929 research outputs found
Gene Turnover and Diversification of the α- and β- Globin Gene Families in Sauropsid Vertebrates
The genes that encode the α- and β-chain subunits of vertebrate hemoglobin have served as a model system for elucidating general principles of gene family evolution, but little is known about patterns of evolution in amniotes other than mammals and birds. Here,we report a comparative genomic analysis of the α- and β-globin gene clusters in sauropsids (archosaurs and nonavian reptiles). The objectives were to characterize changes in the size and membership composition of the α- and β-globin gene families within and among the major sauropsid lineages, to reconstruct the evolutionary history of the sauropsid α- and β-globin genes, to resolve orthologous relationships, and to reconstruct evolutionary changes in the developmental regulation of gene expression. Our comparisons revealed contrasting patterns of evolution in the unlinked α- and β-globin gene clusters. In the α-globin gene cluster,which has remained in the ancestral chromosomal location, evolutionary changes in gene content are attributable to the differential retention of paralogous gene copies that were present in the common ancestor of tetrapods. In the β-globin gene cluster, which was translocated to a new chromosomal location, evolutionary changes in gene content are attributable to differential gene gains (via lineage-specific duplication events) and gene losses (via lineage-specific deletions and inactivations). Consequently, all major groups of amniotes possess unique repertoires of embryonic and postnatally expressed β-type globingenes that diversified independently in each lineage.These independently derived β-type globins descend from a pair of tandemly linked paralogs in the most recent common ancestor of sauropsids
Coronavirus and Pasteurella infections in bovine shipping fever pneumonia and Evans\u27 criteria for causation
Respiratory tract infections with viruses and Pasteurella spp. were determined sequentially among 26 cattle that died during two severe epizootics of shipping fever pneumonia. Nasal swab and serum samples were collected prior to onset of the epizootics, during disease progression, and after death, when necropsies were performed and lung samples were collected. Eighteen normal control cattle also were sampled at the beginning of the epizootics as well as at weekly intervals for 4 weeks. Respiratory bovine coronaviruses (RBCV) were isolated from nasal secretions of 21 and 25 cattle before and after transport. Two and 17 cattle nasally shed Pasteurella spp. before and after transport, respectively. RBCV were isolated at titers of 1 x 103 to 1.2 x 107 PFU per g of lung tissue from 18 cattle that died within 7 days of the epizootics, but not from the lungs of the remaining cattle that died on days 9 to 36. Twenty-five of the 26 lung samples were positive for Pasteurella spp., and their CFU ranged between 4.0 x 105 and 2.3 x 109 per g. Acute and subacute exudative, necrotizing lobar pneumonia characterized the lung lesions of these cattle with a majority of pneumonic lung lobes exhibiting fibronecrotic and exudative changes typical of pneumonic pasteurellosis, but other lung lobules had histological changes consisting of bronchiolitis and alveolitis typical of virus-induced changes. These cattle were immunologically naive to both infectious agents at the onset of the epizootics, but those that died after day 7 had rising antibody titers against RBCV and Pasteurella haemolytica. In contrast, the 18 clinically normal and RBCV isolation-negative cattle had high hemagglutinin inhibition antibody titers to RBCV from the beginning, while their antibody responses to P. haemolytica antigens were delayed. Evans\u27 criteria for causation were applied to our findings because of the multifactorial nature of shipping fever pneumonia. This analysis identified RBCV as the primary inciting cause in these two epizootics. These viruses were previously not recognized as a causative agent in this complex respiratory tract disease of cattle
PANIC: the new panoramic NIR camera for Calar Alto
PANIC is a wide-field NIR camera, which is currently under development for
the Calar Alto observatory (CAHA) in Spain. It uses a mosaic of four Hawaii-2RG
detectors and covers the spectral range from 0.8-2.5 micron(z to K-band). The
field-of-view is 30x30 arcmin. This instrument can be used at the 2.2m
telescope (0.45arcsec/pixel, 0.5x0.5 degree FOV) and at the 3.5m telescope
(0.23arcsec/pixel, 0.25x0.25 degree FOV). The operating temperature is about
77K, achieved by liquid Nitrogen cooling. The cryogenic optics has three flat
folding mirrors with diameters up to 282 mm and nine lenses with diameters
between 130 mm and 255 mm. A compact filter unit can carry up to 19 filters
