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ZUSAMMENFASSUNG Hintergrund Sexualität spielt auch im höheren Lebensalter eine wichtige Rolle und ist mit der Lebensqualität verknüpft, doch wird dieser Zusammenhang weiterhin tabuisiert. Methoden Selektive Literaturübersicht ergänzt durch eigene klinische Erfahrungen zu Bedeutung, Einflussfaktoren und Stigmatisierung von Sexualität im Alter. Ergebnisse Körperliche und psychische Erkrankungen sowie Medikation haben Einfluss auf die Sexualität. Während die sexuelle Aktivität im hohen Lebensalter abnimmt, bleibt die sexuelle Zufriedenheit weiterhin bestehen. Doch haben sich aus objektiven, altersbedingt zunehmenden Einschränkungen Stigmata entwickelt, die das Bild von sexueller Gesundheit im Alter prägen. Neben der öffentlichen Stigmatisierung spielt auch die institutionelle Stigmatisierung eine wichtige Rolle; so fehlt meist ein offenes Ansprechen des sexuellen Erlebens im Arzt-Patienten-Kontakt. Fazit Die medizinischen Bedingungen für eine erfüllte Alterssexualität sind besser denn je. Medizinisches Personal sollte nicht nur mögliche Erkrankungen sowie Polypharmazie als Risikofaktoren für Beeinträchtigung im Blick haben, sondern auch die sexuelle Gesundheit ihrer Patienten in jedem Lebensalter unterstützen.

We study the effect of communication in an experimental game where cooperation is consistent with equilibrium play. We examine two methodological questions which affect many studies of communication in games, particularly those studying the relationship between communication and cooperation in supergames. We show that making it easier for subjects to reach an agreement (by allowing more rounds of communication) does not increase cooperation with a limited message space treatment. Thus, limited message space treatments are not a good substitute for the use of chat. Making the game longer, thereby making the connection between the first period and the continuation game more obvious, also has little impact on cooperation. For both the two- and three-period versions of our game we find substantial amounts of contingent play. This implies that use of a finitely repeated game, which has a number of methodological advantages, maintains the main properties of the underlying supergame.

In 2012–2013 the European Commission has had particularly prominent merger cases, with two prohibitions of transactions and several clearances with far-reaching remedies. In these cases economic analysis has been tightly integrated into the general argument of the Commission and became central to the outcome of the cases. Based on economic theory and supporting data, the Commission has pursued novel economic theories of harm and challenged some economically dubious “common wisdom” in merger assessment. The second area in which economic analysis has had a major impact is in state aid modernization. The new regional aid guidelines of 2013 have moved the rules much closer to economic thinking about effective regional aid and introduced requirements for economic ex-post analysis. Finally, the decisions on the e-books case reflect close cross-Atlantic cooperation with respect to the economic analysis and the design of appropriate remedies. This article reports on a number of examples for the most important cases.

With the widespread use of atypical or second-generation antipsychotics, switching treatment has become current practice and more complicated, as the pharmacological profiles of these agents differ substantially despite their similarity in being 'atypical'. All share the ability to block dopamine D₂ receptors, and most of them also block serotonin 5-HT2A receptors. Apart from these common features, some atypical antipsychotics are also able to block or stimulate other dopamine or serotonin receptors, as well as histaminergic, muscarinergic or adrenergic receptors. As a result of the varying receptor affinities, in switching or discontinuing compounds several possible pitfalls have to be considered, including the occurrence of withdrawal and rebound syndromes. This article reviews the pharmacological background of functional blockade or stimulation of receptors of interest in regard to atypical antipsychotics and the implicated potential withdrawal and rebound phenomena. A MEDLINE search was carried out to identify information on withdrawal or rebound syndromes occurring after discontinuation of atypical antipsychotics. Using the resulting literature, we first discuss the theoretical background to the functional consequences of atypical antipsychotic-induced blockade or stimulation of neurotransmitter receptors and, secondly, we highlight the clinical consequences of this. We then review the available clinical literature on switching between atypical antipsychotics, with respect to the occurrence of withdrawal or rebound symptoms. Finally, we offer practical recommendations based on the reviewed findings. The systematic evaluation of withdrawal or rebound phenomena using randomized controlled trials is still understudied. Knowledge of pharmacological receptor-binding profiles may help clinicians in choosing adequate switching or discontinuation strategies for each agent. Results from large switching trials indicate that switching atypical antipsychotics can be performed in a safe manner. Treatment-emergent adverse events during or after switching are not always considered to be, at least in part, associated with the pre-switch antipsychotic. Further studies are needed to substantiate the evidence gained so far on different switching strategies. The use of concomitant medication, e.g., benzodiazepines or anticholinergic drugs, may help to minimize symptoms arising from the discontinuation or switching of antipsychotic treatment.

