bluuebunny/crossref_metadata_2025_split huggingface dataset:
Methods for the Chemical Synthesis of Fullerenes
Authors: Scott Lawrence T. 
Published: September 2004

AbstractC60 has been synthesized by chemical methods in 12 steps. Lessons learned in the author's laboratory during a decade devoted to the synthesis and study of open geodesic polyarenes strongly influenced the strategy and methodology ultimately employed for preparing a suitable 60‐carbon precursor and for closing it up to the fullerene ball. This review provides a personal account of how the new synthetic tools were developed and put to use.
The theoretical estimation of effective spectral dimension for polymer melts
Authors: Kozlov G. V. , Dolbin I. V. , Zaikov G. E. 
Published: September 2004

AbstractThe theoretical technique of an effective spectral dimension estimation for polymer melts is offered. The comparison of experimental and theoretical values of this parameter has shown their good correspondence. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 1353–1356, 2004
Controlled release of 2‐methyl‐4‐chlorophenoxy acetic acid herbicide from waste gelatin–based blends and composites
Authors: Kandil Sherif , Kenawy El‐Refaie , El‐Maghraby Azza , Elashry Elsayed H. 
Published: September 2004

AbstractThe volume of plastic waste is becoming a serious problem for waste management. Waste management is based on four hierarchical approaches: reduction, reuse, recycling, and energy recovery. We now report on recycling of gelatin scraps that are derived during the production of pharmaceutical capsules, by using the gelatin scraps in the production of controlled‐release systems. This may help to minimize the side effects that often accompany the conventional application of pesticides. More important, the gelatins themselves, when degraded, might be useful to soil solarization and crop growth. Using and recycling these waste materials in the proposed application would save natural resources and consequently would be economically useful. The synthesis of gelatin films, and composites incorporating 2‐methyl‐4‐chlorophenoxy acetic acid (MCPA) as herbicide, will be described. Morphology and mechanical properties of the films were investigated by scanning electron microscopy and tensile tests, respectively. The release of the MCPA herbicide from the prepared blends and composites was investigated. The prepared formulation proved to be useful for agricultural applications. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 1420–1427, 2004
Autoimmune‐associated congenital heart block: Dissecting the cascade from immunologic insult to relentless fibrosis
Authors: Clancy Robert M. , Buyon Jill P. 
Published: September 2004

AbstractFew diseases exemplify the integration of research from bench to bedside as well as neonatal lupus, often described as a model of passively acquired autoimmunity. The signature histologic lesion of autoimmune congenital heart block (CHB) is fibrosis of the conducting tissue and, in some cases, the surrounding myocardium. Although anti‐SSA/Ro‐SSB/La antibodies are detected in > 85% of mothers whose fetuses are identified with conduction abnormalities in a structurally normal heart, the risk for a woman with the candidate antibodies to have a child with CHB is 2%. The mechanism by which maternal anti‐SSA/Ro‐SSB/La antibodies initiate and finally eventuate in atrioventricular nodal scarring is not yet defined, but it is clear that the antibodies alone are insufficient to cause disease and fetal factors are likely contributory. Previous in vitro and in vivo studies suggest that the pathologic cascade is initiated via apoptosis, resulting in translocation of SSA/Ro‐SSB/La antigens to the cell surface where they are bound by maternal autoantibodies. Subsequently, the Fc portion of the bound immunoglobulin engages Fcγ receptors on tissue macrophages, resulting in release of TGF‐β at a threshold favoring a profibrotic milieu and irreversible scarring. This cascade also involves tissue‐specific activation of TGF‐β, which promotes the modulation of fibroblasts into myofibroblasts, a scarring phenotype. Recent findings point to genetic polymorphisms that promote high production of TGF‐β as possible fetal risk factors for CHB. Further elucidation of maternal and fetal contributory factors should provide insight into the pathogenesis of CHB and the rarity of irreversible injury. © 2004 Wiley‐Liss, Inc.
Neural regulation of the hepatic Circadian rhythm
Authors: Shibata Shigenobu 
Published: September 2004

