bluuebunny/crossref_metadata_2025_split huggingface dataset:
Strong Convergence Theorems for Lipschitzian Demicontraction Semigroups in Banach Spaces
Authors: Chang Shih-sen , Cho YeolJe , Lee HWJoseph , Chan ChiKin 
Published: March 2011

AbstractThe purpose of this paper is to introduce and study the strong convergence problem of the explicit iteration process for a Lipschitzian and demicontraction semigroups in arbitrary Banach spaces. The main results presented in this paper not only extend and improve some recent results announced by many authors, but also give an affirmative answer for the open questions raised by Suzuki (2003) and Xu (2005).
Clinical Characteristics and Long-Term Prognosis of Vasospastic Angina Patients Who Survived Out-of-Hospital Cardiac Arrest
Authors: Takagi Yusuke , Yasuda Satoshi , Tsunoda Ryusuke , Ogata Yasuhiro , Seki Atsushi , Sumiyoshi Tetsuya , Matsui Motoyuki , Goto Toshikazu , Tanabe Yasuhiko , Sueda Shozo , Sato Toshiaki , Ogawa Satoshi , Kubo Norifumi , Momomura Shin-ichi , Ogawa Hisao , Shimokawa Hiroaki 
Published: March 2011

Background—
Coronary artery spasm plays an important role in the pathogenesis of ischemic heart disease; however, its role in sudden cardiac death remains to be fully elucidated. We examined the clinical characteristics and outcomes of patients with vasospastic angina (VSA) in our nationwide multicenter registry by the Japanese Coronary Spasm Association.

Methods and Results—

Between September 2007 and December 2008, 1429 patients with VSA (male/female, 1090/339; median, 66 years) were identified. They were characterized by a high prevalence of smoking and included 35 patients who survived out-of-hospital cardiac arrest (OHCA). The OHCA survivors, as compared with the remaining 1394 non-OHCA patients, were characterized by younger age (median, 58 versus 66 years;
P
<0.001) and higher incidence of left anterior descending coronary artery spasm (72% versus 53%,
P
<0.05). In the OHCA survivors, 14 patients underwent implantable cardioverter-defibrillator (ICD) implantation while intensively treated with calcium channel blockers. Survival rate free from major adverse cardiac events was significantly lower in the OHCA survivors compared with the non-OHCA patients (72% versus 92% at 5 years,
P
<0.001), including appropriate ICD shocks for ventricular fibrillation in 2 patients. Multivariable analysis revealed that OHCA events were significantly correlated with major adverse cardiac events (hazard ratio, 3.25; 95% confidence interval, 1.39 to 7.61;
P
<0.01).

Conclusions—
These results from the largest vasospastic angina cohort indicate that vasospasm patients who survived OHCA are high-risk population. Further studies are needed to determine whether implantable cardioverter-defibrillator therapy improves patient prognosis.
High-Resolution Identity by Descent Mapping Uncovers the Genetic Basis for Blood Pressure Differences Between Spontaneously Hypertensive Rat Lines
Authors: Bell Rebecca , Herring Stacy M. , Gokul Nisha , Monita Monique , Grove Megan L. , Boerwinkle Eric , Doris Peter A. 
Published: March 2011

Background—
The recent development of a large panel of genome-wide single nucleotide polymorphisms (SNPs) provides the opportunity to examine genetic relationships between distinct SHR lines that share hypertension but differ in their susceptibility to hypertensive end-organ disease.

Methods and Results—

We compared genotypes at nearly 10 000 SNPs obtained for the hypertension end-organ injury-susceptible spontaneously hypertensive rat (SHR)-A3 (SHRSP, SHR-stroke prone) line and the injury-resistant SHR-B2 line. This revealed that that the 2 lines were genetically identical by descent (IBD) across 86.6% of the genome. Areas of the genome that were not IBD were distributed across 19 of the 20 autosomes and the X chromosome. A block structure of non-IBD comprising a total of 121 haplotype blocks was formed by clustering of SNPs inherited from different ancestors. To test the null hypothesis that distinct SHR lines share a common set of hypertension susceptibility alleles, we compared blood pressure in adult SHR animals from both lines and their F1 and F2 progeny using telemetry. In 16- to 18-week-old animals fed a normal diet, systolic blood pressure (SBP, mm Hg) in SHR-A3 was 205.7±3.86 (mean±SEM, n=26), whereas in similar SHR-B2 animals, SBP was 186.7±2.53 (n=20). In F1 and F2 animals, SBP was 188.2±4.23 (n=19) and 185.6±1.1 (n=211), respectively (
P
<10
−6
, ANOVA). To identify non-IBD haplotype blocks contributing to blood pressure differences between these SHR lines, we developed a high-throughput SNP genotyping system to genotype SNPs marking non-IBD blocks. We mapped a single non-IBD block on chromosome 17 extending over <10 Mb, at which SHR-A3 alleles significantly elevate blood pressure compared with SHR-B2.