Voluntary carbon offset schemes have sprung up in the last decade offering individuals opportunities to neutralize their own carbon footprint. These schemes strongly appeal to the personal responsibility of individuals in reducing the carbon emissions they cause. In this paper we report on a controlled laboratory experiment to better understand the behavioral motivations driving the purchase of carbon offsets, i.e., payments towards the reduction of damages to the environment. We show that the opportunity to offset damages does not affect the total damages created by the individuals when individuals trade in competitive markets. At the same time, we find a stable demand for carbon offsets when the price is sufficiently low. Therefore, introduction of carbon offsets increases efficiency by eliminating some of the damages ex-post. Behavior, however, is very heterogeneous. Individuals with a high (low) personal-responsibility index increase their offset purchases as their own damage (total damages) increases, but do not condition their offsetting behavior on the total damages (own damages) created.

This paper discusses a selection of cases and important policy developments in the enforcement activities of the Directorate General for Competition at the European Commission during the past year (2011–2012). In particular, it illustrates the importance of competition policy in the area of financial markets based on the Deutsche Borse/NYSE Euronext merger decision, discusses the role that the analysis of innovation can play in merger cases based on recent transactions in the hard disk drive industry, and illustrates the rising role of economic analysis in European state aid control.

This paper discusses a selection of cases and important policy developments in the enforcement activities of the Directorate General for Competition at the European Commission during the past year (2010–2011).

Background : Imbalance of glutamatergic neurotransmission has been proposed as a key mechanism underlying symptoms of schizophrenia. The neuropetide N-acetylaspartylglutamate (NAAG) modulates glutamate release. NAAG provides a component of the proton magnetic resonance spectrum (1H-MRS) in humans. The signal of NAAG, however, largely overlaps with its precursor and degrading product N-acetylaspartate (NAA) that by itself does not act in glutamatergic neurotransmission. Methods: We quantified NAAG and NAA separately from the 1H-MRS signal in 20 patients with schizophrenia and 20 healthy comparison subjects on a 3.0 Tesla MR scanner. The 1H-MRS voxels were positioned in the anterior cingulate cortex (ACC) and in the left frontal lobe. Psychopathological symptoms and cognitive performance were assessed. Results: In the ACC, the ratio NAAG/NAA was increased (P = .041) and NAAG was increased at a trend level (P = .066) in patients, while NAA was reduced (P = .030). NAA correlated with attention performance in patients (r = .64, P = .005) in the ACC. There was no group difference of NAAG, NAA, or NAAG/NAA in the frontal lobe but an inverse correlation of NAAG with negatives symptoms (Positive and Negative Symptoms Scale [PANSS] negative, r = −.58, P = .018) and with the total symptom score (PANSS total, r = −.50, P = .049). In addition, there was a positive correlation of frontal lobe NAAG (r = .53, P = .035) and NAAG/NAA (r = .54, P = .030) with episodic memory in patients. Conclusions: In this study, we present the first in vivo evidence for altered NAAG concentration in patients with schizophrenia.

The genetic factors determining the progression of prodromal syndromes to first episode schizophrenia have remained enigmatic to date. In a unique prospective multicentre trial, we assessed whether variants at the d-amino acid oxidase activator (DAOA)/G72 locus influence progression to psychosis. Young subjects with a prodromal syndrome were observed prospectively for up to 2 years to assess the incidence of progression to schizophrenia or first episode psychosis. Of the 82 probands with a prodromal syndrome, 21 probands experienced progression to psychosis within the observation period. Assessment of nine common variants in the DAOA/G72 locus yielded two variants with the predictive value for symptom progression: all four probands with the rs1341402 CC genotype developed psychosis compared with 17 out of 78 probands with the TT or CT genotypes (χ2 = 12.348; df = 2; p = 0.002). The relative risk for progression to psychosis was significantly increased in the CC genotype: RR = 4.588 (95% CI = 2.175–4.588). Similarly, for rs778294, 50% of probands with the AA genotype, but only 22% of probands with a GG or GA genotype progressed to psychosis (χ2 = 7.027; df = 2; p = 0.030). Moreover, haplotype analysis revealed a susceptibility haplotype for progression to psychosis. This is one of the first studies to identify a specific genetic factor for the progression of prodromal syndromes to schizophrenia, and further underscores the importance of the DAOA/G72 gene for schizophrenia. peerReviewed

The serotonin (5-HT) 1A receptor has been found to be dysregulated in prefrontal cortex and other brain regions in schizophrenia, and 5-HT1A receptor levels in the amygdala have been related to negative schizophrenia symptoms. We have assessed the impact of the functional C-1019G variant of the 5-HT1A receptor on the response to risperidone or haloperidol in a prospective, randomized, double-blind study. Patients were treated for 4 weeks and negative symptoms assessed weekly. The variant influenced the response to risperidone: improvement of negative symptoms by 4.38 points for carriers of the C allele, compared with the GG genotype (1.22 points, P=0.046). In a second independent study of 130 schizophrenia patients treated with atypical antipsychotics, this effect was confirmed (P=0.003). The functional variant of the 5-HT1A receptor thus influences the response of schizophrenia patients to atypical antipsychotics and may be useful in the future to predict the pharmacogenetics of negative symptoms.

