Grass rhizosheaths: associated bacterial communities and potential for nitrogen fixation

Rhizosheaths are structures composed of mucilage secreted from plants and adherent soil particles that form a cylinder around the root. Using scanning electron microscopy (SEM), we observed bacteria associated with rhizosheaths of the grasses Achnatherum hymenoides, Calamovilfa longifolia, Hesperostipa comata, and Pascopyrum smithii from a sand dune area in Harding County in northwestern South Dakota. The greatest numbers of bacteria, observed with SEM (529 mm –2 ), and the greatest number of culturable bacteria (9.9 × 10 7 CFU ? g –1 or 5178 CFU ? mm –2 ) were on rhizosheaths of C. longifolia. Rhizosheaths of all the grasses examined contained a higher density of bacteria than the surrounding soil. Nitrogen fixation, as assayed by reduction of acetylene to ethylene, was present in some rhizosheaths. Bacterial nif H gene sequences amplified from bacteria associated with rhizosheaths were most similar to those from Alcaligenes latus and Mesorhizobium loti .     

研制中的新一代仿生人

目前,欧美科学家在仿生学方面进行着广泛地研究,他们即将推出以塑料肌肉和硅芯片有机结合制作的仿生人,令人难以分辨真人与机器人。仿生装置除了替代残疾人体部位外,在防御和治疗疾患上正日益显现出难能可贵的应用潜力。在美国新墨西哥州立大学一所杂乱喧嚣的实验室内,一架人体骨骼复制品轻盈悠然地踩着一辆练习用自行车。这绝非别出心裁的人体技艺展示,人称博尼（Bony）先生的仿生人正在用电池驱动的人工肌肉蹬踏自行车。40年前,瑞典工程师阿尼·拉尔森（ArneLarsson）在首都斯德哥尔摩的卡罗琳斯克研究所研制出第一台完全植入式…     

The earliest record of human activity in northern Europe

The colonization of Eurasia by early humans is a key event after their spread out of Africa, but the nature, timing and ecological context of the earliest human occupation of northwest Europe is uncertain and has been the subject of intense debate. The southern Caucasus was occupied about 1.8 million years (Myr) ago, whereas human remains from Atapuerca-TD6, Spain (more than 780 kyr ago) and Ceprano, Italy (about 800 kyr ago) show that early Homo had dispersed to the Mediterranean hinterland before the Brunhes-Matuyama magnetic polarity reversal (780 kyr ago). Until now, the earliest uncontested artefacts from northern Europe were much younger, suggesting that humans were unable to colonize northern latitudes until about 500 kyr ago. Here we report flint artefacts from the Cromer Forest-bed Formation at Pakefield (52 degrees N), Suffolk, UK, from an interglacial sequence yielding a diverse range of plant and animal fossils. Event and lithostratigraphy, palaeomagnetism, amino acid geochronology and biostratigraphy indicate that the artefacts date to the early part of the Brunhes Chron (about 700 kyr ago) and thus represent the earliest unequivocal evidence for human presence north of the Alps.     

A Bayesian threshold nonlinearity test for financial time series

We propose in this paper a threshold nonlinearity test for financial time series. Our approach adopts reversible‐jump Markov chain Monte Carlo methods to calculate the posterior probabilities of two competitive models, namely GARCH and threshold GARCH models. Posterior evidence favouring the threshold GARCH model indicates threshold nonlinearity or volatility asymmetry. Simulation experiments demonstrate that our method works very well in distinguishing GARCH and threshold GARCH models. Sensitivity analysis shows that our method is robust to misspecification in error distribution. In the application to 10 market indexes, clear evidence of threshold nonlinearity is discovered and thus supporting volatility asymmetry. Copyright © 2005 John Wiley & Sons, Ltd.     

