bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hydrogeological aspects of groundwater drainage of the urban areas in Kuwait City
Authors: Al‐Rashed Muhammad F. , Sherif Mohsen M. 
Published: January 2005

AbstractResidential areas in Kuwait City have witnessed a dramatic rise in subsurface water tables over the last three decades. This water rise phenomenon is attributed mainly to over irrigation practices of private gardens along with leakage from domestic and sewage networks. This paper presents a comprehensive study for urban drainage in two selected areas representing the two hydrogeological settings encountered in Kuwait City. In the first area, a vertical drainage scheme was applied successfully over an area of 1 km2. The system has been under continuous operation and monitoring for more than 4 years without problems, providing a permanent solution for the water rise problem in this area. The hydrogeological system has approached steady state conditions and the water levels have dropped to about 3·5 m below the ground surface. In the second area a dual drainage scheme, composing of horizontal and vertical elements, is proposed. Horizontal elements are suggested in the areas where the deep groundwater contains hazardous gases that may pose environmental problems. The proposed drainage scheme in the second area has not yet been implemented. Field tests were conducted to assess the aquifer parameters in both areas and a numerical model has been developed to predict the long‐term response of the hydrogeological system in the two areas under consideration. Copyright © 2001 John Wiley & Sons, Ltd.
The effect of mining and related activities on the sediment–trace element geochemistry of Lake Coeur d'Alene, Idaho, USA. Part III. Downstream effects: the Spokane River Basin
Authors: Grosbois Cecile A. , Horowitz Arthur J. , Smith James J. , Elrick Kent A. 
Published: January 2005

AbstractDuring 1998/1999, surface and subsurface sediment samples were collected along the entire length of the Spokane River from its outlet at the northern end of Lake Coeur d'Alene (CDA), Idaho, to Lake Roosevelt on the Columbia River, Washington. The study was conducted to determine if the trace element enrichments observed in Lake CDA and on the floodplain and in the CDA River extend through the Spokane River Basin (SRB).As in Lake CDA, surface sediments in the SRB are enriched in Pb, Zn, As, Cd, Sb and Hg relative to local background levels. Pb, Cd and Zn are the most elevated, with maximum enrichment occurring in the upper Spokane River in close proximity to Lake CDA. On average, enrichment decreases downstream, apparently reflecting both increased distance from the inferred source (the CDA River Basin), as well as increased dilution by locally derived but unenriched materials. Only Cd and Zn display marked enrichment throughout the SRB. Pb, Zn and Cd seem to be associated mainly with an operationally defined iron oxide phase, whereas the majority of the As and Sb seem to be matrix‐held.Subsurface sediments also are enriched in Pb, Zn, As, Cd, Sb and Hg relative to background levels. Based on 137Cs and excess 210Pb dating, trace element enrichment began in the middle part of the SRB (Long Lake) between 1900 and 1920. This is contemporaneous with similar enrichments observed in Lake CDA, as well as the completion of Long Lake Dam (1913). In the most downstream part of the basin (Spokane River Arm of Lake Roosevelt), enrichment began substantially later, between 1930 and 1940. The temporal difference in enrichment between Long Lake and the River Arm may reflect the latter's greater distance from the presumed source of the enrichment (the CDA River Basin); however, the difference is more likely the result of the completion of Grand Coulee Dam (1934–1941), which formed Lake Roosevelt, backed up the Spokane River, and increased water levels in the River Arm by about 30 m.
Formation of apatite on poly(α‐hydroxy acid) in an accelerated biomimetic process
Authors: Chen Yun , Mak Arthur F. T. , Li Jiashen , Wang Min , Shum Anita W. T. 
Published: January 2005

AbstractBonelike apatite coating was formed on poly(L‐lactic acid) films and poly(glycolic acid) scaffolds within 24 h through an accelerated biomimetic process. The ion concentrations in the simulated body fluid (SBF) were nearly 5 times of those in the human blood plasma. The apatite formed was characterized by using scanning electron microscopy (SEM), energy dispersive X‐ray spectroscopy (EDX), X‐ray diffraction (XRD), and Fourier transform infrared spectroscopy (FTIR). The apatite formed in 5SBFs was similar in morphology and composition to that formed in the classical biomimetic process using SBF or 1.5SBF and similar to that of natural bone. This indicated that the biomimetic apatite‐coating process could be accelerated by using concentrated simulated body fluid at 37°C. Besides saving time, the accelerated biomimetic process is particularly significant to biodegradable polymers. Some polymers that degrade too fast to be coated with apatite by a classical biomimetic process (e.g., PGA) could be coated with bonelike apatite in an accelerated biomimetic process. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 73B: 68–76, 2005
Presence of MUC4 in human milk and at the luminal surfaces of blood vessels
Authors: Zhang Jin , Perez Aymee , Yasin Mohammad , Soto Pedro , Rong Min , Theodoropoulos George , Carothers Carraway Coralie A. , Carraway Kermit L. 
Published: January 2005

