bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of ELISA D‐dimer test in patients with unstable angina pectoris presenting at the emergency department with a normal electrocardiogram
Authors: Shitrit David , Bar‐Gil Shitrit Ariella , Rudensky Bernard , Sulkes Jaqueline , Gutterer Natan , Zviony Dan 
Published: September 2004

AbstractPatients with unstable angina pectoris and acute myocardial infarction have higher than normal D‐dimer levels. The aim of the study was to determine the value of the D‐dimer test in patients with unstable angina pectoris and a normal electrocardiogram on presentation at the emergency department. The study sample included 81 patients who met these criteria. Blood samples collected at admission were subjected to ELISA D‐dimer. Findings were correlated with coronary risk factors, use of cardiac medications, blood levels of acute phase reactants (fibrinogen and C‐reactive protein), cardiac enzymes levels, length of hospital stay, and catheterization findings. ELISA D‐dimer levels were statistically significantly correlated with cardiac risk factors, namely male sex, older age, smoking, and hypertension (r = 0.25, P = 0.02; r = 0.43, P = 0.0001; r = 0.26, P = 0.03; r = 0.35, P = 0.002, respectively), in addition to use of cardiac medications (beta blockers, aspirin, nitrates), levels of acute phase reactants, length of stay, and catheterization findings. On multivariate analysis, only D‐dimer level, age, and sex were predictors of length of stay (P = 0.018). The study suggests that D‐dimer levels at admission to the emergency department may serve as an additional tool to predict the magnitude of unstable angina pectoris in patients with a normal electrocardiogram. Am. J. Hematol. 77:147–150, 2004. © 2004 Wiley‐Liss, Inc.
Response of myasthenia gravis to rituximab in a patient with non‐Hodgkin lymphoma
Authors: Gajra Ajeet , Vajpayee Neerja , Grethlein Sara J. 
Published: September 2004

AbstractMyasthenia gravis is a B‐cell‐mediated autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles. The underlying defect is an autoantibody‐mediated attack on the acetylcholine receptors (AchRs) at the neuromuscular junction. Rituximab is a genetically engineered chimeric murine/human monoclonal antibody indicated for treatment of patients with low‐grade or follicular, CD20‐positive, B‐cell non‐Hodgkin lymphoma. Based on its potential for elimination of auto‐reactive B‐cell clones, rituximab may have a role in the management of some autoimmune disorders. We report a patient with B‐cell, follicular non‐Hodgkin lymphoma and a long‐standing history of myasthenia gravis and the favorable impact of rituximab on both disorders. Am. J. Hematol. 77:196–197, 2004. © 2004 Wiley‐Liss, Inc.
Hyperhomocysteinemia and deep vein thrombosis in orthotopic heart transplantation: A case report
Authors: Costea Alex , Bhat Geetha 
Published: September 2004

AbstractHomocysteine has been recognized as a risk factor for atherosclerosis and arterial and venous thrombosis. Heart transplant patients have an increased prevalence of hyperhomocysteinemia. High homocysteine levels in transplant patients may promote development of cardiac allograft vasculopathy, but there is minimal information regarding the risk of venous thrombosis. The current case report illustrates the association of increased levels of homocysteine and hypercoagulable syndrome in a 36‐year‐old heart transplant patient with no previous history of clotting disorder. Both elevated homocysteine levels and extensive venous thrombosis responded promptly to treatment with a folate/B12/B6 vitamin combination and enoxaparin. Am. J. Hematol. 77:161–163, 2004. © 2004 Wiley‐Liss, Inc.
Trisomy 21 is associated with variable defects in cytotrophoblast differentiation along the invasive pathway
Authors: Wright Alexi , Zhou Yan , Weier Jingly Fung , Caceres Eduardo , Kapidzic Mirhan , Tabata Takako , Kahn Madelyn , Nash Carl , Fisher Susan J. 
Published: September 2004

