bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increasing the throughput of HomePNA
Authors: Amodei Aurelio , Costa Luís Henrique M. K. , Duarte Otto Carlos M. B. 
Published: February 2008

AbstractIn this paper we propose a new medium access mechanism for HomePNAv2 and HomePNAv3 standards. This mechanism uses a priority aggregation mechanism to avoid collisions, increasing these protocols throughput. Furthermore, this mechanism does not require modifying standards, since it can be implemented over their actual MAC sublayers. Simulation results show that the proposed mechanism is able to increase the throughput up to 44% for HomePNAv2 and 36% for HomePNAv3. Moreover, we also show how this mechanism affects network delay, analyzing average delay and jitter for all protocols presented. Copyright © 2008 John Wiley & Sons, Ltd.
Probabilistic evaluation of seismic performance of 3‐story 3D one‐ and two‐way steel moment‐frame structures
Authors: Tagawa Hiroyuki , MacRae Gregory , Lowes Laura 
Published: February 2008

AbstractThis paper presents the results of a probabilistic evaluation of the seismic performance of 3D steel moment‐frame structures. Two types of framing system are considered: one‐way frames typical of construction in the United States and two‐way frames typical of construction in Japan. For each framing system, four types of beam–column connections are considered: pre‐Northridge welded‐flange bolted‐web, post‐Northridge welded‐flange welded‐web, reduced‐beam‐section, and bolted‐flange‐plate connections. A suite of earthquake ground motions is used to compute the annual probability of exceedence (APE) for a series of drift demand levels and for member plastic‐rotation capacity. Results are compared for the different framing systems and connection details. It is found that the two‐way frames, which have a larger initial stiffness and strength than the one‐way frames for the same beam and column volumes, have a smaller APE for small drift demands for which members exhibit no or minimal yielding, but have a larger APE for large drift demands for which members exhibit large plastic rotations. However, the one‐way frames, which typically comprise a few seismic frames with large‐sized members that have relatively small rotation capacities, may have a larger APE for member failure. The probabilistic approach presented in this study may be used to determine the most appropriate frame configuration to meet an owner's performance objectives. Copyright © 2008 John Wiley & Sons, Ltd.
The effects of cigarette costs on BMI and obesity
Authors: Baum Charles L. 
Published: February 2008

AbstractAbout 30% of Americans are currently obese, which is roughly a 100% increase from 25 years ago. Public health officials have consequently become alarmed because recent research indicates that societal costs of obesity now exceed those of cigarette smoking and alcoholism. Cigarette taxes may have exacerbated the prevalence of obesity. In 1964, the US Surgeon General issued its first report relating smoking and health, and since that time, federal and state governments have increased cigarette taxes in a successful effort to reduce cigarette smoking. However, because cigarette smoking and obesity seem inversely related, cigarette taxes may have simultaneously increased obesity. This paper examines the effects of cigarette costs on BMI and obesity and finds that they have significant positive effects. This paper attempts to reconcile conflicting evidence in the literature by controlling more carefully for correlation with state‐specific time trends using panel data. Results indicate that the net benefit to society of increasing cigarette taxes may not be as large as previously thought, though this research in no way concludes that they should be decreased to prompt weight loss. Copyright © 2008 John Wiley & Sons, Ltd.
The development of attention and response inhibition in early childhood
Authors: Bartgis Jami , Thomas David G. , Lefler Elizabeth K. , Hartung Cynthia M. 
Published: February 2008

AbstractThe goal of this study was to examine the development of attention and response inhibition from ages 5 to 7. Forty children (20 5‐year‐olds and 20 7‐year‐olds) completed four counterbalanced phases of a continuous performance task. Phase 1 was designed to measure attention without distraction, Phase 2 was designed to measure attention with distraction, Phase 3 was designed to measure attention and response inhibition without distraction, and Phase 4 was designed to measure attention and response inhibition with distraction. With regard to attention, 7‐year‐olds performed significantly better than 5‐year‐olds. This age difference was more pronounced when distraction was present. With regard to response inhibition, there were no significant age differences. These results appear to suggest that attention improves between ages 5 and 7 but response inhibition does not. However, conclusions regarding response inhibition were limited because the distraction appeared to have had too powerful an effect on the 5‐year‐olds. Implications and future directions are discussed. Copyright © 2008 John Wiley & Sons, Ltd.
Never look a gift horse in the mouth or should you? Upgrading the Hare Irrigation System in Southern Ethiopia
Authors: Wegerich Kai , Dubale Tesfaye , Bruins Bert 
Published: February 2008

