bluuebunny/crossref_metadata_2025_split huggingface dataset:
3D F–K and finite‐difference dip moveout in cross‐spreads
Authors: Masjukov Andrey V. 
Published: July 2003

ABSTRACTA 3D F–K dip‐moveout (DMO) is developed, which is applicable to data acquired in an elementary single‐fold cross‐spread. The key idea is that a 3D log‐stretch transform and the inherent regularity of the cross‐spread geometry make it possible to transform 3D Fourier DMO. The derived theory generalizes the 2D Fourier shot‐gather DMO in the log‐stretch domain; 2D turns out to be a special case. Similarly to 2D, the cross‐spread DMO becomes convolutional after multidimensional logarithmic stretch. The proposed method works for orthogonal and slanted acquisition geometries; the cross‐spread DMO relationships are found to be independent of the intersection angle of the shot and receiver lines. In contrast to integral (Kirchhoff‐style) methods, the cross‐spread F–K DMO does not degrade from the inevitable irregularity in 3D sampling of offsets in a CMP gather. The newly derived F–K DMO operator can be approximated by finite‐difference (FD) schemes; the low‐order FD cross‐spread DMO equation is shown to be the 3D extension of the Bolondi and Rocca offset continuation. It is shown that F–K and low‐order FD operators are effective in a synthetic case.
Using DC resistivity tomography to detect and characterize mountain permafrost
Authors: Hauck Christian , Vonder Mühll Daniel , Maurer Hansruedi 
Published: July 2003

ABSTRACTDirect‐current (DC) resistivity tomography has been applied to different mountain permafrost regions. Despite problems with the very high resistivities of the frozen material, plausible results were obtained. Inversions with synthetic data revealed that an appropriate choice of regularization constraints was important, and that a joint analysis of several tomograms computed with different constraints was required to judge the reliability of individual features. The theoretical results were verified with three field experiments conducted in the Swiss and the Italian Alps. At the first site, near Zermatt, Switzerland, the location and the approximate lateral and vertical extent of an ice core within a moraine could be delineated. On the Murtel rock glacier, eastern Swiss Alps, a steeply dipping boundary at its frontal part was observed, and extremely high resistivities of several MΩ indicated a high ice content. The base of the rock glacier remained unresolved by the DC resistivity measurements, but it could be constrained with transient EM soundings. On another rock glacier near the Stelvio Pass, eastern Italian Alps, DC resistivity tomography allowed delineation of the rock glacier base, and the only moderately high resistivities within the rock glacier body indicated that the ice content must be lower compared with the Murtel rock glacier.
Phase behaviour of P‐SV converted waves recorded at the sea‐bed
Authors: Dai Hengchang 
Published: July 2003

ABSTRACTShear waves recorded at or near the sea‐bed, i.e. a water–sediment interface, may suffer from unwanted phase change, which is detrimental to velocity analysis and processing and degrades the quality of the final stacked or migrated image. In this study, this phenomenon is analysed for P‐SV converted waves recorded at the sea‐bed. Theoretical analysis shows that phase change does not occur if the converted shear waves always maintain raypaths that lie within the critical angle, provided the subsurface layering is horizontal. A phase change that is asymmetric with offset can readily be explained as being due to dipping layers at targets or the dipping sea‐bed. This analysis is extended to multiple layers and anisotropic media and shows that the same conclusions hold. The analysis performed on two sets of ocean‐bottom‐cable seismic data shows that the majority of observations show little evidence of phase change, and occasionally display the asymmetric phase change with offset. This finding underlines the robustness of converted shear waves for imaging the horizontal subsurfaces and sea‐bed as all of the offset information may be used.
Evidence for post‐transcriptional regulation of interleukin‐5 by dexamethasone
Authors: Staples Karl J. , Bergmann Martin W. , Barnes Peter J. , Newton Robert 
Published: July 2003

