bluuebunny/crossref_metadata_2025_split huggingface dataset:
Percutaneous Coronary Intervention–Related Bleeding Risk Factors in Current Practice
Authors: Mathis A Scott , Gugger James J 
Published: September 2005

BACKGROUND: Bleeding is a common and costly complication of percutaneous coronary intervention (PCI). Little is known about the risk factors for bleeding complications. Objective: To report our PCI-related observations from a single institution and use the information to establish risk factors for short-term bleeding complications, with special focus on examining the importance of renal function. METHODS: A retrospective record review was conducted of the admission of 300 patients grouped according to antithrombotic regimen: unfractionated heparin alone (n = 187), bivalirudin (n = 26), and glycoprotein IIb/IIIa antagonist plus heparin (n = 103). Bleeding and ischemic outcomes were tracked. A model was constructed to predict independent bleeding risk factors. RESULTS: Treatment groups differed significantly regarding any bleeding (p = 0.001), minor bleeding (p < 0.001), and length of stay (p = 0.01). Multivariate predictors of any bleeding included antithrombotic regimen, creatinine clearance (Clcr) <30 mL/min, and hypertension. Any bleeding was associated with prolonged length of stay. Major bleeding was predicted by Clcr <30 mL/min and was associated with prolonged length of stay and death. Minor bleeding was predicted only by choice of antithrombotic regimen. CONCLUSIONS: The major influences on bleeding risk appeared to be Clcr <30 mL/min and choice of antithrombotic regimen. It is important to note that other markers of renal function, including serum creatinine value and serum creatinine at a cutoff level of 1.5 mg/dL, did not predict bleeding events.
Intestinal Pseudo-Obstruction Caused by Diltiazem in a Neutropenic Patient
Authors: Young Rebecca P , Wu Helen 
Published: September 2005

OBJECTIVE: To describe a case of diltiazem-induced intestinal pseudo-obstruction in a neutropenic patient. CASE SUMMARY: A 74-year-old male with newly diagnosed acute myelogenous leukemia developed atrial fibrillation on day 12 of induction chemotherapy. He was initially treated with diltiazem 5 mg intravenously every 5–10 minutes for 5 doses and an amiodarone 150-mg loading dose intravenously. Diltiazem 30 mg orally 4 times daily and amiodarone continuous infusion were started thereafter. Amiodarone therapy was discontinued after one day due to an untoward adverse effect. The diltiazem dose was then escalated. By day 14, the patient was receiving diltiazem 120 mg orally 4 times daily. On day 15, he developed increasing abdominal distention with hyperactive bowel sounds. On day 16, a radiographic examination showed multiple dilated loops of both the small and large bowel representing possible intestinal pseudo-obstruction; diltiazem was discontinued that day. Starting on day 18, the patient showed recovery of intestinal pseudo-obstruction without intervention. No further GI complications developed during his remaining hospital course. DISCUSSION: Intestinal pseudo-obstruction is usually associated with underlying medical conditions such as trauma, infection, cardiac disease, and after surgery. Medications rarely cause such a condition. Detailed examination of the patient's record indicated neither infection nor other medications contributed to the development of intestinal pseudo-obstruction. Additionally, a radiographic examination ruled out neutropenic enterocolitis, a common gastrointestinal complication in neutropenic patients. Use of the Naranjo probability scale indicated a probable relationship between pseudo-obstruction and diltiazem in this patient. CONCLUSIONS: Although calcium-channel blockers rarely cause intestinal pseudo-obstruction, clinicians must be aware of this serious but reversible adverse effect.
Pharmaceutical Care in Community Pharmacy: Practice and Research in the Netherlands
Authors: van Mil JW Foppe 
Published: September 2005

