Optimal nitrogen-to-phosphorus stoichiometry of phytoplankton

Redfield noted the similarity between the average nitrogen-to-phosphorus ratio in plankton (N:P = 16 by atoms) and in deep oceanic waters (N:P = 15; refs 1, 2). He argued that this was neither a coincidence, nor the result of the plankton adapting to the oceanic stoichiometry, but rather that phytoplankton adjust the N:P stoichiometry of the ocean to meet their requirements through nitrogen fixation, an idea supported by recent modelling studies. But what determines the N:P requirements of phytoplankton? Here we use a stoichiometrically explicit model of phytoplankton physiology and resource competition to derive from first principles the optimal phytoplankton stoichiometry under diverse ecological scenarios. Competitive equilibrium favours greater allocation to P-poor resource-acquisition machinery and therefore a higher N:P ratio; exponential growth favours greater allocation to P-rich assembly machinery and therefore a lower N:P ratio. P-limited environments favour slightly less allocation to assembly than N-limited or light-limited environments. The model predicts that optimal N:P ratios will vary from 8.2 to 45.0, depending on the ecological conditions. Our results show that the canonical Redfield N:P ratio of 16 is not a universal biochemical optimum, but instead represents an average of species-specific N:P ratios.     

Chicken welfare is influenced more by housing conditions than by stocking density

Intensive broiler (meat) chicken production now exceeds 800 million birds each year in the United Kingdom and 2 x 10(10) birds worldwide, but it attracts accusations of poor welfare. The European Union is currently adopting standards for broilers aimed at a chief welfare concern--namely, overcrowding--by limiting maximum 'stocking density' (bird weight per unit area). It is not clear, however, whether this will genuinely improve bird welfare because evidence is contradictory. Here we report on broiler welfare in relation to the European Union proposals through a large-scale study (2.7 million birds) with the unprecedented cooperation of ten major broiler producers in an experimental manipulation of stocking density under a range of commercial conditions. Producer companies stocked birds to five different final densities, but otherwise followed company practice, which we recorded in addition to temperature, humidity, litter and air quality. We assessed welfare through mortality, physiology, behaviour and health, with an emphasis on leg health and walking ability. Our results show that differences among producers in the environment that they provide for chickens have more impact on welfare than has stocking density itself.     

加压凝固熔模铸造制备纤维增强铝基复合材料

将熔模精密铸造和预制型液态浸渗技术相结合,开发了一种制备连续(长)纤维增强铝基复合材料的加压凝固熔模精密铸造工艺.该工艺将增强纤维的放置和零件的蜡模制作相结合,可直接生产出高精度的近净形复合材料零件.选定了Sumitomo Chemical公司生产的Altex SN型γ-Al2O3纤维作为复合材料的增强体,并开发了适合加压凝固熔模精密铸造工艺条件的铝合金基体材料AlZn6Mg1Ag1.试验表明这种γ-Al2O3连续纤维增强铝合金复合材料对加压凝固熔模精密铸造工艺有较好的适应性,并有非常理想的强度性能,具有广阔的应用前景.热处理(T6)后复合材料沿纤维方向的抗拉强度σb,0° =1 003 MPa,垂直于纤维方向的抗拉强度σb,90° =220 MPa.     

Field trial of an HTS filter system on a CDMA base station

This paper presents the field trial results of a high temperature superconductor filter system (HTSFS) in a code division multiple access (CDMA) mobile communication base station (BTS) in Tangshan, China. The center frequency of the HTSFS is 830 MHz with 1.4% fractional bandwidth. The noise figure (NF) of the HTSFS, including connectors and cables, is 0.8 dB. The field trial results show that after the HTSFS was installed in the receiver front-end of a CDMA base station, the transmitting power of handset was decreased by 3.1 dB on average. Up to now, the HTSFS has been running steadily in the base station for more than 22 months, demonstrating the reliability and stability of the system.     

A radiation hybrid map of the rat genome containing 5,255 markers.

