bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dynamic analysis of baffled fuel‐storage tanks using the ALE finite element method
Authors: Cho J. R. , Lee S. Y. 
Published: January 2003

AbstractThis paper is concerned with the parametric investigation on the structural dynamic response of moving fuel‐storage tanks with baffles. Since the structural dynamic behaviour is strongly coupled with interior liquid motion, the design of a fuel‐storage tank securing the structural stability becomes the appropriate suppression of the flow motion, which is in turn related to the baffle design. In order to numerically investigate the parametric dynamic characteristics of moving tanks, we employ the arbitrary Lagrangian–Eulerian (ALE) finite element method that is widely being used to deal with the problems with free surface, moving boundary, large deformation and interface contact. Following the theoretical and numerical formulations of fluid‐structure interaction problems, we present parametric numerical results of a cylindrical fuel‐storage tank moving with uniform vertical acceleration, with respect to the baffle number and location, and the inner‐hole diameter. Copyright © 2003 John Wiley & Sons, Ltd.
Approximate simulation of stratospheric flow from aircraft data
Authors: Humi Mayer 
Published: January 2003

AbstractWe show how stratospheric data collected by an aircraft along its flight path can be used to initialize steady state approximate simulations of the stratospheric flow. To this end we reformulate the initial value problem for Boussinesq equations as a large system of stiff ordinary differential equations (using the method of lines). Initial conditions for this system are derived from the aircraft data. As a result we are able to compute the Brunt–Vaisala frequency, Richardson number and the vorticity in the vicinity of the flight path. Copyright © 2003 John Wiley & Sons, Ltd.
The entorhinal cortex of the mouse: Organization of the projection to the hippocampal formation
Authors: van Groen Thomas , Miettinen Pasi , Kadish Inga 
Published: January 2003

AbstractThe origin and the terminations of the projections from the entorhinal cortex to the hippocampal formation of the mouse (C57BL/6J strain) have been studied using anterogradely and retrogradely transported tracers. The entorhinal cortex is principally divided into two areas, the lateral entorhinal area (LEA) and the medial entorhinal area (MEA). LEA is the origin of the lateral perforant path that terminates in the outer one‐third of the molecular layer of the dentate gyrus, and MEA is the origin of the medial perforant path that ends in the middle one‐third of the molecular layer of the dentate gyrus. This projection is mostly to the ispsilateral dentate gyrus; only a few labeled axons and terminals are found in the contralateral dentate gyrus. The projection to the dentate gyrus originates predominantly from neurons in layer II of the entorhinal cortex. The entorhinal cortex also projects to CA3 and CA1 and to subiculum; in both CA3 and CA1, the terminals are present in stratum lacunosum‐moleculare, whereas in the subiculum the terminals are in the outer part of the molecular layer. The projection from the entorhinal cortex to CA3, CA1, and subiculum is bilateral, and it originates predominantly from neurons in layer III, but a small number of neurons in the deeper layers of the entorhinal cortex contributes to this projection. The projection of entorhinal cortex to the hippocampus is topographically organized, neurons in the lateral part of both LEA and MEA project to the dorsal part (i.e., septal pole) of the hippocampus, whereas the projection to the ventral (i.e., temporal pole) hippocampus originates from neurons in medial parts of the entorhinal cortex. Hippocampus 2003;13:133–149. © 2003 Wiley‐Liss, Inc.
Distribution and morphology of serotonin‐immunoreactive axons in the hippocampal region of the New Zealand white rabbit. I. Area dentata and hippocampus
Authors: Bjarkam Carsten R. , Sørensen Jens Christian , Geneser Finn A. 
Published: January 2003