OBJECTIVE: To describe the pharmaceutical care activities and research in community pharmacy in the Netherlands. FINDINGS: Pharmaceutical care is well advanced in Dutch pharmacy practice. This is largely due to the fact that clinical pharmacy was already an integrated part of community pharmacy practice by the end of the 1980s. Activities of the International Pharmaceutical Federation (FIP), some wholesale companies, and influential individuals in the Netherlands stimulated universities and the Royal Society for the Advancement of Pharmacy to advance the implementation of pharmaceutical care. DISCUSSION: Not all pharmacies in the Netherlands provide pharmaceutical care at the same level, although medication surveillance (concurrent and prospective medication analysis) is part of everyday practice. Implementation of quality assurance systems in community pharmacy practice could be helpful in assuring high levels of care. Similar to those in other countries, Dutch pharmacists are torn between the wish to provide pharmaceutical care and economic considerations, although the financial status of most pharmacies is still (very) healthy. New entrants into the market, such as supermarket and pharmacy chains, seem to put little emphasis on care provision. CONCLUSIONS: Pharmaceutical care has been implemented in many Dutch community pharmacies, but not everywhere to the same extent. Due to excellent automated medication surveillance; structured, high-quality medication counseling; and the fact that patients usually visit the same pharmacy, Dutch patients are well protected against many drug-related problems.
Microglial Phagocytosis Induced by Fibrillar β-Amyloid and IgGs Are Differentially Regulated by Proinflammatory Cytokines
Authors: Koenigsknecht-Talboo Jessica , Landreth Gary E. 
Published: September 2005

Microglia undergo a phenotypic activation in response to fibrillar β-amyloid (fAβ) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAβ deposits. However, they can be induced to do so during Aβ vaccination therapy attributable to anti-Aβ antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Aβ plaques.We report that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fAβ or complement receptor 3 and argue that this may, in part, underlie the accumulation of fAβ-containing plaques within the AD brain. The proinflammatory suppression of fAβ-elicited phagocytosis is dependent on nuclear factor κB activation. Significantly, the proinflammatory cytokines do not inhibit phagocytosis elicited by antibody-mediated activation of FcR, which may contribute to the efficiency of Aβ vaccination-based therapy. Importantly, the proinflammatory suppression of fAβ phagocytosis can be relieved by the coincubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinflammatory cytokines induce the production of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis. These findings support anti-inflammatory therapies for the treatment of AD.
Evaluating Human Embryonic Germ Cells: Concord and Conflict as Pluripotent Stem Cells
Authors: Turnpenny Lee , Spalluto Cosma M. , Perrett Rebecca M. , O'Shea Marie , Hanley Karen Piper , Cameron Iain T. , Wilson David I. , Hanley Neil A. 
Published: September 2005

AbstractThe realization of cell replacement therapy derived from human pluripotent stem cells requires full knowledge of the starting cell types as well as their differentiated progeny. Alongside embryonic stem cells, embryonic germ cells (EGCs) are an alternative source of pluripotent stem cell. Since 1998, four groups have described the derivation of human EGCs. This review analyzes the progress on derivation, culture, and differentiation, drawing comparison with other pluripotent stem cell populations.
Can parents adjust to the idea that their child is at risk for a sudden death?: Psychological impact of risk for long QT syndrome
Authors: Hendriks Karin S.W.H. , Grosfeld F.J.M. , van Tintelen J.P. , van Langen I.M. , Wilde A.A.M. , van den Bout J. , ten Kroode H.F.J. 
Published: September 2005

AbstractCan a parent adjust to the idea that its child is at risk for a sudden death? This question is raised by a diagnostic procedure in which children were tested for an inherited Long QT Syndrome (LQTS). This potentially life‐threatening but treatable cardiac arrhythmia syndrome may cause sudden death, especially in children and young adults. The long‐term psychological effects are described for parents whose children were tested for inherited LQTS. The adverse short‐term impact of such testing has been described previously. The goal of this investigation is to determine whether this distress endures. Thirty‐six parents completed measures of psychological distress. With the twenty‐four parents of carrier children, a semi‐structured interview was held 18 months after DNA disclosure. Parents of carrier children reported more distress than parents of non‐carrier children. Parents of carrier children remained vulnerable to high levels of distress; up to one‐third of these parents showed clinically relevant high levels of distress. High levels of distress were reported by parents of carrier children who (1) were highly distressed at previous assessments, (2) were familiar with the disease for a longer time, (3) had experienced a sudden death in the family, (4) were lesser educated, and who (5) were unsatisfied with the given information. Parents were particularly concerned about possible hazardous behavior during puberty. We conclude that the continuous threat of developing LQTS symptoms despite prophylactic treatment affected the psychological well‐being of the parents for a long time. In light of the tempetuous developments in the areas of cardiac genetics, periodical information on new insight and developments may act as a buffer for the parents' (growing) concerns about their child's inherited disorder. © 2005 Wiley‐Liss, Inc.
Alternating penalty trilinear decomposition algorithm for second‐order calibration with application to interference‐free analysis of excitation–emission matrix fluorescence data
Authors: Xia A‐Lin , Wu Hai‐Long , Fang Dong‐Mei , Ding Yu‐Jie , Hu Le‐Qian , Yu Ru‐Qin 
Published: September 2005

