Cryptophytes are a group of unicellular algae with chlorophyll c-containing plastids derived from the uptake of a secondary (i.e., eukaryotic) endosymbiont. Biochemical and molecular data indicate that cryptophyte plastids are derived from red algae, yet the question of whether or not cryptophytes acquired their red algal plastids independent of those in heterokont, haptophyte, and dinoflagellate algae is of long-standing debate. To better understand the origin and evolution of the cryptophyte plastid, we have sequenced the plastid genome of Rhodomonas salina CCMP1319: at 135,854 bp, it is the largest secondary plastid genome characterized thus far. It also possesses interesting features not seen in the distantly related cryptophyte Guillardia theta or in other red secondary plastids, including pseudogenes, introns, and a bacterial-derived gene for the tau/gamma subunit of DNA polymerase III (dnaX), the first time putative DNA replication machinery has been found encoded in any plastid genome. Phylogenetic analyses indicate that dnaX was acquired by lateral gene transfer (LGT) in an ancestor of Rhodomonas, most likely from a firmicute bacterium. A phylogenomic survey revealed no additional cases of LGT, beyond a noncyanobacterial type rpl36 gene similar to that recently characterized in other cryptophytes and haptophytes. Rigorous concatenated analysis of 45 proteins encoded in 15 complete plastid genomes produced trees in which the heterokont, haptophyte, and cryptophyte (i.e., chromist) plastids were monophyletic, and heterokonts and haptophytes were each other's closest relatives. However, statistical support for chromist monophyly disappears when amino acids are recoded according to their chemical properties in order to minimize the impact of composition bias, and a significant fraction of the concatenate appears consistent with a sister-group relationship between cryptophyte and haptophyte plastids.

Pathogenic autoantibodies associated with neuromyelitis optica (NMO) induce disease by targeting aquaporin-4 (AQP4) water channels enriched on astrocytic endfeet at blood–brain interfaces. AQP4 is also expressed at cerebrospinal fluid (CSF)–brain interfaces, such as the pial glia limitans and the ependyma and at the choroid plexus blood–CSF barrier. However, little is known regarding pathology at these sites in NMO. Therefore, we evaluated AQP4 expression, microglial reactivity, and complement deposition at pial and ependymal surfaces and in the fourth ventricle choroid plexus in 23 autopsy cases with clinically and/or pathologically confirmed NMO or NMO spectrum disorder. These findings were compared to five cases with multiple sclerosis, five cases of choroid plexus papilloma, and five control cases without central nervous system disease. In the NMO cases, AQP4 immunoreactivity was reduced relative to control levels in the pia (91%; 21/23), ependyma (56%; 9/16), and choroid plexus epithelium (100%; 12/12). AQP4 immunoreactivity was normal in MS cases in these regions. Compared to MS, NMO cases also showed a focal pattern of pial and ependymal complement deposition and more pronounced microglial reactivity. In addition, AQP4 loss, microglial reactivity, and complement deposition colocalized along the pia and ependyma only in NMO cases. Within the choroid plexus, AQP4 loss was coincident with C9neo immunoreactivity on epithelial cell membranes only in NMO cases. These observations demonstrate that NMO immunopathology extends beyond perivascular astrocytic foot processes to include the pia, ependyma, and choroid plexus, suggesting that NMO IgG-induced pathological alterations at CSF–brain and blood–CSF interfaces may contribute to the occurrence of ventriculitis, leptomeningitis, and hydrocephalus observed among NMO patients. Moreover, disruption of the blood–CSF barrier induced by binding of NMO IgG to AQP4 on the basolateral surface of choroid plexus epithelial cells may provide a unique portal for entry of the pathogenic antibody into the central nervous system.Electronic supplementary materialThe online version of this article (doi:10.1007/s00401-017-1682-1) contains supplementary material, which is available to authorized users.

Clinically, fatigue is a common concern cited by patients following a stroke. While there is a popular notion of what constitutes fatigue, a widely accepted operational definition for scientific study is lacking 1 . Fatigue is subjective, an experience that may be conceptualized on a continuum from normal to pathologic 2 . pathologic fatigue may be differentiated by severity, duration, and functional impairment. the experience of fatigue ABSTRACT: Background: Fatigue affects 33-77% of stroke survivors. there is no consensus concerning risk factors for fatigue poststroke, perhaps reflecting the multifaceted nature of fatigue. We characterized post-stroke fatigue using the Fatigue impact Scale (FiS), a validated questionnaire capturing physical, cognitive, and psychosocial aspects of fatigue. Methods: the Stroke outcomes Study (SoS) prospectively enrolled ischemic stroke patients from [2001][2002]. Measures collected included basic demographics, pre-morbid function (oxford Handicap Scale, oHS), stroke severity (Stroke Severity Scale, SSS), stroke subtype (oxfordshire Community Stroke project Classification, oCSp), and discharge function (oHS; barthel index, bi). an interview was performed at 12 months evaluating function (bi; Modified Rankin Score, mRS), quality of life (Reintegration into Normal living Scale, RNl), depression (geriatric Depression Scale, gDS), and fatigue (FiS). Results: We enrolled 522 ischemic stroke patients and 228 (57.6%) survivors completed one-year follow-up. in total, 36.8% endorsed fatigue (59.5% rated one of worst post-stroke symptoms). linear regression demonstrated younger age was associated with increased fatigue frequency (β=-0.20;p=0.01), duration (β=-0.22;p<0.01), and disability (β=-0.24;p<0.01). younger patients were more likely to describe fatigue as one of the worst symptoms post-stroke (β=-0.24;p=0.001). younger patients experienced greater impact on cognitive (β=-0.27;p<0.05) and psychosocial (β=-0.27;p<0.05) function due to fatigue. Fatigue was correlated with depressive symptoms and diminished quality of life. Fatigue occurred without depression as 49.0% of respondents with fatigue as one of their worst symptoms did not have an elevated gDS. Conclusions: age was the only consistent predictor of fatigue severity at one year. younger participants experienced increased cognitive and psychosocial fatigue.RÉSUMÉ: L'échelle de l'impact de la fatigue démontre la présence d'une fatigue plus importante chez les survivants d'un accident vasculaire cérébral qui sont plus jeunes. Contexte : entre 33 et 77% des patients qui survivent à un accident vasculaire cérébral (avC) éprouvent de la fatigue. il n'existe pas de consensus concernant les facteurs de risque de la fatigue post avC, ce qui témoigne peut-être des multiples facettes de la fatigue. Nous avons caractérisé la fatigue post avC au moyen de l'Échelle des répercussions de la fatigue (eRF), un questionnaire validé qui englobe les aspects physiques, cognitifs et psychosociaux de la fatigue. Méthode : le Stroke outcomes Study a rec...

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