Rsx is a metatherian RNA with Xist-like properties in X-chromosome inactivation

In female (XX) mammals, one of the two X chromosomes is inactivated to ensure an equal dose of X-linked genes with males (XY). X-chromosome inactivation in eutherian mammals is mediated by the non-coding RNA Xist. Xist is not found in metatherians (marsupials), and how X-chromosome inactivation is initiated in these mammals has been the subject of speculation for decades. Using the marsupial Monodelphis domestica, here we identify Rsx (RNA-on-the-silent X), an RNA that has properties consistent with a role in X-chromosome inactivation. Rsx is a large, repeat-rich RNA that is expressed only in females and is transcribed from, and coats, the inactive X chromosome. In female germ cells, in which both X chromosomes are active, Rsx is silenced, linking Rsx expression to X-chromosome inactivation and reactivation. Integration of an Rsx transgene on an autosome in mouse embryonic stem cells leads to gene silencing in cis. Our findings permit comparative studies of X-chromosome inactivation in mammals and pose questions about the mechanisms by which X-chromosome inactivation is achieved in eutherians.     

Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

Frontotemporal dementia (FTD) is the second most common cause of dementia in people under the age of 65 years. A large proportion of FTD patients (35-50%) have a family history of dementia, consistent with a strong genetic component to the disease. In 1998, mutations in the gene encoding the microtubule-associated protein tau (MAPT) were shown to cause familial FTD with parkinsonism linked to chromosome 17q21 (FTDP-17). The neuropathology of patients with defined MAPT mutations is characterized by cytoplasmic neurofibrillary inclusions composed of hyperphosphorylated tau. However, in multiple FTD families with significant evidence for linkage to the same region on chromosome 17q21 (D17S1787-D17S806), mutations in MAPT have not been found and the patients consistently lack tau-immunoreactive inclusion pathology. In contrast, these patients have ubiquitin (ub)-immunoreactive neuronal cytoplasmic inclusions and characteristic lentiform ub-immunoreactive neuronal intranuclear inclusions. Here we demonstrate that in these families, FTD is caused by mutations in progranulin (PGRN) that are likely to create null alleles. PGRN is located 1.7 Mb centromeric of MAPT on chromosome 17q21.31 and encodes a 68.5-kDa secreted growth factor involved in the regulation of multiple processes including development, wound repair and inflammation. PGRN has also been strongly linked to tumorigenesis. Moreover, PGRN expression is increased in activated microglia in many neurodegenerative diseases including Creutzfeldt-Jakob disease, motor neuron disease and Alzheimer's disease. Our results identify mutations in PGRN as a cause of neurodegenerative disease and indicate the importance of PGRN function for neuronal survival.     

Oncogenic pathway signatures in human cancers as a guide to targeted therapies

The development of an oncogenic state is a complex process involving the accumulation of multiple independent mutations that lead to deregulation of cell signalling pathways central to the control of cell growth and cell fate. The ability to define cancer subtypes, recurrence of disease and response to specific therapies using DNA microarray-based gene expression signatures has been demonstrated in multiple studies. Various studies have also demonstrated the potential for using gene expression profiles for the analysis of oncogenic pathways. Here we show that gene expression signatures can be identified that reflect the activation status of several oncogenic pathways. When evaluated in several large collections of human cancers, these gene expression signatures identify patterns of pathway deregulation in tumours and clinically relevant associations with disease outcomes. Combining signature-based predictions across several pathways identifies coordinated patterns of pathway deregulation that distinguish between specific cancers and tumour subtypes. Clustering tumours based on pathway signatures further defines prognosis in respective patient subsets, demonstrating that patterns of oncogenic pathway deregulation underlie the development of the oncogenic phenotype and reflect the biology and outcome of specific cancers. Predictions of pathway deregulation in cancer cell lines are also shown to predict the sensitivity to therapeutic agents that target components of the pathway. Linking pathway deregulation with sensitivity to therapeutics that target components of the pathway provides an opportunity to make use of these oncogenic pathway signatures to guide the use of targeted therapeutics.