bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of multiple human papillomavirus types in the lower genital tract correlates with cervical dysplasia***
Authors: Fife Kenneth H. , Cramer Harvey M. , Schroeder Jill M. , Brown Darron R. 
Published: August 2002

AbstractSome human papillomavirus (HPV) types, such as HPV 16, are clearly associated with cervical dysplasia; however, the role played by other HPV types occasionally found in dysplasia is less certain. In addition, most methods used to detect HPV in clinical specimens cannot easily distinguish among more than two or three HPV types in a single specimen. Therefore, the significance of infection with multiple HPV types is not known. To address this question, we analyzed cervicovaginal lavage specimens from three cohorts of women for HPV DNA using a PCR/reverse blot assay system that permits the detection and partial quantitation of 26 genital HPV types. As expected, 94.1% of women who had dysplasia (n = 34) and 71.4% of women who had atypical squamous cells of uncertain significance (ASCUS) (n = 21) on cytology had HPV DNA detected compared to 54.5% of age matched women with normal cytology. HPV 16 DNA was detected in 35% of dysplasia patients compared to 9% of cytologic normals (P = 0.0044). Dysplasia patients had a mean of 3.29 (range 0–10) different HPV types detected compared to 1.04 (range 0–7) HPV types among those with normal cytology (P < 0.0001). These data support a possible role for multiple HPV types in the development or progression of cervical dysplasia. J. Med. Virol. 64:550–559, 2001. © 2001 Wiley‐Liss, Inc.
Detection of adeno‐associated virus DNA in female genital samples by PCR‐ELISA
Authors: Venturoli S. , Cricca M. , Bonvicini F. , Gallinella G. , Gentilomi G. , Zerbini M. , Musiani M. 
Published: August 2002

AbstractAdeno‐associated viruses (AAV) are human parvoviruses that require helper function for their replication. Several studies have demonstrated that AAV DNA sequences can be found in the female genital tract but the incidence of infection seems very variable. A PCR‐ELISA method detecting AAV DNA was developed for combining the specificity and the sensitivity of conventional PCR with an objective interpretation of the results. In the PCR‐ELISA, a defined number of cells from cervical specimens were digested and amplified with concomitant digoxigenin labeling. Digoxigenin‐labeled amplified products hybridized to a specific biotinylated probe were captured in streptavidin‐coated microtiter wells by a biotin‐streptavidin binding and were visualized by colorimetric immunoenzymatic reaction. PCR‐ELISA was carried out in 110 cervical cytological specimens of women with or without the concomitant detectable presence of papillomavirus (HPV) DNA and the results were compared with those obtained by conventional PCR followed by dot blot hybridization. When compared to conventional PCR considered as reference standard, PCR‐ELISA was found to be 98% sensitive and 96% specific. Out of the total 110 samples examined, 52.7% were positive for AAV DNA by both techniques, demonstrating a high prevalence of AAV infection in the uterine cervix. When analyzing samples with or without the presence of HPV DNA, 63.2 % of the samples were positive for HPV DNA and 41.5% of the samples were negative for HPV proved positive for AAV DNA by both PCR‐ELISA and conventional PCR. Hence, PCR‐ELISA, which can be completed in 1 day, proved to be a reliable method for an objective detection of AAV DNA in clinical samples. The present study showed a frequent infection of the cervical epithelium with AAV both in the presence and absence of HPV infection. J. Med. Virol. 64:577–582, 2001. © 2001 Wiley‐Liss, Inc.
Lack of transmission to polymorphonuclear leukocytes and human umbilical vein endothelial cells as a marker of attenuation of human cytomegalovirus
Authors: Gerna Giuseppe , Percivalle Elena , Baldanti Fausto , Revello Maria Grazia 
Published: August 2002

