bluuebunny/crossref_metadata_2025_split huggingface dataset:
Obesity and hypertension among children after treatment for acute lymphoblastic leukemia
Authors: Chow Eric J. , Pihoker Catherine , Hunt Kathryn , Wilkinson Karen , Friedman Debra L. 
Published: September 2007

AbstractBACKGROUND.The purpose was to determine the prevalence and treatment‐related risk factors for obesity and hypertension among childhood acute lymphoblastic leukemia (ALL) survivors treated with contemporary therapy.METHODS.In a single‐center longitudinal study, serial body mass indices (BMI) and blood pressure (BP) measurements of children ages 2–20 at time of ALL diagnosis and enrolled on pediatric cooperative group trials from 1993–2003 were abstracted from medical records and converted to population‐referenced z‐scores.RESULTS.Among 165 study participants, BMI z‐scores increased significantly between diagnosis (median age 4.8 years) and therapy completion. At the end of therapy, 17.0% of survivors were overweight (BMI of 25–29, or 85–94% for age), 21.2% were obese (BMI ≥30, or ≥95% for age), and 15.3% had BP meeting stage 1+ hypertension thresholds (systolic or diastolic BP ≥140/90 mm Hg, or 95% for age and height plus 5 mm Hg). These proportions were found to be unchanged 2‐3 years later. In multivariate analysis, the highest level of corticosteroid exposure was associated with both obesity (odds ratio [OR] 6.0; 95% confidence interval [95% CI], 1.2–28.5) as well as stage 1+ hypertension (OR 2.4; 95% CI, 1.2–5.1) compared with the lowest level. Females also were more likely to have increased BMI and elevated BP compared with males. Treatment intensity and cranial radiotherapy were not found to be associated with BMI or BP changes.CONCLUSIONS.Despite reductions in the use of cranial radiotherapy, contemporary childhood survivors of ALL remain at an increased risk of obesity and hypertension at least several years after the completion of treatment, with those exposed to higher doses of corticosteroids at greater risk. Cancer 2007. © 2007 American Cancer Society.
Positron emission tomography imaging in nonsmall‐cell lung cancer
Authors: Erasmus Jeremy J. , Macapinlac Homer A. , Swisher Stephen G. 
Published: September 2007

AbstractPositron emission tomography (PET) using 18F‐2‐deoxy‐D‐glucose, a D‐glucose analog labeled with fluorine‐18, complements conventional radiologic assessment in the evaluation of patients with nonsmall‐cell lung cancer (NSCLC). PET is being routinely used to improve the detection of nodal and extrathoracic metastases. PET is also currently being evaluated in the assessment of prognosis and therapeutic response and by potentially allowing an earlier assessment of response may prove invaluable in the oncologic management of patients. The article discusses the diagnosis, staging, and assessment of treatment response and prognosis with an emphasis on the appropriate clinical use of PET in management. Cancer 2007. © 2007 American Cancer Society.
DQ‐based simulation of weakly nonlinear heat conduction processes
Authors: Tomasiello S. 
Published: September 2007

AbstractIn this paper, an explicit form for the numerical solution of problems in the space–time domain by using quadrature rules is proposed. The compact form of the shape functions recently proposed by the author is useful to the scope. Numerical solutions for the time‐dependent one‐dimensional nonlinear heat conduction problem are calculated by means of the iterative differential quadrature method, a method proposed by the author and based on quadrature rules. The accuracy of the solution and stability analysis show good performance of the approach. Copyright © 2007 John Wiley & Sons, Ltd.
Electrochemically Induced Growth of Zinc Oxide
Authors: Palms Dennis , Norwig Jochen , Wegner Gerhard 
Published: September 2007

