bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multiple pathways of maternal effects in black-headed gull eggs: constraint and adaptive compensatory adjustment
Authors: Groothuis T. G. G. , Eising C. M. , Blount J. D. , Surai P. , Apanius V. , Dijkstra C. , Müller W. 
Published: January 2006

Abstract
We investigated in the black-headed gull whether female deposition of antioxidants and immunoglobulins (enhancing early immune function), and testosterone (suppressing immune function and increasing early competitive skills) correlate suggesting that evolution has favoured the mutual adjustment of different pathways for maternal effects. We also took egg mass, the position of the egg in the laying sequence and offspring sex into account, as these affect offspring survival. Yolk antioxidant and immunoglobulin concentrations decreased across the laying order, while yolk testosterone concentrations increased. This may substantially handicap the immune defence of last-hatched chicks. The decrease in antioxidant levels was greater when mothers had a low body mass and when the increase in testosterone concentrations was relatively large. This suggests that female black-headed gulls are constrained in the deposition of antioxidants in last-laid eggs and compensate for this by enhanced testosterone deposition. The latter may be adaptive since it re-allocates the chick's investment from costly immune function to growth and competitive skills, necessary to overcome the consequences of hatching late from an egg of reduced quality.
Making up is hard to do, especially for mothers with high levels of depressive symptoms and their infant sons
Authors: Katherine Weinberg M. , Olson Karen L. , Beeghly Marjorie , Tronick Edward Z. 
Published: January 2006

Background:  The goal of this study was to evaluate the interactions of mothers with normative or high levels of depressive symptomatology on the Center for Epidemiologic Studies‐Depression Scale (CES‐D) and their 3‐month‐old infants. Although successful mutual regulation of affect is critical to children's socio‐emotional development, little is known about the factors that influence dyadic processes such as synchrony, matching, mismatching, and bi‐directionality during early infancy. Therefore, this study evaluated the effects of maternal depressive symptom status, infant gender, and interactional context on mother–infant affective expressiveness and the dyadic features of their interactions.Methods:  Participants were 133 mothers and their healthy full‐term infants. Mothers were classified into three groups on the basis of their total score on the CES‐D at 2 months of infant age: a high symptom group (CES‐D score ≥ 16), a mid symptom control group (CES‐D score = 2–12), and a low symptom group (CES‐D score = 0–1). Mothers and infants were then videotaped in the Face‐to‐Face Still‐Face paradigm at 3 months of infant age. The mothers’ and infants’ affect during the interactions prior to (first play) and following the still‐face (reunion play) were coded microanalytically using Izard's AFFEX system.Results:  Results indicated that male as compared to female infants were more vulnerable to high levels of maternal depressive symptoms and that high symptom mothers and their sons had more difficult interactions in the challenging reunion episode.Conclusions:  The findings suggest that a cycle of mutual regulatory problems may become established between high symptom mothers and their sons, particularly in challenging social contexts. The long‐term consequences of this early social interactive vulnerability in terms of later development need to be further investigated.
Test–retest reliability and criterion validity of the Chinese version of CBCL, TRF, and YSR
Authors: Leung Patrick W.L. , Kwong S.L. , Tang C.P. , Ho T.P. , Hung S.F. , Lee C.C. , Hong S.L. , Chiu C.M. , Liu W.S. 
Published: January 2006

Background: Psychometric properties of the Chinese version of CBCL, TRF, and YSR were understudied. This study aimed at examining their test–retest reliability and criterion validity.Methods: Three Chinese community and clinic samples were recruited in Hong Kong. The parents, teachers, and youths respectively completed the CBCL, TRF, and YSR.Results: The Chinese CBCL, TRF, and YSR were test–retest reliable and valid. However, there was score/case attenuation at retest. CBCL and TRF appeared to screen externalizing and ADHD problems better, while YSR screened internalizing problems better.Conclusions: Clinicians should be cautious about score/case attenuation at retest while using CBCL, TRF, and YSR to chart patients’ progress. They should also recognize their different strengths in screening various disorders.
The prevalence of autistic spectrum disorders in adolescents with a history of specific language impairment (SLI)
Authors: Conti‐Ramsden Gina , Simkin Zoë , Botting Nicola 
Published: January 2006

