bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preparation and characterization of porous cordierite for potential use in cellular ceramics
Authors: Valášková Marta , Martynková Gražyna 
Published: May 2009

AbstractCordierite porous ceramics Z, X, and K were prepared using three mixtures of clay minerals: Z from kaolinite, talc, and aluminum hydroxide, X from kaolinite, talc, vermiculite, and aluminum hydroxide, and K from kaolinite, talc, and magnesium oxide. Ceramics were different in porosity, specific surface area, cordierite polymorphs, and secondary crystalline phases. Vermiculite influenced textural architecture of calcined cordierite ceramics X and predestinated crystallization of the high-temperature hexagonal α-cordierite with secondary minerals enstatite, spinel and corundum. Ceramics Z contained low-temperature orthorhombic β-cordierite, enstatite, and corundum, K was diphase of β-cordierite and forsterite. Total pore area (TPA) and specific surface area (SSA) of X, in spite of the higher porosity and the pore size distribution in the range of 300–1000 nm, were smaller in comparison with TPA and SSA of Z. Ceramics K retained high porosity, two maxima at 300–1000 nm and 50–200 nm in the pores size distribution, and the highest TPA and SSA compared to those observed in ceramics Z and X.
QSAR study of 2,4-disubstituted phenoxyacetic acid derivatives as a CRTh2 receptor antagonists
Authors: Jain Abhishek , Ravichandran Veerasamy , Singh Rajesh , Mourya Vishnukanth , Agrawal Ram 
Published: May 2009

AbstractIn pursuit of better CRTh2 receptor antagonist agents, QSAR studies were performed on a series of 2,4-disubstituted phenoxyacetic acid derivatives. Stepwise multiple linear regression analysis was performed to derive QSAR models which were further evaluated for statistical significance and predictive power by internal and external validation. The best QSAR model was selected; having the correlation coefficient R = 0.904, standard error of estimation SEE = 0.456 and the cross validated squared correlation coefficient Q 2 = 0.739. Predictive ability of the selected model was also confirmed by the leave one out cross validation method and by leave 33 % out Q 2 = 0.688. The QSAR model indicates that the descriptors (logP, SI3, LM, and DVZ) play an important role in the CRTh2 receptor antagonist activities. Results of the present study may be useful in the designing of more potent 2,4-disubstituted phenoxyacetic acid derivatives as CRTh2 receptor antagonist agents.
Fatty acid profile of Trichosanthes kirilowii Maxim. seed oil
Authors: Wang Weifen , Wang Lanzhou , Jiang Jiaxin 
Published: May 2009

AbstractFatty acid profile data for refined cold-pressed Trichosanthes kirilowii Maxim. seed oil, in comparison to other commercially available oils — olive, rapeseed and camellia, are presented. Trichosanthes kirilowii Maxim. seed oil has high oleic and linoleic acid content and high polyunsaturated acid content. Squalene elutes as a distinct peak in the GC chromatograph. For a positive identification, MS detection was used. In the samples analyzed, squalene occurred in the range of 57.4–68.2 mg g−1.
Synthesis, characterization, and anti-tumor activities of some transition metal(II) complexes with podophyllic acid hydrazide
Authors: Qu Jian-Qiang , Qu Ling , Yang Qiu-Hua , Wang Liu-Fang 
Published: May 2009

AbstractFour transition metal(II) complexes with podophyllic acid hydrazide (HL) were prepared and characterized by elemental analysis, complexometric titration, thermal analysis, conductivity, IR, and 1H NMR. The complexes have the general formula ML2 · nH2O, where M = Zn, Cu, Co, and Ni, n = 2 or 0. Anti-tumor activities of podophyllotoxin, HL, ZnL2 · 2H2O, and NiL2 were tested by both the MTT and the SRB method. The results show that the activities of the complexes against the tumor cells tested are superior to HL and the anti-tumor activity of NiL2 is even similar to that of podophyllotoxin.
RANK-RANKL Signaling Pathway Is Critically Involved in the Function of CD4+CD25+ Regulatory T Cells in Chronic Colitis
Authors: Totsuka Teruji , Kanai Takanori , Nemoto Yasuhiro , Tomita Takayuki , Okamoto Ryuichi , Tsuchiya Kiichiro , Nakamura Tetsuya , Sakamoto Naoya , Akiba Hisaya , Okumura Ko , Yagita Hideo , Watanabe Mamoru 
Published: May 2009

