bluuebunny/crossref_metadata_2025_split huggingface dataset:
Timing of removal of pacing wires following paediatric cardiac surgery
Authors: Jowett Victoria , Hayes Nicholas , Sridharan Shankar , Rees Philip , Macrae Duncan 
Published: September 2007

AbstractBackgroundTemporary percutaneous epicardial pacing wires are routinely placed in children following cardiac surgery. There is uncertainty in clinical practice about the optimum timing for their removal, and practice varies widely both within and between different institutions.AimThe aim of our study was to describe the use of temporary pacing in children undergoing cardiac surgery.MethodsWe performed a prospective audit of 140 children following cardiac surgery in two institutions. Information on diagnosis, surgical procedure, occurrence of arrhythmias, use of pacing wires, timing of removal of the wire, and complications related to removal was recorded on a daily basis from clinical records.ResultsWe studied 140 patients undergoing a total of 141 operations. Of these, 39 (28%) required pacing postoperatively. In 38, pacing was required within the first 24 hours. One patient, who was in nodal rhythm for the first 24 hours, required pacing on the second postoperative day, while 29 patients required pacing beyond the first 24 hours. No patient in sinus rhythm on the first postoperative day required new pacing after this time. The median time to removal of the pacing wires was 4.5 days, with an inter-quartile range from 2 to 9 days. Complications included malfunction of atrial wires in 2 patients.ConclusionsOur study shows that no patient who was in sinus rhythm for the first 24 hours post-operatively required pacing before their discharge from hospital. This suggests that, in those patients in a stable state of sinus rhythm, and who have not required pacing within the first 24 hours, it may be safe to remove pacing wires after 24 hours. This could be timed to coincide with the removal of chest drains, thus avoiding the need for multiple distressing procedures.
Biomarker method validation in anticancer drug development
Authors: Cummings J , Ward T H , Greystoke A , Ranson M , Dive C 
Published: September 2007

Over recent years the role of biomarkers in anticancer drug development has expanded across a spectrum of applications ranging from research tool during early discovery to surrogate endpoint in the clinic. However, in Europe when biomarker measurements are performed on samples collected from subjects entered into clinical trials of new investigational agents, laboratories conducting these analyses become subject to the Clinical Trials Regulations. While these regulations are not specific in their requirements of research laboratories, quality assurance and in particular assay validation are essential. This review, therefore, focuses on a discussion of current thinking in biomarker assay validation. Five categories define the majority of biomarker assays from ‘absolute quantitation’ to ‘categorical’. Validation must therefore take account of both the position of the biomarker in the spectrum towards clinical end point and the level of quantitation inherent in the methodology. Biomarker assay validation should be performed ideally in stages on ‘a fit for purpose’ basis avoiding unnecessarily dogmatic adherence to rigid guidelines but with careful monitoring of progress at the end of each stage. These principles are illustrated with two specific examples: (a) absolute quantitation of protein biomarkers by mass spectrometry and (b) the M30 and M65 ELISA assays as surrogate end points of cell death. British Journal of Pharmacology (2008) 153, 646–656; doi:10.1038/sj.bjp.0707441; published online 17 September 2007
Cardioprotection: spotlight on PKG
Authors: Cohen M V , Downey J M 
Published: September 2007

Classical ischaemic preconditioning, delayed or second window preconditioning and postconditioning are forms of cardioprotection that are dependent on cell surface receptors, intracellular signalling molecules and kinases that ultimately block formation of the mitochondrial permeability transition. The latter is presumed to cause myocardial necrosis as well as apoptosis, so prevention of its formation upon resumption of perfusion after a prolonged coronary occlusion should be cardioprotective. In all of these forms of cardioprotection, formation of cGMP and activation of protein kinase G (PKG) are recognized to be key steps in the signal transduction pathway. Burley et al. highlight the roles of cGMP and PKG in their comprehensive review. They describe the basic biology of PKG and emphasize its compartmentalization, which may be responsible for the frustration induced by assays for PKG in whole cell lysates and for the spurious conclusions about the role of PKG in cardioprotection. This review will be useful to both the novice and the seasoned investigator.British Journal of Pharmacology (2007) 152, 833–834; doi:10.1038/sj.bjp.0707453; published online 17 September 2007
Store‐operated calcium entry in vascular smooth muscle
Authors: Leung F P , Yung L M , Yao X , Laher I , Huang Y 
Published: September 2007

