bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of substance P on memory and mood in healthy male subjects
Authors: Herpfer Inga , Katzev Michael , Feige Bernd , Fiebich Bernd L. , Voderholzer Ulrich , Lieb Klaus 
Published: September 2007

AbstractThere is evidence from human and animal studies that substance P (SP) is involved in the etiopathology of depression and anxiety. Furthermore, animal studies have shown effects of SP on memory. In a double‐blind, randomized cross‐over study, 13 healthy young men received SP (1.5 pmol/kg/min) or placebo (NaCl) intravenously over 90 min at two different days. Before and during the infusion, symptoms of anxiety and depression were assessed by different self‐rating questionnaires and cognitive functioning by the Auditory‐Verbal Learning Test (AVLT) as well as by two subtests of the Test for Attentional Performance (TAP). Infusion of SP caused an increase of symptoms of inner tension and of anxiety as assessed by the Acute Panic Inventory (API) and a disturbance of short‐term memory in the AVLT. The results may be interpreted as evidence for an anxiogenic and memory‐disturbing effect of SP. Further studies will focus on the effects of SP in patients with depression, anxiety and cognitive disorders. Copyright © 2007 John Wiley & Sons, Ltd.
Monitoring urban impacts on suspended sediment, trace element, and nutrient fluxes within the City of Atlanta, Georgia, USA: program design, methodological considerations, and initial results
Authors: Horowitz Arthur J. , Elrick Kent A. , Smith James J. 
Published: September 2007

AbstractAtlanta, Georgia (City of Atlanta, COA), is one of the most rapidly growing urban areas in the US. Beginning in 2003, the US Geological Survey established a long‐term water‐quantity/quality monitoring network for the COA. The results obtained during the first 2 years have provided insights into the requirements needed to determine the extent of urban impacts on water quality, especially in terms of estimating the annual fluxes of suspended sediment, trace/major elements, and nutrients.During 2004/2005, suspended sediment fluxes from the City of Atlanta (COA) amounted to about 150 000 t year−1; ≥ 94% of the transport occurred in conjunction with storm‐flow, which also accounted for ≥ 65% of the annual discharge. Typically, storm‐flow averaged ≤20% of the year. Normally, annual suspended sediment fluxes are determined by summing daily loads based on a single calculation step using mean‐daily discharge and a single rating curve‐derived suspended sediment concentration. Due to the small and ‘flashy’ nature of the COAs streams, this approach could produce underestimates ranging from 25% to 64%. Accurate estimates ( ± 15%) require calculation time‐steps as short as every 2–3 h.Based on annual median base‐flow/storm‐flow chemical concentrations, the annual fluxes of ≥ 75% of trace elements (e.g. Cu, Pb, Zn), major elements (e.g. Fe, Al), and total P occur in association with suspended sediment; in turn, ≥ 90% of the transport of these constituents occur in conjunction with storm‐flow. As such, base‐flow sediment‐associated and dissolved contributions represent relatively insignificant portions of the total annual load. An exception is total N, whose sediment‐associated fluxes range from 50% to 60%; even so, storm‐related transport typically exceeds 80%. Hence, in urban environments, non‐point‐sources appear to be the dominant contributors to the fluxes of these constituents. Published in 2007by John Wiley & Sons, Ltd.
The US treasury market in August 1998: untangling the effects of Hong Kong and Russia with high‐frequency data
Authors: Dungey Mardi , Goodhart Charles , Tambakis Demosthenes 
Published: September 2007

AbstractThe second half of August 1998 was dominated by two events. From 14 to 28 August, the Hong Kong Monetary Authority (HKMA) intervened in Hong Kong equity markets to prevent a speculative double play against their currency board. On 17 August, Russia announced its default on sovereign bonds. This paper demonstrates that the HKMA interventions had a substantial impact on the outcomes for US Treasury markets during this period using a careful analysis of high‐frequency bond market data. On this evidence the shocks emanating from Hong Kong provided liquidity to the US Treasury market when it was most needed. Copyright © 2007 John Wiley & Sons, Ltd.
Insights into nuclear localization and dynamic association of CD38 in Raji and K562 cells
Authors: Trubiani Oriana , Guarnieri Simone , Eleuterio Enrica , Di Giuseppe Fabrizio , Orciani Monia , Angelucci Stefania , Di Primio Roberto 
Published: September 2007

