bluuebunny/crossref_metadata_2025 huggingface dataset:
Telomere length is a prognostic factor in neuroblastoma
Authors: Ohali Anat , Avigad Smadar , Ash Shifra , Goshen Yacov , Luria Drorit , Feinmesser Meora , Zaizov Rina , Yaniv Isaac
Published: August 2006

BACKGROUND.

Maintenance of telomeres, in most instances by reactivation of telomerase, is obligatory for the indefinite proliferation of tumor cells. The objective of this study was to evaluate telomere length and telomerase activity (TA) as markers for progression and prognosis in neuroblastoma.

METHODS.

Primary tumor samples from 51 patients were analyzed for telomere length and TA and were correlated with known prognostic parameters and outcome.

RESULTS.

Telomere length had a highly significant correlation with prognosis (P = .007). Short telomeres were predictive of a favorable prognosis, whereas long or unchanged telomeres were predictive of a poor outcome. For the first time to their knowledge, the authors have shown that, within the high‐risk group patients, telomere length could define a favorable subgroup that had a progression‐free survival (PFS) rate of 86% compared with a PFS rate of 36% for patients with more adverse disease, which is the expected PFS rate for such patients (P = .04). In a multivariate analysis, telomere length was the most significant prognostic parameter (P = .032). TA was correlated significantly with outcome and with known prognostic factors. High TA and low TA were associated with adverse and favorable outcomes, respectively (P = .01).

CONCLUSION.

The results of this investigation suggested that telomere length is a highly significant prognostic parameter of clinical relevance in patients with neuroblastoma. In high‐risk patients, telomere length was the sole significant parameter that identified a group of patients who had a favorable prognosis. The authors suggest that telomere length should be included in the recommended diagnostic investigations for patients with neuroblastoma. Cancer 2006. © 2006 American Cancer Society.
Behavioral assessment of neuropathic pain in preclinical models
Authors: Honore Prisca
Published: August 2006

One of the greatest challenges to creating more efficacious medications for pain control has been the heterogeneity of the “chronic pain condition.” It is now appreciated that distinct mechanisms contribute to physiological pain, to pain arising from tissue damage, and to pain arising from injury to the nervous system. Unlike nociceptive pain, neuropathic pain can persist long after the initiating event has healed and is the expression of an abnormal processing of sensory information by the nervous system. Neuropathic pain is very heterogeneous and can originate from nerve injury associated with a wide array of conditions such as direct trauma to nerves, inflammation/nerve compression, metabolic diseases, infections, tumors, toxins, and primary neurological diseases. To study pain transmission, identify new pain targets, and characterize the potential analgesic profile of novel compounds for neuropathic pain relief, an array of experimental animal pain models has been developed mainly in rodents, trying to reflect as many “neuropathic pain conditions” as possible. However, one should remember that even for patients labeled under the same “neuropathic pain disease,” the pain experience is unique and can be very different from one patient to the other, increasing the difficulties of modeling such painful states in animal models. The present review will describe the most utilized animal models of neuropathic pain and the various methods used to assess degrees of hyperalgesia and allodynia in these animals, outlining similarities and differences observed under various preclinical “neuropathic pain conditions.” Drug Dev. Res. 67:302–307, 2006. © 2006 Wiley‐Liss, Inc.
Neural‐glial interaction in the spinal cord for the development and maintenance of nerve injury‐induced neuropathic pain
Authors: Ji Ru‐Rong , Wen Yeong‐Ray
Published: August 2006

Damage to the nervous system often results in neuropathic pain. Current treatment for this disabling state is unsuccessful due to our incomplete understanding of cellular mechanisms causing this pain. Although glial cells were largely ignored in most textbooks of pain, accumulating evidence over the last decade indicates an important role of glial cells in the pathogenesis of pain. Both microglia and astroglia are activated in the spinal cord after peripheral nerve injury. Importantly, activated microglia and astroglia produce multiple inflammatory mediators and neuromodulators, acting on primary afferents or dorsal horn neurons and leading to an enhancement and maintenance of dorsal horn neuron sensitization and subsequent pain sensitization. This neural‐glial interaction after peripheral nerve injury is likely to be triggered by signaling molecules released in the spinal cord from central terminals of damaged sensory neurons, stimulating surrounding glial cells. In addition, there is a microglial‐astroglial interaction; microglia activation occurs before astroglial activation and is known to cause astroglial activation. Glial activation is further enhanced by microglial‐microglial interaction and astroglial‐astroglial interaction. Many signaling molecules (e.g., MAP kinases, ATP receptors, chemokine receptors) are exclusively activated in spinal microglia or astroglia after nerve injury, and an inhibition of these molecules can attenuate neuropathic pain. Since traditional pain‐killers are designed against neuronal targets and are only partially effective to treat neuropathic pain, searching for signaling molecules that are induced in spinal glia in neuropathic pain conditions will identify novel targets for the management of this debilitating chronic pain. Drug Dev. Res. 67:331–338, 2006. © 2006 Wiley‐Liss, Inc.
The endocannabinoid and endovanilloid systems and their interactions in neuropathic pain
Authors: Maione Sabatino , Starowicz Katarzyna , Palazzo Enza , Rossi Francesco , Di Marzo Vincenzo
Published: August 2006

