Equivariant intersection cohomology of the circle actions

In this paper, we prove that the orbit space B and the Euler class of an action of the circle S^1 on X determine both the equivariant intersection cohomology of the pseudomanifold X and its localization. We also construct a spectral sequence converging to the equivariant intersection cohomology of X whose third term is described in terms of the intersection cohomology of B.Comment: Final version as accepted in RACSAM. The final publication is available at springerlink.com; Revista de la Real Academia de Ciencias Exactas, Fisicas y Naturales. Serie A. Matematicas, 201

Strength and uncertainty of phytoplankton metrics for assessing eutrophication impacts in lakes

Phytoplankton constitutes a diverse array of short-lived organisms which derive their nutrients from the water column of lakes. These features make this community the most direct and earliest indicator of the impacts of changing nutrient conditions on lake ecosystems. It also makes them particularly suitable for measuring the success of restoration measures following reductions in nutrient loads. This paper integrates a large volume of work on a number of measures, or metrics, developed for using phytoplankton to assess the ecological status of European lakes, as required for the Water Framework Directive. It assesses the indicator strength of these metrics, specifically in relation to representing the impacts of eutrophication. It also examines how these measures vary naturally at different locations within a lake, as well as between lakes, and how much variability is associated with different replicate samples, different months within a year and between years. On the basis of this analysis, three of the strongest metrics (chlorophyll-a, phytoplankton trophic index (PTI), and cyanobacterial biovolume) are recommended for use as robust measures for assessing the ecological quality of lakes in relation to nutrient-enrichment pressures and a minimum recommended sampling frequency is provided for these three metrics

Association between Frequency of Chromosomal Aberrations and Cancer Risk Is Not Influenced by Genetic Polymorphisms in GSTM1 and GSTT1

To evaluate the role of polymorphisms in glutathione S-transferase M1 (GSTM1) and theta 1 (GSTT1) as effect modifiers of the association between CA and cancer risk. A case-control study was performed pooling data from cytogenetic studies carried out in 1974-1995 in three laboratories in Italy, Norway, and Denmark. The subjects were classified as low, medium, and high by tertile of CA frequency. The data were analysed by setting up a Bayesian model which included prior information about cancer risk by CA frequency

The multidrug resistance 1 (MDR1) gene polymorphism G-rs3789243-A is not associated with disease susceptibility in Norwegian patients with colorectal adenoma and colorectal cancer; a case control study

<p>Abstract</p> <p>Background</p> <p>Smoking, dietary factors, and alcohol consumption are known life style factors contributing to gastrointestinal carcinogenesis. Genetic variations in carcinogen handling may affect cancer risk. The multidrug resistance 1(<it>MDR1/ABCB1</it>) gene encodes the transport protein P-glycoprotein (a phase III xenobiotic transporter). P-glycoprotein is present in the intestinal mucosal lining and restricts absorption of certain carcinogens, among these polycyclic aromatic hydrocarbons. Moreover, P-glycoprotein transports various endogenous substrates such as cytokines and chemokines involved in inflammation, and may thereby affect the risk of malignity. Hence, genetic variations that modify the function of P-glycoprotein may be associated with the risk of colorectal cancer (CRC). We have previously found an association between the <it>MDR1 </it>intron 3 G-rs3789243-A polymorphism and the risk of CRC in a Danish study population. The aim of this study was to investigate if this <it>MDR1 </it>polymorphism was associated with risk of colorectal adenoma (CA) and CRC in the Norwegian population.</p> <p>Methods</p> <p>Using a case-control design, the association between the <it>MDR1 </it>intron 3 G-rs3789243-A polymorphism and the risk of colorectal carcinomas and adenomas in the Norwegian population was assessed in 167 carcinomas, 990 adenomas, and 400 controls. Genotypes were determined by allelic discrimination. Odds ratio (OR) and 95 confidence interval (95% CI) were estimated by binary logistic regression.</p> <p>Results</p> <p>No association was found between the <it>MDR1 </it>polymorphism (G-rs3789243-A) and colorectal adenomas or cancer. Carriers of the variant allele of MDR1 intron 3 had odds ratios (95% CI) of 0.97 (0.72–1.29) for developing adenomas, and 0.70 (0.41–1.21) for colorectal cancer, respectively, compared to homozygous wild type carriers.</p> <p>Conclusion</p> <p>The <it>MDR1 </it>intron 3 (G-rs3789243-A) polymorphism was not associated with a risk of colorectal adenomas or carcinomas in the present Norwegian study group. Thus, this <it>MDR1 </it>polymorphism does not seem to play an important role in colorectal carcinogenesis in this population.</p