Background:  Traditionally, autism and specific language impairment (SLI) have been regarded as distinct disorders but, more recently, evidence has been put forward for a closer link between them: a common set of language problems, in particular receptive language difficulties and the existence of intermediate cases including pragmatic language impairment. The present study aimed to examine the prevalence of autism spectrum disorders in a large sample of adolescents with a history of SLI.Method:  The presence of autism spectrum disorders was examined in seventy‐six 14‐year‐olds with a confirmed history of SLI. A variety of instruments were employed, including the Autism Diagnostic Interview‐Revised (ADI‐R), the Autism Diagnostic Observation Schedule (ADOS) and the Family History Interview (FHI).Results:  The prevalence of autism spectrum disorders in young people with SLI was found to be 3.9%, about 10 times what would be expected from the general population. In addition, a much larger number of young people with a history of SLI showed only some autism spectrum symptoms or showed them in a mild form.Conclusions:  Young people with SLI have an increased risk of autism. The magnitude of this risk is considerable. In addition, a larger proportion (a quarter of individuals) present with a number of behaviours consistent with autism spectrum disorders.
Development of male proactive and reactive physical aggression during adolescence
Authors: Barker Edward D. , Tremblay Richard E. , Nagin Daniel S. , Vitaro Frank , Lacourse Eric 
Published: January 2006

Background:  Different developmental courses have been postulated for proactive and reactive aggression.Objective:  Investigated the developmental course of proactive and reactive aggression in a large sample of adolescent boys from low socioeconomic areas.Method:  A dual group‐based joint trajectory method was used to identify distinct trajectories as well as similarities and differences in intra‐individual changes.Results:  The trajectories for proactive and reactive aggression were similar: the majority of individuals followed infrequent and desisting trajectories. Contrary to expectations, very few adolescents followed trajectories of increasing proactive aggression. Reactive aggression was more common than proactive aggression. The overlap in trajectory group membership of individuals following trajectories of high peaking proactive and reactive aggression was nearly 100%. Across a period of 5 years, the boys on the high peaking trajectories were twice as likely to have affiliated with gangs.Conclusions:  The developmental courses of proactive and reactive aggression are similar during adolescence. Males who tend to frequently use one form of aggression throughout adolescence also tend to frequently use the other and are at an increased risk for contemporaneous delinquent lifestyles.
Predictive validity of ICD‐10 hyperkinetic disorder relative to DSM‐IV attention‐deficit/hyperactivity disorder among younger children
Authors: Lahey Benjamin B. , Pelham William E. , Chronis Andrea , Massetti Greta , Kipp Heidi , Ehrhardt Ashley , Lee Steve S. 
Published: January 2006

Background:  Little is known about the predictive validity of hyperkinetic disorder (HKD) as defined by the Diagnostic Criteria for Research for mental and behavioral disorders of the tenth edition of the International Classification of Diseases (ICD‐10; World Health Organization, 1993), particularly when the diagnosis is given to younger children.Methods:  The predictive validity of HKD was evaluated over a 6‐year period and compared to the predictive validity of DSM‐IV attention‐deficit/hyperactivity disorder (ADHD) in 95 4–6‐year‐old children who met full criteria for at least ADHD and 122 demographically‐matched nonreferred comparison children. Diagnoses were based on structured assessments of both parents and teachers.Results:  All children who met full criteria for HKD also met full DSM‐IV criteria for ADHD, but only 26% of ADHD children met criteria for HKD. Children who met criteria for HKD (N = 24), children who would have met criteria for HKD but were excluded from the diagnosis because they concurrently met criteria for an anxiety disorder or depression (N = 16), and the remaining children who met DSM‐IV criteria for ADHD (N = 55) all exhibited significantly more symptoms of ADHD and greater social and academic impairment during years 2–7 than nonreferred comparison children. Unlike the two other diagnostic groups, however, children who met strict criteria for HKD were not more likely than comparison children to be injured unintentionally or to be placed in special education.Conclusions:  Both ICD‐10 HKD and DSM‐IV ADHD exhibit predictive validity over 6 years, but ICD‐10 HKD appears to under‐identify children with persistent ADHD symptoms and related impairment. Children who met criteria for DSM‐IV ADHD but not HKD exhibited at least as much functional impairment over time as hyperkinetic children.
Event rate and event‐related potentials in ADHD
Authors: Wiersema Roeljan , Van Der Meere Jaap , Roeyers Herbert , Van, Coster Rudy , Baeyens Dieter 
Published: January 2006