Under physiological conditions, nociception has a protective role, allowing an individual to react appropriately to the noxious stimulus and to minimize its effects. On the contrary, chronic pain arises from damage to the nervous system and is persistent. Mechanisms, symptoms, and signs of neuropathic pain have been the subject of extensive studies, but still there is no single, well‐tolerated drug that is effective in all types of neuropathic pain. Currently, there is a growing amount of evidence on the analgesic properties of cannabinoids in nociceptive pathways. Interestingly, recent data also implicate an endogenous cannabinoid ligand, anandamide, as an agonist at the capsaicin VR1/TRPV1 receptor. Herein, we review the available evidence in favour of cannabinoid and vanilloid alleviation of hyperalgesia and allodynia, two typical symptoms of neuropathic pain. The most important findings regarding CB1, TRPV1 receptors, and neuropathic pain are discussed in detail. We also consider the implications of combined studies correlating the endocannabinoid and vanilloid signalling systems as promising therapeutic approaches for new analgesic drugs. Collectively, the investigations reviewed here support the use of drugs targeting the endocannabinoid and endovanilloid systems in the treatment of chronic inflammation and neuropathic pain states. Drug Dev. Res. 67:339–354, 2006. © 2006 Wiley‐Liss, Inc.
Neuronal nicotinic acetylcholine receptors as a target for the treatment of neuropathic pain
Authors: Meyer Michael D.
Published: August 2006

Neuronal nicotinic acetylcholine receptor (nAChR) agonists have been demonstrated to exhibit antinociceptive, antihyperalgesic, and antiallodynic effects across a range of preclinical models of pain. Yet, to date, no drugs have been successfully developed and approved for the treatment of pain from this pharmacological class. In this overview, the mechanism and site of action of nAChR agonists in models of neuropathic pain, as well as the current status and future prospects for the development of drugs from this class for the treatment of neuropathic pain, will be discussed. Drug Dev. Res. 67:355–359, 2006. © 2006 Wiley‐Liss, Inc.
Voltage‐gated sodium channels as molecular targets for neuropathic pain
Authors: Priestley Tony , Hunter John C.
Published: August 2006

The peripheral nervous system relies upon voltage‐gated sodium channels for encoding and transmitting modality‐specific information into and out of the CNS. These channels are powerful transducers, they signal both pleasant and noxious sensations. They are also considered prime suspects for creating and sustaining the inappropriate excitability in neuronal membranes that is a hallmark of any chronic neuropathic pain syndromes. Curtailing such “pathological hyperexcitability” represents a credible approach to the clinical management of neuropathic pain and this review considers the evidence favoring sodium channels as key players in the injury‐induced hyperexcitability and as targets for pharmacological intervention. Currently used sodium channel therapeutics are discussed together with their limitations and issues. Recent developments in sodium channel biology and pathophysiology are reviewed and ideas for next‐generation sodium channel blocking drugs are considered. Drug Dev. Res. 67:360–375, 2006. © 2006 Wiley‐Liss, Inc.
Purinergic control of neuropathic pain
Authors: McGaraughty Steve , Jarvis Michael F.
Published: August 2006

Understanding the purinergic modulation of neurotransmission has been greatly advanced in recent years by the development of receptor‐selective compounds and the ability to manipulate expression of specific receptor subtypes. The use of these tools has resulted in a wealth of evidence demonstrating the importance of adenosine (ADO)‐sensitive and adenosine 5′‐triphosphate (ATP)‐sensitive receptors (P1 and P2, respectively) to the development of pathological nociceptive states, including neuropathic pain. It is likely that more than one of these P1 and P2 receptor subtypes is involved in the modulation and/or transmission of pathological nociceptive signals. ATP, acting at sensory neurons in the periphery and spinal cord as well as on glial cells contributes to neural excitability, is pro‐nociceptive, and likely participates in the sensitization of the central nervous system during chronic pain. ATP is a non‐selective agonist for several ionotropic P2X and metabotropic P2Y receptor subtypes. The homomeric P2X3, P2X4, P2X7, heteromeric P2X2/3, and possibly P2Y2, P2Y4, and P2Y6have all been linked to neuropathic pain in preclinical models. In contrast, ADO generally functions as an endogenous inhibitory neuromodulator and produces these effects by activating on a family of G‐protein coupled cell surface receptors (A1, A2A, A2B, A3). Systemic and intrathecal administration of ADO itself, both preclinically and clinically, reduces neuropathic hypersensitivity, and these effects are likely mediated through activity at the A1receptor subtype. In order to reduce side effects typically related to the administration of ADO, compounds have been identified to allosterically modulate the A1receptor or to limit ADO reuptake. These compounds potently affect neuropathy‐related sensitivity with an improved therapeutic window. Thus, advances in the pharmacology of purinergic neurotransmission have led to the development of new strategies to enhance the endogenous actions of ADO and to limit the neuro‐excitatory effects of ATP. The contributions of the various purinergic receptors to states of neuropathic pain will be reviewed. Drug Dev. Res. 67:376–388, 2006. © 2006 Wiley‐Liss, Inc.
Modulation of neurotrophic growth factors as a therapeutic strategy for neuropathic pain
Authors: Sah Dinah Y.W. , Porreca Frank , Ossipov Michael H.
Published: August 2006