AbstractThis study provides a detailed light microscopic description of the morphology and distribution of immunohistochemically stained serotonergic axons in the hippocampal region of the New Zealand white rabbit. The serotonergic axons were segregated morphologically into three types: beaded fibers, fine fibers, and stem‐axons, respectively. Beaded fibers were thin serotonergic axons with large varicosities, whereas thin axons with small fusiform or granular varicosities were called fine fibers. Finally, thick straight non‐varicose axons were called stem‐axons. Beaded fibers often formed large conglomerates with numerous boutons (pericellular arrays) in close apposition to the cell‐rich layers in the hippocampal region, e.g., the granular and hilar cell layers of the dentate area and the pyramidal cell layer ventrally in CA3. The pericellular arrays in these layers were often encountered in relation to small calbindin‐D28K‐positive cells, as shown by immunohistochemical double staining for serotonin and calbindin‐D28K. The beaded and fine serotonergic fibers displayed a specific innervation pattern in the hippocampal region and were encountered predominantly within the terminal field of the perforant path, e.g., the stratum moleculare hippocampi and the outer two‐thirds of the dentate molecular layer. These fibers were also frequently seen in the deep part of the stratum oriens and the alveus, forming a dense plexus in relation to large multipolar calbindin‐D28K‐positive cells and their basal extensions. Stem‐axons were primarily seen in the fimbria and alveus. This innervation pattern was present throughout the entire hippocampal formation, but there were considerable septotemporal differences in the density of the serotonergic innervation. A high density of innervation prevailed in the ventral/temporal part of the hippocampal formation, whereas the dorsal/septal part received only a moderate to weak serotonergic innervation. These results suggest that the serotonergic system could modulate the internal hippocampal circuitry by way of its innervation in the terminal field of the perforant path, the hilus fasciae dentatae, and ventrally in the zone closely apposed to the mossy fiber layer and the pyramidal cells of CA3. This modulation could be of a dual nature, mediated directly by single serotonergic fibers traversing the hippocampal layers or indirectly by the pericellular arrays and their close relation to the calbindin‐D28K‐positive cells. The marked septotemporal differences in innervation density point toward a difference between the ventral and dorsal parts of the hippocampal formation with respect to serotonergic function and need for serotonergic modulation. Hippocampus 2003;13:21–37. © 2003 Wiley‐Liss, Inc.
Encoding of novel picture pairs activates the perirhinal cortex: An fMRI study
Authors: Pihlajamäki Maija , Tanila Heikki , Hänninen Tuomo , Könönen Mervi , Mikkonen Mia , Jalkanen Ville , Partanen Kaarina , Aronen Hannu J. , Soininen Hilkka 
Published: January 2003

AbstractIt is well established in nonhuman primates that the medial temporal lobe (MTL) structures, the hippocampus and the entorhinal and perirhinal cortices, are necessary for declarative memory encoding. In humans, the neuropathological and neuropsychological changes in early Alzheimer's disease (AD) further support a role for the rhinal cortex in the consolidation of new events into long‐term memory. Little is known, however, regarding the function of the rhinal cortex in humans in vivo. To examine the participation of the interconnected MTL structures as well as the whole‐brain network of activated brain areas in visual associative long‐term memory, functional magnetic resonance imaging (fMRI) was used to determine the brain regions that are activated during encoding and retrieval of paired pictures in 12 young control subjects. The most striking finding in the MTL activation pattern was the consistent activation of the perirhinal cortex in the encoding‐baseline and encoding‐retrieval comparisons with a strict statistical threshold (P < 0.00001). In contrast, no perirhinal cortex activation was detected in the retrieval‐baseline or retrieval‐encoding comparisons even with a low statistical threshold (P < 0.05). The location of the perirhinal activation area was in the transentorhinal part of the perirhinal cortex, in the medial bank of the collateral sulcus. The hippocampus and the more posterior parahippocampal gyrus were activated in both encoding and retrieval conditions. During the encoding processing, MTL activations were more consistent and the hippocampal activation area located more anteriorly than during retrieval. The frontal, parietal, temporal, and occipital association cortices were also activated in the encoding‐baseline and retrieval‐baseline comparisons. The data suggest that encoding, but not retrieval, of novel picture pairs activates the perirhinal cortex. To our knowledge, this is the first fMRI study reporting encoding activation in this transentorhinal part of the perirhinal cortex, the site of the very earliest neuropathological changes in AD. Hippocampus 2003;13:67–80. © 2003 Wiley‐Liss, Inc.
Selective impairment of fornix‐transected rats on a new nonspatial, odor‐guided task
Authors: Hudon C. , Doré F.Y. , Goulet S. 
Published: January 2003

