bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sensing hazardous metal ions using a fluoroionophore calix[4]arene species containing two 8-oxyquinoline groups
Authors: Bagatin Izilda A. , Araki Koiti , Toma Henrique E. 
Published: May 2011

The interaction of a calix[4]arene-based species containing two 8-oxyquinoline chromophore pendants with hazardous metal ions has been investigated using optical absorption and fluorimetric techniques. In the presence of Hg2+, Cd2+, and Pb2+ ions, there is only a small decrease of the calixarene absorption band at 283 nm. The main changes are associated with the absorption band of the 8-oxyquinoline group at 315 nm, undergoing a systematic bathochromic shift to above 350 nm. In addition, a systematic decrease of the oxyquinoline emission at λem = 392 nm (λexc = 315 nm) has been observed. These observations are consistent with the coordination of the metal ions to the quinoline groups attached to the calixarene ligand, providing a useful fluoroinophore species for analytical purposes.
Copper and chromium oxide nanocomposite catalysts for simultaneous elimination of CO and oxygenate VOCs in toxic gas emissions
Authors: Tsoncheva Tanya , Ivanov Krasimir , Dimitrov Dimitar 
Published: May 2011

Copper and chromium oxide nanocomposite materials with different Cu/Cr ratios were prepared by impregnation of a conventional silica support with toluene solutions of the corresponding acetylacetonate precursors and characterized by X-ray diffraction, Fourier transform infrared spectroscopy, UV–vis spectroscopy, X-ray photoelectron spectroscopy, and temperature-programmed reduction–thermogravimetric methods. Their catalytic behaviour in the total oxidation of CO and different oxygenate VOCs (methanol, dimethyl ether, and ethyl acetate) was tested. The relation between the phase composition and catalytic properties of the materials was also analyzed. It was established that materials with a 1:2 CuO/Cr2O3 molar ratio exhibit high catalytic activity for dimethyl ether oxidation, those with 2:1 and 1:1 ratios are suitable for CO and methanol oxidation, respectively, and both of the latter, but at much higher temperatures, are good for ethyl acetate elimination. A catalyst with an optimal composition of 1:1 (mol/mol) CuO/Cr2O3, working in a reactor with three temperature zones of 490–500 K, 570–580 K, and 620–630 K, is proposed for the effective simultaneous elimination of CO, methanol, ethyl acetate, and dimethyl ether in toxic emissions.
Proposition algebra
Authors: Bergstra Jan A. , Ponse Alban 
Published: May 2011

Sequential propositional logic deviates from conventional propositional logic by taking into account that during the sequential evaluation of a propositional statement, atomic propositions may yield different Boolean values at repeated occurrences. We introduce “free valuations” to capture this dynamics of a propositional statement's environment. The resulting logic is phrased as an equationally specified algebra rather than in the form of proof rules, and is named “proposition algebra.” It is strictly more general than Boolean algebra to the extent that the classical connectives fail to be expressively complete in the sequential case. The four axioms for free valuation congruence are then combined with other axioms in order define a few more valuation congruences that gradually identify more propositional statements, up to static valuation congruence (which is the setting of conventional propositional logic).
Proposition algebra is developed in a fashion similar to the process algebra ACP and the program algebra PGA, via an algebraic specification which has a meaningful initial algebra for which a range of coarser congruences are considered important as well. In addition, infinite objects (i.e., propositional statements, processes and programs respectively) are dealt with by means of an inverse limit construction which allows the transfer of knowledge concerning finite objects to facts about infinite ones while reducing all facts about infinite objects to an infinity of facts about finite ones in return.
Angiopoietin-2 TIEs Up Macrophages in Tumor Angiogenesis
Authors: De Palma Michele , Naldini Luigi 
Published: May 2011

