pyruvate carboxylation in neurons
Authors: Hassel Bjørnar 
Published: August 2002

AbstractCarboxylation of pyruvate in the brain was for many years thought to occur only in glia, an assumption that formed much of the basis for the concept of the glutamine cycle. It was shown recently, however, that carboxylation of pyruvate to malate occurs in neurons and that it supports formation of transmitter glutamate. The role of pyruvate carboxylation in neurons is to ensure tricarboxylic acid cycle activity by compensating for losses of α‐ketoglutarate that occur through release of transmitter glutamate and GABA; these amino acids are α‐ketoglutarate derivatives. Available data suggest that neuronal pyruvate carboxylation is quantitatively important. But because there is no net CO2 fixation in the brain, pyruvate carboxylation must be balanced by decarboxylation of malate or oxaloacetate. Such decarboxylation occurs in both neurons and astrocytes. Several in vitro studies have shown a neuroprotective effect of pyruvate supplementation. Pyruvate carboxylation may be one mechanism through which such treatment is effective, because pyruvate carboxylation through malic enzyme is active during energy deficiency and leads to an increase in the level of dicarboxylates that can be metabolized through the tricarboxylic acid cycle for ATP production. © 2001 Wiley‐Liss, Inc.
Light‐induced changes in glutamate release from isolated rat retina is regulated by cyclic guanosine monophosphate
Authors: Barabás Péter , Kovács Ilona , Kovács Richárd , Pálhalmi János , Kardos Julianna , Schousboe Arne 
Published: August 2002

AbstractIsolated rat retina was preloaded with [14C]glutamate and subsequently superfused to follow release of glutamate (Glu). After 20 min of superfusion in the dark, exposure of the [14C]Glu preloaded rat retina to a single train of white light pulses reduced Glu efflux significantly in the absence as well as in the presence of low (4 μM) and high (0.5 mM) concentrations of the Glu uptake inhibitor trans‐L‐pyrrolidine‐2,4‐dicarboxylate (t‐PDC). The dark–light response was the highest in the presence of 4 μM t‐PDC by establishing a plateau at 75% ± 7% of the tonic Glu release in the dark (100%). Displaying transient to saturating responses with increasing relative luminance, time series of four trains of white light pulses arrived at a plateau of 85% ± 10%. The cyclic guanosine monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast (200 μM) antagonized the effect of the light series, leading to a plateau of 115% ± 9%. Exposure of the retina to the guanylyl cyclase inhibitor LY83583 (30 and 100 μM) showed fast, transient responses characterized by peaks at 90% ± 1% and 80% ± 3%, respectively. © 2002 Wiley‐Liss, Inc.
Ultrastructural localization of neuropeptide Y Y1 receptors in the rat medial nucleus tractus solitarius: Relationships with neuropeptide Y or catecholamine neurons
Authors: Glass Michael J. , Chan June , Pickel Virginia M. 
Published: August 2002

