Risk factors for bacterial catheter colonization in regional anaesthesia

BACKGROUND: Although several potential risk factors have been discussed, risk factors associated with bacterial colonization or even infection of catheters used for regional anaesthesia are not very well investigated. METHODS: In this prospective observational trial, 198 catheters at several anatomical sites where placed using a standardized technique. The site of insertion was then monitored daily for signs of infection (secretion at the insertion site, redness, swelling, or local pain). The catheters were removed when clinically indicated (no or moderate postoperative pain) or when signs of potential infection occurred. After sterile removal they were prospectively analyzed for colonization, defined as > 15 colony forming units. RESULTS: 33 (16.7%) of all catheters were colonized, and 18 (9.1%) of these with additional signs of local inflammation. Two of these patients required antibiotic treatment due to superficial infections. Stepwise logistic regression analysis was used to identify factors associated with catheter colonization. Out of 26 potential factors, three came out as statistically significant. Catheter placement in the groin (odds-ratio and 95%-confidence interval: 3.4; 1.5–7.8), and repeated changing of the catheter dressing (odds-ratio: 2.1; 1.4–3.3 per removal) increased the risk for colonization, whereas systemic antibiotics administered postoperatively decreased it (odds ratio: 0.41; 0.12–1.0). CONCLUSION: Colonization of peripheral and epidural nerve catheter can only in part be predicted at the time of catheter insertion since two out of three relevant variables that significantly influence the risk can only be recorded postoperatively. Catheter localisation in the groin, removal of the dressing and omission of postoperative antibiotics were associated with, but were not necessarily causal for bacterial colonization. These factors might help to identify patients who are at increased risk for catheter colonization

Quality of life among Latina breast cancer patients: a systematic review of the literature

Introduction The Latino population is the most rapidly growing ethnic minority in the United States and Latinas have higher rates of advanced breast cancer and more rigorous treatments than White women. However, the literature lacks reviews on quality of life among this population of breast cancer patients. Methods A systematic review of the breast cancer quality of life (QOL) literature was conducted among studies that provided a comparison of mental, physical, social, or sexual QOL between Latinas and other racial/ethnic groups. Of the 375 studies reviewed, 20 quantitative studies and two qualitative studies met criteria for inclusion. Results Latinas were more likely to report poor mental, physical, and social QOL, relative to non-Latinas. Only four studies assessed sexual QOL, making it difficult to draw any conclusions. Of these four QOL domains, the largest disparity was found in the area of mental health in which Latinas reported poorer QOL compared to non-Latina Whites and Blacks. Discussion/conclusions Most quantitative studies revealed either that Latinas consistently evidenced significantly lower QOL than non-Latinas on all measures (6 studies) or reported mixed findings in which Latinas generally demonstrated significantly worse QOL on most, but not all, measures (12 studies) included in the study. Explanatory mechanisms including socio-demographic, treatment-related, and culturally-relevant factors are discussed. Implications for research design, measurement, and clinical work are also included. Implications for cancer survivors Although not entirely consistent, data suggest that Latina breast cancer survivors on average experience worse QOL than non-Latina Whites. Understanding ethnic differences in QOL among breast cancer survivors can inform interventions targeted at improving health status for Latinas

A New (Old), Invasive Ant in the Hardwood Forests of Eastern North America and Its Potentially Widespread Impacts

Biological invasions represent a serious threat for the conservation of biodiversity in many ecosystems. While many social insect species and in particular ant species have been introduced outside their native ranges, few species have been successful at invading temperate forests. In this study, we document for the first time the relationship between the abundance of the introduced ant, Pachycondyla chinensis, in mature forests of North Carolina and the composition, abundance and diversity of native ant species using both a matched pair approach and generalized linear models. Where present, P. chinensis was more abundant than all native species combined. The diversity and abundance of native ants in general and many individual species were negatively associated with the presence and abundance of P. chinensis. These patterns held regardless of our statistical approach and across spatial scales. Interestingly, while the majority of ant species was strongly and negatively correlated with the abundance and presence of P. chinensis, a small subset of ant species larger than P. chinensis was either as abundant or even more abundant in invaded than in uninvaded sites. The large geographic range of this ant species combined with its apparent impact on native species make it likely to have cascading consequences on eastern forests in years to come, effects mediated by the specifics of its life history which is very different from those of other invasive ants. The apparent ecological impacts of P. chinensis are in addition to public health concerns associated with this species due to its sometimes, deadly sting

