bluuebunny/crossref_metadata_2025_split huggingface dataset:
Crystal and molecular structure of 2,6‐bis(4‐fluorobenzylidene)cyclohexanone
Authors: Ompraba G. , Rafi Z. A. , Yogavel M. , Velmurugan D. , Sekar K. , Karthikeyan E. , Perumal S. , Choudhury A. R. , Guru Row T. N. 
Published: August 2003

AbstractThe title compound, C20H16F2O, crystallizes in triclinic system with $ {\rm P} \bar1 $ space group and the unit cell parameters are: a = 9.700(5), b = 11.834(6), c = 14.315(7) Å, α = 78.464(9), β = 74.394(8), γ = 86.186(9)°, V = 1551.0(1) Å3 and Z = 4. The final R‐factor is 4.8%. The cyclohexanone ring adopts a sofa conformation. The different ways of adjusting to steric repulsion results in significant differences between molecule A and B with respect to torsion angles. The steric repulsion between the aromatic groups and hydrogen atoms on the cyclohexanone ring causes increase of the values of bond angles at the C atoms joining the rings and rotation of the corresponding bond, at the expense of conjugation energy of the system. In addition to the van der Waals interactions, C‐H…O, C‐H…F and C‐H…π interactions stabilize the molecular packing. (© 2003 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
The Characterization of LiMn2O4 Thin Film Cathode for Lithium Rechargeable Microbattery Prepared by Liquid Source Misted Chemical Deposition
Authors: Kim K.W. , Kim M.R. , Lee S.‐W. , Han K.‐S. , Woo S.I. 
Published: August 2003

AbstractLiquid source misted chemical deposition was used to fabricate LiMn2O4 film as a cathode for lithium rechargeable microbatteries. The effect of crystallization temperature on the film properties was investigated by X‐ray diffraction (XRD), Raman spectroscopy (RS), X‐ray photoelectron spectroscopy (XPS), scanning electron microscopy (SEM), cyclic voltammetry (CV), and charge/discharge experiments. When the heat treatment for crystallization of the as‐deposited film was carried out at 800 °C in a rapid thermal apparatus (RTA) in an oxygen atmosphere for 5 min, the structural and compositional purity, and the electrochemical activity of the deposited film, were optimized. The LiMn2O4 films prepared by this method exhibited much better electrochemical rechargeability than those deposited by other techniques, such as sputtering, laser ablation, sol–gel coating, etc. The prepared film exhibits an initial discharge capacity of 62.5 μA h cm–2 μm–1 and a low capacity fade of 8.0 % over 100 cycles.
MOCVD of Platinum Films from (CH3)3CH3CpPt and Pt(acac)2: Nanostructure, Conformality, and Electrical Resistivity
Authors: Goswami J. , Wang C.‐G. , Cao W. , Dey S.K. 
Published: August 2003

AbstractA potentially manufacturable liquid‐source MOCVD process was applied to deposit platinum (Pt) films (12–140 nm) on thermally oxidized Si substrates. The deposition of Pt films was carried out at a substrate temperature of 350 °C by oxygen‐assisted pyrolysis of complex precursors in a low‐pressure, hot‐wall reactor. The effects of two different metal–organic precursors, a) trimethyl methyl cyclopentadienyl platinum [(CH3)3CH3CpPt], and b) platinum acetylacetonate [Pt(acac)2], on the properties of Pt films were studied. Although the polycrystalline Pt films deposited from Pt(acac)2 exhibited a preferred (111) orientation with a X‐ray intensity ratio of I(111)/I(200) = 40, the films deposited from (CH3)3CH3CpPt were highly (111) oriented with I(111)/I(200) = 270. The following properties were typical of Pt films from Pt(acac)2 as compared to Pt films from (CH3)3CH3CpPt: finer grain size (25 nm vs. 50 nm), smaller root mean square (rms) surface roughness (5 nm vs. 15 nm), and better step coverage (95 % vs. 35 %). These experimental findings indicated that growth of Pt films from Pt(acac)2 occurred under the kinetically‐limited regime, whereas the deposition of Pt from (CH3)3CH3CpPt was limited by the mass transport rate. Additionally, the temperature (4.2–293 K) dependence of the electrical resistivities (ρ) of Pt films was measured and the electron mean free paths were estimated. It was observed that ρ(T) deviated from Matthiessen's rule.
Synthesis of Boron Nitride Films Using Electron–Cyclotron Resonance Microwave Plasma and an H2–BF3–N2–Ar–He Gas System
Authors: Chan C.‐Y. , Zhang W. , Chan K.‐M. , Bello I. , Lee S.‐T. 
Published: August 2003

