bluuebunny/crossref_metadata_2025_split huggingface dataset:
Twenty‐first‐century check clearing: Are you ready?
Authors: Burnie David A. , Hurtt David , Langsam Sheldon A. 
Published: October 2004

AbstractThe terrorist attacks of 9/11 showed how easy it was to severely disrupt our banking system. The grounding of air flights delayed the transportation
of millions of checks—causing the Federal Reserve Bank's check float to balloon to more than 100 times its normal level.To protect our banking system, Congress passed the Check 21 Act. But what will be the impact on businesses, consumers, and financial institutions? What potential problems will companies face? And what steps can you take to get ready for Check 21? The authors take a close look at these issues and provide some answers. © 2004 Wiley Periodicals, Inc.
Finding cash in the back office
Authors: Reder Dan 
Published: October 2004

AbstractNew approaches to treasury management not only improve cash flow and simplify accounting—they can also save you a lot of money and significantly reduce risk. Improved contract management (CM) software, states the author, offers a high yield and quick payback for treasury managers eager to cut costs. The author explains how CM software works and what to look for when you shop for it. © 2004 Wiley Periodicals, Inc.
Capitalizing interest: What does “material” mean?
Authors: Jordan Charles E. , Clark Stanley J. 
Published: October 2004

AbstractSFAS 34 requires the capitalization of interest as part of the cost of certain assets if the effects of capitalization are deemed material. Yet, U.S. professional standards provide virtually no guidance on what constitutes a material effect. The authors took a close look at recent research and current practice and came up with some simple materiality guidelines for interest capitalization. CEOs and CFOs are now required to certify financial statements; this is enforced with criminal penalties under Sarbanes‐Oxley. So they should read this article carefully. © 2004 Wiley Periodicals, Inc.
Performance management—Making it work
Authors: Cokins Gary 
Published: October 2004

AbstractSenior managers are often frustrated at their lack of direct control. After all, managers can bring about improvement only by influencing their employees, who sometimes don't manage to do what's best for the company as a whole. The solution to this dilemma is performance management, which provides managers and employee teams at all levels the ability to move directly toward their defined strategies. © 2004 Wiley Periodicals, Inc.
Evaluation of intrarenal oxygenation by BOLD MRI at 3.0T
Authors: Li Lu‐Ping , Vu Anthony T. , Li Belinda S.Y. , Dunkle Eugene , Prasad Pottumarthi V. 
Published: October 2004

AbstractPurposeTo examine the benefit of using higher field strengths for BOLD MRI to detect changes in renal medullary oxygenation following pharmacological maneuvers.Materials and MethodsRenal BOLD MRI, primarily at 1.5T, has been shown to be useful for monitoring changes in medullary oxygenation status. We performed the present studies on a 3.0T scanner using a multiple gradient‐echo (mGRE) sequence with a multicoil array to acquire 16 T2*‐weighted images within a single breath‐hold. Data were obtained before and after administration of furosemide (20 mg iv).ResultsThe baseline renal R2* (mean ± SE) at 3.0T was 37.4±1.2 Hz in the medulla, and 21.8 ± 1.2 Hz in the cortex. The BOLD response to furosemide (ΔR2*) at 3.0T was 11.8 ± 1.1 Hz in the medulla, and 3.0 ± 0.5 Hz in the cortex.ConclusionHigher magnetic field strength is beneficial for renal BOLD MRI studies. The cortico‐medullary contrast on the R2* map was significantly improved at 3.0T, with no evidence of increased bulk susceptibility artifacts. Baseline R2* and ΔR2* in the renal medulla at 3.0T were both significantly higher compared to our previously reported data obtained at 1.5T. J. Magn. Reson. Imaging 2004;20:901–904. © 2004 Wiley‐Liss, Inc.
Respiratory reordered UNFOLD perfusion imaging
Authors: Ablitt Nicholas A. , Gatehouse Peter D. , Firmin David N. , Yang Guang‐Zhong 
Published: October 2004