AbstractThe development of a human cytomegalovirus (HCMV) vaccine for the prevention of perinatal disease is urgently needed. However, markers of HCMV attenuation are not defined at present. An in vitro model for the study of interactions of HCMV‐infected human fibroblasts and peripheral blood polymorphonuclear leukocytes showed that (1) known laboratory‐adapted HCMV strains as well as cell culture‐adapted HCMV isolates were not transmitted to polymorphonuclear leukocytes; (2) each of the 80 HCMV recent isolates was consistently transmitted to polymorphonuclear leukocytes as both infectious virus and viral components (nucleic acid and proteins); and (3) all 15 polymorphonuclear leukocyte‐tropic strains tested thus far were also endothelial cell‐tropic. The in vitro transmissibility to polymorphonuclear leukocytes (and endothelial cells) is proposed as a surrogate marker of pathogenicity of HCMV strains. It seems reasonable to assume that a HCMV strain candidate for a vaccine be verified as deprived of the transfer property to polymorphonuclear leukocytes (and endothelial cells) before involvement in clinical trials assessing safety and immunogenicity. J. Med. Virol. 66:335‐339, 2002. © 2002 Wiley‐Liss, Inc.
Changes in neurofilament protein‐immunoreactivity after kainic acid treatment of organotypic hippocampal slice cultures
Authors: Holopainen Irma E. , Lauren Hanna B. , Romppanen Anne , Lopez‐Picon Francisco R. 
Published: August 2002

AbstractNeurofilament (NF) proteins are expressed in the majority of neurons in the central nervous system, and play a crucial role in the organization of neuronal shape and function. In the present study, we have used immunoblotting and immunocytochemical methods to study the light (NF‐L), medium (NF‐M ), and heavy (NF‐H) molecular weight NF proteins in cultured organotypic hippocampal slices during the in vitro maturation and the changes after kainic acid (KA) treatment. In control cultures at 11 DIV throughout 25 DIV, CA3 pyramidal neurons and their proximal dendrites were heavily labeled with the antibodies against all three NF proteins. In CA1 pyramidal neurons, no staining was detected in any age group. A few weakly NF‐L positive granule cells with fibers were detected in each age group, whereas NF‐M and NF‐H positive granule cells first appeared in the older cultures. The application of KA (5 μM) to the cultures for 48 hr, induced a pronounced cell death in the CA3 cell layers, and also moderately damaged granule cells. After the treatment, the immunoblot signal of NF‐L and NF‐M markedly decreased, whereas that of NF‐H almost completely disappeared. The amount of NF‐L positive fibers, however, dramatically increased in the molecular and hilar regions of the dentate gyrus in both age groups. Our results show the cellular heterogeneity in the distribution of NF protein triplet in cultured organotypic hippocampal slices. Kainic acid treatment induced changes, which mimicked those observed in the hippocampal region of epileptic animals. J. Neurosci. Res. 66:620–629, 2001. © 2001 Wiley‐Liss, Inc.
Membrane architecture of mitochondria in neurons of the central nervous system
Authors: Perkins Guy A. , Renken Christian W. , Frey Terrence G. , Ellisman Mark H. 
Published: August 2002

AbstractElectron tomography was used to help redefine the membrane architecture of mitochondria in neurons of the brain. Investigations were conducted on unexplored questions of structural homogeneity between mitochondria in the four intensely studied regions of the brain and in the functionally distinct neuronal sub‐compartments. These mitochondria have the majority of cristae composed of both tubular and lamellar segments with the tubes arranged more peripherally and the lamellae more centrally located. Cristae that are entirely tubular were not commonly seen and those that are entirely lamellar were rare. It was determined that cristae connect through narrow, sometimes very long tubular regions to the peripheral surface of the inner membrane. A structurally distinct type of contact site was revealed in brain mitochondria, which we named the bridge contact site. These bridges may play a role in the structural integrity of the outer and inner membrane systems. It was found that the membrane architecture in the various brain regions and neuronal compartments was strikingly uniform, including consistently tubular crista junctions. The functional consequences of this junctional architecture are discussed in relation to the segregation of proteins between the inner boundary membrane and the cristae membranes, and in relation to the model of microcompartmentation of macromolecules inside cristae. © 2001 Wiley‐Liss, Inc.
Central nervous system myelination in mice with deficient expression of Notch1 receptor
Authors: Givogri Maria I. , Costa Rui M. , Schonmann Vilma , Silva Alcino J. , Campagnoni Anthony T. , Bongarzone Ernesto R. 
Published: August 2002