AbstractBoron nitride (BN) films with high crystallinity and phase purity (>80 %) in the cubic phase were synthesized over large areas using fluorine chemistry and electron–cyclotron resonance (ECR) microwave plasma. Plasma‐enhanced fluorine chemistry was provided by a complex H2–BF3–N2–Ar–He gas mixture. Each component of the mixture was optimized in accordance with its function. Such a procedure allowed the preparation of thick cBN films at a bias voltage as low as –30 V. Micrometer‐thick cBN films exhibiting columnar growth were obtained. However, ion bombardment was still indispensable for the cBN growth. The effects of deposition time and ion bombardment on the phase purity and crystallinity of the cBN films were investigated.
The HIV protease inhibitor Indinavir reduces immature dendritic cell transendothelial migration
Authors: Whelan Kathryn T. , Lin Chen‐Lung , Cella Marina , McMichael Andrew J. , Austyn Jonathan M. , Rowland‐Jones Sarah L. 
Published: August 2003

AbstractIndinavir (IDV) is a protease inhibitor that successfully suppresses HIV‐1 replication as part of anti‐retroviral therapy. There is evidence to suggest that IDV may also act non‐specifically upon host proteases. In this study we investigated whether IDV could modulate protease‐dependent molecules involved in dendritic cell (DC) migration — a pivotal process in immunoregulation. Human monocyte‐derived DC were exposed to IDV (IDV‐DC) and transendothelial migration (TEM) to inflammatory chemokines was determined. TEM of IDV‐DC was significantly impaired compared to non‐treated DC (p<0.01). Phenotypic analysis revealed that IDV‐DC had reduced DC‐SIGN expression, correlating with reduced adhesion to immobilized ICAM‐2. Nevertheless, the reduction in migration following exposure to IDV could not be fully attributable to DC‐SIGN interactions alone. Investigation of IDV‐DC interactions with the underlying matrix protein, fibronectin, demonstrated that IDV significantly impaired DC binding to immobilized fibronectin (p<0.01). IDV appeared to act upon VLA‐4 and VLA‐5 since addition of antagonist monoclonal antibodies (mAb) similarly reduced adhesion ofnon‐treated DC to fibronectin. Combined blockade of DC using anti‐VLA‐4, VLA‐5 and anti‐DC‐SIGN mAb inhibited TEM to a similar extent as IDV. Our results strongly suggest that IDV inhibits host proteases necessary for DC migration and may, therefore, affect DC immunoregulation in HIV‐1‐infected patients.
B cell activation leads to shedding of complement receptor type II (CR2/CD21)
Authors: Masilamani Madhan , Kassahn Daniela , Mikkat Stefan , Glocker Michael O. , Illges Harald 
Published: August 2003