AbstractAneuploid cells in the placenta are associated with poor pregnancy outcomes, but the mechanisms are unclear. Here, we examined the cytotrophoblast (CTB) differentiation pathway that leads to uterine invasion in pregnancies complicated by trisomy 21 (T21) as compared with their normal counterparts. Surprisingly, we observed a wide spectrum of T21 effects. Morphologically, some samples appeared near normal, while others had extensive fibrinoid deposition and apoptosis of CTBs at the maternal–fetal interface (confirmed by TUNEL labeling). At a molecular level, the cells' expression of stage‐specific molecules was variably misregulated. At one end of the spectrum, samples with less apoptosis had relatively normal staining patterns. At the other end, samples with extensive apoptosis showed significantly decreased staining for these antigens. Additional studies confirmed that the effects we observed had functional consequences, because the cells exhibited marked phenotypic alterations in vitro, including a large increase in MMP‐9 production, which distinguishes the effects of T21 on CTBs from those of preeclampsia. The morphologic, phenotypic, and functional differences among CTBs from pregnancies complicated by T21 illustrate the importance of the interplay between fetal/placental genotype and maternal influences on pregnancy outcome. Furthermore, our data may explain why a significant number of these pregnancies end in spontaneous abortion while others survive to term. © 2004 Wiley‐Liss, Inc.
Multiple marker analysis at the promoter region of the DRD4 gene and ADHD: Evidence of linkage and association with the SNP −616
Authors: Lowe Naomi , Kirley Aiveen , Mullins Celine , Fitzgerald Michael , Gill Michael , Hawi Ziarih 
Published: September 2004

AbstractAbnormalities of dopamine neurotransmission have been hypothesized to play an important role in the pathophysiology of attention deficit hyperactivity disorder (ADHD). Support for this has come from numerous association studies on candidate genes including the dopamine D4 receptor gene (DRD4). One of the most replicated associations between ADHD and the dopaminergic system is the 7‐repeat allele of the VNTR polymorphism of this gene. A lack of association between this marker and ADHD has also been reported in several investigations. In the absence of a firm link between the number of the VNTR repeats and the function of the gene, we sought to investigate several additional markers at the 5′‐end of the gene with potential influence on the expression of the DRD4. We observed a significant over transmission of single nucleotide polymorphism (SNP) (χ2 = 7.45, P = 0.008, OR = 1.63). In addition, an excess transmission of the A allele of the −521 SNP was observed, although it did not attain statistical significance (χ2 = 2.14, P = 0.17, OR = 1.25). Linkage disequilibrium (LD) analysis demonstrated a weak level of D' between any of the tested markers implying that this may be a region of high recombination. It also raises the possibility that the new association with ADHD may be independent of the 7‐repeat allele. Further analyses, preferably in samples demonstrating association with the VNTR, or in other ethnic groups, are required to confirm these observations. © 2004 Wiley‐Liss, Inc.
Linkage disequilibrium mapping of bipolar affective disorder at 12q23‐q24 provides evidence for association at CUX2 and FLJ32356
Authors: Glaser Beate , Kirov George , Green Elaine , Craddock Nick , Owen Michael J. 
Published: September 2004

AbstractChromosome 12q23‐q24 has been implicated by several linkage studies as harboring a gene for bipolar affective disorder. We performed linkage disequilibrium (LD) mapping with 17 microsatellite markers across a 1.6 Mb‐wide segment forming the central part of our narrowest linkage region. A significant signal (P = 0.0016) was identified for one microsatellite marker in our UK Caucasian case‐control sample (347 cases, 374 controls). Genes, including regulatory elements, around this marker were screened for mutations and the LD structure of the region determined by genotyping 22 SNPs and insertion/deletion polymorphisms in 94 individuals. A set of 11 haplotype tagging (ht) SNPs was genotyped in our sample using a two‐stage procedure. Two SNPs (rs3847953 and rs933399) and an insertion/deletion with putative functional relevance (which are in high LD with each other and with the microsatellite marker) showed significant or nearly significant association with bipolar disorder after Bonferroni‐correction (reaching nominal P values from P = 0.002 to P = 0.005). In a sample of 110 UK Caucasian parent–offspring trios there was a trend for an over transmission in the same direction that failed to meet conventional levels of statistical significance. Our data provide evidence for association between bipolar mood disorder and markers on chromosome 12q23‐q24 but need replication in independent samples. © 2004 Wiley‐Liss, Inc.
Association analysis of NOTCH 4 polymorphisms with schizophrenia among two independent family based samples
Authors: Prasad S. , Chowdari K.V. , Wood J. , Bhatia T. , Deshpande S.N. , Nimgaonkar V.L. , Thelma B.K. 
Published: September 2004

AbstractThe present study investigated polymorphisms of the NOTCH 4 gene in two independent samples from India and USA, consisting of patients with schizophrenia and their parents (n = 182, and n = 148 ‘trios,’ respectively). Five DNA markers, namely (GAAG)n, (TAA)n, SNP1, SNP2, and (CTG)n were evaluated. Transmission distortion, consistent with a modest association was detected among both samples. Additional association studies at this locus are warranted. © 2004 Wiley‐Liss, Inc.
Association study of neurotrophic tyrosine kinase receptor type 2 (NTRK2) and childhood‐onset mood disorders
Authors: Adams Jennifer H. , Wigg Karen G. , King Nicole , Burcescu Irina , Vetró Ágnes , Kiss Eniko , Baji Ildikó , George Charles J. , Kennedy James L. , Kovacs Maria , Barr Cathy L. 
Published: September 2004