Abstract
Angiopoietin-2 (ANG2), a ligand of the TIE2 receptor, modulates endothelial cell biology and destabilizes blood vessels to facilitate angiogenesis. Recent reports have shown that ANG2 inhibition, for example, by monoclonal antibodies, peptibodies, or CovX-Bodies, may achieve substantial antiangiogenic and antitumor responses in a variety of mouse tumor models, including spontaneous MMTV-PyMT mammary and RIP1-Tag2 pancreatic islet adenocarcinomas. There is also evidence that targeting the ANG2/TIE2 signaling pathway may inhibit the functions of TIE2-expressing macrophages (TEM), a tumor-associated macrophage subset endowed with proangiogenic activity in mouse tumor models. The clinical opportunities afforded by simultaneously targeting the effects of ANG2 on tumor angiogenesis and the proangiogenic activity of TEMs are discussed. Clin Cancer Res; 17(16); 5226–32. ©2011 AACR.
Sphingolipid Modulation of Angiogenic Factor Expression in Neuroblastoma
Authors: Li Mei-Hong , Hla Timothy , Ferrer Fernando 
Published: May 2011

Abstract
Metabolism of sphingolipids into downstream lipid mediators followed by signaling modulates tumor microenvironment and the cancer cells to influence tumor progression. As such, sphingolipid signaling represents a novel way to modulate tumor biology. Neuroblastoma (NB), the most common extracranial solid tumor of childhood, is highly angiogenic and often displays poor prognosis. However, the role of sphingolipid mediators is not known in NB. We found that NB expresses high levels of sphingosine kinase-2, which is essential for the formation of sphingosine-1-phosphate (S1P). S1P induced VEGF expression in SK-N-AS NB cells. The effect occurred at the transcriptional level. Hypoxia in combination with S1P had a synergistic effect on VEGF expression. Strong correlation was detected between S1P receptor-2 (S1P2) and VEGF mRNAs in 11 different cell lines and 17 NB tissues. Blockade of S1P2 with the selective antagonist JTE-013 significantly inhibited S1P-induced VEGF expression. Overexpression and knockdown of S1P2 in SK-N-AS cells increased or inhibited S1P-induced VEGF secretion, respectively. Interestingly, JTE-013 significantly inhibited tumor growth, VEGF mRNA expression, and induced apoptosis in the NB tumor xenografts. Taken together, our data suggest that enhanced formation of sphingolipid mediator S1P in NB profoundly influences tumor microenvironment by inducing VEGF expression via S1P2. Modulation of sphingolipid signaling by inhibiting S1P2 may constitute a novel strategy to control NB. Cancer Prev Res; 4(8); 1325–32. ©2011 AACR.
Left Ventricular Systolic Dysfunction Induced by Ventricular Ectopy
Authors: Huizar Jose F. , Kaszala Karoly , Potfay Jonathan , Minisi Anthony J. , Lesnefsky Edward J. , Abbate Antonio , Mezzaroma Eleonora , Chen Qun , Kukreja Rakesh C. , Hoke Nicholas N. , Thacker Leroy R. , Ellenbogen Kenneth A. , Wood Mark A. 
Published: May 2011

Background—
Premature ventricular contractions (PVCs) commonly coexist with cardiomyopathy. Recently, PVCs have been identified as a possible cause of cardiomyopathy. We developed a PVC-induced cardiomyopathy animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this cardiomyopathy and examine the associated histopathologic abnormalities.

Methods and Results—

Thirteen mongrel dogs were implanted with a specially programmed pacemaker capable of simulating ventricular extrasystoles. Animals were randomly assigned to either 12 weeks of bigeminal PVCs (n=7) or no PVCs (control, n=6). Continuous 24-hour Holter monitoring corroborated ventricular bigeminy in the PVC group (PVC, 49.8% versus control, <0.01%;
P
<0.0001). After 12 weeks, only the PVC group had cardiomyopathy, with a significant reduction in left ventricular ejection fraction (PVC, 39.7±5.4% versus control, 60.7±3.8%;
P
<0.0001) and an increase in left ventricular end-systolic dimension (PVC, 33.3±3.5 mm versus control, 23.7±3.6 mm;
P
<0.001). Ventricular effective refractory period showed a trend to prolong in the PVC group. PVC-induced cardiomyopathy was resolved within 2 to 4 weeks after discontinuation of PVCs. No inflammation, fibrosis, or changes in apoptosis and mitochondrial oxidative phosphorylation were observed with PVC-induced cardiomyopathy.