SummaryInterleukin‐5 (IL‐5) is a T helper type 2 cytokine, which is implicated in the pathogenesis of eosinophilic diseases such as asthma. Both peripheral blood mononuclear cells (PBMC) and primary human T cells display similar patterns of IL‐5 expression when stimulated with both phorbol‐12‐myristate 13‐acetate and phytohaemagglutinin. The expression of IL‐5 stimulated by these agents was shown to require de novo transcription and translation. However, although dexamethasone was a potent inhibitor of both IL‐5 release and messenger RNA accumulation from PBMC and T cells, dexamethasone had no effect on the luciferase activity of a reporter construct under the control of an IL‐5 promoter region transiently transfected into primary human T cells. Furthermore, dexamethasone appeared to decrease the stability of IL‐5 messenger RNA and this effect was dependent upon de novo transcription. Taken together, the results presented here suggest that, whilst transcriptional processes predominantly regulate IL‐5 release, the mechanism by which dexamethasone inhibits IL‐5 is post‐transcriptional.
Role of chemokine ligand 2 in the protective response to early murine pulmonary tuberculosis
Authors: Kipnis Andre , Basaraba Randall J. , Orme Ian M. , Cooper Andrea M. 
Published: July 2003

SummaryChemokines play an important role in the development of immunity to tuberculosis. Chemokine ligand 2 (CCL2, JE, monocyte chemoattractant protein‐1) is thought to be primarily responsible for recruiting monocytes, dendritic cells, natural killer cells and activated T cells, all of which play critical roles in the effective control of tuberculosis infection in mice. We show here that in mice in which the CCL2 gene was disrupted, low‐dose aerosol infection with Mycobacterium tuberculosis resulted in fewer macrophages entering the lungs, but only a minor and transient increase in bacterial load in the lungs; these mice were still able to establish a state of chronic disease. Such animals showed similar numbers of activated T cells as wild‐type mice, as determined by their expression of the CD44hi CD62lo phenotype, but a transient reduction in cells secreting interferon‐γ. These data indicate that the primary deficiency in mice unable to produce CCL2 is a transient failure to focus antigen‐specific T lymphocytes into the infected lung, whereas other elements of the acquired host response are compensated for by different ligands interacting with the chemokine receptor CCR2.
Rat C‐reactive protein activates the autologous complement system
Authors: Padilla Niubel Diaz , Bleeker Wim K. , Lubbers Yvonne , Rigter Gemma M. M. , Van Mierlo Gerard J. , Daha Mohamed R. , Hack C. Erik 
Published: July 2003

SummaryActivation of complement is a biological function of human C‐reactive protein (hCRP), whereas rat CRP (rCRP) has been claimed to be unable to activate complement. As important biological functions of proteins are probably conserved among species, we re‐evaluated, using various ligands, the capability of rCRP to activate complement. The activation of complement by hCRP and rCRP was investigated in solid‐ and fluid‐phase systems. In the solid‐phase system, purified CRP was fixed to enzyme‐linked immunosorbent assay (ELISA) plates and incubated with human or rat recalcified plasma. Dose‐dependent binding of human and rat C3 and C4 was observed to human and rat CRP, respectively. In the fluid‐phase system, recalcified rat plasma, which contains about 500 mg/l of CRP, or human plasma supplemented with hCRP, were incubated with lyso‐phosphatidylcholine. A dose‐dependent activation of complement was observed upon incubation with this ligand, as reflected by the generation of activated C4 as well as of CRP–complement complexes. This activation was, in both cases, inhibited by preincubation of plasma with p‐aminophosphorylcholine, a specific inhibitor of the interaction of CRP with its ligands, or by chelation of calcium ions. We conclude that rat CRP, similarly to human CRP, can activate autologous complement. These results support the notion that opsonization of ligands with complement is an important biological function of CRP.
Allergen‐induced fluctuation in CC chemokine receptor 3 expression on bone marrow CD34+ cells from asthmatic subjects: significance for mobilization of haemopoietic progenitor cells in allergic inflammation
Authors: Sehmi Roma , Dorman Sandra , Baatjes Adrian , Watson Rick , Foley Ronan , Ying Sun , Robinson Douglas S. , Kay A. Barry , O'Byrne Paul M. , Denburg Judah A. 
Published: July 2003

