bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of rotavirus strains from hospitalized and outpatient children with acute diarrhoea in São Paulo, Brazil
Authors: Compagnoli Carmona Rita Cássia , Tavares Timenetsky Maria do Carmo Sampaio , da Silva Fernanda Ferreira , Hernandes Granato Celso Francisco 
Published: July 2004

AbstractFrom August 1994 to July 1995, 234 faecal samples from children with or without acute diarrhoea were collected and tested. The group of children with acute diarrhoea (A) was subdivided into two subgroups: subgroup A1was made up of children with severe diarrhoea, dehydrated and who needed hospitalization and subgroup A2was composed of children who only needed outpatient care. Group B was composed of children without acute diarrhoea (controls). Rotavirus was detected in 36.7% (18/49), 22.0% (15/68) and 1.7% (2/117) patients in groups A1, A2and B, respectively. Of the 35 positive samples in which rotaviruses were detected the VP7 genotypes G1, G2, G3, G5 and the mixture (G2 + G5) were found in 40.0, 11.4, 11.4, 22.9 and 2.9% of the samples, respectively. Also, the VP4 genotypes P[8], P[4] and P[6] were detected in 57.1, 31.4 and 5.7%, respectively. Rotavirus VP6 subgroups I and II were detected at a frequency of 22.4 and 54.3%, respectively. Rotavirus RNA segments had short and long electrophoresis profiles in 20.0 and 51.4% of the cases, respectively. The severity of the disease was not related to a specific G and P types, subgroup or electropherotype. J. Med. Virol. 74:166–172, 2004. © 2004 Wiley‐Liss, Inc.
Differential expression of immunoregulatory genes in male and female Norway rats following infection with Seoul virus
Authors: Klein Sabra L. , Cernetich Amy , Hilmer Sara , Hoffman Eric P. , Scott Alan L. , Glass Gregory E. 
Published: July 2004

AbstractMales of many species are more susceptible than females to infections caused by parasites, bacteria, fungi, and viruses. Following inoculation with Seoul virus, male rats have more virus present in target organs and shed virus longer than females. The goal of this study was to test the hypothesis that variation in the expression of genes associated with immune function mediates sex differences in hantavirus infection. Using DNA microarrays, we examined changes in gene expression in lung tissue during the early (when animals are viremic and shedding virus; Day 15 post‐inoculation (p.i.)) and late (animals have low levels of infectious virus, but high antibody titers; Day 40 p.i.) phases of infection in adult male and female rats. After normalizing the gene expression levels from infected animals to the gene expression levels from same‐sex uninfected controls, our data revealed that 1,813 genes were differentially expressed between the sexes during infection. The expression of key transcriptional factors (e.g., eIF‐2α, NF‐κB, IRF‐1, NF‐IL‐6, and STAT6) and genes that encode for proinflammatory (e.g., TNFαR, IL‐1R, and IL‐1RAcP), antiviral (e.g., IFNγR and Mx proteins), T cell (e.g., CD3 and TCR), and Ig superfamily (e.g., IgM, IgG, and MHC class I and II) proteins was higher in females than males. Conversely, males had higher expression of heat shock protein genes (e.g., hsp70) suggesting that cellular stress is elevated in males. These data provide candidate genes and cellular pathways that may underlie sex differences in responses to Seoul virus and possibly other hemorrhagic fever viruses. J. Med. Virol. 74:180–190, 2004. © 2004 Wiley‐Liss, Inc.
BDNF overexpression produces a long‐term increase in myelin formation in the peripheral nervous system
Authors: Tolwani Ravi J. , Cosgaya José M. , Varma Sushama , Jacob Reza , Kuo Lydia E. , Shooter Eric M. 
Published: July 2004

AbstractThe neurotrophin brain‐derived neurotrophic factor (BDNF) is an endogenous regulator of the myelination process during development in the peripheral nervous system. Enhancement of myelin formation by BDNF is mediated by the neurotrophin receptor p75NTR. Although this neurotrophin is a positive modulator of myelination during early development, the final effects of BDNF on myelin sheaths after active myelination is completed are largely unknown. Using BDNF transgenic mice, we examined the long‐term effects of BDNF on myelination of the peripheral nervous system in vivo. Elevation of BDNF levels in the transgenic mice produced an increase in both the rate and extent of the myelination process. BDNF enhanced and accelerated myelin formation during early development and this increase in myelin content and thickness was maintained in adulthood. Besides enhanced myelination, BDNF also influenced axon caliber size but to a lesser extent. This lagging increase in axon caliber compared to myelin suggests that the axon size is not the only determinant of myelin thickness. © 2004 Wiley‐Liss, Inc.
Developmental shift in expression of netrin receptors in the rat spinal cord: Predominance of UNC‐5 homologues in adulthood
Authors: Manitt Colleen , Thompson Katherine M. , Kennedy Timothy E. 
Published: July 2004