A whole-genome radiation hybrid (RH) panel was used to construct a high-resolution map of the rat genome based on microsatellite and gene markers. These include 3,019 new microsatellite markers described here for the first time and 1,714 microsatellite markers with known genetic locations, allowing comparison and integration of maps from different sources. A robust RH framework map containing 1,030 positions ordered with odds of at least 1,000:1 has been defined as a tool for mapping these markers, and for future RH mapping in the rat. More than 500 genes which have been mapped in mouse and/or human were localized with respect to the rat RH framework, allowing the construction of detailed rat-mouse and rat-human comparative maps and illustrating the power of the RH approach for comparative mapping.     

Spatial proximity of translocation-prone gene loci in human lymphomas

Cancer cells frequently have disease-specific chromosome rearrangements. It is poorly understood why translocations between chromosomes recur at specific breakpoints in the genome. Here we provide evidence that higher-order spatial genome organization is a contributing factor in the formation of recurrent translocations. We show that MYC, BCL and immunoglobulin loci, which are recurrently translocated in various B-cell lymphomas, are preferentially positioned in close spatial proximity relative to each other in normal B cells. Loci in spatial proximity are non-randomly positioned towards the nuclear interior in normal B cells. This locus proximity is the consequence of higher-order genome structure rather than a property of individual genes. Our results suggest that the formation of specific translocations in human lymphomas, and perhaps other tissues, is determined in part by higher-order spatial organization of the genome.     

Generation of functional insulin-producing cells in the gut by Foxo1 ablation

Restoration of regulated insulin secretion is the ultimate goal of therapy for type 1 diabetes. Here, we show that, unexpectedly, somatic ablation of Foxo1 in Neurog3(+) enteroendocrine progenitor cells gives rise to gut insulin-positive (Ins(+)) cells that express markers of mature β cells and secrete bioactive insulin as well as C-peptide in response to glucose and sulfonylureas. Lineage tracing experiments showed that gut Ins(+) cells arise cell autonomously from Foxo1-deficient cells. Inducible Foxo1 ablation in adult mice also resulted in the generation of gut Ins(+) cells. Following ablation by the β-cell toxin streptozotocin, gut Ins(+) cells regenerate and produce insulin, reversing hyperglycemia in mice. The data indicate that Neurog3(+) enteroendocrine progenitors require active Foxo1 to prevent differentiation into Ins(+) cells. Foxo1 ablation in gut epithelium may provide an approach to restore insulin production in type 1 diabetes.     

Nf1;Trp53 mutant mice develop glioblastoma with evidence of strain-specific effects

Astrocytomas are the leading cause of brain cancer in humans. Because these tumours are highly infiltrative, current treatments that rely on targeting the tumour mass are often ineffective. A mouse model for astrocytoma would be a powerful tool for dissecting tumour progression and testing therapeutics. Mouse models of astrocytoma have been designed to express oncogenic proteins in astrocytes, but have had limited success due to low tumour penetrance or limited tumour progression. We present here a mouse model of astrocytomas involving mutation of two tumour-suppressor genes, Nf1 and Trp53. Humans with mutations in NF1 develop neurofibromatosis type I (NF1) and have increased risk of optic gliomas, astrocytomas and glioblastomas. The TP53 tumour suppressor is often mutated in a subset of astrocytomas that develop at a young age and progress slowly to glioblastoma (termed secondary glioblastomas, in contrast to primary glioblastomas that develop rapidly de novo). This mouse model shows a range of astrocytoma stages, from low-grade astrocytoma to glioblastoma multiforme, and may accurately model human secondary glioblastoma involving TP53 loss. This is the first reported mouse model of astrocytoma initiated by loss of tumour suppressors, rather than overexpression of transgenic oncogenes.     

Novel mutations in families with unusual and variable disorders of the skeletal muscle sodium channel.

Mutations in the skeletal muscle sodium channel gene (SCN4A) have been described in paramyotonia congenita (PMC) and hyperkalaemic periodic paralysis (HPP). We have found two mutations in SCN4A which affect regions of the sodium channel not previously associated with a disease phenotype. Furthermore, affected family members display an unusual mixture of clinical features reminiscent of PMC, HPP and of a third disorder, myotonia congenita (MC). The highly variable individual expression of these symptoms, including in some cases apparent non-penetrance, implies the existence of modifying factors. Mutations in SCN4A can produce a broad range of phenotypes in muscle diseases characterized by episodic abnormalities of membrane excitability.