bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low prevalence of TT virus in the cerebrospinal fluid of viremic patients with central nervous system disorders
Authors: Maggi Fabrizio , Fornai Claudia , Vatteroni Maria Linda , Siciliano Gabriele , Menichetti Francesco , Tascini Carlo , Specter Steven , Pistello Mauro , Bendinelli Mauro 
Published: August 2002

AbstractTT virus (TTV) is a widespread infectious agent of humans identified in 1998. In infected individuals, TTV induces persistent viremia but its life cycle and pathogenic potential are still poorly understood. In the present study, the presence of TTV DNA in 32 consecutive paired serum and cerebrospinal fluid (CSF) samples from patients with neurological (mainly multiple sclerosis) disorders was investigated by means of a sensitive quantitative real‐time PCR assay. Of the 24 patients who were found to carry TTV DNA in serum, 3 also had detectable TTV DNA in their CSF. Two TTV positive CSF samples had markers indicative of blood contamination or a disrupted blood‐brain barrier and contained considerably lower TTV loads as compared with the corresponding serum samples, thus suggesting that the virus they contained was of plasma origin. These findings indicated that in general TTV does not permeate effectively an intact blood‐brain barrier. Furthermore, the CNS does not represent a common site of TTV replication and persistence. However, at least one exception was observed: the third TTV positive CSF sample (obtained from a patient with subacute dementia of unknown origin) showed no markers suggestive of disrupted blood‐brain barrier or blood contamination and had a TTV DNA concentration similar to that found in the patient's serum. In addition, the TTV isolates detected in the two body fluids were distinct genetically. The detection of TTV DNA in CSF is of considerable interest but the clinical significance remains unknown. J. Med. Virol. 65:418–422, 2001. © 2001 Wiley‐Liss, Inc.
Inhibition of hepatitis C virus NS3 function by antisense oligodeoxynucleotides and protease inhibitor
Authors: Heintges Tobias , Encke Jens , zu Putlitz Jasper , Wands Jack R. 
Published: August 2002

AbstractHepatitis C Virus (HCV) NS3 protease is an attractive target for antiviral agent development because it is required for viral replication. Because a stable cell culture system or small animal model to study HCV replication is not readily available, we constructed an in vitro model allowing the investigation of NS3 transcription, translation, and protease function. Sequences encoding for full length HCV genomes were cloned and transfected into HuH‐7 human hepatocellular carcinoma cells to analyze NS3 transcription/translation. A plasmid pHCV ORF I luc that expresses the complete HCV coding region upstream of a luciferase reporter gene was designed to enable quantification of translated HCV proteins. Additionally, NS3 protease function was assessed by direct coexpression of NS3 and NS5 in HuH 7 cells, and the subsequent measurement of cleavage products. We found that antisense oligodeoxynucleotides (AS‐ODN) interfered with NS3 translation in a dose dependent fashion; AS‐ODN 5 cotransfection directed against NS3 sequences significantly inhibited protease activity as measured by cleaved NS5A levels. Finally, cleaved NS5A levels served as anindex of protease activity and Chymostatin, a protease inhibitor, almost completely blocked NS3 enzymatic activity. This cell culture system is useful in the assessment of potential antiviral agents on HCV NS3 expression and function. J. Med. Virol. 65:671–680, 2001. © 2001 Wiley‐Liss, Inc.
Clinical evaluation of a single oral dose of human‐bovine (UK) reassortant rotavirus vaccines Wa x UK (P1A[8],G6) and Wa x (DS‐1 x UK) (P1A[8],G2)
Authors: Eichelberger Maryna C. , Sperber Ellen , Wagner Mariam , Hoshino Yasutaka , Dudas Robert , Hodgins Vicki , Marron Jennifer , Nehring Pamela , Casey Roberta , Burns Barbara , Karron Ruth , Clements‐Mann Mary Lou , Kapikian Albert Z. 
Published: August 2002

