bluuebunny/crossref_metadata_2025 huggingface dataset:
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

One 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

Several 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

Mitochondrial 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

Taurine, 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

In 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

Mechanisms 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

Administration 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.
SirT1 fails to affect p53‐mediated biological functions
Authors: Kamel Christopher , Abrol Meena , Jardine Karen , He Xiaohong , McBurney Michael W.
Published: January 2006

The SirT1 gene encodes a protein deacetylase that acts on a number of nuclear substrates. p53 was identified as a SirT1 substrate whose transcriptional activity was reported to be negatively regulated by SirT1‐dependent deacetylation. We set out to determine whether developmental defects and perinatal lethality observed in SirT1‐null mice were caused by p53 hyperactivity by creating mice deficient for both SirT1 and p53. Animals null for both proteins were smaller than normal at birth, had eyelid opening defects and died during the late prenatal and early postnatal periods, a phenotype indistinguishable from mice deficient for SirT1 alone. Upon re‐examination of the role of SirT1 in modulating p53 activity, we found that while SirT1 interacts with p53, the SirT1 protein had little effect on p53‐dependent transcription of transfected or endogenous genes and did not affect the sensitivity of thymocytes and splenocytes to radiation‐induced apoptosis. These findings suggest that SirT1 does not affect many p53‐mediated biological activities despite the fact that acetylated p53 has been shown to be a substrate for SirT1.
Radioiodinated clioquinol as a biomarker for β‐amyloid: Zn2+ complexes in Alzheimer's disease
Authors: Opazo Carlos , Luza Sandra , Villemagne Victor L. , Volitakis Irene , Rowe Christopher , Barnham Kevin J. , Strozyk Dorothea , Masters Colin L. , Cherny Robert A. , Bush Ashley I.
Published: January 2006

Neocortical β‐amyloid (Aβ) aggregates in Alzheimer's disease (AD) are enriched in transition metals that mediate assembly. Clioquinol (CQ) targets metal interaction with Aβ and inhibits amyloid pathology in transgenic mice. Here, we investigated the binding properties of radioiodinated CQ ([125I]CQ) to different in vitro and in vivo Alzheimer models. We observed saturable binding of [125I]CQ to synthetic Aβ precipitated by Zn2+ (Kd = 0.45 and 1.40 nm for Aβ1‐42 and Aβ1‐40, respectively), which was fully displaced by free Zn2+, Cu2+, the chelator DTPA (diethylene triamine pentaacetic acid) and partially by Congo red. Sucrose density gradient of post‐mortem AD brain indicated that [125I]CQ concentrated in a fraction enriched for both Aβ and Zn, which was modulated by exogenous addition of Zn2+ or DTPA. APP transgenic (Tg2576) mice injected with [125I]CQ exhibited higher brain retention of tracer compared to non‐Tg mice. Autoradiography of brain sections of these animals confirmed selective [125I]CQ enrichment in the neocortex. Histologically, both thioflavine‐S (ThS)‐positive and negative structures were labeled by [125I]CQ. A pilot SPECT study of [123I]CQ showed limited uptake of the tracer into the brain, which did however, appear to be more rapid in AD patients compared to age‐matched controls. These data support metallated Aβ species as the neuropharmacological target of CQ and indicate that this drug class may have potential as in vivo imaging agents for Alzheimer neuropathology.
Characterisation of Contact Pressure Distribution in Bolted Joints
Authors: Marshall M. B. , Lewis R. , Dwyer‐Joyce R. S.
Published: January 2006

Abstract:  The quantification of contact area and pressure distribution in a bolted joint is essential information, as it determines the integrity of the coupling. Current bolted joint design standards are based on analytical solutions of the pressure distribution, which, because of the inherent assumptions, frequently do not accurately represent the real conditions in a joint. This study uses a non‐intrusive ultrasonic technique to quantify the contact pressure distribution in a bolted connection. The advantage of this experimental technique is that the effect of actual contact conditions can be determined. An ultrasonic wave is focused onto the clamped interface, and the reflected sound signal recorded. In areas where the contact pressure is high, most of the ultrasound is transmitted, and the reflected sound signal is weak. Whereas, when the contact pressure is low, the vast majority of the ultrasound is reflected back. A parallel experimental calibration is then used to find the relationship between the reflected sound signal and contact pressure. In this way, the pressure distribution in a clamped interface is determined for a series of different bolt torques. Two different interfaces were investigated: the first consisted of two ground surfaces clamped together, and the second a turned profile pressed against a ground surface. The effect of a washer underneath the bolt head was also considered. The turned profile was found to cause the contact to spread; there was also a certain degree of fragmentation leading to higher peak pressures than in the ground interface case. With a washer positioned under the bolt head for the turned case, the clamping performance of the bolt was improved. Good agreement was found when comparing the ultrasonic measurements with previous studies, with respect to the spread of the contact pressure distribution. However, in this study, the peak contact pressure was found to occur away from the edge of the bolt hole, and to be influenced by the edge of the bolt head.
Relative Slip on Contact Surface under Partial Slip Fretting Fatigue Condition
Authors: Sabelkin V. , Mall S.
Published: January 2006