AbstractComplement receptor type II (CR2/CD21) is the major receptor for C3d fragments on immune complexes. CD21 also serves as the receptor for Epstein–Barr virus in humans. On mature B cells, CD21 reduces the threshold of BCR signaling together with CD81, Leu13 and CD19, but it also occurs on other cells of the immune system where it performs unknown functions. A soluble form of CD21 (sCD21) is shed from the cell surface and is found in human blood plasma. An as‐yet‐unknown protease is thought to be responsible for this shedding. Altered levels of sCD21 occur in plasma in certain clinical conditions. We show here by mass spectrometry that sCD21 in human plasma of healthy donors is predominantly a short form of CD21 without the exon‐11‐encoded sequences. Whereas the N terminus of sCD21 was found unmodified, the C terminus is truncated, implying that only the extracellular portion of CD21 is shed. Peripheral blood B cells, but not T cells, contribute to the plasma CD21‐pool. CD21 shedding is induced by stimulation with PMA plus Ca2+ ionophore, or by stimulation of the BCR with anti‐IgM+anti‐CD40.
Trypanosoma cruzi infection modulates intrathymic contents of extracellular matrix ligands and receptors and alters thymocyte migration
Authors: Cotta‐de‐Almeida Vinícius , Bonomo Adriana , Mendes‐da‐Cruz Daniella Arêas , Riederer Ingo , de Meis Juliana , Lima‐Quaresma Kátia Regina Ferreira , Vieira‐de‐Abreu Adriana , Villa‐Verde Déa Maria Serra , Savino Wilson 
Published: August 2003

AbstractSeveral T cell abnormalities have been described in the course of acute Trypanosoma cruzi infection in mice, including severe effects on the thymus. In the present study, looking at the expression of extracellular matrix ligands in the thymus, we observed that deposits of fibronectin and laminin increased progressively during the course of infection, reaching a maximum at the peak of parasitemia and thymic atrophy. Concomitantly, membrane expression of fibronectin and laminin receptors (VLA‐4, VLA‐5 and VLA‐6) was also enhanced on thymocyte subsets of infected mice. These results correlated with changes in intrathymic thymocyte migration ability during the acute phase of infection, when a higher fibronectin‐dependent transmigratory activity of CD4+CD8+ thymocytes was observed. Strikingly, we detected higher frequency of immature and high VLA‐expressing CD4+CD8+ T cells in the peripheral lymphoid organs of infected mice at thepeak of parasitemia. These cells seemed to be thymus dependent, since significantly lower amounts of them were found in thymectomized mice, and some of them carry “prohibited” Vβ segments of the TCR. Our data suggest an imbalance in the intrathymic cell trafficking following acute T. cruzi infection, likely due to dysregulated extracellular matrix‐dependent interactions.
Pathogenesis of Lyme neuroborreliosis: Borrelia burgdorferi lipoproteins induce both proliferation and apoptosis in rhesus monkey astrocytes
Authors: Ramesh Geeta , Alvarez Alida L. , Roberts E. Donald , Dennis Vida A. , Lasater Barbara L. , Alvarez Xavier , Philipp Mario T. 
Published: August 2003

AbstractBrain invasion by Borrelia burgdorferi, the agent of Lyme disease, results in an inflammatory and neurodegenerative disorder called neuroborreliosis. In humans, neuroborreliosis has been correlated with enhanced concentration of glial fibrillary acidic protein in the cerebrospinal fluid, a sign of astrogliosis. Rhesus monkeys infected by us with B. burgdorferi showed evidence of astrogliosis, namely astrocyte proliferation and apoptosis. We formulated the hypothesis that astrogliosis could be caused by spirochetal lipoproteins. We established primary cultures of rhesus monkey astrocytes and stimulated the cells with recombinant lipidated outer surface protein A (L‐OspA), a model B. burgdorferi lipoprotein, and tripalmitoyl‐S‐glyceryl‐Cys‐Ser‐Lys4‐OH (Pam3Cys), a synthetic lipopeptide that mimics the structure of the lipoprotein lipid moiety. L‐OspA elicited not only astrocyte proliferation but also apoptosis, two features observed during astrogliosis. Astrocytes produced both IL‐6 and TNF‐α in response to L‐OspA and Pam3Cys. Proliferation induced by L‐OspA was diminished in the presence of an excess of anti‐IL‐6 antibody, and apoptosis induced by this lipoprotein was completely suppressed with anti‐TNF‐α antibody. Hence, IL‐6 contributes to, and TNF‐α determines, astrocyte proliferation and apoptosis, respectively, as elicited by lipoproteins. Our results provide proof of the principle that spirochetal lipoproteins could be key virulence factors in Lyme neuroborreliosis, and that astrogliosis might contribute to neuroborreliosis pathogenesis.
Tissue‐specific regulation of the human acute‐phase serum amyloid A genes, SAA1 and SAA2, by glucocorticoids in hepatic and epithelial cells
Authors: Thorn Caroline F. , Lu Zhi‐Yong , Whitehead Alexander S. 
Published: August 2003