AbstractThe safety, infectivity, and immunogenicity of two human‐bovine reassortant rotavirus candidate vaccines were evaluated in adults, children, and infants. One of these, Wa x UK, contained a single human rotavirus gene from the Wa strain that encoded VP4 P1A specificity in a background of 10 bovine genes including the VP7 gene that encodes G6 specificity, whereas the other, Wa x (DS‐1 x UK), possessed the human rotavirus VP4 gene from the Wa strain as well as the human VP7 gene from strain DS‐1 that encoded G2 specificity. Each of these vaccines appeared to be well‐tolerated and immunogenic in infants less than 6 months of age following a single oral dose, and therefore should be evaluated further as vaccine candidates. J. Med. Virol. 66:407‐416, 2002. © 2002 Wiley‐Liss, Inc.
Epstein‐Barr virus (EBV) DNA levels in palatine tonsils and autologous serum from EBV carriers
Authors: Nadal David , Blasius Martin , Niggli Felix K. , Meier Gabriela , Berger Christoph 
Published: August 2002

AbstractA real‐time polymerase chain reaction was employed to detect and quantitate Epstein‐Barr virus (EBV) DNA in tonsils and autologous sera from EBV‐seropositive children. EBV DNA was found in 95% of tonsils from 21 children and in 50% from 18 children with serum IgG titers to the virus capsid antigen (VCA) of ≥1:160 and 1:10 to 1:80, respectively (P = 0.002). Tonsils from children with titers ≥1:160 harbored more EBV DNA copies per mg tissue (mean, 1,237; range, < 2–13,998) than from children with titers 1:10 to 1:80 (mean, 23; range, < 2–226; P < 0.0001). By contrast, EBV DNA was detected only in serum from 25% of 20 children with titers ≥ 1:160. Thus, ample differences in tonsillar EBV replication are mirrored inconstantly by detectable EBV in autologous serum suggesting that EBV DNA quantitation in tonsils may serve for refined monitoring of individuals at risk of EBV‐associated lymphoproliferation. J. Med. Virol. 67:54–58, 2002. © 2002 Wiley‐Liss, Inc.
Mother‐to‐infant transmission of hepatitis C virus: Rate of infection and assessment of viral load and IgM anti‐HCV as risk factors*
Authors: Dal Molin Gianna , D'Agaro Pierlanfranco , Ansaldi Filippo , Ciana Giovanni , Fertz Cristina , Alberico Salvatore , Campello Cesare 
Published: August 2002

AbstractOne hundred twenty‐six mother‐infant couples were studied and 105 exposed babies were monitored for at least 12 months to define the risk of mother‐to‐infant HCV transmission. Infection occurred in 5 out of 76 infants (6.6%) born to 69 viraemic mothers and in none of 29 born to 26 non‐viraemic mothers. Only one child was HCV RNA positive one month after birth, while the remaining children became positive at the 3rd to 4th month. HCV genotypes of the babies matched those of their mothers. No difference was found between women who transmitted the virus and those who did not with regard to age, history of drug abuse, HIV infection, ALT abnormal values, HCV genotype, type of delivery, and breast‐feeding. Four out of 5 infected infants were born to mothers with IgM anti‐HCV (P = 0.04). The mean viral titre in transmitting women (107.2) was higher than in non‐transmitting (106.5), and the proportion of mothers with viral load ≥ 107 was statistically higher in transmitting than non‐transmitting women (P = 0.03). These data show that HCV perinatal infection is a rare event and suggest that IgM positivity and high viral load (≥ 107) in the mother are independent variables correlated with HCV transmission (O.R. = 14.5; 95% CI: 1.3–160.7 and O.R. = 16.3; 95% CI: 1.5–179.9, respectively). J. Med. Virol. 67:137–142, 2002. © 2002 Wiley‐Liss, Inc.
Immediate‐early gene response to methamphetamine, haloperidol, and quinolinic acid is not impaired in Huntington's disease transgenic mice
Authors: MacGibbon G.A. , Hamilton L.C. , Crocker S.F. , Costain W.J. , Murphy K.M. , Robertson H.A. , Denovan‐Wright E.M. 
Published: August 2002