Abstract:  A combined experimental–numerical approach was utilized to characterize the relative slip along the contact surface and its features under the partial slip fretting fatigue condition. Relative displacements at two locations on the substrate (specimen) and fretting pad were measured in fretting fatigue tests. These measurements were then utilized to validate finite element analysis. Effects of the coefficient of friction on the relative slip and contact condition were investigated. The stress state along the contact surface was also investigated. Two contact geometries were analysed: cylinder‐on‐flat and flat‐on‐flat. There was no change in relative displacement between locations away from the contact surface because of the change in the coefficient of friction, while relative slip on the contact surface was affected by coefficient of friction. In addition, stick/slip sizes were affected by the change in coefficient of friction. Comparison between present and previous finite element models showed that stress state, as well as a critical plane‐based crack‐initiation parameter, was not much different between these approaches, while relative slip on the contact surface changed considerably.
Prediction of Parasite Infection Dynamics in Primate Metapopulations Based on Attributes of Forest Fragmentation
Authors: GILLESPIE THOMAS R. , CHAPMAN COLIN A.
Published: January 2006

Abstract: Although the effects of forest fragmentation on species and ecological processes have been the focus of considerable research in conservation biology, our capacity to predict how processes will be altered and which taxonomic or functional groups will be most affected by fragmentation is still poor. This problem is exacerbated by inherent temporal and spatial variability in fragment attributes. To improve our understanding of this interplay, we examined how various fragment attributes affect one potentially important ecological process, parasite infection dynamics, and considered how changes in this process affect host metapopulations. From August 1999 to July 2003 we surveyed red colobus (Piliocolobus tephrosceles) metapopulations inhabiting nine fragments (1.2 to 8.7 ha) in western Uganda to determine the prevalence and richness of strongyle and rhabditoid nematodes, a group of potentially pathogenic gastrointestinal parasites. We used noninvasive fecal flotation and sedimentation (n= 536) to detect parasite eggs, cysts, and larvae in colobus fecal samples. To obtain an index of infection risk, we determined environmental contamination withOesophagostomumsp., a representative strongyle nematode, in canopy (n= 30) and ground vegetation plots (n= 30). Concurrently, physical (i.e., size, location, and topography) and biological (i.e., tree diversity, tree density, stump density, and colobine density) attributes were quantified for each fragment. Interfragment comparisons of nine potential factors demonstrated that an index of degradation and human presence (tree stump density) strongly influenced the prevalence of parasitic nematodes. Infection risk was also higher in the fragment with the highest stump density than in the fragment with the lowest stump density. These results demonstrate that host‐parasite dynamics can be altered in complex ways by forest fragmentation and that intensity of extraction (e.g., stump density) best explains these changes.
Designing Large‐Scale Conservation Corridors for Pattern and Process
Authors: ROUGET MATHIEU , COWLING RICHARD M. , LOMBARD AMANDA T. , KNIGHT ANDREW T. , KERLEY GRAHAM I.H.
Published: January 2006