SummaryThere is increasing evidence that primitive progenitors migrate from the bone marrow (BM) via the peripheral circulation to tissue sites where they undergo in situ differentiation to provide a continued source of effector cells, such as eosinophils, during an allergic inflammatory response. To study mechanisms of progenitor cell mobilization in allergic reactions, we investigated fluctuations in the expression of the eotaxin receptor, CC chemokine receptor 3 (CCR3), on CD34+ cells from stable asthmatics following allergen (i.e. antigen) challenge. BM aspirates were taken from seven early responder (ER) and 10 dual responder (DR) asthmatics who, following antigen challenge developed only an early bronchoconstrictor response and an early and late‐ bronchoconstrictor response, respectively. Expression of CCR3 was detected on primitive (CD34+ cells) and eosinophil‐lineage committed progenitors (CD34+ interleukin‐5 receptor alpha‐subunit+ cells) by flow cytometry and confirmed by co‐localization of CCR3 messenger RNA to CD34 immunopositive cells using in situ hybridization. When preantigen levels were compared to 24‐hr postantigen levels, significant increases in BM CD34+ CCR3+ cells were detected in DR, who also developed a significant sputum and blood eosinophilia and increased methacholine airway responsiveness. In contrast, a significant attenuation of BM CD34+ CCR3+ cells was observed in ER. In a dose‐dependent manner eotaxin, but not interleukin (IL)‐5, stimulated CD34+ progenitor cell migration in vitro. This migrational response to eotaxin was abrogated by anti‐CCR3 monoclonal antibody and primed by preincubation with IL‐5. We propose that fluctuations in CCR3 expression on human BM CD34+ cells may facilitate chemokine‐mediated progenitor cell mobilization to the peripheral circulation and the resultant development of pulmonary eosinophilia, a cardinal feature of asthma.
CD8+ immunoregulatory cells in the graft‐versus‐host reaction: CD8 T cells activate dendritic cells to secrete interleukin‐12/interleukin‐18 and induce T helper 1 autoantibody
Authors: Noble Alistair , Leggat Jamie A. , Inderberg Else M. 
Published: July 2003

SummaryInitiation of cell‐mediated immunity or autoimmunity requires secretion of interleukin (IL)‐12 from dendritic cells (DC), which drives the generation of T helper 1 (Th1) effector cells in synergy with IL‐18. Induction of IL‐12 can be triggered by microbial stimuli but also requires signals from activated T cells. We investigated interactions between alloreactive CD4 and CD8 T cells in mixed lymphocyte reactions (MLR) in vitro and in the graft‐versus‐host reaction (GVHR) in vivo. In a parent‐into‐F1 model of GVHR, donor CD8 cells were found to suppress the hyper‐immunoglobulin E (IgE) syndrome, anti‐DNA immunoglobulin G1 (IgG1) autoantibodies and donor CD4‐cell expansion, but were essential for Th1‐dependent immunoglobulin G2a (IgG2a) autoantibody production and release of serum IL‐12 p40. In vitro, addition of alloreactive CD8 cells to CD4 cells and mature DC enhanced Th1 development. CD4 and CD8 T cells induced IL‐18 from DC and primed for IL‐12 p70 secretion via interferon‐γ (IFN‐γ) or tumour necrosis factor‐α (TNF‐α). However CD8 T cells, but not CD4 cells, released IFN‐γ/TNF‐α after primary stimulation. The data suggest that rapid release of inflammatory cytokines from central memory‐type CD8 cells early in immunity is critical for induction of Th1 cells via DC activation and IL‐12 production. This pathway could provide a means for amplification of cell‐mediated autoimmunity in the absence of microbial stimuli.
Host response of platelet‐activating factor receptor‐deficient mice during pulmonary tuberculosis
Authors: Weijer Sebastiaan , Leemans Jaklien C. , Florquin Sandrine , Shimizu Takao , Ishii Satoshi , Van Der Poll Tom 
Published: July 2003

SummaryPlatelet‐activating factor (PAF) is a phospholipid with potent, diverse actions, which has been implicated as an important mediator in host defence against several intracellular pathogens. To determine the role of PAF in host defence in pulmonary tuberculosis, PAF receptor‐deficient (PAFR−/−) and wild‐type (PAFR+/+) mice were infected intranasally with a virulent strain of Mycobacterium tuberculosis. Mycobacterial outgrowth in lungs and liver did not differ significantly between PAFR−/− and PAFR+/+ mice at 2 or 6 weeks postinfection. After 28 weeks, 86% of PAFR−/− mice and 79% of PAFR+/+ mice had died (non‐significant). In addition, both mouse strains were indistinguishable with respect to histopathology, the recruitment and activation of lymphocytes, and cytokine concentrations in the lung. These data suggest that PAF is not involved in the protective immune response to tuberculosis.
Inhibition of B‐cell death does not restore T‐cell‐dependent immune responses in CD40‐deficient mice
Authors: Merino Jesús , Díez Miguel A. , Muñiz María , Buelta Luis , Núñez Gabriel , López‐Hoyos Marcos , Merino Ramón 
Published: July 2003