Background Schizophrenia patients exhibit impairment in prepulse inhibition (PPI) of the acoustic startle response (ASR), suggesting a sensorimotor gating deficit. The serotonin-2A receptor (5-HT 2A R) has been implicated in both the pathogenesis of schizophrenia and the PPI deficits of schizophrenia patients. Moreover, both schizophrenia and PPI are thought to be inheritable. We investigated the impact of three 5-HT 2A R polymorphisms (A-1438G, T102C, H452Y) on PPI in schizophrenia patients. Methods We analyzed the 5-HT 2A R A-1438G, T102C, and H452Y polymorphisms and assessed startle reactivity, habituation, and PPI of ASR in 68 Caucasian schizophrenia inpatients. Patients were also examined with the Positive and Negative Syndrome Scale. Results The 5-HT 2A R A-1438G and T102C polymorphisms were in complete linkage disequilibrium. Patients carrying the T102C TT and the A-1438G AA allele show significantly higher PPI levels and a faster early habituation compared with all other variants. 5-HT 2A R A-1438G and T102C genotype explained approximately 11% of the PPI and early habituation variance. In contrast, the 5-HT 2A R H452Y polymorphism did not affect startle parameters. Conclusions Our findings suggest that PPI and habituation are modulated by 5-HT 2A R A-1438G and T102C genotype in schizophrenia. Consequently, alterations within brain 5-HT 2A Rs may contribute to the PPI deficits in schizophrenia.

Objective Second-generation antipsychotics (SGAs) have proven superior to first-generation antipsychotics regarding relapse prevention, mainly in multiple-episode patients. Practice guidelines recommend SGAs as first-line treatment particularly in first-episode patients, although evidence for this group is still limited. Accordingly, the hypothesis of whether 1-year relapse rate in first-episode schizophrenia under maintenance treatment with risperidone is lower compared to haloperidol in low dose was tested. Method Between November 2000 and May 2004, 1372 patients had been screened for eligibility in the inpatient facilities of 13 German psychiatric university hospitals. 159 remitted patients were enrolled after treatment of an acute first episode of schizophrenia according to ICD-10 F20 criteria. In the randomized controlled trial, double-blind antipsychotic treatment with risperidone or haloperidol was maintained in a targeted dose of 2 to 4 mg/day for 1 year. 151 patients were eligible for analysis. For 127 patients, this was a continuation trial after 8 weeks of randomized, double-blind, acute treatment with the same drugs; 24 patients were additionally randomly assigned after open acute treatment. Results With both antipsychotics (risperidone, N = 77; haloperidol, N = 74), no relapse evolved. Additionally, according to 2 post hoc defined measures of "marked clinical deterioration," significant differences occurred neither in the 2 respective deterioration rates (risperidone = 9%/23%; haloperidol = 8%/22%) nor in time until deterioration. Both antipsychotics were equally effective regarding significant symptom reduction and improvement in quality of life. Extrapyramidal symptoms were slightly higher with haloperidol. The overall dropout rate of 68%, however, was not significantly different between the 2 drug groups. Conclusion Against the background of an overall favorable outcome, the hypothesized difference between risperidone and low-dose haloperidol regarding relapse prevention could not be supported for this sample of patients with first-episode schizophrenia. Possible design-related reasons for this finding are discussed. With regard to the high dropout rate, special programs are needed to keep schizophrenia patients who are in their early acute and postacute illness course in effective and safe treatment. Clinical trials registration ClinicalTrials.gov identifier: NCT00159081.

After years of frustration, the search for genes impacting on schizophrenia is now undergoing some exciting developments. Several proposals of susceptibility genes have been able to be supported by replications. Thus, there are now at least three very strong candidates: the gene for dysbindin (DTNBP1), the gene for neuregulin-1 (NRG1), and a less well-understood gene locus, G72/G30, which are likely to influence manifestations of schizophrenia. Other "hot" candidates such as the disrupted-in-schizophrenia 1 gene (DISC1) and the gene coding for protein kinase B (AKT1) might also prove to be susceptibility genes in the next future. The clinical implications of these findings are not yet fully visible. However, some first insights are possible: most of the genetic findings lack diagnostic specificity, and are also reproduced in bipolar disorder. Strong associations are also obtained on a symptomatic level, not only on a diagnostic level. The pathophysiological role of these hot candidate genes is currently under intensive study.

In this comment the survey by Feuerstein is taken as a point of departure to discuss some of the key challenges facing collusion theory in its application to competition and trade policy. The main issue is one of robustness. It is discussed that the popular use of equilibria with Nash reversion leads to highly non-robust results and contrasts this with a recent approach aimed at detecting robust implications of collusion models. The comment also addresses the challenges posed by renegotiation and tacit collusion.