Abstract:  A major challenge for conservation assessments is to identify priority areas that incorporate biological patterns and processes. Because large‐scale processes are mostly oriented along environmental gradients, we propose to accommodate them by designing regional‐scale corridors to capture these gradients. Based on systematic conservation planning principles such as representation and persistence, we identified large tracts of untransformed land (i.e., conservation corridors) for conservation that would achieve biodiversity targets for pattern and process in the Subtropical Thicket Biome of South Africa. We combined least‐cost path analysis with a target‐driven algorithm to identify the best option for capturing key environmental gradients while considering biodiversity targets and conservation opportunities and constraints. We identified seven conservation corridors on the basis of subtropical thicket representation, habitat transformation and degradation, wildlife suitability, irreplaceability of vegetation types, protected area networks, and future land‐use pressures. These conservation corridors covered 21.1% of the planning region (ranging from 600 to 5200 km2) and successfully achieved targets for biological processes and to a lesser extent for vegetation types. The corridors we identified are intended to promote the persistence of ecological processes (gradients and fixed processes) and fulfill half of the biodiversity pattern target. We compared the conservation corridors with a simplified corridor design consisting of a fixed‐width buffer along major rivers. Conservation corridors outperformed river buffers in seven out of eight criteria. Our corridor design can provide a tool for quantifying trade‐offs between various criteria (biodiversity pattern and process, implementation constraints and opportunities). A land‐use management model was developed to facilitate implementation of conservation actions within these corridors.
Modeling Opportunity Costs of Conservation in Transitional Landscapes
Authors: NAIDOO ROBIN , ADAMOWICZ WIKTOR L.
Published: January 2006

Abstract:  Conservation scientists recognize the urgency of incorporating opportunity costs into conservation planning. Despite this, applications to date have been limited, perhaps partly because of the difficulty in determining costs in regions with limited data on land prices and ownership. We present methods for estimating opportunity costs of land preservation in landscapes or ecoregions that are a changing mix of agriculture and natural habitat. Our approach derives from the literature on estimating land values as opportunity costs of alternate land uses and takes advantage of general availability of necessary data, even in relatively data‐poor regions. The methods integrate probabilities of habitat conversion with region‐wide estimates of economic benefits from agricultural land uses and estimate land values with a discount rate to convert annual values into net present values. We applied our method in a landscape undergoing agricultural conversion in Paraguay. Our model of opportunity costs predicted an independent data set of land values and was consistent with implicit discount rates of 15–25%. Model‐generated land values were strongly correlated with actual land values even after correcting for the effect of property size and proportion of property that was forested. We used the model to produce a map of opportunity costs and to estimate the costs of conserving forest within two proposed corridors in the landscape. This method can be applied to conservation planning in situations where natural habitat is currently being converted to market‐oriented land uses. Incorporating not only biological attributes but also socioeconomic data can help in the design of efficient networks of protected areas that represent biodiversity at minimum costs.
Effects of Restoring Oak Savannas on Bird Communities and Populations
Authors: BRAWN JEFFREY D.
Published: January 2006

Abstract:  Efforts to restore and maintain oak savannas in North America, with emphasis on the use of prescribed fire, have become common. Little is known, however, about how restoration affects animal populations, especially those of birds. I compared the breeding densities, community structure, and reproductive success of birds in oak savannas maintained by prescribed fire (12 sites) with those in closed‐canopy forests (13 sites). All sampling was conducted in Illinois (U.S.A.). Of the 31 bird species analyzed, 12 were more common in savannas, 14 were not affected by habitat structure, and 5 were more common in forest habitat. The species favored by disturbance and restoration included Northern Bobwhites (Colinus virginianus), Mourning Doves ( Zenaida macroura), Red‐headed Woodpeckers ( Melanerpes erythrocephalus), Indigo Buntings ( Passerina cyanea), and Baltimore Orioles (Icterus galbula). Those more common in closed‐canopy forest included Ovenbirds (Seiurus aurocapilla) and Wood Thrushes ( Hylocichla mustelina). Few species were unique to one type of habitat, but overall avian community structure in oak savannas and closed‐canopy forests was generally distinctive. Estimates of nesting success (derived from 785 nests) revealed that 6 of the 13 species considered experienced greater productivity in the savanna habitat. Rates of brood parasitism were unaffected by restoration and habitat structure. Within savannas, tract size had little effect on breeding abundances and reproductive success. My results illustrate that restoration techniques can significantly affect the ecology of constituent animal populations and communities and have key implications regarding avian conservation and the management of forest habitat in fragmented landscapes. Small patches of forest habitat that regularly function as population sinks may offer far better prospects for birds if they are subjected to disturbance and ecosystem restoration.
The Role of Ecolabeling in Fisheries Management and Conservation
Authors: KAISER MICHEL J. , EDWARDS‐JONES GARETH
Published: January 2006