Conclusions—
Thus hypertension in SHR-A3 and -B2 appears to arise from an overlapping set of susceptibility alleles, with SHR-A3 possessing an additional hypertension locus that contributes to further increase blood pressure.
A Complex Double Deletion in
LMNA
Underlies Progressive Cardiac Conduction Disease, Atrial Arrhythmias, and Sudden Death
Authors: Marsman Roos F. , Bardai Abdennasser , Postma Alex V. , Res Jan C.J. , Koopmann Tamara T. , Beekman Leander , van der Wal Allard C. , Pinto Yigal M. , Lekanne Deprez Ronald H. , Wilde Arthur A.M. , Jordaens Luc J. , Bezzina Connie R. 
Published: March 2011

Background—
Cardiac conduction disease is a clinically and genetically heterogeneous disorder characterized by defects in electrical impulse generation and conduction and is associated with sudden cardiac death.

Methods and Results—

We studied a 4-generation family with autosomal dominant progressive cardiac conduction disease, including atrioventricular conduction block and sinus bradycardia, atrial arrhythmias, and sudden death. Genome-wide linkage analysis mapped the disease locus to chromosome 1p22-q21. Multiplex ligation-dependent probe amplification analysis of the
LMNA
gene, which encodes the nuclear-envelope protein lamin A/C, revealed a novel gene rearrangement involving a 24-bp inversion flanked by a 3.8-kb deletion upstream and a 7.8-kb deletion downstream. The presence of short inverted sequence homologies at the breakpoint junctions suggested a mutational event involving serial replication slippage in
trans
during DNA replication.

Conclusions—

We identified for the first time a complex
LMNA
gene rearrangement involving a double deletion in a 4-generation Dutch family with progressive conduction system disease. Our findings underscore the fact that if conventional polymerase chain reaction–based direct sequencing approaches for
LMNA
analysis are negative in suggestive pedigrees, mutation detection techniques capable of detecting gross genomic lesions involving deletions and insertions should be considered.
Oxygen-regulated expression of the erythropoietin gene in the human renal cell line REPC
Authors: Frede Stilla , Freitag Patricia , Geuting Luise , Konietzny Rebecca , Fandrey Joachim 
Published: March 2011

AbstractErythropoietin (EPO), the key hormone in red blood cell renewal, is mainly produced in the adult kidney. Anemia and hypoxia substantially enhance EPO expression to increase erythropoiesis. Investigations of the cellular physiology of renal EPO production have been hampered by the lack of an adequate human cell line. In the present study, we present the human kidney cell line REPC (for renal Epo–producing cells), established from an explanted human kidney exhibiting EPO gene expression and release of the EPO protein in an oxygen-dependent manner. Hypoxic induction of EPO mRNA showed the typical transient increase and peak in expression after 36 hours under continuous conditions of hypoxia. Bioactive EPO protein accumulated in the culture supernatant. The induction of EPO gene expression in REPCs critically depended on the activation of hypoxia-inducible transcription factors (HIFs). SiRNA treatment revealed that the expression of EPO was largely dependent on the activation of the transcription factor complex HIF-2. In addition, hepatic nuclear factor 4α was shown to be critically involved in hypoxia-induced renal EPO expression. Using the human kidney cell line REPC, we provide for the first time a powerful tool with which to study the cellular and molecular regulation of renal EPO production.
Residual sleepiness in obstructive sleep apnoea: phenotype and related symptoms
Authors: Vernet C. , Redolfi S. , Attali V. , Konofal E. , Brion A. , Frija-Orvoen E. , Pottier M. , Similowski T. , Arnulf I. 
Published: March 2011