Mirtazapine belongs to the new generation of antidepressants that is commonly used in clinical routine. Therefore, we feel it mandatory to control compliance in the context of non-response, adverse events or other clinical situations by means of plasma concentration measurements. While controlled clinical studies have evaluated the effect of individual covariates on the pharmacokinetics of mirtazapine, our analysis aims to identify covariates within a naturalistic clinical setting. We performed non-linear mixed-effects modelling with data from 65 depressed inpatients whose plasma concentrations were measured weekly during their stay in hospital. Each patient’s age, height, weight, co-medication, alcohol, coffee and cigarette consumption, weekly serum creatinine concentrations, liver enzyme activity, blood pressure and pulse was noted. From 49 patients, the genotype of cytochrome P 450 (CYP) isoenzymes 2D6, 2C9 and 2C19 was analysed. The clearance of CYP2D6 intermediate metabolisers was reduced by 26% compared with extensive metabolisers. No other factor significantly influenced the clearance of these patients. The variability of mirtazapine plasma concentrations in clinical routine is caused to a relevant degree by CYP2D6. This should be taken into account when therapeutic drug monitoring is carried out to check treatment adherence or when a special clinical situation, such as co-morbidity and add-on medication, demands careful dosing of this drug.

Chronic administration of 3,4-methylenedioxymethamphetamine (MDMA) is associated with long-term depletion of serotonin (5-HT) and loss of 5-HT axons in the brains of rodents and nonhuman primates. Despite the broad database concerning the selective serotonergic neurotoxicity of recreational MDMA consumption by humans, controversy still exists with respect to the question of whether the well-known functional consequences of these neurotoxic effects, such as memory impairment, were caused by chronic 5-HT deficiency. Habituation and prepulse inhibition (PPI) of the acoustic startle response (ASR) can be used as a marker of central serotonergic functioning in rodents and humans. Thus, we investigated the functional status of the central serotonergic system in chronic but abstinent MDMA users by measuring PPI and habituation of ASR. PPI and habituation of ASR were measured in three groups. The first group (MDMA group) included 20 male drug-free chronic users of MDMA; the second group (cannabis group) consisted of 20 male drug-free chronic users of cannabis; and the third group (healthy controls) comprised 20 male participants with no history of illicit drug use. Analysis revealed significantly increased PPI of MDMA users compared to those of cannabis users and healthy controls. Cannabis users and healthy controls showed comparable patterns of PPI. There were no differences in habituation among the three groups. These results suggest that the functional consequences of chronic MDMA use may be explained by 5-HT receptor changes rather than by a chronic 5-HT deficiency condition. Use of cannabis does not lead to alterations of amplitude, habituation, or PPI of ASR.

In this paper, we construct a new basis for insider--outsider theory that acknowledges that insiders are typically easier to organise, so that they can delegate their bargaining decisions to a representative if they want to. We show that harassment or discrimination of new workers by the insider work force is neither individually rational nor needed to explain union formation or inefficient hiring decisions. However, we show that there is a strong tendency for overemployment. Unions tend to increase the efficiency of hiring decisions although union contracts will look like inducing underemployment.

This paper is an attempt to derive priorities for the reform of European merger policy from observed problems with decision making in merger cases. We identify problems in the application of theory and empirical method as well as the impact of resource constraints and the potential for systematic decision bias. In contrast to the intense debate about the merits of a switch from a dominance criterion to a significant lessening of competition test, we find that such a switch would not effectively address any of the problems in Commision decision making on mergers. Similarly, the lack of an efficiency defense does not seem to explain any of the weaknesses of European merger policy. In contrast, we find that most of the problem areas identified in current merger control practice can be effectively addressed by reforming the merger procedure, the internal organization of merger control in the Commission, as well as addressing resource issues. Together with carefully crafted merger guidelines these should have strong priority for the reform of merger policy in Europe.

Fighting collusion Regulation of communication between firms This paper is an attempt to create a coherent approach to the design of competition policy enforcement against collusion based on theoretical considerations, evidence from economic experiments, and case studies. I argue that collusion should primarily be fought indirectly by targeting types of communication between firms that are particularly likely to facilitate collusion. In particular, I identify types of communication which have high potential anti‐competitive effects but where it is unlikely that prohibiting communication will lead to efficiency losses. This analysis leads to some simple rules concerning communication between firms, which could also guide the development of competition rules for B2B electronic market places. — Kai-Uwe Kuhn

We show that the Coase conjecture does not hold when a durable-goods monopolist also sells nondurable goods that are demand related to the durable. The presence of nondurable complements or substitutes reduces the rate at which the monopolist introduces the durable into the market. The price of the durable does not converge to marginal cost. We analyze the incentives of a monopolist to extend his product line to a durable or a nondurable. Most significantly, the profit from adding a durable to the product line disappears as the time between offers becomes short. We study the effects of entry into markets for nondurables and their implications for merger policy.