AbstractCD38 is a type II transmembrane glycoprotein found mainly on the plasma membrane involved in the metabolism of cADPR and NAADP, two nucleotides with calcium mobilizing activity independent of inositol trisphosphate. Recent data report the presence of CD38 in different cellular compartments raising new questions about its effective role in cellular metabolism. In rat hepatocyte nuclei, CD38 has been proposed as a responsive to cADPR integral inner membrane protein suggesting that the nuclear envelope may also be an important source of Ca2+ stores. Further reports indicating that CD38 is localized in nuclear compartments in a variety of cell types and tissues including brain, liver, eye, spleen, and bone raise the condition of resolving the question concerning the effective presence of CD38 within the nucleus. Here we report data supporting the presence of CD38 at nuclear level independently of expression of surface CD38. We utilized two different human leukemia cell lines expressing or not expressing CD38 molecule on their cell surface. The morphological and biochemical results including enzymatic activity and proteomic determinations explain the effective nuclear localization of CD38 in human Raji and K562 cells. Since cell nucleus is a complex and highly dynamic environment with many functionally specialized regions, the nuclear localization of specific proteins represents an important mechanism in signal transduction. The presence of CD38 at the interchromatin region whether linked to nuclear scaffold or stored in nuclear structures as micronuclei and Cajal bodies co‐localizing with coilin, suggests its involvement in nuclear processes including transcription, replication, repairing and splicing. J. Cell. Biochem. 103: 1294–1308, 2008. © 2007 Wiley‐Liss, Inc.
Cloning and characterisation of Ifi206: A new murine HIN‐200 family member
Authors: Ludlow Louise E. , Hii Linda L. , Thorpe Janine , Newbold Andrea , Tainton Kellie M. , Trapani Joseph A. , Clarke Christopher J.P. , Johnstone Ricky W. 
Published: September 2007

AbstractHIN‐200 proteins are interferon‐inducible proteins capable of regulating cell growth, senescence, differentiation and death. Using a combination of in silico analysis of NCBI EST databases and screening of murine C57BL/6 cDNA libraries we isolated novel murine HIN‐200 cDNAs designated Ifi206S and Ifi206L encoding two putative mRNA splice variants. The p206S and p206L protein isoforms have a modular domain structure consisting of an N‐terminal PAAD/DAPIN/Pyrin domain, a region rich in serine, threonine and proline residues and a C‐terminal 200 B domain characteristic of other HIN‐200 proteins. Ifi206 mRNA was detected only in the spleen and lung of BALB/c and C57BL/6 mice and expression was up‐regulated by both types I and II IFN subtypes. p206 protein was predominantly expressed in the cytoplasm and addition of LMB, a CRM1 dependent nuclear export inhibitor, caused p206 to accumulate in the nucleus. Unlike other human and mouse HIN‐200 proteins that contain only a single 200 amino acid domain, overexpression of p206 impaired the clonogenic growth of tumour cell lines. Thus, p206 represents the newest HIN‐200 family member discovered. It has distinct and restricted pattern of expression however maintains many of the hallmarks of HIN‐200 proteins including the presence of a characteristic 200 X domain, induction by interferon and an ability to suppress tumour cell growth. J. Cell. Biochem. 103: 1270–1282, 2008. © 2007 Wiley‐Liss, Inc.
Secretion without Golgi
Authors: Prudovsky Igor , Tarantini Francesca , Landriscina Matteo , Neivandt David , Soldi Raffaella , Kirov Aleksandr , Small Deena , Kathir Karuppanan Muthusamy , Rajalingam Dakshinamurthy , Kumar Thallapuranam Krishnaswamy Suresh 
Published: September 2007

AbstractA growing number of proteins devoid of signal peptides have been demonstrated to be released through the non‐classical pathways independent of endoplasmic reticulum and Golgi. Among them are two potent proangiogenic cytokines FGF1 and IL1α. Stress‐induced transmembrane translocation of these proteins requires the assembly of copper‐dependent multiprotein release complexes. It involves the interaction of exported proteins with the acidic phospholipids of the inner leaflet of the cell membrane and membrane destabilization. Not only stress, but also thrombin treatment and inhibition of Notch signaling stimulate the export of FGF1. Non‐classical release of FGF1 and IL1α presents a promising target for treatment of cardiovascular, oncologic, and inflammatory disorders. J. Cell. Biochem. 103: 1327–1343, 2008. © 2007 Wiley‐Liss, Inc.
Biochemical analysis of the interaction of calcium with toposome: A major protein component of the sea urchin egg and embryo
Authors: Hayley Michael , Sun Ming , Merschrod S Erika F. , Davis Philip J. , Robinson John J. 
Published: September 2007