AbstractMUC4 is a heterodimeric membrane mucin, composed of a mucin subunit ASGP‐1 (MUC4α) and a transmembrane subunit ASGP‐2 (MUC4β), which has been implicated in the protection of epithelial cell surfaces. Surprisingly, development and characterization of a new monoclonal antibody (mAb), called 1G8, against ASGP‐2 demonstrated by immunohistochemistry the presence of MUC4 at the luminal surfaces of blood vessels of both normal tissues and tumors. Muc4 was detected with 1G8 and other Muc4 antibodies in blood vessels from humans, rats and mice. This expression of MUC4 in endothelial cells was confirmed by immunoblotting with 1G8 in human umbilical vein endothelial cells (HUVECs), human iliac artery endothelial cells (HIAECs), and human microvascular endothelial cells (HMVECs). MUC4 could be observed on HUVECs grown on either plastic or Matrigel. Finally, MUC4 expression in the three types of endothelial cell lines was confirmed by reverse transcription‐polymerase chain reaction (RT‐PCR). These results provide, to our knowledge, the first demonstration of a member of the MUC gene family and membrane mucin in blood vessels. As a luminal surface component, the MUC4 is situated to contribute to the non‐adhesive luminal surface and to act as an intrinsic protection and survival factor. © 2005 Wiley‐Liss, Inc.
Hypoxia/reoxygenation reduces microvascular endothelial cell coupling by a tyrosine and MAP kinase dependent pathway
Authors: Rose Keeley , Ouellette Yves , Bolon Michael , Tyml Karel 
Published: January 2005

AbstractCommunication of electrical signals along the microvascular endothelium plays a key role in integrating microvascular function required for local regulation of blood flow. The aim of the present study was to examine the effect of a short‐term hypoxia (0.1% O2, 1 h) plus reoxygenation (H/R) on electrical coupling in cultured monolayers of microvascular endothelial cells (rat skeletal muscle origin). To assess coupling, we used a current injection technique and a Bessel function model to compute the intercellular resistance (an inverse measure of coupling) and cell membrane resistivity (a measure of resistance to current leakage across the cell membrane). H/R resulted in rapid (within 4 min after reoxygenation) and sustained (up to 100 min) reduction in intercellular coupling, but it did not alter membrane resistivity. H/R did not alter gap junction protein connexin 43 expression nor its tyrosine phosphorylation as determined by immunoblot and immunoprecipitation analyses. Inhibition of mitochondrial respiration (1 mM NaCN) did not mimic the effect of H/R. However, pre‐treatment of monolayers with tyrphostin A48 (1.5 μM), PP2 (10 nM) (tyrosine kinase inhibitors), U 0126 (20 μM), and PD 98059 (5 μM) (MEK1/2 inhibitors) inhibited the H/R‐induced reduction in coupling. These results indicate that endothelial cell coupling was reduced quickly after reoxygenation, via activation of a tyrosine and MAP kinase dependent pathway. We predict that a short‐term H/R can rapidly compromise microvascular function in terms of reduced cellular communication along the vascular wall. © 2005 Wiley‐Liss, Inc.
Sodium ascorbate (vitamin C) induces apoptosis in melanoma cells via the down‐regulation of transferrin receptor dependent iron uptake
Authors: Kang Jae Seung , Cho Daeho , Kim Young‐In , Hahm Eunsil , Kim Yeong Seok , Jin Shun Nu , Kim Ha Na , Kim Daejin , Hur Daeyoung , Park Hyunjeong , Hwang Young Il , Lee Wang Jae 
Published: January 2005