AbstractPurposeTo propose a respiratory reordered UNFOLD (RR‐UNFOLD) imaging sequence to significantly reduce the amount of k‐space data required for first‐pass MR myocardial perfusion imaging.Materials and MethodsRapid acquisition of high‐resolution imaging data is essential to detailed quantitative analysis of first‐pass myocardial perfusion. Existing MR sequences have explored the full capacity of the imaging hardware to reduce the acquisition window within each cardiac cycle while maintaining the desired spatial resolution. Further improvement in perfusion imaging will require a more efficient use of the information content of the k‐space data. The method uses prospective diaphragmatic navigator echoes to ensure that temporal filtering of UNFOLD is carried out on a series of images that are spatially registered. An adaptive real‐time rebinning algorithm is developed for the creation of static image subseries related to different levels of respiratory motion. Issues concerning the temporal smoothing of tracer kinetic signals are discussed, and a solution based on oversampling of the central k‐space is provided. The method is assessed in 10 normal subjects without the administration of contrast agent, and further validated by administration of Gd‐DTPA in 10 patients at rest.ResultsThe results of this study show that RR‐UNFOLD significantly extends the applicability of UNFOLD to perfusion imaging, which yields a 40% reduction in image artifact when the same amount of k‐space information is used.ConclusionThe scan efficiency achieved can be used in combination with MR hardware improvements for extending the three‐dimensional spatial coverage and shortening the data acquisition window to provide detailed information on regional myocardial perfusion abnormalities. J. Magn. Reson. Imaging 2004;20:817–825. © 2004 Wiley‐Liss, Inc.
Magnetic resonance imaging of knee cartilage using a water selective balanced steady‐state free precession sequence
Authors: Kornaat Peter R. , Doornbos Joost , van der Molen Aart J. , Kloppenburg Margreet , Nelissen Rob G. , Hogendoorn Pancras C.W. , Bloem Johan L. 
Published: October 2004

AbstractPurposeTo compare an optimized water selective balanced steady‐state free precession sequence (WS‐bSSFP) with conventional magnetic resonance (MR) sequences in imaging cartilage of osteoarthritic knees.Materials and MethodsFlip angles of sagittal and axial WS‐bSSFP sequences were optimized in three volunteers. Subsequently, the knees of 10 patients with generalized osteoarthritis were imaged using sagittal and axial WS‐bSSFP and conventional MR imaging techniques. We calculated contrast‐to‐noise ratios (CNR) between cartilage and its surrounding tissues to quantitatively analyze the various sequences. Using dedicated software we compared, in two other patients, the accuracy of cartilage volume measurements with anatomic sections of the tibial plateau.ResultsCNRtotal eff (CNR efficiency between cartilage and its surrounding tissue) using WS‐bSSFP was maximal with a 20–25° flip angle. CNRtotal eff was higher in WS‐bSSFP than in conventional images: 6.1 times higher compared to T1‐weighted gradient echo (GE) images, 5.1 compared to proton‐density (PD) fast spin echo (FSE) images, and 4.8 compared to T2‐weighted FSE images. The mean difference of cartilage volume measurement on WS‐bSSFP and anatomic sections was 0.06 mL compared to 0.24 mL for T1‐GE and anatomic sections.ConclusionA WS‐bSSFP sequence is superior to conventional MR imaging sequences in imaging cartilage of the knee in patients with osteoarthritis. J. Magn. Reson. Imaging 2004;20:850–856. © 2004 Wiley‐Liss, Inc.
Dynamic near‐real‐time magnetic resonance imaging for analyzing the velopharyngeal closure in comparison with videofluoroscopy
Authors: Beer Ambros J. , Hellerhoff Paul , Zimmermann Angela , Mady Katalin , Sader Robert , Rummeny Ernst J. , Hannig Christian 
Published: October 2004