In non‐excitable cells, activation of G‐protein‐coupled phospholipase C (PLC)‐linked receptors causes the release of Ca2+from intracellular stores, which is followed by transmembrane Ca2+entry. This Ca2+entry underlies a small and sustained phase of the cellular [Ca2+]iincreases and is important for several cellular functions including gene expression, secretion and cell proliferation. This form of transmembrane Ca2+entry is supported by agonist‐activated Ca2+‐permeable ion channels that are activated by store depletion and is referred to as store‐operated Ca2+entry (SOCE) and represents a major pathway for agonist‐induced Ca2+entry. In excitable cells such as smooth muscle cells, Ca2+entry mechanisms responsible for sustained cellular activation are normally considered to be mediated via either voltage‐operated or receptor‐operated Ca2+channels. Although SOCE occurs following agonist activation of smooth muscle, this was thought to be more important in replenishing Ca2+stores rather than acting as a source of activator Ca2+for the contractile process. This review summarizes our current knowledge of SOCE as a regulator of vascular smooth muscle tone and discusses its possible role in the cardiovascular function and disease. We propose a possible hypothesis for its activation and suggest that SOCE may represent a novel target for pharmacological therapeutic intervention.British Journal of Pharmacology(2008)153, 846–857; doi:10.1038/sj.bjp.0707455; published online 17 September 2007
The complications of promiscuity: endocannabinoid action and metabolism
Authors: Alexander S P H , Kendall D A 
Published: September 2007

In this review, we present our understanding of the action and metabolism of endocannabinoids and related endogenous molecules. It is clear that the interactions between the multiple endocannabinoid‐like molecules (ECLs) are highly complex, both at the level of signal transduction and metabolism. Thus, ECLs are a group of ligands active at 7‐transmembrane and nuclear receptors, as well as transmitter‐gated and ion channels. ECLs and their metabolites can converge on common endpoints (either metabolic or signalling) through contradictory or reinforcing pathways. We highlight the complexity of the endocannabinoid system, based on the promiscuous nature of ECLs and their metabolites, as well as the synthetic modulators of the endocannabinoid system.British Journal of Pharmacology(2007)152, 602–623; doi:10.1038/sj.bjp.0707456; published online 17 September 2007
The orphan receptor GPR55 is a novel cannabinoid receptor
Authors: Ryberg E , Larsson N , Sjögren S , Hjorth S , Hermansson N‐O , Leonova J , Elebring T , Nilsson K , Drmota T , Greasley P J 
Published: September 2007

Background:The endocannabinoid system functions through two well characterized receptor systems, the CB1 and CB2 receptors. Work by a number of groups in recent years has provided evidence that the system is more complicated and additional receptor types should exist to explain ligand activity in a number of physiological processes.Experimental approach:Cells transfected with the human cDNA for GPR55 were tested for their ability to bind and to mediate GTPγS binding by cannabinoid ligands. Using an antibody and peptide blocking approach, the nature of the G‐protein coupling was determined and further demonstrated by measuring activity of downstream signalling pathways.Key results:We demonstrate that GPR55 binds to and is activated by the cannabinoid ligand CP55940. In addition endocannabinoids including anandamide and virodhamine activate GTPγS binding via GPR55 with nM potencies. Ligands such as cannabidiol and abnormal cannabidiol which exhibit no CB1or CB2 activity and are believed to function at a novel cannabinoid receptor, also showed activity at GPR55. GPR55 couples to Gα13 and can mediate activation of rhoA, cdc42 and rac1.Conclusions:These data suggest that GPR55 is a novel cannabinoid receptor, and its ligand profile with respect to CB1 and CB2 described here will permit delineation of its physiological function(s).British Journal of Pharmacology (2007) 152, 1092–1101; doi:10.1038/sj.bjp.0707460; published online 17 September 2007
Extraction and Characterization of Lipids from the Kernels, Leaves, and Stalks of Nine Grain Sorghum Parent Lines
Authors: Christiansen K. L. , Weller C. L. , Schlegel V. L. , Cuppett S. L. , Carr T. P. 
Published: September 2007