AbstractThe electrolytically induced precipitation of zinc oxide from zinc nitrate solution on gold surfaces in the presence of water‐soluble polymers was examined for reaction times between 0.5 and 600 seconds. Regardless of the additive, polycrystalline films of zinc oxide have formed after 30 seconds, but polymeric additives dramatically change the morphology of the ZnO films. Amperometric analysis and fitting the diffusion reduced the current density‐time curve according to Avrami kinetics and it reveals that polymers bearing methacrylic acid groups result in spherical growth whereas such with sulfonic acid groups lead to a platelike growth of crystallites. Without additive prisms grow predominantly in one dimension. These findings are confirmed also by scanning electron microscopy (SEM) and X‐ray diffraction (XRD) analysis.
Inhibitory effects and target genes of bone morphogenetic protein 6 in Jurkat TAg cells
Authors: Sivertsen Einar A. , Huse Kanutte , Hystad Marit E. , Kersten Christian , Smeland Erlend B. , Myklebust June H. 
Published: September 2007

AbstractBone morphogenetic proteins (BMP) are multifunctional cytokines that belong to the TGF‐β superfamily. BMP have been shown to regulate haematopoietic stem cells, B lymphopoiesis and early thymocyte differentiation. In the present study we explored the role of BMP‐6 in Jurkat TAg cells. BMP‐6 rapidly induced phosphorylation of Smad1/5/8, p38 and ERK1/2, followed by a potent up‐regulation of ID1, ID2 and ID3. ID1 and ID3 were also induced at the protein level. Genome‐wide expression profiling of cells treated with BMP‐6 compared to medium confirmed that ID1–ID3 were target genes of BMP‐6 together with Noggin and Smad6. Furthermore, several genes involved in transcriptional regulation were also identified, including NFKBIA, HEY1, DLX2, KLF10 and early growth response 1. Stimulation with BMP‐6 exerted an antiproliferative effect that was counteracted by inhibitor of DNA binding (Id)1 siRNA, indicating that Id1 is an important downstream mediator in Jurkat TAg cells. A subset of CD4+ T cells were found to express the BMP receptors Alk‐2 and Alk‐3 (type I), in addition to BMPRII (type II). BMP‐6 also induced phosphorylation of Smad1/5/8, followed by transcriptional increase in ID1–ID3 mRNA expression. However, we did not observe significant changes in Id protein expression in CD4+ T cells. Altogether, the data indicate a role for BMP‐6 in human T lineage cells.
Immune modulation of human dendritic cells by complement
Authors: Castellano Giuseppe , Woltman Andrea M. , Schlagwein Nicole , Xu Wei , Schena Francesco P. , Daha Mohamed R. , van Kooten Cees 
Published: September 2007

AbstractDeficiency in complement proteins such as C1q is associated with the development of systemic lupus erythematosus (SLE). Here, we show that the differentiation of dendritic cells (DC) in the presence of C1q (C1qDC) gives rise to CD1a+/DC‐SIGN+ cells with high phagocytic capacity and low expression of CD80, CD83 and CD86. Further, when C1qDC were exposed to LPS, a significant reduction in the production of IL‐6, TNF‐α and IL‐10 occurred with a limited up‐regulation of CD80, CD83 and CD86. In addition, C1qDC were less responsive to activation by CD40L in terms of IL‐12p70 secretion and CD86 expression. C1qDC showed an impaired ability to stimulate alloreactive T cells, with a reduced production of IFN‐γ. In conclusion, we have shown that C1q is a potent modulator of DC, resulting in cells characterized by an impaired capacity of cytokine production and an impaired up‐regulation of costimulatory molecules, leading to a limited T cell response. Therefore, we hypothesize that, next to a pivotal role in the safe clearance of apoptotic cells, C1q regulates the threshold of DC activation and thereby prevents hyperactivation of the overall immune response.
Calcium dependence of T cell proliferation following focal stimulation
Authors: Schwarz Eva C. , Kummerow Carsten , Wenning Anna S. , Wagner Kerstin , Sappok Anne , Waggershauser Katherina , Griesemer Désirée , Strauß Bettina , Wolfs Melodie‐Jo , Quintana Ariel , Hoth Markus 
Published: September 2007