Background:  It has been repeatedly found that performance of children with attention deficit hyperactivity disorder (ADHD) is more impaired when a long inter‐stimulus interval (ISI) is used than when a short ISI is used. According to the cognitive‐energetic model, this may reflect difficulty in remaining in an optimal motor activation state because of insufficient effort allocation.Method:  Event‐related potentials (ERPs) were evaluated during a Go/No‐Go task that incorporates a condition with a fast and a slow presentation rate.Results:  ADHD, whether or not comorbid with oppositional defiant/conduct disorder (ODD/CD), was associated with a steeper increase in reaction time (RT) from the fast to the slow condition accompanied by a missing increment of the parietal P3. Speed of responding was found to be correlated with P3 amplitude. In the fast condition, children with ADHD made more errors of commission, accompanied by a smaller No‐Go N2, a component thought to be related to inhibition; however, after controlling for ODD/CD these differences disappeared.Conclusions:  The association between the steeper increase in RT and reduced parietal P3s may indicate that the children with ADHD did not allocate enough extra effort to adjust to a potentially under‐activated state. However, the event rate effects could not account for all of the differences between groups and also early automatic information processing stages seem disturbed in this disorder as indexed by larger P2 amplitudes. Alternative explanations are discussed.
Gene expression profiling reveals that peripheral nerve regeneration is a consequence of both novel injury‐dependent and reactivated developmental processes
Authors: Bosse Frank , Hasenpusch‐Theil Kerstin , Küry Patrick , Müller Hans Werner 
Published: January 2006

AbstractOne of the most striking features of the injured mature peripheral nervous system is the ability to regenerate. The lesioned peripheral nervous system displays stereotypic histopathological reactions indicating the activation of a co‐ordinated lesion‐induced gene expression programme. Previous research has already identified molecular components of this axonal switch from a mature transmitting to a regenerative growth mode. The observed alterations in gene expression within the lesioned distal nerve stump were largely attributed to recapitulated developmental processes. However, to our knowledge, this hypothesis has not been proven systematically. Most of the stereotypic molecular and cellular reactions during nerve development and repair can be assigned to specific time windows. Consequently, we have compared gene expression profiles of both paradigms at six different time‐points each by means of cDNA array hybridization. Our data identified injury‐specific molecular reactions and revealed to what extent developmental mechanisms are reactivated in response to nerve lesion. Ninety‐one genes (47% of the regeneration‐associated genes) were found to be significantly regulated in both paradigms, suggesting that regeneration only partially recapitulates development and that approximately half of the regulated genes are part of a regeneration‐dependent programme. Interestingly, mainly genes encoding signal transducers or factors involved in processes such as cell death, immune response, transport and transcriptional regulation showed injury‐specific gene expression.
The interaction between dopamine D2‐like and beta‐adrenergic receptors in the prefrontal cortex is altered by mood‐stabilizing agents
Authors: Montezinho Liliana P. , Castro M. Margarida C. A. , Duarte Carlos B. , Penschuck Silke , Geraldes Carlos F. G. C. , Mørk Arne 
Published: January 2006

AbstractSeveral studies have suggested the involvement of biogenic monoaminergic neurotransmission in bipolar disorder and in the therapy for this disease. In this study, the effects of the mood‐stabilizing drugs lithium, carbamazepine or valproate on the dopaminergic and adrenergic systems, particularly on D2‐like and β‐adrenergic receptors, were studied both in cultured rat cortical neurones and in rat prefrontal cortex. In vitro and in vivo data showed that stimulation of β‐adrenergic receptors with isoproterenol increased cyclic adenosine monophosphate (cAMP) levels and this effect was significantly inhibited by lithium, carbamazepine or valproate. The activation of dopamine D2‐like receptors with quinpirole decreased the isoproterenol‐induced rise in cAMP in control conditions. This inhibition was observed in vivo after chronic treatment of the rats with carbamazepine or valproate, but not after treatment with lithium or in cultured rat cortical neurones after 48 h exposure to the three mood stabilizers. Dopamine D2 and β1‐adrenergic receptors were found to be co‐localized in prefrontal cortical cells, as determined by immunohistochemistry, but western blot experiments revealed that receptor levels were differentially affected by treatment with the three mood stabilizers. These data show that mood stabilizers affect D2 receptor‐mediated regulation of β‐adrenergic signalling and that each drug acts by a unique mechanism.
Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn‐superoxide dismutase mutant mice
Authors: Damiano Maria , Starkov Anatoly A. , Petri Susanne , Kipiani Kathuna , Kiaei Mahmoud , Mattiazzi Marina , Flint Beal M. , Manfredi Giovanni 
Published: January 2006

