bluuebunny/crossref_metadata_2025_split huggingface dataset:
Technical and Clinical Characterization of the Bio-PTH (1–84) Immunochemiluminometric Assay and Comparison with a Second-Generation Assay for Parathyroid Hormone
Authors: Inaba Masaaki , Nakatsuka Kiyoshi , Imanishi Yasuo , Watanabe Masakazu , Mamiya Yuji , Ishimura Eiji , Nishizawa Yoshiki 
Published: February 2004

Abstract
Background: The Bio-Intact parathyroid hormone (1–84) assay (Bio-PTH), a newly developed two-site immunochemiluminometric assay, measures exclusively PTH (1–84) in contrast to second-generation “intact PTH” (I-PTH) assays. We investigated the technical performance and clinical significance of this new assay.
Methods: PTH was measured simultaneously by the Bio-PTH assay and Allegro intact PTH IRMA in sera from Japanese patients with calcium disorders.
Results: Measured Bio-PTH in serum was unaffected by six freeze-thaw cycles and was stable at 4 °C for 7 days and during storage at −20 or −80 °C over 28 days. The calibration curve was linear to 1800 ng/L. The detection limit was 3.9 ng/L. The intra- and interassay imprecision was &lt;2.8% and 3.5%, respectively, for analyte concentrations spanning the range of the calibration curve. Bio-PTH was unaffected by a 1000-fold excess of PTH (7–84), although I-PTH reacted equally with PTH (7–84) and PTH (1–84). Bio-PTH was correlated with I-PTH in healthy individuals (r = 0.953; P &lt;0.0001; n = 26) and in the full population without renal dysfunction (r = 0.994; P &lt;0.0001; n = 62). In 72 volunteers, mean (SD) Bio-PTH was 22.2 (7.1) ng/L, or 62% of the mean I-PTH [36.1 (22.3) ng/L]. This ratio was 51% in hemodialysis patients (n = 177). Mean Bio-PTH was high in patients with primary hyperparathyroidism [121 (85) ng/L; n = 18] and hemodialysis patients [102 (104) ng/L; n = 177], low in idiopathic hypoparathyroidism [5.5 (2.8) ng/L; n = 4], and within 2 SD of the mean for healthy controls in Paget disease of the bone [34 (15) ng/L; n = 9] and bone metastasis [24 (12) ng/L; n = 8].
Conclusion: The Bio-PTH assay is sensitive and precise and produces expected results for patients with the studied disorders of calcium metabolism.
Agreeableness as a predictor of aggression in adolescence
Authors: Gleason Katie A. , Jensen‐Campbell Lauri A. , South Richardson Deborah 
Published: January 2004

AbstractThis multi‐method research linked the Big Five personality dimensions to aggression in early adolescence. Agreeableness was the personality dimension of focus because this dimension is associated with motives to maintain positive interpersonal relations. In two studies, middle school children were assessed on the Big Five domains of personality. Study 1 showed that agreeableness was associated with both indirect and direct aggression. In addition, the link between agreeableness and aggression was strongest for direct strategies. Study 2 examined the hypotheses that agreeableness predicts social cognitions associated with aggression, peer reports of direct aggression, and teacher reports of adjustment. Agreeableness predicted peer reports of aggression and social cognitions associated with aggression. In addition, aggression mediated the link between agreeableness and adjustment. Results suggest that of the Big Five dimensions, Agreeableness is most closely associated with processes and outcomes related to aggression in adolescents. Aggr. Behav. 30:43–61, 2004. © 2004 Wiley‐Liss, Inc.
Effects of acute, subchronic and intermittent MDMA (‘ECSTASY’) administration on agonistic interactions between male mice
Authors: Navarro José Francisco , Maldonado Enrique 
Published: January 2004