The characteristics of residual excessive sleepiness (RES), defined by an Epworth score >10 in adequately treated apnoeic patients, are unknown.
40 apnoeic patients, with (n = 20) and without (n = 20) RES, and 20 healthy controls underwent clinical interviews, cognitive and biological tests, polysomnography, a multiple sleep latency test, and 24-h sleep monitoring.
The marked subjective sleepiness in the RES group (mean± sd score 16.4±3) contrasted with moderately abnormal objective measures of sleepiness (90% of patients with RES had daytime sleep latencies >8 min). Compared with patients without RES, the patients with RES had more fatigue, lower stage N3 percentages, more periodic leg movements (without arousals), lower mean sleep latencies and longer daytime sleep periods. Most neuropsychological dimensions (morning headaches, memory complaints, spatial memory, inattention, apathy, depression, anxiety and lack of self-confidence) were not different between patients with and without RES, but gradually altered from controls to apnoeic patients without and then with RES.
RES in apnoeic patients differs markedly from sleepiness in central hypersomnia. The association between RES, periodic leg movements, apathy and depressive mood parallels the post-hypoxic lesions in noradrenaline, dopamine and serotonin systems in animals exposed to intermittent hypoxia.
Adaptive support ventilation for faster weaning in COPD: a randomised controlled trial
Authors: Kirakli C. , Ozdemir I. , Ucar Z.Z. , Cimen P. , Kepil S. , Ozkan S.A. 
Published: March 2011

Adaptive support ventilation (ASV) is a closed-loop ventilation mode that can act both as pressure support ventilation (PSV) and pressure-controlled ventilation. Weaning with ASV shows promising results, mainly in post-cardiac surgery patients. The aim of the present randomised controlled study was to test the hypothesis that weaning with ASV could reduce the weaning duration in patients with chronic obstructive pulmonary disease (COPD) when compared with PSV.From among 435 COPD patients admitted to the intensive care unit (ICU) during a 20-month period, 97 were enrolled. Patients were assigned at random to either ASV or PSV as a weaning mode.Compared with PSV, ASV provided shorter weaning times (median 24 (interquartile range 20–62) hversus72 (24–144) h, p=0.041) with similar weaning success rates (35 out of 49 for ASV and 33 out of 48 for PSV). Length of stay in the ICU was also shorter with ASV but the difference was not statistically significant.This study suggests that ASV may be used in the weaning of COPD patients with the advantage of shorter weaning times. Further studies are needed to investigate the role and potential advantages of ASV in the weaning period of different patient groups.
Physician judgement is a crucial adjunct to pneumonia severity scores in low-risk patients
Authors: Choudhury G. , Chalmers J.D. , Mandal P. , Akram A.R. , Murray M.P. , Short P. , Singanayagam A. , Hill A.T. 
Published: March 2011

This study investigates the reasons for hospitalisation in patients with low-risk (CURB-65 score 0–1) community-acquired pneumonia (CAP), with a view to identifying the potential for improving outpatient management.As part of a prospective observational study of CAP, we evaluated reasons for hospitalisation in these low-risk patients.565 patients had low-risk CAP and 420 of these were admitted (for >12 h). 39.3% had additional markers of severity justifying admission, 29.5% of the admissions were required for further management that could not be provided rapidly in the community, 11.9% had unsafe social circumstances and 19.3% had no clinical reason justifying hospitalisation. 30-day mortality was increased in patients with additional severity markers (6.7%), which was significantly higher compared with 0% for patients awaiting investigations (p=0.009) and 0% without a clear indication for hospitalisation (p=0.04). In a logistic regression analysis, parameters associated with 30-day mortality were chronic cardiac comorbidity (adjusted odds ratio (aOR) 5.73, 95% CI 1.52–21.6; p=0.01), acidosis (aOR 5.14, 95% CI 1.44–18.3; p=0.01), hypoxia (aOR 9.86, 95% CI 2.39–40.7; p=0.002) and multilobar chest radiograph shadowing (aOR 4.54, 95% CI 1.21–17.1; p=0.03).This study supports recommendations from international guidelines that pneumonia severity scores should be used as an adjunct to clinical judgement, when deciding on hospitalisation.
Comparing Global Initiative for Asthma (GINA) criteria with the Childhood Asthma Control Test (C-ACT) and Asthma Control Test (ACT)
Authors: Koolen B.B. , Pijnenburg M.W.H. , Brackel H.J.L. , Landstra A.M. , van den Berg N.J. , Merkus P.J.F.M. , Hop W.C.J. , Vaessen-Verberne A.A.P.H. 
Published: March 2011