Abstract
It is now clear that functional CD4+CD25+ regulatory T (TR) cells exist as part of the normal immune population and prevent the development of intestinal inflammation. We have recently shown that CD4+CD25+ TR cells reside in the intestine and control intestinal homeostasis in humans and mice. In this study, we demonstrate that the TNF family molecule RANKL and its receptor RANK are critically involved in controlling the function of CD4+CD25+ TR cells in the intestine. We first found that RANKL was preferentially expressed on both CD4+CD25+ TR cells and colitogenic CD4+ T cells, whereas RANK was expressed on dendritic cells. Although neutralizing anti-RANKL mAb did not affect TR activity of CD4+CD25+ TR cells to suppress the proliferation of CD4+ responder cells in vitro, in vivo administration of anti-RANKL mAb abrogated CD4+CD25+ TR cell-mediated suppression of colitis induced by adoptive transfer of CD4+CD45RBhigh T cells into SCID mice. Interestingly, an adoptive transfer experiment using Ly5.1+CD4+CD45RBhigh cells and Ly5.2+CD4+CD25+ TR cells revealed that the ratio of CD4+CD25+ TR cells in total CD4+ T cells in inflamed mucosa was significantly decreased by anti-RANKL mAb treatment. Consistent with this, the expression of RANK on lamina propria CD11c+ cells from colitic mice was significantly increased as compared with that from normal mice, and in vitro treatment with anti-RANKL mAb suppressed the expansion of CD4+Foxp3+ TR cells in culture with colitic lamina propria CD11c+ cells. Together, these results suggest that the RANK-RANKL signaling pathway is critically involved in regulating the function of CD4+CD25+ TR cells in colitis.
Protein Kinase Cθ Focusing at the cSMAC Is a Consequence rather than Cause of TCR Signaling and Is Dependent on the MEK/ERK Pathway
Authors: Praveen Kesavannair , Zheng Yan , Rivas Fabiola , Gajewski Thomas F. 
Published: May 2009

Abstract
Correlation between protein kinase Cθ focusing within the central supramolecular activation cluster (cSMAC) of the immunological synapse and optimal TCR/costimulatory receptor ligation was interpreted to imply that PKCθ focusing is required for productive signaling. However, this notion has been called into question and competing data suggest that the cSMAC contributes to receptor down-modulation. The observation that PKCθ focusing at the cSMAC is promoted by CD28 coligation, and also that it occurs late after proximal tyrosine phosphorylation events have been initiated, has led us to investigate an alternative possibility that PKCθ focusing might be a consequence rather than a cause of productive integrated signaling. Indeed, we found that inhibition of the downstream signaling molecules MEK and PI3K (but not of calcineurin, NF-κB, JNK, or p38 MAPK) significantly prevented the focusing of PKCθ at the cSMAC. It recently has been suggested that the cSMAC may be associated with TCR degradation and signal termination. Using MEK inhibition as a tool, we observed that absence of detectable PKCθ focusing had no significant effect on TCR down-modulation or duration of CD3ζ phosphorylation. Our results suggest that PKCθ focusing at the cSMAC occurs as a consequence of productive integrated downstream signaling at least at the level of MEK. If PKCθ focusing accurately reflects the cSMAC as a whole, then our data also argue against the cSMAC as being required for proximal TCR signal termination.
Proteasome Regulation of ULBP1 Transcription
Authors: Butler James E. , Moore Mikel B. , Presnell Steven R. , Chan Huei-Wei , Chalupny N. Jan , Lutz Charles T. 
Published: May 2009

