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  1. Fulltext Cardiovascular health decline in adolescent girls in the NGHS cohort, 1987-1997
    Gooding HC, Ning H, Perak AM, Allen N, Lloyd-Jones D, Moore LL, et al.
    Prev Med Rep, 2020 Dec;20:101276.
    PMID: 33344149 DOI: 10.1016/j.pmedr.2020.101276
    Adolescence is a critical time for the preservation or loss of cardiovascular health. We aimed to describe trajectories of cardiovascular health in adolescent girls and identify early adolescent factors associated with cardiovascular health in young adulthood. We used data from the National Growth and Health Study, a longitudinal cohort of 2,379 girls followed annually from ages 9-19 years. We classified participants as having ideal, intermediate, or poor levels of the seven cardiovascular health metrics at four developmental stages: early (ages 9-11), middle (ages 12-14), and late (ages 15-17) adolescence, and early young adulthood (ages ≥ 18). We calculated total cardiovascular health scores (range 0-14) at each stage and empirically identified patterns of cardiovascular health trajectories. We examined associations between trajectory group membership and various demographic, behavioral, and physiological factors. Mean cardiovascular health scores declined with age from 10.8 to 9.4 in white girls and 10.3 to 8.9 in black girls; 17% of white girls and 23% of black girls had low cardiovascular health (score 
  2. Gigantic chloroplasts, including bizonoplasts, are common in shade-adapted species of the ancient vascular plant family Selaginellaceae
    Liu JW, Li SF, Wu CT, Valdespino IA, Ho JF, Wu YH, et al.
    Am J Bot, 2020 04;107(4):562-576.
    PMID: 32227348 DOI: 10.1002/ajb2.1455
    PREMISE: Unique among vascular plants, some species of Selaginella have single giant chloroplasts in their epidermal or upper mesophyll cells (monoplastidy, M), varying in structure between species. Structural variants include several forms of bizonoplast with unique dimorphic ultrastructure. Better understanding of these structural variants, their prevalence, environmental correlates and phylogenetic association, has the potential to shed new light on chloroplast biology unavailable from any other plant group.

    METHODS: The chloroplast ultrastructure of 76 Selaginella species was studied with various microscopic techniques. Environmental data for selected species and subgeneric relationships were compared against chloroplast traits.

    RESULTS: We delineated five chloroplast categories: ME (monoplastidy in a dorsal epidermal cell), MM (monoplastidy in a mesophyll cell), OL (oligoplastidy), Mu (multiplastidy, present in the most basal species), and RC (reduced or vestigial chloroplasts). Of 44 ME species, 11 have bizonoplasts, cup-shaped (concave upper zone) or bilobed (basal hinge, a new discovery), with upper zones of parallel thylakoid membranes varying subtly between species. Monoplastidy, found in 49 species, is strongly shade associated. Bizonoplasts are only known in deep-shade species (<2.1% full sunlight) of subgenus Stachygynandrum but in both the Old and New Worlds.

    CONCLUSIONS: Multiplastidic chloroplasts are most likely basal, implying that monoplastidy and bizonoplasts are derived traits, with monoplastidy evolving at least twice, potentially as an adaptation to low light. Although there is insufficient information to understand the adaptive significance of the numerous structural variants, they are unmatched in the vascular plants, suggesting unusual evolutionary flexibility in this ancient plant genus.

  3. Fulltext FAT1 mutations cause a glomerulotubular nephropathy
    Gee HY, Sadowski CE, Aggarwal PK, Porath JD, Yakulov TA, Schueler M, et al.
    Nat Commun, 2016 Feb 24;7:10822.
    PMID: 26905694 DOI: 10.1038/ncomms10822
    Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney disease (CKD). Here we show that recessive mutations in FAT1 cause a distinct renal disease entity in four families with a combination of SRNS, tubular ectasia, haematuria and facultative neurological involvement. Loss of FAT1 results in decreased cell adhesion and migration in fibroblasts and podocytes and the decreased migration is partially reversed by a RAC1/CDC42 activator. Podocyte-specific deletion of Fat1 in mice induces abnormal glomerular filtration barrier development, leading to podocyte foot process effacement. Knockdown of Fat1 in renal tubular cells reduces migration, decreases active RAC1 and CDC42, and induces defects in lumen formation. Knockdown of fat1 in zebrafish causes pronephric cysts, which is partially rescued by RAC1/CDC42 activators, confirming a role of the two small GTPases in the pathogenesis. These findings provide new insights into the pathogenesis of SRNS and tubulopathy, linking FAT1 and RAC1/CDC42 to podocyte and tubular cell function.
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