bluuebunny/crossref_metadata_2025_split huggingface dataset:
Linearized and non‐linear acoustic/viscous splitting techniques for low Mach number flows
Authors: Farshchi Mohammad , Hannani Siamak K. , Ebrahimi Mohammad 
Published: July 2003

AbstractComputation of the acoustic disturbances generated by unsteady low‐speed flow fields including vortices and shear layers is considered. The equations governing the generation and propagation of acoustic fluctuations are derived from a two‐step acoustic/viscous splitting technique. An optimized high order dispersion–relation–preserving scheme is used for the solution of the acoustic field. The acoustic field generated by a corotating vortex pair is obtained using the above technique. The computed sound field is compared with the existing analytic solution. Results are in good agreement with the analytic solution except near the centre of the vortices where the acoustic pressure becomes singular. The governing equations for acoustic fluctuations are then linearized and solved for the same model problem. The difference between non‐linear and linearized solutions falls below the numerical error of the simulation. However, a considerable saving in CPU time usage is achieved in solving the linearized equations. The results indicate that the linearized acoustic/viscous splitting technique for the simulation of acoustic fluctuations generation and propagation by low Mach number flow fields seems to be very promising for three‐dimensional problems involving complex geometries. Copyright © 2003 John Wiley & Sons, Ltd.
Steady/unsteady aerodynamic analysis of wings at subsonic, sonic and supersonic Mach numbers using a 3D panel method
Authors: Cho Jeonghyun , Han Cheolheui , Cho Leesang , Cho Jinsoo 
Published: July 2003

AbstractThis paper treats the kernel function of an integral equation that relates a known or prescribed upwash distribution to an unknown lift distribution for a finite wing. The pressure kernel functions of the singular integral equation are summarized for all speed range in the Laplace transform domain. The sonic kernel function has been reduced to a form, which can be conveniently evaluated as a finite limit from both the subsonic and supersonic sides when the Mach number tends to one. Several examples are solved including rectangular wings, swept wings, a supersonic transport wing and a harmonically oscillating wing. Present results are given with other numerical data, showing continuous results through the unit Mach number. Computed results are in good agreement with other numerical results. Copyright © 2003 John Wiley & Sons, Ltd.
Numerical simulation of time‐dependent hydrodynamic removal of a contaminated fluid from a cavity
Authors: Fang Lih‐Chuan , Nicolaou Dimitri , Cleaver John W. 
Published: July 2003

AbstractThe time‐dependent hydrodynamic removal of a contaminated fluid from a rectangular cavity on the floor of a duct is analysed numerically. Laminar duct flows are considered for Reynolds numbers of 50 and 1600 where the characteristic length is the duct height. Two cases are considered where: (1) the fluid density in the cavity is the same as that for the duct fluid and (2) the cavity fluid has a higher density than the duct fluid but the two fluids are miscible. The flow is solved by a numerical solution of the time‐dependent Navier–Stokes equations. Attention is focused on the convective transport of contaminated fluid out from the cavity and the effect of duct flow velocity profile on the cleaning process. Passive markers are used in the numerical simulation for the purpose of identifying the contaminated cavity fluid. The results show that the flow patterns in the cavity are influenced by the type of duct flow. From a cleaning perspective, the results suggest that it is easier for the duct flow to penetrate a cavity and to remove contaminated cavity fluid when the duct flow is of the Poiseuille type and the aspect ratio is large. Copyright © 2003 John Wiley & Sons, Ltd.
Numerical simulation of mold filling in foam reaction injection molding
Authors: Seo Dongjin , Ryoun Youn Jae , Tucker Charles L. 
Published: July 2003

AbstractA numerical simulation of reaction injection molding (RIM) of polymeric foam is developed, using a finite volume method (FVM). In this study we predict mold filling with a variable‐density fluid that fills a mold by self‐expansion. We deal with two‐dimensional, isothermal cases. With the assumptions of ideal mixing and rapid bubble nucleation, the foam is modelled as a continuum with a time‐dependent density. The continuum is assumed to be a Newtonian fluid. We develop a pressure‐based FVM for unstructured meshes that includes the SIMPLE algorithm with treatment of fluid compressibility. Cell‐based, co‐located storage is used for all physical variables. To treat the moving interface, an explicit high‐resolution interface capturing method is used. Foam flow in a slit is investigated, and the numerical calculations are in good agreement with an approximate analytic solution. For fountain flow in a rectangular cavity, the shape of the flow front is flatter and the traces of the particles are more complicated for an expanding foam than for a constant‐density fluid. An example of mold filling by an expanding foam demonstrates the geometric flexibility of the method. Copyright © 2003 John Wiley & Sons, Ltd.
Solution adaptive grids applied to low Reynolds number flow
Authors: de With G. , Holdø A. E. , Huld T. A. 
Published: July 2003