AbstractThe upgrading of the Hare Irrigation System was a joint undertaking of the governments of Ethiopia and the People's Republic of China. After completion of the primary and the secondary canals, farmers refused to take over responsibility of the system. Existing literature on the Hare Irrigation System does not differentiate between various farmer groups and their interests. This study highlights the differences in perception of head‐end, middle and tail‐end farmers. The main group that is not satisfied with the system are the head‐enders, because they are partly excluded from using it. While the middle and tail‐end farmers are satisfied with the new irrigation system, they are unhappy because they have not received the “promised” compensation. Overall, the paper highlights the lack of transparency and communication between the local community, the government and the Chinese design and construction agency, which appears to be the main reason for the dissatisfaction of parts of the local community. Copyright © 2008 John Wiley & Sons, Ltd.
PSM/SH2B1 splice variants: Critical role in src catalytic activation and the resulting STAT3s‐mediated mitogenic response
Authors: Zhang Manchao , Deng Youping , Riedel Heimo 
Published: February 2008

AbstractA role of PSM/SH2B1 had been shown in mitogenesis and extending to phenotypic cell transformation, however, the underlying molecular mechanism remained to be established. Here, four alternative PSM splice variants and individual functional protein domains were compared for their role in the regulation of Src activity. We found that elevated cellular levels of PSM variants resulted in phenotypic cell transformation and potentiated cell proliferation and survival in response to serum withdrawal. PSM variant activity presented a consistent signature pattern for any tested response of highest activity observed for gamma, followed by delta, alpha, and beta with decreasing activity. PSM‐potentiated cell proliferation was sensitive to Src inhibitor herbimycin and PSM and Src were found in the same immune complex. PSM variants were substrates of the Src Tyr kinase and potentiated Src catalytic activity by increasing the Vmax and decreasing the Km for ATP with the signature pattern of variant activity. Dominant‐negative PSM peptide mimetics including the SH2 or PH domains inhibited Src catalytic activity as well as Src‐mediated phenotypic cell transformation. Activation of major Src substrate STAT3 was similarly potentiated by the PSM variants in a Src‐dependent fashion or inhibited by PSM domain‐specific peptide mimetics. Expression of a dominant‐negative STAT3 mutant blocked PSM variant‐mediated phenotypic cell transformation. Our results implicate an essential role of the PSM variants in the activation of the Src kinase and the resulting mitogenic response—extending to phenotypic cell transformation and involving the established Src substrate STAT3. J. Cell. Biochem. J. Cell. Biochem. 104: 105–118, 2008. © 2008 Wiley‐Liss, Inc.
Src‐Tyrosine kinases are major agents in mitochondrial tyrosine phosphorylation
Authors: Tibaldi Elena , Brunati Anna Maria , Massimino Maria Lina , Stringaro Annarita , Colone Marisa , Agostinelli Enzo , Arancia Giuseppe , Toninello Antonio 
Published: February 2008

AbstractMitochondrial tyrosine phosphorylation is emerging as an important mechanism in regulating mitochondrial function. This article, aimed at identifying which kinases are the major agents in mitochondrial tyrosine phosphorylation, shows that this role should be attributed to Src family members. Indeed, various members of this family, for example, Fgr, Fyn, Lyn, c‐Src, are constitutively present in the internal structure of mitochondria as well as Csk, a key enzyme in the regulation of the activity of this family. By means of different approaches, biochemical fractioning, Western blotting and immunogold analysis “in situ” of phosphotyrosine signaling, evidence is reported on the existence of a signal transduction pathway from plasma membrane to mitochondria, resulting in increasing Src‐dependent mitochondrial tyrosine phosphorylation. The activation of Src kinases at mitochondrial level is associated with the proliferative status where several mitochondrial proteins are specifically tyrosine‐phosphorylated. J. Cell. Biochem. 104: 840–849, 2008. © 2008 Wiley‐Liss, Inc.
Effect of UV irradiation on colorectal cancer cells with acquired TRAIL resistance
Authors: Kim Seong C. , Park Sung‐Soo , Lee Yong J. 
Published: February 2008

AbstractTumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) is a member of the TNF superfamily. TRAIL shows strong cytotoxicity to many cancer cells but minimal cytotoxicity to most normal cells. Interestingly, our recent studies have demonstrated that pretreatment with TRAIL induces acquired resistance to TRAIL (Song et al. 2007 J Biol Chem 282: 319). Acquired TRAIL resistance develops within 1 day and gradually decays within 5 days after TRAIL treatment. In our current study, we examined whether human colorectal carcinoma CX‐1 cells with acquired TRAIL resistance are resistant to UV irradiation as well. CX‐1 cells were treated with 200 ng/ml TRAIL for 6 h and incubated various times (0.25–5 days) and then challenged to UV irradiation. Unexpectedly, we observed an increase in apoptosis in acquired TRAIL resistant cells after UVC as well as UVB exposure. This was due to an increase in caspase activation which was mediated through cytochrome c release. These results suggest that cells with acquired TRAIL resistance are sensitive to UV irradiation. J. Cell. Biochem. 104: 1172–1180, 2008. © 2008 Wiley‐Liss, Inc.
Intracellular GSH level is a factor in As4.1 juxtaglomerular cell death by arsenic trioxide
Authors: Han Yong Hwan , Kim Sung Zoo , Kim Suhn Hee , Park Woo Hyun 
Published: February 2008

AbstractArsenic trioxide has been known to regulate many biological functions such as cell proliferation, apoptosis, differentiation, and angiogenesis in various cell lines. We investigated the involvement of GSH and ROS such as H2O2 and O in the death of As4.1 cells by arsenic trioxide. The intracellular ROS levels were changed depending on the concentration and length of incubation with arsenic trioxide. The intracellular O level was significantly increased at all the concentrations tested. Arsenic trioxide reduced the intracellular GSH content. Treatment of Tiron, ROS scavenger decreased the levels of ROS in 10 µM arsenic trioxide‐treated cells. Another ROS scavenger, Tempol did not decrease ROS levels in arsenic trioxide‐treated cells, but slightly recovered the depleted GSH content and reduced the level of apoptosis in these cells. Exogenous SOD and catalase did not reduce the level of ROS, but did decrease the level of O. Both of them inhibited GSH depletion and apoptosis in arsenic trioxide‐treated cells. In addition, ROS scavengers, SOD and catalase did not alter the accumulation of cells in the S phase induced by arsenic trioxide. Furthermore, JNK inhibitor rescued some cells from arsenic trioxide‐induced apoptosis, and this inhibitor decreased the levels of O and reduced the GSH depletion in these cells. In summary, we have demonstrated that arsenic trioxide potently generates ROS, especially O, in As4.1 juxtaglomerular cells, and Tempol, SOD, catalase, and JNK inhibitor partially rescued cells from arsenic trioxide‐induced apoptosis through the up‐regulation of intracellular GSH levels. J. Cell. Biochem. 104: 995–1009, 2008. © 2008 Wiley‐Liss, Inc.
Merging molecular imaging and RNA interference: Early experience in live animals
Authors: Bogdanov Alexei A. 
Published: February 2008

AbstractThe rapid development of non‐invasive imaging techniques and imaging reporters coincided with the enthusiastic response that the introduction of RNA interference (RNAi) techniques created in the research community. Imaging in experimental animals provides quantitative or semi‐quantitative information regarding the biodistribution of small interfering RNAs and the levels of gene interference (i.e., knockdown of the target mRNA) in living animals. In this review we give a brief summary of the first imaging findings that have potential for accelerating the development and testing of new approaches that explore RNAi as a method for achieving loss‐of‐function effects in vivo and as a promising therapeutic tool. J. Cell. Biochem. 104: 1113–1123, 2008. © 2008 Wiley‐Liss, Inc.
Lack of insulin impairs Mg2+ homeostasis and transport in cardiac cells of streptozotocin‐injected diabetic rats
Authors: Reed Grant , Cefaratti Christie , Berti‐Mattera Liliana N. , Romani Andrea 
Published: February 2008