AbstractThe human acute‐phase protein serum amyloid A (A‐SAA), encoded by the SAA1 and SAA2 genes, is dramatically induced by pro‐inflammatory mediators during the acute‐phase response to infection or injury. Circulating A‐SAA is predominantly synthesized by the liver. However, other tissues are the source of locally produced A‐SAA. Here, we establish that the qualitative and kinetic aspects of SAA1 and SAA2 transcription following treatment of HepG2 hepatoma cells and KB epithelial cells with glucocorticoids and cytokines are quite distinct. Untreated HepG2 cells do not express A‐SAA mRNA and glucocorticoids, when administered alone, fail to induce either SAA1 or SAA2. In contrast, untreated KB cells constitutively express SAA1 mRNA. Following cytokine stimulation, both A‐SAA genes are rapidly up‐regulated to similar extents. As in the hepatoma cell line, co‐stimulation of KB cells with glucocorticoids places SAA1 at a transcriptional advantage over SAA2. Interestingly, SAA1 can be significantly induced by glucocorticoids alone in KB cells. The effects of glucocorticoids on SAA1 in both cell lines is glucocorticoid receptor‐dependent. Differential regulation of A‐SAA expression in these cell lines may reflect different temporal and spatial requirements for A‐SAA synthesis in response to different inflammatory challenges.
Cruzipain induces autoantibodies against cardiac muscarinic acetylcholine receptors. Functional and pathological implications
Authors: Sterin‐Borda Leonor , Giordanengo Laura , Joensen Lilian , Gea Susana 
Published: August 2003

AbstractThe goal of this study was to investigate whether cruzipain, a Trypanosoma cruzi immunodominant antigen, was able to induce antibodies reactive to the cardiac M2 muscarinic acetylcholine receptor (M2 mAChR). Immunization with cruzipain that was devoid of enzyme activity triggered IgG antibodies against cardiac M2 mAChR. By radioligand competition assay we proved that the anti‐cruzipain IgG fraction, purified from serum, inhibited binding of the specific M2 mAChR radioligand [3H]quinuclidinyl benzilate. We also demonstrated that anti‐cruzipain IgG reacted against the second extracellular loop of the M2 mAChR. The corresponding affinity‐purified serum anti‐M2e2 IgG (reacting against a synthetic peptide corresponding to this loop in humans) displayed agonist‐like activity associated with specific M2 mAChR activation — increase of cGMP, inositol phosphate accumulation and nitric oxide synthase activity — triggering a decrease in myocardial contractility. Moreover, the same IgG fraction decreased heart frequency, related to inhibition of adenylate cyclase activity. These results imply thatcruzipain plays a role in the production of antibodies against M2 mAChR, which have been related to the pathogenesis of dysautonomic syndrome described in Chagas' disease.
OX40 (CD134) and OX40 ligand interaction plays an adjuvant role during in vivo Th2 responses
Authors: Ishii Naoto , Ndhlovu Lishomwa C. , Murata Kazuko , Sato Takayuki , Kamanaka Masahito , Sugamura Kazuo 
Published: August 2003