AbstractWe have investigated the biochemical and functional properties of toposome, a major protein component of sea urchin eggs and embryos. Atomic force microscopy was utilized to demonstrate that a Ca2+‐driven change in secondary structure facilitated toposome binding to a lipid bilayer. Thermal denaturation studies showed that toposome was dependent upon calcium in a manner paralleling the effect of this cation on secondary and tertiary structure. The calcium‐induced, secondary, and tertiary structural changes had no effect on the chymotryptic cleavage pattern. However, the digestion pattern of toposome bound to phosphatidyl serine liposomes did vary as a function of calcium concentration. We also investigated the interaction of this protein with various metal ions. Calcium, Mg2+, Ba2+, Cd2+, Mn2+, and Fe3+ all bound to toposome. In addition, Cd2+ and Mn2+ displaced Ca2+, prebound to toposome, while Mg2+, Ba2+, and Fe3+ had no effect. Collectively, these results further enhance our understanding of the role of Ca2+ in modulating the biological activity of toposome. J. Cell. Biochem. 103: 1464–1471, 2008. © 2007 Wiley‐Liss, Inc.
Regulation of monocarboxylate transporter 1 (MCT1) promoter by butyrate in human intestinal epithelial cells: Involvement of NF‐κB pathway
Authors: Borthakur Alip , Saksena Seema , Gill Ravinder K. , Alrefai Waddah A. , Ramaswamy Krishnamurthy , Dudeja Pradeep K. 
Published: September 2007

AbstractButyrate, a short chain fatty acid (SCFA) produced by bacterial fermentation of undigested carbohydrates in the colon, constitutes the major fuel for colonocytes. We have earlier shown the role of apically localized monocarboxylate transporter isoform 1 (MCT1) in transport of butyrate into human colonic Caco‐2 cells. In an effort to study the regulation of MCT1 gene, we and others have cloned the promoter region of the MCT1 gene and identified cis elements for key transcription factors. A previous study has shown up‐regulation of MCT1 expression, and activity by butyrate in AA/C1 human colonic epithelial cells, however, the detailed mechanisms of this up‐regulation are not known. In this study, we demonstrate that butyrate, a substrate for MCT1, stimulates MCT1 promoter activity in Caco‐2 cells. This effect was dose dependent and specific to butyrate as other predominant SCFAs, acetate, and propionate, were ineffective. Utilizing progressive deletion constructs of the MCT1 promoter, we showed that the putative butyrate responsive elements are in the −229/+91 region of the promoter. Butyrate stimulation of the MCT1 promoter was found to be independent of PKC, PKA, and tyrosine kinases. However, specific inhibitors of the NF‐κB pathway, lactacystein (LC), and caffeic acid phenyl ester (CAPE) significantly reduced the MCT1 promoter stimulation by butyrate. Also, butyrate directly stimulated NF‐κB‐dependent luciferase reporter activity. Histone deacetylase (HDAC) inhibitor trichostatin A (TSA) also stimulated MCT1 promoter activity, however, unlike butyrate, this stimulation was unaltered by the NF‐κB inhibitors. Further, the combined effect of butyrate, and TSA on MCT1 promoter activity was additive, indicating that their mechanisms of action were independent. Our results demonstrate the involvement of NF‐κB pathway in the regulation of MCT1 promoter activity by butyrate. J. Cell. Biochem. 103: 1452–1463, 2008. © 2007 Wiley‐Liss, Inc.
Empirical bond‐order potential for hydrocarbons: Adaptive treatment of van der Waals interactions
Authors: Liu Aibing , Stuart Steven J. 
Published: September 2007

AbstractBond‐order potentials provide a powerful class of models for simulating chemically reactive systems with classical potentials. In these models, the covalent bonding interactions adapt to the environment, allowing bond strength to change in response to local chemical changes. However, the non‐bonded interactions should also adapt in response to chemical changes, an effect which is neglected in current bond‐order potentials. Here the AIREBO potential is extended to include adaptive Lennard‐Jones terms, allowing the van der Waals interactions to vary adaptively with the chemical environment. The resulting potential energy surface and its gradient remain continuous, allowing it to be used for dynamics simulations. This new potential is parameterized for hydrocarbons, and is fit to the energetics and densities of a variety of condensed phase molecular hydrocarbons. The resulting model is more accurate for modeling aromatic and other unsaturated hydrocarbon species, for which the original AIREBO potential had some deficiencies. Testing on compounds not used in the fitting procedure shows that the new model performs substantially better in predicting heats of vaporization and pressures (or densities) of condensed‐phase molecular hydrocarbons. © 2007 Wiley Periodicals, Inc. J Comput Chem, 2008
Paxillin's LD4 motif interacts with bcl‐2
Authors: Sheibani Nader , Tang Yixin , Sorenson Christine M. 
Published: September 2007