AbstractChildhood‐onset mood disorders (COMD) are often familial, and twin studies of COMD provide compelling evidence that genetic factors are involved. Deficits in neural plasticity have been suggested to underlie the development of depression. The receptor tropomyosin related kinase B (TrkB) and its ligand, brain derived neurotrophic factor (BDNF), play essential roles in neural plasticity, and mRNA expression of both of these genes has been shown to be influenced by stress and chronic antidepressant treatment. In addition, TrkB knock‐out mice display inappropriate stress coping mechanisms. Having previously shown that BDNF is associated with COMD, in this study we investigated the gene encoding TrkB, neurotrophic tyrosine kinase, receptor, type 2 (NTRK2) as a susceptibility factor in COMD. We tested for association of NTRK2 with COMD in two independent samples: (a) a case‐control sample matched on ethnicity and gender, consisting of 120 cases who met DSM III/IV criteria for major depressive or dysthymic disorder before age 14 or bipolar I/II before the age of 18, and controls, and (b) a family based control sample of 113 families collected in Hungary, identified by a proband between the age of 7 and 14 who met DSM IV criteria for major depressive disorder or bipolar I/II disorder. There was no evidence for an allelic or genotypic association of three polymorphisms of NTRK2 with COMD in the case‐control sample. Also, in the family based sample, using the transmission disequilibrium test (TDT), we did not identify any evidence of allelic association for each marker individually or when haplotypes were analyzed. Based on these results, using these three polymorphisms, we do not find support for NTRK2 as a susceptibility gene for COMD. © 2004 Wiley‐Liss, Inc.
Association of the −141C Del variant of the dopamine D2 receptor (DRD2) with positive family history and suicidality in German alcoholics
Authors: Johann Monika , Putzhammer Albert , Eichhammer Peter , Wodarz Norbert 
Published: September 2004

AbstractSeveral lines of evidence indicate an involvement of the dopaminergic system in alcoholism, withdrawal, suicidality, and attention‐deficit hyperactivity disorder (ADHD). The functionally relevant −141C Ins/Del polymorphism located upstream to exon 1 in the 5′‐region of the dopamine D2 receptor (DRD2) gene might be an interesting candidate gene. We investigated a sample of 1,126 well‐characterized, primary chronic alcoholics of German descent according to a phenotype–genotype strategy, i.e., alcoholics suffering from severe withdrawal complications such as seizure or delirium, family history positive (FH+) alcoholics, alcoholics with an antisocial personality disorder (ASPD), alcoholics with an ADHD, and type 1 or type 2 alcoholics according to Cloninger's typology. Compared to the control subjects, there was a significant excess of the −141C Del allele in alcoholics with a paternal and grandpaternal history of alcoholism and in alcoholic subgroups with suicidality or without a history of withdrawal symptoms. There were no significant differences in allele frequency between the entire group or subgroups of alcoholics and healthy controls. Therefore, the −141C Del variant of the DRD2 might be a protective factor against the development of withdrawal symptoms. However, it might also be a risk factor in a highly burdened subgroup of alcoholics with a paternal and grandpaternal history of alcoholism and it might contribute to the substantially higher likelihood of suicide in alcoholics. © 2004 Wiley‐Liss, Inc.
APOE and other loci affect age‐at‐onset in Alzheimer's disease families with PS2 mutation
Authors: Wijsman Ellen M. , Daw E. Warwick , Yu Xuesong , Steinbart Ellen J. , Nochlin David , Bird Thomas D. , Schellenberg Gerard D. 
Published: September 2004

