bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cumulative sum (CUSUM) analysis in the assessment of trainee competence in fetal biometry measurement
Authors: Weerasinghe S. , Mirghani H. , Revel A. , Abu‐Zidan F. M. 
Published: July 2006

AbstractObjectiveTo determine the value of cumulative sum (CUSUM) analysis in assessing trainee proficiency in fetal biometry measurement.MethodsThree primary healthcare doctors with no prior ultrasound training were recruited. Each trainee measured the fetal biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC) and femur length (FL) on 100 consecutive pregnant women. The supervisor repeated the measurements. The CUSUM for each set of trainee measurements was calculated at a set failure rate of 10%. The point at which the graph fell below two consecutive boundary lines indicated the number of examinations required to achieve competence.ResultsThe CUSUM graphs showed that the rate of learning measurement skills varied among the three trainees. The graph for the CUSUM series for BPD and HC measurement for all trainees fell below two consecutive boundary lines and remained there, indicating competence. The CUSUM series for AC measurement for two of the trainees indicated that competence was achieved; however, for the third trainee, while the graph fell below two consecutive boundary lines, indicating competence, it rose again, crossing two consecutive boundary lines. This indicated a loss of competence and the need for further training. FL measurements for the same trainee never fell below two consecutive boundary lines, indicating failure to achieve competence; the other two achieved competence, but failed to maintain it.ConclusionsCUSUM is a useful tool for identifying points of competence and for quantifying the duration of ultrasound training required for each trainee. It provides an early indication of performance, and highlights difficulties in individual performance. Copyright © 2006 ISUOG. Published by John Wiley & Sons, Ltd.
Cord insertion into the lower third of the uterus in the first trimester is associated with placental and umbilical cord abnormalities
Authors: Hasegawa J. , Matsuoka R. , Ichizuka K. , Otsuki K. , Sekizawa A. , Farina A. , Okai T. 
Published: July 2006

AbstractObjectivesTo assess the feasibility of detecting the cord insertion site during the late first trimester, and to investigate the possible association between perinatal complications and a cord insertion in the lower third of the uterus in the first trimester.MethodsThis was a prospective cohort study in which the positional relationship between the uterus and the cord insertion site was examined using gray‐scale transvaginal sonography at 9–11 weeks of gestation. The distance between the internal os and the fundus was divided equally into three parts. Cord insertions located in the upper or middle thirds were defined as normal (controls), and those located in the lower third were defined as cases, regardless of their relationship to the chorion villosum. Third‐trimester sonography and pathological examination of the placenta and cord at delivery were performed to check for placental/cord abnormalities. The univariate association between the location of the cord insertion in the first trimester and placental and umbilical cord abnormalities and perinatal complications was assessed.ResultsThe cord insertion site was identified in 318/340 (93.5%) cases at 9–11 weeks of gestation and it was in the lower third of the uterus in 35 (11.0%) cases. Of these 35, the cord insertion was found at delivery to be low in nine cases (26%) and the placenta was low‐lying at delivery in eight (23%). None of the 283 cases with a normal cord insertion in the first trimester was found to have a low‐lying placenta at delivery (P < 0.0001). Ten (29%) of the cases with a low cord insertion and four (1.4%) with a normal cord insertion in the first trimester had a velamentous or marginal cord insertion at delivery (P < 0.0001). At delivery, five (14%) of the low cord insertion cases and four (1.4%) of the normal cord insertion cases (P < 0.0001) had some form of placental malformation, including accessory placenta and infarction of the placenta. An emergency Cesarean section was performed in four (11%) and six (2.1%) of the low and normal cord insertion cases, respectively (P = 0.003).ConclusionDevelopmental abnormalities of the placenta and umbilical cord occur frequently in cases in which the cord insertion is in the lower third of the uterus in the first trimester. We suggest that screening for the cord insertion site at 9–11 weeks of gestation may have clinical significance for predicting abnormalities of the cord and the placenta at delivery. Copyright © 2006 ISUOG. Published by John Wiley & Sons, Ltd.
New Directions in Pediatric Neuro-Oncology Practice: Impact of the Children's Cancer Group Study 9933, a Phase II Study of High-Dose Chemotherapy Before Radiation in Children with Newly Diagnosed High-Grade Astrocytoma
Authors: MacDonald Tobey J. 
Published: July 2006