AbstractRecent studies suggest that acute administration of 3,4‐methylenedioxymethamphetamine (MDMA), an amphetamine derivative popularly known as “ecstasy,” produces an antiaggressive effect in male mice. However, there is no evidence with respect to the development of tolerance or sensitization after its subchronic or intermittent administration. In this study, we examined the action of low to moderate doses of MDMA (1.25, 2.5 and 5 mg/kg, i.p), administered acutely, subchronically (for 7 days) or intermittently, on agonistic behavior elicited by isolation in male mice. Individually housed mice were exposed to anosmic “standard opponents” 30 minutes after the drug administration, and the encounters were videotaped and evaluated using an ethologically based analysis. Acute treatment with MDMA provoked a significant reduction of aggressive behaviors, without altering immobility. However, this action was only selective at 1.25 mg/kg. With the intermediate (2.5 mg/kg) and the highest doses (5 mg/kg) of the drug, it was observed a significant decrease of offensive behaviors, accompanied by an increase of exploration from a distance, avoidance/flee and defense/submission behaviors. This ethopharmacological profile could indicate the existence of an anxiogenic‐like effect of MDMA. The overall picture of the effects of MDMA was very similar in the acutely, intermittently and daily treated animals. No tolerance or sensitization to the actions of the drug was developed after its repeated or intermittent administration.
Effects of viewing videos of bullfights on Spanish children
Authors: Graña J.L. , Cruzado J.A. , Andreu J.M. , Muñoz‐Rivas M.J. , Peña M.E. , Brain P.F. 
Published: January 2004

AbstractSome of the psychological effects of viewing bullfights on children 8–12 years old are described. Two hundred and forty subjects (120 girls and 120 boys) aged between eight and twelve from a variety of socioeconomic backgrounds were selected from three public or private elementary / secondary schools in Madrid, Spain. The first study used a questionnaire to examine the children's attitudes towards bullfighting by looking at their acceptance and cognitive‐emotional appraisal of the event. Videotapes of bullfights with differing commentaries were then used, along with a battery of questionnaires, to assess the emotional impact of these events, as well as the impact of narrative explanations on aggression and anxiety. Most children were not very positive about bullfights in the initial questionnaire. Viewing of tapes with ‘festive’ or aggressive dialogues (but not tapes without a justification) resulted in more expressed aggression in boys than girls. There was also evidence that age had a significant effect, and that some children appeared disturbed by the exposure. Aggr. Behav. 30:16–28, 2004. © 2004 Wiley‐Liss, Inc.
Friendship and loneliness among bullies and victims: Data from seven countries
Authors: Eslea Mike , Menesini Ersilia , Morita Yohji , O'Moore Mona , Mora‐Merchán Joaquin A. , Pereira Beatriz , Smith Peter K. 
Published: January 2004

AbstractResearch suggests that the relationship between school bullying and its various risk factors should be clearer among girls than boys, and should become stronger with age, as roles within the peer group stabilise. This paper tests this theory by comparing sex, school type, and bully/victim status differences in friendships and playground social interactions, using data from nine surveys in seven countries: China, England, Ireland, Italy, Japan, Portugal, and Spain. A total of approximately 48,000 children completed various translations of the Olweus Bullying Questionnaire. Small but generally consistent main effects were found for sex and school type (boys and primary pupils enjoyed playtimes more and had more friends, but were also more likely to spend playtimes alone). Larger effects were consistently found for bully/victim status (victims were significantly worse off on all the measures in all the samples where a difference was found, while bullies and neutrals did not differ consistently), but the interactions between these factors varied widely between samples and there were few consistent patterns. It is concluded that bullying is a universal phenomenon with many negative correlates for victims and few (if any) for bullies, but that there are cultural variations in the way that bullying is related to sex, age, and social support. Aggr. Behav. 30:71–83, 2004. © 2004 Wiley‐Liss, Inc.
Nongenetic pathologic developments of brain‐wave patterns in monozygotic twins discordant and concordant for schizophrenia
Authors: Weisbrod M. , Hill H. , Sauer H. , Niethammer R. , Guggenbühl S. , Hell D. , Stassen H.H. 
Published: January 2004

AbstractEvidence from previous studies has suggested that the inter‐individual differences in human brain‐wave patterns (EEG) are predominantly determined by genetic factors. In particular, the within‐pair EEG concordance of monozygotic (mz) twins was found to be typically as high as r = 0.81 across channels and frequency bands, thus being comparable to that between repeated assessments on the same individual with typically r = 0.83. Yet our investigations into mz twins discordant and concordant for schizophrenia yielded a significantly reduced within‐pair EEG concordance for both, the pairs discordant for schizophrenia and the pairs concordant for schizophrenia (with concordance for schizophrenia assessed through a syndrome‐oriented approach). A multivariate discriminant function of EEG parameters distinguished in a reproducible way between affected and unaffected subjects at an overall performance of >75% correctly classified subjects, while the severity of illness, as derived from EEG‐differences between affected and unaffected subjects, was closely related to the severity of illness as provided by psychopathology syndrome scores. Consequently, EEG anomalies associated with schizophrenia and manifested differently in the mz co‐twins concordant for schizophrenia are likely the effect of nongenetic, pathologic processes that evolved independently in the co‐twins' genetically identical brains once the illness began to progress. The existence of such nongenetic processes would suggest a modification of the standard phenotype‐to‐genotype search strategies of molecular‐genetic studies that aim to link the schizophrenia phenotype to genetic vulnerability factors. © 2003 Wiley‐Liss, Inc.
Evidence of a founder effect in families with frontotemporal dementia that harbor the tau +16 splice mutation
Authors: Pickering‐Brown Stuart , Baker Matt , Bird Thomas , Trojanowski John , Lee Virginia , Morris Huw , Rossor Martin , Janssen John C. , Neary David , Craufurd David , Richardson Anna , Snowden Julie , Hardy John , Mann David , Hutton Mike 
Published: January 2004

