bluuebunny/crossref_metadata_2025_split huggingface dataset:
A simple method for compressible multiphase mixtures and interfaces
Authors: Andrianov Nikolai , Saurel Richard , Warnecke Gerald 
Published: January 2003

AbstractWe develop a Godunov‐type scheme for a non‐conservative, unconditional hyperbolic multiphase model. It involves a set of seven partial differential equations and has the ability to solve interface problems between pure materials as well as compressible multiphase mixtures with two velocities and non‐equilibrium thermodynamics (two pressures, two temperatures, two densities, etc.).Its numerical resolution poses several difficulties. The model possesses a large number of acoustic and convective waves (seven waves) and it is not easy to upwind all these waves accurately and simply. Also, the system is non‐conservative, and the numerical approximations of the corresponding terms need to be provided. In this paper, we focus on a method, based on a characteristic decomposition which solves these problems in a simple way and with good accuracy. The robustness, accuracy and versatility of the method is clearly demonstrated on several test problems with exact solutions. Copyright © 2003 John Wiley & Sons, Ltd.
Positivity‐preserving, flux‐limited finite‐difference and finite‐element methods for reactive transport
Authors: MacKinnon Robert J. , Carey Graham F. 
Published: January 2003

AbstractA new class of positivity‐preserving, flux‐limited finite‐difference and Petrov–Galerkin (PG) finite‐element methods are devised for reactive transport problems.The methods are similar to classical TVD flux‐limited schemes with the main difference being that the flux‐limiter constraint is designed to preserve positivity for problems involving diffusion and reaction. In the finite‐element formulation, we also consider the effect of numerical quadrature in the lumped and consistent mass matrix forms on the positivity‐preserving property. Analysis of the latter scheme shows that positivity‐preserving solutions of the resulting difference equations can only be guaranteed if the flux‐limited scheme is both implicit and satisfies an additional lower‐bound condition on time‐step size. We show that this condition also applies to standard Galerkin linear finite‐element approximations to the linear diffusion equation. Numerical experiments are provided to demonstrate the behavior of the methods and confirm the theoretical conditions on time‐step size, mesh spacing, and flux limiting for transport problems with and without nonlinear reaction. Copyright © 2003 John Wiley & Sons, Ltd.
Temporal specific patterns of semaphorin gene expression in rat brain after kainic acid‐induced status epilepticus
Authors: Barnes Gregory , Puranam Ram S. , Luo Yuling , McNamara James O. 
Published: January 2003

AbstractMossy fiber sprouting and other forms of synaptic reorganization may form the basis for a recurrent excitatory network in epileptic foci. Four major classes of axon guidance molecules—the ephrins, netrins, slits, and semaphorins—provide targeting information to outgrowing axons along predetermined pathways during development. These molecules may also play a role in synaptic reorganization in the adult brain and thereby promote epileptogenesis. We studied semaphorin gene expression, as assessed by in situ hybridization, using riboprobes generated from rat cDNA in an adult model of synaptic reorganization, kainic acid (KA)‐induced status epilepticus (SE). Within the first week after KA‐induced SE, semaphorin 3C, a class III semaphorin, mRNA content is decreased in the CA1 area of the hippocampus and is increased in the upper layers of cerebral cortex. Another class III semaphorin, semaphorin 3F, is also decreased in CA1 and CA3 of hippocampus within the first week after KA‐SE. These changes in gene expression are principally confined to neurons. By contrast, there was little change in the semaphorin 4C mRNA content of CA1 neurons at this time. No changes in expression of semaphorin 3A and 4C genes were detected 28 days after KA‐induced SE. Regulation of semaphorin gene expression after KA‐induced SE suggests that neurons may regulate the expression of axonal guidance molecules and thereby contribute to synaptic reorganization after injury of the mature brain. The anatomic locale of the altered semaphorin gene expression may serve as a marker for specific networks undergoing synaptic reorganization in the epileptic brain. Hippocampus 2003;13:1–20. © 2003 Wiley‐Liss, Inc.
The role of NMDA glutamate receptors, PKA, MAPK, and CAMKII in the hippocampus in extinction of conditioned fear
Authors: Szapiro German , Vianna Monica R.M. , McGaugh James L. , Medina Jorge H. , Izquierdo Ivan 
Published: January 2003