Expression of NDRG2 is down-regulated in high-risk adenomas and colorectal carcinoma

<p>Abstract</p> <p>Background</p> <p>It has recently been shown that <it>NDRG2 </it>mRNA is down-regulated or undetectable in several human cancers and cancer cell-lines. Although the function of NDRG2 is unknown, high <it>NDRG2 </it>expression correlates with improved prognosis in high-grade gliomas. The aim of this study has been to examine <it>NDRG2 </it>mRNA expression in colon cancer. By examining affected and normal tissue from individuals with colorectal adenomas and carcinomas, as well as in healthy individuals, we aim to determine whether and at which stages <it>NDRG2 </it>down-regulation occurs during colonic carcinogenesis.</p> <p>Methods</p> <p>Using quantitative RT-PCR, we have determined the mRNA levels for <it>NDRG2 </it>in low-risk (n = 15) and high-risk adenomas (n = 57), colorectal carcinomas (n = 50) and corresponding normal tissue, as well as control tissue from healthy individuals (n = 15). <it>NDRG2 </it>levels were normalised to <it>β-actin</it>.</p> <p>Results</p> <p><it>NDRG2 </it>mRNA levels were lower in colorectal carcinomas compared to normal tissue from the control group (p < 0.001). When comparing adenomas/carcinomas with adjacent normal tissue from the same individual, <it>NDRG2 </it>expression levels were significantly reduced in both high-risk adenoma (p < 0.001) and in colorectal carcinoma (p < 0.001). There was a trend for <it>NDRG2 </it>levels to decrease with increasing Dukes' stage (p < 0.05).</p> <p>Conclusion</p> <p>Our results demonstrate that expression of <it>NDRG2 </it>is down-regulated at a late stage during colorectal carcinogensis. Future studies are needed to address whether <it>NDRG2 </it>down-regulation is a cause or consequence of the progression of colorectal adenomas to carcinoma.</p

Haplotype frequencies in a sub-region of chromosome 19q13.3, related to risk and prognosis of cancer, differ dramatically between ethnic groups

<p>Abstract</p> <p>Background</p> <p>A small region of about 70 kb on human chromosome 19q13.3 encompasses 4 genes of which 3, <it>ERCC1</it>, <it>ERCC2</it>, and <it>PPP1R13L </it>(aka <it>RAI</it>) are related to DNA repair and cell survival, and one, <it>CD3EAP</it>, aka <it>ASE1</it>, may be related to cell proliferation. The whole region seems related to the cellular response to external damaging agents and markers in it are associated with risk of several cancers.</p> <p>Methods</p> <p>We downloaded the genotypes of all markers typed in the 19q13.3 region in the HapMap populations of European, Asian and African descent and inferred haplotypes. We combined the European HapMap individuals with a Danish breast cancer case-control data set and inferred the association between HapMap haplotypes and disease risk.</p> <p>Results</p> <p>We found that the susceptibility haplotype in our European sample had increased from 2 to 50 percent very recently in the European population, and to almost the same extent in the Asian population. The cause of this increase is unknown. The maximal proportion of overall genetic variation due to differences between groups for Europeans versus Africans and Europeans versus Asians (the F_stvalue) closely matched the putative location of the susceptibility variant as judged from haplotype-based association mapping.</p> <p>Conclusion</p> <p>The combined observation that a common haplotype causing an increased risk of cancer in Europeans and a high differentiation between human populations is highly unusual and suggests a causal relationship with a recent increase in Europeans caused either by genetic drift overruling selection against the susceptibility variant or a positive selection for the same haplotype. The data does not allow us to distinguish between these two scenarios. The analysis suggests that the region is not involved in cancer risk in Africans and that the susceptibility variants may be more finely mapped in Asian populations.</p

On extensions of some classes of algebras

The paper consists of three parts. In the first part we discuss on extensions of Lie algebras and their importance in Physics. Then we deal with the extensions of some classes of algebras with one binary operation. The third part is devoted to the study of extensions of two classes of algebras, possessing two algebraic operations, called dialgebras. In all the cases we propose 2-cocycles and respective extensions. The motivation to study the extensions is to use them further for the classification problem of the classes algebras considered in low dimensional cases

Effect of occupational exposure to cytostatics and nucleotide excision repair polymorphism on chromosomal aberrations frequency

