994 resultados para 126-792C
Resumo:
Numerous marine tephra layers cored at Sites 792 and 793 in the Izu-Bonin forearc region offer additional information about the timing and spatial characteristics of arc volcanism and the evolution of island arcs. Explosive volcanism along the Izu-Bonin Arc, with maxima just before rifting of the arc at ~40 and 5-0 Ma, produced black and white tephras of variable grain sizes and chemical compositions. Most of the tephras belong chemically to low-K and low-alkali tholeiitic rock series with a few tephra of the high-K and alkalic rock series. Most of the tephras (low-K series) were derived from the Izu-Bonin Arc, although a few were produced far to the west of the Izu-Bonin Arc (e.g., from the Ryukyu Arc). Black tephras may have come from nearby sources, such as Aogashima, Sumisu, and Torishima islands. The high-K series of tephras, within the sediments younger than 3 Ma, may reflect thickening of the island-arc crust.
Resumo:
Radiolarians occur at five Leg 126 sites. Well-preserved radiolarians were recovered from Miocene and Pliocene through Holocene sections. The results of this study may help to fill the informational gap on Quaternary radiolarian distribution at mid-latitudes in the western Pacific. Radiolarian preservation is discontinuous, and, although present in Oligocene sections, specimens are poorly preserved.
Resumo:
miR-126 has been implicated in the processes of inflammation and angiogenesis. Through these processes, miR-126 is implicated in cancer biology, but its role there has not been well reviewed. The aim of this review is to examine the molecular mechanisms and clinicopathological significance of miR-126 in human cancers. miR-126 was shown to have roles in cancers of the gastrointestinal tract, genital tracts, breast, thyroid, lung and some other cancers. Its expression was suppressed in most of the cancers studied. The molecular mechanisms that are known to cause aberrant expression of miR-126 include alterations in gene sequence, epigenetic modification and alteration of dicer abundance. miR-126 can inhibit progression of some cancers via negative control of proliferation, migration, invasion, and cell survival. In some instances, however, miR-126 supports cancer progression via promotion of blood vessel formation. Downregulation of miR-126 induces cancer cell proliferation, migration, and invasion via targeting specific oncogenes. Also, reduced levels of miR-126 are a significant predictor of poor survival of patients in many cancers. In addition, miR-126 can alter a multitude of cellular mechanisms in cancer pathogenesis via suppressing gene translation of numerous validated targets such as PI3K, KRAS, EGFL7, CRK, ADAM9, HOXA9, IRS-1, SOX-2, SLC7A5 and VEGF. To conclude, miR-126 is commonly down-regulated in cancer, most likely due to its ability to inhibit cancer cell growth, adhesion, migration, and invasion through suppressing a range of important gene targets. Understanding these mechanisms by which miR-126 is involved with cancer pathogenesis will be useful in the development of therapeutic targets for the management of patients with cancer.
Resumo:
A genome-wide association study (GWAS) of educational attainment was conducted in a discovery sample of 101,069 individuals and a replication sample of 25,490. Three independent single-nucleotide polymorphisms (SNPs) are genome-wide significant (rs9320913, rs11584700, rs4851266), and all three replicate. Estimated effects sizes are small (coefficient of determination R(2) approximately 0.02%), approximately 1 month of schooling per allele. A linear polygenic score from all measured SNPs accounts for approximately 2% of the variance in both educational attainment and cognitive function. Genes in the region of the loci have previously been associated with health, cognitive, and central nervous system phenotypes, and bioinformatics analyses suggest the involvement of the anterior caudate nucleus. These findings provide promising candidate SNPs for follow-up work, and our effect size estimates can anchor power analyses in social-science genetics.