AbstractClonal T cell expansion through proliferation is a central process of the adaptive immune response. Apoptosis of activated T cells is required to avoid chronic inflammation. T cell proliferation and apoptosis are often analyzed with stimuli that do not induce formation of a functional immunological synapse. Here we analyze the Ca2+ dependence of proliferation and apoptosis in primary human CD4+ T cells following stimulation with anti‐CD3/anti‐CD28‐coated beads, which induce a tight interaction similar to the immunological synapse. We found this focal stimulation to be much more efficient for stimulating IL‐2 production and proliferation than non‐focal TCR stimuli. Surprising little Ca2+ entry through Ca2+ channels was required for T cell proliferation. Transient free intracellular calcium concentration ([Ca2+]i) elevations of up to 220 nM from a baseline level of around 40 nM were sufficient for maximal proliferation in primary human CD4+ T cells. We also show that proliferation was very Ca2+ sensitive in the range 90–120 nM, whereas apoptosis was basically constant for [Ca2+]i levels of 90–120 nM. We conclude that very small changes in [Ca2+]i can dramatically change the ratio between proliferation and apoptosis, thus keeping the balance between overshooting and inefficient immune responses.
Specific TLR ligands regulate APRIL secretion by dendritic cells in a PKR‐dependent manner
Authors: Hardenberg Gijs , Planelles Lourdes , Schwarte Carla M. , van Bostelen Liesbeth , Le Huong Tran , Hahne Michael , Medema Jan Paul 
Published: September 2007

AbstractA proliferation inducing ligand (APRIL) and B cell activating factor belonging to the TNF family (BAFF/BLyS) have been implicated in IgA class switch recombination in thymus‐independent (TI) B cell responses. Dendritic cells (DC) are thought to regulate Ig class switching in TI B cell responses by providing B cells with cytokines, including APRIL and BAFF. We therefore set out to analyze the regulation of APRIL and BAFF expression by human monocyte‐derived DC (moDC). We observed that moDC produce and secrete APRIL, but could not detect expression of BAFF. Importantly, stimulation with the Toll‐like receptor ligands CpG and poly I:C specifically induced APRIL production, while other Toll‐like receptor ligands were ineffective. The increase in APRIL was dependent on translation, but surprisingly not transcription. Instead, enhanced APRIL production and secretion resulted from activation of protein kinase receptor (PKR), as it was completely inhibited by the specific inhibitor of PKR, 2‐aminopurine. This suggests that the specific induction of APRIL by CpG and poly I:C, and the signal integration by PKR, are regulated by translational modification and hint at a role for APRIL in the TI B cell response to viral infections.
Functional role of phosphatidylcholine‐specific phospholipase C in regulating CD16 membrane expression in natural killer cells
Authors: Cecchetti Serena , Spadaro Francesca , Lugini Luana , Podo Franca , Ramoni Carlo 
Published: September 2007

AbstractCD16, the low‐affinity FcIgG receptor (FcγRIIIA), is predominantly expressed in human NK cells. Our recent findings indicate that CD16 expression on the outer membrane surface of NK cells is correlated with the membrane expression of phosphatidylcholine‐specific phospholipase C (PC‐PLC). In the present study we analyzed the trafficking of CD16 from the plasma membrane to cytoplasmic regions, after stimulation with specific mAb. The CD16 receptor is internalized, likely degraded and newly synthesized; its endocytosis is independent of ATP, but requires an integral and functional actin cytoskeleton. Antibody‐mediated CD16 cross‐linking results in an approximately twofold increase in PC‐PLC enzymatic activity within 10 min. Analysis of PC‐PLC and CD16 distribution in NK cell plasma membrane demonstrates that the proteins are physically associated and partially accumulated in lipid rafts. Pre‐incubation of NK cells with a PC‐PLC inhibitor, D609, causes a dramatic decrease both in CD16 receptor and PC‐PLC enzyme expression on the plasma membrane. Interestingly, among phenotype PBL markers, only CD16 is strongly down‐modulated by D609 treatment. CD16‐mediated cytotoxicity is also reduced after D609 incubation. Taken together, these data suggest that the PC‐PLC enzyme could play an important role in regulating CD16 membrane expression, the CD16‐mediated cytolytic mechanism and CD16‐triggered signal transduction.
Endoglycosidase treatment abrogates IgG arthritogenicity: Importance of IgG glycosylation in arthritis
Authors: Nandakumar Kutty Selva , Collin Mattias , Olsén Arne , Nimmerjahn Falk , Blom Anna M. , Ravetch Jeffrey V. , Holmdahl Rikard 
Published: September 2007

