bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hepatitis C virus–Epstein‐barr virus interaction in patients with AIDS
Authors: Challine Dominique , Buisson Marlyse , Cadilhac Michel , Germanidis Georgios , Joab Irene , Eliaszewicz Muriel , Caumes Eric , Flahault Antoine , Fillet Anne‐Marie , Pawlotsky Jean‐Michel , Seigneurin Jean‐Marie 
Published: September 2002

AbstractImmortalization of B cells by Epstein‐Barr virus (EBV) and their subsequent proliferation leads to B‐cell non‐Hodgkin's lymphoma in immunocompromised patients. The role of hepatitis C virus (HCV) in B‐cell non‐Hodgkin's lymphoma has recently been raised, and an interaction between HCV and EBV is supported by recent in vitro experiments. The aim of this study was to investigate in vivo interactions between HCV and EBV in patients with AIDS, i.e., patients exposed to the risk of EBV‐related B‐cell non‐Hodgkin's lymphoma. A total of 135 patients were prospectively studied. Serological and molecular markers of HCV, EBV, and human immunodeficiency virus (HIV) infection were sought. All the patients harbored latent EBV infection, and 20% had detectable HCV RNA in serum. No significant relationship was found between HIV, HCV, and EBV viral load in peripheral blood mononuclear cells or plasma. There was no difference between anti‐HCV‐positive and ‐negative patients or between HCV RNA‐positive and ‐negative patients with regard to the prevalence of EBV markers, especially EBV replication markers. The presence of EBV replication markers was not related to HCV RNA seropositivity or to HCV viral load. Five patients subsequently developed B‐cell non‐Hodgkin's lymphoma, none of whom had markers of EBV or HCV replication. These results argue against an in vivo interaction between HCV and EBV in patients with AIDS, and against a role of HCV infection in the occurrence of B‐cell non‐Hodgkin's lymphoma in these patients. J. Med. Virol. 67:510–515, 2002. © 2002 Wiley‐Liss, Inc.
Prolonged shedding of rotavirus in a geriatric inpatient
Authors: Mori Isamu , Matsumoto Kazuo , Sugimoto Kazunori , Kimura Makiko , Daimon Nagomu , Yokochi Takashi , Kimura Yoshinobu 
Published: September 2002

AbstractThis study concerns a nosocomial rotaviral infection of a geriatric patient with clinical symptoms of acute gastroenteritis. The virological diagnosis was based on the detection of rotaviral antigens using a Rota kit, viral genome RNA by reverse transcription‐polymerase chain reaction method, and viral particles by electron microscopy in the stool samples. Prolonged rotaviral shedding was suggested to be due to impaired natural killer cell activity, possibly together with deficiency of specific local immune response of the patient. J. Med. Virol. 67:613–615, 2002. © 2002 Wiley‐Liss, Inc.
Direct cell–cell interactions control apoptosis and oligodendrocyte marker expression of neuroepithelial cells
Authors: Hugnot J.P. , Mellodew K. , Pilcher H. , Uwanogho D. , Price J. , Sinden J.D. 
Published: September 2002

AbstractDuring brain development, the neuroepithelium generates neurons and glial cells. Proliferation and differentiation of neuroepithelial cells are controlled by a complex combination of secreted factors and more intrinsic or local mechanisms, such as lateral inhibition and asymmetric division. To obtain further insights into the signals governing neuroepithelial cell fate, we used the immortomouse to derive conditionally immortalised cell lines from mouse E10 neuroepithelium. We isolated a nestin‐positive basic fibroblast growth factor (bFGF)‐responsive cell line (SVE10‐23) which mostly differentiate into astrocytes when cocultured with primary cortical cells. We found that, by simply lowering the cell density, SVE10‐23 cells embarked on oligodendrocytic differentiation as indicated by the strong expression of galactocerebroside C and 2′3′‐cyclic nucleotide 3′‐phosphodiesterase. Apoptosis accompanied the differentiation, and all cells died within 1 week. We present here evidence that direct interactions between cells are the main mechanism regulating this oligodendrocytic differentiation. We demonstrate that SVE10‐23 cells contact or proximity inhibit their differentiation, prevent apoptosis, and promote their proliferation. Similarly, others nestin‐positive precursor cell lines and nonimmortalised bFGF‐grown E10 cells were found to spontaneously differentiate at low density, thus generalising the idea that neural precursor fate is regulated by direct cell–cell interactions. The SVE10‐23 cell line provides a valuable tool with which to study further the molecular components implicated in this mode of regulation. J. Neurosci. Res. 65:195–207, 2001. © 2001 Wiley‐Liss, Inc.
Modulation of HSP25 expression during anterior horn motor neuron degeneration in the paralysé mouse mutant
Authors: Pieri Isabelle , Cifuentes‐Diaz Carmen , Oudinet Jean Paul , Blondet Brigitte , Rieger François , Gonin Sandrine , Arrigo André‐Patrick , Thomas Yolène 
Published: September 2002