ABSTRACTThe objectives of this study were to identify and quantify lipid classes extracted from the stalk, leaves, and the whole kernels of nine different sorghum parent lines. All extractions were performed with a Soxtec using n‐hexane as the extraction solvent. Analytical methods including high‐performance liquid chromatography (HPLC), gas chromatography (GC), and thin‐layer chromatography (TLC) were used to identify and quantify the extracted lipid classes: triacylglycerides (TAG), diglycerides (DG), policosanols (PA), free sterols (FS), phytosterols (PS), free fatty acids (FFA), tocopherols (T), and fatty aldehydes. Overall, extracts from the leaves had higher amounts of soluble matter. Extracts from leaves contained more alcohols and sterols, whereas extracts from the stalks and the whole kernels contained the greatest amount of free fatty acids and fatty aldehydes, respectively. Trace amounts of tocopherol were detected by HPLC in all 27 samples. The lipid profiles of extracts from the whole kernels, leaves, and stalks from the same plant differed. The lipid profiles of extracts from each anatomical part of the sorghum plant differed between the nine parent lines.
Molecular Weight Distribution of (1→3)(1→4)‐β‐Glucan Affects Pasting Properties of Flour from Oat Lines with High and Typical Amounts of β‐Glucan
Authors: Yao Ni , Jannink Jean‐Luc , White Pamela J. 
Published: September 2007

ABSTRACTExperimental (N979‐5‐2‐4 and IA95111) and traditional oat lines (Jim and Paul) with average %β‐glucan of 7.5, 7.8, 4.9, and 4.4%, respectively, were grown in 2002, 2003, and 2004. Molecular weight (MW) distributions of the β‐glucans were examined for potential variations among growing years and for relationships with pasting properties measured by Rapid ViscoAnalyser under three separate conditions: 1) in silver nitrate (SN) solution to inactivate enzymes; 2) hydrolyzed by α‐amylase to eliminate the effect of starch; and 3) treated with lichenase to remove β‐glucan. The β‐glucan was extracted by a process involving multiple precipitation and dialysis steps, and the MW distributions were determined by HPLC. %β‐Glucan in N979‐5‐2‐4 and IA95111 lines were consistently and significantly greater (P < 0.05) than in Jim and Paul lines during three growing years. The contribution of β‐glucan to peak viscosity on the RVA was substantially greater than that of the starch for all three years. The molecular number average and peak MW of β‐glucan from N979‐5‐2‐4 and IA95111 were greater than these values for Jim and Paul, and values were consistent among years. The MW of extracted β‐glucan was associated with pasting properties after amylase hydrolysis, but not after treatment with lichenase or in SN solution.
Experimental Determination of Longitudinal Expansion During Extrusion of Starches
Authors: Kumar A. , Ganjyal G. M. , Jones D. D. , Hanna M. A. 
Published: September 2007

ABSTRACTExpansion during extrusion of starches is a unique phenomenon used extensively in the food industry. Sectional expansion index is usually determined as the ratio of the square of the diameter of the final extrudate to the square of diameter of the die through which the product is expelled. Longitudinal expansion index is calculated indirectly by doing a mass balance across the extruder and making an assumption for density of the dough melt in the die. The objective of this research was to determine the longitudinal expansion index experimentally using a die designed to measure the velocity of the melt dough inside the die. A tracer was induced to change the conductivity of the melt dough. The velocity inside the die was then determined by measuring the time of travel of a tracer with the help of electrical probes. Corn starch (25% amylose and 30% moisture content) was extruded in a twin‐screw extruder at a barrel temperature of 140°C, screw speeds of 80, 120, and 160 rpm, and feed rates corresponding to the screw speeds varying from 7.35 to 13. 35 kg/hr. An inverse relationship was observed between the longitudinal expansion and the sectional expansion indices.
The effects of iron deficiency on neutrophil/monocyte apoptosis in children
Authors: Berrak S. G. , Angaji M. , Turkkan E. , Canpolat C. , Timur C. , Eksioglu‐Demiralp E. 
Published: September 2007