AbstractA numerical study has been undertaken to investigate the use of a solution adaptive grid for flow around a cylinder in the laminar flow regime. The main purpose of this work is twofold. The first aim is to investigate the suitability of a grid adaptation algorithm and the reduction in mesh size that can be obtained. Secondly, the uniform asymmetric flow structures are ideal to validate the mesh structures due to mesh refinement and consequently the selected refinement criteria. The refinement variable used in this work is a product of the rate of strain and the mesh cell size, and contains two variables Cm and Cstr which determine the order of each term. By altering the order of either one of these terms the refinement behaviour can be modified. Copyright © 2003 John Wiley & Sons, Ltd.
Differential modulation of hippocampal chemical‐induced injury response by ebselen, pentoxifylline, and TNFα‐, IL‐1α‐, and IL‐6‐neutralizing antibodies
Authors: Jean Harry G. , Bruccoleri Alessandra , Lefebvre d'Hellencourt Christian 
Published: July 2003

AbstractThe proinflammatory cytokines tumor necrosis factor (TNFα), interleukin‐1 (IL‐1α), and interleukin‐6 (IL‐6) have been associated with various models of hippocampal damage. To examine their role in initiation of an acute hippocampal injury response, 21‐day‐old male CD‐1 mice received an acute intraperitoneal (i.p.) injection of trimethyltin hydroxide (TMT; 2.0 mg/kg) to produce necrosis of dentate granule neurons, astrocyte, and microglia reactivity. Tremors and intermittent seizures were evident at 24 hr. Intercellular adhesion molecule‐1 (ICAM‐1), glial fibrillary acidic protein (GFAP), anti‐apoptotic TNFα‐inducible early response gene (A‐20), macrophage inflammatory protein (MIP)‐1α, TNFα, IL‐1α, IL‐6, and caspase 3 mRNA levels were significantly elevated. Pretreatment with the antioxidant, ebselen, decreased ICAM‐1, A‐20, and TNFβ elevations. Pentoxifylline blocked elevations in A‐20 and decreased elevations in GFAP mRNA levels. Neither prevented histopathology or behavioral effects. Intracisternal injection of TNFα‐neutralizing antibody significantly inhibited both behavioral effects and histopathology. RNase protection assays showed that TMT‐induced elevations in mRNA levels for ICAM‐1, A‐20, GFAP, MIP‐1α, IL‐1α, TNFα, TNFβ, and caspase 3 were blocked by anti‐TNFα. These data demonstrate a significant role for TNFα in an acute neuro‐injury in the absence of contribution from infiltrating cells. The cerebellum shows limited if any damage after TMT; however, in combination with the i.c.v. injection, elevations were seen in GFAP and in EB‐22, a murine acute‐phase response gene homologous to the alpha (1)‐antichymotrypsin gene. Elevations were similar for artificial cerebral spinal fluid and anti‐IL‐1α, and significantly increased with anti‐TNFα, anti‐IL‐6, or the combination of antibodies. Responses seen in the cerebellum suggest synergistic interactions between the baseline state of the cell and manipulations in the cytokine environment. Data suggests a role for TNFα in the pathogenesis of hippocampal injury induced by TMT. Published 2003 Wiley‐Liss, Inc.
Spatiotemporal changes of apolipoprotein E immunoreactivity and apolipoprotein E mRNA expression after transient middle cerebral artery occlusion in rat brain
Authors: Kamada Hiroshi , Sato Keiko , Zhang Wen Ri , Omori Nobuhiko , Nagano Isao , Shoji Mikio , Abe Koji 
Published: July 2003

AbstractApolipoprotein E (ApoE) is a constituent of lipoprotein and plays an important role in the maintenance of neural networks. However, spatiotemporal differences in ApoE expression and its long‐term role in neural process after brain ischemia have not been studied. We investigated changes of ApoE immunoreactivity and ApoE mRNA expression both in the core and in the periischemic area at 1, 7, 21, or 56 days after 90 min of transient middle cerebral artery occlusion. Double stainings for ApoE plus NeuN or plus ED1 were performed in order to identify cell type of ApoE‐positive stainings. The maximal increase of ApoE expression was observed at 7 days in the core and at 7 and 21 days in the periischemic area. In the core, ApoE plus NeuN double‐positive cells increased at 1 and 7 days, without ApoE mRNA expression, whereas they increased in the periischemic area, with a peak at 21 days, with ApoE mRNA expression in glial cells but not in neurons. On the other hand, ApoE plus ED1 double‐positive cells increased only in the core, with a peak in number at 7 and 21 days and marked ApoE mRNA expression in macrophages. The present study suggests that ApoE plays various important roles in different type of cells, reflecting spatiotemporal dissociation between degenerative and regenerative processes after brain ischemia, and that ApoE is profoundly involved in pathological conditions, such as brain ischemia. © 2003 Wiley‐Liss, Inc.
Potential roles of Alzheimer precursor protein A4 and β‐amyloid in survival and function of aged spinal motor neurons after axonal injury
Authors: Xie Yuanyun , Yao Zhibin , Chai Hong , Wong Wai‐Man , Wu Wutian 
Published: July 2003