ABSTRACTBackground: Despite the use of surgery, radiotherapy (RT) and standard chemotherapy, childhood high-grade astrocytoma (HGA) continues to carry a dismal prognosis. In an attempt to identify effective drug combinations and an alternative treatment strategy, the Children's Cancer Group (CCG) conducted a nationwide clinical trial that prospectively evaluated 102 children with HGA and post-operative residual disease for efficacy and toxicity of four courses of high-dose chemotherapy (HDCT) before RT. Design and methods: Patients were randomly assigned to one of three couplets of drugs: carboplatin/etoposide (Regimen A); ifosfamide/etoposide (Regimen B); or cyclophosphamide/etoposide (Regimen C). After HDCT, all patients received local RT followed by lomustine and vincristine. Results: Of 76 evaluable patients (median age 11.95 years, range 3–20 years), 30 patients relapsed during HDCT and 11 others did not complete HDCT due to toxicity. Non-hematologic serious toxicities were common (29%) and 21% of patients did not receive RT. Objective response rates were not associated with amount of residual disease and did not statistically differ between regimens: 27% (Regimen A), 8% (Regimen B), and 29% (Regimen C). Overall survival (OS) was 24 ± 5% at 5 years and did not differ between groups. The 5-year, event-free survival (EFS) for all patients was 8 ± 3% and 14 ± 7% for Regimen A (p = 0.07). Patients who responded to HDCT had a nominally higher survival rate (p = 0.03 for trend). Interpretation: HDCT prior to RT provides no additional clinical benefit to conventional treatment in HGA, regardless of the amount of measurable residual tumor, and adversely effects ability to complete RT. Strong consideration should be given to investigating alternative strategies and novel biologic agents for this disease.
A Double-Blind, Randomized Clinical Trial to Assess the Augmentation with Nimodipine of Antidepressant Therapy in the Treatment of “Vascular Depression”
Authors: Taragano F.E. , Bagnati P.M. , Allegri R.F. 
Published: July 2006

ABSTRACTThere is evidence for an association between vascular disease and depression, and in particular between cerebrovascular disease and depression, especially that occurring later in life. Among the diverse psychiatric diseases, the one which is most widely studied concerning the relationship with the vascular system, is depression. The risk relationship between depression and vascular events is a two-way road: the presence of depression increases the cerebrovascular and cardiovascular event risk (worsening its evolution and prognosis, as well) and a patient evidencing cerebrovascular or heart disease, will also show an increase in the risk of suffering depression (Taragano et al., 2005). Depression is a common cause of disability in the elderly. It reduces quality of life and represents a serious public health problem (Beekman et al., 2001; Steffens et al., 2000). Its prevalence in late life is 2–3% for major depression and 12–15% for all depressive syndromes (Beekman et al., 1999).
Evidence for specific regional patterns of responses to different vasoconstrictors and vasodilators in sheep isolated pulmonary arteries and veins
Authors: Kemp B. K. , Smolich J. J. , Cocks T. M. 
Published: July 2006

Responses of large (5–7 mm in diameter) and medium sized (3–4 mm in diameter) branches of sheep isolated intrapulmonary arteries and veins and three groups of small pulmonary arteries (200, 500 and 1000 μm diameter) to the vasoconstrictors endothelin‐1, 5‐hydroxytryptamine (5‐HT), noradrenaline and the thromboxane A2 mimetic, U46619, were examined. Also, relaxation responses to the endothelium‐dependent vasodilators, acetylcholine (ACh), bradykinin and ionomycin and the endothelium‐independent vasodilator, sodium nitroprusside (SNP), were studied to determine their predominant site of action within the pulmonary vasculature.
Endothelin‐1 was the most potent vasoconstrictor tested in all vessels. The maximum response to endothelin‐1, expressed as a percentage of the maximum contraction to KCl depolarization, did not differ significantly between the different vessels. By contrast, pulmonary arteries greater than 200 μm in diameter failed to contract to U46619, whereas U46619 was a potent constrictor of large and medium‐sized veins.
5‐HT caused similar contractions in all arteries >200 μm in diameter, but the maximum response was significantly diminished in smaller arteries. By contrast, the maximum response to noradrenaline was progressively attenuated with decreasing arterial diameter. Both 5‐HT and noradrenaline caused poor contractions in veins. Pulmonary veins were less sensitive to 5‐HT than arteries and at low concentrations 5‐HT caused relaxation. No change in sensitivity to noradrenaline was noted between the arteries and veins.
Relaxation responses to bradykinin and ionomycin decreased progressively along the pulmonary vascular tree and were nearly absent in large veins. Also, ACh was a poor relaxing agent of large and medium‐sized arteries and failed to mediate any relaxation response in other vessel segments. Surprisingly the smallest arteries examined (∼200 μm in diameter) failed to relax to ionomycin, bradykinin and SNP. However, both the sensitivity and maximum relaxation to SNP were similar in all other arterial and venous segments.
In conclusion, marked regional differences in reactivity to both vasoconstrictors and vasodilators occur in arterial and venous segments of the sheep isolated pulmonary vasculature. Such specialization may have important implications for the regulation of resistance in this low tone vascular bed.
Evidence that NO acts as a redundant NANC inhibitory neurotransmitter in the guinea‐pig isolated taenia coli
Authors: Selemidis S. , Satchell D. G. , Cocks T. M. 
Published: July 2006