Abstract:  The Marine Stewardship Council (MSC) regulates the ecolabeling of products from fisheries with the aim of promoting sustainable fishery practices. To date 11 fisheries have attained full certification and a further 7 are under review. Together these fisheries offer 220 ecolabeled marine products to consumers. Despite great potential to encourage sustainable fisheries, and thereby bring conservation benefits to marine systems, a range of issues may limit the wider uptake of MSC ecolabeled products. These include a general lack of consumer concern for marine fishes and sustainable fisheries, an absence of guaranteed continued financial benefits to participating fishers, and difficulties of quality assurance that are related to complexities of monitoring compliance of marine fisheries. In addition, it is apparent that property rights over the fishery seem to be an essential prerequisite for engagement in MSC, and this is one major impediment to wider uptake of the scheme in current marine fisheries, which tend to be open access. Some modifications to the current scheme may be needed if wider participation of marine fishers is to be achieved. These may include a tiered approach to certification, certification of fishers rather than fisheries, governmental facilitation to assist the latter, and greater engagement with retailers and buyers rather than individual consumers. None of these changes will occur without constructive engagement of government, retailers, and the fishing industry.
Progressive Cardiac Conduction Defect is the Prevailing Phenotype in Carriers of a Brugada Syndrome SCN5A Mutation
Authors: PROBST VINCENT , ALLOUIS MARIE , SACHER FREDERIC , PATTIER SABINE , BABUTY DOMINIQUE , MABO PHILIPE , MANSOURATI JACQUES , VICTOR JACQUES , NGUYEN JEAN‐MICHEL , SCHOTT JEAN‐JACQUES , BOISSEAU PIERRE , ESCANDE DENIS , LE MAREC HERVÉ
Published: January 2006

Introduction: Loss‐of‐function mutations in the SCN5A gene encoding the cardiac sodium channel are responsible for Brugada syndrome (BS) and also for progressive cardiac conduction disease (inherited Lenègre disease). In an attempt to clarify the frontier between these two entities, we have characterized cardiac conduction defect and its evolution with aging in a cohort of 78 patients carrying a SCN5A mutation linked to Brugada syndrome.

Methods and Results: Families were included in the study if a SCN5A mutation was identified in a BS proband and if at least two family members were mutation carriers. Sixteen families met the study criteria, representing 78 carriers. Resting ECG showed a spontaneous BS ECG pattern in 28 of 78 (36%) gene carriers. Intraventricular conduction anomalies were identified in 59 of 78 gene carriers including complete (17) or incomplete (24) right bundle branch block, right bundle branch block plus hemiblock (6), left bundle branch block (1), hemiblock (1), and parietal block (10). PR and QRS duration were longer in the gene carrier cohort in comparison with their relatives carrying no mutation. Finally, in the gene carrier cohort conduction defect progressively aggravated with aging leading in five occasions to pacemaker implantations.

Conclusion: The present study shows that the most common phenotype of gene carriers of a BS‐type SCN5A mutation is progressive cardiac conduction defects similar to the Lenègre disease phenotype. In consequence, we propose that carriers of a SCN5A mutation need a clinical and ECG follow‐up because of the risk associated with severe conduction defects.
The Effect of Induction Method on Defibrillation Threshold and Ventricular Fibrillation Cycle Length
Authors: ZIMA ENDRE , GERGELY MIHÁLY , SOÓS PÁL , GELLÉR LÁSZLÓ ALAJOS , NEMES ATTILA , ACSÁDY GYÖRGY , MERKELY BÉLA
Published: January 2006

Introduction: Since no clinical data are available on the comparison of the “shock on T‐wave” and “high frequency burst” ventricular fibrillation (VF) induction modes during defibrillation threshold (DFT) testing, we aimed to compare these two methods during implantable cardioverter defibrillator implantation.

Methods: The DFT was determined with a step‐down protocol using biphasic, anodal polarity (100%, 40%, 20% voltage control) shocks. Patients were randomized: VF was induced by 50 Hz burst in group B (n = 45) and T‐wave shock in group T (n = 41). The DFT was defined as the lowest energy level that terminated VF; confirmed DFT (DFTc) was defined as the minimal energy level that consecutively terminated VF twice. Success rate of DFTc was calculated during an intraindividual test for the alternate induction method.

Results: A total of 546 episodes of VF were induced: n = 278 (B) vs n = 268 (T). Incidence of VT during inductions was 9.9% (B) vs 2.7% (T), P < 0.05. Neither the DFT, 8.8 ± 4.0 J (B) vs 9.7 ± 4.2 J (T), nor the DFTc, 10.6 ± 5.1 J (B) vs 10.8 ± 4.2 J (T), proved to be significantly different. A significant correlation was found between VF cycle length (CL) and the concomitant DFT (r = 0.298, P < 0.05) in group T only. Subgroup analysis of patients under chronic class III antiarrhythmic treatment showed no increase of the DFT in either group and significantly lower incidence of VT induction in group T regardless of antiarrhythmic treatment.