Neurotrophic growth factors have tremendous untapped potential for the treatment of neurological injuries and diseases. In contrast to specific neurotransmitter modulators or ion channel blockers, a neurotrophic growth factor profoundly impacts multiple molecular pathways within a cell, with the possibility of exerting broad, and potentially “disease‐modifying” effects that may counteract the underlying pathology. Although numerous clinical trials have been carried out with the prototypic neurotrophic growth factors, including most notably NGF for diabetic neuropathy and GDNF for Parkinson's disease, none of these trials have been successful to date in providing compelling data for drug approval. The apparent lack of translation from the bench to the clinic may be considered in the context of our current understanding of the neurotrophic growth factors, especially mechanism of action, efficacy in animal models of disease, and safety and tolerability, and how these factors relate to clinical trial design. The application of this new knowledge to future clinical trials of neuropathic pain may provide opportunities for successful clinical development of neurotrophic growth factor modulators. Drug Dev. Res. 67:389–403, 2006. © 2006 Wiley‐Liss, Inc.
T‐type calcium channels: an emerging therapeutic target for the treatment of pain
Authors: Snutch Terrance P. , David Laurence S.
Published: August 2006

It has become generally accepted that presynaptic high voltage–activated N‐type calcium channels located in the spinal dorsal horn are a validated clinical target for therapeutic interventions associated with severe intractable pain. Low voltage–activated (T‐type) calcium channels play a number of critical roles in nervous system function, including controlling thalamocortical bursting behaviours and the generation of spike wave discharges associated with slow wave sleep patterns. There is a growing body of evidence that T‐type calcium channels also contribute in several ways to both acute and neuropathic nociceptive behaviours. In the one instance, the Cav3.1 T‐type channel isoform likely contributes an anti‐nociceptive function in thalamocortical central signalling, possibly through the activation of inhibitory nRT neurons. In another instance, the Cav3.2 T‐type calcium channel subtype acts at the level of primary afferents in a strongly pro‐nociceptive manner in both acute and neuropathic models. While a number of classes of existing clinical agents non‐selectively block T‐type calcium channels, there are no subtype‐specific drugs yet available. The development of agents selectively targeting peripheral Cav3.2 T‐type calcium channels may represent an attractive new avenue for therapeutic intervention. Drug Dev. Res. 67:404–415, 2006. © 2006 Wiley‐Liss, Inc.
Rapid three‐dimensional imaging and analysis of the beating embryonic heart reveals functional changes during development
Authors: Liebling Michael , Forouhar Arian S. , Wolleschensky Ralf , Zimmermann Bernhard , Ankerhold Richard , Fraser Scott E. , Gharib Morteza , Dickinson Mary E.
Published: August 2006

We report an accurate method for studying the functional dynamics of the beating embryonic zebrafish heart. The fast cardiac contraction rate and the high velocity of blood cells have made it difficult to study cellular and subcellular events relating to heart function in vivo. We have devised a dynamic three‐dimensional acquisition, reconstruction, and analysis procedure by combining (1) a newly developed confocal slit‐scanning microscope, (2) novel strategies for collecting and synchronizing cyclic image sequences to build volumes with high temporal and spatial resolution over the entire depth of the beating heart, and (3) data analysis and reduction protocols for the systematic extraction of quantitative information to describe phenotype and function. We have used this approach to characterize blood flow and heart efficiency by imaging fluorescent protein‐expressing blood and endocardial cells as the heart develops from a tube to a multichambered organ. The methods are sufficiently robust to image tissues within the heart at cellular resolution over a wide range of ages, even when motion patterns are only quasiperiodic. These tools are generalizable to imaging and analyzing other cyclically moving structures at microscopic scales. Developmental Dynamics 235:2940–2948, 2006. © 2006 Wiley‐Liss, Inc.
Germ cell restricted expression of chick Nanog
Authors: Cañón Susana , Herranz Cristina , Manzanares Miguel
Published: August 2006

Nanog is a pluripotency‐associated factor expressed in embryonic stem cells and in the epiblast and primordial germ cells of the mouse embryo. We have identified the chick orthologue of Nanog and found that its expression is limited to primordial germ cells in the early embryo and is not found throughout the epiblast. Genomic analysis has shown that Nanog is an amniote‐specific gene and is absent from anamniotes and invertebrates. Furthermore, other pluripotency associated genes that are located in close proximity to Nanog in human and mouse are absent from the chick genome. Such observations lead to a scenario of sequential addition of novel genes to a genomic region associated to pluripotency. These results have profound implications for the study of the evolution of pluripotent lineages in the embryo and of vertebrate stem cells. Developmental Dynamics 235:2889–2894, 2006. © 2006 Wiley‐Liss, Inc.
Endotoxin modulates the capacity of CpG‐activated liver myeloid DC to direct Th1‐type responses
Authors: Abe Masanori , Tokita Daisuke , Raimondi Giorgio , Thomson Angus W.
Published: August 2006