AbstractA new method, alternating penalty trilinear decomposition (APTLD), is developed for the decomposition of three‐way data arrays. By utilizing the alternating least squares principle and alternating penalty constraints to minimize three different alternating penalty errors simultaneously, the intrinsic profiles are found. The APTLD algorithm can avoid the two‐factor degeneracy problem and relieve the slow convergence problem, which is difficult to handle for the traditional parallel factor analysis (PARAFAC) algorithm. It retains the second‐order advantage of quantification for analytes of interest even in the presence of potentially unknown interferents. In additions, it is insensitive to the estimated component number, thus avoiding the difficulty of determining a correct component number for the model, which is intrinsic in the PARAFAC algorithm. The results of treating one simulated and one real excitation–emission spectral data set showed that the proposed algorithm performs well as long as the model dimensionality chosen is not less than the actual number of components. Furthermore, the performance of the APTLD algorithm sometimes surpasses that of the PARAFAC algorithm in the prediction of concentration profiles even if the component number chosen is the same as the actual number of underlying factors in real samples. Copyright © 2005 John Wiley & Sons, Ltd.
Survival of metastatic breast carcinoma patients over a 20‐year period
Authors: Gennari Alessandra , Conte PierFranco , Rosso Riccardo , Orlandini Cinzia , Bruzzi Paolo 
Published: September 2005

AbstractBACKGROUNDThe expectation of improvement in patient survival with administration of new chemotherapy agents for metastatic breast carcinoma (MBC) is not consistently supported by data from clinical trials, which are often underpowered and have not detected moderate survival advantage. The aim of this study was to evaluate the impact of new agents on prognosis of MBC patients enrolled in clinical trials of first‐line chemotherapy.METHODSBetween 1983 and 2001, 640 MBC patients were entered into 6 consecutive trials; the present analysis was limited to patients. The date of diagnosis of metastatic breast disease was used to define 5 arbitrarily chosen 3‐year time cohorts, 1983–1986, 1987–1989, 1992–1994, 1995–1997, and 1998–2001. Multivariate proportion of hazard (PH) models were used to evaluate changes in overall survival (OS) and progression‐free survival (PFS) over time and to detect changes associated with the use of taxanes, while adjusting for differences in baseline factors among 5 cohorts.RESULTSPatient characteristics were evenly distributed across the 5 cohorts. Median OS was 18 months, 17.2 months, 19.2 months, 26.1 months, and 23.6 months, respectively, in cohorts 1983–1986, 1987–1989, 1992–1994, 1995–1997, 1998–2001 (P< 0.0001). Age, performance status, relapse‐free survival, type of adjuvant treatment, metastatic site, and taxane first‐line chemotherapy were all associated with survival. These data failed to provide an indication of temporal trend and suggested a reduction in hazard of death in two cohorts (1995–1997 and 1998–2001) where taxane was added to first‐line chemotherapy.CONCLUSIONSThe analysis provided evidence of improvement in prognosis of MBC patients that was associated with use of modern chemotherapeutic agents independent of time. Cancer 2005. © 2005 American Cancer Society.
Synthesis and Structure of the Group 12 Pyrimidinethiolate Complexes ∞3[Zn(S‐2‐N2C4H3)2], ∞2[Cd(S‐2‐N2C4H3)2], [Hg(S‐2‐N2C4H3)2] and[Cd(S‐2‐N2C4H3)2(tmeda)]
Authors: Eichhöfer Andreas , Buth Gernot 
Published: September 2005

