3,998 research outputs found

    The Milliarcsecond Structure of Radio Galaxies and Quasars

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    Hybrid maps of the nuclei of radio galaxies and quasars show a variety of morphologies. Among compact sources, two structures are common: an asymmetric, “core-jet” morphology (eg, 3C 273), and an “equal double” morphology with two separated, similar components (eg, CTD 93). The nuclei of extended, double radio galaxies generally have a core-jet morphology with the jet directed toward one of the outer components

    Scaling leaf respiration with nitrogen and phosphorus in tropical forests across two continents

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    Leaf dark respiration (Rdark) represents an important component controlling the carbon balance in tropical forests. Here, we test how nitrogen (N) and phosphorus (P) affect Rdark and its relationship with photosynthesis using three widely separated tropical forests which differ in soil fertility. Rdark was measured on 431 rainforest canopy trees, from 182 species, in French Guiana, Peru and Australia. The variation in Rdark was examined in relation to leaf N and P content, leaf structure and maximum photosynthetic rates at ambient and saturating atmospheric CO2 concentration. We found that the site with the lowest fertility (French Guiana) exhibited greater rates of Rdark per unit leaf N, P and photosynthesis. The data from Australia, for which there were no phylogenetic overlaps with the samples from the South American sites, yielded the most distinct relationships of Rdark with the measured leaf traits. Our data indicate that no single universal scaling relationship accounts for variation in Rdark across this large biogeographical space. Variability between sites in the absolute rates of Rdark and the Rdark : photosynthesis ratio were driven by variations in N- and P-use efficiency, which were related to both taxonomic and environmental variability

    Barriers and Facilitators to Staying Smoke-Free after Having a Baby, a Qualitative Study: Women’s Views on Support Needed to Prevent Returning to Smoking Postpartum

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    Background: Postpartum return to smoking (PPRS) is a common and important public health problem. Interventions to prevent PPRS have not been shown to be effective. We aimed to qualitatively explore the barriers and facilitators to staying smoke-free after having a baby, and women’s views on the support needed to avoid PPRS to inform future intervention development. Methods: We conducted semi-structured telephone interviews (n = 26) with pregnant women who quit smoking (n = 9), and postpartum women who were abstinent at delivery and returned to smoking (n = 7) or stayed smoke-free (n = 10). Inductive thematic analysis was used. Results: Five overarching themes were identified: (i) smoking intentions; (ii) facilitators to staying smoke-free; (iii) barriers to staying smoke-free; (iv) support to avoid relapse; and (v) e-cigarettes, nicotine replacement therapy, and varenicline. Facilitators to staying smoke-free were the health benefits to their baby, whilst barriers included stress, cravings, and being in environments where they would previously have smoked. Women wanted continuous offers of support to stay smoke-free throughout the extended postpartum period, with a particular interest in support for partners to quit smoking and self-help support. Women expressed safety concerns for e-cigarettes, nicotine replacement therapy, and varenicline. Conclusions: Offers of support to stay smoke-free should continue throughout the postpartum and engage with partners or other household members who smoke. Reassuring women about the relative safety of nicotine replacement therapy and e-cigarettes by a health professional, particularly for those who are breastfeeding, could be beneficial

    Gene expression profiling in the Cynomolgus macaque Macaca fascicularis shows variation within the normal birth range

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    BACKGROUND: Although an adverse early-life environment has been linked to an increased risk of developing the metabolic syndrome, the molecular mechanisms underlying altered disease susceptibility as well as their relevance to humans are largely unknown. Importantly, emerging evidence suggests that these effects operate within the normal range of birth weights and involve mechanisms of developmental palsticity rather than pathology. METHOD: To explore this further, we utilised a non-human primate model Macaca fascicularis (Cynomolgus macaque) which shares with humans the same progressive history of the metabolic syndrome. Using microarray we compared tissues from neonates in the average birth weight (50-75(th )centile) to those of lower birth weight (5-25(th )centile) and studied the effect of different growth trajectories within the normal range on gene expression levels in the umbilical cord, neonatal liver and skeletal muscle. RESULTS: We identified 1973 genes which were differentially expressed in the three tissue types between average and low birth weight animals (P < 0.05). Gene ontology analysis identified that these genes were involved in metabolic processes including cellular lipid metabolism, cellular biosynthesis, cellular macromolecule synthesis, cellular nitrogen metabolism, cellular carbohydrate metabolism, cellular catabolism, nucleotide and nucleic acid metabolism, regulation of molecular functions, biological adhesion and development. CONCLUSION: These differences in gene expression levels between animals in the upper and lower percentiles of the normal birth weight range may point towards early life metabolic adaptations that in later life result in differences in disease risk