Conclusions—
This novel PVC animal model demonstrates that frequent PVCs alone can induce a reversible form of cardiomyopathy in otherwise structurally normal hearts. PVC-induced cardiomyopathy lacks gross histopathologic and mitochondrial abnormalities seen in other canine models of cardiomyopathy.
Molecular Analysis of Patterning of Conduction Tissues in the Developing Human Heart
Authors: Sizarov Aleksander , Devalla Harsha D. , Anderson Robert H. , Passier Robert , Christoffels Vincent M. , Moorman Antoon F.M. 
Published: May 2011

Background—
Recent studies in experimental animals have revealed some molecular mechanisms underlying the differentiation of the myocardium making up the conduction system. To date, lack of gene expression data for the developing human conduction system has precluded valid extrapolations from experimental studies to the human situation.

Methods and Results—
We performed immunohistochemical analyses of the expression of key transcription factors, such as ISL1, TBX3, TBX18, and NKX2–5, ion channel HCN4, and connexins in the human embryonic heart. We supplemented our molecular analyses with 3-dimensional reconstructions of myocardial TBX3 expression. TBX3 is expressed in the developing conduction system and in the right venous valve, atrioventricular ring bundles, and retro-aortic nodal region. TBX3-positive myocardium, with exception of the top of the ventricular septum, is devoid of fast-conducting connexin40 and connexin43 and hence identifies slowly conducting pathways. In the early embryonic heart, we found wide expression of the pacemaker channel HCN4 at the venous pole, including the atrial chambers. HCN4 expression becomes confined during later developmental stages to the components of the conduction system. Patterns of expression of transcription factors, known from experimental studies to regulate the development of the sinus node and atrioventricular conduction system, are similar in the human and mouse developing hearts.

Conclusions—
Our findings point to the comparability of mechanisms governing the development of the cardiac conduction patterning in human and mouse, which provide a molecular basis for understanding the functioning of the human developing heart before formation of a discrete conduction system.
Modulation of Novel Cardiorenal and Inflammatory Biomarkers by Intravenous Nitroglycerin and Nesiritide in Acute Decompensated Heart Failure
Authors: Chow Sheryl L. , O'Barr Stephen A. , Peng Jessica , Chew Eric , Pak Firooz , Quist Ryan , Patel Paryus , Patterson J. Herbert , Heywood J. Thomas 
Published: May 2011

Background—
Modulation of novel cardiorenal and inflammatory markers may provide insight into the disease process and outcomes of patients with acute decompensated heart failure.

Methods and Results—

In this open-labeled, prospective, randomized study, 89 patients received either nesiritide (NES) or nitroglycerin (NTG) infusion by standard protocol. The serum or plasma concentrations of cystatin-C and inflammatory markers (high-sensitivity C-reactive protein, tumor necrosis factor-α, transforming growth factor-β1, and interleukin-6) were measured in 66 patients with acute decompensated heart failure at baseline and during drug infusion. Mean baseline values for demographics were not significantly different between NTG and NES groups; however, baseline inflammatory markers were elevated on admission. In NES compared with NTG groups, lower cystatin-C (1449 versus 2739 ng/mL,
P
<0.05) and IL-6 (25 versus 50 pg/mL,
P
<0.05) were observed. There were no significant differences in concentrations of high-sensitivity C-reactive protein, tumor necrosis factor-α, and transforming growth factor-β1 between groups over time.