AbstractStriatal neurons in symptomatic Huntington's disease (HD) transgenic mice are resistant to a variety of toxic insults, including quinolinic acid (QA), kainic acid and 3‐nitropropionic acid. The basis for this resistance is currently unknown. To investigate the possibility that the immediate‐early gene (IEG) response is defective in symptomatic HD mice leading to a lack of response to these compounds, we examined the expression of c‐Fos and Krox 24 after administration of the indirect dopamine agonist methamphetamine, the dopamine D2 receptor antagonist haloperidol and the neurotoxin QA in 5‐ and 10‐week‐old R6/2 transgenic HD and wild‐type mice. Unlike wild‐type and pre‐symptomatic R6/2 transgenic HD mice, 10‐week‐old symptomatic HD mice were resistant to methamphetamine‐induced gliosis and QA lesion. There was, however, no difference in the number or distribution of c‐Fos‐immunoreactive nuclei 2 hr after single injections of methamphetamine or haloperidol among 5‐ and 10‐week‐old wild‐type mice and 5‐ and 10‐week‐old R6/2 HD mice. Similarly, despite their resistance to QA‐induced lesioning and lower basal levels of krox‐24 mRNA, the symptomatic R6/2 mice had equivalent increases in the amount of c‐fos and krox‐24 mRNA compared to wild‐type and pre‐symptomatic R6/2 HD mice as determined by in situ hybridization and densitometry 2 hr after QA administration. These data demonstrate that the c‐Fos and Krox 24 IEG response to dopamine agonists, dopamine antagonists and neurotoxic insult is functional in symptomatic R6/2 HD mice. Resistance to toxic insult in R6/2 mice may be conferred by interactions of mutant huntingtin with proteins or transcriptional processes further along the toxic cascade. © 2002 Wiley‐Liss, Inc.
α1‐Antichymotrypsin/Alzheimer's peptide Aβ1–42 complex perturbs lipid metabolism and activates transcription factors PPARγ and NFκB in human neuroblastoma (Kelly) cells
Authors: Sun Yong‐Xin , Wright H.T. , Janciauskiene S. 
Published: August 2002

AbstractAmyloid‐beta peptide (Aβ) and the serpin proteinase inhibitor α1‐antichymotrypsin (ACT) are components of the amyloid plaques associated with Alzheimer's disease (AD). Aβ exists in soluble monomeric and oligomeric forms and in an insoluble polymerised fibrillar form, but it is not clear which of these plays the most important role in the etiology of AD. In vitro, Aβ1–42 interacts with ACT, and as a result of this, ACT loses its proteinase inhibitor activity and polymerisation of Aβ1–42 is promoted. Here we provide evidence that new molecular forms resulting from incubation of ACT with Aβ1–42 have multiple cellular level effects on neuronal cells. The mixture of soluble Aβ and an ACT/Aβ complex formed by 2 hr incubation at a 10:1 molar ratio of Aβ:ACT strongly induce cellular proliferation and expression of transcription factors peroxisome proliferator‐activated receptor‐gamma (PPARγ) and NFκB, and also increase uptake and depress degradation of native and oxidised low‐density lipoprotein (LDL) by cells. Similar but less pronounced effects are seen when cells are exposed to the Aβ peptide alone preincubated for 2 hr. Aβ1–42 and to a lesser extent ACT/Aβ1–42 complex mixture prepared by 2 hr incubation both inhibit association of native LDL with cells. Neither ACT alone nor the Aβ1–42 and ACT/Aβ1–42 forms prepared by 24‐hr incubation show any significant effects in these assays. We propose that specific molecular forms of Aβ1–42 and ACT/Aβ1–42 complex mixture, both dependent on the abundances of Aβ1–42 and ACT/Aβ1–42 in vivo and on their time of exposure to each other, have cellular effects which are important for the initiation and progression of the pathologies associated with AD. © 2002 Wiley‐Liss, Inc.
Changes of KCl sensitivity of proliferating neural progenitors during in vitro neurogenesis
Authors: Herberth Balázs , Pataki Ágnes , Jelitai Márta , Schlett Katalin , Deák Ferenc , Spät András , Madarász Emília 
Published: August 2002