    Occupational illnesses in the 2009 Zambian labour force survey

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    <p>Abstract</p> <p>Background</p> <p>Occupational health has received limited research attention in the Southern African Development Community (SADC). Much of the published data in this region come from South Africa and little has been reported north of the Limpopo. The present study was conducted to estimate the burden of occupational illnesses in Zambia and assess factors associated with their occurrence.</p> <p>Methods</p> <p>Data were obtained from the Zambian Labour Force Survey of 2009. Frequencies were used to estimate the prevalence of occupational diseases. Logistic regression analyses were conducted to determine the associations between demographic, social and economic factors and reported illness resulting from occupational exposures. Odds ratios (OR) from bivariate analyses and adjusted odds ratios (AOR) from the multivariate analysis together with their 95% Confidence Intervals (CI) are reported.</p> <p>Results</p> <p>Data on 59,118 persons aged 18 years or older were available for analysis, of which 29805 (50.4%) were males. The proportions of the sample that reported to have suffered from an occupational illness were 12.7% among males and 10.4% among females (p < 0.001). Overall the proportions of respondents who reported suffering from fatigue, fever and chest infections were 38.8%, 21.7% and 17.1%, respectively. About two thirds (69.7%) of the study participants had stayed away from work due to the illness suffered at work; there was no sex differences (p = 0.216). Older age, being male, lower education level, married/cohabiting or once married (separated/divorced/widowed), and paid employee or employer/self employed were positively associated with having suffered from illness.</p> <p>Conclusions</p> <p>The findings from this study call for urgent effort for specific measures to prevent and mitigate the effects of occupational injuries. These interventions may include: public health campaigns, enforcement or change in work policies and regulations. Special attention may have to be made towards those who were more likely to suffer from occupational illnesses.</p

    Phenotypic and molecular assessment of seven patients with 6p25 deletion syndrome: Relevance to ocular dysgenesis and hearing impairment

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    BACKGROUND: Thirty-nine patients have been described with deletions involving chromosome 6p25. However, relatively few of these deletions have had molecular characterization. Common phenotypes of 6p25 deletion syndrome patients include hydrocephalus, hearing loss, and ocular, craniofacial, skeletal, cardiac, and renal malformations. Molecular characterization of deletions can identify genes that are responsible for these phenotypes. METHODS: We report the clinical phenotype of seven patients with terminal deletions of chromosome 6p25 and compare them to previously reported patients. Molecular characterization of the deletions was performed using polymorphic marker analysis to determine the extents of the deletions in these seven 6p25 deletion syndrome patients. RESULTS: Our results, and previous data, show that ocular dysgenesis and hearing impairment are the two most highly penetrant phenotypes of the 6p25 deletion syndrome. While deletion of the forkhead box C1 gene (FOXC1) probably underlies the ocular dysgenesis, no gene in this region is known to be involved in hearing impairment. CONCLUSIONS: Ocular dysgenesis and hearing impairment are the two most common phenotypes of 6p25 deletion syndrome. We conclude that a locus for dominant hearing loss is present at 6p25 and that this locus is restricted to a region distal to D6S1617. Molecular characterization of more 6p25 deletion patients will aid in refinement of this locus and the identification of a gene involved in dominant hearing loss

    Lack of correlation of stem cell markers in breast cancer stem cells

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    BACKGROUND: Various markers are used to identify the unique sub-population of breast cancer cells with stem cell properties. Whether these markers are expressed in all breast cancers, identify the same population of cells, or equate to therapeutic response is controversial. METHODS: We investigated the expression of multiple cancer stem cell markers in human breast cancer samples and cell lines in vitro and in vivo, comparing across and within samples and relating expression with growth and therapeutic response to doxorubicin, docetaxol and radiotherapy. RESULTS: CD24, CD44, ALDH and SOX2 expression, the ability to form mammospheres and side-population cells are variably present in human cancers and cell lines. Each marker identifies a unique rather than common population of cancer cells. In vivo, cells expressing these markers are not specifically localized to the presumptive stem cell niche at the tumour/stroma interface. Repeated therapy does not consistently enrich cells expressing these markers, although ER-negative cells accumulate. CONCLUSIONS: Commonly employed methods identify different cancer cell sub-populations with no consistent therapeutic implications, rather than a single population of cells. The relationships of breast cancer stem cells to clinical parameters will require identification of specific markers or panels for the individual cancer

    Cancer stem cell heterogeneity in hereditary breast cancer

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    The cancer stem cell hypothesis proposes that tumors arise in stem or progenitor cells generating in tumors driven by a subcomponent that retains cancer stem cell properties. Recent evidence supports the hypothesis that the BRCA1 gene involved in hereditary breast cancer plays a role in breast stem cell function. Furthermore, studies using mouse BRCA1 knockout models provide evidence for the existence of heterogeneous cancer stem cell populations in tumors generated in these mice. Although these populations may arise from different stem/progenitor cells, they share the expression of a common set of stem cell regulatory genes and show similar characteristics in in vitro mammosphere assays and xenograft models. Furthermore, these 'cancer stem cells' display resistance to chemotherapeutic agents. These studies suggest that breast tumors may display intertumor stem cell heterogeneity. Despite this heterogeneity, cancer stem cells may share common characteristics that can be used for their identification and for therapeutic targeting
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