Conclusions—
The differential modulation effects of cystatin-C and interleukin-6 but not other inflammatory markers, in response to NES compared with NTG therapy, may provide important implications for vasodilator therapy. Further studies are warranted to confirm these findings.

Clinical Trial Registration—

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT00842023.
Incidence, Risk Factors, and Clinical Sequelae of Angiographic Peri-Stent Contrast Staining After Sirolimus-Eluting Stent Implantation
Authors: Imai Masao , Kadota Kazushige , Goto Tsuyoshi , Fujii Satoki , Yamamoto Hiroyuki , Fuku Yasushi , Hosogi Shingo , Hirono Akitoshi , Tanaka Hiroyuki , Tada Takeshi , Morimoto Takeshi , Shiomi Hiroki , Kozuma Ken , Inoue Katsumi , Suzuki Nobuaki , Kimura Takeshi , Mitsudo Kazuaki 
Published: May 2011

Background—
We have noted abnormal angiographic findings—at the sites of drug-eluting stent implantation, suggesting contrast staining outside the stent struts—that do not fulfill the classic definition of coronary artery aneurysm. We propose a new term, peri-stent contrast staining (PSS), for these abnormal angiographic findings and assess their incidence, risk factors, and clinical sequelae.

Methods and Results—

Peri-stent contrast staining was defined as contrast staining outside the stent contour extending to ≥20% of the stent diameter. The study population consisted of 3081 lesions (1998 patients) that were treated exclusively with sirolimus-eluting stents and were evaluated by follow-up angiography within 12 months after sirolimus-eluting stent implantation in a single center. Late acquired PSS was observed in 58 lesions (1.9%) in 49 patients (2.5%). Independent risk factors of PSS included chronic total occlusion, whereas negative risk factors for PSS were left circumflex coronary artery lesion and in-stent restenosis lesion. Stent fracture was more frequently observed in lesions with PSS than in lesions without PSS (43.1% versus 5.4%,
P
<0.0001). Excluding 269 lesions with target-lesion revascularization within 12 months, the study population for long-term follow-up consisted of 51 lesions (42 patients) with PSS and 2761 lesions (1751 patients) without PSS. Cumulative incidence of target-lesion revascularization and definite very late stent thrombosis at 3 years in the PSS group was higher than that in the non-PSS group (15.0% versus 6.5%, and 8.2% versus 0.2%, respectively).

Conclusions—
Peri-stent contrast staining found within 12 months after sirolimus-eluting stent implantation appeared to be associated with subsequent target-lesion revascularization and very late stent thrombosis.
Casein Kinase-2α1 Induces Hypertrophic Response by Phosphorylation of Histone Deacetylase 2 S394 and its Activation in the Heart
Authors: Eom Gwang Hyeon , Cho Young Kuk , Ko Jeong-Hyeon , Shin Sera , Choe Nakwon , Kim Yoojung , Joung Hosouk , Kim Hyung-Seok , Nam Kwang-Il , Kee Hae Jin , Kook Hyun 
Published: May 2011

Background—
Cardiac hypertrophy is characterized by transcriptional reprogramming of fetal gene expression, and histone deacetylases (HDACs) are tightly linked to the regulation of those genes. We previously demonstrated that activation of HDAC2, 1 of the class I HDACs, mediates hypertrophy. Here, we show that casein kinase-2α1 (CK2α1)–dependent phosphorylation of HDAC2 S394 is required for the development of cardiac hypertrophy.