AbstractA microarray analysis experiment has revealed that there are many genes, including so‐called clock genes, expressing a circadian rhythm in the liver. The clock genes mentioned above are expressed not only in the suprachiasmatic nucleus (SCN) of the hypothalamus, where the master clock exists, but also in other brain regions and various peripheral tissues. In the liver, clock genes are abundantly expressed and show a clear circadian rhythm. Thus, clock genes seem to play a critical role in the molecular clockworks of both the SCN and the liver. Although oscillation of clock genes in the liver is controlled under the circadian clock mechanism in the SCN, we do not know the resetting signals on liver clock function. Over the past few years, use of the pseudorabies virus, a transsynaptic tract tracer, has allowed us to map neural connections between the SCN and peripheral tissues in several physiological systems. Communication between the SCN and peripheral tissues occurs through autonomic nervous systems involving the sympathetic and parasympathetic neurons. This review mainly describes both anatomical and physiological experiments to reveal the sympathetic control over liver clock function. Although further study is necessary to produce the precise mechanism underlying neural control of liver clock systems, evolution of this mechanism will help our understanding of liver clock functions such as drug metabolism and energy metabolism. © 2004 Wiley‐Liss, Inc.
Function follows form: Cardiac conduction system defects in Nkx2‐5 mutation
Authors: Jay Patrick Y. , Harris Brett S. , Buerger Antje , Rozhitskaya Olga , Maguire Colin T. , Barbosky Laura A. , McCusty Ellen , Berul Charles I. , O'Brien Terrence X. , Gourdie Robert G. , Izumo Seigo 
Published: September 2004

AbstractMutations of Nkx2‐5 cause congenital heart disease and atrioventricular block in man. The altered expression of an electrophysiologic protein regulated by Nkx2‐5 was originally presumed to cause the conduction defect, but when no such protein was found, an alternative hypothesis was considered. In pediatric patients, the association of certain cardiac malformations with congenital atrioventricular block suggests that errors in specific developmental pathways could cause both an anatomic and a physiologic defect. We therefore hypothesized that Nkx2‐5 insufficiency perturbs the conduction system during development, which in turn manifests as a postnatal conduction defect. Experimental results from Nkx2‐5 knockout mouse models support the developmental hypothesis. Hypoplasia of the atrioventricular node, His bundle, and Purkinje system can explain in whole or in part specific conduction and electrophysiologic defects present in Nkx2‐5 haploinsufficiency. © 2004 Wiley‐Liss, Inc.
Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus
Authors: Petri Michelle A. , Mease Philip J. , Merrill Joan T. , Lahita Robert G. , Iannini Mark J. , Yocum David E. , Ginzler Ellen M. , Katz Robert S. , Gluck Oscar S. , Genovese Mark C. , Van Vollenhoven Ronald , Kalunian Kenneth C. , Manzi Susan , Greenwald Maria W. , Buyon Jill P. , Olsen Nancy J. , Schiff Michael H. , Kavanaugh Arthur F. , Caldwell Jacques R. , Ramsey‐Goldman Rosalind , St. Clair E. William , Goldman Allan L. , Egan Rita M. , Polisson Richard P. , Moder Kevin G. , Rothfield Naomi F. , Spencer Robert T. , Hobbs Kathryn , Fessler Barri J. , Calabrese Leonard H. , Moreland Larry W. , Cohen Stanley B. , Quarles Betty J. , Strand Vibeke , Gurwith Marc , Schwartz Kenneth E. 
Published: September 2004

AbstractObjectiveTo determine whether prasterone administration results in improvement or stabilization of systemic lupus erythematosus (SLE) disease activity and its symptoms.MethodsWomen with active SLE were treated with prasterone 200 mg/day plus standard SLE treatments or with placebo plus standard SLE treatments for up to 12 months in this randomized, double‐blind investigation conducted at 27 centers. Standard SLE treatments included prednisone (≤10 mg/day), antimalarials, and immunosuppressive agents; dosages were required to be stable for ≥6 weeks prior to enrollment and remain unchanged during protocol treatment. Responders were patients who experienced no clinical deterioration and had improvement or stabilization over the duration of the study in 2 disease activity measures (the SLE Disease Activity Index [SLEDAI] and the Systemic Lupus Activity Measure) and 2 quality of life measures (patient's global assessment and the Krupp Fatigue Severity Scale).ResultsA total of 381 women with SLE were enrolled. Among patients with clinically active disease at baseline (SLEDAI score >2), 86 of 147 in the prasterone group (58.5%) demonstrated improvement or stabilization without clinical deterioration, as compared with 65 of 146 in the placebo group (44.5%) (P = 0.017). Acne and hirsutism were reported in 33% and 16%, respectively, of the prasterone group and in 14% and 2%, respectively, of the placebo group (P < 0.05 for both comparisons). However, most cases of acne and hirsutism were mild and did not require withdrawal from therapy. Myalgias and oral stomatitis were reported less frequently in the prasterone group (22% and 15%, respectively) than in the placebo group (36% and 23%, respectively) (P < 0.05 for both comparisons). Serum levels of high‐density lipoprotein cholesterol, triglycerides, and C3 complement significantly decreased, while levels of testosterone and, to a lesser extent, estradiol increased in the prasterone group.ConclusionIn adult women with active SLE, administration of prasterone at a dosage of 200 mg/day improved or stabilized signs and symptoms of disease and was generally well tolerated.
Platelet‐activating factor–acetylhydrolase and other novel risk and protective factors for cardiovascular disease in systemic lupus erythematosus
Authors: Cederholm Anna , Svenungsson Elisabet , Stengel Dominique , Fei Guo‐Zhong , Pockley A. Graham , Ninio Ewa , Frostegård Johan 
Published: September 2004