AbstractSerum and tissue Mg2+ content are markedly decreased in diabetic patients and animals. At the tissue level, Mg2+ loss progresses over time and affects predominantly heart, liver and skeletal muscles. In the present study, alterations in Mg2+ homeostasis and transport in diabetic cardiac ventricular myocytes were evaluated. Cardiac tissue and isolated cardiac ventricular myocytes from diabetic animals displayed a decrease in total Mg2+ content that affected all cellular compartments. This decrease was associated with a marked reduction in cellular protein and ATP content. Diabetic ventricular myocytes were unable to mobilize Mg2+ following β‐adrenergic receptor stimulation or addition of cell permeant cyclic‐AMP. Sarcolemma vesicles purified from diabetic animals, however, transported Mg2+ normally as compared to vesicles from non‐diabetic animals. Treatment of diabetic animals with exogenous insulin for 2 weeks restored ATP and protein levels as well as Mg2+ homeostasis and transport to levels comparable to those observed in non‐diabetic animals. These results suggest that in diabetic cardiac cells Mg2+ homeostasis and extrusion via β‐adrenergic/cAMP signaling are markedly affected by the concomitant decrease in protein and ATP content. As Mg2+ regulates numerous cellular enzymes and functions, including protein synthesis, these results provide a new rationale to interpret some aspects of the cardiac dysfunctions observed under diabetic conditions. J. Cell. Biochem. 104: 1034–1053, 2008. © 2008 Wiley‐Liss, Inc.
Proteomics investigation of protein expression changes in ouabain induced apoptosis in human umbilical vein endothelial cells
Authors: Qiu Jie , Gao Hai‐Qing , Li Bao‐Ying , Shen Lin 
Published: February 2008

AbstractOuabain is Na+/K+_ATPase inhibitor and an endogenous regulator of blood pressure, it has dual effect on vascular endothelial cells(VEC) cell growth and VEC apoptosis is contributed to vascular dysfunction involved in vascular remolding. However, the precise mechanisms of apoptosis induced by ouabain remained unclear. The objective of this study was to identify the differently expressed proteins involved in VEC apoptosis induced by ouabain in order to explore cellular and subcellular mechanisms related to ouabain actions. Human umbilical vein endothelial cells (HUVEC) were exposed to increasing concentrations (0.1 nM to 10 µM) of ouabain at 12–48 h intervals. Cell viability tests revealed that high concentrations of ouabain inhibited cell growth. Flow cytometry and caspase‐3 activity analysis confirmed that apoptosis was primarily responsible for ouabain induced cell death. Two‐dimensional electrophoresis in conjunction with mass spectrometry revealed that the ouabain‐induced apoptosis was accompanied by regulated expression of programmed cell death protein 6, cytochrome C1, endothelin converting enzyme, claudin‐1, reticulon‐4, galectin‐1, ras‐related protein rab‐11B, calnexin, profilin‐1 and heat shock protein 60 (HSP60). Further study on cytochrome c and HSP60 demonstrated that levels of mitochondria and cytosol cytochrome c and HSP60 changed in response to ouabain treatment. Data showed that mitochondria proteins such as HSP60 interferes with HSP60‐Bax interactions played an important role in ouabain induced apoptosis. These data bring new sights into physiological role for ouabain in VEC apoptosis and vascular remodeling, thus provide new strategies for new anti‐cardiovascular disease drug development or the identification of biomarkers for vascular dysfunction in ouabain related hypertension. J. Cell. Biochem. 104: 1054–1064, 2008. © 2008 Wiley‐Liss, Inc.
Binding of RFX2 and NF‐Y to the testis‐specific histone H1t promoter may be required for transcriptional activation in primary spermatocytes
Authors: vanWert Jane M. , Wolfe Steven A. , Grimes Sidney R. 
Published: February 2008

AbstractThe testis‐specific linker histone H1t is transcribed exclusively in pachytene spermatocytes during spermatogenesis. The H1t promoter contains two imperfect inverted repeats which together comprise the X‐box motif that is known to bind the transcription factor regulatory factor X (RFX). Out of all the histone H1 family promoters this motif appears only in the H1t promoter and may contribute to H1t tissue‐specific expression. We show by Western blotting, EMSA, ChIP analysis, and real‐time RT‐PCR that the rat H1t X‐box is bound by RFX2 in vivo in spermatocytes. We demonstrate that transcription factor NF‐Y binds to the CCAAT‐box motif that is located downstream and adjacent to the X‐box and that testis NF‐Y interacts either directly or indirectly with RFX2. Furthermore, we show that both the X‐box and CCAAT‐box are required for promoter activity and that co‐expression of RFX2 greatly enhances testis histone H1t promoter activity in the GC‐1spg germinal cell line. J. Cell. Biochem. 104: 1087–1101, 2008. © 2008 Wiley‐Liss, Inc.
Lysophosphatidic acid promotes cell invasion by up‐regulating the urokinase‐type plasminogen activator receptor in human gastric cancer cells
Authors: Kim Mi Ha , Park Jung Sun , Chang Hee Jung , Baek Min Kyung , Kim Hyeong Rok , Shin Boo Ahn , Ahn Bong Whan , Jung Young Do 
Published: February 2008