AbstractPurposeTo demonstrate the feasibility of dynamic magnetic resonance imaging (MRI) with near‐real‐time temporal resolution (“real‐time MRI”) for analyzing the velopharyngeal closure in comparison with multiview videofluoroscopy.Materials and MethodsSeven patients (three females and four males, 5–21 years old, mean age = 11.3 years) with suspected velopharyngeal insufficiency, and one healthy volunteer were examined with videofluoroscopy and real‐time MRI using a turbo‐spin‐echo (TSE) sequence (TR = 170 msec, TE = 21 msec, slice thickness = 6 mm, six images per second). Imaging was done during phonation in all three image planes. The results were analyzed by two radiologists in comparison with videofluoroscopy as the standard of reference for overall image quality and the pattern of velopharyngeal closure.ResultsReal‐time MRI correctly depicted the pattern of velopharyngeal closure in correspondence to videofluoroscopy in all cases. Concerning the movement of the pharyngeal walls, real‐time MRI falsely depicted a general movement of the dorsal pharyngeal wall in one case, whereas videofluoroscopy showed no movement. In one patient, real‐time MRI provided additional information by showing an asymmetric movement of the lateral pharyngeal walls that could not be depicted by videofluoroscopy due to technical limitations. Concerning image quality, the coronal plane was more difficult to evaluate with real‐time MRI compared to videofluoroscopy. The axial plane was easier to analyze in real‐time MRI compared to videofluoroscopy.ConclusionReal‐time MRI has the potential to depict the pattern of velopharyngeal closure in close correlation with videofluoroscopy, and may deliver additional information in selected cases. J. Magn. Reson. Imaging 2004;20:791–797. © 2004 Wiley‐Liss, Inc.
Profound increase in sensitivity to glutamatergic‐ but not cholinergic agonist‐induced seizures in transgenic mice with astrocyte production of IL‐6
Authors: Samland Helen , Huitron‐Resendiz Salvador , Masliah Eliezer , Criado Jose , Henriksen Steven J. , Campbell Iain L. 
Published: October 2004

AbstractTransgenic mice with glial fibrillary acidic protein (GFAP) promoter driven‐astrocyte production of the cytokines interleukin‐6 (IL‐6) and tumor necrosis factor (TNF) were used to determine whether the pre‐existing production of these cytokines in vivo might modulate the sensitivity of neurons to excitotoxic agents. Low doses of kainic acid (5 mg/kg) that produced little or no behavioral or electroencephalogram (EEG) alterations in wild type or glial fibrillary acidic protein (GFAP)‐TNF animals induced severe tonic‐clonic seizures and death in GFAP‐IL6 transgenic mice of 2 or 6 months of age. GFAP‐IL6 mice were also significantly more sensitive to N‐methyl‐D‐aspartate (NMDA)‐ but not pilocarpine‐induced seizures. Kainic acid uptake in the brain of the GFAP‐IL6 mice was higher in the cerebellum but not in other regions. Kainic acid binding in the brain of GFAP‐IL6 mice had a similar distribution and density as wild type controls. In the hippocampus of GFAP‐IL6 mice that survived low dose kainic acid, there was no change in the extent of either neurodegeneration or astrocytosis. Immunostaining revealed degenerative changes in gamma aminobutyric acid (GABA)‐ and parvalbumin‐positive neurons in the hippocampus of 2‐month‐old GFAP‐IL6 mice which progressed to the loss of these cells at 6 months of age. Thus, GFAP‐IL6 but not GFAP‐TNF mice showed markedly enhanced sensitivity to glutamatergic‐ but not cholinergic‐induced seizures and lethality. This may relate, in part, to a compromise of inhibitory interneuron function. Therefore, pre‐existing IL‐6 production and inflammation in the central nervous system (CNS) not only causes spontaneous neurodegeneration but also synergizes with other neurotoxic insults to induce more severe acute functional neurological impairment. © 2003 Wiley‐Liss, Inc.
Characterisation of a sphingosine 1‐phosphate‐activated Ca2+ signalling pathway in human neuroblastoma cells
Authors: Villullas Israel Ramos , Smith Alison J. , Heavens Robert P. , Simpson Peter B. 
Published: October 2004