AbstractObjectiveThere is an important inflammatory component to atherosclerosis and cardiovascular disease (CVD). It is therefore interesting that the risk of CVD is high in inflammatory diseases such as systemic lupus erythematosus (SLE). In this study, we investigated nontraditional risk factors for the development of CVD in patients with SLE.MethodsTwenty‐six women (mean age 52 years) with SLE and a history of CVD were compared with 26 age‐matched women with SLE and no clinical manifestations of CVD (SLE controls) and 26 age‐matched healthy women (population controls). Serum levels of several novel nontraditional risk and protective factors were determined: heat‐shock protein (HSP)–related factors (Hsp60, Hsp70, anti–human Hsp60, anti–human Hsp70, and anti–mycobacterial Hsp65), platelet‐activating factor–acetylhydrolase (PAF‐AH) activity, secretory phospholipase A2 GIIA (sPLA2), and anti–endothelial cell antibody (AECA). The intima‐media thickness and the presence of plaques in the common carotid arteries were determined by B‐mode ultrasound as a surrogate measure of atherosclerosis.ResultsLevels of PAF‐AH, but not HSP‐related factors, AECA, or sPLA2, were significantly increased in SLE cases. Only PAF‐AH discriminated between SLE cases and SLE controls (P = 0.005). PAF‐AH was significantly associated with low‐density lipoprotein (LDL) cholesterol and total cholesterol in the SLE cases (r = 0.50, P = 0.0093 and r = 0.54, P = 0.0045), but not in either control group.ConclusionThe increased levels of PAF‐AH in SLE cases and the association between PAF‐AH and LDL cholesterol adds support to the notion that PAF‐AH may promote atherothrombosis in SLE. The role of HSPs in CVD is complex, since anti‐Hsp65 appears to be associated with the presence of CVD, whereas Hsp70 might protect against it. In this cross‐sectional study, levels of HSP‐related factors, AECA, and sPLA2 were not associated with CVD in SLE.
Intracellular events in platelet activation induced by antiphospholipid antibodies in the presence of low doses of thrombin
Authors: Vega‐Ostertag Mariano , Harris E. Nigel , Pierangeli Silvia S. 
Published: September 2004

AbstractObjectiveThrombosis and thrombocytopenia are features of the antiphospholipid syndrome (APS), suggesting that antiphospholipid antibodies (aPL) may bind platelets, causing activation and aggregation of platelets and thrombosis. The intracellular events involved in aPL‐mediated platelet activation are not fully understood and are therefore the subject of this study.MethodsIgG fractions and their F(ab′)2 fragments were purified from the sera of 7 patients with APS and from the pooled sera of 10 healthy subjects (as controls). Phosphorylation of p38 MAPK, ERK‐1/2, and [Ca2+]‐dependent cytosolic phospholipase A2 (cPLA2) was determined in lysates of washed platelets pretreated with low doses of thrombin and aPL or control IgG or their F(ab′)2 fragments, by immunoblot. The effects of aPL on platelet aggregation in the presence or absence of a p38 MAPK inhibitor, SB203580, were examined. Thromboxane B2 (TXB2) production was detected by enzyme‐linked immunosorbent assay on gel‐filtered platelets treated with aPL and thrombin, with or without SB203580. Calcium mobilization studies were done utilizing a fluorometric assay.ResultsTreatment of platelets with IgG aPL, or their F(ab′)2 fragments, in conjunction with subactivating doses of thrombin resulted in a significant increase in phosphorylation of p38 MAPK. Neither the IgG aPL nor their F(ab′)2 fragments increased significantly the phosphorylation of ERK‐1/2 MAPKs. Furthermore, pretreatment of platelets with SB203580 completely abrogated the aPL‐mediated enhanced aggregation of the platelets. Platelets treated with F(ab′)2 aPL and thrombin produced significantly larger amounts of TXB2 when compared with controls, and this effect was completely abrogated by treatment with SB203580. In addition, cPLA2 was also significantly phosphorylated in platelets treated with thrombin and F(ab′)2 aPL. There were no significant changes in intracellular [Ca2+] when platelets were treated with aPL and low doses of thrombin.ConclusionThe data strongly indicate that aPL in the presence of subactivating doses of thrombin induce the production of TXB2 mainly through the activation of p38 MAPK and subsequent phosphorylation of cPLA2. The ERK‐1/2 pathway does not seem to be involved in this process, at least in the early stages of aPL‐mediated platelet activation.
The etiologic diagnosis of infectious discitis is improved by amplification‐based DNA analysis
Authors: Lecouvet Frédéric , Irenge Leonid , Vandercam Bernard , Nzeusseu Adrien , Hamels Sandrine , Gala Jean‐Luc 
Published: September 2004