AbstractThere is a strong correlation between the overexpression of urokinase‐type plasminogen activator receptor (uPAR) and gastric cancer invasion. This study examined the effect of phospholipid lysophosphatidic acid (LPA) on uPAR expression in human gastric cancer AGS cells and the underlying signal transduction pathways. Treating human gastric AGS cells with LPA induced the expression of uPAR mRNA and promoter activity in both a time‐ and dose‐dependent manner. Small interfering RNA targeting for LPA receptors, dominant negative Rho‐family GTPase (RhoA, Rac1, and Cdc42) and an expression vector encoding a mutated c‐jun (TAM67) partially blocked the LPA‐induced uPAR expression. Site‐directed mutagenesis and electrophoretic mobility shift studies showed that the transcription factors activation protein‐1 (AP‐1) and nuclear factor (NF)‐κB are essential for the LPA‐induced uPAR transcription. In addition, AGS cells treated with LPA showed enhanced invasion, which was partially abrogated by the uPAR‐neutralizing antibodies and inhibitors of Rho kinase, JNK, and NF‐κB. This suggests that LPA induces uPAR expression through the LPA receptors, Rho‐family GTPase, JNK, AP‐1 and NF‐κB signaling pathways, which in turn stimulates the cell invasiveness of human gastric cancer AGS cells. J. Cell. Biochem. 104: 1102–1112, 2008. © 2008 Wiley‐Liss, Inc.
Roles of Wnt signalling in bone growth, remodelling, skeletal disorders and fracture repair
Authors: Macsai Carmen E. , Foster Bruce K. , Xian Cory J. 
Published: February 2008

AbstractWnt signalling has an essential role in regulating bone formation and remodelling during embryonic development and throughout postnatal and adult life. Specifically, Wnt signalling regulates bone formation by controlling embryonic cartilage development and postnatal chondrogenesis, osteoblastogenesis, osteoclastogenesis, endochondral bone formation, and bone remodelling. Abnormalities in the function of Wnt genes give rise to or contribute to the development of several pathological bone conditions, including abnormal bone mass, osteosarcomas and bone loss in multiple myeloma. Furthermore, Wnt signalling is activated during bone fracture repair and plays a crucial role in regulating bone regeneration. J. Cell. Physiol. 215: 578–587, 2008. © 2008 Wiley‐Liss, Inc.
HIV‐1 Tat inhibits NGF‐Induced Egr‐1 transcriptional activity and consequent p35 expression in neural cells
Authors: Darbinian Nune , Darbinyan Armine , Czernik Marta , Peruzzi Francesca , Khalili Kamel , Reiss Krzysztof , Gordon Jennifer , Amini Shohreh 
Published: February 2008

AbstractInfection with HIV‐1 causes degeneration of neurons leading to motor and cognitive dysfunction in AIDS patients. One of the key viral regulatory proteins, Tat, which is released by infected cells, can be taken up by various uninfected cells including neurons and by dysregulating several biological events induces cell injury and death. In earlier studies, we demonstrated that treatment of neuronal cells with Tat affects the nerve growth factor (NGF) signaling pathway involving MAPK/ERK. Here we demonstrate that a decrease in the level of Egr‐1, one of the targets for MAPK, by Tat has a negative impact on the level of p35 expression in NGF‐treated neural cells. Further, we demonstrate a reduced level of Egr‐1 association with the p35 promoter sequence in NGF‐treated cells expressing Tat. As p35, by associating with Cdk5, phosphorylates several neuronal proteins including neurofilaments and plays a role in neuronal differentiation and survival, we examined kinase activity of p35 complexes obtained from cells expressing Tat. Results from H1 kinase assays showed reduced activity of the p35 complex from Tat‐expressing cells in comparison to that from control cells. Accordingly, the level of phosphorylated neurofilaments was diminished in Tat‐expressing cells. Similarly, treatment of PC12 cells with Tat protein or supernatant from HIV‐1 infected cells decreased kinase activity of p35 in these cells. These observations ascribe a role for Tat in altering p35 expression and its activity that affects phosphorylation of proteins involved in neuronal cell survival. J. Cell. Physiol. 216: 128–134, 2008. © 2008 Wiley‐Liss, Inc.