AbstractSeveral kindreds of Volga German (VG) ancestry have a single PS2 mutation that causes an autosomal dominant form of Alzheimer's disease (AD). These families show a wide range in age‐at‐onset, which suggests the existence of modifying factors other than the PS2 mutation. To examine evidence for a genetic basis of variation in onset age, we performed a Bayesian oligogenic segregation and linkage analysis on nine VG families confirmed to have at least one affected PS2 carrier. This analysis simultaneously estimated the effects of APOE and PS2 and the number and effects of additional loci affecting AD age‐at‐onset. In addition, a family effect accounted for shared environmental effects. This analysis approach has the advantage of full use of the complete pedigree structure, as well as use of information on unsampled individuals with phenotypic data. These analyses provide evidence that APOE plays a small, but significant, role in modifying the age‐at‐onset in these VG families. The effects estimated for the APOE ε3 and ε4 genotypes were consistent with those estimated in previous analysis of late‐onset AD families, with evidence for a dose‐dependent relationship between number of ε4 alleles and age‐at‐onset. We estimated an ∼83% posterior probability of at least one modifier locus in addition to APOE, and that the fraction of the variance in age‐at‐onset attributable to PS2, APOE, other loci, and family effects is ∼70, ∼2, ∼6.5, and ∼8.5%, respectively. These results provide evidence that APOE and other loci modify onset in AD caused by PS2 mutation. © 2004 Wiley‐Liss, Inc.
DAT1, DRD4, and DRD5 polymorphisms are not associated with ADHD in Dutch families
Authors: Bakker Steven C. , van der Meulen Emma M. , Oteman Nicole , Schelleman Hedi , Pearson Peter L. , Buitelaar Jan K. , Sinke Richard J. 
Published: September 2004

AbstractRecent meta‐analyses have indicated that the dopamine transporter gene (DAT1) and the dopamine receptor genes D4 (DRD4) and D5 (DRD5) are associated with attention‐deficit hyperactivity disorder (ADHD), although single studies frequently failed to show significant association. In a family‐based sample of 236 Dutch children with ADHD, we have investigated the previously described variable number of tandem repeat (VNTR) polymorphisms and two additional microsatellites at the DAT1 and DRD4 loci. DRD5 was investigated using the microsatellite that was previously found to be associated. Transmission disequilibrium tests (TDTs) did not show preferential transmission of alleles or two‐marker haplotypes to affected offspring. These data suggest that DAT1, DRD4, and DRD5 do not contribute substantially to ADHD in the Dutch population. © 2004 Wiley‐Liss, Inc.
A genome scan of neuroticism in nicotine dependent smokers
Authors: Neale Benjamin M. , Sullivan Patrick F. , Kendler Kenneth S. 
Published: September 2004

AbstractNeuroticism is a personality factor that has consistently been demonstrated to be associated with anxiety, depression, and other “internalizing” disorders. We analyzed a genome scan for neuroticism on a sample of 129 sib‐pair families (113 with a single sibling pair, 18 with multiple sibling pairs) containing a total of 201 possible sibling pairs, ascertained for concordance on nicotine dependence. Using Merlin‐Regress, we replicated peaks for neuroticism described by prior studies, on chromosomes 1 and 11 with LOD scores of 2.52 and 1.97 (P‐value of 0.003 and 0.0108) respectively, and have some evidence for a novel finding on chromosome 12 with a LOD of 2.85 (P‐value of 0.0014). © 2004 Wiley‐Liss, Inc.
Brain perfusion and dopaminergic genes in boys with attention‐deficit/hyperactivity disorder
Authors: Szobot Claudia , Roman Tatiana , Cunha Renato , Acton Paul , Hutz Mara , Rohde Luis Augusto 
Published: September 2004

AbstractNeuroimaging studies have suggested the involvement of several brain areas in attention‐deficit/hyperactivity disorder (ADHD). Genetic investigations have supported the role of both dopamine D4 receptor gene (DRD4) and dopamine transporter gene (DAT1) in the vulnerability to the disorder. This study evaluates whether the presence of risk alleles at DRD4 and/or DAT1 genes is associated with differences in regional cerebral blood flow (rCBF) in a sample of ADHD boys. The rCBF was compared between ADHD patients with and without risk alleles at DRD4 (7‐repeat allele) and/or at DAT1 (homozygosis for the 10‐repeat allele) genes by single photon emission computed tomography (SPECT) during continuous performance test. Images were analyzed using statistical parametric mapping (SPM‐99). No significant differences in rCBF were found both between ADHD boys with and without the 7‐repeat allele at DRD4 locus, as well as between ADHD boys homozygous for the 10‐repeat allele and ADHD subjects with other genotypes at the DAT1 locus. However, a significantly higher perfusion in the right middle temporal gyrus was found in the group with risk alleles at both DRD4 and DAT1 loci (n = 6) compared to ADHD boys without risk alleles at both loci (n = 28) (P < 0.05). Our findings suggest that a higher recruitment in middle temporal gyrus, an area associated to working memory and selective attention, should exist to compensate a putative effect of the interaction between these dopaminergic genes. © 2004 Wiley‐Liss, Inc.
MCP‐1 gene (SCYA2) and schizophrenia: A case‐control association study
Authors: Mundo Emanuela , Altamura A. Carlo , Vismara Serena , Zanardini Roberta , Bignotti Stefano , Randazzo Roberto , Montresor Claudio , Gennarelli Massimo 
Published: September 2004

