High Fill-Out, Extreme Mass Ratio Overcontact Binary Systems. X. The new discovered binary XY Leonis Minoris

The new discovered short-period close binary star, XY LMi, was monitored photometrically since 2006. It is shown that the light curves are typical EW-type and show complete eclipses with an eclipse duration of about 80 minutes. By analyzing the complete B, V, R, and I light curves with the 2003 version of the W-D code, photometric solutions were determined. It is discovered that XY LMi is a high fill-out, extreme mass ratio overcontact binary system with a mass ratio of q=0.148 and a fill-out factor of f=74.1%, suggesting that it is on the late evolutionary stage of late-type tidal-locked binary stars. As observed in other overcontact binary stars, evidence for the presence of two dark spots on both components are given. Based on our 19 epoches of eclipse times, it is found that the orbital period of the overcontact binary is decreasing continuously at a rate of dP/dt=-1.67\times10^{-7}\,days/year, which may be caused by the mass transfer from the primary to the secondary or/and angular momentum loss via magnetic stellar wind. The decrease of the orbital period may result in the increase of the fill-out, and finally, it will evolve into a single rapid-rotation star when the fluid surface reaching the outer critical Roche Lobe.Comment: 19 pages, 4 figures, 9 table

An evaluation of membrane properties and process characteristics of a scaled-up pressure retarded osmosis (PRO) process

YesThis work presents a systematic evaluation of the membrane and process characteristics of a scaled-up pressure retarded osmosis (PRO). In order to meet pre-defined membrane economic viability ( ≥ 5 W/m2), different operating conditions and design parameters are studied with respect to the increase of the process scale, including the initial flow rates of the draw and feed solution, operating pressure, membrane permeability-selectivity, structural parameter, and the efficiency of the high-pressure pump (HP), energy recovery device (ERD) and hydro-turbine (HT). The numerical results indicate that the performance of the scaled-up PRO process is significantly dependent on the dimensionless flow rate. Furthermore, with the increase of the specific membrane scale, the accumulated solute leakage becomes important. The membrane to achieve the optimal performance moves to the low permeability in order to mitigate the reverse solute permeation. Additionally, the counter-current flow scheme is capable to increase the process performance with a higher permeable and less selectable membrane compared to the co-current flow scheme. Finally, the inefficiencies of the process components move the optimal APD occurring at a higher dimensionless flow rate to reduce the energy losses in the pressurization and at a higher specific membrane scale to increase energy generation

Linear and non-linear dependencies between copy number aberrations and mRNA expression reveal distinct molecular pathways in breast cancer

<p>Abstract</p> <p>Background</p> <p>Elucidating the exact relationship between gene copy number and expression would enable identification of regulatory mechanisms of abnormal gene expression and biological pathways of regulation. Most current approaches either depend on linear correlation or on nonparametric tests of association that are insensitive to the exact shape of the relationship. Based on knowledge of enzyme kinetics and gene regulation, we would expect the functional shape of the relationship to be gene dependent and to be related to the gene regulatory mechanisms involved. Here, we propose a statistical approach to investigate and distinguish between linear and nonlinear dependences between DNA copy number alteration and mRNA expression.</p> <p>Results</p> <p>We applied the proposed method to DNA copy numbers derived from Illumina 109 K SNP-CGH arrays (using the log R values) and expression data from Agilent 44 K mRNA arrays, focusing on commonly aberrated genomic loci in a collection of 102 breast tumors. Regression analysis was used to identify the type of relationship (linear or nonlinear), and subsequent pathway analysis revealed that genes displaying a linear relationship were overall associated with substantially different biological processes than genes displaying a nonlinear relationship. In the group of genes with a linear relationship, we found significant association to canonical pathways, including purine and pyrimidine metabolism (for both deletions and amplifications) as well as estrogen metabolism (linear amplification) and BRCA-related response to damage (linear deletion). In the group of genes displaying a nonlinear relationship, the top canonical pathways were specific pathways like PTEN and PI13K/AKT (nonlinear amplification) and Wnt(B) and IL-2 signalling (nonlinear deletion). Both amplifications and deletions pointed to the same affected pathways and identified cancer as the top significant disease and cell cycle, cell signaling and cellular development as significant networks.</p> <p>Conclusions</p> <p>This paper presents a novel approach to assessing the validity of the dependence of expression data on copy number data, and this approach may help in identifying the drivers of carcinogenesis.</p

Molecular alterations associated with liver metastases development in colorectal cancer patients