AbstractThe effects of KCl‐treatment on the survival and proliferation of NE‐4C self‐renewing neural progenitor cells were investigated during early phases of in vitro induced neurogenesis. NE‐4C cells, derived from the anterior brain vesicles of embryonic mouse (E9), divided continuously under non‐inducing conditions, but acquired neuronal features within 6 days, if induced by all‐trans retinoic acid (RA). During the first 2 days of induction, the cells went on proliferating and did not show signs of morphological differentiation. In this stage, the resting membrane potential of RA‐induced cells adopted more negative values in comparison to non‐induced ones. Despite the increased membrane polarity and K+ conductance, addition of 20–50 mM KCl failed to elicit inward Na+ currents and did not induce an increase in the intracellular Ca+ level. Long‐term treatment with 25 mM KCl, on the other hand, resulted in a selective loss of cells committed to neuronal fate by both decreasing the rate of cell proliferation and increasing the rate of cell death. The data indicate that the viability and proliferation of neural progenitors are influenced by extracellular K+‐level in a differentiation stage‐dependent manner. © 2002 Wiley‐Liss, Inc.
Effects of chronic nicotine administration on nitric oxide synthase expression and activity in rat brain
Authors: Weruaga Eduardo , Balkan Burcu , Koylu Ersin O. , Pogun Sakire , Alonso José R. 
Published: August 2002

AbstractAlthough there is substantial evidence concerning the influence of nicotine on nitric oxide (NO) synthesis in the vascular system, there are fewer studies concerning the central nervous system. Although NO metabolites (nitrates/nitrites) increase in several rat brain regions after chronic injection of nicotine, the cellular origin of this rise in NO levels is not known. The aim of the present work was to assess the effects of repetitive nicotine administration on nitric oxide synthase (NOS) expression and activity in male and female rat brains. To determine levels of nitrate/nitrite, the Griess reaction was carried out in tissue micropunched from the frontal cortex, striatum, and accumbens of both male and female rats untreated (naïve) or injected with saline or nicotine (0.4 mg/kg for 15 days). In parallel, coronal sections of fixed brains from equally treated animals were immunostained for neuronal NOS or histochemically labelled for NADPH‐diaphorase activity. Nicotine treatment increased NO metabolites significantly in all brain regions compared with naïve or saline‐treated rats. By contrast, analysis of the planimetric counting of NOS/NADPH‐diaphorase‐positive neurons failed to demonstrate any significant effect of the nicotine treatment. A significant decrease was observed with both techniques employed in saline‐injected female rats compared with naïve animals, suggesting a stress response. The mismatch between the biochemical and the histological data after chronic nicotine treatment is discussed. The up‐regulation of NO sources other than neurons is proposed. © 2002 Wiley‐Liss, Inc.
BDNF activated TrkB/IRR receptor chimera promotes survival of sympathetic neurons through Ras and PI‐3 kinase signaling
Authors: Kelly‐Spratt Karen S. , Klesse Laura J. , Parada Luis F. 
Published: August 2002