Abstract.  Objectives: Iron is essential for DNA synthesis; its deficiency may lead to impaired DNA synthesis and subsequent alterations in levels of apoptosis. Here, we have aimed to investigate effects of iron deficiency anaemia (IDA) on apoptotic response of phagocytic cells and to understand whether the effect is reversible after iron supplementation. Materials and methods: Forty‐nine IDA patients and 26 healthy controls, aged between 6 months and 12 years with similar demographic status, were considered. Neutrophil‐ and monocyte‐apoptotic responses of IDA patients and the control group were compared by flow cytometry. Then, IDA patients were provided with oral iron supplementation. On day 15 of iron therapy, neutrophil‐ and monocyte‐apoptotic responses of IDA patients were rechecked and were compared to those of control group. Results: Neutrophil‐ and monocyte‐apoptotic responses in terms of early and late percentages of apoptosis, and percentages of necrotic cells, were significantly less in IDA patients compared to the control group. The significantly low apoptotic responses of IDA patients rose to levels of the control group by day 15 of iron therapy. Besides, the effect of IDA on apoptotic responses was found to be more enhanced in severe IDA patients that those of mild IDA patients. Conclusion: Correction of differences after iron supplementation therapy implies that IDA might be a cause for changes in neutophil‐ and monocyte‐apoptotic responses. The impact of this diminution of apoptotic cellular function in IDA should be further investigated, with longitudinal studies, in order to document the impact of any severe and/or long‐lasting IDA on autoimmunity and malignancy.
Simulated microgravity inhibits the proliferation and osteogenesis of rat bone marrow mesenchymal stem cells
Authors: Dai Z. Q. , Wang R. , Ling S. K. , Wan Y. M. , Li Y. H. 
Published: September 2007

Abstract. Objectives: Microgravity is known to affect the differentiation of bone marrow mesenchymal stem cells (BMSCs). However, a few controversial findings have recently been reported with respect to the effects of microgravity on BMSC proliferation. Thus, we investigated the effects of simulated microgravity on rat BMSC (rBMSC) proliferation and their osteogeneic potential.Materials and methods: rBMSCs isolated from marrow using our established effective method, based on erythrocyte lysis, were identified by their surface markers and their proliferation characteristics under normal conditions. Then, they were cultured in a clinostat to simulate microgravity, with or without growth factors, and in osteogenic medium. Subsequently, proliferation and cell cycle parameters were assessed using methylene blue staining and flow cytometry, respectively; gene expression was determined using Western blotting and microarray analysis.Results: Simulated microgravity inhibited population growth of the rBMSCs, cells being arrested in the G0/G1phase of cell cycle. Growth factors, such as insulin‐like growth factor‐I, epidermal growth factor and basic fibroblastic growth factor, markedly stimulated rBMSC proliferation in normal gravity, but had only a slight effect in simulated microgravity. Akt and extracellular signal‐related kinase 1/2 phosphorylation levels and the expression of core‐binding factor α1 decreased after 3 days of clinorotation culture. Microarray and gene ontology analyses further confirmed that rBMSC proliferation and osteogenesis decreased under simulated microgravity.Conclusions: The above data suggest that simulated microgravity inhibits population growth of rBMSCs and their differentiation towards osteoblasts. These changes may be responsible for some of the physiological changes noted during spaceflight.
Plasma aldosterone response to the low‐dose adrenocorticotrophin (ACTH 1–24) stimulation test
Authors: Honour J. W. , Bridges N. A. , Conway‐Phillips E. , Hindmarsh P. C. 
Published: September 2007