AbstractIn the present experiment, sham‐operated (SH) and fornix‐transected (FX) rats were trained on a new nonspatial, odor‐guided task. On each session, eight odor pairs were presented twice. On the first occurrence of a pair, rats were reinforced for pushing the container (go response) in which the olfactory stimuli were placed. On the second occurrence, they were not reinforced and had to refrain from responding (no‐go response) to be scored as success. Rats were first trained to criterion on odor pairs made of replicates of the same odor (S pairs). Then they were trained to criterion on pairs made of different odors, each member of the pair overlapping with that of another pair (O pairs) and finally, on pairs of different odors with no overlap (NO pairs). The results showed that the number of sessions to reach criterion was significantly higher in FX than in SH rats during training on O pairs, but not during training on S or on NO pairs. These findings are consistent with the configural (Rudy and Sutherland, 1995: Hippocampus 5:375–389) or relational (Eichenbaum et al., 1994: Behav Brain Sci 17:449–518) account of the hippocampal memory function. Hippocampus 2003;13:48–52. © 2003 Wiley‐Liss, Inc.
Regional analysis of hippocampal activation during memory encoding and retrieval: fMRI study
Authors: Greicius Michael D. , Krasnow Ben , Boyett‐Anderson Jesse M. , Eliez Stephan , Schatzberg Alan F. , Reiss Allan L. , Menon Vinod 
Published: January 2003

AbstractInvestigators have recently begun to examine the differential role of subregions of the hippocampus in episodic memory. Two distinct models have gained prominence in the field. One model, outlined by Moser and Moser (Hippocampus 1998;8:608–619), based mainly on animal studies, has proposed that episodic memory is subserved by the posterior two‐thirds of the hippocampus alone. A second model, derived by Lepage et al. (Hippocampus 1998;8:313–322) from their review of 52 PET studies, has suggested that the anterior hippocampus is activated by memory encoding while the posterior hippocampus is activated by memory retrieval. Functional magnetic resonance imaging (fMRI) studies have tended to show limited activation in the anteriormost regions of the hippocampus, providing support for the Moser and Moser model. A potential confounding factor in these fMRI studies, however, is that susceptibility artifact may differentially reduce signal in the anterior versus the posterior hippocampus. In the present study, we examined activation differences between hippocampal subregions during encoding and retrieval of words and interpreted our findings within the context of these two models. We also examined the extent to which susceptibility artifact affects the analysis and interpretation of hippocampal activation by demonstrating its differential effect on the anterior versus the posterior hippocampus. Both voxel‐by‐voxel and region‐of‐interest analyses were conducted, allowing us to quantify differences between the anterior and posterior aspects of the hippocampus. We detected significant hippocampal activation in both the encoding and retrieval conditions. Our data do not provide evidence for regional anatomic differences in activation between encoding and retrieval. The data do suggest that, even after accounting for susceptibility artifact, both encoding and retrieval of verbal stimuli activate the middle and posterior hippocampus more strongly than the anterior hippocampus. Finally, this study is the first to quantify the effects of susceptibility‐induced signal loss on hippocampal activation and suggests that this artifact has significantly biased the interpretation of earlier fMRI studies. Hippocampus 2003;13:164–174. © 2003 Wiley‐Liss, Inc.
Cellular mechanisms underlying the rhythmic bursts induced by NMDA microiontophoresis at the apical dendrites of CA1 pyramidal neurons
Authors: Bonansco Christian , Buño Washington 
Published: January 2003