Assessment of interactions between 205 breast cancer susceptibility loci and 13 established risk factors in relation to breast cancer risk, in the Breast Cancer Association Consortium.

BACKGROUND: Previous gene-environment interaction studies of breast cancer risk have provided sparse evidence of interactions. Using the largest available dataset to date, we performed a comprehensive assessment of potential effect modification of 205 common susceptibility variants by 13 established breast cancer risk factors, including replication of previously reported interactions. METHODS: Analyses were performed using 28 176 cases and 32 209 controls genotyped with iCOGS array and 44 109 cases and 48 145 controls genotyped using OncoArray from the Breast Cancer Association Consortium (BCAC). Gene-environment interactions were assessed using unconditional logistic regression and likelihood ratio tests for breast cancer risk overall and by estrogen-receptor (ER) status. Bayesian false discovery probability was used to assess the noteworthiness of the meta-analysed array-specific interactions. RESULTS: Noteworthy evidence of interaction at ≤1% prior probability was observed for three single nucleotide polymorphism (SNP)-risk factor pairs. SNP rs4442975 was associated with a greater reduction of risk of ER-positive breast cancer [odds ratio (OR)int = 0.85 (0.78-0.93), Pint = 2.8 x 10-4] and overall breast cancer [ORint = 0.85 (0.78-0.92), Pint = 7.4 x 10-5) in current users of estrogen-progesterone therapy compared with non-users. This finding was supported by replication using OncoArray data of the previously reported interaction between rs13387042 (r2 = 0.93 with rs4442975) and current estrogen-progesterone therapy for overall disease (Pint = 0.004). The two other interactions suggested stronger associations between SNP rs6596100 and ER-negative breast cancer with increasing parity and younger age at first birth. CONCLUSIONS: Overall, our study does not suggest strong effect modification of common breast cancer susceptibility variants by established risk factors

Genome-wide association and transcriptome studies identify target genes and risk loci for breast cancer

Genome-wide association studies (GWAS) have identified more than 170 breast cancer susceptibility loci. Here we hypothesize that some risk-associated variants might act in non-breast tissues, specifically adipose tissue and immune cells from blood and spleen. Using expression quantitative trait loci (eQTL) reported in these tissues, we identify 26 previously unreported, likely target genes of overall breast cancer risk variants, and 17 for estrogen receptor (ER)-negative breast cancer, several with a known immune function. We determine the directional effect of gene expression on disease risk measured based on single and multiple eQTL. In addition, using a gene-based test of association that considers eQTL from multiple tissues, we identify seven (and four) regions with variants associated with overall (and ER-negative) breast cancer risk, which were not reported in previous GWAS. Further investigation of the function of the implicated genes in breast and immune cells may provide insights into the etiology of breast cancer.Peer reviewe

How Do They Do It? – Understanding the Success of Marine Invasive Species

From the depths of the oceans to the shallow estuaries and wetlands of our coasts, organisms of the marine environment are teeming with unique adaptations to cope with a multitude of varying environmental conditions. With millions of years and a vast volume of water to call their home, they have become quite adept at developing specialized and unique techniques for survival and – given increasing human mediated transport – biological invasions. A growing world human population and a global economy drives the transportation of goods across the oceans and with them invasive species via ballast water and attached to ship hulls. In any given 24-hour period, there are about 10,000 species being transported across different biogeographic regions. If any of them manage to take hold and establish a range in an exotic habitat, the implications for local ecosystems can be costly. This review on marine invasions highlights trends among successful non-indigenous species (NIS), from vectors of transport to ecological and physiological plasticity. Apart from summarizing patterns of successful invasions, it discusses the implications of how successfully established NIS impact the local environment, economy and human health. Finally, it looks to the future and discusses what questions need to be addressed and what models can tell us about what the outlook on future marine invasions is