INTRODUCTION: 3,4-Methylenedioxymethamphetamine (MDMA, "ecstasy") is a recreational club drug with supposed neurotoxic effects selectively on the serotonin system. MDMA users consistently exhibit memory dysfunction but there is an ongoing debate if these deficits are induced mainly by alterations in the prefrontal or mediotemporal cortex, especially the hippocampus. Thus, we investigated the relation of verbal memory deficits with alterations of regional cerebral brain glucose metabolism (rMRGlu) in recreational MDMA users. METHODS: Brain glucose metabolism in rest was assessed using 2-deoxy-2-((18)F)fluoro-D-glucose positron emission tomography ((18)FDG PET) in 19 male recreational users of MDMA and 19 male drug-naïve controls. (18)FDG PET data were correlated with memory performance assessed with a German version of the Rey Auditory Verbal Learning Test. RESULTS: As previously shown, MDMA users showed significant impairment in verbal declarative memory performance. PET scans revealed significantly decreased rMRGlu in the bilateral dorsolateral prefrontal and inferior parietal cortex, bilateral thalamus, right hippocampus, right precuneus, right cerebellum, and pons (at the level of raphe nuclei) of MDMA users. Among MDMA users, learning and recall were positively correlated with rMRGlu predominantly in bilateral frontal and parietal brain regions, while recognition was additionally related to rMRGlu in the right mediotemporal and bihemispheric lateral temporal cortex. Moreover, cumulative lifetime dose of MDMA was negatively correlated with rMRGlu in the left dorsolateral and bilateral orbital and medial PFC, left inferior parietal and right lateral temporal cortex. CONCLUSIONS: Verbal learning and recall deficits of recreational MDMA users are correlated with glucose hypometabolism in prefrontal and parietal cortex, while word recognition was additionally correlated with mediotemporal hypometabolism. We conclude that memory deficits of MDMA users arise from combined fronto-parieto-mediotemporal dysfunction.

Financial constraints are an important impediment to the growth of small businesses. We study theoretically and empirically how the financial constraints of agents affect their decisions to exert effort, and, hence the organizational decisions and growth of principals, in the context of franchising. We find that a 30 percent decrease in average collateralizable housing wealth in a region delays chains' entry into franchising by 0.28 years on average, 9 percent of the average waiting time, and slows their growth by around 10 percent, leading to a 10 percent reduction in franchised chain employment.

Financial constraints are considered an important impediment to growth for small businesses. We study theoretically and empirically the relationship between the financial constraints of agents and the organizational decisions and growth of principals, in the context of franchising. We find that a 30 percent decrease in average collateralizable housing wealth in an area is associated with a delay in chains’ entry into franchising by 0.33 years on average, or 10 percent of the average waiting time, and a reduction in chain growth and hence a reduction in franchised chain employment of about 9 percent.

In standard durable-goods monopoly models, both the set of buyers and the set of prices are assumed to be continua. If the set of buyers is finite, the perfectly discriminating monopoly outcome is a unique subgame perfect equilibrium when the seller is sufficiently patient. Introducing instead a smallest unit of account yields the Coasian outcome as a generically unique subgame perfect equilibrium for patient enough buyers. A folk theorem is obtained if both sets are finite. These results reflect a strategic disadvantage of having to make moves with a large impact on other players' payoffs. The analysis is extended to durable-goods oligopoly. Copyright 1995 by University of Chicago Press.

To evaluate the predictive validity of early response compared to other well-known predictor variables in acutely ill first-episode patients.112 patients were treated with a mean dosage of 4.14 mg (±1.70) haloperidol and 112 patients with a mean dosage of 4.17 mg (±1.55) risperidone for a mean inpatient treatment duration of 42.92 days (±16.85) within a double-blind, randomized controlled trial. Early response was defined as a ≥ 30% improvement in the PANSS total score by week 2, response as a ≥ 50% reduction in the PANSS total score from admission to discharge and remission according to the consensus criteria. Univariate tests and logistic regression models were applied to identify significant predictors of response and remission.52% of the patients were responders and 59% remitters at discharge. Non-remitters at discharge were hindered from becoming remitters mainly by the presence of negative symptoms. Univariate tests revealed several significant differences between responders/non-responders and remitters/non-remitters such as age, severity of baseline psychopathology as well as the frequency of early response. Both early response (p0.0001) and a higher PANSS positive subscore at admission (p=0.0002) were identified as significant predictors of response at discharge, whereas a shorter duration of untreated psychosis (p=0.0167), a lower PANSS general psychopathology subscore (p0.0001), and early treatment response (p=0.0002) were identified as significant predictors of remission.Together with the finding that early response is a significant predictor of response and remission, the relevance and predictive validity of negative and depressive symptoms for outcome is also highlighted.

To determine whether well-described patterns of altered perfusion in schizophrenia can be identified by using continuous arterial spin labeling (CASL) with a whole-brain imaging sequence.This study was approved by the ethics committee of the local institutional review board, and written informed consent was obtained from all subjects. CASL was used to compare cerebral perfusion between 11 nonmedicated patients with schizophrenia and 25 healthy control subjects. Since antipsychotic medication may affect perfusion, only drug-free subjects were examined. Resting-state perfusion, as measured in terms of regional cerebral blood flow, was compared voxel wise by using an analysis of variance design in a statistical parametric mapping program, with patient age and sex as covariates.Compared with the healthy control subjects, the schizophrenic patients had extensive areas of hypoperfusion in the frontal lobes bilaterally, in the anterior and medial cingulate gyri, and in the parietal lobes bilaterally. Increased perfusion was observed in the cerebellum, brainstem, and thalamus of the schizophrenic patients as compared with the perfusion in these areas in the control subjects.CASL in schizophrenia revealed patterns of hypo- and hyperperfusion similar to the perfusion patterns in previously published positron emission tomographic and single photon emission computed tomographic studies. The advantages of CASL, including independence from injected contrast agents, no irradiation, and fast acquisition time, may facilitate intensive perfusion studies of the early recognition of schizophrenia and other psychiatric disorders, as well as longitudinal disease-monitoring research of these conditions.