AbstractThe paralysé spontaneous mutation in mice involves degeneration and death of anterior horn motor neurons. Mutant mice are not viable past postnatal day 16. At present, the mechanisms involved in motor neuron death are unknown. Here, we investigate the expression of the small heat shock protein Hsp25, in the spinal cord of paralysé at two different stages during postnatal development, i.e., day 11 and day 14. Western blot analysis reveals that the level of Hsp25 was strikingly different in paralysé as compared to control littermates. Hsp25 expression level in paralysé at day 11 was much lower than in control mice. At day 14, an opposite pattern was observed. Such pattern seems to be restricted to spinal cord, since level of Hsp25 in other tissues (lung, brain, liver, and heart) was quite similar. Immunofluorescence examination of the lumbar spinal cord sections reveals that in control mice, Hsp25 was expressed at high level in motor neurons located in the ventral horn at both day 11 and day 14. By contrast, in paralysé mice, Hsp25 staining within the motor neurons was barely detectable except as a spot in the nucleolus (day 11). At the end stage of the disease (day 14), not only was Hsp25 staining even less intense in motor neurons, but also a strong Hsp25 staining was observed in reactive astrocytes within the gray matter. Taken together, these data suggest that Hsp25 expression is differently modulated in neuronal and glial cells during neurodegenerative processes leading to motor neuron death. J. Neurosci. Res. 65:247–253, 2001. © 2001 Wiley‐Liss, Inc.
IL‐6 deficiency allows for enhanced therapeutic value after bone marrow transplantation across a minor histocompatibility barrier in the twitcher (globoid cell leukodystrophy) mouse
Authors: Biswas Sangita , Pinson David M. , Bronshteyn Illya G. , LeVine Steven M. 
Published: September 2002

AbstractBone marrow transplantation (BMT) has therapeutic value for twitcher (globoid cell leukodystrophy) mice, which suffer from a genetic deficiency of the lysosomal enzyme galactosylceramidase that leads to progressive demyelination and early death. Preliminary investigations indicated that a semiallogeneic BMT resulted in graft vs. host disease (GVHD) in twitcher mice but not normal mice. Increased production of the cytokine IL‐6 has been demonstrated in twitcher mice, and it has been linked with induction of GVHD. We investigated the effects of BMT in twitcher/IL‐6 deficient mice and compared these findings with those from transplanted twitcher and control mice. After a semiallogeneic BMT, 11.4% of controls died within few weeks while the rest survived >100 days without GVHD. In contrast, 85% of the transplanted twitcher mice died by 70 days and 65% developed clinical signs of GVHD, e.g., alopecia and weight loss. In transplanted twitcher/IL‐6 deficient mice, only 21% died by Day 70, none had alopecia, and 23% had weight loss. There was no difference in the onset day and severity of twitching between twitcher and twitcher/IL‐6 deficient mice after BMT. In transplanted twitcher/IL‐6 deficient mice, there was improvement of BBB integrity and a decrease in globoid cell number compared with nontransplanted twitcher/IL‐6 deficient mice. In summary, these results demonstrate that an underlying pathology like globoid cell leukodystrophy leads to activation of GVHD responses in a donor–host combination that would not normally induce GVHD. Furthermore, IL‐6 seems to play a key role because a deficiency of IL‐6 results in a better prognosis. J. Neurosci. Res. 65:298–307, 2001. © 2001 Wiley‐Liss, Inc.
Induction of the proinflammatory cytokine interleukin‐18 by axonal injury
Authors: Menge Til , Jander Sebastian , Stoll Guido 
Published: September 2002