Several tools are useful in detecting uncontrolled asthma in children. The aim of this study was to compare Global Initiative for Asthma (GINA) guidelines with the Childhood Asthma Control Test (C-ACT) and the Asthma Control Test (ACT) in detecting uncontrolled asthma in children.145 children with asthma filled in a web-based daily diary card for 4 weeks on symptoms, use of rescue medication and limitations of activities, followed by either the C-ACT or ACT. For predicting uncontrolled asthma, score cut-off points of 19 were used for C-ACT and ACT.According to GINA guidelines, asthma was uncontrolled in 71 (51%) children and completely controlled in 19 (14%) children. The area under the curve in the receiver operating characteristic curves for C-ACT and ACTversusGINA guidelines were 0.89 and 0.92, respectively. Cut-off points of 19 for C-ACT and ACT resulted in a sensitivity of 33% and 66% in predicting uncontrolled asthma, respectively.C-ACT and ACT correlate well with GINA criteria in predicting uncontrolled asthma, but commonly used cut-off points for C-ACT and ACT seem to underestimate the proportion of children with uncontrolled asthma as defined by GINA.
Accuracy of cell typing in nonsmall cell lung cancer by EBUS/EUS–FNA cytological samples
Authors: Wallace W.A.H. , Rassl D.M. 
Published: March 2011

Endoscopic ultrasound-guided transbronchial or transoesophageal lymph node aspiration is increasingly used as a method of diagnosing nonsmall cell carcinoma. Data validating the accuracy of cell typing of nonsmall cell carcinoma using these cytological samples has not been assessed.23 samples were identified in Edinburgh, UK and a further 25 in Cambridge, UK, with matching histological samples. The morphological cell type, as assessed on the cytological preparations and cell blocks, was recorded and immunohistochemical staining was performed, where possible, as an adjunct. The final cell type, as assessed by morphology with or without immunohistochemistry, was correlated with that reported in the paired histological samples.Cell blocks with tumour were available in 39 out of 48 cases. The accuracy of cell typing when no cell block was available was four out of nine cases. This increased to 25 out of 39 when a cell block was available, increasing to 33 out of 39 with the addition of immunohistochemistry. The overall accuracy of classification was 37 out of 48 cases.Accurate cell typing of nonsmall cell carcinomas can be performed using endoscopically derived fine-needle aspirates. The importance of obtaining sufficient material for the production of cell blocks is critical in allowing optimal assessment.
Role of growth hormone-releasing hormone in sleep and growth impairments induced by upper airway obstruction in rats
Authors: Tarasiuk A. , Berdugo-Boura N. , Troib A. , Segev Y. 
Published: March 2011

Upper airway obstruction (UAO) can lead to abnormal growth hormone (GH) homeostasis and growth retardation but the mechanisms are unclear. We explored the effect of UAO on hypothalamic GH-releasing hormone (GHRH), which has a role in both sleep and GH regulation.The tracheae of 22-day-old rats were narrowed; UAO and sham-operated animals were sacrificed 16 days post-surgery. To stimulate slow-wave sleep (SWS) and GH secretion, rats were treated with ritanserin (5-HT2receptor antagonist). Sleep was measured with a telemetric system. Hypothalamic GHRH, hypothalamic GHRH receptor (GHRHR) and GH receptor, and orexin were analysed using ELISA, real-time PCR and Western blot.UAO decreased hypothalamic GHRH, GHRHR and GH receptor levels, while orexin mRNA increased (p<0.01). In UAO rats, the duration of wakefulness was elevated and the duration of SWS, paradoxical sleep and slow-wave activity was reduced (p<0.001). Ritanserin alleviated these effects,i.e.normalised hypothalamic GHRH content, decreased wake duration, increased duration and depth of SWS, and attenuated growth impairment (p<0.001).Here, we present evidence that growth retardation in UAO is associated with a reduction in hypothalamic GHRH content. Our findings show that abnormalities in the GHRH/GH axis underlie both growth retardation and SWS-disorder UAO.
Mometasone and desloratadine additive effect on eosinophil survival and cytokine secretion from epithelial cells
Authors: Mullol Joaquim , de Borja Callejas Francisco , Martínez-Antón Maria Asunción , Méndez-Arancibia Eva , Alobid Isam , Pujols Laura , Valero Antonio , Picado Cesar , Roca-Ferrer Jordi 
Published: March 2011

Abstract

Background
Although antihistamines and topical corticosteroids are used in combination to treat allergic rhinitis, their additive effect has not been yet demonstrated. The aim was investigate the antiinflammatory additive effect of mometasone and desloratadine on cytokine and sICAM-1 secretion by epithelial cells, and on eosinophil survival stimulated by human epithelial cells secretions from nasal mucosa and polyps.