AbstractNetrins are a family of secreted proteins required for normal neural development. Netrin‐1 is expressed at similar levels in the adult rat spinal cord and the embryonic CNS, suggesting that it contributes to adult CNS function. Here we show that the netrin receptors dcc, neogenin, unc5h1, unc5h2, and unc5h3 are also expressed in the adult rat spinal cord. Lower levels of DCC and neogenin were detected in the adult relative to the embryonic CNS. Conversely, the adult spinal cord contains increased levels of UNC‐5 homologues in comparison with the embryo. Multiple mRNA transcripts detected by Northern blot analysis suggested that netrin receptors might be encoded by alternatively spliced mRNAs. We have identified a novel alternatively spliced mRNA encoding UNC5H1, UNC5H1ΔTSP1, which lacks the first of the two extracellular thrombospondin domains. This novel splice variant is the major transcript detected in the early embryonic CNS, although both splice variants are expressed in the adult. Previously identified alternatively spliced mRNAs encoding DCC and neogenin were also detected. Dcc, neogenin, unc5h1, unc5h2, and unc5h3 are expressed by subsets of neurons. Robust expression of unc5h2 was found in glia. These findings suggest that unc‐5 homologues constitute a major mode of netrin‐1 signal transduction in the adult spinal cord and may be involved in phenomena analogous to axon repulsion, such as inhibiting process extension and collateral sprouting. © 2004 Wiley‐Liss, Inc.
T‐cell hybridoma specific for myelin oligodendrocyte glycoprotein‐35–55 peptide produced from HLA‐DRB1*1501‐transgenic mice
Authors: Chou Yuan K. , Culbertson Nicole , Rich Cathleen , LaTocha Dorian , Buenafe Abigail C. , Huan Jianya , Link Jason , Wands J.M. , Born Willi K. , Offner Halina , Bourdette Dennis N. , Burrows Gregory G. , Vandenbark Arthur A. 
Published: July 2004

AbstractThe goal of this study was to establish an unlimited and standardized source of humanized myelin peptide‐specific T cells for in vitro testing of biological function. Thus, we perpetuated myelin oligodendrocyte glycoprotein (MOG)‐35–55 peptide‐specific T cells obtained from immunized HLA‐DRB1*1501‐transgenic (Tg) mice by somatic fusions with BW5147 thymoma cells or BW5147 T‐cell receptor (TCR) α−β− variant (BW5147 variant) cells. The resulting T‐cell hybridomas responded strongly to both mouse MOG‐35–55 (42S) and human MOG‐35–55 peptide (42P), regardless of which peptide was used for initial immunization, and were DRB1*1501 restricted. The MOG‐35–55‐reactive T‐cell hybridomas were CD3+CD4+CD8− and expressed intracellular Th1 cytokines upon concanavalin A stimulation. Clones from either human MOG‐35–55‐ or mouse MOG‐35–55‐selected hybridomas uniquely expressed the TCR BV8 gene in combination with AV17 and AV11 genes. V gene analyses confirmed the expression of TCR AV1, AV11, AV16, BV1, and BV5 gene segments in the widely used fusion partner BW5147 and demonstrated deletion of TCR AV1, AV11, and BV1 in the BW5147 variant. T‐cell hybridomas were positively stained with anti‐TCR β‐chain antibody on the cell surface, whereas neither BW5147 nor its variant had positive TCR surface expression. For functional application, we found that a monomeric form of the human HLA‐DR2‐derived recombinant T‐cell receptor ligand (RTL) covalently linked to human MOG‐35–55 peptide specifically inhibited proliferation of a hybridoma clone selected with human MOG‐35–55 but not a different hybridoma clone selected with myelin basic protein. The RTL‐induced inhibition in vitro of the human MOG‐35–55 peptide‐specific hybridoma reflected the ability of the RTL to inhibit experimental autoimmune encephalomyelitis induced by human MOG‐35–55 peptide in HLA‐DR2 transgenic mice. Thus, the MOG‐35–55 peptide‐specific T‐cell hybridoma from DR2‐Tg mice represents a novel humanized T‐cell reagent useful for standardized biological screening of both DR2‐restricted stimulation and RTL‐dependent inhibition of response to human MOG‐35–55 peptide. © 2004 Wiley‐Liss, Inc.
Oxidative stress‐induced death in the nervous system: Cell cycle dependent or independent?
Authors: Langley Brett , Ratan Rajiv R. 
Published: July 2004