AbstractTo study the potential role of Alzheimer precursor protein A4 (APP) and β‐amyloid (A/β) on aging motor neuron survival, expression of APP, A/β, and choline acetyltransferase (ChaT) were investigated in aged rats after either distal axotomy or root avulsion injury. Approximately 45% in number of total aged spinal motor neuron were normally APP‐positive. A/β‐positive neurites were observed normally in the spinal ventral horn of aged rats. After distal axotomy, without apparent neurodegeneration such as cell loss and decreased ChaT‐immunoreactivity, increased levels of APP expression were observed in the spinal cords of aged rats post‐injury. In contrast, after avulsion, expression of APP and A/β were downregulated in the spinal ventral horn of aged rats, and marked loss of spinal motor neurons and downregulated ChaT expression were observed. Our data indicate that APP and A/β might play beneficial roles in neuronal survival of aged spinal motor neurons after axonal injury. © 2003 Wiley‐Liss, Inc.
Administration of the p38 MAPK inhibitor SB203580 affords brain protection with a wide therapeutic window against focal ischemic insult
Authors: Piao Chun Shu , Kim Jung‐Bin , Han Pyung‐Lim , Lee Ja‐Kyeong 
Published: July 2003

AbstractWe have reported previously the delayed and differential induction of p38α and p38β mitogen‐activated protein kinases (MAPKs) in microglia and astrocytes, respectively, in brain after transient global ischemia. We report here the sustained induction and activation of p38α MAPK in activating microglia in rat brain after transient middle cerebral artery occlusion (MCAO). The intraventricular administration of SB203580, a p38 MAPK inhibitor, 30 min before MCAO reduced the infarct volume to 50% of the control, which was accompanied by the significant improvement of neurological deficits. More interestingly, the infarct volume was reduced to 72% and 77% when SB203580 was administered 6 hr and 12 hr after MCAO, respectively. The induction of various factors involved in inflammatory processes, such as inducible nitric oxide synthase (iNOS), tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β) and cyclooxygenase‐2 (COX‐2), was suppressed by the administration of SB203580 at 6 hr after MCAO. These results suggest that sustained activation of p38 MAPK pathway and p38 MAPK‐associated inflammatory processes play a crucial role in postischemic brain. © 2003 Wiley‐Liss, Inc.
FGF‐2 modulates expression and distribution of GAP‐43 in frog retinal ganglion cells after optic nerve injury
Authors: Soto Ileana , Marie Bruno , Baro Deborah J. , Blanco Rosa E. 
Published: July 2003

AbstractBasic fibroblast growth factor (bFGF or FGF‐2) has been implicated as a trophic factor that promotes survival and neurite outgrowth of neurons. We found previously that application of FGF‐2 to the proximal stump of the injured axon increases retinal ganglion cell (RGC) survival. We determine here the effect of FGF‐2 on expression of the axonal growth‐associated phosphoprotein (GAP)‐43 in retinal ganglion cells and tectum of Rana pipiens during regeneration of the optic nerve. In control retinas, GAP‐43 protein was found in the optic fiber layer and in optic nerve; mRNA levels were low. After axotomy, mRNA levels increased sevenfold and GAP‐43 protein was significantly increased. GAP‐43 was localized in retinal axons and in a subset of RGC cell bodies and dendrites. This upregulation of GAP‐43 was sustained through the period in which retinal axons reconnect with their target in the tectum. FGF‐2 application to the injured nerve, but not to the eyeball, increased GAP‐43 mRNA in the retina but decreased GAP‐43 protein levels and decreased the number of immunopositive cell bodies. In the tectum, no treatment affected GAP‐43 mRNA but FGF‐2 application to the axotomized optic nerve increased GAP‐43 protein in regenerating retinal projections. We conclude that FGF‐2 upregulates the synthesis and alters the distribution of the axonal growth‐promoting protein GAP‐43, suggesting that it may enhance axonal regrowth. © 2003 Wiley‐Liss, Inc.
Expression and subcellular localization of Ror tyrosine kinase receptors are developmentally regulated in cultured hippocampal neurons
Authors: Paganoni Sabrina , Ferreira Adriana 
Published: July 2003