AbstractActivity of the Notch1 gene is known to inhibit oligodendrocyte (OL) differentiation in vitro. We tested the hypothesis that the Notch1 pathway regulates in vivo myelin formation, by examining brain myelination of Notch1 receptor null heterozygotes mutant animals (Notch1+/–). We show that a deficiency in Notch1 expression leads to increased abundance of products of specific myelin genes in myelinated areas of the brain during the first 2 weeks of postnatal life. We observed increased numbers of myelinated axons in optic nerves and the presence of myelinated fibers in the molecular layer (ML) of the Notch1+/– cerebella. These findings were accompanied by up‐regulation of Mash1 and down‐regulation of Hes5 proteins. In addition, we found expression of Jagged1, one of the Notch1 activators, in unmyelinated axons of the cerebellar ML during normal development. Our findings indicate that the Jagged/Notch signaling pathway might actively participate in the regulation of myelination during central nervous system development and suggest that certain neuronal populations might regulate whether their axons are myelinated by the expression of inhibitory signals such as Jagged1. © 2002 Wiley‐Liss, Inc.
Neurotoxic effects of apolipoprotein E4 are mediated via dysregulation of calcium homeostasis
Authors: Veinbergs Isaac , Everson Analisa , Sagara Yutaka , Masliah Eliezer 
Published: August 2002

AbstractThe association of the E4 allele of apolipoprotein E (apoE4) as a genetic risk factor for Alzheimer's disease (AD) has been well established. Although recent studies in neuronal cell lines and transgenic mice have shown that apoE4 promotes neurodegeneration, the mechanisms through which apoE4 impairs neuronal viability are not completely understood. In this context, the main objective of the present study was to determine whether the neurotoxic effects of apoE4 are mediated by an alteration in calcium homeostasis. For this purpose, effects of recombinant apoE3 and apoE4 on cell viability and intracellular calcium levels were analyzed in a murine hippocampal cell line (HT22) and in primary rat cortical neurons, in the presence or absence of calcium inhibitors. Under basal conditions, apoE4‐treated cells displayed increased levels of cytosolic calcium associated with cell death in a dose‐dependent manner. Furthermore, apoE4 treatment potentiated the rise in cytosolic calcium and cell death following the administration of a calcium ionophore. The effects of apoE4 on cell viability and calcium homeostasis were inhibited by calcium chelators or by blocking calcium channels, but not by inhibitors of intracellular calcium reserves. Taken together, these results indicate that the neurotoxic effects of apoE4 are dependent on extracellular calcium influx via calcium channels. © 2002 Wiley‐Liss, Inc.
Effects of cytokine deficiency on chemokine expression in CNS of mice with EAE
Authors: Matejuk Agata , Dwyer Jami , Ito Atsushi , Bruender Zachary , Vandenbark Arthur A. , Offner Halina 
Published: August 2002

AbstractAlthough both cytokines and chemokines have been implicated in the pathogenesis of clinical and histological EAE, their interactions in vivo have not yet been clearly established. To address this issue, we evaluated expression of chemokines and receptors in the CNS of wild‐type control and cytokine deficient mice at the peak of EAE induced with MOG‐35–55 peptide in CFA. Our results demonstrate that: 1) expression of most chemokines/receptors was drastically inhibited in TNF‐α deficient mice, and was reflective of delayed onset and reduced severity of EAE; 2) distinct patterns of chemokine expression occurred in various other cytokine knockout mice that did not significantly affect expression of clinical EAE; 3) there was a strong association between expression of MIP‐1α, MIP‐2 and MCP‐1 in CNS and overall severity of EAE in wild‐type and cytokine knockout mice; and 4) among CNS infiltrating cells at the peak of EAE, macrophages and CD8+ T cells were the primary cellular source of most of the chemokines. Of note, we present evidence that TNF‐α may be involved in regulating RANTES and MIP‐1α, and that IL‐4 may be involved in regulating MCP‐1. Our results not only identify the cellular source of chemokines in CNS, but also implicate MIP‐1α, MIP‐2, and MCP‐1 in controlling CNS inflammation and severity of EAE. © 2002 Wiley‐Liss, Inc.
Gender‐dependent hypoxic tolerance mediated via gender‐specific mechanisms
Authors: von Arnim C.A.F. , Etrich S.M. , Timmler M. , Riepe M.W. 
Published: August 2002