AbstractInsulin receptor‐related receptor (IRR) expression is tightly coupled to the nerve growth factor (NGF) receptor, TrkA, throughout development. Expression of both receptors is primarily localized to neural crest derived sensory and sympathetic neurons. In contrast to TrkA, however, the physiological ligand for IRR is unknown. To analyze the intracellular signaling and potential function of the orphan IRR in neurons, an adenovirus expressing a TrkB/IRR chimeric receptor was used to infect cultured mouse superior cervical ganglion neurons that normally require NGF for survival. Brain derived neurotrophic factor (BDNF)‐activated TrkB/IRR induced neuronal survival. We utilized numerous receptor mutants in order to identify the intracellular domains of IRR necessary for signaling and neuron survival. Finally, we employed adenovirus encoding dominant negative forms of the extracellular signal‐regulated kinase (ERK) signaling cascade to demonstrate that IRR, like TrkA, requires ras activation to promote neuron survival. Therefore, by use of the chimeric TrkB/IRR receptor, we have demonstrated the ability of IRR to elicit activation of signaling cascades resulting in a biological response in superior cervical ganglion (SCG) neurons. © 2002 Wiley‐Liss, Inc.
Protective effect of apolipoprotein E against ischemic neuronal injury is mediated through antioxidant action
Authors: Kitagawa Kazuo , Matsumoto Masayasu , Kuwabara Keisuke , Takasawa Ken‐Ichiro , Tanaka Shigeru , Sasaki Tsutomu , Matsushita Kohji , Ohtsuki Toshiho , Yanagihara Takehiko , Hori Masatsugu 
Published: August 2002

AbstractRecent studies have demonstrated that apolipoprotein E (APOE) deficiency worsened neuronal injuries after transient focal and global cerebral ischemia. However, the molecular mechanism underlying the protective effect of APOE remains uncertain, even though several mechanisms, including excitotoxicty, free radicals, and apoptosis, have been cited as causes of selective neuronal vulnerability in cerebral ischemia. In the present study, we first compared the vulnerability of cultured neurons prepared from APOE‐knockout mice upon exposure to glutamate, hydrogen peroxide, and staurosporine. No significant difference in cell viability was observed after exposure to glutamate or staurosporine between APOE‐deficient and wild‐type mice. However, exposure to hydrogen peroxide significantly increased the level of cell death in APOE‐deficient mice compared with that in wild‐type mice. After transient forebrain ischemia for 12 min, APOE‐deficient mice showed more neuronal death than wild‐type mice. Pretreatment of APOE‐deficient mice with vitamin E for 2 months markedly reduced neuronal death caused by ischemia. The results suggest that APOE exerted its neuroprotective effect against ischemia through its antioxidant action but not through mitigation of glutamate toxicity or blocking of apoptosis. © 2002 Wiley‐Liss, Inc.
Growth factor regulation of cytoplasmic dynein intermediate chain subunit expression preceding neurite extension
Authors: Salata Mark W. , Dillman James F. , Lye R. John , Pfister K. Kevin 
Published: August 2002

AbstractCytoplasmic dynein is a motor protein responsible for intracellular movements toward the minus ends of microtubules. The intermediate chains are one of the subunits important for binding dynein to cargo. The intermediate chains are encoded by two genes and are translated into at least five different polypeptide isoforms in rat brain. In rat optic nerve, dynein with only one of the intermediate chain polypeptides is found associated with membrane bounded organelles in fast anterograde transport. Dynein containing the other intermediate chain polypeptides associates with a different set of proteins, in the slow transport component. To determine if the intermediate chain expression levels are regulated during neurite differentiation, we analyzed the protein levels by two‐dimensional SDS‐PAGE and intermediate chain mRNA by RT‐PCR in cultured rat pheochromocytoma (PC12) cells. In the absence of nerve growth factor, the major intermediate chain isoform is the IC74‐2C polypeptide. IC74‐2C is ubiquitous and is utilized for constitutive dynein function and association with membrane bounded organelles. Within 24 hr of the addition of nerve growth factor to the cultures, there is an increased expression of the developmentally regulated isoforms that are associated with the actin cytoskeleton. This change in intermediate chain isoform expression preceded neurite growth. Nerve growth factor induced differentiation also results in increased light intermediate chain phosphorylation. The growth factor induced changes in the expression of dynein intermediate chains suggests that specific intermediate chain isoforms are utilized during axon growth. J. Neurosci. Res. 65:408–416, 2001. © 2001 Wiley‐Liss, Inc.
Dscam is associated with axonal and dendritic features of neuronal cells
Authors: Agarwala Kishan Lal , Ganesh Subramaniam , Suzuki Toshimitsu , Akagi Takumi , Kaneko Kumi , Amano Kenji , Tsutsumi Yukie , Yamaguchi Kazuhiko , Hashikawa Tsutomu , Yamakawa Kazuhiro 
Published: August 2002