AbstractObjectiveBlood cultures and cultures of disc material are required to identify and treat bacterial agents responsible for septic spondylodiscitis, but these methods have limited sensitivities. We undertook this study to compare nonculture amplification‐based DNA analysis with conventional culture of disc aspirate.MethodsNineteen patients with spondylodiscitis, including 11 with a history of spinal surgery, presented with negative blood cultures and underwent percutaneous disc or epidural abscess puncture for bacterial diagnosis. Amplification by polymerase chain reaction was performed on 16S ribosomal DNA universal target genes and femA staphylococci‐specific target genes in all patients, and on the upstream p34 mycobacterial gene in 1 patient. Species identification relied on amplicon sequencing and comparison with templates from GenBank. Amplification of the femA gene led to subsequent testing for methicillin resistance by amplification of the mecA gene. Further assessment using a staphylococci‐ and methicillin resistance–specific DNA array was performed on 3 samples.ResultsMicrobiologic and molecular assays identified the causative organism in 14 of 19 patients (74%) and 19 of 19 patients (100%), respectively. In culture‐positive patients, DNA‐based and microbiologic results were highly correlated. Five agents (Staphylococcus simulans, Staphylococcus sciuri, Brucella species, Actinomyces israelii, and Mycobacterium tuberculosis complex) were identified only by DNA‐based methods. In 1 sample, Corynebacterium jeikeium and coagulase‐negative Staphylococcus were both cultured, whereas DNA analysis identified only Staphylococcus hominis.ConclusionDNA‐based methods are highly sensitive and specific. They can usefully complement standard microbiologic methods for identifying the cause of infectious spondylodiscitis and contribute to species‐specific therapeutic orientation in patients with negative blood and disc aspirate cultures.
Proximity of residence to trichloroethylene‐emitting sites and increased risk of offspring congenital heart defects among older women
Authors: Yauck Jennifer S. , Malloy Marsha E. , Blair Kathleen , Simpson Pippa M. , McCarver D. Gail 
Published: September 2004

AbstractBACKGROUNDPrevious studies suggest that trichloroethylene (TCE) is a selective cardiac teratogen. We tested the hypothesis that the odds of maternal residence close to TCE‐emitting sites would be greater among infants with congenital heart defects (CHDs) than among infants without CHDs.METHODSWe conducted a case‐control study of 4025 infants, identified from hospital and birth records, born from 1997 to 1999 to Milwaukee, Wisconsin mothers. A geographic information system was used to calculate distances between maternal residences and TCE sites. We used classification tree analysis to determine appropriate values by which to dichotomously categorize mothers by TCE exposure (exposed: residence within 1.32 miles of at least one TCE site) and age (older: ≥38 years), and logistic regression to test for CHD risk factors.RESULTSThe proportion of mothers who were both older and had presumed TCE exposure was more than six‐fold greater among case infants than among control infants (3.3% [8/245] versus 0.5% [19/3780]). When adjusted for other variables, CHD risk was over three‐fold greater among infants of older, exposed mothers compared to infants of older, nonexposed mothers (adjusted OR, 3.2; 95% CI, 1.2–8.7). Older maternal age, alcohol use, chronic hypertension, and preexisting diabetes were each associated with CHDs (adjusted ORs, 1.9, 2.1, 2.8, 4.1; 95% CIs, 1.1–3.5, 1.1–4.2, 1.2–6.7, 1.5–11.2, respectively), but residence close to TCE sites alone was not.CONCLUSIONSOur findings suggest that maternal age and TCE exposure interact to increase CHD risk, although the mechanism by which this occurs is unknown. A prospective study is underway to confirm this finding. Birth Defects Research (Part A), 2004. © 2004 Wiley‐Liss, Inc.
Organizing population data into complex family pedigrees: Application of a second‐order data linkage to state birth defects registries
Authors: Tu Shihfen , Mason Craig A. 
Published: September 2004