AbstractPrimary hypoxic tolerance and preconditioning are gender dependent and modulated in females during the estrus cycle. The underlying mechanisms, however, remain to be determined. mRNA of estrogen receptor‐α (EAR), progesterone receptor (PR), and adenosine receptor subtypes A1 and A3 (A1R and A3R) were investigated with reverse transcriptase‐PCR in hippocampi from control male and female mice and animals treated in vivo with a single i.p. injection of 20 mg/kg body weight 3‐nitropropionate (3NP) 1 or 24 hr prior to preparation. Results were analyzed relative to expression in hippocampi from untreated males. mRNA levels of EAR and A1R were alike in males and females and unaltered by preconditioning with 3NP. In contrast, PR mRNA levels were alike in males and females during proestrus but lower during estrus and diestrus (85% ± 15%, P < 0.05; and 80% ± 10%, P < 0.05, respectively). Upon preconditioning, PR mRNA decreased to 67% ± 19% (P < 0.05) and 56% ± 13% (P < 0.05) during proestrus and diestrus, respectively, but was unaltered during estrus and in males. On preconditioning, A3R mRNA decreased from 115% ± 16% to 86% ± 29% (P < 0.05) during diestrus but remained at the control level during proestrus and estrus. With low‐level expression of PRs, as achieved upon preconditioning, hypoxic tolerance is increased. Other than in males, adenosine A3 receptors are not up‐regulated upon preconditioning in females. Thus, not only is net hypoxic tolerance gender dependent but mechanisms conferring hypoxic tolerance are gender specific. © 2002 Wiley‐Liss, Inc.
Arctigenin protects cultured cortical neurons from glutamate‐induced neurodegeneration by binding to kainate receptor
Authors: Jang Young P. , Kim So R. , Choi Young H. , Kim Jinwoong , Kim Sang G. , Markelonis George J. , Oh Tae H. , Kim Young C. 
Published: August 2002

AbstractWe previously reported that arctigenin, a lignan isolated from the bark of Torreya nucifera, showed significant neuroprotective activity against glutamate‐induced toxicity in primary cultured rat cortical cells. In this study, the mode of action of arctigenin was investigated using primary cultures of rat cortical cells as an in vitro system. Arctigenin significantly attenuated glutamate‐induced neurotoxicity when added prior to or after an excitotoxic glutamate challenge. The lignan protected cultured neuronal cells more selectively from neurotoxicity induced by kainic acid than by N‐methyl‐D‐aspartate. The binding of [3H]‐kainate to its receptors was significantly inhibited by arctigenin in a competitive manner. Furthermore, arctigenin directly scavenged free radicals generated by excess glutamate and successfully reduced the level of cellular peroxide in cultured neurons. These results suggest that arctigenin exerted significant neuroprotective effects on glutamate‐injured primary cultures of rat cortical cells by directly binding to kainic acid receptors and partly scavenging of free radicals. © 2002 Wiley‐Liss, Inc.
Glial transporters for glutamate, glycine and GABA I. Glutamate transporters
Authors: Gadea Ana , López‐Colomé Ana María 
Published: August 2002

AbstractThe termination of chemical neurotransmission in the CNS involves the rapid removal of neurotransmitter from synapses by specific transport systems. Such mechanism operates for the three major amino acid neurotransmitters glutamate, γ‐aminobutyric acid (GABA) and glycine. To date, five different high‐affinity Na+‐dependent glutamate (Glu) transporters have been cloned: GLT1, GLAST, EAAC1, EAAT4 and EAAT5. The first two are expressed mainly by glial cells, and seem to be the predominant Glu transporters in the brain. A major function of Glu uptake in the nervous system is to prevent extracellular Glu concentrations from raising to neurotoxic levels in which glial transporters seem to play a critical role in protecting neurons from glutamate‐induced excitotoxicity. Under particular conditions, glial GluTs have been shown to release Glu by reversal of activity, in a Ca2+‐ and energy‐independent fashion. Furthermore, an activity of these transporters as ion channels or transducing units coupled to G‐proteins has recently been reported. The localization, stoichiometry, and regulation of glial GluTs are outlined, as well as their possible contributions to nervous system diseases as ALS, AD and ischemic damage. J. Neurosci. Res. 63:453–460, 2001. © 2001 Wiley‐Liss, Inc.
Neurons and glial cells of the embryonic human brain and spinal cord express multiple and distinct isoforms of laminin
Authors: Liesi Päivi , Fried Gabriel , Stewart Randall R. 
Published: August 2002