AbstractThe pyrimidinethiolate complexes ∞3[Zn(S‐2‐N2C4H3)2],∞2[Cd(S‐2‐N2C4H3)2] and [Hg(S‐2‐N2C4H3)2] have been prepared by reaction of MCl2 (M = Zn, Cd, Hg) with 2 equiv. of Me3SiS‐2‐N2C4H3 in organic solvents, whilst [Cd(S‐2‐N2C4H3)2(tmeda)] was obtained by recrystallisation of∞2[Cd(S‐2‐N2C4H3)2] in TMEDA at 40 °C. The structures of the complexes were determined by single‐crystal X‐ray crystallography, which shows that the different metal atoms each have different coordination environments. The zinc atom in ∞3[Zn(S‐2‐N2C4H3)2] exhibits a tetrahedral coordination with one sulfur and three nitrogen atoms from pyrimidinethiolate ligands, whereas the cadmium atoms in ∞2[Cd(S‐2‐N2C4H3)2] and [Cd(S‐2‐N2C4H3)2(tmeda)] are six‐coordinate with either three sulfur and three nitrogen atoms or two sulfur and four nitrogen atoms. In contrast, the mercury atoms in [Hg(S‐2‐N2C4H3)2] display a distorted square‐planar coordination to a pair of chelating –S‐2‐N2C4H3 ligands with additional weak Hg–S interactions to adjacent molecules. While known cadmium and zinc pyrimidinethiolate complexes consist of one‐dimensional chains, ∞3[Zn(S‐2‐N2C4H3)2] and ∞2[Cd(S‐2‐N2C4H3)2] form either three‐ or two‐dimensional polymeric networks of metal atoms. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Synthesis of (R)‐(–)‐2‐Fluoronorapomorphine — A Precursor for the Synthesis of (R)‐(–)‐2‐Fluoro‐N‐[11C]propylnorapomorphine for Evaluation as a Dopamine D2 Agonist Ligand for PET Investigations
Authors: Søndergaard Kåre , Langgaard Kristensen Jesper , Gillings Nic , Begtrup Mikael 
Published: September 2005

Abstract2‐Fluoronorapomorphine, the PET labelling precursor to 2‐fluoro‐N‐[11C]propylnorapomorphine, was prepared in 13 steps from codeine in a total yield of 10 %. Codeine was converted in four steps into N‐benzylnorcodeine which was oxidised by using the Swern protocol. Subsequent acid‐catalysed rearrangement afforded N‐benzylnormorphothebaine which was selectively triflylated at the 2‐position and pivaloylated at the 11‐position. The triflate underwent palladium‐catalysed amination with benzophenone imine. Amination conditions required sequential base addition to give substantial conversion of the triflate to the corresponding N‐substituted benzophenone imine. After acidic hydrolysis the resulting aniline was transformed into the 2‐fluoro compound via the Balz–Schiemann reaction. Hydrogenolysis of the N‐benzyl group followed by deprotection of the catechol moiety using BBr3 provided 2‐fluoronorapomorphine. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Combined genome‐wide allelotyping and copy number analysis identify frequent genetic losses without copy number reduction in medulloblastoma
Authors: Langdon Jacqueline A. , Lamont Jayne M. , Scott Debbie K. , Dyer Sara , Prebble Emma , Bown Nick , Grundy Richard G. , Ellison David W. , Clifford Steven C. 
Published: September 2005

