7 research outputs found

    Control Transaction Governance: Collective Action and Asymmetric Information Problems and Ex post Policing

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    Why, when and how should control transactions be policed ex post and by a judiciary? This article is the first to 1) articulate the doctrinal prerequisites for effective ex post judicial policing of fiduciaries in control transactions, and 2) theoretically unify two seemingly distinct approaches to police control transactions: the ex post judicial policing in the United States and the ex ante policing by the Takeover Panel in the United Kingdom. Shareholder collective action and asymmetric information problems, and the extent of gatekeeping by fiduciaries together determine the mode of third-party interventions, such as those by judiciaries and the Takeover Panel, in control transactions. The Article’s analysis yields normative conclusions about how judiciaries in the United States, including Delaware’s, should fine-tune gatekeeping by corporate fiduciaries in control transactions. It predicts that multijurisdictional shareholder litigation that seeks anticipatory adjudication will produce negative consequences. Further, it gives policy makers outside of the United States the theoretical foundation for crafting third-party interventions in both types of control transactions, i.e., third-party acquisitions of control and controller freeze-outs, that are optimal for their own jurisdictions

    Control Transaction Governance: Collective Action and Asymmetric Information Problems and Ex post Policing

    Get PDF
    Why, when and how should control transactions be policed ex post and by a judiciary? This article is the first to 1) articulate the doctrinal prerequisites for effective ex post judicial policing of fiduciaries in control transactions, and 2) theoretically unify two seemingly distinct approaches to police control transactions: the ex post judicial policing in the United States and the ex ante policing by the Takeover Panel in the United Kingdom. Shareholder collective action and asymmetric information problems, and the extent of gatekeeping by fiduciaries together determine the mode of third-party interventions, such as those by judiciaries and the Takeover Panel, in control transactions. The Article’s analysis yields normative conclusions about how judiciaries in the United States, including Delaware’s, should fine-tune gatekeeping by corporate fiduciaries in control transactions. It predicts that multijurisdictional shareholder litigation that seeks anticipatory adjudication will produce negative consequences. Further, it gives policy makers outside of the United States the theoretical foundation for crafting third-party interventions in both types of control transactions, i.e., third-party acquisitions of control and controller freeze-outs, that are optimal for their own jurisdictions

    Variants associated with Gaucher disease in multiple system atrophy

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    International audienceObjective : Glucocerebrosidase gene (GBA) variants that cause Gaucher disease are associated with Parkinson disease (PD) and dementia with Lewy bodies (DLB). To investigate the role of GBA variants in multiple system atrophy (MSA), we analyzed GBA variants in a large case–control series.Methods : We sequenced coding regions and flanking splice sites of GBA in 969 MSA patients (574 Japanese, 223 European, and 172 North American) and 1509 control subjects (900 Japanese, 315 European, and 294 North American). We focused solely on Gaucher-disease-causing GBA variants.Results : In the Japanese series, we found nine carriers among the MSA patients (1.65%) and eight carriers among the control subjects (0.89%). In the European series, we found three carriers among the MSA patients (1.35%) and two carriers among the control subjects (0.63%). In the North American series, we found five carriers among the MSA patients (2.91%) and one carrier among the control subjects (0.34%). Subjecting each series to a Mantel–Haenszel analysis yielded a pooled odds ratio (OR) of 2.44 (95% confidence interval [CI], 1.14–5.21) and a P-value of 0.029 without evidence of significant heterogeneity. Logistic regression analysis yielded similar results, with an adjusted OR of 2.43 (95% CI 1.15–5.37) and a P-value of 0.022. Subtype analysis showed that Gaucher-disease-causing GBA variants are significantly associated with MSA cerebellar subtype (MSA-C) patients (P = 7.3 × 10−3).Interpretation : The findings indicate that, as in PD and DLB, Gaucher-disease-causing GBA variants are associated with MSA

    Mutations in COQ2 in familial and sporadic multiple-system atrophy the multiple-system atrophy research collaboration

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    Background: Multiple-system atrophy is an intractable neurodegenerative disease characterized by autonomic failure in addition to various combinations of parkinsonism, cerebellar ataxia, and pyramidal dysfunction. Although multiple-system atrophy is widely considered to be a nongenetic disorder, we previously identified multiplex families with this disease, which indicates the involvement of genetic components. Methods: In combination with linkage analysis, we performed whole-genome sequencing of a sample obtained from a member of a multiplex family in whom multiple-system atrophy had been diagnosed on autopsy. We also performed mutational analysis of samples from members of five other multiplex families and from a Japanese series (363 patients and two sets of controls, one of 520 persons and one of 2383 persons), a European series (223 patients and 315 controls), and a North American series (172 patients and 294 controls). On the basis of these analyses, we used a yeast complementation assay and measured enzyme activity of parahydroxybenzoate-polyprenyl transferase. This enzyme is encoded by the gene COQ2 and is essential for the biosynthesis of coenzyme Q10. Levels of coenzyme Q10 in lymphoblastoid cells and brain tissue were measured on high-performance liquid chromatography. Results: We identified a homozygous mutation (M78V-V343A/M78V-V343A) and compound heterozygous mutations (R337X/V343A) in COQ2 in two multiplex families. Furthermore, we found that a common variant (V343A) and multiple rare variants in COQ2, all of which are functionally impaired, are associated with sporadic multiple-system atrophy. The V343A variant was exclusively observed in the Japanese population. Conclusions: Functionally impaired variants of COQ2 were associated with an increased risk of multiple-system atrophy in multiplex families and patients with sporadic disease, providing evidence of a role of impaired COQ2 activities in the pathogenesis of this disease.12 page(s
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