AbstractWe have identified by immunocytochemistry, Western blotting, and RT‐PCR the isoforms of laminin expressed by glial cells and neurons cultured from human embryonic brain and spinal cord. We show that most of the known laminins are present in human neurons and glial cells. Importantly, Western analysis demonstrates that the isoforms of laminin present in embryonic human brain differ from those expressed in human spinal cord. Neurons of the brain and spinal cord also express their distinct and characteristic isoforms of laminin compared to the glial cells of the same CNS regions. These results suggest that, in addition to the known laminins, several novel isoforms may exist in the human embryonic CNS. The observed differences between the isoforms of laminin in brain and spinal cord neurons and glial cells may result from primary structural changes or from posttranslational modifications, e.g., variations in glycosylation. Thus, identification of these novel laminins and determination of their function(s) should further our understanding of the mechanisms of aging, disease, and trauma in the human CNS. J. Neurosci. Res. 64:144–167, 2001. © 2001 Wiley‐Liss, Inc.
Biological characterization and optical imaging of brain‐derived neurotrophic factor‐green fluorescent protein suggest an activity‐dependent local release of brain‐derived neurotrophic factor in neurites of cultured hippocampal neurons
Authors: Kojima Masami , Takei Nobuyuki , Numakawa Tadahiro , Ishikawa Yasuyuki , Suzuki Shingo , Matsumoto Tomoya , Katoh‐Semba Ritsuko , Nawa Hiroyuki , Hatanaka Hiroshi 
Published: August 2002

AbstractTo visualize the release dynamics of the brain‐derived neurotrophic factor (BDNF) involved in neural plasticity, we constructed a plasmid encoding green fluorescent protein (GFP) fused with BDNF. First, several biological studies confirmed that this fusion protein (BDNF‐GFP) mimics the biological functions and the release kinetics of unfused (native) BDNF. Second, when BDNF‐GFP was expressed in cultured hippocampal neurons, we observed that this protein formed striking clusters in the neurites of mature neurons and colocalized with the PSD‐95 immunoreactivity. Such a clustered BDNF‐GFP rapidly disappeared in response to depolarization with KCl, as revealed by confocal microscopic studies. These data suggest that BDNF is locally and rapidly released at synaptic sites in an activity‐dependent manner. Optical studies using BDNF‐GFP may provide important evidence regarding the participation of BDNF in synaptic plasticity. J. Neurosci. Res. 64:1–10, 2001. © 2001 Wiley‐Liss, Inc.
Subtropical cold surges: regional aspects and global distribution
Authors: Garreaud René D. 
Published: August 2002

AbstractShallow surges of cold dry air are frequently observed to the east of the major mountain ranges, moving from mid‐latitudes well into the Tropics in about 4 days. Because of their strong impact on weather, regional aspects of cold surges have received considerable attention, particularly over Southeast Asia, to the east of the Rockies and Mexican Sierras, and to the east of the subtropical Andes. Both observational and numerical studies reveal a similar structure and evolution of cold surges in different regions. These common aspects are reviewed in this work, as well as the mechanisms responsible for the development and subsequent advance of cold surges over the subtropics. Atmospheric reanalysis data are used to document the global distribution of cold surges on the basis of their continental‐scale imprints on relevant fields, as well as to estimate their contribution on the regional and global energy balances. It is found that cold surges have a major cooling and drying effect over the regions where they are prevalent (e.g. subtropical South America) and represent a sizeable sink of energy for the Tropics. Copyright © 2001 Royal Meteorological Society
Seasonal prediction of European spring precipitation from El Niño–Southern Oscillation and Local sea‐surface temperatures
Authors: Lloyd‐Hughes Benjamin , Saunders Mark A. 
Published: August 2002

AbstractThe extent to which European seasonal precipitation is predictable is a topic of scientific and societal importance. Although the potential for seasonal prediction is much less over Europe than in the tropics, it is not negligible. Previous studies suggest that European seasonal precipitation skill may peak in the spring (March–April–May) period, this being the season when El Niño–Southern Oscillation (ENSO) teleconnections to the North Atlantic and European sector are at their strongest. Examination of the correlation significance and temporal stability of contemporaneous and lagged ENSO links to European and North African precipitation over 98 years confirms this to be the case. The strongest ENSO links are found across the central European region (45°N–55°N,35°E–5°W). These links are symmetric with the sign of ENSO. Using a linear statistical model employing temporally stable lagged ENSO and lagged local North Atlantic sea surface temperatures as predictors, we compute the forecast skill and significance of central European spring precipitation over 30 independent years. For early March forecasts our model skill is 14–18% better than climatology, which is significant at the 95% level. Copyright © 2002 Royal Meteorological Society