AbstractDysregulation of the inflammatory response system has been linked to the pathophysiology of schizophrenia. Abnormal levels of proinflammatory cytokines and their receptors have been found in peripheral blood and cerebrospinal fluid of schizophrenic patients, suggesting the presence of immune activation. Monocyte chemoattractant protein 1 (MCP‐1) influences the expression of cytokines related to T helper responses. MCP‐1 also exerts several effects on monocytes, including the expression of several proinflammatory genes. The A‐2518G polymorphism of the MCP‐1 gene (SCYA2) appears to affect the transcriptional activity and monocyte MCP‐1 production. The aim of this case‐control study was to investigate the potential role of SCYA2 (A‐2518G polymorphism) in conferring susceptibility to schizophrenia and to the resistance to antipsychotic treatment. The sample studied consisted of 191 DSM‐IV schizophrenia or schizoaffective disorder (depressive subtype) patients and 161 matched healthy controls. No significant genotypic (χ2 = 0.278, df = 2, P = 0.986) or allelic (χ2 = 0.021, df = 1, P = 0.884) association was found between the A‐2518G variant of the SCYA2 and the diagnosis. No differences in the age at onset of schizophrenia were found between the three genotype groups identified. Significant genotypic association was found between the A‐2518G variant of the SCYA2 and the resistance to antipsychotic treatment (χ2 = 6.26, df = 2, P = 0.04), with resistant patients more frequently carrying the G allele. The odds ratio associated to the presence of the G allele was 2.39 (95% CI = 1.14–4.98). These data suggest that the A‐2518G variant of the SCYA2 has not a major role in the pathogenesis of schizophrenia, while it could be implicated in the resistance to antipsychotic treatment. © 2004 Wiley‐Liss, Inc.
Magnetic characterization of cobalt nanoparticles by temperature‐dependent magnetic relaxation measurements
Authors: Romanus E. , Matoussevitch N. , Prass S. , Heinrich J. , Müller R. , Berkov D. V. , Bönnemann H. , Weber P. 
Published: September 2004

AbstractA recently introduced method for the characterization of magnetic nanoparticles based on the analysis of the dependence of the Néel relaxation signal on the sample temperature (temperature‐dependent magnetorelaxometry, TMRX) has been applied to characterize air‐stable cobalt particles made by decomposition of Co2(CO)8 in the presence of aluminium‐organic compounds. The influence of small changes in the preparation process on the magnetic relaxation behaviour has been studied.A mean magnetically relevant particle size has been derived from TMRX, zero‐field cooled magnetisation and low‐temperature coercivity measurements and has been compared with a mean physical size determined by transmission electron microscopy investigations. Copyright © 2004 John Wiley & Sons, Ltd.
Cure kinetics of epoxy/anhydride nanocomposite systems with added reactive flame retardants
Authors: Torre L. , Lelli G. , Kenny J. M. 
Published: September 2004

AbstractMontmorillonite nanocomposite systems obtained from epoxy cured using anhydride and the addition of a reacting flame retardant are studied in this paper. In particular, a thermokinetic analysis of the behavior of five different compounds was performed, using a differential scanning calorimeter. The isothermal tests showed double reaction peaks, due to the cure reactions of DGEBA/acid anhydride systems. The comparisons between dynamic thermograms (and between isothermal ones, too) for the different mixtures also showed that the addition of other active substances (such as a nanofiller or a flame retardant additive) does not change the mechanism of crosslinking from a qualitative point of view, but both the nanoreinforcement and the flame retardant seemed to exert an evident catalytic action on the cure reactions. A model describing the cure behavior of the aforementioned materials is proposed in this work. This model takes into account the fact that the reaction mechanism of each analyzed system is composed of a couple of parallel phenomena: the fast opening of anhydride ring (corresponding to a first exothermic peak and characterized by “n‐th order” kinetics) and resin networking (corresponding to a second exothermic peak and characterized by an “auto‐catalytic with zero initial velocity” behavior). The verification of the proposed model was performed by means of a comparison between experimental data (normalized curves derived from DSC thermograms) and theoretical data (derived from a numerical integration—using the second order Runge–Kutta method—of the model‐representative equation) and provided very good results. This allows one to apply such a model to any engineering process problem concerning the cure of DGEBA/acid anhydride/phyllosilicate nanocomposite systems. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 1676–1689, 2004