DC are believed to play important roles in the induction and regulation of immune responses in the liver, an organ implicated in peripheral tolerance. Since the liver is located downstream of the gut, it is constantly exposed to bacterial LPS. Our recent observations indicate that prior exposure to endotoxin modulates subsequent liver DC responses to this TLR4 ligand. In this study, we demonstrate that endotoxin modifies the capacity of mouse liver myeloid DC (MDC) activated by CpG (TLR9 ligand) to direct Th1‐type responses. IL‐12 production by liver MDC was significantly lower than that of spleen MDC following CpG or Imiquimod (R837; TLR7 ligand) activation in vitro. In addition, allogeneic T cells stimulated by CpG‐activated liver MDC secreted significantly lower levels of IFN‐γ than T cells stimulated with CpG‐activated spleen MDC. A similar effect on liver DC was observed in response to in vivo CpG administration. This effect may be explained by exposure of the DC to endotoxin, because LPS attenuated IL‐12 production by CpG‐stimulated liver MDC, both in vitro and in vivo. Moreover, attenuation of the response to CpG was not observed in liver MDC from TLR4‐mutant (C3H/HeJ) mice, in which TLR4 signaling is impaired. These data suggest that endotoxin‐induced ‘cross‐tolerance’ to TLR ligands in liver DC may contribute to down‐regulation of hepatic immune responses.
The co‐expression of 2B4 (CD244) and CD160 delineates a subpopulation of human CD8+ T cells with a potent CD160‐mediated cytolytic effector function
Authors: Rey Jérôme , Giustiniani Jérôme , Mallet Francoise , Schiavon Valèrie , Boumsell Laurence , Bensussan Armand , Olive Daniel , Costello Régis T
Published: August 2006

Within human CD8+ T lymphocytes, the CD27−CD45RAhigh or CD56+ phenotypes contribute to precisely define the cells with CTL effector function. Novel markers were demonstrated to correlate with CTL properties, such as the 2B4 (CD244) receptor, a member of the CD2 subset of the immunoglobulin superfamily or the glycosylphosphatidylinositol‐anchored CD160 receptor. We performed a study of these markers to further define the population of effectors with CTL functions. Here we show that cytotoxic subpopulations defined by surface markers CD160, CD56 and CD57 are mostly contained in the 2B4+CD8+ T cell population. Expression of CD160 identifies two populations in the 2B4+ population. The 2B4+CD160+ subset expresses a bona fide CTL phenotype. The co‐expression of 2B4 and CD160 defines T cells containing high amounts of perforin and granzyme B. During CTL ontogeny, an up‐regulation of 2B4 and CD160 is observed from a naive to a terminally differentiated phenotype. Finally, we demonstrated that CD160 triggering failed to induce cytotoxicity per se, but costimulated CD3‐redirected killing. We conclude that the co‐expression of 2B4 and CD160 defines a CD8+ T lymphocyte subpopulation with high CTL activity.
Contribution of the PD‐1 ligands/PD‐1 signaling pathway to dendritic cell‐mediated CD4+ T cell activation
Authors: Kuipers Harmjan , Muskens Femke , Willart Monique , Hijdra Daniëlle , van Assema Friso B. J. , Coyle Anthony J. , Hoogsteden Henk C. , Lambrecht Bart N.
Published: August 2006

Dendritic cells (DC) are extremely proficient inducers of naïve CD4+ T cell activation due to their high expression level of peptide‐MHC and an array of accessory molecules involved in cell migration, adhesion and co‐signaling, including PD‐1 ligand 1 (PD‐L1) and PD‐1 ligand 2 (PD‐L2). Whether PD‐L1 and PD‐L2 have a stimulatory or inhibitory function is a matter of debate, and could be partially dependent on the model system used. In this study we examined the role of PD‐L1 and PD‐L2 expressed by DC in naïve CD4+ T cell activation in a more physiologically relevant model system, using OVA‐specific T cells in combination with various levels of TCR stimulation. Overexpression of PD‐L1 or PD‐L2 by DC did not inhibit T cell proliferation, even when B7–1 and B7–2 mediated costimulation was absent, although IL‐2 production was consistently decreased. Surprisingly, blocking PD‐L1 and PD‐L2 with soluble programmed death‐1 (sPD‐1) also inhibited T cell activation, probably via reverse signaling via PD‐L1 and/or PD‐L2 into DC, leading to reduced DC maturation. This study suggests a relatively minor contribution of PD‐1 ligands in DC‐driven CD4+ T cell activation and provides evidence for reverse signaling by PD‐L1 and PD‐L2 into DC, resulting in a suppressive DC phenotype.
NK cells of human secondary lymphoid tissues enhance T cell polarization via IFN‐γ secretion
Authors: Morandi Barbara , Bougras Gwenola , Muller William A. , Ferlazzo Guido , Münz Christian
Published: August 2006

Human secondary lymphoid tissues harbor NK cells that predominantly secrete cytokines in response to activation. Here, we demonstrate that these immunoregulatory NK cells assist in the Th1 polarization of primary immune responses, induced by dendritic cells. Tonsilar, but not peripheral blood NK cells enhanced the expansion of IFN‐γ‐producing CD4+ T cells via their superior ability to produce IFN‐γ. Addition of IFN‐γ increased Th1 polarization while antibody blocking of this cytokine abolished NK cell‐dependent Th1 polarization. Our data suggest that NK cells in secondary lymphoid organs assist priming of Th1 cells via cytokine secretion and this effect should be harnessed during vaccination against viruses and tumors.
Organocatalytic Asymmetric Michael Addition of 2,2‐Dimethyl‐1,3‐dioxan‐5‐one to Nitro Alkenes Employing Proline‐Based Catalysts
Authors: Enders Dieter , Chow Sharon
Published: August 2006