We use experiments to analyze what type of communication is most effective in achieving cooperation in a simple collusion game. Consistent with the existing literature on communication and collusion, even minimal communication leads to a short run increase in collusion. However, in a limited message-space treatment where subjects cannot communicate contingent strategies, this initial burst of collusion rapidly collapses. When unlimited pre-game communication is allowed via a chat window, an initial decline in collusion is reversed over time. Content analysis is used to identify multiple channels by which communication improves collusion in this setting. Explicit threats to punish cheating prove to be by far the most important factor to successfully establish collusion, consistent with the existing theory of collusion. However, collusion is even more likely when we allow for renegotiation, contrary to standard theories of renegotiation. What appears critical for the success of collusion with renegotiation is that cheaters are often admonished in strong terms. Allowing renegotiation therefore appears to increase collusion by allowing for an inexpensive and highly effective form of punishment.

Sustained attention as measured by the Continuous Performance Test (CPT) has proved a valuable endophenotype for schizophrenia. Recently pharmacological studies suggested a role of the serotonin (5-HT) 3 receptor in schizophrenia. The 5-HT3 receptors are the only ligand-gated ion channels within the 5-HT receptor family. Applying an endophenotype approach, we investigated a potential impact of the genes of the 5-HT3A and 5-HT3B subunits as well as the novel 5-HT3C, 5-HT3D, and 5-HT3E subunits on CPT performance in subjects with schizophrenia. The study included 196 patients with schizophrenia, 113 of their parents, and 205 healthy controls recruited from community registers. Sustained attention was assessed with the Continuous Performance Test-Identical Pairs (CPT-IP). Assessing functional and coding variants of the 5-HT3 receptor subunit genes, we found the GG genotype of the 5-HT3E subunit gene (rs7627615; Thr86Ala) to be associated with better attentional capacities in subjects with schizophrenia and healthy controls. This study provides additional evidence for a role of the serotonergic system and the 5-HT3 receptor in schizophrenia.

OBJECTIVES Among serotonin (5 HT) receptors the 5 HT3 receptor is the only ligand gated ion channel. 5 HT3 antagonists such as ondansetron and tropisetron may improve auditory gating and neurocognitive deficits in schizophrenic patients. Moreover many antipsychotic drugs are antagonists at 5 HT3 receptors. However the role of 5 HT3 receptor variants on response to antipsychotic drugs in schizophrenic patients is still unclear. METHODS In a prospective randomized double blind study we have assessed six functional and coding variants of the subunit genes HTR3A HTR3B as well as the novel HTR3C HTR3D and HTR3E subunits in the response to haloperidol or risperidone. Seventy patients were treated for 4 weeks and positive symptoms negative symptoms and general psychopathology were measured by the Positive and Negative Syndrome Scale (PANSS). RESULTS HTR3E had an effect on the speed of response to antipsychotics. GG allele carriers responded more quickly to treatment on the PANSS negative symptom subscale (P = 0.03) and on the total PANSS score (P = 0.04) irrespective of medication. In a second independent study of 144 schizophrenia patients treated with atypical antipsychotics this effect could not be confirmed. CONCLUSION Our findings argue against a major effect of HTR3 variants in response to antipsychotics. Solely the HTR3E and also the HTR3A variant could exert a weak effect on the speed of response to antipsychotics.

This report concerns the case of a 29-year-old male patient suffering from severe psychotic illness who had been satisfactorily treated with clozapine for 4 months. Clozapine had also been successfully administered during a psychotic episode 5 years previously. Though symptoms of psychosis were successfully controlled following the most recent psychotic episode, a medical consultation assessed that exacerbation of pancreatitis warranted discontinuation of the current antipsychotic treatment regime. Following a series of unsuccessful courses of neuroleptic medication, a magnetic resonance cholangiopancreaticography (MRCP) revealed marked cholecystolithiasis suggesting a biliary pancreatitis. Clozapine treatment was readministered following cholecystectomy. After 4 weeks of antipsychotic treatment the patient was discharged from hospital on clozapine monotherapy.