AbstractResearchers and health officials are increasingly using electronic linkage of large‐scale health data systems as a tool for assembling a comprehensive picture of birth defects at a population level. Current linkage and database techniques are limited to first‐order linkage – linking information on a single individual in one database with information on that same individual in another database. For example, while current strategies may indicate whether a child with a certain birth defect also has a specific metabolic disorder or risk factor, they are unable to readily determine whether he or she also has any siblings or other relatives with the same pattern. In contrast, the current manuscript proposes a second‐order linkage—one that organizes data so that individual‐level data can readily be organized into families or extended family pedigrees across an entire population. The ability to link and organize population data into family pedigrees can have significant, broad impact upon health research and service delivery. This can lead to large‐scale analysis of genetic factors and, with the linking of environmental data, the potential for large‐scale studies of gene‐environment interactions. In addition, it expands the potential for epidemiological research by readily allowing the examination of familial effects upon population rates of birth defects, and provides valuable information that can assist in applied public health. An example of a second order database incorporating an electronic birth defects registry is presented. Birth Defects Research (Part A) 70:603–608, 2004. © 2004 Wiley‐Liss, Inc.
Vertrauensvorschuß und wissenschaftliches Fehlhandeln — Eine reliabilistische Modellierung der Fälle Abderhalden, Goldschmidt, Moewus und Waldschmidt‐Leitz
Authors: Charpa Ulrich , Deichmann Ute 
Published: September 2004

AbstractReliabilist philosophy of science considers scientific misconduct a transgression against the principles of good cognitive practice. Good practice in research is characterised by the reliability, efficiency and fertility of the cognitive processes involved. The reliabilist approach is closely connected to the idea of mutual cognitive dependency of the research community. Trust in the testimony of others is not an inevitable but a favouring factor of scientific progress — and misconduct damages the testimonial chain, respectively the principle of trustworthiness. Within the reliabilist framework, the main focus on questionable research is not on whether or not there are fraudulent intentions (that means particular mental events of the past), but on recognisable consequences for the research community. Criticising the constructivist modeling of questionable research, we reconstruct certain contributions by Emil Abderhalden, Richard Goldschmidt, Franz Moewus, and Ernst Waldschmitz‐Leitz as serious misconducts respectively frauds. We also show that specific social factors — often regarded as “apologising” conditions — decisively interfere with the principle of trustworthiness in the scientific community.
Der Scharlatan auf dem Rechtsweg — und was vielleicht zu seiner Umlenkung getan werden könnte
Authors: Schneider Christoph 
Published: September 2004

AbstractA number of recent allegations of scientific misconduct in Germany have led to judicial proceedings. Two examples are analyzed in depth, showing evidence for mutual incompatibilities between the legal system and the scientific system. In particular, it seems doubtful whether basic rules of good scientific practice are adequately and consistently taken into account by the courts when assessing the burden of proof. Strengths and weaknesses of some alternatives to judicial proceedings in such cases are discussed.
Solid‐phase synthesis of second‐generation polyproline dendrimers
Authors: Sanclimens Glòria , Crespo Laia , Giralt Ernest , Royo Miriam , Albericio Fernando 
Published: September 2004

AbstractSecond‐generation dendrimers have been prepared on solid phase by successive additions of branched polyproline building blocks starting from two different branching units anchored to the solid support. The preparation of Pro‐rich building blocks was carried out by stepwise solid‐phase synthesis and their iterative addition was performed by a convergent approach, also using solid‐phase synthesis. cis‐4‐Amino‐L‐proline and imidazolidine‐2‐carboxylic acid were used as branching units due to their structural resemblance to proline. The optimized strategy allowed the target compounds to be obtained with high purities without the need for purification steps. © 2004 Wiley Periodicals, Inc. Biopolymers (Pept Sci), 2004