The organocatalytic asymmetric Michael addition of 2,2‐dimethyl‐1,3‐dioxan‐5‐one (1) was performed with various nitro alkenes 2 using a number of proline‐based catalysts (A–M) affording polyfunctional nitro ketones 3. Reverse diastereoselectivity was observed with the diphenylprolinol catalyst J, and the best diastereo‐ and enantiomeric excesses were achieved with the sulfonamide catalyst M (de = 84–98 %, ee = 81–86 %). (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Why minority group members resent impostors
Authors: Warner Ruth , Hornsey Matthew J. , Jetten Jolanda
Published: August 2006

An impostor is defined as somebody who publicly lays claim to an identity while simultaneously disguising their failure to fulfill key criteria for group membership. The current study aimed to identify why minority group members feel negatively toward impostors. In two experiments, gay participants evaluated a person who claimed to be either gay or straight. In half of the conditions the target's claims for identity were consistent with their behavior, and in the other half the target's claims for identity were inconsistent with their behavior (impostors). Participants perceived a straight target that claimed to be gay to be doing more damage to the group than a consistent straight target. This effect was mediated by ratings of the extent to which the target was threatening the distinctiveness of gay identity. Furthermore, a gay target who claimed to be straight was seen to be less likeable and was seen to be doing more damage to the group than a consistent gay target, effects that were mediated by the extent to which the target was perceived to feel shame about their group identity. Implications of the results for our understanding of impostorism are discussed. Copyright © 2006 John Wiley & Sons, Ltd.
Opinion‐based group membership as a predictor of commitment to political action
Authors: Bliuc Ana‐Maria , McGarty Craig , Reynolds Katherine , Muntele Daniela
Published: August 2006

Research on group identification has shown it to be a surprisingly weak predictor of intentions to take large‐scale social action. The weak links may exist because researchers have not always examined identification with the type of group that is most relevant for predicting action. Our focus in two studies (one in Romania and one in Australia, both Ns = 101) was on opinion‐based groups (i.e. groups formed around shared opinions). We found that social identification with opinion‐based groups was an excellent predictor of political behavioural intentions, particularly when items measuring identity certainty were included. The results provide clear evidence of the role of social identity constructs for predicting commitment to social action and complement analyses of politicised collective identity and crowd behaviour. Copyright © 2006 John Wiley & Sons, Ltd.
Development of the positive–negative asymmetry effect: in‐group exclusion norm as a mediator of children's evaluations on negative attributes
Authors: Rutland Adam , Brown Rupert J. , Cameron Lindsey , Ahmavaara Anni , Arnold Katie , Samson Jenni
Published: August 2006

Two studies were conducted that go beyond previous research by examining when and why children might show intergroup bias in the attribution of positive, but not negative traits (PNAE: the positive–negative asymmetry effect, Mummendey & Otten, 1998, European review of social psychology, Vol. 9). In Study 1 (n = 107) children completed a ‘mixed’ trait attribution task in a dichotomous group context. As predicted there was a developmental trend between 7 and 12 years of age in the PNAE. The 7‐year olds were the only age group not to show the effect. Study 1 also found a quadratic developmental trend in children's national intergroup bias. Study 2 (n = 62) replicated the developmental path of the PNAE found in Study 1 using a wider age range of 6–16 years. This study used a ‘mixed’ list of traits which were not only antonyms and a procedure that made the positive and negative trait dimensions explicitly independent. Significantly, Study 2 found in‐group exclusion norm partially mediated the development of the PNAE. These findings support an account of the positive–negative asymmetry effect based upon normative processes. Copyright © 2006 John Wiley & Sons, Ltd.
How regulatory focus influences consumer behavior
Authors: Werth Lioba , Foerster Jens
Published: August 2006

According to Higgins (1997) the theory of regulatory focus says that in terms of both information processing and motivation it makes a difference whether people have a promotion or prevention focus. In this paper, this theory will be applied to the area of consumer psychology. In three experiments we show that consumer's regulatory focus either measured or induced in a given situation influences product evaluations. Study 1 shows that consumers are interested in different product features depending on their focus; whereas in the prevention focus they are more interested in safety‐oriented aspects, in the promotion focus they concentrate more on comfort‐oriented qualities. In Study 2, a typical prevention product and a typical promotion product are compared with one another and data shows that focus compatible products are evaluated more positively. In Study 3 we demonstrate that advertisments that correspond to the focus of the consumer lead to more positive evaluations of the product than advertisments that are incompatible with the focus of the consumer. Theoretical and practical implications will be discussed. Copyright © 2006 John Wiley & Sons, Ltd.
Group polarization and choice‐dilemmas: how important is self‐categorization?
Authors: Krizan Zlatan , Baron Robert S.
Published: August 2006

Self‐categorization proponents (e.g., Turner, 1991) assume that group polarization occurs because discussants wish to differentiate themselves from outgroup positions and implicitly think of such groups even when they are not specifically mentioned. Ingroup/outgroup salience is thought to heighten such effects. To examine this view, we had participants discuss Choice Dilemma items either with or without explicit knowledge of outgroup positions. Contrary to a self‐categorization account, this manipulation of outgroup salience did not affect the degree of group polarization. In addition, rating measures revealed little spontaneous consideration of outgroup positions on the part of participants, nor was consideration of outgroup positions related to degree of polarization. Group members did show evidence of ingroup identification, but this identification was unrelated to participants' post‐discussion conformity to the group consensus. Taken as a whole, these results suggest distinct limits to the self‐categorization interpretation of group polarization involving Choice Dilemmas. Copyright © 2006 John Wiley & Sons, Ltd.
Social identity and the attitude–behaviour relationship: effects of anonymity and accountability
Authors: Smith Joanne R. , Terry Deborah J. , Hogg Michael A.
Published: August 2006