The relative contribution of the putative transmitters, nitric oxide (NO) and an apamin‐sensitive factor, possibly ATP, to inhibitory responses evoked by electrical field stimulation (EFS; 0.2–5 Hz, 0.2 ms duration, supra‐maximal voltage for 10 s) of non‐adrenergic, non‐cholinergic (NANC) nerves was investigated in the guinea‐pig isolated taenia coli contracted with histamine (1 μM).
Peak relaxations to EFS (0.2–5 Hz) were tetrodotoxin (1 μM)‐sensitive, maximal at 0.2 Hz and completely resistant to the nitric oxide synthase inhibitor, NG‐nitro‐L‐arginine (L‐NOARG; 100 μM) in either the presence or absence of atropine (1 μM). Furthermore, the specific inhibitor of soluble guanylyl cyclase, 1H‐[1,2,4] oxadiazolo [4,3‐a] quinoxaline‐1‐one (ODQ; 10 μM), the cytochrome P450 inhibitor and free radical generator, 7‐ethoxyresorufin (7‐ER; 10 μM) and the NO scavenger, oxyhaemoglobin (HbO; 30 μM) had no effect on EFS‐induced relaxations alone and in combination with L‐NOARG (100 μM).
Maximum relaxation to the NO donor, sodium nitroprusside (SNP; 1 μM) was significantly reduced by HbO (30 μM), abolished by 7‐ER (10 μM) and ODQ (10 μM) but was unaffected by apamin (0.1 μM), an inhibitor of small conductance Ca2+‐activated K+ channels.
The relaxation to EFS at 0.2 Hz was resistant to apamin but those to 0.5 and 5 Hz were significantly reduced. EFS (0.2–5 Hz)‐evoked relaxations that persisted in the presence of apamin were further significantly inhibited by L‐NOARG (100 μM) or ODQ (10 μM), but not by HbO (30 μM) or 7‐ER (10 μM).
ATP (1–30 μM) produced concentration‐dependent relaxations that were abolished by apamin (0.1 μM), unaffected by ODQ (10 μM) but only significantly reduced by L‐NOARG (100 μM) at the lowest concentration of ATP (1 μM) used.
Nifedipine (0.3 μM), abolished contractions to 67 mM KCl, histamine (10 μM), endothelin‐1 (0.03 μM), 5‐hydroxytryptamine (5‐HT; 10 μM) and the thromboxane‐mimetic, 9‐11‐dideoxy‐9α, 11α‐methano‐epoxy‐prostaglandin F2α (U46619; 0.1 μM).
The findings of the present study suggest that NO is released during NANC nerve stimulation, but plays no role in NANC relaxations in the guinea‐pig taenia coli unless the effects of another apamin‐sensitive, nerve‐derived hyperpolarizing factor (NDHF) are blocked. Thus, we propose that in this tissue, NO acts as a ‘backup’ or redundant NANC nerve inhibitory transmitter and like NDHF mediates relaxation via hyperpolarization.
Effect of interleukin‐1β, tumour necrosis factor‐α and interferon‐γ on the induction of cyclo‐oxygenase‐2 in cultured human airway smooth muscle cells
Authors: Pang Linhua , Knox Alan J. 
Published: July 2006