AbstractNeuropeptide Y (NPY) Y1 receptor (Y1‐R) agonists influence cardiovascular regulation. These actions may involve NPY‐ and catecholamine‐containing neurons in the medial nucleus of the solitary tract (mNTS), at the level of the area postrema. The cellular sites through which Y1‐R agonists may interact with NPY and catecholamines in the mNTS, however, are not known. To determine potential sites of action for Y1‐R agonists, and their relationship to NPY or catecholamines in the mNTS, we used electron microscopic immunocytochemistry for the detection of sequence‐specific antipeptide antisera against Y1‐R alone or in combination with antisera against NPY or the catecholamine‐synthesizing enzyme tyrosine hydroxylase (TH). Analyses were conducted in the rat mNTS, at the level of the area postrema. Y1‐R was found mainly in small unmyelinated axons and axon terminals but also in some somata and dendrites as well as a small number of glia. Within axon terminals, labeling for Y1‐R was often present on dense core vesicles and small synaptic vesicles as well as extrasynaptic areas of the plasmalemma. Some Y1‐R‐labeled terminals also contained NPY or TH, suggesting that agonists of Y1‐R may influence the release of NPY or catecholamines in the mNTS. In addition, Y1‐R was found in dendrites that received asymmetric excitatory‐type synapses from unlabeled axon terminals. Some of these dendrites contained NPY or TH, which indicates that Y1‐R may be targeted for functional activation within NPY‐ or catecholamine‐expressing neurons in the mNTS. These results demonstrate that Y1‐R is a presynaptic receptor in NPY‐ or catecholamine‐containing axon terminals within the mNTS as well as a postsynaptic receptor on NPY‐ or catecholamine‐containing neurons that are contacted by axon terminals that likely contain excitatory amino acid transmitters. Agonists of Y1‐R in the mNTS may thus affect cardiovascular regulation by modulating NPY, catecholamine, and excitatory amino acid transmission. © 2002 Wiley‐Liss, Inc.
Interleukin‐4, interleukin‐10, and interleukin‐1‐receptor antagonist but not transforming growth factor‐β induce ramification and reduce adhesion molecule expression of rat microglial cells
Authors: Wirjatijasa Florentina , Dehghani Faramarz , Blaheta Roman A. , Korf Horst‐Werner , Hailer Nils P. 
Published: August 2002

AbstractThe activity of microglial cells is strictly controlled in order to maintain central nervous system (CNS) immune privilege. We hypothesized that several immunomodulatory factors present in the CNS parenchyma, i.e., the Th2‐derived cytokines interleukin (IL)‐4 and IL‐10, interleukin‐1‐receptor‐antagonist (IL‐1‐ra), or transforming growth factor (TGF)‐β can modulate microglial morphology and functions. Microglial cells were incubated with IL‐4, IL‐10, IL‐1‐ra, TGF‐β, or with astrocyte conditioned media (ACM) and were analyzed for morphological changes, expression of intercellular adhesion molecule (ICAM)‐1, and secretion of IL‐1β or tumor necrosis factor (TNF)‐α. Whereas untreated controls showed an amoeboid morphology both Th2‐derived cytokines, IL‐1‐ra, and ACM induced a morphological transformation to the ramified phenotype. In contrast, TGF‐β‐treated microglial cells showed an amoeboid morphology. Even combined with the neutralizing antibodies against IL‐4, IL‐10, or TGF‐β ACM induced microglial ramification. Furthermore, ACM did not contain relevant amounts of IL‐4 and IL‐10, as measured by enzyme‐linked immunosorbent assay (ELISA). Flow cytometry showed that lipopolysaccharide (LPS)‐induced ICAM‐1‐expression on microglial cells was strongly suppressed by ACM, significantly modulated by IL‐4, IL‐10, or IL‐1‐ra, but not influenced by TGF‐β. The LPS‐induced secretion of IL‐1β and TNF‐α was only reduced after application of ACM, whereas IL‐4 or IL‐10 did not inhibit IL‐1β‐ or TNF‐α secretion. TGF‐β enhanced IL‐1β‐ but not TNF‐α secretion. In summary, we demonstrate that IL‐4, IL‐10, and IL‐1‐ra induce microglial ramification and reduce ICAM‐1‐expression, whereas the secretion of proinflammatory cytokines is not prevented. TGF‐β has no modulating effects. Importantly, unidentified astrocytic factors that are not identical with IL‐4, IL‐10, or TGF‐β possess strong immunomodulatory properties. © 2002 Wiley‐Liss, Inc.
Protective effects of atypical antipsychotic drugs on PC12 cells after serum withdrawal
Authors: Bai Ou , Wei Zelan , Lu Wenfu , Bowen Rudy , Keegan David , Li Xin‐Min 
Published: August 2002