Introduction The cases in the US and Europe against Microsoft have been perhaps the most high-profile antitrust cases in the last twenty years. In the various Microsoft cases, antitrust authorities in the US and Europe took on what was at some points the most valuable company in the world and its CEO Bill Gates, the world's richest man. After five years of investigation, on 24 March 2004, the European Commission held Microsoft guilty of an abuse of a dominant position under Article 82 and imposed the largest fine ever for such an antitrust violation in Europe – €497 million. The Commission also demanded major forward-looking behavioural remedies including compulsory licensing of intellectual property and forced unbundling. This degree of behavioural intervention is highly unusual and led to continued conflict about the implementation of the remedies. The Decision found that Microsoft had abused its dominant position in the PC operating system market in two ways: ‘deliberately restricting interoperability between Windows PCs and non-Microsoft workgroup servers, and by tying its Windows Media Player (WMP), a product where it faced competition, with its ubiquitous Windows operating system.' As remedies for these violations the European Commission ordered Microsoft: ‘within 120 days, to disclose complete and accurate interface documentation which would allow non-Microsoft workgroup servers to achieve full interoperability with Windows PCs and servers’; ‘within 90 days, to offer to PC manufacturers a version of its Windows client PC operating system without Windows Media Player’. The case is fascinating as it touches on one of the key issues concerning the conduct of modern competition policy': how should we think about the role of antitrust in high-tech industries dominated by rapid innovation?

We use experiments to analyze what type of communication is most effective in achieving cooperation in a simple collusion game. Consistent with the existing literature on communication and collusion, even minimal communication leads to a short run increase in collusion. However, in a limited message-space treatment where subjects cannot communicate contingent strategies, this initial burst of collusion rapidly collapses. When unlimited pre-game communication is allowed via a chat window, an initial decline in collusion is reversed over time. Content analysis is used to identify multiple channels by which communication improves collusion in this setting. Explicit threats to punish cheating prove to be by far the most important factor to successfully establish collusion, consistent with the existing theory of collusion. However, collusion is even more likely when we allow for renegotiation, contrary to standard theories of renegotiation. What appears critical for the success of collusion with renegotiation is that cheaters are often admonished in strong terms. Allowing renegotiation therefore appears to increase collusion by allowing for an inexpensive and highly effective form of punishment.

Suicidal ideation has been related to cognitive rigidity whereas suicidal behaviour itself was associated with specific executive deficits. Yet it remains unclear if a distinct cognitive suicidal phenotype does exist. The aim of the present study was to further investigate the role of suicidal thinking for the neuropsychological performance in depressive suicide attempters. Depressive inpatients after a recent suicide attempt, who either had present suicidal ideation (n = 14) or not (n = 15) and healthy controls (n = 29) were recruited. The groups were assessed by means of executive tasks designed to capture impulsive decision-making, and with verbal memory and attention tests. Self-rating measures of impulsivity and aggression were further applied. Only patients with current suicidal ideation showed executive dysfunctions with impaired decision-making being the most salient. Verbal memory and attention were reasonably intact in all patients. All patients reported increased aggression. Suicidal ideation is clearly associated with impaired cognitive performance. Our results suggest that executive deficits seen in depressive suicide attempters have a state-dependent component.

It has been recently shown that Catechol O-methyltransferase (COMT) Val 158 Met polymorphism strongly influences prepulse inhibition (PPI) of the acoustic startle response (ASR) in healthy human volunteers. Given that schizophrenia patients exhibit impairment in PPI and that COMT is a putative susceptibility gene for schizophrenia, we investigated the impact of the COMT Val 158 Met polymorphisms on PPI in schizophrenic inpatients. We analyzed COMT Val 158 Met polymorphisms and assessed startle reactivity, habituation, and PPI of ASR in 68 Caucasian schizophrenia inpatients. Clinical symptoms were measured with the Positive and Negative Syndrome Scale (PANSS). Patients carrying the Val 158 Met Met/Met allele showed elevated PPI levels whereas startle reactivity and habituation did not differ from the other two genotypes. These preliminary results imply that PPI is influenced by COMT Val 158 Met genotype in schizophrenia as well. In concert with other findings, our data suggest that PPI is a polygenic trait.

Introduction Sexual dysfunction is a frequent side effect of antipsychotic treatment. Increased prolactin levels are believed to be responsible for this sexual impairment despite contradictory results. Aim The primary objective of the present study was to examine the relationship between sexual dysfunction, subjective well‐being and prolactin levels in patients with schizophrenia treated either with risperidone or quetiapine. The secondary objective was to explore the relationship between testosterone and the severity of positive and negative symptoms of schizophrenia in male patients. Methods In a 4‐week nonrandomized open label observational study, 102 inpatients with schizophrenia were recruited. Sexual functioning, subjective well‐being and endocrinological parameters were assessed as well as psychopathological characteristics. Main Outcome Measures Two self‐rating questionnaires concerned with sexual functioning (“Essener Fragebogen zur Sexualitat”) and Subjective Well‐Being Under Neuroleptic Treatment Scale (SWN) were completed by the patients. Plasma levels of prolactin in male and female patients were measured. Furthermore, in male patients testosterone, luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) were determined. Positive and Negative Symptom Scale (PANSS) was applied. Results After 4 weeks, patients treated with quetiapine reported less severe sexual impairment, as well as lower PANSS negative and general score compared with patients treated with risperidone. Additionally, emotional regulation as measured with the SWN was higher in patients treated with quetiapine. Risperidone was significantly associated with elevated prolactin levels. Prolactin levels were not correlated either with sexual dysfunction or PANSS. However, in the group of patients treated risperidone, sexual impairment was significantly associated with the SWN subscale emotional regulation. Conclusions Increased prolactin levels do not seem to be decisive for antipsychotic induced sexual dysfunction. Improvement of severity of illness and regaining the ability to regulate one's own emotion have positive influence on sexual functioning. Westheide J, Cvetanovska G, Albrecht C, Bliesener N, Cooper‐Mahkorn D, Creutz C, Hornung W‐P, Klingmuller D, Lemke MR, Maier W, Schubert M, Strater B, and Kuhn K‐U. Prolactin, subjective well‐being and sexual dysfunction: An open label observational study comparing Quetiapine with Risperidone. J Sex Med **;**:**–**.