Background: Understanding the molecular biology of colorectal cancer (CRC) provides opportunities for effective personalised patient management. We evaluated whether chromosomal aberrations, mutations in the PI(3)K signalling pathway and the CpG-island methylator phenotype (CIMP) in primary colorectal tumours can predict liver metastases. Methods: Formalin-fixed paraffin-embedded material from primary colorectal tumours of three different groups were investigated: patients with CRC without metastases (M0, n=39), patients who were treated with hyperthermal intraperitoneal chemotherapy for CRC metastases confined to the peritoneum (PM, n=46) and those who had isolated hepatic perfusion for CRC metastases confined to the liver (LM, n=48). Results: All samples were analysed for DNA copy number changes, PIK3CA, KRAS, BRAF mutations, CIMP and microsatellite instability. The primary CRCs of the LM group had significantly higher frequency of amplified chromosome 20q (P=0.003), significantly fewer mutations in the PI(3)K signalling pathway (P=0.003) and fewer CIMP high tumours (P=0.05). There was a strong inverse correlation between 20q and the PI(3)K pathway mutations. Conclusion: The development of CRC liver metastases is associated with amplification of chromosome 20q and not driven by mutations in the PI(3)K signalling pathway.S C Bruin, Y He, I Mikolajewska-Hanclich, G-J Liefers, C Klijn, A Vincent, V J Verwaal, K A de Groot, H Morreau, M-L F van Velthuysen, R A E M Tollenaar and L J van' t Vee

Recent translational research: microarray expression profiling of breast cancer – beyond classification and prognostic markers?

Genomic expression profiling has greatly improved our ability to subclassify human breast cancers according to shared molecular characteristics and clinical behavior. The logical next question is whether this technology will be similarly useful for identifying the dominant signaling pathways that drive tumor initiation and progression within each breast cancer subtype. A major challenge will be to integrate data generated from the experimental manipulation of model systems with expression profiles obtained from primary tumors. We highlight some recent progress and discuss several obstacles in the use of expression profiling to identify pathway signatures in human breast cancer

Meta-Analysis and Gene Set Enrichment Relative to ER Status Reveal Elevated Activity of MYC and E2F in the “Basal” Breast Cancer Subgroup

10.1371/journal.pone.0004710PLoS ONE43

Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer

Abstract Introduction In breast cancer, gene expression analyses have defined five tumor subtypes (luminal A, luminal B, HER2-enriched, basal-like and claudin-low), each of which has unique biologic and prognostic features. Here, we comprehensively characterize the recently identified claudin-low tumor subtype. Methods The clinical, pathological and biological features of claudin-low tumors were compared to the other tumor subtypes using an updated human tumor database and multiple independent data sets. These main features of claudin-low tumors were also evaluated in a panel of breast cancer cell lines and genetically engineered mouse models. Results Claudin-low tumors are characterized by the low to absent expression of luminal differentiation markers, high enrichment for epithelial-to-mesenchymal transition markers, immune response genes and cancer stem cell-like features. Clinically, the majority of claudin-low tumors are poor prognosis estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and epidermal growth factor receptor 2 (HER2)-negative (triple negative) invasive ductal carcinomas with a high frequency of metaplastic and medullary differentiation. They also have a response rate to standard preoperative chemotherapy that is intermediate between that of basal-like and luminal tumors. Interestingly, we show that a group of highly utilized breast cancer cell lines, and several genetically engineered mouse models, express the claudin-low phenotype. Finally, we confirm that a prognostically relevant differentiation hierarchy exists across all breast cancers in which the claudin-low subtype most closely resembles the mammary epithelial stem cell. Conclusions These results should help to improve our understanding of the biologic heterogeneity of breast cancer and provide tools for the further evaluation of the unique biology of claudin-low tumors and cell lines

No common denominator for breast cancer lymph node metastasis

The axillary lymph node status is the most powerful prognostic factor for breast cancer patients to date. The molecular mechanisms that control lymph node metastasis, however, remain poorly understood. To define patterns of genes or gene regulatory pathways that drive breast cancer lymph node metastasis, we compared the gene expression profiles of 15 primary breast carcinomas and their matching lymph node metastases using microarrays. In general, primary breast carcinomas and lymph node metastases do not differ at the transcriptional level by a common subset of genes. No classifier or single gene discriminating the group of primary tumours from those of the lymph node metastases could be identified. Also, in a series of 295 breast tumours, no classifier predicting lymph node metastasis could be developed. However, subtle differences in the expression of genes involved in extracellular-matrix organisation and growth factor signalling are detected in individual pairs of matching primary and metastatic tumours. Surprisingly, however, different sets of these genes are either up- or downregulated in lymph node metastases. Our data suggest that breast carcinomas do not use a shared gene set to accomplish lymph node metastasis