AbstractThe role of OX40‐OX40 ligand (OX40L) interaction in Th cell differentiation remains contentious. In vitro studies have revealed a Th2‐biased effect by OX40 signals in T cells. However, in vivo studies demonstrated that OX40‐OX40L interaction is involved in responses either Th1 or Th2, or both, which appears to be dependent on the experimental conditions used. We document in our report Th cell differentiation in OX40L‐deficient and OX40L‐transgenic (Tg) mice in response to protein antigens (Ag) and to Leishmania major (L. major) infection. Upon immunization with protein Ag, we demonstrate the adjuvant effect of OX40 signals during in vivo Th2 responses. However, adjuvant treatment to mice ameliorates the Th2‐specific effect of OX40‐OX40L interaction and rather induces concurrent promotion of both Th1 and Th2 responses via OX40 signals. Thus, previous reports showing promotion of Th1 response by OX40‐OX40L interaction may in actual fact be affected by the adjuvant effects mediated by the various experimental conditions. Indeed, constitutive OX40–OX40L interactions in OX40L‐Tg mice converted the normally resistant C57BL/6 strain, into a susceptible status following L. major infection due to an extraordinary elevated Th2 response. These results provide convincing evidence demonstrating that the OX40‐OX40L interaction is paramount in the development of Th2 responses in vivo.
Aging‐dependent generation of suppressive CD4+CD25–R123loCD103+ T cells in mice
Authors: Shimizu Jun , Moriizumi Eiko 
Published: August 2003

AbstractAdvancing age is associated with significant alterations in immune functions, including a decline in CD4 T cell function, in both mice and humans. In our previous report, we showed that CD4+CD25– T cells in aged (24‐month‐old) mice, especially after in vitro pre‐stimulation of these cells, exhibit hyporesponsive and suppressive properties. We examined here whether the suppressive activity of aged CD4+CD25– T cells is ascribable to a particular population within these cells. In vitro analyses revealed that cell populations rapidly extruding Rhodamine‐123 (R123) (referred to as R123lo cells) in aged CD4+CD25– T cells have a more potent suppressive function compared with R123hi populations.In addition, CD103+ cells in freshly prepared aged CD4+CD25–R123lo T cells had a most potent suppressive activity. Both R123hi and R123lo populations had individually stronger suppressive activity after pre‐stimulation than before pre‐stimulation. Furthermore, the R123lo population in young CD4+CD25– T cells also had different properties from R123hi T cells: low responsiveness, no additive effect in proliferation assays, and the gain of a suppressive function after in vitro pre‐stimulation. Takentogether, these results suggest that CD4+CD25–R123lo T cells are a unique population within whole CD4+CD25– T cells. This population exists in the earlystage of the life span, and the properties in this population become obvious with aging, that is the gain of their suppressive activity.
Activation of Epstein‐Barr virus/C3d receptor (gp140, CR2, CD21) on human cell surface triggers pp60src and Akt‐GSK3 activities upstream and downstream to PI 3‐kinase, respectively
Authors: Barel Monique , Balbo Michelle , Le Romancer Muriel , Frade Raymond 
Published: August 2003

AbstractWe previously demonstrated that CR2 activation on human B lymphocyte surface specifically triggered tyrosine phosphorylation of the 95‐kDa nucleolin, this leading to its binding on SH2 domainsof p85 sub‐unit of PI 3‐kinase and to activation of this enzyme. The specificity of CR2 pathway was clearly demonstrated as neither CD19 nor BCR could induce tyrosine phosphorylation of nucleolin in normal B lymphocytes. These data led us to investigate herein additional molecular events, which were triggered by CR2 activation, upstream and downstream to PI 3‐kinase activation. Upstream, we demonstrated that pp60src, a tyrosine kinase of the src family, was involved in tyrosine phosphorylation of nucleolin, while syk tyrosine kinase was not. We also demonstrated a direct protein‐proteininteraction of pp60src with nucleolin in a CR2‐dependent and CD19‐independent pathway. Downstream, we demonstrated that CR2 activation also triggered Akt and GSK3 enzyme activation, this pathway being under the control of pp60src tyrosine kinase activation. These regulatory functions of activated CR2 were specific as independent of syk tyrosine kinase and of CD19 and BCR activation. Thus, CR2 activation recruits a specific mechanism to activate PI 3‐kinase and its subsequent pathways, this mechanism being different to those recruited by CD19 and BCR.
NK T cells stimulated with a ligand for TLR2 at least partly contribute to liver injury caused by Escherichia coli infection in mice
Authors: Hiromatsu Takashi , Matsuguchi Tetsuya , Shimizu Hideyuki , Yajima Toshiki , Nishimura Hitoshi , Arai Toshiyuki , Nimura Yuji , Yoshikai Yasunobu 
Published: August 2003