AbstractDscam, a novel cell‐adhesion molecule belonging to the Ig‐superfamily mediates homophilic intercellular adhesion and is expressed abundantly in the nervous system during development. To gain better understanding on the role of Dscam in neuronal differentiation, we raised an antibody and characterized its protein product. Anti‐Dscam antibody detected an ∼200‐kDa protein band in human and mouse brain lysates. Immunohistochemical studies showed that during embryonic development of mice, mouse Dscam is expressed throughout the neuronal tissues and also in nonneuronal tissues such as lung, liver, and limb buds. In adult brain Dscam expression is predominant in the cerebellum, hippocampus, and olfactory bulb. Immunofluorescence double labeling of hippocampal and cerebellar primary cultures revealed that Dscam is associated with axonal and dendritic processes. In view of its cellular localization and spatiotemporal expression pattern, we suggest that Dscam is involved in cell–cell interactions during axonal‐dendritic development, and maintenance of functional neuronal networks. J. Neurosci. Res. 66:337–346, 2001. © 2001 Wiley‐Liss, Inc.
Variability of total and solid precipitation in the Canadian Arctic from 1950 to 1995
Authors: Przybylak Rajmund 
Published: August 2002

AbstractTrends in solid and total precipitation, as well as in the ratio of solid to total precipitation (hereinafter S/T ratio), in the Canadian Arctic in recent decades have been investigated. In addition, the influence of air temperature and circulation factors (atmospheric and oceanic) on the above‐mentioned precipitation characteristics have been examined. Recently updated and adjusted data by the Canadian Climate Centre from 16 stations located in the Canadian Arctic and two stations from the sub‐Arctic were used for the investigation. The southern boundary of the study area was taken after Atlas Arktiki (Tresjinkov, A. 1985. Glavnoye Upravlenye Geodeziy i Kartografiy: Moscow; 204 pp). The majority of the data cover the period from 1950 to 1995.A statistically significant increase in all kinds of areally averaged seasonal and annual precipitation for the Canadian Arctic over the period 1950–95 has been found. On the other hand, the S/T ratio did not change significantly, except for summer values, and its behaviour was also in accord with small variations noted in air temperature.An increase in air temperature in the Canadian Arctic most often led to a rise in all kinds of annual precipitation sums, but only when the warmest and coldest years were chosen based on individual stations. The pattern of the relationship is significantly more complicated, and can even be opposite to that presented above, when the sets of the warmest and coldest years are chosen based on the areally averaged annual temperature for the Canadian Arctic. Significantly more stable results of changes were found for the S/T ratio, which in warmer periods was usually lower. However, more detailed and reliable investigations of temperature–precipitation relationships conducted for individual stations showed that though the S/T ratio in warmer periods may well be lower, this only applies to the southern (warmer) part of the Canadian Arctic (<70 °N).During periods with high positive values of the North Atlantic Oscillation Index (NAOI), a decrease in precipitation is observed in the south‐eastern part of the Canadian Arctic, i.e. in the area where strong cooling was also observed. During El Niño events most of the Canadian Arctic had both greater precipitation and a higher S/T ratio than during La Niña events.The most unequivocal results of precipitation and S/T ratio changes were found for changes in the Arctic Ocean circulation regimes. In almost the whole study area, a lower precipitation and S/T ratio were noted during the anticyclonic circulation regime in the Arctic Ocean. Copyright © 2002 Royal Meteorological Society