Conclusion: The DFT and the VFCL proved to be independent of the VF induction method. The T‐wave shock was more unlikely to induce VT during DFT testing. These results suggest that both methods are reliable in DFT determination, though T‐wave shock application is a more reliable method for DFT testing.
Pseudosinus Tachycardias Originating from Left Pulmonary Veins
Authors: MATSUO SEIICHIRO , YAMANE TEIICHI , DATE TARO , MOCHIZUKI SEIBU
Published: January 2006

The case of a 55‐year‐old man with LV dysfunction in whom the baseline cardiac rhythm falsely mimicked a sinus rhythm (SR) but actually originated from the left superior and inferior pulmonary vein (PV) is reported. The P waves before ablation were flat in leads I and V1, negative in lead aVL, and positive in leads II, III, aVF. After the left superior PV was isolated from the left atrium, another ectopic rhythm newly appeared from the left inferior PV. Interestingly, the LV systolic function improved after the resumption of the SR, thus suggesting that tachycardia‐induced cardiomyopathy might be involved in the mechanism of LV systolic disturbance.
The direct contribution of fish to lake phosphorus cycles
Authors: Griffiths D.
Published: January 2006

Abstract –  Published data are synthesised to assess the direct contribution of fish to the recycling of phosphorus across a lake productivity gradient. Phosphorus excretion rates by fish assemblages are more or less directly proportional to fish biomass, despite changes in mean body mass, species composition and diet with increasing lake productivity. Piecewise linear regression of published data shows for the first time that lacustrine fish biomass increases with total phosphorus (TP) concentration in the water column up to around 140 μg·TP·l−1 but levels off above that value, suggesting that fish contribute less to nutrient recycling as lake productivity increases. The results confirm previous findings that water column nutrient recycling by fish is much less important than by plankton and that fish are important nutrient stores in lakes. The contribution of fish to nutrient recycling is small because of their low turnover rates relative to other taxa.
Behaviour and growth of juvenile brown trout exposed to fluctuating flow
Authors: Flodmark L. E. W. , Forseth T. , L'Abée‐Lund J. H. , Vøllestad L. A.
Published: January 2006

Abstract – Parr of brown trout (Salmo truttaL.) were exposed to constant or fluctuating water level and flow in artificial outdoor stream channels during 21 days in three consecutive runs, and their individual behaviour and social interactions were monitored. Despite the large variation in flow, no clear differences in growth, which was generally poor, and behaviour were found between treatments. The signs of a social structure in the stream channels were very subtle and there were no clear relation between growth rate and aggressive/dominant behaviour in any of the treatments in accordance with findings in studies of growth and dominance in the wild. Thus, in regulated rivers, daily fluctuations in flow and water level (hydropeaking) are not likely to alter the behaviour of juvenile brown trout or affect their energy turnover negatively. Several studies now indicate that if stranding can be avoided, hydropeaking has relatively small direct effects on stream salmonids. Therefore, future research should focus on cascading ecological effects that may influence the productivity of the ecosystems in regulated rivers.
The prolactin family and pregnancy‐dependent adaptations
Authors: SOARES Michael J. , ALAM S. M. Khorshed , KONNO Toshihiro , HO‐CHEN Jennifer K. , AIN Ruparsri
Published: January 2006

The prolactin gene family represents species‐specific expansions of hormones/cytokines contributing to the regulation of pregnancy‐dependent adaptations. In this review, we discuss the prolactin family expansion in the mouse and rat, its linkage with viviparity and its potential role in regulating adaptations to physiological stressors.
Biology of the prolactin family in bovine placenta. II. Bovine prolactin‐related proteins: Their expression, structure and proposed roles
Authors: USHIZAWA Koichi , HASHIZUME Kazuyoshi
Published: January 2006