Authors evaluated the incidence of total chromosomal aberrations (CA) and their types – chromatid-type (CTA) and chromosome-type (CSA) in peripheral blood lymphocytes from 72 oncologic unit's workers occupationally exposed to cytostatics in relationship to polymorphisms of DNA repair genes XPD, XPG and XPC. The cytogenetic analysis was used for determination of chromosomal aberrations frequency and PCR-RFLP method for polymorphisms of genes. Statistically higher frequency of total CA was detected in exposed group as compared to control (1.90±1.34% vs. 1.26±0.93%; Mann-Whitney U-test, p=0.001). There was not detected any difference between CTA and CSA (0.92±1.04% vs. 0.98±1.17%). Similarly, in genes XPD exon 23 and XPC exon 15 wasn't detected any difference neither in total chromosomal aberrations nor in CTA and CSA types. Statistically significant decrease of total chromosomal aberrations and CTA-type with presence of variant allele C was detected in gene XPG exon 15. Authors pointed out the importance of individual susceptibility factors in evaluation of effects of genotoxic agents, in that event, when the concentration does not meet the occupational exposure limit

Increased mRNA expression levels of ERCC1, OGG1 and RAI in colorectal adenomas and carcinomas

BACKGROUND: The majority of colorectal cancer (CRC) cases develop through the adenoma-carcinoma pathway. If an increase in DNA repair expression is detected in both early adenomas and carcinomas it may indicate that low repair capacity in the normal mucosa is a risk factor for adenoma formation. METHODS: We have examined mRNA expression of two DNA repair genes, ERCC1 and OGG1 as well as the putative apoptosis controlling gene RAI, in normal tissues and lesions from 36 cases with adenomas (mild/moderat n = 21 and severe n = 15, dysplasia) and 9 with carcinomas. RESULTS: Comparing expression levels of ERCC1, OGG1 and RAI between normal tissue and all lesions combined yielded higher expression levels in lesions, 3.3-fold higher (P = 0.005), 5.6-fold higher(P < 3·10(-5)) and 7.7-fold higher (P = 0.0005), respectively. The levels of ERCC1, OGG1 and RAI expressions when comparing lesions, did not differ between adenomas and CRC cases, P = 0.836, P = 0.341 and P = 0.909, respectively. When comparing expression levels in normal tissue, the levels for OGG1 and RAI from CRC cases were significantly lower compared to the cases with adenomas, P = 0.012 and P = 0.011, respectively. CONCLUSION: Our results suggest that increased expression of defense genes is an early event in the progression of colorectal adenomas to carcinomas

Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of colorectal adenoma and carcinoma, in a Norwegian cohort: a case control study

BACKGROUND: Genetic polymorphisms in DNA repair genes may influence individual variation in DNA repair capacity, which may be associated with risk of developing cancer. For colorectal cancer the importance of mutations in mismatch repair genes has been extensively documented. Less is known about other DNA repair pathways in colorectal carcinogenesis. In this study we have focused on the XRCC1, XRCC3 and XPD genes, involved in base excision repair, homologous recombinational repair and nucleotide excision repair, respectively. METHODS: We used a case-control study design (157 carcinomas, 983 adenomas and 399 controls) to test the association between five polymorphisms in these DNA repair genes (XRCC1 Arg(194)Trp, Arg(280)His, Arg(399)Gln, XRCC3 Thr(241)Met and XPD Lys(751)Gln), and risk of colorectal adenomas and carcinomas in a Norwegian cohort. Odds ratio (OR) and 95% confidence interval (95% CI) were estimated by binary logistic regression model adjusting for age, gender, cigarette smoking and alcohol consumption. RESULTS: The XRCC1 280His allele was associated with an increased risk of adenomas (OR 2.30, 95% CI 1.19–4.46). The XRCC1 399Gln allele was associated with a reduction of risk of high-risk adenomas (OR 0.62, 95% CI 0.41–0.96). Carriers of the variant XPD 751Gln allele had an increased risk of low-risk adenomas (OR 1.40, 95% CI 1.03–1.89), while no association was found with risk of carcinomas. CONCLUSION: Our results suggest an increased risk for advanced colorectal neoplasia in individuals with the XRCC1 Arg(280)His polymorphism and a reduced risk associated with the XRCC1 Arg(399)Gln polymorphism. Interestingly, individuals with the XPD Lys(751)Gln polymorphism had an increased risk of low-risk adenomas. This may suggest a role in regression of adenomas