AbstractThe +16 exon 10 splice mutation of the tau gene (microtubule‐associated protein tau, MAPT) has been reported in numerous families with frontotemporal dementia (FTD). To date, the majority of these families are from England and Wales in the UK, although families with this mutation have been reported from Australia and the USA. Our own analysis has identified eight families with the +16 MAPT splice mutation from around the Manchester and North Wales areas of the UK. Given the proximity of the UK families to one another it is likely that they are related and represent a single extended pedigree. In order to investigate this possibility, and the possibility that the families with this mutation from London, the USA, and Australia are related, we genotyped 11 microsatellite markers around the tau locus. In most cases (20/25, 80%), a common haplotype, approximately 3 cM in size, was identified. In the remaining cases, this haplotype appears to have been varyingly reduced in size by recombination. We demonstrate that the +16 mutation is on the H1 tau haplotype and that H1 specific polymorphisms are also shared by these families. These data provide evidence that the MAPT +16 splice mutation cases from around the world analyzed in this study are indeed related and represent a single pedigree that probably originated in the North Wales area of the UK. Furthermore, this single large pedigree may be of use in the identification of disease modifying loci in FTD. © 2003 Wiley‐Liss, Inc.
No evidence of association or linkage disequilibrium between polymorphisms in the 5′ upstream and coding regions of the dopamine D4 receptor gene and schizophrenia in a Portuguese population
Authors: Ambrósio Alda M. , Kennedy James L. , Macciardi Fabio , Barr Cathy , Soares Maria J. , Oliveira Catarina R. , Pato Carlos N. 
Published: January 2004

AbstractAlterations in dopaminergic system have been implicated in the pathophysiology of this disease for many years, and this study was performed to assess the possible involvement of the dopamine D4 receptor (DRD4) gene polymorphisms either in the 5′ upstream or in the coding regions, in the etiology of schizophrenia. The approach included an association study with 90 Portuguese trios by doing the analysis of the individual alleles and the haplotypes. For the polymorphisms in the 5′ upstream region (−C616G and −C521T) and in the coding region (48 bp repeat) of the DRD4 gene, negative results were obtained with both haplotype relative risk (HRR) and transmission disequilibrium test (TDT), as well as transmit. These data suggest that polymorphisms (−C616G, −C521T, and 48 bp repeat) at the DRD4 gene do not have a minor effect in the susceptibility to schizophrenia in our sample. © 2003 Wiley‐Liss, Inc.
Association study of cannabinoid receptor gene (CNR1) alleles and anorexia nervosa: Differences between restricting and bingeing/purging subtypes
Authors: Siegfried Z. , Kanyas K. , Latzer Y. , Karni O. , Bloch M. , Lerer B. , Berry E.M. 
Published: January 2004

AbstractAnorexia nervosa (AN) is a severe and disabling psychiatric disorder, characterized by profound weight loss and body image disturbance. Family and twin studies indicate a significant genetic contribution to this disorder although no genetic mutation has yet been identified. The endocannabinoid system has recently been implicated in many physiological functions including appetite regulation. We, therefore, undertook a family based study to test the hypothesis whether a polymorphism of the CNR1 gene, which encodes human CB1 receptor, a subclass of the central cannabinoid receptor, contributes to the susceptibility to AN. Fifty two families (parents with one or two affected siblings) were genotyped for the (AAT) trinucleotide repeat of CNR1 gene. Using the haplotype relative risk (HRR) method, the distribution of alleles transmitted to the patients was not found to be significantly different from the non‐transmitted parental alleles. However, upon dividing the samples to restricting and bingeing/purging subtypes of AN, the extended transmission disequilibrium test (ETDT) revealed that there is preferential transmission of different alleles in each of the subtypes. The 14 repeat allele was preferentially transmitted in the bingeing/purging AN group (P = 0.05) but not in the restricting AN group, whereas the 13 repeat allele was preferentially transmitted in the restricting AN group (almost significant, P = 0.07) but not in the bingeing/purging AN group. Our study suggests that restricting AN and bingeing/purging AN may be associated with different alleles of the CNR1 gene. © 2003 Wiley‐Liss, Inc.
Genetic mapping using haplotype and model‐free linkage analysis supports previous evidence for a locus predisposing to severe bipolar disorder at 5q31‐33
Authors: Hong Kyung Sue , McInnes L. Alison , Service Susan K. , Song Terry , Lucas Jennifer , Silva Sandra , Fournier Eduardo , León Pedro , Molina Julio , Reus Victor I. , Sandkuijl Lodewijk A. , Freimer Nelson B. 
Published: January 2004