Abstractbcl‐2 is the founding member of a family of proteins which influences cell survival in response to a variety of stimuli including those from growth factor receptors and integrins. However, how these activities are coordinated through bcl‐2 requires further investigation. bcl‐2 interacts with paxillin, potentially linking cell survival and cell adhesive pathways. Paxillin is an adapter protein implicated in growth factor and integrin‐mediated signal transduction pathways. Previous work in this laboratory demonstrated that loss of bcl‐2 affects cell adhesion and migration characteristics of renal epithelial cells, perhaps through disruption of its interaction with paxillin. Here studies were performed to determine the bcl‐2 binding motif in paxillin. The amino‐terminal portion of paxillin, specifically its LD4 motif, was found to associate with bcl‐2. However, the amino‐terminal portion of paxillin with the LD4 domain deleted did not associate with bcl‐2. The corresponding LD motif in other paxillin family members, Hic‐5 and leupaxin, did not associate with bcl‐2. Mutations in paxillin's LD4 motif made to mimic Hic‐5 and leupaxin LD4‐like motifs (E268 → R or S272 → H) abolished its association with bcl‐2. Incubation of embryonic kidneys with paxillin's LD4 motif disrupted ureteric bud branching and morphogenesis, while incubation with the comparable Hic‐5 LD motif did not significantly affect morphogenesis. These data suggest that paxillin's association with bcl‐2 plays a unique role during kidney development that other paxillin family members may not be able to fulfill. J. Cell. Physiol. 214: 655–661, 2008. © 2007 Wiley‐Liss, Inc.
Ajulemic acid, a nonpsychoactive cannabinoid acid, suppresses osteoclastogenesis in mononuclear precursor cells and induces apoptosis in mature osteoclast‐like cells
Authors: George Kerri L. , Saltman Laura H. , Stein Gary S. , Lian Jane B. , Zurier Robert B. 
Published: September 2007

AbstractOral administration of ajulemic acid (AjA), a cannabinoid acid devoid of psychoactivity, prevents joint tissue injury in rats with adjuvant induced arthritis. Because activation of osteoclasts is central to the pathogenesis of bone erosion in patients with rheumatoid arthritis (RA), we investigated the influence of AjA on osteoclast differentiation and survival. Osteoclast cultures were established by stimulation of RAW264.7 cells and primary mouse bone marrow cultures with receptor activator of NF‐κB ligand (RANKL). Simultaneous addition of AjA (15 and 30 µM) and RANKL to both culture systems significantly suppressed development of multinucleated osteoclasts (osteoclastogenesis) in a dose dependent manner, as determined by quantification of multinuclear, tartrate‐resistant acid phosphatase (TRAP)‐positive cells. AjA impaired growth of RAW264.7 monocytes and prevented further osteoclast formation in cultures in which osteoclastogenesis had already begun. Reduction by AjA of both monocyte growth and osteoclast formation was associated with apoptosis, assayed by annexin V and propidium iodide staining, and caspase activity. The anti‐osteoclastogenic effects of AjA did not require the continuous presence of AjA in the cell cultures. Based on these findings, we propose that AjA or other nonpsychoactive synthetic analogs ofCannabisconstituents may be useful therapy for diseases such as RA and osteoporosis in which bone resorption is a central feature. J. Cell. Physiol. 214: 714–720, 2008. © 2007 Wiley‐Liss, Inc.
HDLs activate ADAM17‐dependent shedding
Authors: Tellier Edwige , Canault Matthias , Poggi Marjorie , Bonardo Bernadette , Nicolay Alain , Alessi Marie‐Christine , Nalbone Gilles , Peiretti Franck 
Published: September 2007