AbstractMitochondrial respiratory chain dysfunction, impaired intracellular Ca2+ homeostasis and activation of the mitochondrial apoptotic pathway are pathological hallmarks in animal and cellular models of familial amyotrophic lateral sclerosis associated with Cu/Zn‐superoxide dismutase mutations. Although intracellular Ca2+ homeostasis is thought to be intimately associated with mitochondrial functions, the temporal and causal correlation between mitochondrial Ca2+ uptake dysfunction and motor neuron death in familial amyotrophic lateral sclerosis remains to be established. We investigated mitochondrial Ca2+ handling in isolated brain, spinal cord and liver of mutant Cu/Zn‐superoxide dismutase transgenic mice at different disease stages. In G93A mutant transgenic mice, we found a significant decrease in mitochondrial Ca2+ loading capacity in brain and spinal cord, as compared with age‐matched controls, very early on in the course of the disease, long before the onset of motor weakness and massive neuronal death. Ca2+ loading capacity was not significantly changed in liver G93A mitochondria. We also confirmed Ca2+ capacity impairment in spinal cord mitochondria from a different line of mice expressing G85R mutant Cu/Zn‐superoxide dismutase. In excitable cells, such as motor neurons, mitochondria play an important role in handling rapid cytosolic Ca2+ transients. Thus, mitochondrial dysfunction and Ca2+‐mediated excitotoxicity are likely to be interconnected mechanisms that contribute to neuronal degeneration in familial amyotrophic lateral sclerosis.
Regulation of taurine transport in rat hippocampal neurons by hypo‐osmotic swelling
Authors: Olson James E. , Martinho Eduardo 
Published: January 2006

AbstractTaurine, an important mediator of cellular volume regulation in the central nervous system, is accumulated into neurons and glia by means of a highly specific sodium‐dependent membrane transporter. During hyperosmotic cell shrinkage, net cellular taurine content increases as taurine transporter activity is enhanced via elevated gene expression of the transporter protein. In hypo‐osmotic conditions, taurine is rapidly lost from cells by means of taurine‐conducting membrane channels. We reasoned that changes in taurine transporter activity also might accompany cell swelling to minimize re‐accumulation of taurine from the extracellular space. Thus, we determined the kinetic and pharmacological characteristics of neuronal taurine transport and the response to osmotic swelling. Accumulation of radioactive taurine is strongly temperature dependent and occurs via saturable and non‐saturable pathways. At concentrations of taurine expected in extracellular fluidin vivo, 98% of taurine accumulation would occur via the saturable pathway. This pathway obeys Michaelis–Menten kinetics with aKmof 30.0 ± 8.8 μm(mean ± SE) andJmaxof 2.1 ± 0.2 nmol/mg protein min. The saturable pathway is dependent on extracellular sodium with an effective binding constant of 80.0 ± 3.1 mmand a Hill coefficient of 2.1 ± 0.1. This pathway is inhibited by structural analogues of taurine and by the anion channel inhibitors, 4,4′‐diisothiocyanostilbene‐2, 2′‐disulfonic acid (DIDS) and 5‐nitro‐2‐(3 phenylpropylamino) benzoic acid (NPPB). NPPB, but not DIDS, also reduces the ATP content of the cell cultures. Osmotic swelling at constant extracellular sodium concentration reduces theJmaxof the saturable transport pathway by approximately 48%, increasesKdifffor the non‐saturable pathway by 77%, but has no effect on cellular ATP content. These changes in taurine transport occurring in swollen neuronsin vivowould contribute to net reduction of taurine content and resulting volume regulation.
Stimulation of ubiquitin–proteasome pathway through the expression of amidohydrolase for N‐terminal asparagine (Ntan1) in cultured rat hippocampal neurons exposed to static magnetism
Authors: Hirai Takao , Taniura Hideo , Goto Yasuaki , Ogura Masato , Sng Judy C. G. , Yoneda Yukio 
Published: January 2006