AbstractWe report further evidence for our previous suggestion [Garner et al., 2001: Am J Hum Genet 68:1061–1064] of a locus on 5q predisposing to bipolar I disorder (BP‐I) in an extended Costa Rican pedigree. We genotyped additional microsatellite markers in this region and applied a multi‐point non‐parametric linkage analysis (SimWalk2). Significant identity‐by‐descent allele sharing among affected relatives was observed for all of the 20 markers tested in a segment of approximately 15 cM. Most affected individuals shared a single haplotype over this region; breaks within this haplotype may suggest a more restricted candidate location for a BP‐I gene. These results support the suggestion that a locus at 5q31‐33, together with a previously reported locus at 18q22‐23, may provide the major genetic risk for BP‐I in this family. © 2003 Wiley‐Liss, Inc.
CALCYONgene variation, schizophrenia, and cocaine dependence
Authors: Luo Xingguang , Kranzler Henry , Lappalainen Jaakko , Rosenheck Robert , Charney Dennis , Zuo Lingjun , Erdos Joseph , van Kammen Daniel P. , Gelernter Joel 
Published: January 2004

AbstractCalcyon is a brain‐specific D1 dopamine receptor‐interacting protein, with a potential role in D1‐mediated physiological processes, including motor control, reward mechanisms, and cognitive processes. Our objective was to investigate the relationship between polymorphism of theCALCYONgene and (1) schizophrenia and (2) cocaine dependence in African‐American (AA) and European‐American (EA) subjects. Two single nucleotide polymorphisms (SNPs) at theCALCYONlocus were genotyped in 70 AA and 206 EA individuals with schizophrenia and 90 AA and 118 EA individuals with cocaine dependence. The control group was comprised of 46 AA and 207 EA subjects screened to exclude those with psychiatric or substance use disorders. The specific polymorphisms studied were markers +295214G/A and +297151T/G. Comparisons of allele and haplotype frequencies between cases and controls were performed with the Fisher's Exact Test. Linkage disequilibrium (LD) between these two SNPs was calculated with the 3LOCUS program. No alleles or haplotypes were found to be associated with schizophrenia or cocaine dependence either in AA or EA subjects. The markers +295214G/A and +297151T/G are in the same haplotype block in all subgroups. Allele and haplotype frequencies differed significantly between EA and AA subjects. These results suggest that these two genetic variants in theCALCYONgene do not play a major role in predisposition to either schizophrenia or cocaine dependence in AA or EA subjects. Furthermore, these findings begin to establish a haplotype map for this gene in the AA and EA populations. © 2003 Wiley‐Liss, Inc.
An investigation into sub‐telomeric deletions of chromosome 22 and pervasive developmental disorders
Authors: Nair‐Miranda Kumudini , Murch Ashleigh , Petterson Beverly , Hill Wayne , Nikolova‐Hill Amelia , Bradley Linda , Jackson Sandy , Hallmayer Joachim 
Published: January 2004

AbstractDeletions of the sub‐telomeric region of chromosome 22 have been associated with mental retardation, developmental delay, and autistic behaviors. This study investigated sub‐telomeric anomalies of chromosome 22 using fluorescent in situ hybridization (FISH) probes in 82 subjects diagnosed with autism and atypical autism. No microdeletions were detected in this group. Similar FISH analyses were undertaken on two children with developmental delay, who were ascertained to be ring 22 during routine cytogenetic investigations. One subject was shown to have a microdeletion in the sub‐telomeric region tested. Both children met the social and communication cut off for autism on the ADI and but did not meet the cut off for restrictive and repetitive behaviors. Only one of the two children met the criteria for PDD on the ADOS. © 2003 Wiley‐Liss, Inc.
Multiple missense mutations in the diazepam binding inhibitor (DBI) gene identified in schizophrenia but lack of disease association
Authors: Niu N. , Rice S.R. , Heston L.L. , Sobell J.L. 
Published: January 2004