AbstractThe tumor necrosis factor‐alpha (TNF) converting enzyme (ADAM17) is a metalloprotease that cleaves several transmembrane proteins, including TNF and its receptors (TNFR1 and TNFR2). We recently showed that the shedding activity of ADAM17 is sequestered in lipid rafts and that cholesterol depletion increased the shedding of ADAM17 substrates. These data suggested that ADAM17 activity could be regulated by cholesterol movements in the cell membrane. We investigated if the membrane cholesterol efflux induced by high‐density lipoproteins (HDLs) was able to modify the shedding of ADAM17 substrates. HDLs added to different cell types, increased the ectodomain shedding of TNFR2, TNFR1, and TNF, an effect reduced by inhibitors active on ADAM17. The HDLs‐stimulated TNF release occurred also on cell‐free isolated plasma membranes. Purified apoA1 increased the shedding of TNF in an ABCA1‐dependent manner, suggesting a role for the cholesterol efflux in this phenomenon. HDLs reduced the cholesterol and proteins (including ADAM17) content of lipid rafts and triggered the ADAM17‐dependent cleavage of TNF in the non‐raft region of the membrane. In conclusion, these data demonstrate that HDLs alter the lipid raft structure, which in turn activates the ADAM17‐dependent processing of transmembrane substrates. J. Cell. Physiol. 214: 687–693, 2008. © 2007 Wiley‐Liss, Inc.
1α,25‐dihydroxy vitamin D3‐enhanced expression of the osteocalcin gene involves increased promoter occupancy of basal transcription regulators and gradual recruitment of the 1α,25‐dihydroxy vitamin D3 receptor‐SRC‐1 coactivator complex
Authors: Carvallo Loreto , Henríquez Berta , Paredes Roberto , Olate Juan , Onate Sergio , van Wijnen Andre J. , Lian Jane B. , Stein Gary S. , Stein Janet L. , Montecino Martin 
Published: September 2007

AbstractBinding of 1α,25‐dihydroxy vitamin D3 to the C‐terminal ligand‐binding domain (LBD) of its receptor (VDR) induces a conformational change that enables interaction of VDR with transcriptional coactivators such as members of the p160/SRC family or the DRIP (vitamin D receptor‐interacting complex)/Mediator complex. These interactions are critical for VDR‐mediated transcriptional enhancement of target genes. The p160/SRC members contain intrinsic histone acetyl transferase (HAT) activities that remodel chromatin at promoter regulatory regions, and the DRIP/Mediator complex may establish a molecular bridge between the VDR complex and the basal transcription machinery. Here, we have analyzed the rate of recruitment of these coactivators to the bone‐specific osteocalcin (OC) gene in response to short and long exposures to 1α,25‐dihydroxy vitamin D3. We report that in intact osteoblastic cells VDR, in association with SRC‐1, rapidly binds to the OC promoter in response to the ligand. The recruitment of SRC‐1 correlates with maximal transcriptional enhancement of the OC gene at 4 h and with increased histone acetylation at the OC promoter. In contrast to other 1α,25‐dihydroxy vitamin D3‐enhanced genes, binding of the DRIP205 subunit, which anchors the DRIP/Mediator complex to the VDR, is detected at the OC promoter only after several hours of incubation with 1α,25‐dihydroxy vitamin D3, concomitant with the release of SRC‐1. Together, our results support a model where VDR preferentially recruits SRC‐1 to enhance bone‐specific OC gene transcription. J. Cell. Physiol. 214: 740–749, 2008. © 2007 Wiley‐Liss, Inc.
Differential signaling mechanisms of HNP‐induced IL‐8 production in human lung epithelial cells and monocytes
Authors: Syeda Farisa , Liu Hui‐Yu , Tullis Elizabeth , Liu Mingyao , Slutsky Arthur S. , Zhang Haibo 
Published: September 2007

AbstractHuman neutrophil peptides (HNP) kill microorganisms but also modulate immune responses through upregulation of the chemokine IL‐8 by activation of the nucleotide P2Y6 receptor. However, the intracellular signaling mechanisms remain yet to be determined. Human lung epithelial cells (A549) and monocytes (U937) were stimulated with HNP in the absence and presence of the specific kinase inhibitors for Src, extracellular signal‐regulated kinase‐1 and ‐2 (ERK1/2), p38 mitogen‐activated protein kinase (MAPK), c‐Jun‐N‐terminal kinases (JNK), and Akt. HNP induced a rapid phosphorylation of the kinases in both cell types associated with a dose‐dependent, selective production of IL‐8 among 10 cytokines assayed. The HNP‐induced IL‐8 production was blocked by the Src tyrosine kinase inhibitor PP2, MEK1/2 inhibitor U0126, and the phosphatidylinositol 3 kinase (PI3K) inhibitor LY294002, but not by the JNK inhibitor SP600125 in both cell types. Treatment with the p38 inhibitor SB203580 attenuated the HNP‐induced IL‐8 production only in monocytes. Blockade of Src kinase blunted HNP‐induced phosphorylation of the ERK1/2 and Akt but not p38 in monocytes. In contrast, Src inhibition had no effect on phosphorylation of the other kinases in the lung epithelial cells. We conclude that the activation of ERK1/2 and PI3K/Akt pathways is required for HNP‐induced IL‐8 release which occurs in a Src‐independent manner in lung epithelial cells, while is Src‐dependent in monocytes. J. Cell. Physiol. 214: 820–827, 2008. © 2007 Wiley‐Liss, Inc.