SummarySignalling through CD40 is essential for the development of immunoglobulin G (IgG) antibody responses, germinal centres and B‐cell memory against T‐dependent antigens. In addition, engagement of CD40 in B cells promotes cell survival by inducing the expression of anti‐apoptotic members of the bcl‐2 family of cell‐death regulators. In the present study we analysed whether T‐dependent immune responses can be developed in mice deficient in CD40 if the anti‐apoptotic activity mediated by the engagement of CD40 in B cells is compensated by the constitutive over‐expression of anti‐apoptotic genes of the bcl‐2 family. We showed that the over‐expression of either hbcl‐2 or hbcl‐xL transgenes in B cells is not sufficient to restore IgG antibody responses and germinal centre formation in CD40‐deficient mice. These results indicate that CD40 functions, other than those mediated through survival, are required for the establishment of T‐dependent B‐cell responses.
αβ T‐cell development is not affected by inversion of TCRβ gene enhancer sequences: polar enhancement of gene expression regardless of enhancer orientation
Authors: Huang Fang , Cabaud Olivier , Verthuy Christophe , Hueber Anne‐Odile , Ferrier Pierre 
Published: July 2003

SummaryV(D)J recombination and expression of the T‐cell receptor β (TCRβ) gene are required for the development of the αβ T lymphocyte lineage. These processes depend on a transcriptional enhancer (Eβ) which acts preferentially on adjacent upstream sequences, and has little impact on the 5′ distal and 3′ proximal regions of the TCRβ locus. Using knock‐in mice, we show that αβ T‐cell differentiation and TCRβ gene recombination and expression are not sensitive to the orientation of Eβ sequences. We discuss the implication of these results regarding the mode of enhancer function at this locus during T lymphocyte development.
The membrane attack complex of complement contributes to plasmin‐induced synthesis of platelet‐activating factor by endothelial cells and neutrophils
Authors: Lupia Enrico , Del Sorbo Lorenzo , Bergerone Serena , Emanuelli Giorgio , Camussi Giovanni , Montrucchio Giuseppe 
Published: July 2003

SummaryThrombolytic agents, used to restore blood flow to ischaemic tissues, activate several enzymatic systems with pro‐inflammatory effects, thus potentially contributing to the pathogenesis of ischaemia–reperfusion injury. Platelet‐activating factor (PAF), a phospholipid mediator of inflammation, has been implicated in the pathogenesis of this process. We previously showed that the infusion of streptokinase (SK) induces the intravascular release of PAF in patients with acute myocardial infarction (AMI), and that cultured human endothelial cells (EC) synthesized PAF in response to SK and plasmin (PLN). In the present study, we investigated the role of the membrane attack complex (MAC) of complement in the PLN‐induced synthesis of PAF. In vivo, we showed a correlation between the levels of soluble terminal complement components (sC5b‐9) and the concentrations of PAF detected in blood of patients with AMI infused with SK. In vitro both EC and polymorphonuclear neutrophils (PMN), incubated in the presence of PLN and normal human serum, showed an intense staining for the MAC neoepitope, while no staining was detected when they were incubated with PLN in the presence of heat‐inactivated normal human serum. Moreover, the insertion of MAC on EC and PMN plasmamembrane elicited the synthesis of PAF. In conclusion, our results elucidate the mechanisms involved in PAF production during the activation of the fibrinolytic system, showing a role for complement products in this setting. The release of PAF may increase the inflammatory response, thus limiting the beneficial effects of thrombolytic therapy. Moreover, it may have a pathogenic role in other pathological conditions, such as transplant rejection, tumoral angiogenesis, and septic shock, where fibrinolysis is activated.
Murine lymph node‐derived stromal cells effectively support survival but induce no activation/proliferation of peripheral resting T cells in vitro
Authors: Zhou Yan‐wen , Aritake Sayoko , Tri Endharti Agustina , Wu Jianghong , Hayakawa Akemi , Nakashima Izumi , Suzuki Haruhiko 
Published: July 2003

