Roduction of active, cleaved BID on cardiolipin platforms that serve for the assembly of active caspase-8 and in the GUV “mimicking system”. (a) The order ZK-36374 diagram depicts the sequence of events in cells of type II according to Gonzalvez et al. [25]. The CL (red heads)/caspase-8 platform at the contact sites between inner and outer mitochondrial membranes (enriched in CL) binds BID resulting in the production of the active truncated, C-termimal part of BID (tcBID). This in turn causes CL induced perturbations of the membrane curvature, BAK/BAX oligomerization and cytochrome c release. (b) Schematic representation 1531364 of the reconstituted functional platform on giant unilamellar vesicles containing CL with the p18/p10. DD, death domain; DED, death effector domain; p10 and p18 form the catalytic core of the caspase. The p43/p10 caspase-8 isoform comprises two DEDs, one p10 domain and one p18 domain. IMM, inner mitochondrial membrane; IMS, inter membrane space; OM, outer mitochondrial membrane. Red dots in the intermembrane espace, cytochrome c and the violet head correspond to the cardiolipin at the contact sites between outer and inner membrane. doi:10.1371/journal.pone.0055250.order BIBS39 gfamily members, but also as key players in recognition processes as demonstrated by the example cardiolipin triggering the activation of caspase-8 in the apoptotic process.Author ContributionsConceived and designed the experiments: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Performed the experiments: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Analyzed the data: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Contributed reagents/materials/analysis tools: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Wrote the paper: OJ AJGS BK PXP.AcknowledgmentstBid was provided to BK and PXP by Bruno Antonsson (Serono Pharmaceutical Research Institute, Geneva, Switzerland) or by JeanClaude Martinou (University Geneva, Zwitzerland) which also provided us with active caspase-8 (P10/P18). Thanks also to Lawrence Aggerbeck for help writing the manuscript.The Mitosome: Cardiolipin-Caspase-8-Bid
Migraine is a neurological disease characterized by recurrent episodes of headache [1]. The reported prevalence in men and women is 8.6 and 17.5 , respectively [2]. While migraine has been associated with an increased risk of ischemic stroke [3?], it remains controversial whether it is also linked to an increased risk of hemorrhagic stroke (HS). While retrospective studies have suggested a link between migraine and HS in women [6,7] and prospective data from the Women’s Health Study showed an increased risk of HS in migraineurs with aura [8], several other studies were unable to identify a higher risk of HS in patients with migraine [5,9,10]. Such inconsistency may be partly due to small sample size and partly to the retrospective case-control design adopted in the majority of studies, which makes it difficult to establish a temporal relationship between migraine and HS. In addition, research on the association between migraine and HS in men is sparse. We therefore performed this large-scale, population-based, age- and sex-matched follow-up study to investigatewhether migraine is associated with increased risk of developing HS.Materials and Methods Data sourceThe data used in this study were obtained from the complete National Health Insurance (NHI) claim database in Taiwan for the period 2000 to 2003. The NHI program has been implemented in Taiwan since 1995, and the coverage rate was 96 of the whole population in 2000 and.Roduction of active, cleaved BID on cardiolipin platforms that serve for the assembly of active caspase-8 and in the GUV “mimicking system”. (a) The diagram depicts the sequence of events in cells of type II according to Gonzalvez et al. [25]. The CL (red heads)/caspase-8 platform at the contact sites between inner and outer mitochondrial membranes (enriched in CL) binds BID resulting in the production of the active truncated, C-termimal part of BID (tcBID). This in turn causes CL induced perturbations of the membrane curvature, BAK/BAX oligomerization and cytochrome c release. (b) Schematic representation 1531364 of the reconstituted functional platform on giant unilamellar vesicles containing CL with the p18/p10. DD, death domain; DED, death effector domain; p10 and p18 form the catalytic core of the caspase. The p43/p10 caspase-8 isoform comprises two DEDs, one p10 domain and one p18 domain. IMM, inner mitochondrial membrane; IMS, inter membrane space; OM, outer mitochondrial membrane. Red dots in the intermembrane espace, cytochrome c and the violet head correspond to the cardiolipin at the contact sites between outer and inner membrane. doi:10.1371/journal.pone.0055250.gfamily members, but also as key players in recognition processes as demonstrated by the example cardiolipin triggering the activation of caspase-8 in the apoptotic process.Author ContributionsConceived and designed the experiments: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Performed the experiments: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Analyzed the data: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Contributed reagents/materials/analysis tools: OJ LFM AJGS MP TG FG EG JAS BK PS PXP. Wrote the paper: OJ AJGS BK PXP.AcknowledgmentstBid was provided to BK and PXP by Bruno Antonsson (Serono Pharmaceutical Research Institute, Geneva, Switzerland) or by JeanClaude Martinou (University Geneva, Zwitzerland) which also provided us with active caspase-8 (P10/P18). Thanks also to Lawrence Aggerbeck for help writing the manuscript.The Mitosome: Cardiolipin-Caspase-8-Bid
Migraine is a neurological disease characterized by recurrent episodes of headache [1]. The reported prevalence in men and women is 8.6 and 17.5 , respectively [2]. While migraine has been associated with an increased risk of ischemic stroke [3?], it remains controversial whether it is also linked to an increased risk of hemorrhagic stroke (HS). While retrospective studies have suggested a link between migraine and HS in women [6,7] and prospective data from the Women’s Health Study showed an increased risk of HS in migraineurs with aura [8], several other studies were unable to identify a higher risk of HS in patients with migraine [5,9,10]. Such inconsistency may be partly due to small sample size and partly to the retrospective case-control design adopted in the majority of studies, which makes it difficult to establish a temporal relationship between migraine and HS. In addition, research on the association between migraine and HS in men is sparse. We therefore performed this large-scale, population-based, age- and sex-matched follow-up study to investigatewhether migraine is associated with increased risk of developing HS.Materials and Methods Data sourceThe data used in this study were obtained from the complete National Health Insurance (NHI) claim database in Taiwan for the period 2000 to 2003. The NHI program has been implemented in Taiwan since 1995, and the coverage rate was 96 of the whole population in 2000 and.