AbstractPavlovian conditioning involves the association of initially neutral conditioned stimuli (CS) with unconditioned stimuli (US) that elicit a response. In contextual fear conditioning in rodents, the CS is the context of a training apparatus and the US is a foot shock. Retrieval of memory of the training is tested by presenting the CS alone. But a retrieval test also initiates extinction of the conditioned response. That is, presentation of the CS alone results in new learning, i.e., the CS no longer predicts the US. Here we report that extinction is triggered by two hippocampal signaling pathways underlying retrieval (the cAMP‐dependent protein kinase and the mitogen‐activated protein kinase pathways) and two other mechanisms that become activated at the same time and are not necessary for retrieval (N‐methyl‐D‐aspartate glutamatergic receptors and the calcium/calmodulin‐dependent protein kinase II signaling pathway). Thus, the molecular mechanisms underlying acquisition and/or consolidation of the memory for extinction are similar to those described for the acquisition and/or consolidation of the original contextual fear. Hippocampus 2003;13:53–58. © 2003 Wiley‐Liss, Inc.
Effect of halothane on type 2 immobility‐related hippocampal theta field activity and theta‐on/theta‐off cell discharges
Authors: Bland Brian H. , Bland Cheryl E. , Colom Luis V. , Roth Sheldon H. , DeClerk Shandra , Dypvik Audny , Bird Jenn , Deliyannides Alexandra 
Published: January 2003

AbstractRats were studied in acute and chronic (freely moving) recording conditions during exposure to different levels of the volatile anesthetic halothane, in order to assess effects on hippocampal theta field activity in the chronic condition and on theta‐related cellular discharges in the acute condition. Previous work has shown that the generation of hippocampal type 2 theta depends on the coactivation of cholinergic and GABAergic inputs from the medial septum. Based on these data and recent findings that halothane acts on interneuron GABAA receptors, we predicted that exposure of rats to subanesthetic levels would result in the induction of type 2 theta field activity. In the chronic condition, exposure to subanesthetic levels of halothane (0.5–1.0 vol %) was found to induce theta field activity during periods of immobility (type 2 theta) with a mean increase of 39% in amplitude (mV) compared to control levels during movement. The total percentage of signal power (V2) associated with peak theta frequencies (80% compared to control levels of 47%) was also increased by halothane. Over the whole range of administered halothane concentrations, theta field frequency progressively declined from a mean peak frequency of 6.5 ± 0.8 Hz at 0.5 vol % halothane to a mean peak frequency of 4.0 ± 1.8 Hz at 2.0 vol % halothane. Subsequent administration of a muscarinic cholinergic antagonist, atropine sulfate, selectively abolished all type 2 immobility‐related theta field activity, while type 1 movement‐related theta was still intact. At anesthetic levels (1.5–2.0 vol %) in acute experiments, hippocampal field activity spontaneously cycled between theta and large‐amplitude irregular activity. Analysis of depth profiles in four experiments revealed they were identical to those previously described for rats under urethane anesthesia conditions. In addition, the discharge properties of 31 theta‐related cells, classified as tonic and phasic theta‐on and tonic and phasic theta‐off cells, did not differ significantly from those described previously in rats anesthetized with urethane. These data provide further support for an involvement of GABAA receptors in the generation of hippocampal theta. Hippocampus 2003;13:38–47. © 2003 Wiley‐Liss, Inc.
Type II glucocorticoid receptor immunoreactivity in the mossy cells of the rat and the mouse hippocampus
Authors: Patel Anisha , Bulloch Karen 
Published: January 2003

AbstractHippocampal principal neurons, granule and pyramidal cells, are known to express type II glucocorticoid receptors (GR) and it is believed that glucocorticoids (GC) mediate at least some of their effects through GR. Under conditions of severe stress and trauma, these principal cells are vulnerable to damage and this mechanism may be exacerbated by GR. The mossy cell, an excitatory dentate gyrus neuron, is also damaged following trauma, with over 50% reported loss in rats after kainate‐induced seizures. However, it has not been determined if GC play any role in protecting or exacerbating damage to this important hippocampal cell type. In the present study, we have undertaken an evaluation of the presence of GR in mossy cells of the rat and mouse utilizing an immunocytochemical double‐labeling technique. To identify mossy cells in the rat, we utilized an antibody to the glutamate receptor subunit 2/3 (GluR2/3). In addition to GluR2/3 antibodies, in the mouse, an antibody to the calcium‐binding protein, calretinin (CR), to identify mossy cells was also employed. Our results show that GR immunoreactivity (IR) was colocalized with GluR2/3‐IR in approximately 90% of the rat and the mouse mossy cells. In addition, GR‐IR was identified in the CR‐IR mossy cells in the mouse hippocampus, whereas the CR‐IR interneurons of rat and mouse were negative for GR‐IR. The presence of GR on mossy cells may indicate the ability of GC to mediate cellular activity of these cells. Hippocampus 2003;13:59–66. © 2003 Wiley‐Liss, Inc.
Theta‐ and movement velocity‐related firing of hippocampal neurons is disrupted by lesions centered on the perirhinal cortex
Authors: Muir Gary M. , Bilkey David K. 
Published: January 2003