Methods
Epithelial cells obtained from nasal mucosa or polyps were stimulated with 10% fetal bovine serum in presence of mometasone (10-11M-10-5M) with/without desloratadine (10-5M). Cytokine and sICAM-1 concentrations in supernatants were measured by ELISA. Peripheral blood eosinophils were incubated during 4 days with epithelial cell secretions with (10-11M-10-5M) and/or desloratadine (10-5M) and survival assessed by Trypan blue. Results are expressed as percentage (mean ± SEM) compared to control.

Results
Fetal bovine serum stimulated IL-6, IL-8, GM-CSF and sICAM-1 secretion. In mucosa and polyp epithelial cells, mometasone inhibited this induced secretion while desloratadine inhibited IL-6 and IL-8. The combination of 10-5M desloratadine and 10-9M mometasone reduced IL-6 secretion (48 ± 11%, p < 0.05) greater extent than mometasone alone (68 ± 10%) compared to control (100%). Epithelial cell secretions induced eosinophil survival from day 1 to 4, this effect being inhibited by mometasone. At day 4, the combination of mometasone (10-11M) and desloratadine (10-5M) provoked an increased inhibition of eosinophil survival induced by cell secretions (27 ± 5%, p < 0.01) than mometasone (44 ± 7%) or desloratadine (46 ± 7%) alone.

Conclusions
These results suggest that the combination of desloratadine and mometasone furoate have a greater antinflammatory effect in an in vitro model of eosinophil inflammation than those drugs administered alone.
The MAP kinase ERK and its scaffold protein MP1 interact with the chromatin regulator Corto during Drosophilawing tissue development
Authors: Mouchel-Vielh Emmanuèle , Rougeot Julien , Decoville Martine , Peronnet Frédérique 
Published: March 2011

AbstractBackgroundMitogen-activated protein kinase (MAPK) cascades (p38, JNK, ERK pathways) are involved in cell fate acquisition during development. These kinase modules are associated with scaffold proteins that control their activity. InDrosophila,dMP1, that encodes an ERK scaffold protein, regulates ERK signaling during wing development and contributes to intervein and vein cell differentiation. Functional relationships during wing development between a chromatin regulator, the Enhancer of Trithorax and Polycomb Corto, ERK and its scaffold protein dMP1, are examined here.ResultsGenetic interactions show thatcortoanddMP1act together to antagonizerolled(which encodes ERK) in the future intervein cells, thus promoting intervein fate. Although Corto, ERK and dMP1 are present in both cytoplasmic and nucleus compartments, they interact exclusively in nucleus extracts. Furthermore, Corto, ERK and dMP1 co-localize on several sites on polytene chromosomes, suggesting that they regulate gene expression directly on chromatin. Finally, Corto is phosphorylated. Interestingly, its phosphorylation pattern differs between cytoplasm and nucleus and changes upon ERK activation.ConclusionsOur data therefore suggest that the Enhancer of Trithorax and Polycomb Corto could participate in regulating vein and intervein genes during wing tissue development in response to ERK signaling.
Serum response factor is required for cell contact maintenance but dispensable for proliferation in visceral yolk sac endothelium
Authors: Holtz Mary L , Misra Ravi P 
Published: March 2011

Abstract
Background
Endothelial-specific knockout of the transcription factor serum response factor (SRF) results in embryonic lethality by mid-gestation. The associated phenotype exhibits vascular failure in embryos as well as visceral yolk sac (VYS) tissues. Previous data suggest that this vascular failure is caused by alterations in cell-cell and cell-matrix contacts. In the current study, we sought to more carefully address the role of SRF in endothelial function and cell contact interactions in VYS tissues.

Results
Tie2-Cre recombinase-mediated knockout of SRF expression resulted in loss of detectable SRF from VYS mesoderm by E12.5. This loss was accompanied by decreased expression of smooth muscle alpha-actin as well as vascular endothelial cadherin and claudin 5, endothelial-specific components of adherens and tight junctions, respectively. Focal adhesion (FA) integrins alpha5 and beta1 were largely unchanged in contrast to loss of the FA-associated molecule vinculin. The integrin binding partner fibronectin-1 was also profoundly decreased in the extracellular matrix, indicating another aspect of impaired adhesive function and integrin signaling. Additionally, cells in SRF-null VYS mesoderm failed to reduce proliferation, suggesting not only that integrin-mediated contact inhibition is impaired but also that SRF protein is not required for proliferation in these cells.

Conclusions
Our data support a model in which SRF is critical in maintaining functional cell-cell and cell-matrix adhesion in endothelial cells. Furthermore, we provide evidence that supports a model in which loss of SRF protein results in a sustained proliferation defect due in part to failed integrin signaling.