Abstract
Killer lymphocytes recognize stress-activated NKG2D ligands on tumors. We examined NKG2D ligand expression in head and neck squamous cell carcinoma (HNSCC) cells and other cell lines. HNSCC cells typically expressed MHC class I chain-related gene A (MICA), MICB, UL16-binding protein (ULBP)2, and ULBP3, but they were uniformly negative for cell surface ULBP1 and ULBP4. We then studied how cancer treatments affected NKG2D ligand expression. NKG2D ligand expression was not changed by most cancer-relevant treatments. However, bortezomib and other proteasome inhibitor drugs with distinct mechanisms of action dramatically and specifically up-regulated HNSCC ULBP1 mRNA and cell surface protein. Proteasome inhibition also increased RNA for ULBP1 and other NKG2D ligands in nontransformed human keratinocytes. Proteasome inhibitor drugs increased ULBP1 transcription by acting at a site in the 522-bp ULBP1 promoter. Although the DNA damage response pathways mediated by ATM (ataxia-telangiectasia, mutated) and ATR (ATM and Rad3-related) signaling had been reported to up-regulate NKG2D ligand expression, we found that ULBP1 up-regulation was not inhibited by caffeine and wortmannin, inhibitors of ATM/ATR signaling. ULBP1 expression in HNSCC cells was not increased by several ATM/ATR activating treatments, including bleomycin, cisplatin, aphidicolin, and hydroxyurea. Ionizing radiation caused ATM activation in HNSCC cells, but high-level ULBP1 expression was not induced by gamma radiation or UV radiation. Thus, ATM/ATR signaling was neither necessary nor sufficient for high-level ULBP1 expression in human HNSCC cell lines and could not account for the proteasome effect. The selective induction of ULBP1 expression by proteasome inhibitor drugs, along with variable NKG2D ligand expression by human tumor cells, indicates that NKG2D ligand genes are independently regulated.
IgE-FcεRI Interactions Determine HIV Coreceptor Usage and Susceptibility to Infection during Ontogeny of Mast Cells
Authors: Sundstrom J. Bruce , Hair Gregory A. , Ansari Aftab A. , Secor W. Evan , Gilfillan Alasdair M. , Metcalfe Dean D. , Kirshenbaum Arnold S. 
Published: May 2009

Abstract
Progenitor mast cells (prMCs), derived from CD34+ precursors are CD4+/CCR5+/CXCR4+ and susceptible to CCR5(R5)-tropic virus but only marginally susceptible to CXCR4(X4)-tropic HIV. As infected prMCs mature within extravascular compartments, they become both latently infected and HIV-infection resistant, and thus capable of establishing an inducible reservoir of CCR5-tropic infectious clones. In this report we provide the first evidence that IgE-FcεRI interactions, occurring during a unique period of mast cell (MC) ontogeny, enhance prMC susceptibility to X4 and R5X4 virus. IgE-FcεRI interactions significantly increased expression of CXCR4 mRNA (∼400- to 1800-fold), enhanced prMC susceptibility to X4 and R5X4 virus (∼3000- to 16,000-fold), but had no significant effect on CD4, CCR3, or CCR5 expression, susceptibility to R5 virus, or degranulation. Enhanced susceptibility to infection with X4 virus occurred during the first 3–5 wk of MC ontogeny and was completely inhibited by CXCR4-specific peptide antagonists and omalizumab, a drug that inhibits IgE-FcεRI interactions. IgE-FcεRI coaggregation mediated by HIVgp120 or Schistosoma mansoni soluble egg Ag accelerated maximal CXCR4 expression and susceptibility to X4 virus by prMCs. Our findings suggest that for HIV-positive individuals with atopic or helminthic diseases, elevated IgE levels could potentially influence the composition of CXCR4-tropic and R5X4-tropic variants archived within the long-lived tissue MC reservoir created during infection.
Novel Human Transitional B Cell Populations Revealed by B Cell Depletion Therapy
Authors: Palanichamy Arumugam , Barnard Jennifer , Zheng Bo , Owen Teresa , Quach Tam , Wei Chungwen , Looney R. John , Sanz Iñaki , Anolik Jennifer H. 
Published: May 2009