AbstractSphingosine 1‐phosphate (S1P) has assumed great importance within neuroscience research because of putative links between S1P‐sensitive Edg receptors and neuroregeneration, cell survival, and alterations in neurite outgrowth. In the present study, we examined the mechanisms by which the endogenous complement of S1P‐sensitive human Edg receptors can elevate Ca2+ in the human neuroblastoma cell line, SH‐SY5Y. Reverse transcriptase‐polymersase chain reaction (RT‐PCR) confirmed the expression of mRNA for Edg 3, 5, and 8 subtypes of S1P‐responsive Edg receptors in SH‐SY5Y cells. Neither S1P nor the muscarinic agonist methacholine were able to cause a change in SH‐SY5Y cell morphology, whereas retinoic acid caused a range of changes, including an increase in neurite outgrowth, under similar test conditions. Stimulation with S1P resulted in a slowly rising increase in cytosolic Ca2+ levels. These responses were dependent upon inositol‐1,4,5‐trisphosphate receptors, thapsigargin‐sensitive endoplasmic reticulum, and also intact functional mitochondria. S1P‐evoked Ca2+ responses were similar in mechanism to those of methacholine, which activated a much faster responding, larger amplitude Ca2+ response. These studies indicate that in an endogenous human expression system, S1P appears to be an efficacious agonist of Edg receptors. Despite its slow time course of response, S1P appears to activate the same single Ca2+ store in SH‐SY5Y cells as is activated by methacholine and other G protein coupled receptors. © 2003 Wiley‐Liss, Inc.
Presenilin 1 mediates retinoic acid‐induced differentiation of SH‐SY5Y cells through facilitation of Wnt signaling
Authors: Uemura Kengo , Kitagawa Naoyuki , Kohno Ryuichi , Kuzuya Akira , Kageyama Takashi , Shibasaki Hiroshi , Shimohama Shun 
Published: October 2004

AbstractPresenilin 1 interacts with β‐catenin, an essential component of the Wnt signaling pathway. To elucidate the role of presenilin 1‐β‐catenin interaction in neuronal differentiation, we established SH‐SY5Y cells stably expressing wild‐type presenilin 1, P117L mutant presenilin 1, which is linked to the early‐onset familial form of Alzheimer's disease, and D385A mutant presenilin 1, which has no aspartyl proteinase activity. We demonstrate that SH‐SY5Y cells stably expressing D385A mutant presenilin 1 failed to differentiate in response to retinoic acid treatment. Retinoic acid caused an increase in nuclear β‐catenin levels in SH‐SY5Y cells, which was followed by an increase in cyclin D1 protein levels. Abnormal cellular accumulation of β‐catenin was observed in D385A mutant transfected cells, whereas nuclear β‐catenin and cellular cyclin D1 levels failed to increase. Conversely, SH‐SY5Y cells expressing the P117L mutant differentiated normally and showed increased nuclear β‐catenin and cellular cyclin D1 levels. These findings suggest that neuronal differentiation of SH‐SY5Y cells involves the Wnt signaling pathway and that presenilin 1 plays a crucial role in Wnt signal transduction by regulating the nuclear translocation of β‐catenin. © 2003 Wiley‐Liss, Inc.
ERK and SAPK signaling in auditory brainstem neurons after unilateral cochlear ablation
Authors: Suneja Sanoj K. , Potashner Steven J. 
Published: October 2004