AbstractRor1 and Ror2 are two novel receptor tyrosine kinases that have been implicated in neuronal differentiation in Caenorhabditis elegans. As a first step toward elucidating their role in the mammalian brain, we analyzed their expression and localization patterns in hippocampal neurons. Our results showed that both receptors are expressed from early stages of development and that their protein levels peak during periods of active synapse formation. Immunocytochemical analysis indicated that Ror1 and Ror2 are highly concentrated in the growth cones of immature neurons and are present throughout the somatodendritic compartment of mature hippocampal cells. Further analysis indicated that they are present not only in the cell membrane but also in Triton‐ and saponin‐insoluble fractions, suggesting that they may be associated with both the cytoskeleton and membrane‐bound organelles. Taken collectively, our results suggest that Ror1 and Ror2 might play a role during early stages of development in mammalian central neurons. © 2003 Wiley‐Liss, Inc.
Dysregulation of axonal sodium channel isoforms after adult‐onset chronic demyelination
Authors: Rasband Matthew N. , Kagawa Tetsushi , Park Eunice W. , Ikenaka Kazuhiro , Trimmer James S. 
Published: July 2003

AbstractDemyelination results in conduction block through changes in passive cable properties of an axon and in the expression and localization of axonal ion channels. We show here that adult‐onset chronic demyelination, such as occurs in demyelinating disorders and after nerve injury, alters the complement of axonal voltage‐dependent Na+ (Nav) channel isoforms and their localization. As a model, we used heterozygous transgenic mice with two extra copies of the proteolipid protein gene (Plp/−). Retinal ganglion cell axons in these mice myelinate normally, with young Plp/− and wild‐type mice expressing Nav1.2 at low levels, whereas Nav1.6 is clustered in high densities at nodes of Ranvier. At 7 months of age, however, Plp/− mice exhibit severe demyelination and oligodendrocyte cell death, leading to a profound reduction in Nav1.6 clusters, loss of the paranodal axoglial apparatus, and a marked increase in Nav1.2. We conclude that myelin is crucial not only for node of Ranvier formation, but also to actively maintain the proper localization and complement of distinct axonal Nav channel isoforms throughout life. The altered Nav channel isoform localization and complement induced by demyelination may contribute to the pathophysiology of demyelinating disorders and nerve injury. © 2003 Wiley‐Liss, Inc.
Hyperalgesic effects of γ‐aminobutyric acid transporter I in mice
Authors: Hu Jia‐Hua , Yang Na , Ma Ying‐Hua , Zhou Xiao‐Gang , Jiang Jie , Duan Shu‐hui , Mei Zhen‐Tong , Fei Jian , Guo Li‐He 
Published: July 2003

AbstractThe present study focused on the involvement of γ‐aminobutyric acid transporter I (GAT1) in pain. We found that GABA uptake was increased in mouse spinal cord at 20 min and 120 min after formalin injection and in mouse brain at 120 min, but not 20 min, after formalin injection. In addition, the antinociceptive effects of GAT1‐selective inhibitors were examined using assays of thermal (tail‐flick) and chemical (formalin and acetic acid) nociception in C57BL/6J mice. The GAT1‐selective inhibitors, ethyl nipecotate and NO‐711, exhibited significant antinociceptive effects in these nociceptive assays. To study further the effects of GAT1 on pain, we used two kinds of GAT1‐overexpressing transgenic mice (under the control of a CMV promoter or a NSE promoter) to examine the nociceptive responses in these mice. In the thermal, formalin, and acetic acid assays, both kinds of transgenic mice displayed significant hyperalgesia after nociceptive stimuli. In addition, the μ opioid receptor antagonist naloxone had no influence on nociceptive responses in wild‐type and transgenic mice. The results indicate that GAT1 is involved in the regulation of pain processes, and point to the possibility of developing analgesic drugs that target GAT1 other than opioid receptors. © 2003 Wiley‐Liss, Inc.
Expression of 2′,3′‐cyclic nucleotide 3′‐phosphodiesterase (CNPase) in the developing olfactory bulb and subventricular zone rostral extension
Authors: Gomes Silvana S. , Carvalho Sergio L. , Santiago Marcelo F. , Lopez Luciane B. , Barradas Penha C. , Cavalcante Leny A. 
Published: July 2003