The placenta produces various peptides and steroid hormones that regulate placental function and fetal growth. Prolactin‐related proteins are peptides that are produced by the placenta and belong to the growth hormone/prolactin family, and have structural similarity to prolactin and placental lactogen. Although several prolactin‐related protein genes have been detected in bovine placenta, their expression profiles and functions are not clear. The main difficulties in examining their biological function is the similarity between their genes and the lack of information about their proteins. Recently, molecular biology methods have been used to detect some new bovine prolactin‐related proteins, and elucidate their biological functions. This review focuses on the structures, expression profiles and conceivable functions of prolactin‐related proteins in bovine placenta. With respect to their expression profiles, bovine prolactin‐related proteins fall into four groups: (i) those expressed around the implantation period; (ii) those that reach peak expression in the middle of gestation; (iii) those that increase with the progress of gestation, reaching a peak in late gestation; and (iv) those that reach a plateau in early gestation and are maintained at that level throughout gestation. Data indicate that bovine prolactin‐related proteins have different biological roles in different periods of gestation.  In situ monitoring suggests that bovine prolactin‐related protein‐I has a role in the attachment of trophoblast cells to endometrium during the early implantation period.
Comparison of homogeneity and heterogeneity of residual variance using random regression test‐day models for first lactation Japanese Holstein cows
Authors: FUJII Chie , SUZUKI Mitsuyoshi
Published: January 2006

Using a large‐scale data set that included first lactation test day records from 1975 to 2000 for Japanese Holsteins, genetic parameters for milk yield were estimated by using random regression (RR) test‐day models (TDM) with heterogeneous and homogeneous residual variances. It is necessary for the RR‐TDM to include a function that explains the shape of the lactation curve. The RR‐TDM with the LW curve, which combined Wilmink's curve and a Legendre polynomial, was used for fitting the model for milk yield. In recent years, increases in residual variance have been noted for Japanese dairy cattle. Thus, three kinds of heterogeneous residual variance over the calving year were considered: H1, H2 and HG. Linear and quadratic exponential functions for the calving year were used in H1 and H2, respectively. Residual variance of HG was divided into five groups according to calving year. Homogeneous residual variance was HO. All heterogeneous residual variances increased with calving year in an almost linear fashion. Residual variance increased over the study period. However, there is no need to consider heterogeneous residual variances in genetic evaluations, because the heterogeneity of residual variance over the years did not affect the ranking of top sires and cows.
Mapping of expressed sequence tag markers with a cDNA‐amplified fragment length polymorphism method in Japanese quail (Coturnix japonica)
Authors: SASAZAKI Shinji , HINENOYA Tomoko , FUJIMA Daisuke , KIKUCHI Shinichi , FUJIWARA Akira , MANNEN Hideyuki
Published: January 2006

In our previous study, a Kobe‐NIBS Japanese quail (KNQ) linkage map was constructed mainly using amplified fragment length polymorphism (AFLP) markers. In order to compare chicken and quail chromosomes, we developed expressed sequence tag (EST) markers derived from cDNA‐AFLP fragments and localized these markers on the linkage map. Using a total of 128 AFLP primer combinations, 24 polymorphic bands were obtained between a neurofilament‐deficient mutant quail line male and a muscular disorder quail line female, which were the parents of the KNQ resource family. Nine of the 24 markers were mapped by linkage analysis. These markers were mapped to seven linkage groups, namely 1, 2, 3, 6, 8, 15 and 42. A subsequent homology search using chicken genome sequences strongly suggests that these linkage groups correspond with chicken chromosomes 1, 2, 3, 5, 15, 23 and 26.
Effects of leptin and leptin peptide amide on the release of luteinizing hormone, growth hormone and prolactin from cultured porcine anterior pituitary cells
Authors: NONAKA Sumie , HASHIZUME Tsutomu , YAMASHITA Tetsuro
Published: January 2006

The present study was carried out to determine whether leptin or leptin (116–130) peptide amide (lep (116–130)), an active fragment of the native protein in rats, is able to stimulate the release of luteinizing hormone (LH), growth hormone (GH) or prolactin (PRL) from cultured porcine anterior pituitary (AP) cells in vitro. The AP cells were obtained from 6 month‐old pigs and were incubated for 3 h with 10−11−10−7 mol/L leptin or lep (116–130) after being cultured in Dulbecco's modified Eagle's medium for 3–4 days. Leptin significantly increased the concentration of LH and GH in the culture medium at concentrations of 10−8 and 10−7 mol/L, respectively, compared with the controls (P < 0.05). Leptin did not increase the concentration of PRL in the culture medium. In contrast to these results, no effects of lep (116–130) on the release of LH, GH or PRL were seen in the cultured cells. These results suggest that leptin stimulates the release of LH and GH by acting directly on porcine AP cells, and that a fragment of leptin protein comprising amino acids 116–130 is not associated with the secretion of hormones in pigs.