AbstractThe hippocampus is critically involved in spatial memory and navigation. It has previously been proposed that, as part of this process, the hippocampus might have access to self‐motion information. The possibility that some of this information may originate from the perirhinal cortex, a region involved in high‐order multimodal processing, was tested in the present study by recording the responses of hippocampal complex‐spike (place cells) and theta cells (putative interneurons) to movement velocity and to the movement‐related theta rhythm EEG while rats with bilateral ibotenic acid lesions centered on the perirhinal cortex (n = 5), or control surgeries (n = 5), foraged in a rectangular environment. Perirhinal cortex lesions altered several characteristics of place and theta cell firing. First, the proportion of theta cells recorded was significantly lower in perirhinal lesion animals (8/39 units) compared to controls (22/53 units). Second, the firing of place cells recorded from lesion animals was phase‐shifted so as to occur significantly earlier during the theta rhythm cycle than in place cells from controls (mean difference = 48.73°). Third, the firing rates of a significantly lower proportion of place cells from lesion animals were modulated by the movement velocity of the animal compared to place cells from controls. These results indicate that the perirhinal cortex contributes to the responses of hippocampal CA1 place cells by providing information about self‐movement and by controlling the timing of firing of these cells. This information may normally be utilized by the hippocampus during spatial memory and navigation processes. Hippocampus 2003;13:93–108. © 2003 Wiley‐Liss, Inc.
Reward value invariant place responses and reward site associated activity in hippocampal neurons of behaving rats
Authors: Tabuchi E. , Mulder A.B. , Wiener S.I. 
Published: January 2003

AbstractTo investigate the involvement of the hippocampal‐accumbens system in goal‐oriented displacement behaviors, hippocampal neuronal activity was recorded in rats learning and recalling new distributions of different volumes of liquid reward among the arms of a plus maze. Each arm had a reward box containing a water trough and identical visual cues that could be illuminated independently. As the water‐restricted rat successively visited the respective boxes, it received 7, 5, and 3 drops of water, and then 1 drop, provided at 1‐s intervals. (Reward distributions were reassigned daily and mid‐session.) In the training phase, reward boxes were lit individually. In the recall phase, the lamps on all arms were lit and then turned off as the rat visited the boxes in order of descending value. Neuronal firing rates were analyzed for changes related to reward value or to shifts between learning and recall phases. The principal finding is that place responses remained unchanged after these manipulations and that these neurons showed no evidence of explicit coding of reward value. In addition, two other types of responses appeared while the rat was stationary at the reward boxes awaiting multiple rewards. These were observed primarily in neurons within the dentate gyrus, but also in CA1. Position‐selective reward site responses were regular at 20–60 impulses per second, while position‐independent discharges bursted irregularly at about 5 impulses per second. Such responses could explain controversial reports of reward dependence in hippocampal neurons. The higher incidence of the latter responses in the temporal (“ventral”) hippocampus is consistent with the distinctive anatomical and functional properties of this subregion. Hippocampus 2003;13:117–132. © 2003 Wiley‐Liss, Inc.
Stimulation‐induced reset of hippocampal theta in the freely performing rat
Authors: Williams J.M. , Givens B. 
Published: January 2003