AbstractThe olfactory bulb (OB) presents a unique pattern of permanent acquisition of primary afferents and interneurons, but not much detail is known about the differentiation of its oligodendroglial cells. We studied the expression of 2′,3′‐cyclic nucleotide 3′‐phosphodiesterase (CNPase), a protein related to axonal ensheathment by myelinating cells. Expression of CNPase in OB follows a general caudorostral gradient, with the exception of the glomerular layer (GL). At postnatal day 5–6 (P5–P6), the first CNPase+ profiles appeared in the dorsal lateral olfactory tract adjacent to the accessory OB (AOB), followed by rare cell bodies and processes in AOB internal plexiform layer at P7. At P9, the main OB (MOB) granular cell layer (GrCL) already showed intensely stained CNPase+ processes. From P5 to P12, small numbers of CNPase+ cells were found in the subventricular zone (SVZ), throughout its rostral extension (SVZ‐RE), and in the intrabulbar subependymal layer. The appearance of CNPase+ profiles delimiting glomeruli started in the GL rostralmost region at P12, extending to all GL levels, but glomeruli remained open caudally at P15. At P18, oligodendroglial glomeruli were evident throughout OB, but the adult pattern was established only after P30. There was no age‐related loss of CNPase immunoreactivity in glial cell bodies, possibly indicating de novo ensheathment of neurites. Our results show an earlier onset of oligodendroglial differentiation in OB than previously reported and a rostrocaudal gradient of formation of oligodendroglial glomeruli. They also raise the possibility that a minor fraction of OB oligodendrocytes might derive from the SVZ‐RE. © 2003 Wiley‐Liss, Inc.
Microarray analysis of gene expression in proliferating Schwann cells: Synergistic response of a specific subset of genes to the mitogenic action of heregulin plus forskolin
Authors: Schworer Charles M. , Masker Kathryn K. , Wood G. Craig , Carey David J. 
Published: July 2003

AbstractCultured Schwann cells treated with heregulin growth factor require costimulation with a cyclic adenosine monophosphate‐elevating agent to produce maximal cell proliferation. Gene chip expression analysis was used to identify genes that are induced or repressed when Schwann cells are treated with heregulin and/or forskolin. By utilizing arrays that contained 8,799 probes, the expression of over 1,000 genes was found to be significantly changed after 30 hr of treatment with heregulin, forskolin, or heregulin plus forskolin. Hierarchical clustering revealed groups of genes with distinct expression patterns. Of particular interest was a cluster of 140 genes that were up‐regulated by heregulin plus forskolin but not by heregulin or forskolin alone. Many of the genes in this group have roles in cell division, such as cyclin B, cyclin D3, E2F‐5, cdc 25B, polo‐like kinase, and protein kinase C type III. These findings identify a profile of gene expression for Schwann cell proliferation. © 2003 Wiley‐Liss, Inc.
Astrocyte‐targeted expression of interleukin‐6 protects the central nervous system during neuroglial degeneration induced by 6‐aminonicotinamide
Authors: Penkowa Milena , Camats Jordi , Hadberg Hanne , Quintana Albert , Rojas Santiago , Giralt Mercedes , Molinero Amalia , Campbell Iain L. , Hidalgo Juan 
Published: July 2003

Abstract6‐Aminonicotinamide (6‐AN) is a niacin antagonist, which leads to degeneration of gray matter astrocytes mainly in the brainstem. We have examined the role of interleukin‐6 (IL‐6) in this degenerative process by using transgenic mice with astrocyte‐targeted IL‐6 expression (GFAP‐IL6 mice). This study demonstrates that transgenic IL‐6 expression significantly increases the 6‐AN‐induced inflammatory response of reactive astrocytes, microglia/macrophages, and lymphocytes in the brainstem. Also, IL‐6 induced significant increases in proinflammatory cytokines IL‐1, IL‐12, and tumor necrosis factor‐α as well as growth factors basic fibroblast growth factor (bFGF), transforming growth factor‐β, neurotrophin‐3, angiopoietin, vascular endothelial growth factor, and the receptor for bFGF. In accordance, angiogenesis was increased in GFAP‐IL6 mice relative to controls after 6‐AN. Moreover, oxidative stress and apoptotic cell death were significantly reduced by transgenic IL‐6 expression. IL‐6 is also a major inducer in the CNS of metallothionein I and II (MT‐I+II), which were significantly increased in the GFAP‐IL6 mice. MT‐I+II are antioxidants and neuroregenerative factors in the CNS, so increased MT‐I+II levels in GFAP‐IL6 mice could contribute to the reduction of oxidative stress and cell death in these mice. © 2003 Wiley‐Liss, Inc.