Abstract
Transitional cells represent a crucial step in the differentiation and selection of the mature B cell compartment. Human transitional B cells have previously been variably identified based on the high level of expression of CD10, CD24, and CD38 relative to mature B cell populations and are expanded in the peripheral blood following rituximab-induced B cell-depletion at reconstitution. In this study, we take advantage of the gradual acquisition of the ABCB1 transporter during B cell maturation to delineate refined subsets of transitional B cells, including a late transitional B cell subset with a phenotype intermediate between T2 and mature naive. This late transitional subset appears temporally following the T1 and T2 populations in the peripheral compartment after rituximab-induced B cell reconstitution (and is thus termed T3) and is more abundant in normal peripheral blood than T1 and T2 cells. The identity of this subset as a developmental intermediate between early transitional and mature naive B cells was further supported by its ability to differentiate to naive during in vitro culture. Later transitional B cells, including T2 and T3, are found at comparatively increased frequencies in cord blood and spleen but were relatively rare in bone marrow. Additional studies demonstrate that transitional B cells mature across a developmental continuum with gradual up-regulation of mature markers, concomitant loss of immature markers, and increased responsiveness to BCR cross-linking in terms of proliferation, calcium flux, and survival. The characterization of multiple transitional B cell subpopulations provides important insights into human B cell development.
A Programmed Switch from IL-15- to IL-2-Dependent Activation in Human NK Cells
Authors: Pillet Anne-Hélène , Bugault Florence , Thèze Jacques , Chakrabarti Lisa A. , Rose Thierry 
Published: May 2009

Abstract
IL-2 and IL-15 differentially control the development, activation and proliferation of human NK cells, although they share common signal-transducing receptor chains CD122 and common γ. To explore this issue, we analyzed in detail the kinetics of cytokine receptor expression, cytokine binding, and signaling responses in human NK cells treated with common γ-chain family cytokines. We provide evidence for the sequential expression of IL-15Rα and IL-2Rα at the surface of cytokine-stimulated human NK cells, independent of the cytokine used for stimulation (IL-2, IL-15, or IL-7). Binding experiments confirmed the switch of high-affinity receptor from IL-15R to IL-2R between 18 and 48 h after stimulation. Consequently, phospho-STAT5 signaling responses to IL-15 were efficient in human NK cells pretreated with cytokines for 18 h, but were abolished at 48 h. Functional NK cell responses to IL-15, including IFN-γ secretion and CD107a expression, followed a similar pattern, indicating the physiological relevance of the cytokine receptor switch. Importantly, IL-15 complexed to soluble IL-15Rα preserved the capacity to activate cytokine-stimulated human NK cells at 48 h, suggesting that human NK cells remained competent for IL-15 trans-presentation, while they had become refractory to free diffusible IL-15. These findings define a common cytokine receptor expression program, which increases human NK cell sensitivity to free IL-15 in early activation and redirects responses toward IL-2 and trans-presented IL-15 at later stages. Such a program may prevent excessive human NK cell activation by effectors of innate immunity and regulate the transition between the innate and adaptive stages of immune responses.
Central Memory CD8+ T Cells Induce Graft-versus-Host Disease and Mediate Graft-versus-Leukemia
Authors: Zheng Hong , Matte-Martone Catherine , Jain Dhanpat , McNiff Jennifer , Shlomchik Warren D. 
Published: May 2009