AbstractNeuronal death, attributable to perturbed redox homeostasis, is the underlying factor in many acute and chronic neurological disorders. The mechanisms employed by oxidatively stressed neurons to commit to cell death pathways are beginning to be characterized, but this is hampered by a lack of good models that extrapolate readily to redox‐dependent neuronal death paradigms. In this Mini‐Review, we discuss mechanisms by which oxidative stress can result in neurodegeneration. We examine evidence on which terminally differentiated neurons might commit to death under conditions of oxidative stress. In some cases, death may be linked to an aberrant and uncoordinated reentry into the cell cycle and mitotic catastrophe. Other evidence suggests that cell cycle reentry is not mandatory for death execution. Rather, the reexpression of cell cycle proteins may induce apoptotic pathways in a cell cycle‐independent manner. In contrast to these models, there is also evidence that oxidative neuronal death is independent of cell cycle proteins. We conclude that oxidative stress‐induced neuronal death may be promoted via several pathways, which may be cycle protein dependent or independent. The determining factor for which or how many pathways are induced appears to be context dependent and determined by the level and duration of oxidative stress. © 2004 Wiley‐Liss, Inc.
Modulation of CREB expression and phosphorylation in the rat nucleus accumbens during nicotine exposure and withdrawal
Authors: Pluzarev Olivera , Pandey Subhash C. 
Published: July 2004

AbstractThe nucleus accumbens region of the brain has been shown to play a role in reward and reinforcing mechanisms of drugs of abuse. To understand the molecular mechanisms of nicotine addiction, the present investigation examined the effects of acute and chronic nicotine treatment and its withdrawal on cAMP‐responsive element binding (CREB) protein expression and phosphorylation (serine‐133) in nucleus accumbens (NAc) structures of rats. it was found that acute treatment (1 and 18 hr of withdrawal) with nicotine had no effects on total creb and phosphorylated CREB (p‐CREB) protein levels in shell or core structures of rat NAc. On the other hand, 18‐hr withdrawal after chronic nicotine exposure produced significant reductions in the total CREB and p‐CREB protein levels in the shell but not in core structures of nac. interestingly, nicotine withdrawal (1 hr) after chronic exposure maintained normal levels of total CREB and p‐CREB protein levels in the shell and core structures of NAc. These results suggest the possibility that decreased CREB activity in the shell of NAc may be associated with abnormal reward mechanisms during nicotine withdrawal after chronic exposure. © 2004 Wiley‐Liss, Inc.
Microarray analysis of acute and delayed gene expression profile in rats after focal ischemic brain injury and reperfusion
Authors: Lu X.‐C. May , Williams Anthony J. , Yao Changping , Berti Rossana , Hartings Jed A. , Whipple Rebecca , Vahey Maryanne T. , Polavarapu Ratna G. , Woller Kimberly L. , Tortella Frank C. , Dave Jitendra R. 
Published: July 2004

AbstractTemporal changes in gene expression were measured using DNA microarrays after 30‐min or 2‐hr transient middle cerebral artery occlusion (MCAo) in rats. Total RNA was extracted from the injured hemisphere at 30 min, 4 hr, 8 hr, 24 hr, 3 days, and 7 days after MCAo for GeneChip analysis using Affymetrix U34 Rat Neurobiology arrays (1,322 functional genes). In total, 267 genes were expressed differentially: 166 genes were upregulated, 94 genes were downregulated, and 7 genes were biphasically up‐ and downregulated. Among all differentially expressed genes, 88 were newly identified as associated with ischemic brain injury. Most affected genes were distributed among 12 functional categories. Immediate early genes, transcription factors, and heat shock proteins were upregulated as early as 30 min after MCAo, followed by the upregulation of inflammation, apoptosis, cytoskeletal, and metabolism genes, which peaked within 4–24 hr of injury. Neurotrophic growth factors exhibited a sustained upregulation beginning 24 hr after MCAo and persisting through 7 days post‐injury. Three classes of genes were downregulated with distinct temporal patterns: ion channel genes and neurotransmitter receptor genes were downregulated between 8–24 hr after injury, whereas synaptic proteins genes were downregulated between 3–7 days after MCAo. Downregulation of synaptic protein gene expression after ischemic injury is of particular interest because of its conspicuously delayed pattern as a functional group, which has not been reported previously and may play a role in post‐injury recovery. © 2004 Wiley‐Liss, Inc.
Dietary silicon affects bone turnover differently in ovariectomized and sham‐operated growing rats
Authors: Nielsen Forrest H. , Poellot Rhonda 
Published: July 2004

