1,327 research outputs found
Genetic Polymorphism in Evolving Population
We present a model for evolving population which maintains genetic
polymorphism. By introducing random mutation in the model population at a
constant rate, we observe that the population does not become extinct but
survives, keeping diversity in the gene pool under abrupt environmental
changes. The model provides reasonable estimates for the proportions of
polymorphic and heterozygous loci and for the mutation rate, as observed in
nature
Historic genetic structuring and paraphyly within the Great-tailed Grackle
The Great-tailed Grackle (Quiscalus mexicanus) and Boat-tailed Grackle (Q. major) are sister species that have expanded their ranges during historical times. This expansion has created an area of sympatry between these species in Texas and Louisiana, and between distinctive Great-tailed Grackle subspecies in the southwestern United States and northern Mexico. We investigated the evolutionary histories of both species using mitochondrial DNA sequence data and modern phylogenetic methods. Our results reveal genetic structure within Great-tailed, but not Boat-tailed Grackles. Great-tailed Grackles are separated into two clades, but range expansion in the north has led to secondary contact between them. Boat-tailed Grackles are monophyletic and are embedded within the Great-tailed Grackle assemblage, rendering the latter paraphyletic. These results reveal a complex phylogeographic pattern caused by recent range expansion and secondary contact of once allopatric units
Mutators and long-term molecular evolution of pathogenic Escherichia coli O157:H7.
It has been proposed that an increased mutation rate (indicated by the frequency of hypermutable isolates) has facilitated the emergence of Escherichia coli O157:H7. Analysis of the divergence of 12 genes shows no evidence that the pathogen has undergone an unusually high rate of mutation and molecular evolution
Employer's management of employees affected by cancer
Return to work (RTW) following treatment can be problematic for cancer survivors. Although some people affected by cancer are able to continue working, a greater proportion of these survivors end up unemployed, retire early or change jobs than those without a diagnosis of cancer. One of the reasons for not returning to work is the lack of understanding and support from employers and supervisors. Currently, it is not clear what factors are likely to influence the employer’s management of employees recovering from cancer. This article reports the outcome from a review of the published literature on factors related to the current employer management of employed cancer survivors
Co-Transport of Polycyclic Aromatic Hydrocarbons by Motile Microorganisms Leads to Enhanced Mass Transfer under Diffusive Conditions.
The
environmental chemodynamics of hydrophobic organic chemicals
(HOCs) are often rate-limited by diffusion in stagnant boundary layers.
This study investigated whether motile microorganisms can act as microbial
carriers that enhance mass transfer of HOCs through diffusive boundary
layers. A new experimental system was developed that allows (1) generation
of concentration gradients of HOCs under the microscope, (2) exposure
and direct observation of microorganisms in such gradients, and (3)
quantification of HOC mass transfer. Silicone O-rings were integrated
into a Dunn chemotaxis chamber to serve as sink and source for polycyclic
aromatic hydrocarbons (PAHs). This resulted in stable concentration
gradients in water (>24 h). Adding the model organism <i>Tetrahymena
pyriformis</i> to the experimental system enhanced PAH mass transfer
up to hundred-fold (benzo[a]pyrene). Increasing mass transfer enhancement
with hydrophobicity indicated PAH co-transport with the motile organisms.
Fluorescence microscopy confirmed such transport. The effective diffusivity
of <i>T. pyriformis</i>, determined by video imaging microscopy,
was found to exceed molecular diffusivities of the PAHs up to four-fold.
Cell-bound PAH fractions were determined to range from 28% (naphthalene)
to 92% (pyrene). Motile microorganisms can therefore function as effective
carriers for HOCs under diffusive conditions and might significantly
enhance mobility and availability of HOCs
A Computational and Experimental Study of the Regulatory Mechanisms of the Complement System
The complement system is key to innate immunity and its activation is necessary for the clearance of bacteria and apoptotic cells. However, insufficient or excessive complement activation will lead to immune-related diseases. It is so far unknown how the complement activity is up- or down- regulated and what the associated pathophysiological mechanisms are. To quantitatively understand the modulatory mechanisms of the complement system, we built a computational model involving the enhancement and suppression mechanisms that regulate complement activity. Our model consists of a large system of Ordinary Differential Equations (ODEs) accompanied by a dynamic Bayesian network as a probabilistic approximation of the ODE dynamics. Applying Bayesian inference techniques, this approximation was used to perform parameter estimation and sensitivity analysis. Our combined computational and experimental study showed that the antimicrobial response is sensitive to changes in pH and calcium levels, which determines the strength of the crosstalk between CRP and L-ficolin. Our study also revealed differential regulatory effects of C4BP. While C4BP delays but does not decrease the classical complement activation, it attenuates but does not significantly delay the lectin pathway activation. We also found that the major inhibitory role of C4BP is to facilitate the decay of C3 convertase. In summary, the present work elucidates the regulatory mechanisms of the complement system and demonstrates how the bio-pathway machinery maintains the balance between activation and inhibition. The insights we have gained could contribute to the development of therapies targeting the complement system.Singapore. Ministry of Education (Grant T208B3109)Singapore. Agency for Science, Technology and Research (BMRC 08/1/21/19/574)Singapore-MIT Alliance (Computational and Systems Biology Flagship Project)Swedish Research Counci
Fine-Scale Mapping of the 4q24 Locus Identifies Two Independent Loci Associated with Breast Cancer Risk
Background: A recent association study identified a common variant (rs9790517) at 4q24 to be associated with breast cancer risk. Independent association signals and potential functional variants in this locus have not been explored.
Methods: We conducted a fine-mapping analysis in 55,540 breast cancer cases and 51,168 controls from the Breast Cancer Association Consortium.
Results: Conditional analyses identified two independent association signals among women of European ancestry, represented by rs9790517 [conditional P = 2.51 × 10−4; OR, 1.04; 95% confidence interval (CI), 1.02–1.07] and rs77928427 (P = 1.86 × 10−4; OR, 1.04; 95% CI, 1.02–1.07). Functional annotation using data from the Encyclopedia of DNA Elements (ENCODE) project revealed two putative functional variants, rs62331150 and rs73838678 in linkage disequilibrium (LD) with rs9790517 (r2 ≥ 0.90) residing in the active promoter or enhancer, respectively, of the nearest gene, TET2. Both variants are located in DNase I hypersensitivity and transcription factor–binding sites. Using data from both The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), we showed that rs62331150 was associated with level of expression of TET2 in breast normal and tumor tissue.
Conclusion: Our study identified two independent association signals at 4q24 in relation to breast cancer risk and suggested that observed association in this locus may be mediated through the regulation of TET2.
Impact: Fine-mapping study with large sample size warranted for identification of independent loci for breast cancer risk
Parthenogenesis In The Tropical Gekkonid Lizard, Nactus Arnouxii (Sauria: Gekkonidae)
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137400/1/evo02464.pd
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