AbstractThe glycosylation status of IgG has been implicated in the pathology of rheumatoid arthritis. Earlier, we reported the identification of a novel secreted endo‐β‐N‐acetylglucosaminidase (EndoS), secreted by Streptococcus pyogenes that specifically hydrolyzes the β‐1,4‐di‐N‐acetylchitobiose core of the asparagine‐linked glycan of human IgG. Here, we analyzed the arthritogenicity of EndoS‐treated collagen type II (CII)‐specific mouse mAb in vivo. Endoglycosidase treatment of the antibodies inhibited the induction of arthritis in (BALB/c × B10.Q) F1 mice and induced a milder arthritis in B10.RIII mice as compared with the severe arthritis induced by non‐treated antibodies. Furthermore, EndoS treatment did not affect the binding of IgG to CII and their ability to activate complement, but it resulted in reduced IgG binding to FcγR and disturbed the formation of stable immune complexes. Hence, the asparagine‐linked glycan on IgG plays a crucial role in the development of arthritis.
Programmed cell death 1 (PD‐1) and its ligand PD‐L1 are required for allograft tolerance
Authors: Wang Liqing , Han Rongxiang , Hancock Wayne W. 
Published: September 2007

AbstractProgrammed cell death‐1 (PD‐1, CD279) and its widely expressed, inducible ligand, PD‐L1 (CD274), together dampen T cell activation, but whether they are essential for allograft tolerance is unknown. We show, using gene‐deficient mice and blocking mAbs in wild‐type mice, that costimulation blockade is ineffectual in PD‐1–/– or PD‐L1–/– allograft recipients, or in wild‐type allograft recipients treated with anti‐PD‐1 or anti‐PD‐L1 mAb. Alloreactive PD‐1–/– CD4 and CD8 T cells had enhanced proliferation and cytokine production compared to wild‐type controls, and anergy could not be induced in PD‐1‐deficient CD4 T cells. We conclude that without inhibitory signals from PD‐1 ligation, alloantigen‐induced T cell proliferation and expansion cannot be regulated by costimulation blockade, and peripheral tolerance induction cannot occur.
Cover Picture: TLR agonists induce the differentiation of human bone marrow CD34+ progenitors into CD11c+ CD80/86+ DC capable of inducing a Th1‐type response – Eur. J. Immunol. 10/2007
Authors: Sioud Mouldy , Fløisand Yngvar 
Published: September 2007

AbstractIt has recently been shown that TLR are capable of regulating the differentiation of haematopoietic progenitor cells. Specifically, R848 (resquimod, a specific TLR7/8 agonist) is capable of stimulating the differentiation of human bone marrow CD34+ progenitors into myeloid DC. Sioud and Fløisand (pp. 2834–2846) investigate the differentiation induced by other TLR agonists (loxoribine (TLR7) and Pam3CSK4 (TLR2)), as well as further investigating the effects of R848. The cover image (a composite, artificially coloured figure) is based on May‐Grünwald‐Giesma staining of the CD11c– CD14– (green section of the image), CD11c+ CD14+ (yellow section) and CD11c+ CD14– (red section) cell subsets induced following stimulation of CD34+ progenitors with R848 for seven days. Importantly, around 30% of cells of the CD11c+ CD14– subset display DC morphology (multiple fine dendrites) and, furthermore, this CD11c+ CD14– subset is shown to be capable of activating allogeneic T cells.
[Bis(catechol)salen]MnIII Coordination Polymers as Support‐Free Heterogeneous Asymmetric Catalysts for Epoxidation
Authors: Cho So‐Hye , Gadzikwa Tendai , Afshari Mitra , Nguyen SonBinh T. , Hupp Joseph T. 
Published: September 2007