AbstractSodium ascorbate (vitamin C) has a reputation for inconsistent effects upon malignant tumor cells, which vary from growth stimulation to apoptosis induction. Melanoma cells were found to be more susceptible to vitamin C toxicity than any other tumor cells. The present study has shown that sodium ascorbate decreases cellular iron uptake by melanoma cells in a dose‐ and time‐dependent fashion, indicating that intracellular iron levels may be a critical factor in sodium ascorbate‐induced apoptosis. Indeed, sodium ascorbate‐induced apoptosis is enhanced by the iron chelator, desferrioxamine (DFO) while it is inhibited by the iron donor, ferric ammonium citrate (FAC). Moreover, the inhibitory effects of sodium ascorbate on intracellular iron levels are blocked by addition of transferrin, suggesting that transferrin receptor (TfR) dependent pathway of iron uptake may be regulated by sodium ascorbate. Cells exposed to sodium ascorbate demonstrated down‐regulation of TfR expression and this precedes sodium ascorbate‐induced apoptosis. Taken together, sodium ascorbate‐mediated apoptosis appears to be initiated by a reduction of TfR expression, resulting in a down‐regulation of iron uptake followed by an induction of apoptosis. This study demonstrates the specific mechanism of sodium ascorbate‐induced apoptosis and these findings support future clinical trial of sodium ascorbate in the prevention of human melanoma relapse. © 2005 Wiley‐Liss, Inc.
Application of the TLM technique to integrated optic component modelling
Authors: Jacquin O. , Ndagijimana F. , Cachard A. , Benech P. 
Published: January 2005

AbstractThe TLM algorithm is of high interest to simulate new integrated optical devices as a ‘photonic band gap’ (PBG) structures. These components are realized with semiconductor material and constituted by a set of abrupt optical discontinuities. The electromagnetic behaviour of these structures does not allow the use of usual simulation methods of integrated optics. Indeed, their validity conditions are not satisfied. Then, we have to use unusual simulation method for integrated optics as TLM software which allows the visualization and understanding of the behaviour of electromagnetic field in the PBG structures. In this paper, the simulation results of different optical devices made from the TLM method are presented. Copyright © 2001 John Wiley & Sons, Ltd.
γ‐Glutamylcysteine ethyl ester protection of proteins from Aβ(1–42)‐mediated oxidative stress in neuronal cell culture: A proteomics approach
Authors: Boyd‐Kimball Debra , Sultana Rukhsana , Poon H. Fai , Mohmmad‐Abdul Hafiz , Lynn Bert C. , Klein Jon B. , Butterfield D. Allan 
Published: January 2005

AbstractProtein oxidation mediated by amyloid β‐peptide (1–42) (Aβ[1–42]) has been proposed to play a central role in the pathogenesis of Alzheimer's disease (AD), a neurodegenerative disorder associated with aging and the loss of cognitive function. The specific mechanism by which Aβ(1–42), the primary component of the senile plaque and a pathologic hallmark of AD, contributes to the oxidative damage evident in AD brain is unknown. Moreover, the specific proteins that are vulnerable to oxidative damage induced by Aβ(1–42) are unknown. Identification of such proteins could contribute to our understanding of not only the role of Aβ(1–42) in the pathogenesis of AD, but also provide insight into the mechanisms of neurodegeneration at the protein level in AD. We report the proteomic identification of two proteins found to be oxidized significantly in neuronal cultures treated with Aβ(1–42): 14‐3‐3ζ and glyceraldehyde‐3‐phosphate dehydrogenase. We also report that pretreatment of neuronal cultures with γ‐glutamylcysteine ethyl ester, a compound that supplies the limiting substrate for the synthesis of glutathione and results in the upregulation of glutathione in neuronal cultures, protects both proteins against Aβ(1–42)‐mediated protein oxidation. © 2005 Wiley‐Liss, Inc.
Inactivation of bad by site‐specific phosphorylation: The checkpoint for ischemic astrocytes to initiate or resist apoptosis
Authors: Chen Xiao Qian , Lau Lok Ting , Fung Yin‐Wan Wendy , Yu Albert Cheung Hoi 
Published: January 2005

AbstractBcl‐2‐associated death protein (Bad), a member of the Bcl family, directs astrocytes in primary cultures to enter or resist apoptosis during ischemia in vitro. Under ischemia, Bad was the only Bcl family member whose expression was upregulated significantly during the early stages of an ischemic insult. Increased endogenous Bad was translocated from the cytoplasm to mitochondria to induce apoptosis in astrocytes. Concurrently, ischemia also induced Bad phosphorylation specifically on Ser112 to promote survival. This site‐specific phosphorylation of Bad was mediated by an early activation of the mitogen‐activated protein kinase/extracellular signal‐regulated protein kinase (MAPK/ERK) intracellular signaling pathway. This study demonstrates that ischemia‐induced Bad plays a dual role in determining whether astrocytes enter or resist apoptosis after an ischemic insult. © 2005 Wiley‐Liss, Inc.
PLCγ signaling underlies BDNF potentiation of Purkinje cell responses to GABA
Authors: Cheng Qing , Yeh Hermes H. 
Published: January 2005