AbstractInterleukin‐18 (IL‐18) is an important cytokine in innate immunity and in the induction phase of autoimmunity. We report the expression of IL‐18 mRNA and protein after nerve crush during Wallerian degeneration (WD) of the rat nervous system. In normal optic nerves (ON) constitutive IL‐18 mRNA levels as revealed by semiquantitative reverse transcriptase polymerase chain reaction were higher than in sciatic nerves (SN). After nerve crush, steady‐state levels moderately increased in the distal nerve part of the SN but not the ON. By immunocytochemistry no SN or faint ON IL‐18 protein expression was detectable in normal nerves. In contrast, IL‐18 expression dramatically increased after SN and ON crush. On the cellular level, ED1+ macrophages infiltrating the crush site strongly expressed IL‐18 at days 2 and 4 after SN crush. By days 4 and 8, in addition, the entire distal nerve part was covered by IL‐18+ macrophages. At day 16, IL‐18 immunoreactivity had disappeared despite the presistence of large numbers of ED1+ macrophages. A similar infiltration of IL‐18+ macrophages was seen at the crush site in the ON. Moreover, microglia in the distal ON stump lacking macrophage infiltration and undergoing delayed myelin degradation up‐regulated IL‐18. In conclusion this study shows that IL‐18 is involved in the cytokine network associated with the robust inflammatory response during WD of the SN. Despite up‐regulation of the proinflammatory cytokine IL‐18, major histocompatiblity complex class II, and CD4 molecules similar to macrophages in the PNS, microglial activation after ON injury appears to be insufficient to mount an effective phagocytic response as a prerequisite for successful regeneration in the CNS. J. Neurosci. Res. 65:332–339, 2001. © 2001 Wiley‐Liss, Inc.
CB1 cannabinoid receptor‐mediated neurite remodeling in mouse neuroblastoma N1E‐115 cells
Authors: Zhou Dan , Song Z.H. 
Published: September 2002

AbstractThe morphological remodeling of neuronal cells influences neurogenesis and brain functions. We hypothesize that psychoactive and neurotoxic effects of cannabinoids may be mediated, at least in part, by their morphoregulatory activities. In the present study, mouse neuroblastoma N1E‐115 cells were used as an in vitro model to investigate cannabinoid‐induced neurite remodeling effects and to identify the involvement of cannabinoid receptors in this neurite remodeling process. Using reverse transcription‐polymerase chain reaction and immunofluorescence microscopy, the endogenously expressed CB1, but not CB2, cannabinoid receptors were detected in morphologically differentiated N1E‐115 cells. Activation of these natively expressed CB1 cannabinoid receptors by cannabinoid agonist HU‐210 led to a concentration‐dependent inhibition of adenylate cyclase activity. Importantly, HU‐210 treatment induced neurite retraction in a concentration‐dependent manner. Pretreatment of N1E‐115 cells with a CB1 antisense oligodeoxynucleotide (ODN) suppressed HU‐210‐induced inhibition of forskolin‐stimulated cAMP accumulation, indicating that the knocking down of functional CB1 cannabinoid receptor expression was achieved. Antisense ODN pretreatment also abolished HU‐210‐induced neurite retraction, demonstrating the involvement of CB1 cannabinoid receptors in mediating the neurite remodeling effects of HU‐210. In addition, reversing HU‐210‐induced intracellular cAMP declination by 8‐Br‐cAMP partially prevented HU‐210‐induced neurite retraction, indicating the involvement of cAMP‐dependent signaling pathways in mediating the neurite remodeling function of CB1 cannabinoid receptors in N1E‐115 cells. These data demonstrate that neurite remodeling is a newly discovered function of CB1 cannabinoid receptors. This morphoregulatory function of CB1 cannabinoid receptors might be a new mechanism that mediates the psychoactive and neurotoxic effects of cannabinoids in developing and adult brain. J. Neurosci. Res. 65:346–353, 2001. © 2001 Wiley‐Liss, Inc.
Ethanol exposure inhibits the cytotoxic effect induced by gp120 in CHP100 human neuroblastoma cells
Authors: Navarra Michele , Romano Caterina , Lorenzon Tatiana , Rotiroti Domenicantonio , Di Renzo Gianfranco 
Published: September 2002