Methods and Results—

Hypertrophic stimuli phosphorylated HDAC2 S394, which was necessary for its enzymatic activation, and therefore the development of hypertrophic phenotypes in rat neonatal cardiomyocytes or in isoproterenol-administered mice hearts. Transgenic mice overexpressing HDAC2 wild type exhibited cardiac hypertrophy, whereas those expressing phosphorylation-resistant HDAC2 S394A did not. Compared with that in age-matched normal human hearts, phosphorylation of HDAC2 S394 was dramatically increased in patients with hypertrophic cardiomyopathy. Hypertrophy-induced phosphorylation of HDAC2 S394 and its enzymatic activity were completely blocked either by CK2 blockers or by
CK2
α
1 short interfering RNA
. Hypertrophic stimuli led CK2α1 to be activated, and its chemical inhibitors blocked hypertrophy in both phenylephrine-treated cardiomyocytes and isoproterenol-administered mice. CK2α1-transgenic mice developed hypertrophy, which was attenuated by administration of trichostatin A, an HDAC inhibitor. Overexpression of CK2α1 caused hypertrophy in cardiomyocytes, whereas chemical inhibitors of both CK2 and HDAC as well as HDAC2 S394A blunted it. Hypertrophy in CK2α1-transgenic mice was exaggerated by crossing these mice with wild-type-HDAC2-overexpressing mice. By contrast, however, it was blocked when CK2α1-transgenic mice were crossed with HDAC2 S394A-transgenic mice.

Conclusions—
We have demonstrated a novel mechanism in the development of cardiac hypertrophy by which CK2 activates HDAC2 via phosphorylating HDAC2 S394.
Renin-Angiotensin-Aldosterone Genotype Influences Ventricular Remodeling in Infants With Single Ventricle
Authors: Mital Seema , Chung Wendy K. , Colan Steven D. , Sleeper Lynn A. , Manlhiot Cedric , Arrington Cammon B. , Cnota James F. , Graham Eric M. , Mitchell Michael E. , Goldmuntz Elizabeth , Li Jennifer S. , Levine Jami C. , Lee Teresa M. , Margossian Renee , Hsu Daphne T. 
Published: May 2011

Background—
We investigated the effect of polymorphisms in the renin-angiotensin-aldosterone system (RAAS) genes on ventricular remodeling, growth, renal function, and response to enalapril in infants with single ventricle.

Methods and Results—

Single ventricle infants enrolled in a randomized trial of enalapril were genotyped for polymorphisms in 5 genes: angiotensinogen, angiotensin-converting enzyme, angiotensin II type 1 receptor, aldosterone synthase, and chymase. Alleles associated with renin-angiotensin-aldosterone system upregulation were classified as risk alleles. Ventricular mass, volume, somatic growth, renal function using estimated glomerular filtration rate, and response to enalapril were compared between patients with ≥2 homozygous risk genotypes (high risk), and those with <2 homozygous risk genotypes (low risk) at 2 time points: before the superior cavopulmonary connection (pre-SCPC) and at age 14 months. Of 230 trial subjects, 154 were genotyped: Thirty-eight were high risk, and 116 were low risk. Ventricular mass and volume were elevated in both groups pre-SCPC. Ventricular mass and volume decreased and estimated glomerular filtration rate increased after SCPC in the low-risk (
P
<0.05), but not the high-risk group. These responses were independent of enalapril treatment. Weight and height z-scores were lower at baseline, and height remained lower in the high-risk group at 14 months, especially in those receiving enalapril (
P
<0.05).

Conclusions—
Renin-angiotensin-aldosterone system–upregulation genotypes were associated with failure of reverse remodeling after SCPC surgery, less improvement in renal function, and impaired somatic growth, the latter especially in patients receiving enalapril. Renin-angiotensin-aldosterone system genotype may identify a high-risk subgroup of single ventricle patients who fail to fully benefit from volume-unloading surgery. Follow-up is warranted to assess long-term impact.

Clinical Trial Registration—

http://www.clinicaltrials.gov
. Unique identifier: NCT00113087.
Risk of Bleeding With 2 Doses of Dabigatran Compared With Warfarin in Older and Younger Patients With Atrial Fibrillation
Authors: Eikelboom John W. , Wallentin Lars , Connolly Stuart J. , Ezekowitz Mike , Healey Jeff S. , Oldgren Jonas , Yang Sean , Alings Marco , Kaatz Scott , Hohnloser Stefan H. , Diener Hans-Christoph , Franzosi Maria Grazia , Huber Kurt , Reilly Paul , Varrone Jeanne , Yusuf Salim 
Published: May 2011

Background—
Dabigatran 150 and 110 mg twice a day and warfarin are effective for stroke prevention in atrial fibrillation. The purpose of this study was to compare their risks of bleeding in the Randomized Evaluation of Long-Term Anticoagulant Therapy (RE-LY) trial.