AbstractBrain‐derived neurotrophic factor (BDNF) regulates neuronal survival, neurite outgrowth, and excitatory synaptic transmission. We reported recently that acute BDNF exposure decreased γ‐aminobutyric acid (GABA) responses in cultured mouse cerebellar granule cells through tyrosine receptor kinase B (TrkB) receptor‐mediated signaling. In the present study, we extend this work to investigate BDNF‐induced modulation of GABA responses and GABAA receptor‐mediated synaptic events in cerebellar slices. Thin (200 μm) parasagittal slices of cerebellum were prepared from postnatal Day 7 and 14 mice. Purkinje cells and granule cells, both of which express TrkB‐like immunoreactivity, were identified for whole‐cell recording. BDNF promptly enhanced GABA responses in Purkinje cells but, consistent with our previous finding in culture, attenuated those recorded in granule cells. In Purkinje cells, BDNF exposure shifted rightward the cumulative peak amplitude distribution for miniature inhibitory postsynaptic currents (mIPSCs) without changing the mIPSC frequency. BDNF‐induced potentiation of Purkinje cell responses to GABA was blocked by TrkB‐Fc (receptor body that sequesters BDNF), K252a (inhibitor of TrkB receptor autophosphorylation), U73122 (inhibitor of phospholipase‐Cγ [PLCγ]), KN62 (specific inhibitor of calcium/calmodulin‐dependent kinase), KT5720 (specific cyclic AMP‐dependent kinase inhibitor), and by intracellular dialysis of Rp‐cyclic AMP or BAPTA (1,2‐bis(o‐aminophenoxy)ethane‐N,N, N′,N′‐tetraacetic acid). Overall, our results indicate that BDNF acutely potentiates GABAA receptor function in cerebellar Purkinje cells via the TrkB receptor‐PLCγ signal transduction cascade. In addition, we propose that cyclic AMP‐mediated intracellular signaling mechanisms may facilitate manifestation of the BDNF‐induced modulatory outcome. © 2005 Wiley‐Liss, Inc.
Dynamic expression of de novo DNA methyltransferases Dnmt3a and Dnmt3b in the central nervous system
Authors: Feng Jian , Chang Hua , Li En , Fan Guoping 
Published: January 2005

AbstractTo explore the role of DNA methylation in the brain, we examined the expression pattern of de novo DNA methyltransferases Dnmt3a and Dnmt3b in the mouse central nervous system (CNS). By comparing the levels of Dnmt3a and Dnmt3b mRNAs and proteins in the CNS, we showed that Dnmt3b is detected within a narrow window during early neurogenesis, whereas Dnmt3a is present in both embryonic and postnatal CNS tissues. To determine the precise pattern of Dnmt3a and Dnmt3b gene expression, we carried out X‐gal histochemistry in transgenic mice in which the lacZ marker gene is knocked into the endogenous Dnmt3a or Dnmt3b gene locus (Okano et al. [1999] Cell 99:247–257). In Dnmt3b‐lacZ transgenic mice, X‐gal‐positive cells are dispersed across the ventricular zone of the CNS between embryonic days (E) 10.5 and 13.5 but become virtually undetectable in the CNS after E15.5. In Dnmt3a‐lacZ mice, X‐gal signal is initially observed primarily in neural precursor cells within the ventricular and subventricular zones between E10.5 and E17.5. However, from the newborn stage to adulthood, Dnmt3a X‐gal signal was detected predominantly in postmitotic CNS neurons across all the regions examined, including olfactory bulb, cortex, hippocampus, striatum, and cerebellum. Furthermore, Dnmt3a signals in CNS neurons increase during the first 3 weeks of postnatal development and then decline to a relatively low level in adulthood, suggesting that Dnmt3a may be of critical importance for CNS maturation. Immunocytochemistry experiments confirmed that Dnmt3a protein is strongly expressed in neural precursor cells, postmitotic CNS neurons, and oligodendrocytes. In contrast, glial fibrillary acidic protein‐positive astrocytes exhibit relatively weak or no Dnmt3a immunoreactivity in vitro and in vivo. Our data suggest that whereas Dnmt3b may be important for the early phase of neurogenesis, Dnmt3a likely plays a dual role in regulating neurogenesis prenatally and CNS maturation and function postnatally. © 2005 Wiley‐Liss, Inc.
Expression profiling of sciatic nerve in a Charcot‐Marie‐Tooth disease type 1a mouse model
Authors: ten Asbroek Anneloor L.M.A. , Verhamme Camiel , van Groenigen Marjon , Wolterman Ruud , de Kok‐Nazaruk Maryla M. , Baas Frank 
Published: January 2005