AbstractThe aim of present study was to investigate the acute effects of ethanol on cytotoxicity induced by HIV‐1 coat protein gp120 in CHP100 human neuroblastoma cell line. We demonstrate that ethanol, within a range of clinically relevant concentrations (15–90 mM) prevents cell death elicited by gp120 (10 pM) in a dose dependent manner. This protective action seems to be mediated by a reduction of free intracellular Ca2+ levels because ethanol, at concentrations ranging from 0.1–0.5%, is able to decrease gp120‐stimulated Ca2+ uptake up to 24%. Furthermore, our data show an involvement of NO/cGMP messenger system pathway, because ethanol is also able to reduce gp120‐stimulated NO release (up to 45%) and cyclic GMP accumulation (up to 73%). These findings suggest that the protective effect of ethanol against gp120‐induced cytotoxicity in CHP100 cells underlies a Ca2+‐activated, NO/cGMP‐dependent mechanism. J. Neurosci. Res. 65:354–361, 2001. © 2001 Wiley‐Liss, Inc.
Identity salience: a moderator of the relationship between group gender composition and work group conflict
Authors: Randel Amy E. 
Published: September 2002

AbstractThis study proposes and tests models in which the salience of gender serves as a moderator of the relationship between group gender composition and work group conflict. The numerical distinctiveness of gender group composition was found to trigger the salience of group members' gender identities for men in the group. Identity salience was found to affect work group conflict beyond what one would predict on the basis of gender diversity alone. Support was found for gender identity salience as a moderator variable with respect to the linkage between numerical distinctiveness in gender work group composition and relationship conflict in work groups for men. This study offers an explanation for the differing effects found across studies regarding the effect of group composition on work group conflict: the extent to which gender is relied upon by group members in describing those in their group. Copyright © 2002 John Wiley & Sons, Ltd.
To stay or to go: voluntary survivor turnover following an organizational downsizing
Authors: Spreitzer Gretchen M. , Mishra Aneil K. 
Published: September 2002

AbstractThis paper examines the relationship between survivor reactions to a downsizing and retention subsequent to a downsizing. We hypothesize that survivors who experience the downsizing as distributively, procedurally, and interactionally just and who see top management as trustworthy will feel more attached to the organization because each reduces the threat inherent in downsizing. In addition, we hypothesize that survivors who feel empowered will also feel more attached to the organization because they feel better able to cope with the downsizing. We further hypothesize that those survivors who feel more attached to the organization following the downsizing will be more likely to remain with the organization in the coming year. The theoretical model is tested on a sample of aerospace employees who survived an organizational downsizing. The trustworthiness of management, distributive justice, procedural justice, and three dimensions of empowerment are found to facilitate more organizational attachment. Higher levels of attachment are found, in turn, to facilitate less voluntary turnover in the year following the downsizing. Copyright © 2002 John Wiley & Sons, Ltd.
The influence of large‐scale atmospheric circulation on the surface energy balance of the King George Island ice cap
Authors: Braun Matthias , Saurer Helmut , Vogt Steffen , Simões Jefferson Cardia , Goßmann Hermann 
Published: September 2002

AbstractDuring the austral summer 1997–1998 three automatic weather stations were operated at different altitudes on the sub‐Antarctic ice cap of King George Island (South Shetland Islands). Snowmelt was derived from energy balance computations. Turbulent heat fluxes were calculated from meteorological measurements using the bulk aerodynamic approach, with net radiation being measured directly. Modelled ablation rates were compared with readings at ablation stakes and continuously measured snow height at a reference site. Snow depletion and daily snowmelt cycles could be well reproduced by the model. Generally, radiation balance provided the major energy input for snowmelt at all altitudes, whereas sensible heat flux was a second heat source only in lower elevations. The average latent heat flux was negligible over the entire measuring period. A strong altitudinal gradient of available energy for snowmelt was observed. Sensible heat flux as well as latent heat flux decreased with altitude. The measurements showed a strong dependence of surface energy fluxes and ablation rates on large‐scale atmospheric conditions. Synoptic weather situations were analysed based on AVH RR infrared quicklook composite images and surface pressure charts. Maximum melt rates of up to 20 mm per day were recorded during a northwesterly advection event with meridional air mass transport. During this northwesterly advection, the contribution of turbulent heat fluxes to the energy available for snowmelt exceeded that of the radiation balance. For easterly and southerly flows, continentally toned, cold dry air masses dominated surface energy balance terms and did not significantly contribute to ablation. The link between synoptic situations and ablation is especially valuable, as observed climatic changes along the Antarctic Peninsula are attributed to changes in the atmospheric circulation. Therefore, the combination of energy balance calculations and the analysis of synoptic‐scale weather patterns could improve the prediction of ablation rates for climate change scenarios. Copyright © 2001 Royal Meteorological Society
Retro‐active skill of multi‐tiered forecasts of summer rainfall over southern Africa
Authors: Landman Willem A. , Mason Simon J. , Tyson Peter D. , Tennant Warren J. 
Published: September 2002