distributed over four filter wheels. Narrow band (1%) filters can be used. The
instrument has a diameter of 1.1 m and it is about 1 m long. The weight limit
of 400 kg at the 2.2m telescope requires a light-weight cryostat design. The
aluminium vacuum vessel and radiation shield have wall thicknesses of only 6 mm
and 3 mm respectively.Comment: This paper has been presented in the SPIE of Astronomical Telescopes
and Instrumentation 2008 in Marseille (France
Aggregation Patterns in Stressed Bacteria
We study the formation of spot patterns seen in a variety of bacterial
species when the bacteria are subjected to oxidative stress due to hazardous
byproducts of respiration. Our approach consists of coupling the cell density
field to a chemoattractant concentration as well as to nutrient and waste
fields. The latter serves as a triggering field for emission of
chemoattractant. Important elements in the proposed model include the
propagation of a front of motile bacteria radially outward form an initial
site, a Turing instability of the uniformly dense state and a reduction of
motility for cells sufficiently far behind the front. The wide variety of
patterns seen in the experiments is explained as being due the variation of the
details of the initiation of the chemoattractant emission as well as the
transition to a non-motile phase.Comment: 4 pages, REVTeX with 4 postscript figures (uuencoded) Figures 1a and
1b are available from the authors; paper submitted to PRL
Dietary acid load and risk of cancer: new insights from a nationwide case-control study
Objective: Dietary acid load can contribute to metabolic acidosis, which is closely linked to cancer development through inflammation and cell transformation mechanisms. However, limited epidemiologic evidence is still linking diet-dependent acid load and cancer risk. Since we published nine studies specifically focusing on dietary acid load and the risk of cancer development, we decided to explore its potential role more deeply through the analysis of all databases combined.
Materials and methods: A case-control study was performed on 13270 subjects (3736 cases and 9534 age-frequency and residence-matched controls) drawn from the major public hospitals in Uruguay. Participants were interviewed through a multi-topic questionnaire, including a food frequency questionnaire. Food-derived nutrients were calculated from available databases. The dietary acid load was calculated based on validated measures, including Potential Renal Acid Load and Net Endogenous Acid Production scores. Odds ratios (OR) were estimated by logistic regression, adjusting for potential confounders.
Results: We found significant and direct associations between dietary acid load and cancer risk (OR= 1.44 and OR= 1.64 for the highest scores). The estimated methionine intake was found also significantly and directly associated (OR= 1.97), while the plant fiber was significantly and inversely associated (OR= 0.49).
Conclusions: Results confirm that an acidogenic dietary style may increase the risk of cancer. Our findings suggest that both Met and plant fiber intakes might be independent factors influencing the risk linked to acid-base disbalance which turn into a metabolic stress, but acting in opposite directions. Furthermore, Met intake displayed comparable odds ratios as the scores themselves
Dietary acid load and risk of gastric cancer: a case-control study
Objective: The dietary acid load can contribute to metabolic acidosis, which is closely linked to cancer development through mechanisms of inflammation and cell transformation. However, very limited epidemiologic evidence is linking diet-dependent acid load and cancer risk. Since no published studies focused on dietary acid load and gastric cancer (GC) risk, we explored this association in the present study.
Patients and Methods: A case-control study was performed in 1370 patients (274 cases and 1096 age-frequency, sex, and urban/rural residence matched controls) through a multi-topic inquiry, including a food frequency questionnaire. Food-derived nutrients were calculated from available databases. The dietary acid load was calculated based on two validated measures: Potential Renal Acid Load (PRAL) score and Net Endogenous Acid Production (NEAP) score. Odds ratios (OR) and their 95% confidence intervals (95% CI) were estimated by unconditional logistic regression, adjusting for potential confounders.
Results: We found direct, significant associations between dietary acid load and GC risk: (OR=1.74, 95% CI 1.13-2.66) and (OR=1.90, 95% CI 1.26-2.84) for highest PRAL and NEAP, respectively. Both risk estimates also displayed linear trends. Both acid load scores were directly associated with animal-based foods (mainly meat) and inversely associated with the intake of plant-based foods.