AbstractExpression profiling was performed on sciatic nerve of normal mice and of transgenic mice overexpressing the peripheral myelin protein 22 kDa (PMP22). These mice represent a model for the hereditary peripheral neuropathy Charcot‐Marie Tooth type 1A. Comparison of the profiles reveals that the proteasomal degradation pathway and various signaling mechanisms are up‐regulated in the diseased nerve. The down‐regulated processes represent cell shape and adhesion as well as cellular activity and metabolism. In addition, we found that the most significantly up‐regulated differences could not be mapped on known transcripts and thus might represent not identified transcripts. Our data will be helpful to direct future research aimed at deciphering the molecular pathogenesis of the most prevalent hereditary peripheral neuropathy. © 2005 Wiley‐Liss, Inc.
Effect of tumor necrosis factor‐α on the reciprocal G‐protein‐induced regulation of norepinephrine release by the α2‐adrenergic receptor
Authors: Reynolds Jessica L. , Ignatowski Tracey A. , Spengler Robert N. 
Published: January 2005

Abstractα2‐Adrenergic receptors control norepinephrine (NE) release and tumor necrosis factor‐α (TNF) production from neurons. TNF regulates NE release, depending on α2‐adrenergic receptor functioning. The relationship between TNF production in the brain and α2‐adrenergic receptor activation could have profound control over NE release. TNF and α2‐adrenergic regulation of NE release was investigated in rat hippocampal slices incubated with pertussis toxin (PTX). The α2‐adrenergic receptor couples to Gαi/o‐proteins to inhibit NE release; however, in slices preexposed to PTX, α2‐adrenergic receptor activation facilitates NE release. TNF exposure subsequent to PTX restores α2‐adrenergic inhibition of NE release. PTX exposure of hippocampal slices prevents agonist‐induced increases in Gαi/o labeling with a GTP analog; after subsequent TNF exposure, agonist‐induced increases in Gαi/o labeling are restored. TNF regulation of NE release transforms from inhibition to facilitation depending on α2‐adrenergic receptor activation following PTX exposure. Therefore, TNF directs the coupling of the α2‐adrenergic receptor, ultimately affecting NE release. © 2005 Wiley‐Liss, Inc.
Effects of an absenteeism feedback intervention on employee absence behavior†
Authors: Gaudine Alice P. , Saks Alan M. 
Published: January 2005

AbstractThe purpose of this study was to test the effects of an Absenteeism Feedback Intervention (AFI) on employee absenteeism. Three hundred and seventy‐one employees working in 14 experimental and 13 control groups in a medium sized hospital participated in the study. Employees working in the experimental groups received absenteeism feedback at three time periods that provided them with information about their own number of absent days and episodes (sequential days counted as a single absence episode) as well as the average of their work and occupational group. Comparisons of absent days and episodes between the AFI and control groups indicate some support for the effectiveness of the intervention. In particular, there was a reduction in absent days and episodes for employees with higher than average absenteeism during the previous year but who were not extreme offenders. The research and practical implications of the AFI for reducing employee absenteeism are discussed. Copyright © 2001 John Wiley & Sons, Ltd.
ENSO variability, teleconnections and climate change
Authors: Diaz Henry F. , Hoerling Martin P. , Eischeid Jon K. 
Published: January 2005

AbstractAn overview is presented of the principal features of the El Niño–Southern Oscillation (ENSO) teleconnections in terms of regional patterns of surface temperature, precipitation and mid‐tropospheric atmospheric circulation. The discussion is cast in the context of variations in the associations over time, with decadal scale changes emphasized. In the five decades or so for which we have adequate records to reliably analyse the global aspects of ENSO effects on regional climates around the world, we have witnessed one major decadal scale change in the overall pattern of sea‐surface temperatures (SST) in the global ocean, and concomitant changes in the atmospheric response to those changes. The analysis underscores the connection between low frequency changes in tropical SST, ENSO and decadal scale changes in the general atmospheric circulation, pointing to the complex interplay between the canonical ENSO system, slow changes in SST in the Indo‐Pacific over the last century, and long‐term changes in the atmospheric circulation itself. Published in 2001 by John Wiley & Sons, Ltd.