Methods and Results—

The RE-LY trial randomized 18 113 patients to receive dabigatran 110 or 150 mg twice a day or warfarin dose adjusted to an international normalized ratio of 2.0 to 3.0 for a median follow-up of 2.0 years. Compared with warfarin, dabigatran 110 mg twice a day was associated with a lower risk of major bleeding (2.87% versus 3.57%;
P
=0.002), whereas dabigatran 150 mg twice a day was associated with a similar risk of major bleeding (3.31% versus 3.57%;
P
=0.32). There was a significant treatment-by-age interaction, such that dabigatran 110 mg twice a day compared with warfarin was associated with a lower risk of major bleeding in patients aged <75 years (1.89% versus 3.04%;
P
<0.001) and a similar risk in those aged ≥75 years (4.43% versus 4.37%;
P
=0.89;
P
for interaction <0.001), whereas dabigatran 150 mg twice a day compared with warfarin was associated with a lower risk of major bleeding in those aged <75 years (2.12% versus 3.04%;
P
<0.001) and a trend toward higher risk of major bleeding in those aged ≥75 years (5.10% versus 4.37%;
P
=0.07;
P
for interaction <0.001). The interaction with age was evident for extracranial bleeding, but not for intracranial bleeding, with the risk of the latter being consistently reduced with dabigatran compared with warfarin irrespective of age.

Conclusions—
In patients with atrial fibrillation at risk for stroke, both doses of dabigatran compared with warfarin have lower risks of both intracranial and extracranial bleeding in patients aged <75 years. In those aged ≥75 years, intracranial bleeding risk is lower but extracranial bleeding risk is similar or higher with both doses of dabigatran compared with warfarin.

Clinical Trial Registration—

http://www.clinicaltrials.gov
. Unique identifier: NCT00262600.
T and B lymphocyte abnormalities in bone marrow biopsies of common variable immunodeficiency
Authors: Ochtrop Manuella L. Gomes , Goldacker Sigune , May Annette M. , Rizzi Marta , Draeger Ruth , Hauschke Dieter , Stehfest Claudia , Warnatz Klaus , Goebel Heike , Technau-Ihling Katja , Werner Martin , Salzer Ulrich , Eibel Hermann , Schlesier Michael , Peter Hans Hartmut 
Published: May 2011

AbstractIn common variable immunodeficiency (CVID) defects in early stages of B-cell development, bone marrow (BM) plasma cells and T lymphocytes have not been studied systematically. Here we report the first morphologic and flow cytometric study of B- and T-cell populations in CVID BM biopsies and aspirates. Whereas the hematopoietic compartment showed no major lineage abnormalities, analysis of the lymphoid compartment exhibited major pathologic alterations. In 94% of the patients, BM plasma cells were either absent or significantly reduced and correlated with serum immunoglobulin G levels. Biopsies from CVID patients had significantly more diffuse and nodular CD3+ T lymphocyte infiltrates than biopsies from controls. These infiltrates correlated with autoimmune cytopenia but not with other clinical symptoms or with disease duration and peripheral B-cell counts. Nodular T-cell infiltrates correlated significantly with circulating CD4+CD45R0+ memory T cells, elevated soluble IL2-receptor and neopterin serum levels indicating an activated T-cell compartment in most patients. Nine of 25 patients had a partial block in B-cell development at the pre-B-I to pre-B-II stage. Because the developmental block correlates with lower transitional and mature B-cell counts in the periphery, we propose that these patients might form a new subgroup of CVID patients.