Personal Character and Firm Performance. The Economic Implications of Having Fraudulent Board Members

Unique proprietary data on Swedish board members reveal that a non-trivial proportion of board members in Swedish listed firms have been convicted of serious crimes. Analyzing the data shows that board members with personal fraudulent behavior are more likely to be males than females. We also find that the greater the proportion of fraudulent board members, the lower is the profitability and the higher are the earnings (and cash flows) volatility of the firm. However, the negative effect of fraudulent behavior on profitability is mitigated when fraudulent board members have a larger stake in the firm’s equity. Finally, we find that the earnings of firms with more fraudulent board members are lower and less value-relevant. Given the strong legal enforcement in Sweden, our results raise serious concerns about the effects of board members’ personal fraudulent behavior on firm performance and risk-taking in other countries, particularly the United States and the United Kingdom.Fraudulent behavior; Fraud; Crimes; Convicted board members; Corporate governance; Profitability; Earnings volatility

Entrepreneurial Stock Brokering and Switching Costs

Stock brokers are entrepreneurs who incur switching costs when the change brokerage houses. We use Helsinki Stock Exchange data to investigate these costs by examining whether investors are loyal to their brokers when brokers move. We find that investors who have extant relationships with the new house are more likely to attract the investors from the old houses, and savvy (knowledgeable) investors are more likely to stay with their broker

Sotataloustietoutta XI : Sotatalous 2020-luvulla

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A mouse model of the schizophrenia-associated 1q21.1 microdeletion syndrome exhibits altered mesolimbic dopamine transmission

Abstract 1q21.1 hemizygous microdeletion is a copy number variant leading to eightfold increased risk of schizophrenia. In order to investigate biological alterations induced by this microdeletion, we generated a novel mouse model (Df(h1q21)/+) and characterized it in a broad test battery focusing on schizophrenia-related assays. Df(h1q21)/+ mice displayed increased hyperactivity in response to amphetamine challenge and increased sensitivity to the disruptive effects of amphetamine and phencyclidine hydrochloride (PCP) on prepulse inhibition. Probing of the direct dopamine (DA) pathway using the DA D1 receptor agonist SKF-81297 revealed no differences in induced locomotor activity compared to wild-type mice, but Df(h1q21)/+ mice showed increased sensitivity to the DA D2 receptor agonist quinpirole and the D1/D2 agonist apomorphine. Electrophysiological characterization of DA neuron firing in the ventral tegmental area revealed more spontaneously active DA neurons and increased firing variability in Df(h1q21)/+ mice, and decreased feedback reduction of DA neuron firing in response to amphetamine. In a range of other assays, Df(h1q21)/+ mice showed no difference from wild-type mice: gross brain morphology and basic functions such as reflexes, ASR, thermal pain sensitivity, and motor performance were unaltered. Similarly, anxiety related measures, baseline prepulse inhibition, and seizure threshold were unaltered. In addition to the central nervous system-related phenotypes, Df(h1q21)/+ mice exhibited reduced head-to tail length, which is reminiscent of the short stature reported in humans with 1q21.1 deletion. With aspects of both construct and face validity, the Df(h1q21)/+ model may be used to gain insight into schizophrenia-relevant alterations in dopaminergic transmission

Persistent gating deficit and increased sensitivity to NMDA receptor antagonism after puberty in a new mouse model of the human 22q11.2 micro-deletion syndrome – a study in male mice