AbstractAn experiment was performed to test the hypothesis that low dietary silicon affects blood, bone, and urine indices associated with bone formation and breakdown, bone strength and physical characteristics, and the circulating amount of an extracellular matrix protein (osteopontin) involved in bone cell adhesion and activation. A second objective was to ascertain whether ovariectomy (estrogen deficiency) alters the effects of low dietary silicon on bone formation. Female rats weighing about 56 g were assigned to groups of 10 in a factorially arranged experiment. The variables were supplemental dietary silicon at 0 or 35 mg/kg and ovariectomy (estrogen‐deficient) or sham operation at the start of the experiment. The basal silicon‐low diet contained about 2 mg Si/kg. Low dietary silicon compared with adequate silicon decreased plasma osteopontin concentration, increased plasma sialic acid concentration, and increased urinary helical peptide excretion. Low dietary silicon also affected the response to estrogen deficiency. Ovariectomy increased plasma alkaline phosphatase in the silicon‐supplemented, but not in the silicon‐low rats. In contrast, ovariectomy decreased liver ornithine aminotransferase in silicon‐low but not in silicon‐supplemented rats. Ovariectomy increased the urinary excretion of deoxypyridinoline and decreased the femur concentration of sialic acid more markedly in silicon‐supplemented than silicon‐low rats. Silicon and an interaction between silicon and ovariectomy only mildly changed bone strength and physical measurements and did not affect femur calcium concentration. The findings suggest that silicon has a biochemical function that affects bone growth processes before bone crystal formation by affecting bone collagen turnover and sialic acid‐containing extracellular matrix proteins such as osteopontin. J. Trace Elem. Exp. Med. 17:137–149, 2004. Published 2004 Wiley‐Liss, Inc.
Comparative quantative analysis of zinc, magnesium, and copper content in the scalp hair of healthy people and breast cancer patients
Authors: Kilic Eser , Demiroglu Asuman , Saraymen Recep , Ok Engin 
Published: July 2004

AbstractA quantitative elemental analysis of scalp hair of female breast cancer patients (n = 26) and female controls (n = 27) was used to study to find out correlation and possible changes, between breast cancer and healthy controls. Atomic absorption spectrophotometer analysis of the quantitative method was used to determine copper, magnesium, and zinc levels. There were no differences in magnesium concentrations (P > 0.05) in breast cancer patients and healthy subjects. However, comparison of mean elemental contents of the breast cancer patients with controls showed a significant enhancement of copper (P < 0.05) but declining trends for zinc (P < 0.05) in breast cancer patients. The usefulness and significance of element status in cancer patients should be discussed more detailed in the light of the most these recent data. J. Trace Elem. Exp. Med. 17:175–180, 2004. © 2004 Wiley‐Liss, Inc.
Oriented Quiescent Crystallization of Polyethylene Studied by USAXS.
Authors: Stribeck Norbert , Camarillo Armando Almendarez , Bayer Rüdiger K. 
Published: July 2004

AbstractSummary: In a series of papers the crystallization of a commercial polyethylene (PE) material has been studied by in situ ultra small‐angle X‐ray scattering (USAXS) and it has been found that the placement of crystallites is predominantly a random car parking process, dealt with in the field of random sequential adsorption. Here we investigate the secondary effect, the generation of order from the chaos, and characterize how lamellae agglomerate to form clusters. Owing to the chaotic principle, clusters are of different size and thus the nanostructure is, in general, heterogeneous. During isothermal crystallization, we only find order inside sparse clusters of lamellae. Globally the nanostructure resembles a random blend of these clusters. A geometric relation couples the number fraction of lamellae to the size of the cluster they belong to. More longitudinal order is achieved if the material is subsequently quenched. Amorphous gaps of favorable width act as nests in which thin crystals are preferentially generated (harmonic completion). Together with their neighboring parents they imprint excess order. During continuous non‐isothermal crystallization we have observed that clusters with several members are selectively built from thinner crystals. Order is growing in the late state of crystallization. This violation of the common assumption of homogeneity makes the classic notion of a distorted lattice (convolution polynomial, paracrystal) become restricted to a subset of the global crystallite thickness distribution.A weak (a) and a strong (b) order generating mechanism found during PE crystallization.magnified imageA weak (a) and a strong (b) order generating mechanism found during PE crystallization.
Fragmentation pathways of protonated peptides
Authors: Paizs Béla , Suhai Sándor 
Published: July 2004

