Changes in carbon dioxide during an oceanic anoxic event linked to intrusion into Gondwana coals

The marine sedimentary record exhibits evidence for episodes of enhanced organic carbon burial known as 'oceanic anoxic events' (OAEs). They are characterized by carbon-isotope excursions in marine and terrestrial reservoirs and mass extinction of marine faunas. Causal mechanisms for the enhancement of organic carbon burial during OAEs are still debated, but it is thought that such events should draw down significant quantities of atmospheric carbon dioxide. In the case of the Toarcian OAE (approximately 183 million years ago), a short-lived negative carbon-isotope excursion in oceanic and terrestrial reservoirs has been interpreted to indicate raised atmospheric carbon dioxide caused by oxidation of methane catastrophically released from either marine gas hydrates or magma-intruded organic-rich rocks. Here we test these two leading hypotheses for a negative carbon isotopic excursion marking the initiation of the Toarcian OAE using a high-resolution atmospheric carbon dioxide record obtained from fossil leaf stomatal frequency. We find that coincident with the negative carbon-isotope excursion carbon dioxide is first drawn down by 350 +/- 100 p.p.m.v. and then abruptly elevated by 1,200 +/- 400 p.p.m.v, and infer a global cooling and greenhouse warming of 2.5 +/- 0.1 degrees C and 6.5 +/- 1 degrees C, respectively. The pattern and magnitude of carbon dioxide change are difficult to reconcile with catastrophic input of isotopically light methane from hydrates as the cause of the negative isotopic signal. Our carbon dioxide record better supports a magma-intrusion hypothesis, and suggests that injection of isotopically light carbon from the release of thermogenic methane occurred owing to the intrusion of Gondwana coals by Toarcian-aged Karoo-Ferrar dolerites.     

Analysis of the DNA sequence and duplication history of human chromosome 15

Here we present a finished sequence of human chromosome 15, together with a high-quality gene catalogue. As chromosome 15 is one of seven human chromosomes with a high rate of segmental duplication, we have carried out a detailed analysis of the duplication structure of the chromosome. Segmental duplications in chromosome 15 are largely clustered in two regions, on proximal and distal 15q; the proximal region is notable because recombination among the segmental duplications can result in deletions causing Prader-Willi and Angelman syndromes. Sequence analysis shows that the proximal and distal regions of 15q share extensive ancient similarity. Using a simple approach, we have been able to reconstruct many of the events by which the current duplication structure arose. We find that most of the intrachromosomal duplications seem to share a common ancestry. Finally, we demonstrate that some remaining gaps in the genome sequence are probably due to structural polymorphisms between haplotypes; this may explain a significant fraction of the gaps remaining in the human genome.     

神奇的心理暗示

<正>很多时候,失败并不是单纯地因为力量薄弱,还有可能是失去了平和的心态,以至乱了方寸。由此可见,心理暗示的作用不容小觑。你有过这样的经历吗?某天,你穿了一双自认为很酷的鞋出门,结果却接二连三地被同学们嫌弃。当第一个同学说不好看的时候,你可能还觉得这只是他的个人看法而己,可是当越来越多的人这么说了之后,你也就慢慢开始怀疑自己的审美眼光了。于是心里     

Rapid appearance and local toxicity of amyloid-beta plaques in a mouse model of Alzheimer's disease

Senile plaques accumulate over the course of decades in the brains of patients with Alzheimer's disease. A fundamental tenet of the amyloid hypothesis of Alzheimer's disease is that the deposition of amyloid-beta precedes and induces the neuronal abnormalities that underlie dementia. This idea has been challenged, however, by the suggestion that alterations in axonal trafficking and morphological abnormalities precede and lead to senile plaques. The role of microglia in accelerating or retarding these processes has been uncertain. To investigate the temporal relation between plaque formation and the changes in local neuritic architecture, we used longitudinal in vivo multiphoton microscopy to sequentially image young APPswe/PS1d9xYFP (B6C3-YFP) transgenic mice. Here we show that plaques form extraordinarily quickly, over 24 h. Within 1-2 days of a new plaque's appearance, microglia are activated and recruited to the site. Progressive neuritic changes ensue, leading to increasingly dysmorphic neurites over the next days to weeks. These data establish plaques as a critical mediator of neuritic pathology.     

Genome-wide genetic analysis of polyploidy in yeast

Polyploidy, increased sets of chromosomes, occurs during development, cellular stress, disease and evolution. Despite its prevalence, little is known about the physiological alterations that accompany polyploidy. We previously described 'ploidy-specific lethality', where a gene deletion that is not lethal in haploid or diploid budding yeast causes lethality in triploids or tetraploids. Here we report a genome-wide screen to identify ploidy-specific lethal functions. Only 39 out of 3,740 mutations screened exhibited ploidy-specific lethality. Almost all of these mutations affect genomic stability by impairing homologous recombination, sister chromatid cohesion, or mitotic spindle function. We uncovered defects in wild-type tetraploids predicted by the screen, and identified mechanisms by which tetraploidization affects genomic stability. We show that tetraploids have a high incidence of syntelic/monopolar kinetochore attachments to the spindle pole. We suggest that this defect can be explained by mismatches in the ability to scale the size of the spindle pole body, spindle and kinetochores. Thus, geometric constraints may have profound effects on genome stability; the phenomenon described here may be relevant in a variety of biological contexts, including disease states such as cancer.