AbstractDetailed analysis of mechanisms of genetic loss for specific tumor suppressor genes (TSGs; e.g., RB1, APC and NF1) indicates that TSG inactivation can occur by allelic loss of heterozygosity (LOH), without any alteration in DNA copy number. However, the role and prevalence of such events in the pathogenesis of specific malignancies remains to be established on a genome‐wide basis. We undertook a detailed molecular assessment of chromosomal defects in a panel of nine cell lines derived from primary medulloblastomas, the most common malignant brain tumors of childhood, by parallel genome‐wide assessment of LOH (allelotyping) and copy number aberrations (comparative genomic hybridization and fluorescence in situ hybridization). The majority of genetic losses observed were detected by both copy number and LOH methods, indicating they arise through the physical deletion of chromosomal material. However, a significant proportion of losses (17/42, 40%) represented regions of allelic LOH without any associated copy number reduction; these events involved both whole chromosomes (10/17) and sub‐chromosomal regions (7/17). Using this approach, we identified medulloblastoma‐characteristic alterations, e.g., isochromosome for 17q, MYC amplification and losses on chromosomes 10, 11, and 16, alongside novel regions of genetic loss (e.g., 10q21.1‐26.3, 11q24.1‐qter). This detailed genetic characterization of the majority of medulloblastoma cell lines provides important precedent for the widespread involvement of copy number‐neutral genetic losses in medulloblastoma and demonstrates that combined assessment of copy number aberrations and LOH will be necessary to accurately determine the contribution of chromosomal defects to tumor development. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat. © 2005 Wiley‐Liss, Inc.
Visualizing levels of osteoblast differentiation by a two‐color promoter‐GFP strategy: Type I collagen‐GFPcyan and osteocalcin‐GFPtpz
Authors: Bilic‐Curcic I. , Kronenberg M. , Jiang X. , Bellizzi J. , Mina M. , Marijanovic I. , Gardiner E.M. , Rowe D.W. 
Published: September 2005

AbstractA 3.9 kb DNA fragment of human osteocalcin promoter and 3.6 kb DNA fragment of the rat collagen type1a1 promoter linked with visually distinguishable GFP isomers, topaz and cyan, were used for multiplex analysis of osteoblast lineage progression. Three patterns of dual transgene expression can be appreciated in primary bone cell cultures derived from the transgenic mice and by histology of their corresponding bones. Our data support the interpretation that strong pOBCol3.6GFPcyan alone is found in newly formed osteoblasts, while strong pOBCol3.6GFPcyan and hOC‐GFPtpz are present in osteoblasts actively making a new matrix. Osteoblasts expressing strong hOC‐GFPtpz and weak pOBCol3.6GFPcyan are also present and may or may not be producing mineralized matrix. This multiplex approach reveals the heterogeneity within the mature osteoblast population that cannot be appreciated by current histological methods. It should be useful to identify and isolate populations of cells within an osteoblast lineage as they progress through stages of differentiation. genesis 43:87–98, 2005. © 2005 Wiley‐Liss, Inc.
Why worry about awareness in choice problems? Econometric analysis of screening for cervical cancer
Authors: Belkar Rochelle , Fiebig Denzil G. , Haas Marion , Viney Rosalie 
Published: September 2005

AbstractThe decision to undertake a screening test is conditional upon awareness of screening. From an econometric perspective there is a potential selection problem, if no distinction is made between aware and unaware non‐screeners. This paper explores this problem through analysis of the determinants of cervical screening in Australia. Cervical cancer is one of the most preventable and curable forms of cancer. Since 1991 there has been a concerted effort in Australia to recommend and encourage women to have Pap smears every two years. The success of this program can be partly gauged by exploring the determinants of screening for cervical cancer. Using unit record data from the 1995 National Health Survey, an econometric model is developed for whether women have ever screened or not. A proportion of women in the sample contend that they have never heard of a Pap test. The analysis characterizes this group of women and accounts for their presence in the modelling. The paper demonstrates failing to model awareness can result in inconsistent parameter estimates even when the degree of censoring in the sample is relatively small. Copyright © 2005 John Wiley & Sons, Ltd.
Smoke‐free laws and bar revenues in California – the last call
Authors: Cowling David W. , Bond Philip 
Published: September 2005

AbstractCalifornia was the first state to implement smoke‐free restaurant and bar laws, in 1995 and 1998, respectively. We analyze how these laws affected the distribution of revenues between bars and restaurants. Critics of smoke‐free bar laws have often claimed that a prohibition on smoking reduces bar revenues. Similar claims are made for the effects of smoke‐free restaurant laws. Such claims implicitly assume that a smoke‐free law reduces expenditures by smokers by more than it increases expenditures by non‐smokers. Using tax revenue data from 1990 to 2002, our analysis suggests that the actual effect is just the opposite: the 1995 smoke‐free restaurant law is associated with anincreasein restaurant revenues, while the 1998 smoke‐free bar law is associated with an increase in bar revenues. Copyright © 2005 John Wiley & Sons, Ltd.