Genome-wide association and transcriptome studies identify target genes and risk loci for breast cancer

Genome-wide association studies (GWAS) have identified more than 170 breast cancer susceptibility loci. Here we hypothesize that some risk-associated variants might act in non-breast tissues, specifically adipose tissue and immune cells from blood and spleen. Using expression quantitative trait loci (eQTL) reported in these tissues, we identify 26 previously unreported, likely target genes of overall breast cancer risk variants, and 17 for estrogen receptor (ER)-negative breast cancer, several with a known immune function. We determine the directional effect of gene expression on disease risk measured based on single and multiple eQTL. In addition, using a gene-based test of association that considers eQTL from multiple tissues, we identify seven (and four) regions with variants associated with overall (and ER-negative) breast cancer risk, which were not reported in previous GWAS. Further investigation of the function of the implicated genes in breast and immune cells may provide insights into the etiology of breast cancer

Association analysis identifies 65 new breast cancer risk loci

Breast cancer risk is influenced by rare coding variants in susceptibility genes, such as BRCA1, and many common, mostly non-coding variants. However, much of the genetic contribution to breast cancer risk remains unknown. Here we report the results of a genome-wide association study of breast cancer in 122,977 cases and 105,974 controls of European ancestry and 14,068 cases and 13,104 controls of East Asian ancestry. We identified 65 new loci that are associated with overall breast cancer risk at P < 5 × 10-8. The majority of credible risk single-nucleotide polymorphisms in these loci fall in distal regulatory elements, and by integrating in silico data to predict target genes in breast cells at each locus, we demonstrate a strong overlap between candidate target genes and somatic driver genes in breast tumours. We also find that heritability of breast cancer due to all single-nucleotide polymorphisms in regulatory features was 2-5-fold enriched relative to the genome-wide average, with strong enrichment for particular transcription factor binding sites. These results provide further insight into genetic susceptibility to breast cancer and will improve the use of genetic risk scores for individualized screening and prevention.We thank all the individuals who took part in these studies and all the researchers, clinicians, technicians and administrative staff who have enabled this work to be carried out. Genotyping of the OncoArray was principally funded from three sources: the PERSPECTIVE project, funded by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research, the ‘Ministère de l’Économie, de la Science et de l’Innovation du Québec’ through Genome Québec, and the Quebec Breast Cancer Foundation; the NCI Genetic Associations and Mechanisms in Oncology (GAME-ON) initiative and Discovery, Biology and Risk of Inherited Variants in Breast Cancer (DRIVE) project (NIH Grants U19 CA148065 and X01HG007492); and Cancer Research UK (C1287/A10118 and C1287/A16563). BCAC is funded by Cancer Research UK (C1287/A16563), by the European Community’s Seventh Framework Programme under grant agreement 223175 (HEALTH-F2-2009-223175) (COGS) and by the European Union’s Horizon 2020 Research and Innovation Programme under grant agreements 633784 (B-CAST) and 634935 (BRIDGES). Genotyping of the iCOGS array was funded by the European Union (HEALTH-F2-2009-223175), Cancer Research UK (C1287/A10710), the Canadian Institutes of Health Research for the ‘CIHR Team in Familial Risks of Breast Cancer’ program, and the Ministry of Economic Development, Innovation and Export Trade of Quebec, grant PSR-SIIRI-701. Combining of the GWAS data was supported in part by The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative grant U19 CA 148065 (DRIVE, part of the GAME-ON initiative)