AbstractThe diazepam binding inhibitor (DBI), alternatively known as the acyl‐CoA binding protein (ACBP), is involved in multiple biological actions. The polypeptide binds to the peripheral, or mitochondrial, benzodiazepine receptor and facilitates transport of cholesterol to the inner membrane to stimulate steroid synthesis. Through this action, DBI indirectly modulates gamma‐aminobutyric acid (GABA)‐mediated inhibitory neurotransmission. DBI can be postulated as a candidate gene for psychiatric phenotypes including anxiety, mood, and psychotic disorders. In an examination of the DBI gene among 112 individuals with schizophrenia, our laboratory has identified 18 novel single nucleotide polymorphisms (SNPs), including three missense changes in conserved amino acids, a coding region microdeletion, and multiple SNPs in the putative promoter region. Case‐control association analyses were performed for the missense changes, but none was found to be significantly associated with disease. © 2003 Wiley‐Liss, Inc.
Clinical features of psychotic disorders and polymorphisms in HT2A, DRD2, DRD4, SLC6A3 (DAT1), and BDNF: A family based association study
Authors: Fanous Ayman H. , Neale M.C. , Straub R.E. , Webb B.T. , O'Neill A.F. , Walsh D. , Kendler K.S. 
Published: January 2004

AbstractSchizophrenia is clinically heterogeneous and multidimensional, but it is not known whether this is due to etiological heterogeneity. Previous studies have not consistently reported association between any specific polymorphisms and clinical features of schizophrenia, and have primarily used case‐control designs. We tested for the presence of association between clinical features and polymorphisms in the genes for the serotonin 2A receptor (HT2A), dopamine receptor types 2 and 4, dopamine transporter (SLC6A3), and brain‐derived neurotrophic factor (BDNF). Two hundred seventy pedigrees were ascertained on the basis of having two or more members with schizophrenia or poor outcome schizoaffective disorder. Diagnoses were made using a structured interview based on the SCID. All patients were rated on the major symptoms of schizophrenia scale (MSSS), integrating clinical and course features throughout the course of illness. Factor analysis revealed positive, negative, and affective symptom factors. The program QTDT was used to implement a family‐based test of association for quantitative traits, controlling for age and sex. We found suggestive evidence of association between the His452Tyr polymorphism in HT2A and affective symptoms (P = 0.02), the 172‐bp allele of BDNF and negative symptoms (P = 0.04), and the 480‐bp allele in SLC6A3 (= DAT1) and negative symptoms (P = 0.04). As total of 19 alleles were tested, we cannot rule out false positives. However, given prior evidence of involvement of the proteins encoded by these genes in psychopathology, our results suggest that more attention should be focused on the impact of these alleles on clinical features of schizophrenia. © 2003 Wiley‐Liss, Inc.
Haplotypes of the monoamine oxidase genes and the risk for substance use disorders
Authors: Vanyukov Michael M. , Maher Brion S. , Devlin Bernie , Tarter Ralph E. , Kirillova Galina P. , Yu Ling‐Mei , Ferrell Robert E. 
Published: January 2004

AbstractMonoamine oxidase A (MAOA) locus is an attractive candidate for exploring genetic contribution to the variation in the risk for substance use disorders (SUD) because of its important role in the metabolism of neurotransmitters, including dopamine and serotonin. Prior findings have suggested an association of the MAOA gene with the risk for early onset SUD. To extend this research, we genotyped four MAOA markers (two VNTR polymorphisms and two SNPs) and built a cladogram reflecting the evolutionary history of MAOA haplotypes [Nguyen et al., under review]. The cladogram served as the framework for nested ANOVA and logit analyses of association between MAOA and indices of liability to SUD (diagnosis, age of onset, and a dimensional index of substance use related problems) in a sample of adult males of European ancestry. Whereas no association was found for the categorical diagnosis, a significant relationship was detected between the dimensional liability indices and MAOA haplotypes. Overall, our results, albeit not definitive, are consistent with the hypothesis that variants in MAOA account for a small portion of the variance of SUD risk, possibly mediated by liability to early onset behavioral problems. © 2003 Wiley‐Liss, Inc.