Abstract
In allogeneic hemopoietic stem cell transplantation, mature donor αβ T cells in the allograft promote T cell reconstitution in the recipient and mediate the graft-vs-leukemia (GVL) effect. Unfortunately, donor T cells can attack nonmalignant host tissues and cause graft-vs-host disease (GVHD). It has previously been shown that effector memory T cells not primed to alloantigen do not cause GVHD yet transfer functional T cell memory and mediate GVL. Recently, central memory T cells (TCM) have also been reported to not cause GVHD. In contrast, in this study, we demonstrate that purified CD8+ TCM not specifically primed to alloantigens mediate GVHD in the MHC-mismatched C57BL/6 (B6)→BALB/c and the MHC-matched, multiple minor histocompatibility Ag-mismatched C3H.SW→B6 strain pairings. CD8+ TCM and naive T cells (TN) caused similar histological disease in liver, skin, and bowel. B6 CD8+ TCM and TN similarly expanded in BALB/c recipients, and the majority of their progeny produced IFN-γ upon restimulation. However, in both models, CD8+ TCM induced milder clinical GVHD than did CD8+ TN. Nonetheless, CD8+ TCM and TN were similarly potent mediators of GVL against a mouse model of chronic-phase chronic myelogenous leukemia. Thus, in contrast to what was previously thought, CD8+ TCM are capable of inducing GVHD and are substantially different from TEM but only subtly so from TN.
Role of Marginal Zone B Lymphocytes in Invariant NKT Cell Activation
Authors: Bialecki Emilie , Paget Christophe , Fontaine Josette , Capron Monique , Trottein François , Faveeuw Christelle 
Published: May 2009

Abstract
Splenic marginal zone B (MZB) lymphocytes represent, along with dendritic cells (DC) a first line of defense against blood-borne pathogens. MZB cells express high levels of MHC class II and CD1d molecules but so far their ability to activate and orientate conventional and innate-like T lymphocytes, such as invariant NKT (iNKT) cells, is still elusive. In the present study, we show that murine MZB cells proliferate, mature phenotypically, and secrete cytokines in response to TLR (except TLR3) agonists. When pulsed with OVA peptide (but not whole OVA), MZB cells promote the release of IFN-γ and IL-4 by Ag-specific CD4+ T lymphocytes and their stimulation with the TLR9 agonist CpG oligodeoxynucleotide (ODN), a potent MZB cell activator, biases them toward more Th1 inducers. Unlike DC, CpG ODN-stimulated MZB cells fail to stimulate iNKT cells. Although able to activate iNKT hybridomas, MZB cells sensitized with free α-galactosylceramide (α-GalCer), a CD1d-restricted glycolipid Ag, do not directly activate ex vivo sorted iNKT cells unless DC are added to the culture system. Interestingly, MZB cells amplify the DC-mediated activation of iNKT cells and depletion of MZB cells from total splenocytes strongly reduces iNKT cell activation (cytokine production) in response to α-GalCer. Thus, DC and MZB cells provide help to each other to optimize iNKT cell stimulation. Finally, in vivo transfer of α-GalCer-loaded MZB cells potently activates iNKT and NK cells. This study confirms and extends the concept that MZB cells are important players in immune responses, a property that might be exploited.
Neonatal Exposure to Low-Dose 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Causes Autoimmunity Due to the Disruption of T Cell Tolerance
Authors: Ishimaru Naozumi , Takagi Atsuya , Kohashi Masayuki , Yamada Akiko , Arakaki Rieko , Kanno Jun , Hayashi Yoshio 
Published: May 2009