AbstractFas ligand (Fas L) expression was induced on intrahepatic NK1.1+ T cells in vivo after an intraperitoneal inoculation of Escherichia coli. Liver injury after E. coli infection, as assessed by serum GPT level and histological examination, was significantly reduced in Jα281–/– mice lacking NK1.1+ T cells or in gld/gld mice bearing mutated Fas L, indicating that NK T cells at least partly contribute to E. coli‐induced liver injury in a Fas/Fas L‐dependent manner. Bacterial numbers in organs and cytokine levelsin serum of Jα281–/– mice did not differ from those of Jα281+/+ mice following E. coli infection. Intrahepatic NK1.1+ T cells, which preferentially expressed Toll‐like receptor 2 (TLR2) mRNA, responded in vitro to synthetic lipoprotein, a ligand for TLR2, by inducing Fas L expression on their surface. In a manner analogous to E. coli infection, lipoprotein and LPS could additively induce Fas L expression on NK1.1+ T cells, leading to liver injury in vivo in normal mice but not in gld/gld mice. In conclusion, it is suggested that induction of Fas L on NK T cells in response to bacterial components such as lipoproteins plays an important role in pathogenesis of E. coli‐induced liver injuryin mice.
Contrasting roles for IL‐10 in protective immunity to different life cycle stages of intestinal nematode parasites
Authors: Helmby Helena , Grencis Richard K. 
Published: August 2003

AbstractExpulsion of the gastro‐intestinal nematode Trichinella spiralis is associated with a pronounced mastocytosis mediated by a T helper (Th) 2 type response involving interleukin (IL)‐4 and IL‐13. Here we demonstrate that IL‐10 is a key regulator of protective immune responses against T. spiralis in vivo. IL‐10 knockout mice or normal mice treated with a neutralizing anti‐IL‐10 receptor antibody are highly susceptible to a primary T. spiralis infection and show significantly delayed adult worm expulsion. Depletion of IL‐10 resulted in elevated Th1 and Th2 cytokine responses but significantly reduced numbers of mucosal mast cells in the jejunum. Interestingly, the increase in IFN‐γ detected in the absence of IL‐10 resulted in increased immunity to larval stages. Hence, IL‐10 has a negative effect on immunity to the tissue dwelling larval stages of T. spiralis but plays a significant biological role as an in vivo regulator of intestinal mast cell responses and is crucially involved in protection against adult stages of intestinal parasites in vivo.
The impaired NK cell cytolytic function in viremic HIV‐1 infection is associated with a reduced surface expression of natural cytotoxicity receptors (NKp46, NKp30 and NKp44)
Authors: De Maria Andrea , Fogli Manuela , Costa Paola , Murdaca Giuseppe , Puppo Francesco , Mavilio Domenico , Moretta Alessandro , Moretta Lorenzo 
Published: August 2003

AbstractSignals leading to NK cell triggering are primarily mediated by natural cytotoxicity receptors (NCR) upon binding to as‐yet‐undefined cell surface ligand(s) on normal hematopoietic cells, pathogen‐infected cells or tumor cells. In this study we tried to determine whether the decreased NK cell cytolytic function that is observed in HIV‐1‐infected patients may be related to a decreased expression of NCR. In HIV‐1‐infected patients, freshly drawn, purified NK cells expressed significantly decreased surface densities of NKp46 and NKp30 NCR. The low surface density of NKp46, NKp30 and NKp44 was also confirmed in in‐vitro‐activated NK cell populations and NK cell clones derived from HIV‐1 patients compared with uninfected donors. This defective NCR expression in HIV‐1 patients was associated with a parallel decrease of NCR‐mediated killing of different tumor target cells. Thus, the present study indicates that the defective expression of NCR represents at least one of the possible mechanisms leading to the impaired NK cell function in HIV‐1 infection and it can contribute to explain the relatively high frequency of opportunistic tumors reported in cohorts of untreated patients before the occurrence of profound immunosuppression (<200 CD4+ cells/mm3).