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101.
Steven W Kembel Evan Jones Jeff Kline Dale Northcutt Jason Stenson Ann M Womack Brendan JM Bohannan G Z Brown Jessica L Green 《The ISME journal》2012,6(8):1469-1479
Buildings are complex ecosystems that house trillions of microorganisms interacting with each other, with humans and with their environment. Understanding the ecological and evolutionary processes that determine the diversity and composition of the built environment microbiome—the community of microorganisms that live indoors—is important for understanding the relationship between building design, biodiversity and human health. In this study, we used high-throughput sequencing of the bacterial 16S rRNA gene to quantify relationships between building attributes and airborne bacterial communities at a health-care facility. We quantified airborne bacterial community structure and environmental conditions in patient rooms exposed to mechanical or window ventilation and in outdoor air. The phylogenetic diversity of airborne bacterial communities was lower indoors than outdoors, and mechanically ventilated rooms contained less diverse microbial communities than did window-ventilated rooms. Bacterial communities in indoor environments contained many taxa that are absent or rare outdoors, including taxa closely related to potential human pathogens. Building attributes, specifically the source of ventilation air, airflow rates, relative humidity and temperature, were correlated with the diversity and composition of indoor bacterial communities. The relative abundance of bacteria closely related to human pathogens was higher indoors than outdoors, and higher in rooms with lower airflow rates and lower relative humidity. The observed relationship between building design and airborne bacterial diversity suggests that we can manage indoor environments, altering through building design and operation the community of microbial species that potentially colonize the human microbiome during our time indoors. 相似文献
102.
Douglas P. Chivers Xiaoxia Zhao Grant E. Brown Tracy A. Marchant Maud C. O. Ferrari 《Evolutionary ecology》2008,22(4):561-574
In a series of experiments, we investigated the effects of food availability and risk frequency on the dynamics of predator-induced
changes in growth and morphology of prey fish using goldfish (Carassius auratus) as our test species. In experiment 1, we fed goldfish high or low food rations and exposed them to either alarm cues from
conspecifics, cues from swordtails or a water control. After 60 days, goldfish in the alarm cue treatment significantly increased
their body depth and body weight but had smaller body length than goldfish exposed to swordtails cues or water, likely reducing
their vulnerability to gape-limited predators. Importantly, food level had an impact on the amplitude of the morphological
changes. In experiment 2, goldfish were exposed to two different frequencies of predation cues or a water control for 50 days.
The cues were either continued or discontinued from day 51 to 100, and all cues were resumed from day 101 to 150. We found
that goldfish exposed to predation cues increased their depth and weight at a faster rate than did the goldfish exposed to
water, and of particular significance was the fact that frequency of risk had an effect on the amplitude of the change. When
the cues were interrupted, the increase in growth rate parameters was reduced to the level of the goldfish exposed to water.
However, when the cues were resumed, the rate increased to match the growth rate of the goldfish that were continuously exposed
to the cues. Finally, we staged encounters between goldfish of differing morphologies and yellow perch (Perca flavescens) and found that deep-bodied goldfish had better survival than the shallow-bodied ones. These experiments illustrate the dynamic
nature of inducible morphological defences. 相似文献
103.
Savvas Saouros Kovilen Sawmynaden Jan Marchant Peter Simpson Stephen Matthews 《Biomolecular NMR assignments》2008,2(2):175-177
Microneme protein complexes are important for invasion of host cells by Toxoplasma gondii. We report the resonance assignment of the galectin-like domain of microneme protein 1 in complexes with the second and third
EGF domains from microneme protein 6.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
104.
Kovilen Sawmynaden Savvas Saouros Jan Marchant Peter Simpson Stephen Matthews 《Biomolecular NMR assignments》2008,2(2):187-189
Toxoplasma gondii is the causative agent of toxoplasmosis. Here we present a complete set of NMR assignments for the second EGF domain from
microneme protein 6 and its re-assignment in complex with the galectin-like domain from microneme protein 1. 相似文献
105.
Jan Marchant Kovilen Sawmynaden Savvas Saouros Peter Simpson Stephen Matthews 《Biomolecular NMR assignments》2008,2(2):119-121
Microneme protein 4 is involved in cell binding by the important parasite Toxoplasma gondii. We present here the backbone and side-chain assignments of the first two apple domains together with a new graphical aid
for their assignment using NMRView.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
106.