Two experiments examined the impact of anonymity and accountability on the expression of group‐mediated attitude‐behaviour consistency. In Study 1, low and high identifiers (N = 106) were exposed to an attitude‐congruent norm and provided information about their intentions under anonymous and in‐group accountable conditions. In Study 2, salience of identity was manipulated, and participants (N = 185) were exposed to either an attitude‐congruent or an attitude‐incongruent norm, and provided information on their intentions and behaviour under anonymous and in‐group accountable conditions. In both studies, accountability elicited group‐normative attitudes and behaviour among individuals for whom the group was not a salient basis for self‐definition. When the group was a salient basis for self‐definition, the expression of attitude‐consistent intentions and behaviour was greater in anonymous conditions. It is suggested that strategic effects, such as those that occur in the presence of an in‐group audience, influence displays of group‐normative attitude–behaviour consistency. Copyright © 2006 John Wiley & Sons, Ltd.
Sex ratio and mate preferences: a cross‐cultural investigation
Authors: Stone Emily A. , Shackelford Todd K. , Buss David M.
Published: August 2006

Sex ratio is the number of men per 100 reproductive‐age women within a specified mating pool. We generated and tested two hypotheses about the cross‐cultural relationships between sex ratio and mate preferences using preference ratings of 18 characteristics provided by 9809 participants and corresponding sex ratio data secured from an international organization. The Classical Sex Ratio Mate Preference Shifts Hypothesis predicts that in imbalanced sex ratio societies, the more numerous sex will lower their standards, to facilitate acquisition of a partner of the less numerous sex. The Alternative Sex Ratio Mate Preference Shifts Hypothesis predicts that in lower sex ratio societies, men will lower their standards to secure more short‐term matings, whereas women will raise their standards to avoid deception by men seeking short‐term relationships. Results supported the Classical Sex Ratio Mate Preference Shifts Hypothesis for men, and the Alternative Sex Ratio Mate Preference Shifts Hypothesis for women. Discussion addresses limitations of the current research and highlights future directions for research on the relationships between sex ratio and mating psychology and behavior. Copyright © 2006 John Wiley & Sons, Ltd.
The impact of regulatory focus on affective responses to social discrimination
Authors: Sassenberg Kai , Hansen Nina
Published: August 2006

The impact of individuals' regulatory focus and the domain of outcomes (non‐gains vs. losses) on the target's affective responses to social discrimination were tested. Based on regulatory focus theory (Higgins, 1997), it was predicted that a prevention focus would lead to more anger and agitation after social discrimination, because experiencing social discrimination is similar to experiencing failure. This pattern was predicted to be more pronounced when social discrimination was based on losses than when social discrimination was based on non‐gains (i.e., when the in‐group was evaluated more negatively vs. less positively compared to the out‐group). The results of three studies using chronic and situationally induced regulatory focus confirmed these predictions. No effect was found for the promotion focus. Copyright © 2006 John Wiley & Sons, Ltd.
Retracted:When different is better: performance following upward comparison
Authors: Johnson Camille S. , Stapel Diederik A.
Published: August 2006

The attainability of upward social comparisons is known to affect self‐evaluative responses. The consequences for performance, however, are less well understood. We suggest that demoralizing upward comparisons with unattainable targets may lead to improved performance when the target and performance domains are mismatched. For example, comparison with a target that has been successful in an analytic domain should lead to better performance in a verbal domain. This improvement in performance occurs because increased performance in alternative domains provides an opportunity for self‐evaluation maintenance. In three studies, we demonstrate that upward comparisons to targets whose successes are perceived as threatening lead to improved performance when the task and performance domain do not match, but no improvements when the domains match. Copyright © 2006 John Wiley & Sons, Ltd.
Altruism and egoism: prosocial motivations for helping depend on relationship context
Authors: Maner Jon K. , Gailliot Matthew T.
Published: August 2006

Findings from the current study suggest that the link between helping and empathic concern—a hypothesized motivator of altruistic behavior—may be more pronounced in the context of kinship relationships than among strangers. Participants expressed their willingness to help a kin‐member or stranger in specific need situations. Putative mediators of helping (empathic concern, general negative affect, perceptions of oneness) were measured. Empathic concern appeared to partially mediate effects of relationship context on willingness to help. Moreover, while controlling for egoistic motivators (negative affect, oneness), empathic concern was linked to participants' willingness to help a kin‐member but not a stranger. Findings suggest that factors motivating prosocial action in close relationships may be different from those that motivate helping among strangers. Copyright © 2006 John Wiley & Sons, Ltd.
When the rich contribute more in public good dilemmas: the role of provision point level
Authors: De Cremer David
Published: August 2006