AbstractAtypical antipsychotic drugs are widely used in the treatment of schizophrenia, and clinical evidence has shown that early and prolonged intervention with these drugs will improve the long‐term outcome. It is still unclear, however, whether the atypical antipsychotic drugs are also neuroprotective. To clarify this matter, we used PC12 cell cultures and the MTT assay for cell viability to determine whether various concentrations of the atypical antipsychotics clozapine, quetiapine, and risperidone are neuroprotective after serum withdrawal. In addition, to explore the drugs' actions, Northern blot was used to examine the gene expression of SOD1 (Cu/Zn superoxide dismutase) and p75NTR (p75 neurotrophin receptor). The results demonstrated that 1) the antipsychotic drugs can protect PC12 cells from death after serum withdrawal; cell viability in these drug treatment groups is significantly different from that in the groups without serum in the medium (P < 0.01); and 2) these drugs up‐regulated the SOD1 gene expression to more than 120% (P < 0.05) and also down‐regulated p75NTR mRNA levels to less than 65% of their respective control values (P < 0.05). These findings suggest that the atypical antipsychotics clozapine, quetiapine, and risperidone may exert a neuroprotective function through the modulation of SOD1 and p75NTR expression. © 2002 Wiley‐Liss, Inc.
Distribution in ocular structures and optic pathways of immunocompetent and glial cells in an experimental allergic encephalomyelitis (EAE) relapsing model
Authors: Villarroya Henri , Klein Christophe , Thillaye‐Goldenberg Brigitte , Eclancher Françoise 
Published: August 2002

AbstractRelapsing experimental allergic encephalomyelitis (EAE) was induced in DA rats and the ocular pathologic events were examined at the various phases of the illness. About 80% of EAE rats presented anterior uveitis (AU), even after complete EAE recovery. We studied the phenotype and localization of immunocompetent cells, the major histocompatibility complex (MHC) class I and II antigen expression, as well as the chemokine monocyte chemoattractant protein‐1 (MCP‐1) appearance. In control animals, there were many glial fibrillary acidic protein (GFAP)+ cells and OX42+ cells in the ciliary body, retina, optic nerve and chiasma. Except in retina, we observed constitutive MHC class I and II expression. During the EAE acute phase, there was up‐regulation of MHC class II and GFAP antigens in iris, ciliary body, limbus, and optic pathways. MHC class I and ED2 antigens were expressed in meninges and in the prechiasmatic cisterna, by cells which could have a role in immune surveillance. MCP‐1 mRNA was highly expressed in optic pathways during the acute phase and the protein was expressed by astrocytes, macrophages, and lymphocytes. During the relapsing phase, MCP‐1 was weakly expressed to disappear almost completely during the final recovery phase. The expression of MHC class II on astrocytes was increased during the relapsing and final recovery phase in which the inflammatory lesions persisted. These findings suggest that ocular areas and optic pathways, mainly optic chiasma, are important targets in the relapsing EAE. J. Neurosci. Res. 63:525–535, 2001. © 2001 Wiley‐Liss, Inc.
Age‐ and concentration‐dependent neuroprotection and toxicity by TNF in cortical neurons from β‐amyloid
Authors: Viel J.J. , McManus D.Q. , Smith Sherry S. , Brewer G.J. 
Published: August 2002

AbstractThe induction of an inflammatory response and release of cytokines such as TNF may be involved in the age‐related etiology of Alzheimer disease (AD). In the brain, microglia have been shown to produce a wide variety of immune mediators, including the pro‐inflammatory cytokine tumor necrosis factor (TNF). We hypothesize that with age there is increased ability of microglia to produce TNF or that age decreases the neuroprotective effect of TNF against beta‐amyloid (Aβ) toxicity in neurons. We investigated the effects of Aβ(1–40) on TNF secretion from forebrain cultures of microglia from embryonic, middle‐age (9‐month) and old (36‐month) rats. Over the first 12 hr of exposure to 10 μM Aβ (1–40), microglia from embryonic and old rats increase TNF secretion, although microglia from middle‐age rats did not produce detectable levels of TNF. When low concentrations of TNF are added to neurons together with Aβ (1–40) in the absence of exogenous antioxidants, neuroprotection for old neurons is significantly less than neuroprotection for middle‐age neurons. In neurons from old rats, high levels of TNF together with Aβ are more toxic than in neurons from middle‐age or embryonic rats. These results are discussed in relation to neuroprotection and toxicity of the age‐related pathology of AD. J. Neurosci. Res. 64:454–465, 2001. © 2001 Wiley‐Liss, Inc.
Expression of a voltage‐dependent potassium channel protein (Kv3.1) in the embryonic development of the auditory system
Authors: Zhou Xiangning , Baier Christopher , Hossain Waheeda Amin , Goldenson Mark , Morest D. Kent 
Published: August 2002

