Decreased pericellular matrix production and selection for enhanced cell membrane repair may impair osteocyte responses to mechanical loading in the aging skeleton

Transient plasma membrane disruptions (PMD) occur in osteocytes with in vitro and in vivo loading, initiating mechanotransduction. The goal here was to determine whether osteocyte PMD formation or repair is affected by aging. Osteocytes from old (24 months) mice developed fewer PMD (?76% females, ?54% males) from fluid shear than young (3 months) mice, and old mice developed fewer osteocyte PMD (?51%) during treadmill running. This was due at least in part to decreased pericellular matrix production, as studies revealed that pericellular matrix is integral to formation of osteocyte PMD, and aged osteocytes produced less pericellular matrix (?55%). Surprisingly, osteocyte PMD repair rate was faster (+25% females, +26% males) in osteocytes from old mice, and calcium wave propagation to adjacent nonwounded osteocytes was blunted, consistent with impaired mechanotransduction downstream of PMD in osteocytes with fast PMD repair in previous studies. Inducing PMD via fluid flow in young osteocytes in the presence of oxidative stress decreased postwounding cell survival and promoted accelerated PMD repair in surviving cells, suggesting selective loss of slower‐repairing osteocytes. Therefore, as oxidative stress increases during aging, slower‐repairing osteocytes may be unable to successfully repair PMD, leading to slower‐repairing osteocyte death in favor of faster‐repairing osteocyte survival. Since PMD are an important initiator of mechanotransduction, age‐related decreases in pericellular matrix and loss of slower‐repairing osteocytes may impair the ability of bone to properly respond to mechanical loading with bone formation. These data suggest that PMD formation and repair mechanisms represent new targets for improving bone mechanosensitivity with aging.     

Novel homozygous mutations in the genes ARL6 and BBS10 underlying Bardet–Biedl syndrome

Bardet–Biedl syndrome (BBS) is an autosomal recessive disorder resulting from structural and functional defects in numerous organs. Frequent manifestations reported in the syndrome include obesity, renal dysplasia, cognitive impairment, postaxial polydactyly, pigmentary retinal degeneration and hypogonadism. To date, 17 genes causing BBS have been identified. Two of these BBS1 and BBS10 are the most frequently mutated genes.     

大鼠产前手机辐射对子代小脑白质的影响

目的:探讨大鼠产前850～1 900 MHz手机辐射对成年子代小脑白质的影响。方法:孕鼠随机分为短时产前手机辐射组、长时产前手机辐射组和对照组,短时和长时辐射组于孕期第1～17日分别进行每天6 h和24 h手机辐射,各组雄性子代大鼠(n＝8)于3月龄取小脑组织,进行苏木精-伊红(HE)染色观察小脑皮质细胞形态,免疫组化和Western blot检测髓鞘碱性蛋白(MBP)、神经微丝-L(NF-L)和胶质纤维酸性蛋白(GFAP)表达。结果:与对照组比较,短时程和长时程产前手机辐射组子代大鼠小脑浦肯野细胞出现形态学改变;与对照组比较,长时程辐射组MBP、NF-L表达明显减少(P均＜0.05),而GFAP表达明显增多(P＜0.05);与短时程辐射组比较,长时程组子代大鼠小脑MBP、NF-L表达明显减少(P均＜0.05),而GFAP表达明显增多(P＜0.05)。结论:产前手机辐射会导致雄性子代大鼠小脑髓鞘和轴突的损害,以及星形胶质细胞的活化,且这种改变与产前手机辐射的时程相关。     

Origin and evolution of chromosomal sperm proteins

In the eukaryotic cell, DNA compaction is achieved through its interaction with histones, constituting a nucleoprotein complex called chromatin. During metazoan evolution, the different structural and functional constraints imposed on the somatic and germinal cell lines led to a unique process of specialization of the sperm nuclear basic proteins (SNBPs) associated with chromatin in male germ cells. SNBPs encompass a heterogeneous group of proteins which, since their discovery in the nineteenth century, have been studied extensively in different organisms. However, the origin and controversial mechanisms driving the evolution of this group of proteins has only recently started to be understood. Here, we analyze in detail the histone hypothesis for the vertical parallel evolution of SNBPs, involving a “vertical” transition from a histone to a protamine‐like and finally protamine types (H → PL → P), the last one of which is present in the sperm of organisms at the uppermost tips of the phylogenetic tree. In particular, the common ancestry shared by the protamine‐like (PL)‐ and protamine (P)‐types with histone H1 is discussed within the context of the diverse structural and functional constraints acting upon these proteins during bilaterian evolution.     

Apparatus Composition, Growth, And Survivorship Of The Lower Ordovician Conodont paracordylodus Gracilis Lindström, 1955

Analysis of numerous conodont element clusters from the Lower Ordovician cherts of the Burubaital Formation in central Kazakhstan reveals that the apparatus of Paracordylodus gracilis Lindstro¨m, 1955 consisted of 15 elements: two M elements, nine S elements (including 1 S₀), and four P elements (2 P₁, 2 P₂). The clusters probably originated as faecal pellets, but the best preserved indicate that the architecture of the apparatus of P. gracilis was comparable to that of ozarkodinid conodonts, providing strong support for the hypothesis that the 15-element 2M-9S-4P apparatus plan was plesiomorphic for conodonts with morphologically complex elements. All the elements within the P. gracilis clusters appear to be at a similar stage of ontogeny, and there is no evidence for late addition or replacement of elements. Analysis of element growth suggests that the relative dimensions of some elements changed during ontogeny, but the available data support the hypothesis that the growth of the apparatus as a whole was isometric. The size distribution of P. gracilis in the Burubaital Formation suggests that individuals in a particular size range were preferentially selected for consumption by predators. The identity of these predators is unknown, but they may have included other P. gracilis .