Background: The hemizygous 22q11.2 micro-deletion is a common copy number variant in humans. The deletion confers high risk of neurodevelopmental disorders including autism and schizophrenia. Up to 41% of deletion carriers experience psychotic symptoms. Methods: We present a new mouse model (Df(h22q11)/+) of the deletion syndrome (22q11.2DS) and report on the most comprehensive study undertaken in 22q11.2DS models. The study was conducted in male mice. Results: We found elevated post-pubertal NMDA receptor antagonist induced hyper-locomotion, age-independent prepulse inhibition (PPI) deficits and increased acoustic startle response (ASR). The PPI deficit and increased ASR was resistant to antipsychotic treatment. The PPI deficit was not a consequence of impaired hearing measured by auditory brain stem responses. The Df(h22q11)/+ mice also displayed increased amplitude of loudness-dependent auditory evoked potentials. Prefrontal cortex and dorsal striatal (DStr) elevations of the dopamine metabolite DOPAC and increased DStr expression of the AMPA receptor subunit GluR1 was found. The Df(h22q11)/+ mice did not deviate from wild-type mice in a wide range of other behavioural and biochemical assays. Limitations: The 22q11.2 micro-deletion has incomplete penetrance in humans and the severity of disease depends on the complete genetic makeup in concert with environmental factors. In order to obtain more marked phenotypes reflecting the severe conditions related to 22q11.2DS it is suggested to expose the Df(h22q11)/+ mice to environmental stressors which may unmask latent psychopathology. Conclusion: The Df(h22q11)/+ model will be a valuable tool for increasing our understanding of the aetiology of schizophrenia and other psychiatric disorders associated with the 22q11DS.The research leading to these results was conducted as part of NEWMEDS and received support from the Innovative Medicine Initiative Joint Undertaking under grant agreement n° 115008 of which resources are composed of EFPIA in-kind contribution and financial contribution from the European Union’s Seventh Framework Programme (FP7/2007-2013). This work was further supported by grants from the Danish Advanced Technology Foundation (File no. 001-2009-2) and by the Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM)

Tekijänoikeus työsuhteessa

Tutkimuksessa selvitetään kenelle tekijänoikeus työsuhteessa luotuun teokseen lähtökohtaisesti kuuluu ja millä perusteella oikeudet voivat siirtyä. Tekijänoikeuslaista sen paremmin kuin työsopimuslaistakaan ei tähän ongelmaan löydy suoraa vastausta. Oikeuskäytännössä ja oikeuskirjallisuudessa ei asiaan ole juuri otettu yksiselitteistä kantaa. Tutkimuksessa analysoidaan tekijänoikeuden ja työoikeuden välillä olevaa ristiriitaa. Tekijänoikeuslain mukaan tekijänoikeudet kuuluvat aina teoksen tekijälle ja työoikeudellisten periaatteiden mukaan työn tulos kuuluu työnantajalle. Työsuhdetekijänoikeudesta on keskusteltu Suomessa erityisesti viime vuosina. Keskustelu on johtanut usein kysymykseen: tulisiko säätää erillinen laki, joka sääntelisi työsuhdetekijän-oikeudellisia kysymyksiä vai voidaanko ongelma ratkaista lisäämällä tekijänoikeuslakiin olettamasäännös tekijänoikeuden siirtymisestä työsuhteessa. Opetusministeriön aloitteesta vuonna 2002 käynnistetyllä tekijänoikeusselvi-tyksellä pyrittiin kartoittamaan tekijänoikeus-lain uudistustarpeita tältä osin. Tekijänoikeus-selvitys toimii tämän tutkimuksen yhtenä merkittävänä tukijalkana. Tutkimuksen tuloksista käy ilmi, että ongelmat työsuhdetekijänoikeudellisissa kysymyksissä aiheutuvat lainsäädännöllisten aukkojen lisäksi epäselvistä sopimuksista sekä siitä, ettei oikeuksien siirtymisestä ole nimenomaista sopimusta. Tällaisessa tilanteessa oikeudel-linen ennakoitavuus on heikkoa. Voidaan kuitenkin todeta tietyillä toimialoilla teki-jänoikeuksien siirtymisestä sovitun joko nimenomaisesti tai konkludenttisesti. Tutkimuksen mukaan tekijänoikeuksien siirty-minen työsuhteessa on tulevaisuudessa entistä merkityksellisempi asia ja sen vuoksi siitä tulisi säätää erikseen lailla.fi=Kokotekstiversiota ei ole saatavissa.|en=Fulltext not available.|sv=Fulltext ej tillgänglig