AbstractSea‐surface temperature (SST) variations of the oceans surrounding southern Africa are associated with seasonal rainfall variability, especially during austral summer when the tropical atmospheric circulation is dominant over the region. Because of instabilities in the linear association between summer rainfall over southern Africa and SSTs of the tropical Indian Ocean, the skilful prediction of seasonal rainfall may best be achieved using physically based models. A two‐tiered retro‐active forecast procedure for the December–February (DJF) season is employed over a 10‐year period starting from 1987/1988. Rainfall forecasts are produced for a number of homogeneous regions over part of southern Africa. Categorized (below‐normal, near‐normal and above‐normal) statistical DJF rainfall predictions are made for the region to form the baseline skill level that has to be outscored by more elaborate methods involving general circulation models (GCMs). The GCM used here is the Centre for Ocean–Land–Atmosphere Studies (COLA) T30, with predicted global SST fields as boundary forcing and initial conditions derived from the National Centres for Environmental Prediction (NCEP) reanalysis data. Bias‐corrected GCM simulations of circulation and moisture at certain standard pressure levels are downscaled to produce rainfall forecasts at the regional level using the perfect prognosis approach.In the two‐tiered forecasting system, SST predictions for the global oceans are made first. SST anomalies of the equatorial Pacific (NIÑO3.4) and Indian oceans are predicted skilfully at 1‐ and 3‐month lead‐times using a statistical model. These retro‐active SST forecasts are accurate for pre‐1990 conditions, but predictability seems to have weakened during the 1990s. Skilful multi‐tiered rainfall forecasts are obtained when the amplitudes of large events in the global oceans (such as El Niño and La Niña episodes) are described adequately by the predicted SST fields. GCM simulations using persisted August SST anomalies instead of forecast SSTs produce skill levels similar to those of the baseline for longer lead‐times. Given high‐skill SST forecasts, the scheme has the potential to provide climate forecasts that outscore the baseline skill level substantially. Copyright © 2001 Royal Meteorological Society
In search of zonal circulations in the equatorial Atlantic sector from the NCEP–NCAR reanalysis
Authors: Hastenrath Stefan 
Published: September 2002

AbstractThe National Center for Environmental Prediction–National Center for Atmospheric Research (NCEP–NCAR) 1958–1997 upper‐air dataset has been evaluated for evidence of equatorial zonal circulation cells over the Atlantic and adjacent continents. For January, April, July and October, maps are presented of mid‐tropospheric vertical motion, upper‐tropospheric divergent flow, and zonal–vertical cross‐sections of vertical and divergent zonal motion and total zonal flow. In the boreal winter half‐year, a centre of intense ascending motion and upper‐tropospheric, mainly northward‐directed outflow is located off the mouth of the Amazon. From this centre there is also some outflow into centres of upper‐tropospheric convergence and subsidence over the equatorial eastern Pacific and eastern Atlantic, respectively. From January to April, the near‐equatorial band of ascending motion shifts southward, and the upper‐tropospheric convergence centre is displaced from the Equator into the South Atlantic. In the boreal summer half‐year, the band of strongest ascending motion is displaced northward, and two separate centres of upper‐tropospheric divergent outflow are found over northern hemispheric Africa and the Central American Seas. From these centres, the outflow is directed approximately southward into the southern hemisphere. The analysis points to the existence of an equatorial zonal circulation cell in the Atlantic sector confined to around January. Copyright © 2001 Royal Meteorological Society