AbstractIn order to elucidate mechanisms underlying modulation by static magnetism of the cellular functionality and/or integrity in the brain, we screened genes responsive to brief magnetism in cultured rat hippocampal neurons using differential display analysis. We have for the first time cloned and identified Ntan1 (amidohydrolase for N‐terminal asparagine) as a magnetism responsive gene in rat brain. Ntan1 is an essential component of a protein degradation signal, which is a destabilizing N‐terminal residue of a protein, in the N‐end rule. In situ hybridization histochemistry revealed abundant expression of Ntan1 mRNA in hippocampal neurons in vivo. Northern blot analysis showed that Ntan1 mRNA was increased about three‐fold after 3 h in response to brief magnetism. Brief magnetism also increased the transcriptional activity of Ntan1 promoter by luciferase reporter assay. Brief magnetism induced degradation of microtubule‐associated protein 2 (MAP2) without affecting cell morphology and viability, which was prevented by a selective inhibitor of 26S proteasome in hippocampal neurons. Overexpression of Ntan1 using recombinant Ntan1 adenovirus vector resulted in a marked decrease in the MAP2 protein expression in hippocampal neurons. Our results suggest that brief magnetism leads to the induction of Ntan1 responsible for MAP2 protein degradation through ubiquitin–proteasome pathway in rat hippocampal neurons.
Odorant receptors directly activate phospholipase C/inositol‐1,4,5‐trisphosphate coupled to calcium influx in Odora cells
Authors: Liu Guang , Badeau Robert M. , Tanimura Akihiko , Talamo Barbara R. 
Published: January 2006

AbstractMechanisms by which odorants activate signaling pathways in addition to cAMP are hard to evaluate in heterogeneous mixtures of primary olfactory neurons. We used single cell calcium imaging to analyze the response to odorant through odorant receptor (OR) U131 in the olfactory epithelial cell line Odora (Murrell and Hunter 1999), a model system with endogenous olfactory signaling pathways. Because adenylyl cyclase levels are low, agents activating cAMP formation do not elevate calcium, thus unmasking independent signaling mediated by OR via phospholipase C (PLC), inositol‐1,4,5‐trisphosphate (IP3), and its receptor. Unexpectedly, we found that extracellular calcium is required for odor‐induced calcium elevation without the release of intracellular calcium, even though the latter pathway is intact and can be stimulated by ATP. Relevant signaling components of the PLC pathway and G protein isoforms are identified by western blot in Odora cells as well as in olfactory sensory neurons (OSNs), where they are localized to the ciliary zone or cell bodies and axons of OSNs by immunohistochemistry. Biotinylation studies establish that IP3receptors type 2 and 3 are at the cell surface in Odora cells. Thus, individual ORs are capable of elevating calcium through pathways not directly mediated by cAMP and this may provide another avenue for odorant signaling in the olfactory system.
Acute amphetamine down‐regulates RGS4 mRNA and protein expression in rat forebrain: distinct roles of D1 and D2 dopamine receptors
Authors: Schwendt Marek , Gold Stephen J. , McGinty Jacqueline F. 
Published: January 2006

AbstractAdministration of psychostimulants modulates mRNA of several regulators of guanine nucleotide‐binding protein signaling (RGSs) proteins in the brain. In the present study, the regulation of amphetamine‐induced decrease of RGS4 expression in the rat forebrain was evaluated. RGS4 mRNA was reduced by amphetamine in an inverse, dose‐dependent manner. The lowest dose (2.5 mg/kg) decreased RGS4 mRNA in caudate putamen for up to 6 h after injection whereas the decrease in several frontal cortical areas was detected at 3 h only. Analysis of RGS4 immunoreactivity by western blotting revealed a decrease 3 h after amphetamine solely in the caudate putamen. Systemic administration of D1 (SCH23390) or D2 (eticlopride) receptor antagonists blocked amphetamine‐induced locomotion but amphetamine augmented both the SCH23390‐induced increase and the eticlopride‐induced decrease in RGS4 mRNA in the caudate putamen. Further, the down‐regulation of RGS4 immunoreactivity by eticlopride was robust whereas the effect of SCH23390 was blunted as compared with its effect on mRNA. These data suggest that, by decreasing RGS4 expression in the caudate putamen via D1 receptors, acute amphetamine could disinhibit RGS4‐sensitive guanine nucleotide‐binding protein α‐subunit i‐ and/or q‐coupled signaling pathways and favor mechanisms that counterbalance D1 receptor stimulation.