Increased levels of several pro‐inflammatory cytokines including interleukin‐1β (IL‐1β) and tumour necrosis factor‐α (TNFα) have been found in bronchoalveolar lavage fluid from symptomatic asthmatic patients. IL‐1β, TNFα and interferon‐γ (IFNγ) are known to stimulate a number of cells to produce inflammatory mediators such as prostaglandins. Although airway smooth muscle (ASM) is known to be a rich source of prostaglandins, the regulation of cyclo‐oxygenase (COX) isoforms and prostanoid production by proinflammatory cytokines have not been studied in human airway smooth muscle.
We studied the effects of IL‐1β, TNFα and IFNγ on the induction of two isoforms of cyclo‐oxygenase and its relation to prostaglandin E2 (PGE2) release and COX activity (reflected by PGE2 synthesis from exogenous arachidonic acid) in human cultured airway smooth muscle cells.
IL‐1β, but not TNFα or IFNγ, caused a time‐ and concentration‐dependent enhancement in PGE2 and other prostanoid (6‐keto‐PGF1α, PGF2α, thromboxane B2 (TXB2) and PGD2) production, with PGE2 and 6‐keto‐PGF1α as the principal products. This stimulation was accompanied by a corresponding increase in COX activity.
COX‐2 protein measured by Western blot analysis was not detectable in untreated cells, but was increased in a time‐ and concentration‐dependent manner by IL‐1β, but not TNFα or IFNγ. In contrast, no variation in the expression of COX‐1 protein was observed.
Pretreatment with the conventional non‐steroidal anti‐inflammatory drugs (NSAIDs), indomethacin and ibuprofen, and the selective COX‐2 inhibitors, NS‐398 and nimesulide, completely blocked IL‐1β‐induced PGE2 release and COX activity. The glucocorticosteroid dexamethasone and protein synthesis inhibitors, cycloheximide and actinomycin D, not only markedly inhibited IL‐1β‐stimulated PGE2 release and COX activity but also suppressed IL‐1β‐induced COX‐2 induction.
This study demonstrates that human cultured ASM cells release prostanoids in response to IL‐1β stimulation and that the response is mostly mediated by the induction of COX‐2 rather than COX‐1 isoenzyme, implying that airway smooth muscle may be an important source of prostaglandins in human airways and that COX‐2 may play an important role in the regulation of the inflammatory process in asthma.
Effects of delayed treatment with nebracetam on neurotransmitters in brain regions after microsphere embolism in rats
Authors: Takeo Satoshi , Hayashi Hideki , Miyake Keiko , Takagi Kaori , Tadokoro Mina , Takagi Norio , Oshikawa Sayuri 
Published: July 2006

The effects of delayed treatment with nebracetam, a novel nootropic drug, on neurotransmitters of brain regions were examined in rats with microsphere embolism‐induced cerebral ischaemia.
Cerebral ischaemia was induced by administration of 900 microspheres (48 μm) into the internal carotid artery. The rats with stroke‐like symptoms were treated p.o. with 30 mg kg−1 nebracetam twice daily. The levels of acetylcholine, dopamine, noradrenaline, 5‐hydroxytryptamine (5‐HT) and their metabolites in the cerebral cortex, striatum and hippocampus of animals with microsphere embolism were determined by high performance liquid chromatography (h.p.l.c.) on the 3rd and 7th days after the operation.
Although the microsphere embolism induced significant changes in most of the neurotransmitters and some of their metabolites in the brain regions, the delayed treatment with nebracetam partially restored only the hippocampal 5‐HT and the striatal dopamine metabolite contents on the 3rd day.
The hippocampal in vivo 5‐HT synthesis, but not the striatal dopamine synthesis, was attenuated in rats with microsphere embolism on the 3rd day, but was restored by treatment with nebracetam. In vivo striatal dopamine turnover rate of the rats with microsphere embolism was inhibited on the 3rd day irrespective of treatment with nebracetam.
The present study provides evidence for a possible action of nebracetam on 5‐HT metabolism in the ischaemic brain.
The effect of continuous versus intermittent treatment with transdermal nitroglycerin on pacing‐induced preconditioning in conscious rabbits
Authors: Szilvassy Z. , Ferdinandy P. , Nagy I. , Jakab I. , Koltai M. 
Published: July 2006