AbstractPrevious research has suggested that visual and auditory stimuli in a working memory task have the ability to reset hippocampal theta, perhaps allowing an organism to encode the incoming information optimally. The present study examined two possible neural pathways involved in theta resetting. Rats were trained on a visual discrimination task in an operant chamber. At the beginning of a trial, a light appeared over a centrally located lever that the rat was required to press to receive a water reward. There was a 30‐s intertrial interval before the next light stimulus appeared. After learning the task, all rats received surgical implantation of stimulating electrodes in both the fornix and the perforant path and recording electrodes, bilaterally in the hippocampus. After surgery, theta was recorded before and after the light stimulus to determine whether resetting to the visual stimulus occurred. During the intertrial interval, rats received single‐pulse electrical stimulation of either the fornix or perforant path. Theta was recorded both before and after the electrical stimulation to determine whether resetting occurred. In this experiment, hippocampal theta was reset after all three stimulus conditions (light, perforant path, and fornix stimulation), with the greatest degree of reset occurring after the fornix stimulation. The results suggest that activation of the perforant path and fornix may underlie theta reset and provide a mechanism by which the hippocampus may enhance cognitive processing. Hippocampus 2003;13:109–116. © 2003 Wiley‐Liss, Inc.
Long‐term potentiation and long‐term depression induced by local application of ATP to hippocampal CA1 neurons of the Guinea pig
Authors: Yamazaki Yoshihiko , Kaneko Kenya , Fujii Satoshi , Kato Hiroshi , Ito Ken‐Ichi 
Published: January 2003

AbstractThe present study has investigated the role of ATP in the induction of synaptic plasticity, using local application of ATP by picopump administration into the stratum radiatum of guinea pig hippocampal region CA1. Excitatory postsynaptic currents (EPSCs) evoked by stimulation of Schaffer collateral/commissural afferents synapsing on CA1 pyramidal cells of hippocampal slices were monitored in voltage‐clamp mode, using whole‐cell recording. Brief local application of ATP (1 mM) induced an inward current, usually consisting of early‐ and late‐phase components. Because the late‐phase component of an ATP‐induced current was largely inhibited by Ca2+‐free solution, this component is supposed to depend on extracellular Ca2+. After local application of ATP, long‐term synaptic modification of EPSCs was induced: LTP was detected in neurons exhibiting a small late Ca2+ current, while LTD was obtained from recordings showing a large late Ca2+ current in response to ATP application. There was a statistically significant correlation between the magnitude of long‐term plastic changes and the size of Ca2+ currents in response to ATP application. Furthermore, there was significant difference between the average size of the Ca2+ current in the LTP group and the size in the LTD group. These results suggest that a small Ca2+ influx in response to ATP application induces LTP, whereas a large one induces LTD in guinea pig hippocampal CA1 neurons. Hippocampus 2003;13:81–92. © 2003 Wiley‐Liss, Inc.
Tyrosine‐nitration of caspase 3 and cytochrome c does not suppress apoptosis induction in squamous cell carcinoma cells
Authors: Ueta Eisaku , Kamatani Takaaki , Yamamoto Tetsuya , Osaki Tokio 
Published: January 2003

AbstractThe influence of tyrosine nitration of cytochrome c and caspase 3 on apoptosis induction was investigated in an established squamous carcinoma cell line, OSC‐4. The intracellular NO and O levels were increased up to about 110–120% and 140–180% of the control levels, respectively, after the treatment of OSC‐4 cells with 5‐FU (100 μg/ml), PLM (10 μg/ml), CDDP (10 μg/ml), or γ‐rays (20 Gy). The treatment of OSC‐4 cells with ONOO− (1 mM) and the above anticancer agents induced tyrosine nitration of 14, 32 kDa protein among others and nitration of tyrosine residues of cytochrome c and caspase 3 was identified by the Western blotting of immunoprecipitates obtained by antibodies to these proapoptotic proteins. When cytochrome c and procaspase 3 were treated with ONOO−, tyrosine nitration was increased in a ONOO−‐dose dependent manner. Tyrosine nitration of cleaved (17 kDa) caspase 3, however, was not induced by ONOO−. Procaspase 3 in the cytosol of HeLa cells was activated by the addition of ONOO−‐treated as well as ONOO−‐untreated cytochrome c. In addition, cleavage of ICAD and PARP were not suppressed in OSC‐4 cells by pretreatment with ONOO−. Activity of cleaved caspase 3 was not suppressed at low concentrations or by treatment with ONOO− or NO donors, SIN‐1 and SNP. Furthermore, apoptosis of OSC‐4 cells by the anticancer agents was not suppressed by ONOO−. In conclusion, these results suggest that nitration of tyrosine residues of cytochrome c and procaspase 3 is induced by chemoradiotherapy but their nitration does not suppress cancer cell apoptosis. © 2002 Wiley‐Liss, Inc.
Genetic susceptibility to nasopharyngeal carcinoma within the HLA‐A locus in Taiwanese
Authors: Lu Cheng‐Chan , Chen Jung‐Chin , Jin Ying‐Tai , Yang Hsiao‐Bai , Chan Shih‐Huang , Tsai Sen‐Tien 
Published: January 2003