AbstractUnilateral cochlear ablation (UCA) in adults deafferented one cochlear nucleus (CN) and induced several plasticities in central auditory pathways. To assess whether signal transduction could contribute to these changes, we determined if UCA induced activity in the extracellular signal‐regulated kinase (ERK) and the stress‐activated protein kinase (SAPK) signal transduction pathways. Using Western blots, we measured phosphorylated ERK1 (ERK1‐P), ERK2 (ERK2‐P), p46 and p54 SAPK (SAPK‐P) and c‐Jun (c‐Jun‐P) levels in the major subdivisions of the CN, the principal nuclei of the superior olivary complex (SOC) and the central nucleus of the inferior colliculus (ICc) for up to 145 days postablation. ERK1‐P and ERK2‐P were typically elevated at 7 and 145 days but depressed at 30 days, 60 days, or both. In addition, ERK1‐P and ERK2‐P were elevated at 3 days in the anteroventral (AVCN) and posteroventral CN (PVCN). Immunohistochemical labeling indicated that after 5 days, most ERK1/2‐P in the CN was in neuronal nuclei. Only minor changes were evident in total ERK1 and ERK2 levels. Several correlations were evident between the postablation plasticities observed previously and altered ERK1‐P and ERK2‐P levels. Few changes were found in SAPK‐P and c‐Jun‐P levels. Concomitant elevations of SAPK‐P and c‐Jun‐P were not evident, except in the superficial dorsal CN (DCN) at postablation day 3, consistent with a cell‐stress response. These findings suggest that signals induced as a consequence of UCA are transduced mainly through the neuronal ERK pathway. This activity probably influenced gene expression and cytoplasmic regulatory mechanisms that contributed to the plasticities induced by UCA. © 2003 Wiley‐Liss, Inc.
Pyruvate protection against β‐amyloid‐induced neuronal death: Role of mitochondrial redox state
Authors: Alvarez Gema , Ramos Milagros , Ruiz Francisca , Satrústegui Jorgina , Bogónez Elena 
Published: October 2004

AbstractThe mechanism by which β‐amyloid protein (Aβ) causes degeneration in cultured neurons is not completely understood, but several lines of evidence suggest that Aβ‐mediated neuronal death is associated with an enhanced production of reactive oxygen species (ROS) and oxidative damage. In the present study, we address whether supplementation of glucose‐containing culture media with energy substrates, pyruvate plus malate (P/M), protects rat primary neurons from Aβ‐induced degeneration and death. We found that P/M addition attenuated cell death evoked by β‐amyloid peptides (Aβ25–35 and Aβ1–40) after 24 hr treatment and that this effect was blocked by α‐ciano‐3‐hydroxycinnamate (CIN), suggesting that it requires mitochondrial pyruvate uptake. P/M supply to control and Aβ‐treated neuronal cultures increases cellular reducing power, as indicated by the ability to reduce the dye 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT). The early increases in ROS levels, measured by dichlorofluorescein (DCF) fluorescence, and caspase‐3 activity that follow exposure to Aβ were notably reduced in the presence of P/M. These results place activation of caspase‐3 most likely downstream of oxidative damage to the mitochondria and indicate that mitochondrial NAD(P) redox status plays a central role in the neuroprotective effect of pyruvate. Inhibition of respiratory chain complexes and mitochondrial uncoupling did not block the early increase in ROS levels, suggesting that Aβ could initiate oxidative stress by activating a source of ROS that is not accesible to the antioxidant defenses fueled by mitochondrial substrates. © 2003 Wiley‐Liss, Inc.
Protective role of the cytokine‐inducible isoform of nitric oxide synthase induction and nitrosative stress in experimental autoimmune encephalomyelitis of the DA rat
Authors: Kahl Kai G. , Zielasek Jürgen , Uttenthal L. Otto , Rodrigo Jose , Toyka Klaus V. , Schmidt Harald H.H.W. 
Published: October 2004

AbstractThe pathogenic role of nitric oxide (NO) in multiple sclerosis (MS) remains controversial. Some groups have reported a pathogenic role of NO in experimental autoimmune encephalomyelitis (EAE), an animal model of some aspects of MS, whereas we and others have found a disease‐suppressive effect of NO in EAE. Because the previously used EAE models have a mainly monophasic inflammatory disease course, distinct from MS, we here studied EAE in the DA rat, which better models the demyelinating and relapsing disease course of human MS. The induction of EAE in DA rats led to 1) severe inflammatory infiltrates mainly in the lumbar spinal cord; 2) an up‐regulation of the activity of the cytokine‐inducible isoform of NO synthases (NOS‐II); and 3) increased tissue protein tyrosine nitration, as indicated by peroxynitrite (ONOO−), as a marker of nitrosative stress. Sources of superoxide metabolism, i.e., NADPH oxidase, myeloperoxidase, and superoxide dismutase, remained unchanged. Early treatment of animals with aminoguanidine, a relatively selective inhibitor of NOS‐II, lowered nitrotyrosine immunoreactivity but at the same time led to more severe disease and pronounced inflammatory infiltrates in the lumbar spinal cord. Our results suggest a rather protective role of NOS‐II induction and nitrosative stress in EAE in DA rats and support the hypothesis of a disease‐mitigating immunomodulatory role of NO in this animal model of MS. © 2003 Wiley‐Liss, Inc.
β‐amyloid peptide binding protein does not couple to G protein in a heterologous Xenopus expression system
Authors: Lee Yong , Chang Deok‐Jin , Lee Yong‐Seok , Chang Keun‐A , Kim Hyoung , Yoon Jeung‐Sook , Lee Seungbok , Suh Yoo‐Hun , Kaang Bong‐Kiun 
Published: October 2004