AbstractThis article reports the cellular mechanisms underlying a form of intracellular “theta‐like” (θ‐like) rhythm evoked in vitro by microiontophoresis of N‐methyl‐D‐aspartate (NMDA) at the apical dendrites of CA1 pyramidal neurons. Rhythmic membrane potential (Vm) oscillations and action potential (AP) bursts (≈6 Hz; ≈20 mV; ≈2–5 APs) were evoked in all cells. The response lasted ≈2 s, and the initial oscillations were usually small (<20 mV) and below AP threshold. Rhythmic bursts were never evoked by imposed depolarization in the absence of NMDA. Block of Na+ conductance with tetrodotoxin (TTX) (1.5 μM), of non‐NMDA receptors with 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) (20 μM) and of synaptic inhibition by bicuculline (50 μM) and picrotoxin (50 μM) did not prevent NMDA oscillation. Inhibition of the voltage dependence of the NMDA conductance in Mg2+‐free Ringer's solution blocked oscillations. Preventing Ca2+ influx with Ca2+‐free and Co2+ (2‐mM) solutions and block of the slow Ca2+‐dependent afterhyperpolarization (sAHP) by carbamilcholine (5 μM), isoproterenol (10 μM), and intracellular BAPTA blocked NMDA oscillations. Inhibition of L‐type Ca2+ conductance with nifedipine (30 μM) reduced oscillation amplitude. Block of tetraethylammonium (TEA) (10 mM) and 4AP (10 mM)‐sensitive K+ conductance increased the duration and amplitude, but not the frequency, of oscillations. In conclusion, θ‐like bursts relied on the voltage dependence of the NMDA conductance and on high‐threshold Ca2+ spikes to initiate and boost the depolarizing phase of oscillations. The repolarization is initiated by TEA‐sensitive K+ conductance and is controlled by the sAHP. These results suggest a role of interactions between NMDA conductance and intrinsic membrane properties in generating the CA1 θ‐rhythm. Hippocampus 2003;13:10067. © 2003 Wiley‐Liss, Inc.
Early life risk factors in cancer: The relation of birth weight to adult obesity
Authors: Leong Nicole M. , Mignone Laura I. , Newcomb Polly A. , Titus‐Ernstoff Linda , Baron John A. , Trentham‐Dietz Amy , Stampfer Meir J. , Willett Walter C. , Egan Kathleen M. 
Published: January 2003

AbstractThe intrauterine environment appears to play a role in the development of adult diseases, including several prominent cancers. Our study aims to characterize the relationship between birth weight, a measure of the intrauterine environment, and adult obesity. A population‐based sample of women aged 50–79, living in the states of Massachusetts, New Hampshire or Wisconsin, were randomly selected from lists of licensed drivers and Medicare beneficiaries to participate as controls in a case‐control study of breast cancer. Information on birth weight, adult height and adult weight were collected through structured telephone interviews from 1992–1995. Our analysis was based on 1,850 interviews. A U‐shaped relationship between birth weight and adult BMI was observed. Median adult BMI for the birth weight categories (in kilograms) <2.3, 2.3<2.5, 2.5<3.2, 3.2<3.9, 3.9<4.5 and ≥4.5 were 26.6, 24.4, 25.1, 25.5, 25.4 and 26.6 kg/m respectively. Compared to women 2.5<3.2 kg at birth, women in highest birth weight category (≥4.5 kg) had an odds ratio of 1.99 (95% CI 1.13–3.48) of being obese (≥30 kg/m2) as adults. The odds ratio for women in the <2.3 kg birth weight category was 1.67 (95% CI 1.01–2.76). These data suggest that both low and high birth weights are associated with higher adult BMI and support the hypothesis that fetal experience may influence adult obesity with potential consequences for risk of several major cancers. © 2002 Wiley‐Liss, Inc.
Does skin fibroblast radiosensitivity predict squamous cancer cell radiosensitivity of the same individual?
Authors: Haikonen Johanna , Rantanen Virpi , Pekkola Kirsi , Kulmala Jarmo , Grénman Reidar 
Published: January 2003

AbstractIndividualization of radiation doses is presumed to result in better radiotherapy outcome. Success rate in measuring radiosensitivity is probably the most limiting factor for present radiosensitivity assays to be introduced into clinical routine. To find a simpler predictive parameter, we compared the radiosensitivity of dermal fibroblasts and head and neck squamous cell carcinoma (SCC) cell lines established from the same individuals. The radiosensitivity was tested using the clonogenic 96‐well plate assay. The surviving fraction at 2.0 Gy (SF2) was determined, as well as the mean inactivation dose (AUC) of cancer cells. SF2 of SCC cell lines and skin fibroblasts were 0.25–0.44 and 0.11–0.43, respectively. AUC of SCC cells was 1.4–2.1 Gy. Dermal fibroblasts were more radiosensitive than SCC cells in 14 of 15 cases. In 1 patient (UT‐SCC‐8), cancer cells were found to be more radiosensitive than corresponding dermal fibroblasts. There was a clear tendency to a correlation between radiosensitivities of these 2 cell types, but statistical significance was reached only when the data of UT‐SCC‐8 was excluded. In our material, the intrinsic radiosensitivity of head and neck SCC cells could in most cases be predicted from the intrinsic radiosensitivity of dermal fibroblasts established from the same individual. © 2002 Wiley‐Liss, Inc.
Expression of the coxsackie and adenovirus receptor in human astrocytic tumors and xenografts
Authors: Fuxe Jonas , Liu Lu , Malin Stephen , Philipson Lennart , Collins V. Peter , Pettersson Ralf F. 
Published: January 2003