Matthews HK Marchant L Carmona-Fontaine C Kuriyama S Larraín J Holt MR Parsons M Mayor R 《Development (Cambridge, England)》2008,135(10):1771-1780
Directed cell migration is crucial for development, but most of our current knowledge is derived from in vitro studies. We analyzed how neural crest (NC) cells migrate in the direction of their target during embryonic development. We show that the proteoglycan Syndecan-4 (Syn4) is expressed in the migrating neural crest of Xenopus and zebrafish embryos. Loss-of-function studies using an antisense morpholino against syn4 show that this molecule is required for NC migration, but not for NC induction. Inhibition of Syn4 does not affect the velocity of cell migration, but significantly reduces the directional migration of NC cells. Furthermore, we show that Syn4 and PCP signaling control the directional migration of NC cells by regulating the direction in which the cell protrusions are generated during migration. Finally, we perform FRET analysis of Cdc42, Rac and RhoA in vitro and in vivo after interfering with Syn4 and PCP signaling. This is the first time that FRET analysis of small GTPases has been performed in vivo. Our results show that Syn4 inhibits Rac activity, whereas PCP signaling promotes RhoA activity. In addition, we show that RhoA inhibits Rac in NC cells. We present a model in which Syn4 and PCP control directional NC migration by, at least in part, regulating membrane protrusions through the regulation of small GTPase activities. 相似文献
107.
QTL detection experiments in livestock species commonly use the half-sib design. Each male is mated to a number of females, each female producing a limited number of progeny. Analysis consists of attempting to detect associations between phenotype and genotype measured on the progeny. When family sizes are limiting experimenters may wish to incorporate as much information as possible into a single analysis. However, combining information across sires is problematic because of incomplete linkage disequilibrium between the markers and the QTL in the population. This study describes formulæ for obtaining MLEs via the expectation maximization (EM) algorithm for use in a multiple-trait, multiple-family analysis. A model specifying a QTL with only two alleles, and a common within sire error variance is assumed. Compared to single-family analyses, power can be improved up to fourfold with multi-family analyses. The accuracy and precision of QTL location estimates are also substantially improved. With small family sizes, the multi-family, multi-trait analyses reduce substantially, but not totally remove, biases in QTL effect estimates. In situations where multiple QTL alleles are segregating the multi-family analysis will average out the effects of the different QTL alleles. 相似文献
108.
Judith van Holten Kris Reedquist Pascale Sattonet-Roche Tom JM Smeets Christine Plater-Zyberk Margriet J Vervoordeldonk Paul P Tak 《Arthritis research & therapy》2004,6(3):R239
We investigated the therapeutic potential and mechanism of action of IFN-β protein for the treatment of rheumatoid arthritis
(RA). Collagen-induced arthritis was induced in DBA/1 mice. At the first clinical sign of disease, mice were given daily injections
of recombinant mouse IFN-β or saline for 7 days. Disease progression was monitored by visual clinical scoring and measurement
of paw swelling. Inflammation and joint destruction were assessed histologically 8 days after the onset of arthritis. Proteoglycan
depletion was determined by safranin O staining. Expression of cytokines, receptor activator of NF-κB ligand, and c-Fos was
evaluated immunohistochemically. The IL-1-induced expression of IL-6, IL-8, and granulocyte/macrophage-colony-stimulating
factor (GM-CSF) was studied by ELISA in supernatant of RA and osteoarthritis fibroblast-like synoviocytes incubated with IFN-β.
We also examined the effect of IFN-β on NF-κB activity. IFN-β, at 0.25 μg/injection and higher, significantly reduced disease
severity in two experiments, each using 8–10 mice per treatment group. IFN-β-treated animals displayed significantly less
cartilage and bone destruction than controls, paralleled by a decreased number of positive cells of two gene products required
for osteoclastogenesis, receptor activator of NF-κB ligand and c-Fos. Tumor necrosis factor α and IL-6 expression were significantly
reduced, while IL-10 production was increased after IFN-β treatment. IFN-β reduced expression of IL-6, IL-8, and GM-CSF in
RA and osteoarthritis fibroblast-like synoviocytes, correlating with reduced NF-κB activity. The data support the view that
IFN-β is a potential therapy for RA that might help to diminish both joint inflammation and destruction by cytokine modulation. 相似文献
109.
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