AbstractThe fragmentation pathways of protonated peptides are reviewed in the present paper paying special attention to classification of the known fragmentation channels into a simple hierarchy defined according to the chemistry involved. It is shown that the ‘mobile proton’ model of peptide fragmentation can be used to understand the MS/MS spectra of protonated peptides only in a qualitative manner rationalizing differences observed for low‐energy collision induced dissociation of peptide ions having or lacking a mobile proton. To overcome this limitation, a deeper understanding of the dissociation chemistry of protonated peptides is needed. To this end use of the ‘pathways in competition’ (PIC) model that involves a detailed energetic and kinetic characterization of the major peptide fragmentation pathways (PFPs) is proposed. The known PFPs are described in detail including all the pre‐dissociation, dissociation, and post‐dissociation events. It is our hope that studies to further extend PIC will lead to semi‐quantative understanding of the MS/MS spectra of protonated peptides which could be used to develop refined bioinformatics algorithms for MS/MS based proteomics. Experimental and computational data on the fragmentation of protonated peptides are reevaluated from the point of view of the PIC model considering the mechanism, energetics, and kinetics of the major PFPs. Evidence proving semi‐quantitative predictability of some of the ion intensity relationships (IIRs) of the MS/MS spectra of protonated peptides is presented. © 2004 Wiley Periodicals, Inc., Mass Spec Rev 24:508–548, 2005
Cover Picture: Macromol. Theory Simul. 6/2004
Authors: Kornherr Andreas , Olaj Oskar Friedrich , Schnöll‐Bitai Irene , Zifferer Gerhard 
Published: July 2004

Cover: The picture on the cover shows theoretical PLP‐SEC‐distributions (characteristic parameters as indicated) assuming various extents of axial dispersion (small: red; moderate: green and large: blue).Further details can be found in the Full Paper by A. Kornherr, O. F. Olaj,* I. Schnöll‐Bitai, and G. Zifferer* on page 560.
Proto oncogene/eukaryotic translation initiation factor (eIF) 4E attenuates mevalonate‐mediated regulation of 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase synthesis
Authors: Buechler Robbie D. , Peffley Dennis M. 
Published: July 2004

AbstractThe rate‐limiting enzyme for mevalonate synthesis in mammalian cells is 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase. Products of mevalonate synthesis are required for cell cycle progression as well as cell growth and survival. In tumor cells, HMG‐CoA reductase is generally elevated because of attenuated sterol‐mediated regulation of transcription. However, tumor cell HMG‐CoA reductase remains sensitive to post‐transcriptional regulation by mevalonate‐derived isoprenoid intermediates of cholesterol synthesis. Isoprenoids suppress HMG‐CoA reductase synthesis through a mechanism that reduces initiation of translation on HMG‐CoA reductase mRNA. Because HMG‐CoA reductase mRNA transcripts have 5′‐untranslated regions (UTR) that are GC rich and contain stable secondary structure, we tested the hypothesis that overexpression of eIF4E would attenuate isoprenoid‐mediated regulation of HMG‐CoA reductase. eIF4E is elevated in many tumor cells and behaves as a proto‐oncogene by aberrantly translating mRNAs whose translation is normally suppressed by 5‐UTRs that are GC rich. A CHO cell line expressing high levels of eIF4E (rb4E) was developed by infecting cells with retroviruses containing a full‐length mouse cDNA for eIF4E. Levels of reductase synthesis were elevated fivefold in rb4E cells compared to noninfected CHO cells; HMG‐CoA reductase mRNA levels were not increased in rb4E cells compared to normal CHO cells. Total cellular protein synthesis was only increased by approximately 15% in rb4E cells compared to CHO cells. The mTOR inhibitor rapamycin lowered HMG‐CoA reductase synthesis by 50 and 60% in rb4E and CHO cells, respectively; no equivalent effect was observed for HMG‐CoA reductase mRNA levels with rapamycin treatment. These results indicate that HMG‐CoA reductase mRNA is in a class of mRNAs with highly structured 5′‐UTRs whose m7GpppX cap‐dependent translation is closely linked to the rapamycin‐sensitive mitogen activated pathway for protein synthesis. © 2004 Wiley‐Liss, Inc.