The present research examined the effects of endowment size, provision point level and the opportunity to voice one's opinion on contributions in asymmetric public good dilemmas. Results from a first experiment showed that group members endowed with more resources contributed more when the required threshold for obtaining a public good was high rather than low. ‘Rich’ participants who reported that their personal contribution was more critical for success contributed more. However, most groups failed to surpass the high provision point threshold level. Results from a second experiment reveal that ‘rich’ participants given voice, contributed more than ‘rich’ participants not given a voice. Voice contributed to greater feelings of inclusiveness, higher contributions and increased the likelihood that the group surpassed the high provision point level. Copyright © 2006 John Wiley & Sons, Ltd.
Considering reasons for a value influences behaviour that expresses related values: an extension of the value‐as‐truisms hypothesis
Authors: Karremans Johan C.
Published: August 2006

Previous research has demonstrated that value‐congruent behaviour is increased after people have considered reasons for or against the value (since values typically lack cognitive support). The present research importantly extends these previous findings. Specifically, based on the reasoning that values can be categorised into different motivational types, it was predicted that considering reasons (i.e. providing cognitive support) for or against a specific value should increase behaviour that expresses a related value. Two studies provided strong support for this central prediction. In Study 1, participants who were asked to consider reasons for or against the values of honesty and loyalty were especially likely to engage in helping behaviour. In Study 2, participants who considered reasons for the value of helpfulness were especially likely to behave in an egalitarian manner (compared to participants who did not consider reasons, and participants who were merely primed with helpfulness). The implications of these findings for when and why considering reasons for a value influences value‐expressive behaviour, as well as some practical implications, are discussed. Copyright © 2006 John Wiley & Sons, Ltd.
DNA damage in Pakistani pesticide‐manufacturing workers assayed using the Comet assay
Authors: Bhalli Javed A. , Khan Q.M. , Nasim A.
Published: August 2006

The production and use of chemical pesticides has increased in recent years. Although the increased use of pesticides may benefit agriculture, they are also the potential source of environmental pollution, and exposure to pesticides can have negative consequences for human health. In the present study, we have assessed DNA damage in blood leukocytes from 29 Pakistani pesticide‐factory workers and 35 controls of similar age and smoking history. The workers were exposed to various mixtures of organophosphates, carbamates, and pyrethroids. DNA damage was measured with the single cell gel electrophoresis (SCGE) assay or Comet assay, using the mean comet tail length (μm) as the DNA damage metric. Exposed workers had significantly longer comet tail lengths than the controls (mean ± SD 19.98 ± 2.87 vs. 7.38 ± 1.48, P < 0.001). Of the possible confounding factors, smokers had significantly longer mean comet tail lengths than nonsmokers and exsmokers for both the workers (21.48 ± 2.58 vs.18.37 ± 2.28, P < 0.001) and the controls (8.86 ± 0.56 vs. 6.79 ± 1.31, P < 0.001), while age had a minimal effect on DNA damage (P > 0.05 and P < 0.05 for workers and controls, respectively). The results of this study indicate that occupational exposure to pesticides causes DNA damage. Environ. Mol. Mutagen., 2006. © 2006 Wiley‐Liss, Inc.
Simultaneous estimation of gene‐gene and gene‐environment interactions for numerous loci using double penalized log–likelihood
Authors: Tanck Michael W.T. , Wouter Jukema J. , Zwinderman Aeilko H.
Published: August 2006

Many common human diseases are considered to be caused by complex multifactorial processes. For these diseases, it is expected that numerous genetic and environmental factors and, possibly, their interactions play a role. Therefore, simultaneously analyzing the effects of numerous genes and environmental factors is a more realistic approach compared to single gene analyses, but the large number of genes and environmental factors pose a challenge, not in the least due to the limitations created by the tools available for analyzing such high‐dimensional models. In the present manuscript we propose a method that is capable of identifying “true” interactions in a setting where the number of effects to be estimated is very large and can even surpass the number of observations. Basically, all possible (interaction) effects are entered in a double penalized model, where main effects are ridge penalized, whereas the interactions are subjected to a least absolute shrinkage and selection operator (lasso) penalty. Results from the simulations and real data show that the proposed method is capable of detecting interactions even with relative small effect sizes.Genet.Epidemiol. 2006. © 2006 Wiley‐Liss, Inc.
Gene‐dropping vs. empirical variance estimation for allele‐sharing linkage statistics
Authors: Jung Jeesun , Weeks Daniel E. , Feingold Eleanor
Published: August 2006

In this study, we compare the statistical properties of a number of methods for estimating P‐values for allele‐sharing statistics in non‐parametric linkage analysis. Some of the methods are based on the normality assumption, using different variance estimation methods, and others use simulation (gene‐dropping) to find empirical distributions of the test statistics. For variance estimation methods, we consider the perfect variance approximation and two empirical variance estimates. The simulation‐based methods are gene‐dropping with and without conditioning on the observed founder alleles. We also consider the Kong and Cox linear and exponential models and a Monte Carlo method modified from a method for finding genome‐wide significance levels. We discuss the analytical properties of these various P‐value estimation methods and then present simulation results comparing them. Assuming that the sample sizes are large enough to justify a normality assumption for the linkage statistic, the best P‐value estimation method depends to some extent on the (unknown) genetic model and on the types of pedigrees in the sample. If the sample sizes are not large enough to justify a normality assumption, then gene‐dropping is the best choice. We discuss the differences between conditional and unconditional gene‐dropping. Genet. Epidemiol. 2006. © 2006 Wiley‐Liss, Inc.
Estimating haplotype relative risks in complex disease from unphased SNPs data in families using a likelihood adjusted for ascertainment
Authors: Carayol J. , Philippi A. , Tores F.
Published: August 2006