SummaryLittle is known about the homeostatic mechanisms by which the levels of peripheral lymphocytes are maintained. The survival of naïve T cells in vivo must be maintained by some factors that have not been characterized in an in vitro culture system. In this study, we established a culture system of stromal cells derived from murine lymph nodes and investigated the action of the stromal cells in supporting the survival of resting T cells in vitro. Most of the T cells cocultured with the stromal cells did not die, and the supernatant of cultured stromal cells increase the viability of T cells. This T‐cell survival‐supporting activity was maintained for more than 7 days. Although interleukin (IL)‐4, IL‐6, IL‐7, and interferon‐β also rescued peripheral T cells from spontaneous cell death, medium‐soluble and heat‐sensitive factor(s) derived from the stromal cells supported the survival of T cells more effectively and for a longer time than did these cytokines. T cells maintained in the culture system with the stromal cells appeared to remain in a resting G0/G1 state and did not show remarkable DNA synthesis. From these results, it is presumed that some soluble factor(s) other than the tested cytokines that have been identified as supporting T‐cell survival are produced from lymph node stromal cells. These factor(s) play an important role in maintenance of resting T cells.
Up‐regulation of matrix metalloproteinase‐1 expression in U937 cells by low‐density lipoprotein‐containing immune complexes requires the activator protein‐1 and the Ets motifs in the distal and the proximal promoter regions
Authors: Maldonado Alejandro , Game Bryan A. , Song Lanxi , Huang Yan 
Published: July 2003

SummaryWe reported previously that low‐density lipoprotein (LDL)‐containing immune complexes (LDL‐IC) stimulated matrix metalloproteinase‐1 (MMP‐1) expression in U937 histiocytes through Fc gamma receptor (FcγR)‐mediated extracellular signal‐regulated kinase pathway. The present study has explored the transcriptional mechanisms involved in the stimulation. Deletion analysis showed that LDL‐IC stimulated MMP‐1 promoter activity in cells transfected with the Construct 1 that contained a 4,334‐bp MMP‐1 promoter fragment, but had no effect in cells transfected with other constructs that had shorter MMP‐1 promoter (2685‐bp or less), suggesting that cis‐acting elements located between −4334 and −2685 are required for the promoter stimulation. The mutation study further indicated that the activator protein‐1 (AP‐1) (−3471) or Ets (−3836) motifs in this distal region were essential for the LDL‐IC‐stimulated MMP‐1 expression. Moreover, although above deletion analysis showed that LDL‐IC did not stimulate MMP‐1 promoter activity in cells transfected with constructs that contained the proximal AP‐1 (−72) and Ets (−88) in the promoter fragments that are 2685‐bp or less, the mutations of the −72 AP‐1 or the −88 Ets motif in the construct 1 abolished the stimulation of MMP‐1 expression by LDL‐IC, suggesting that a long promoter sequence is required for the −72 AP‐1 and −88 Ets motifs to be involved in the stimulation. Finally, electrophoretic mobility shift assay showed that LDL‐IC stimulated the activities of transcription factors AP‐1 and Ets. In conclusion, the present study shows that both the distal and proximal AP‐1 and Ets motifs are required for LDL‐IC‐stimulated MMP‐1 expression in U937 histiocytes.
Genomic structure around joining segments and constant regions of swine T‐cell receptor α/δ (TRA/TRD) locus
Authors: Uenishi Hirohide , Hiraiwa Hideki , Yamamoto Ryuji , Yasue Hiroshi , Takagaki Yohtaroh , Shiina Takashi , Kikkawa Eri , Inoko Hidetoshi , Awata Takashi 
Published: July 2003

SummaryA complete genomic region of 131·2 kb including the swine T‐cell receptor α/δ constant region (TRAC/TRDC) and joining segments (TRAJ/TRDJ) was sequenced. The structure of this region was strikingly conserved in comparison to that of human or mouse. All of the 61 TRAJ segments detected in the human genomic sequence were detected in the swine sequence and the sequence of the protein binding site of T early alpha, the sequence of the α enhancer element and the conserved sequence block between TRAJ3 and TRAJ4 are highly conserved. Insertion of the repetitive sequences that interspersed after the differentiation of the species in mammals such as short interspersed nucleotide elements is markedly suppressed in comparison to other genomic regions, while the composition of the mammalian‐wide interspersed sequences is relatively conserved in human and swine. This observation indicates the existence of a highly selective pressure to conserve this genomic region around TRAJ throughout the evolution of mammals.