AbstractThe sensitivity of human tissues and tumors to infection with type C adenoviruses correlates with the expression of the human coxsackie B‐ and adenovirus receptor, hCAR. HCAR is heterogeneously expressed in various tissues and types of human cancer cells, which has implications for the use of adenoviruses as vectors in cancer gene therapy. Using immunoblotting, real‐time PCR, FACS‐analysis and sensitivity to infection with adenovirus‐lacZ, we analyzed the expression level of hCAR in glioma Grade IV cell lines. With real‐time PCR, we also analyzed hCAR expression in primary human astrocytomas of different malignancy grades, as well as in their xenograft derivatives. Analysis of a set of 10 cell lines showed great variation in hCAR expression. Susceptibility to Ad5lacZ correlated well with hCAR expression, whereas no correlation was observed with the expression of αvβ3/αvβ5 integrins, proposed to function as co‐receptors for adenoviruses. A great variation of CAR expression was also observed in primary astrocytomas of different malignancy grades. The mean value of CAR expression was significantly lower in 22 Grade IV tumors as compared to the values for 6 Grade II (p = 0.01) and 6 Grade III (p = 0.01) tumors. When the hCAR expression in 11 xenografts derived from Grade IV gliomas were compared to the levels detected in the original parental tumors, a mean 12‐fold higher expression was seen in the xenografts (P = 0.01). Two xenografts with low hCAR expression grew considerably faster than the hCAR‐expressing cells. Our results have relevance for the use of adenoviruses in gene therapy against astrocytomas. © 2002 Wiley‐Liss, Inc.
Ectopic p21sdi1 gene transfer induces retinoic acid receptor β expression and sensitizes human cancer cells to retinoid treatment
Authors: Teraishi Fuminori , Kadowaki Yoshihiko , Tango Yasuhisa , Kawashima Takeshi , Umeoka Tatsuo , Kagawa Shunsuke , Tanaka Noriaki , Fujiwara Toshiyoshi 
Published: January 2003

AbstractThe biological effects of retinoic acid (RA) are mediated by nuclear retinoic acid receptors (RARs) that function as ligand‐activated transcriptional factors. The response of human cancer cells to RA is known to be associated with the expression of RARβ. Recent studies have demonstrated that the loss of RARβ expression is involved in the development of a variety of human malignancies. We show that recombinant adenovirus‐mediated p21sdi1 gene transfer enhances RARβ mRNA expression as well as protein expression and induces the sensitivity to all‐trans RA (ATRA) in human cancer cells. Semi‐quantitative reverse transcription‐polymerase chain reaction analysis demonstrated that infection with adenovirus carrying human p21sdi1 gene (Ad5CMV‐p21), which encodes a cyclin‐dependent kinase inhibitor, induced RARβ mRNA and protein expression in H1299 human non‐small cell lung cancer cells and DLD‐1 human colorectal cancer cells. We also found that exogenous introduction of the p21sdi1 gene transcriptionally activated the upstream promoter function of the RARβ gene. Treatment with 1 μM of ATRA showed no significant inhibitory effects on the growth of H1299 and DLD‐1 cells; after Ad5CMV‐p21 infection, however, cells underwent apoptosis with ATRA treatment at the same concentration, suggesting that p21sdi1 gene transfer sensitized H1299 and DLD‐1 cells, presumably, through RARβ upregulation. We also demonstrated the efficacy of intratumoral injection of Ad5CMV‐p21 in combination with systemic administration of ATRA in a nude mice xenograft model. Our results indicate that recombinant adenovirus‐mediated p21sdi1 gene transfer could be potentially useful for the local induction of RA sensitivity in human premalignant and malignant lesions lacking appropriate RARβ expression. © 2002 Wiley‐Liss, Inc.