The understanding of complex diseases and insights to improve their medical management may be achieved through the deduction of how specific haplotypes may play a joint effect to change relative risk information. In this paper we describe an ascertainment adjusted likelihood‐based method to estimate haplotype relative risks using pooled family data coming from association and/or linkage studies that were used to identify specific haplotypes. Haplotype‐based analysis tends to require a large amount of parameters to capture all the information that leads to efficiency problems. An adaptation of the Stochastic Expectation Maximization algorithm is used for haplotypes inference from genotypic data and to reduce the number of nuisance parameters for risk estimation. Using different simulations, we show that this method provides unbiased relative risk estimates even in case of departure from Hardy‐Weinberg equilibrium.Genet. Epidemiol. 2006. © 2006 Wiley‐Liss, Inc.
Retroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiation
Authors: Zhou Yong‐Xing , Flint Nicole C. , Murtie Joshua C. , Le Tuan Q. , Armstrong Regina C.
Published: August 2006

Fibroblast growth factor 2 (FGF2) inhibits oligodendrocyte progenitor cell (OPC) differentiation during development and limits remyelination following chronic demyelination. The current study examines the mechanism underlying this effect of FGF2 expression on OPC differentiation. Retroviral lineage tracing demonstrates a direct in vivo effect of FGF receptor (FGFR) signaling on OPC differentiation. Retrovirus expressing a dominant negative FGFR construct (FGFRdn) and green fluorescent protein (GFP) was injected into the dorsal columns of postnatal day 7 (P7) mice followed by perfusion at P28. Among the GFP‐labeled cells, FGFRdn retrovirus generated a higher proportion of oligodendrocytes than did control infections. This result from FGFRdn expression in OPCs was similar to the result obtained in our previous study using control retrovirus in FGF2 null mice. Further, in vitro retroviral siRNA expression distinguishes the function of specific FGFR isoforms in OPC responses to FGF2. FGF2 inhibition of OPC differentiation was effectively blocked by siRNA targeted to FGFR1, but not FGFR2 or FGFR3. We propose a model of direct FGF2 activation of FGFR1 leading to inhibition of OPC differentiation. This signaling pathway may be an important regulator of oligodendrocyte generation during myelination in development and may perturb OPC generation of remyelinating oligodendrocytes in demyelinating disease. Published 2006 Wiley‐Liss, Inc.
TGF‐β1 potentiates astrocytic nitric oxide production by expanding the population of astrocytes that express NOS‐2
Authors: Hamby Mary E. , Hewett James A. , Hewett Sandra J.
Published: August 2006

Both transforming growth factor‐β1 (TGF‐β1) and nitric oxide synthase‐2 (NOS‐2) are upregulated under various neuropathological states. Evidence suggests that TGF‐β1 can either attenuate or augment NOS‐2 expression, with the prevailing effect dependent on the experimental paradigm employed and the cell‐type under study. The purpose of the present study was to determine the effect of TGF‐β1 on astrocytic NOS‐2 expression. In purified astrocyte cultures, TGF‐β1 alone did not induce NOS‐2 or NO production. However, NO production induced by lipopolysaccharide (LPS) plus IFNγ was enhanced by TGF‐β1 in a concentration‐dependent manner between 10 and 1,000 pg/mL. The presence of IFNγ was not necessary for this effect to occur, as TGF‐β1 enhanced NO production induced by LPS in a similar fashion. In cultures stimulated with LPS plus IFNγ, the enhancement of NO production by TGF‐β1 was associated with a corresponding increase in NOS‐2 mRNA and protein expression. Interestingly, immunocytochemical assessment of NOS‐2 protein expression demonstrated that TGF‐β1 augmented astrocytic NO production, specifically by increasing the pool of astrocytes capable of expressing NOS‐2 induced by either LPS (∼threefold) or LPS plus IFNγ (∼sevenfold). In a broader sense, our results suggest that TGF‐β1 recruits a latent population of astrocytes to respond to stimulation by pro‐inflammatory mediators. © 2006 Wiley‐Liss, Inc.
Hippocampal and cortical place cell plasticity: Implications for episodic memory
Authors: Frank Loren M. , Brown Emery N. , Stanley Garrett B.
Published: August 2006

In humans, the hippocampus is essential for storing episodic memories. These event memories require the rapid storage of novel associations, but little is known about the cellular correlates of such rapid plasticity. We studied patterns of activity and plasticity in the CA1 region of the hippocampus and in anatomically adjacent cortical regions as rats explored a novel arm of a maze to identify the neural correlates of hippocampally dependent memory formation. We found that hippocampal place fields exhibited three phenomena that may have direct relevance to the encoding of episodic memories: (1) very rapid plasticity upon exposure to the new environment, (2) instability in representations formed after short periods of exploration, and (3) a dissociation between the stability of a hippocampal representation and the apparent familiarity of a location. In contrast, cortical regions showed less dramatic changes. Taken together, these findings suggest that hippocampal activity undergoes a period of rapid reorganization during the encoding of novel information, and that even after this reorganization is complete, areas outside the hippocampus have not yet formed stable memories. © 2006 Wiley‐Liss, Inc.