Abstract
Although 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to influence immune responses, the effects of low-dose TCDD on the development of autoimmunity are unclear. In this study, using NFS/sld mice as a model for human Sjögren’s syndrome, in which the lesions are induced by the thymectomy on day 3 after birth, the autoimmune lesions in the salivary glands, and in later phase, inflammatory cell infiltrations in the other organs were developed by neonatal exposure to nonapoptotic dosage of TCDD without thymectomy on day 3 after birth. We found disruption of thymic selection, but not thymic atrophy, in TCDD-administered mice. The endogenous expression of aryl hydrocarbon receptor in the neonatal thymus was significantly higher than that in the adult thymus, suggesting that the neonatal thymus may be much more sensitive to TCDD compared with the adult thymus. In addition, the production of TH1 cytokines such as IL-2 and IFN-γ from splenic CD4+ T cells and the autoantibodies relevant for Sjögren’s syndrome in the sera from TCDD-exposed mice were significantly increased compared with those in control mice. These results suggest that TCDD/aryl hydrocarbon receptor signaling in the neonatal thymus plays an important role in the early thymic differentiation related to autoimmunity.
Hypoxia-Inducible Factor (HIF) 1α Accumulation and HIF Target Gene Expression Are Impaired after Induction of Endotoxin Tolerance
Authors: Frede Stilla , Stockmann Christian , Winning Sandra , Freitag Patricia , Fandrey Joachim 
Published: May 2009

Abstract
The oxygen-sensitive transcription factor hypoxia-inducible factor 1 (HIF-1) is known as the key regulator of hypoxia-induced gene expression. In addition to hypoxia, endotoxins such as bacterial LPS as well as proinflammatory cytokines have been shown to induce HIF-1, suggesting an integrative role for HIF-1 in conditions of hypoxia and inflammation. Cells can become tolerant to endotoxins by repetitive exposure to LPS. Herein, we studied the effect of endotoxin tolerance on HIF-1α accumulation and expression of HIF target genes in human monocytic cells and primary mouse peritoneal macrophages. Tolerant cells had reduced levels of HIF-1α under hypoxia, which was due to lowered levels of HIF-1α mRNA. HIF-1α expression is under control of NF-κB and increased DNA binding of the p52 subunit of NF-κB was found in tolerant cells. Knock down of p52 abolished the effects of endotoxin tolerance on HIF-1α expression, which suggest a negative regulatory role of p52 on HIF-1α transcription during endotoxin tolerance. Endotoxin tolerant cells showed diminished expression of the HIF target genes phosphoglycerate kinase 1 and adrenomedullin and reduced viability under hypoxic conditions, as well as a significantly reduced invasion. Peritoneal macrophages from endotoxin-tolerant mice made showed significantly reduced HIF-1α protein accumulation and subsequent HIF target gene expression. We conclude that endotoxin tolerance impairs HIF-1α induction which reduces the ability of monocytic cells to survive and function under hypoxic conditions.
Withdrawal of Sex Steroids Reverses Age- and Chemotherapy-Related Defects in Bone Marrow Lymphopoiesis
Authors: Dudakov Jarrod A. , Goldberg Gabrielle L. , Reiseger Jessica J. , Chidgey Ann P. , Boyd Richard L. 
Published: May 2009

Abstract
A significant decline in immune function is characteristic of aging. Along with the involution of the thymus and associated impaired architecture, which contributes to profound loss of naive T cell production, there are also significant declines in B cell development and the progenitors that support lymphopoiesis. These collectively lead to a reduced peripheral immune repertoire, increase in opportunistic infections, and limited recovery following cytoablation through chemo- or radiotherapy. We have previously shown that sex steroid ablation (SSA) causes a major reversal of age-related thymic atrophy and improves recovery from hematopoietic stem cell transplant. This study focused on the impact of SSA on the B cell compartment and their progenitors in middle-aged and cyclophosphamide-treated mice. In both models, SSA enhanced the number of lymphoid progenitors and developing B cells in the bone marrow (BM) as well as reversing age-related defects in the cycling kinetics of these cells. Enhanced BM lymphopoiesis was reflected in the periphery by an increase in recent BM emigrants as well as immature and mature plasma cells, leading to an enhanced humoral response to challenge by hepatitis B vaccine. In conclusion, SSA improves lymphoid progenitor and B cell recovery from age- and chemotherapy-induced immunodepletion, complimenting the effects on T cells. Since SSA has been achieved clinically for over 25 years, this provides a novel, rational basis for approaching the need for immune recovery in many clinical conditions.