AbstractNPC is an epithelial tumor that is highly prevalent among the southern Chinese. Numerous studies have indicated that specific HLA haplotypes and genes within the HLA complex are associated with NPC. As a first effort to localize the gene responsible for susceptibility, the HLA‐A, ‐B, and ‐A2 subtypes were examined for their association to NPC. Consistent with previous reports, frequencies of HLA‐A2 [OR = 2.50, pc = 0.020 (study population); OR = 3.73, pc = 0.0030 (≥40 years old)] were significantly higher in patients with NPC than in healthy controls. Two‐locus analysis indicated that A2+B46+ individuals are at greater risk for NPC than A2−B46− individuals in both the population studied and the ≥40‐year‐old group. This, however, may be due to the close linkage of these 2 genes. Moreover, A2+B38+ individuals were at higher risk than A2−B38− individuals in both the population studied and the ≥40‐year‐old group; A2 and B38 are not genetically linked. These findings suggest that B38 or B46 alone cannot confer a high risk of NPC but that, in conjunction with A2, B38 or B46 positivity greatly increases risk. None of 5 A2 subtypes identified from studied populations was significantly associated with NPC. Microsatellite marker D6S211, located 97 kb telomeric to HLA‐A, was analyzed for its association with NPC. Allele 4 of D6S211 was significantly associated with NPC (OR = 3.97, pc = 0.0042). These results strongly support the hypothesis that genes associated with susceptibility to NPC in the HLA region are within the HLA‐A locus. © 2002 Wiley‐Liss, Inc.
Relationship between steroid hormone contraceptives and HPV, cervical intraepithelial neoplasia and cervical carcinoma
Authors: de Villiers Ethel‐Michele 
Published: January 2003

AbstractAvailable data demonstrate an increase in the transcription of high‐risk papillomaviruses by the 16α‐hydroxylation of estrogens, which is in line with the epidemiologic data showing an increased cervical carcinogenesis risk for long‐term contraceptive‐using, HPV‐infected women. No evidence exists for an increase in HPV‐negative contraceptive users. © 2002 Wiley‐Liss, Inc.
Impact of comorbidity on lung cancer survival
Authors: Tammemagi C. Martin , Neslund‐Dudas Christine , Simoff Michael , Kvale Paul 
Published: January 2003

AbstractLung cancer is associated with smoking and age, both of which are associated with comorbidity. We evaluated the impact of comorbidity on lung cancer survival. Data on 56 comorbidities were abstracted from the records of a cohort of 1,155 patients. Survival effects were evaluated with Cox regression (outcome crude death). The adjustedR2statistic was used to compare the survival variation explained by predictive variables. No comorbidity was observed in 11.7% of patients, while 54.3% had 3 or more (mean 2.97) comorbidities. In multivariate analysis, 19 comorbidities were associated with survival: HIV/AIDS, tuberculosis, previous metastatic cancer, thyroid/glandular diseases, electrolyte imbalance, anemia, other blood diseases, dementia, neurologic disease, congestive heart failure, COPD, asthma, pulmonary fibrosis, liver disease, gastrointestinal bleeding, renal disease, connective tissue disease, osteoporosis and peripheral vascular disease. Only the latter was protective. Some of the hazards of comorbidities were explained by more directly acting comorbidities and/or receipt of treatment. Stage explained 25.4% of the survival variation. In addition to stage, the 19 comorbidities explained 6.1%, treatments 9.2%, age 3.7% and histology 1.3%. Thirteen uncommon comorbidities (prevalence <6%) affected 21.2% of patients and explained 3.5% of the survival variation. Comorbidity count and the Charlson index were significant predictors but explained only 2.5% and 2.0% of the survival variation, respectively. Comorbidity has a major impact on survival in early‐ and late‐stage disease, and even infrequent deleterious comorbidities are important collectively. Comorbidity count and the Charlson index failed to capture much information. Clinical practice and trials need to consider the effect of comorbidity in lung cancer patients. © 2002 Wiley‐Liss, Inc.