Tolerance to the hypotensive effect of nitroglycerin (NG) blocks preconditioning induced by rapid ventricular pacing (RVP) in rabbits. In the present work the effect of continuous versus intermittent treatment with transdermal nitroglycerin on the pacing‐induced preconditioning phenomenon was studied in conscious rabbits.
RVP (500 beats min−1 over 5 min) increased left ventricular end‐diastolic pressure (LVEDP) from baseline 4.1±0.9 to postpacing 13.8±2.9 mmHg (P<0.001) with a right intraventricular ST‐segment elevation of 1.25±0.13 mV, two indicators of myocardial ischaemia. These changes were significantly attenuated when the RVP period was preceded by a preconditioning pacing of the same rate and duration with an interpacing interval of 5 min.
Protection by preconditioning was abolished when the animals had been made tolerant to the vasodilator effect of 30 μg kg−1 NG by the application of transdermal NG (approx. 0.07 mg kg−1 h−1) over 7 days. Furthermore, transdermal NG per se attenuated both RVP‐induced ST‐segment elevation and LVEDP‐increase over the 7 day period.
With intermittent transdermal NG treatment (12 h ‘patch on’ vs ‘patch off’), neither development of vascular tolerance nor attenuation of the NG‐ or preconditioning‐induced anti‐ischaemic effects were observed. However, the severity of pacing‐induced myocardial ischaemia was significantly increased during the ‘patch off’ periods.
In a second set of experiments, postpacing changes in cardiac cyclic GMP and cyclic AMP levels were determined by means of radioimmunoassay in chronically instrumented anaesthetized open‐chest rabbits with the same NG‐treatment protocols. Preconditioning reduced postpacing increase in cyclic AMP with an increase in cyclic GMP concentrations in hearts of the untreated animals and in those given patches intermittently during both ‘patch on’ and ‘patch off’ periods. However, the preconditioning effect on either cyclic nucleotide was blocked in the tolerant animals.
Transdermal NG increased resting levels of both cardiac cyclic nucleotides in the non‐tolerant but not in the tolerant state. The postpacing increase in cyclic AMP content was inhibited by transdermal NG, independent of vascular tolerance development, whereas, an increase in cyclic GMP content was exclusively seen in the non‐tolerant animals.
We conclude that the anti‐ischaemic effect of NG is independent of the cyclic GMP mechanism in the tolerant state. While intermittent NG therapy prevents development of vascular tolerance and preserves preconditioning, the nitrate‐free periods yield an increased susceptibility of the heart to ischaemic challenges.
Inferring gene regulatory networks from multiple microarray datasets
Authors: Wang Yong , Joshi Trupti , Zhang Xiang-Sun , Xu Dong , Chen Luonan 
Published: July 2006

Abstract
Motivation: Microarray gene expression data has increasingly become the common data source that can provide insights into biological processes at a system-wide level. One of the major problems with microarrays is that a dataset consists of relatively few time points with respect to a large number of genes, which makes the problem of inferring gene regulatory network an ill-posed one. On the other hand, gene expression data generated by different groups worldwide are increasingly accumulated on many species and can be accessed from public databases or individual websites, although each experiment has only a limited number of time-points.
Results: This paper proposes a novel method to combine multiple time-course microarray datasets from different conditions for inferring gene regulatory networks. The proposed method is called GNR (Gene Network Reconstruction tool) which is based on linear programming and a decomposition procedure. The method theoretically ensures the derivation of the most consistent network structure with respect to all of the datasets, thereby not only significantly alleviating the problem of data scarcity but also remarkably improving the prediction reliability. We tested GNR using both simulated data and experimental data in yeast and Arabidopsis. The result demonstrates the effectiveness of GNR in terms of predicting new gene regulatory relationship in yeast and Arabidopsis.
Availability: The software is available from , and or upon request from the authors.
Contact: chen@eic.osaka-sandai.ac.jp, xudong@missouri.edu, zxs@amt.ac.cn
Supplementary information: Supplementary data are available at Bioinformatics online.
Postoperative Infusion of Amino Acids Induces a Positive Protein Balance Independently of the Type of Analgesia Used
Authors: Donatelli Francesco , Schricker Thomas , Mistraletti Giovanni , Asenjo Francisco , Parrella Piervirgilio , Wykes Linda , Carli Franco 
Published: July 2006

Background
Net loss of body protein is a prominent feature of the catabolic response to surgical tissue trauma. Epidural analgesia with hypocaloric dextrose has been demonstrated to attenuate leucine oxidation but was unable to make protein balance positive. The current study was set to determine whether an infusion of amino acids on the second day after colon surgery would revert the catabolic state and promote protein synthesis while maintaining glucose homeostasis in patients receiving epidural analgesia as compared with patient-controlled analgesia with morphine (PCA).

Methods
Sixteen patients undergoing colorectal surgery were randomly assigned to receive epidural blockade or PCA as analgesic techniques and underwent a 6-h stable isotope infusion study (3 h fasted, 3 h fed) on the second postoperative day. Whole body glucose kinetics and protein turnover were measured using [6,6-2H2]glucose and l-[1-13C]leucine as tracer.

Results
The infusion of amino acids caused a decrease in endogenous glucose rate of appearance in both groups (P < 0.05), with greater changes in the PCA group (P < 0.05). Administration of amino acids suppressed the appearance of leucine from protein breakdown in both groups (P < 0.05), although the decrease was greater in the PCA group (P < 0.05). Leucine oxidation increased in both groups (P < 0.05), with greater change in the epidural group (P < 0.05). Protein synthesis increased to the same extent in both groups (P < 0.05). Protein balance became positive after the infusion of amino acids, and the effect was greater in the PCA group (P < 0.05).

Conclusions
Infusion of amino acids decreased the endogenous glucose production and induced a positive protein balance independent of the type of anesthesia provided, although such effects were greater in the PCA group.