Conclusions: A high dietary acid load may contribute to GC development. To the best of our knowledge, the present is the first epidemiologic case-control study analyzing associations of dietary acid load and GC risk in a Western population. Further research is warranted to confirm our findings
Law of Genome Evolution Direction : Coding Information Quantity Grows
The problem of the directionality of genome evolution is studied. Based on
the analysis of C-value paradox and the evolution of genome size we propose
that the function-coding information quantity of a genome always grows in the
course of evolution through sequence duplication, expansion of code, and gene
transfer from outside. The function-coding information quantity of a genome
consists of two parts, p-coding information quantity which encodes functional
protein and n-coding information quantity which encodes other functional
elements except amino acid sequence. The evidences on the evolutionary law
about the function-coding information quantity are listed. The needs of
function is the motive force for the expansion of coding information quantity
and the information quantity expansion is the way to make functional innovation
and extension for a species. So, the increase of coding information quantity of
a genome is a measure of the acquired new function and it determines the
directionality of genome evolution.Comment: 16 page
Origin of Complexity in Hemoglobin Evolution
Most proteins associate into multimeric complexes with specific architectures, which often have functional properties such as cooperative ligand binding or allosteric regulation. No detailed knowledge is available about how any multimer and its functions arose during evolution. Here we use ancestral protein reconstruction and biophysical assays to elucidate the origins of vertebrate hemoglobin, a heterotetramer of paralogous α- and β-subunits that mediates respiratory oxygen transport and exchange by cooperatively binding oxygen with moderate affinity. We show that modern hemoglobin evolved from an ancient monomer and characterize the historical “missing link” through which the modern tetramer evolved—a noncooperative homodimer with high oxygen affinity that existed before the gene duplication that generated distinct α- and β-subunits. Reintroducing just two post-duplication historical substitutions into the ancestral protein is sufficient to cause strong tetramerization by creating favorable contacts with more ancient residues on the opposing subunit. These surface substitutions markedly reduce oxygen affinity and even confer cooperativity because an ancient linkage between the oxygen binding site and the multimerization interface was already an intrinsic feature of the protein’s structure. Our findings establish that evolution can produce new complex molecular structures and functions via simple genetic mechanisms that recruit existing biophysical features into higher-level architectures.
The interfaces that hold molecular complexes together typically involve sterically tight, electrostatically complementary interactions among many amino acids. Similarly, allostery and cooperativity usually depend on numerous residues that connect surfaces to active sites. The acquisition of such complicated machinery would seem to require elaborate evolutionary pathways. The classical explanation of this process, by analogy to the evolution of morphological complexity, is that multimerization conferred or enhanced beneficial functions, allowing selection to drive the many substitutions required to build and optimize new interfaces.
Whether this account accurately describes the evolution of any natural molecular complex requires a detailed reconstruction of the historical steps by which it evolved. Hemoglobin (Hb) is a useful model for this purpose, because the structural mechanisms that mediate its multimeric assembly, cooperative oxygen binding, and allosteric regulation are well established. Moreover, its subunits descend by duplication and divergence from the same ancestral proteins, so their history can be reconstructed in a single analysis. Despite considerable speculation, virtually nothing is known about the evolutionary origin of Hb’s heterotetrameric architecture and the functions that depend on it
Slogging and Stumbling Toward Social Justice in a Private Elementary School: The Complicated Case of St. Malachy
This case study examines St. Malachy, an urban Catholic elementary school primarily serving children traditionally marginalized by race, class, linguistic heritage, and disability. As a private school, St. Malachy serves the public good by recruiting and retaining such traditionally marginalized students. As empirical studies involving Catholic schools frequently juxtapose them with public schools, the author presents this examination from a different tack. Neither vilifying nor glorifying Catholic schooling, this study critically examines the pursuit of social justice in this school context. Data gathered through a 1-year study show that formal and informal leaders in St. Malachy adapted their governance, aggressively sought community resources, and focused their professional development to build the capacity to serve their increasingly pluralistic student population. The analysis confirms the deepening realization that striving toward social justice is a messy, contradictory, and complicated pursuit, and that schools in both public and private sectors are allies in this pursuit
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