SummaryBackground  Endocrine tests for adrenal insufficiency use pharmacological doses of stimulant such as ACTH. More physiological tests have often used high‐dose protocols for sampling frequency.Aims  To evaluate the response of plasma aldosterone concentration to low doses (125, 250 and 500 ng/m2 body surface area) of synthetic ACTH.Design  A randomised trial in six normal adult males aged 18–27 years.Materials and methods  Aldosterone concentration was measured by radioimmunoassay in serum from blood samples taken at 10 min intervals for 90 min.Results  All three doses produced a significant rise in plasma aldosterone concentration (125 ng/m2, P = 0·003; 250 ng/m2, P < 0·001; 500 ng/m2, P < 0·001) but there was no effect of dose on either the peak or incremental plasma aldosterone concentration. Mean time to peak was similar between the doses and the two higher doses were associated with a longer secretory profile (125 ng/m2 56 (26 SD) mins, 250 ng/m2 74 (19) mins, 500 ng/m2 77 (21) mins; F = 3·39; P = 0·04). Peaks of 100% were detected within 30 min of drug administration and peak response was associated with the prestimulation plasma aldosterone concentration (r = 0·45; P = 0·003). The between‐ and within‐individual coefficients of variation for prestimulation concentrations were 37·0% and 32·8%, and for the peak response were 27·2% and 27·2%, respectively.Conclusions  The response of plasma aldosterone concentrations to low‐dose ACTH administration requires a blood sampling protocol of 0, 10, 20 and 30 min to capture concentrations near the peak response. The high‐dose protocol would have missed the response. Over the dose range studied no dose–response was observed so the selection of dose should be based on the dose effective to release steroids in the glucocorticoid pathway if this study is to be used in conjunction with such evaluation.
Testing the differential predation hypothesis for the invasion of rusty crayfish in a stream community: laboratory and field experiments
Authors: KUHLMANN MARK L. , BADYLAK STEPHANIE M. , CARVIN ERIN L. 
Published: September 2007

Summary1. We tested the hypothesis that the non‐native rusty crayfish (Orconectes rusticus) is less vulnerable to predators than two native species (O. propinquus and O. obscurus) it is replacing in streams of the upper Susquehanna River catchment (New York, U.S.A.).2. We used laboratory experiments to compare species‐specific predation rates by smallmouth bass (Micropterus dolomieu) on crayfish of equal size and field tethering experiments to compare relative predation rates between native O. propinquus and non‐native O. rusticus by the suite of crayfish predators in our system. We predicted that crayfish size would affect predation rate but that predation rates would be equal among species when size was controlled.3. We also tested for two potential artefacts of tethering. We tethered crayfish in cages to test whether the ability to escape from tethers is size specific, and we tested whether tethering alters differential predation among crayfish species by the smallmouth bass.4. In the laboratory, smallmouth bass predation on rusty crayfish was lower than on either of the native species. In the field, predation risk for tethered crayfish was inversely related to size but did not differ among species when size was taken into account. Because rusty crayfish in the field experiment were slightly larger than the native species, as in nature, mortality was overall lower for the rusty crayfish.5. In cages, smaller crayfish were more probably to escape from tethers than larger ones, an artefact that may partially confound results from our tethering experiments. Unexpectedly, tethering nearly eliminated predation by smallmouth bass. This artefact prevented us from testing for an interaction of tethering with differential predation and means that the results of field tethering experiments do not include any contribution from smallmouth bass predation.6. Our experiments highlight the importance of explicitly considering potential artefacts that could confound results.7. Our results indicate that differential predation contributes to the rusty crayfish's invasion of a stream community. In our study system, predation rates on rusty crayfish are lower than for native species mostly because of selection by predators for smaller crayfish; species‐specific characteristics such as behaviour that further reduce predation may also contribute, especially where smallmouth bass predation is important.