AbstractThe formation of coordination polymers by the reaction of [bis(catechol)salen]MnIII with several di‐ and trivalent metal ions is reported. These polymers are insoluble in a wide range of organic solvents and water but can be dissolved upon addition of excess pyrocatechol. They function as enantioselective heterogeneous epoxidation catalysts and exhibit catalytic activity comparable to that of the homogeneous[bis(catechol)salen]MnIII building block alone when used for the enantioselective epoxidation of 2,2‐dimethyl‐2H‐chromene. After catalysis, catalyst isolation from the reaction mixture can be readily achieved by centrifugation and decantation. Under practical oxidant concentrations, the catalyst can be recycled up to ten times with little loss of activity and no loss of enantioselectivity. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Substitution, Addition, and Recombination Reactions of Precursor Complexes with Ferrocenyl Carboxylate Units
Authors: Wang Xia , Li Linke , Hou Hongwei , Wu Jie , Fan Yaoting 
Published: September 2007

AbstractWith the use of sodium β‐ferrocenylacrylate and sodium p‐ferrocenylbenzoate as functional ligands, we synthesized mononuclear precursor complexes containing facile leaving groups or coordinatively unsaturated metal ions: [Cd(η2‐OOCCH=CHFc)2(C2H5OH)2] (1), {[Cd(η2‐OOCC6H4Fc)2(dmf)2(H2O)]} (2), {[Cd(η2‐OOCC6H4Fc)2 (phen)(H2O)](CH3OH)} (3), and {[Zn(OOCC6H4Fc)2(phen)](H2O)} (4) (phen = 1,10‐phenanthroline). Investigation of the fourprecursor ferrocenyl carboxylate complexes as building blocks resulted in ten complexes. The complexes{[Cd(η2‐OOCCH=CHFc)2(bbbm)](H2O)}n (1a), {[Cd2(η2‐OOCCH=CHFc)4 (pbbm)2](CH3OH)6(H2O)4} (1b), {[Cd(η2‐OOCC6H4Fc)2(py)3] (CH3OH)4} (2a), {[Cd2(η2‐OOCC6H4Fc)4(btx)2](thf)3(CH3OH)2} (2b), {[Cd2(η2‐OOCC6H4Fc)2(OOCC6H4Fc)2(phen)2(bbbm)] (CH3OH)4(thf)2} (3a), and [Zn(OOCC6H4Fc)2(phen)(H2O)] (4a) were obtained by the substitution or addition reactions of the precursor complexes under moderate conditions. As anticipated, the structural integrity of the precursor complexes can be maintained from the precursors to these complexes. We designed the structures of the complexes by controlling the number of leaving groups in the precursor complexes. In addition, a recombination may have taken place in the reactions of the precursor complexes with organic ligands under severe conditions. The “recombinant” complexes {[Cd2(η2‐OOCCH=CHFc)2(μ2‐η2‐OOCCH=CHFc)2(L)2](CH3OH)4}n [L = 1,4‐bis(imidazol‐1‐ylmethyl)benzene (bix), 1c; L = btx, 1d], {[Cd(η2‐OOCC6H4Fc)2(pbbm)(H2O)](H2O)}n (3b) and {[Zn(OOCC6H4Fc)2(bbbm)](CH3OH)3}n (4b) were also obtained under reflux conditions. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Pressure‐assisted field‐amplified sample injection with reverse migrating micelles for analyzing trace steroids in MEKC
Authors: Fang Huaifang , Yang Fangxing , Sun Junling , Zeng Zhaorui , Xu Ying 
Published: September 2007

AbstractThis paper describes a novel method that applies pressure‐assisted field‐amplified sample injection with reverse migrating micelles (PA‐FASI‐RMM) for the online concentration of neutral analytes in MEKC with a low‐pH BGE. After injection of a plug of water into the separation capillary, negative voltage and positive pressure were simultaneously applied to initialize PA‐FASI‐RMM injection. The hydrodynamic flow generated by the positive pressure compensated the reverse EOF in the water plug and allowed the water plug to remain in the capillary during FASI with reverse migrating micelles (FASI‐RMM) to obtain a much longer injection time than usual, which improved stacking efficiency greatly. Equations describing this injection mode were introduced and were supported by experimental results. For a 450‐s online PA‐FASI‐RMM injection, three orders of magnitude sample enhancement in terms of peak area could be observed for the steroids and an achievement of detection limits was between 1 and 10 ng/mL.
Mutations in the lungs of gpt delta transgenic mice following inhalation of diesel exhaust
Authors: Hashimoto Akiko H. , Amanuma Kimiko , Hiyoshi Kyoko , Sugawara Yoshiki , Goto Sataro , Yanagisawa Rie , Takano Hirohisa , Masumura Ken‐ichi , Nohmi Takehiko , Aoki Yasunobu 
Published: September 2007