AbstractAlzheimer's disease is a neurodegenerative disorder related to the formation of protein aggregates. β‐Amyloid protein (Aβ), generated by enzymatic cleavage of amyloid precursor protein (APP), can cause such aggregation, and these aggregates may cause neuronal cell death by inducing apoptosis. However, Aβ‐induced intracellular signaling pathways involved in the neuronal death are not well understood. Recently it was shown that Aβ aggregates induce neuronal cell death via β‐amyloid peptide‐binding protein (BBP), a receptor for Aβ in BBP‐transfected cells, which is known to be sensitive to pertussis toxin, a Gαi/o family inhibitor. However, the actual coupling of BBP to the pertussis‐sensitive G protein was not demonstrated. In this study, we performed electrophysiological recordings using the two‐electrode voltage‐clamp technique to test whether human or Drosophila BBPs, singly or in combination with APP, are coupled to a specific type of G protein. Our results suggest that BBP is not directly coupled to Gαi/o, Gαs, or Gαq proteins and that BBP may need a component other than APP to exert its toxic effect in concert with Aβ. © 2003 Wiley‐Liss, Inc.
Diazoxide pretreatment induces delayed preconditioning in astrocytes against oxygen glucose deprivation and hydrogen peroxide‐induced toxicity
Authors: Rajapakse Nishadi , Kis Bela , Horiguchi Takashi , Snipes James , Busija David 
Published: October 2004

AbstractRecent studies suggest that activation of mitochondrial ATP‐sensitive potassium channels (mKATP) with diazoxide can protect neurons against ischemic stress. However, it is not yet known whether astrocytes, which are more resilient against ischemia, respond similarly to diazoxide. We exposed cultured astrocytes to oxygen‐glucose deprivation (OGD) or hydrogen peroxide (H2O2) with or without pretreatment with the mKATP opener diazoxide. Marked decreases in astrocyte viability were evident after 9 and 12 hr of OGD [76% ± 3% (n = 50) and 60% ± 1% (n = 50)] and 400 and 600 μM H2O2 [40% ± 2% (n = 16) and 25% ± 2% (n = 16)], respectively, compared with no treatment (100% ± 1%). Diazoxide treatment (3 days of sequential application) dramatically reversed the negative effects of OGD and H2O2, resulting in complete blockade of astrocyte cell death. Effects of diazoxide were blocked by the mKATP blocker 5‐hydroxydecanoic acid (5‐HD). Furthermore, incubation of astrocytes with diazoxide resulted in loss of mitochondrial membrane potential monitored by tetramethylrhodamineethylester fluorescence. Additionally, generation of reactive oxygen species was observed in response to diazoxide, assessed using the oxidation‐sensitive dye hydroethidine, and this effect was abolished by antioxidants, catalase, and a superoxide dismutase mimetic, M40401. Finally, diazoxide increased the protein level of phosphorylated protein kinase C (PKC) revealed by immunoblot analysis. Our findings demonstrate that opening of mKATP by diazoxide identifies a delayed preconditioning effect that is protective against two types of injury in astrocytes and that diazoxide may deliver protection via mitochondrial depolarization, free radical production, and PKC activation. © 2003 Wiley‐Liss, Inc.