AbstractThe present study traces the development of a voltage‐dependent potassium channel protein (Kv3.1) in the avian homologue of the cochlear nucleus, in the cochleovestibular ganglion, and in the otic epithelium from early developmental stages until near hatching. Immunohistochemistry with antibodies to the carboxy terminus (recognizing the Kv3.1b splice variant) and to the amino terminus (recognizing either form of Kv3.1) was used on Hamburger‐Hamilton‐staged chicken embryos. There were three periods in the relative levels of immunostaining in these regions. Early (E2–6), when precursor cells proliferate, migrate, and form axons, there was staining when using either antibody. In the middle period (E6–11), marked by hair cell differentiation, dendritic growth, and early synapse formation, staining levels decreased. In the late period (E11–19), when auditory function begins, staining increased rapidly, especially for Kv3.1b. Early Kv3.1 expression occurs in neuronal and hair cell precursors before they differentiate or function. Later, in the otic epithelium, a high level of Kv3.1 in cilia may precede or coincide with the onset of hair cell function. In neurons, some features of its localization correlate with axon outgrowth and synapse formation, others with the onset of neural activity and function. J. Neurosci. Res. 65:24–37, 2001. © 2001 Wiley‐Liss, Inc.
Transplants of cells genetically modified to express neurotrophin‐3 rescue axotomized Clarke's nucleus neurons after spinal cord hemisection in adult rats
Authors: Himes B. Timothy , Liu Yi , Solowska Joanna M. , Snyder Evan Y. , Fischer Itzhak , Tessler Alan 
Published: August 2002

AbstractTo test the idea that genetically engineered cells can rescue axotomized neurons, we transplanted fibroblasts and immortalized neural stem cells (NSCs) modified to express neurotrophic factors into the injured spinal cord. The neurotrophin‐3 (NT‐3) or nerve growth factor (NGF) transgene was introduced into these cells using recombinant retroviral vectors containing an internal ribosome entry site (IRES) sequence and the β‐galactosidase or alkaline phosphatase reporter gene. Bioassay confirmed biological activity of the secreted neurotrophic factors. Clarke's nucleus (CN) axons, which project to the rostral spinal cord and cerebellum, were cut unilaterally in adult rats by T8 hemisection. Rats received transplants of fibroblasts or NSCs genetically modified to express NT‐3 or NGF and a reporter gene, only a reporter gene, or no transplant. Two months postoperatively, grafted cells survived at the hemisection site. Grafted fibroblasts and NSCs expressed a reporter gene and immunoreactivity for the NGF or NT‐3 transgene. Rats receiving no transplant or a transplant expressing only a reporter gene showed a 30% loss of CN neurons in the L1 segment on the lesioned side. NGF‐expressing transplants produced partial rescue compared with hemisection alone. There was no significant neuron loss in rats receiving grafts of either fibroblasts or NSCs engineered to express NT‐3. We postulate that NT‐3 mediates survival of CN neurons through interaction with trkC receptors, which are expressed on CN neurons. These results support the idea that NT‐3 contributes to long‐term survival of axotomized CN neurons and show that genetically modified cells rescue axotomized neurons as efficiently as fetal CNS transplants. J. Neurosci. Res. 65:549–564, 2001. © 2001 Wiley‐Liss, Inc.