AbstractDiesel exhaust (DE) is a major airborne pollutant of urban areas. It contains various polycyclic aromatic hydrocarbons (PAH) and nitrated PAHs. In this study, gpt delta mice were treated with inhalation of 1 or 3 mg m−3 DE, or a single intratracheal instillation of diesel exhaust particles (DEP) or DEP extract. In the lungs of mice treated with inhalation of 3 mg m−3 DE for 12 weeks, the mutant frequency (MF) was 3.2‐fold higher than that of the control group (1.90 × 10−5 and 0.59 × 10−5, respectively). An instillation of DEP and DEP extract resulted in a significant dose‐dependent linear increase in MF. In mice treated with 0.5 mg DEP and 0.2 mg DEP extract, the MFs were 3.0‐ and 2.7‐fold higher than that of the control group, respectively. The mutagenic potency (MF mg−1) of DEP extract (5.6 × 10−5) was double that of DEP (2.7 × 10−5), suggesting that the mutagenicity of the latter is derived primarily from compounds in the extract, which itself is responsible for ca. 50% of the weight of DEP. G:C→A:T transitions were the predominant gpt mutation induced by all three treatments and G:C→T:A transversions were induced by DEP and DEP extract. Guanine bases centered in nucleotide sequences such as GGA, TGA, CGG, and CGT were the major mutation targets of all three treatments. Thus, our results suggest that the mutagens contained in DEP such as PAH and nitrated PAHs induce mutations and may be responsible for carcinogenesis caused by inhalation of DE. Environ. Mol. Mutagen., 2007. © 2007 Wiley‐Liss, Inc.
Enhanced mutagenesis of Salmonella tester strains due to deletion of genes other than uvrB
Authors: Swartz Carol D. , Parks Nick , Umbach David M. , Ward William O. , Schaaper Roel M. , DeMarini David M. 
Published: September 2007

AbstractThe standard Salmonella mutagenicity (Ames) tester strains are missing 15–119 genes due to the extended Δ(gal‐bio‐uvrB) mutations that render the strains excision‐repair deficient (ΔuvrB). We constructed strains of Salmonella that are homologous to tester strains TA98 and TA100 except that in place of the uvrB deletion, they contain single‐gene defects in either uvrB, moaA, moeA, or both uvrB and moeA. We then tested the following mutagens in these strains: 2‐acetylaminofluorene, Glu‐P‐1, 4‐aminobiphenyl, benzo[a]pyrene, MX, 1‐nitropyrene, 6‐hydroxylaminopurine (HAP), and 2‐amino‐6‐hydroxylaminopurine (AHAP). We confirmed in Salmonella a previous finding in Escherichia coli that the enhanced mutagenicity of the purine analogues HAP and AHAP is not due to the deletion of the uvrB gene but due to the deletion of moeA and/or moaA, which are involved in molybdenum cofactor biosynthesis. The spontaneous mutant frequency and induced mutagenic potency of mutagens due to the extended ΔuvrB mutation are due largely to the deletion of uvrB and to some extent of moeA/moaA at the frameshift hisD3052 allele of TA98 but involve other genes in addition to uvrB and moeA/moaA at the base‐substitution hisG46 allele of TA100. The extended ΔuvrB mutation does not prevent the detection of mutagens that would have been detected in a strain containing a single uvrB defect. Because of the deletion of moeA/moaA, the extended uvrB deletion generally enhanced spontaneous and induced mutagenicity, especially at the base‐substitution allele. This enhanced sensitivity may underlay the severe health effects in humans who have mutations in molybdenum cofactor biosynthesis genes. Environ. Mol. Mutagen., 2007. © 2007 Wiley‐Liss, Inc.