Patients with first-episode schizophrenia appear to respond to lower doses of neuroleptics, and to be more sensitive to developing extrapyramidal side-effects. The authors therefore compared in such patients the efficacy and extrapyramidal tolerability of comparatively low dosages of the atypical neuroleptic risperidone and of the conventional neuroleptic haloperidol. Risperidone was hypothesized to have better extrapyramidal tolerability and efficacy in treating negative symptoms. Patients were randomly assigned under double-blind conditions to receive risperidone (n=143) or haloperidol (n=146) for 8 wk. The primary efficacy criterion was the estimated difference in the mean change in the Positive and Negative Symptom Scale (PANSS) negative score between treatment groups; secondary efficacy criteria were changes on the PANSS total score and other PANSS subscores, and several other measures of psychopathology and general functioning. The primary tolerability criterion was the difference in baseline-adjusted occurrence rates of extrapyramidal side-effects measured with the Simpson-Angus Scale (SAS) compared between treatment groups. The main hypothesis was that risperidone would be superior in terms of improving negative symptoms and lowering the risk of extrapyramidal symptoms. Secondary tolerability criteria were the other extrapyramidal symptoms, measured with the Hillside Akathisia Scale (HAS) and the Abnormal Involuntary Movement Scale (AIMS). The average mean daily doses were 3.8 mg (s.d.=1.5) for risperidone and 3.7 mg (s.d.=1.5) for haloperidol. There were similar, significant improvements in both treatment groups in the primary and secondary efficacy criteria. At week 8 nearly all scores of extrapyramidal side-effects indicated a significantly higher prevalence of extrapyramidal side-effects with haloperidol than with risperidone [SAS: risperidone 36.5% of patients; haloperidol 51.5% of patients; likelihood ratio test, chi2(1)=7.8, p=0.005]. There were significantly fewer drop-outs [risperidone n=55, drop-out rate=38.5%; haloperidol n=79, drop-out rate=54.1%, chi2(1)=7.1, p=0.009] and a longer non-discontinuation time [risperidone: average of 50.8 d to drop-out; haloperidol: average of 44.0 d to drop-out; log rank test, chi2(1)=6.4, p=0.011] in the risperidone group. Risperidone and haloperidol appear to be equally effective in treating negative and other symptoms of first-episode schizophrenia. Risperidone has better extrapyramidal tolerability and treatment retention rate than the equivalent dose of haloperidol in these patients.

In recent years, evidence has been accumulating indicating a major role of glutamate in the pathogenesis and pathophysiology of schizophrenia. Of particular importance in this regard are the metabotropic glutamate receptors (GRM). Thus, a recently published trial of the amino acid analogue LY2140023, which exerts its effects through the activation of the glutamate receptors GRM3/GRM2, showed an improvement of positive and negative symptoms comparable to treatment with olanzapine. A functional variant of GRM3 has been described which modulates synaptic glutamate levels. We assessed whether this functional variant rs6465084 is related to schizophrenia in a large sample of patients and controls. We found an increased frequency of the A allele (p=0.027) and the AA genotype (p=0.024) in schizophrenia patients. Moreover, in an assessment of schizophrenia endophenotypes, patients of the AA genotype performed poorly in the digit symbol test, a measure of attention (p=0.008). Our results provide further evidence for the potential importance of the glutamate receptor GRM3 in schizophrenia, and indicate that the novel antipsychotic LY2140023 may actually be targeting a pathogenic pathway of schizophrenia.

Scrutiny of potential mergers by the European Commission often focuses on unilateral effects or single firm dominance. But some cases have involved concerns over coordinated effects: the concern that the merger could increase the likelihood of consumer harm through tacit collusion by the reduced number of firms in the industry (this is known as collective dominance). The economic and legal issues are far less certain in these cases and a particular challenge is how to bring empirical evidence to bear on the decision. In this chapter we examine a case in newsprint and magazine paper - UPM Kymmene/Norske Skog/Haindl . Here, coordinated effects were at the centre of the Commission's concerns. We discuss how collusion theory and evidence were used to help clear the merger without remedies in the final Decision.