Study of odd-mass N=82 isotones with realistic effective interactions

The microscopic quasiparticle-phonon model, MQPM, is used to study the energy spectra of the odd $Z=53 - 63$, N=82 isotones. The results are compared with experimental data, with the extreme quasiparticle-phonon limit and with the results of an unrestricted $2s1d0g_{7/2}0h_{11/2}$ shell model (SM) calculation. The interaction used in these calculations is a realistic two-body G-matrix interaction derived from modern meson-exchange potential models for the nucleon-nucleon interaction. For the shell model all the two-body matrix elements are renormalized by the $\hat{Q}$-box method whereas for the MQPM the effective interaction is defined by the G-matrix.Comment: Elsevier latex style espart, 26 pages, submitted to Nuclear Physics

Emerging evidence for CHFR as a cancer biomarker : from tumor biology to precision medicine

Novel insights in the biology of cancer have switched the paradigm of a "one-size-fits-all" cancer treatment to an individualized biology-driven treatment approach. In recent years, a diversity of biomarkers and targeted therapies has been discovered. Although these examples accentuate the promise of personalized cancer treatment, for most cancers and cancer subgroups no biomarkers and effective targeted therapy are available. The great majority of patients still receive unselected standard therapies with no use of their individual molecular characteristics. Better knowledge about the underlying tumor biology will lead the way toward personalized cancer treatment. In this review, we summarize the evidence for a promising cancer biomarker: checkpoint with forkhead and ring finger domains (CHFR). CHFR is a mitotic checkpoint and tumor suppressor gene, which is inactivated in a diverse group of solid malignancies, mostly by promoter CpG island methylation. CHFR inactivation has shown to be an indicator of poor prognosis and sensitivity to taxane-based chemotherapy. Here we summarize the current knowledge of altered CHFR expression in cancer, the impact on tumor biology and implications for personalized cancer treatment

Turn the tide: scientific research towards an integrated plan for the Upper-Seascheldt

During the last 150 years the Scheldt estuary has seen many changes either to claim land for urban or agricultural development or to improve the navigability. From the 1950’s onwards the most important changes to the character of the estuary could be attributed to infrastructural works such as dike construction and deepening. Even though cause–effect relationships are difficult to determine it is largely accepted that, besides reclamations, the main contribution to the loss of habitat can be attributed to the increase in tidal amplitude. In various studies the relationship between tidal amplification and large scale engineering works, including deepening, (downstream) sand extraction, embankments and straightening works, has been pointed out. It is clear that anthropogenic changes to the system can have serious consequences to the state of the estuary and that future works need to be prepared in a conscious and sustainable manner in order to avoid further tidal amplification.Within the framework of the project “Integrated Plan Upper-Seascheldt” commissioned by the Seascheldt division of the Waterwegen & Zeekanaal NV, it is investigated how navigability can be improved (to class Va) without negative effects to nature and safety against flooding. It is the goal of this integrated study to look for synergy in order to mitigate negative impacts of the proposed measures or even to improve the functioning of the system. In the last 10 years already various environmental measures like de-poldering are being implemented under the SIGMA-Plan.This paper will discuss the evolution of the Seascheldt in relation to historical anthropogenic changes. It will focus on the observed changes in water level, bathymetry, habitats (salt marshes) and sediment concentrations. In addition, the paper will outline the project plan to investigate whether de-poldering projects and other solutions or strategies can be identified that may ‘turn the tide’. This study involves applied scientific research to improve knowledge on (ecological) functioning of the Scheldt Estuary by means of a chain of model developments by the project partners (INBO, UA and FHR)

Mitochondrial DNA copy number in colorectal cancer: between tissue comparisons, clinicopathological characteristics and survival

Low mitochondrial DNA (mtDNA) copy number in tumors has been associated with worse prognosis in colorectal cancer (CRC). This study further deciphers the role of mtDNA copy number in CRC by comparing mtDNA copy number between healthy, adenoma and carcinoma tissue, by investigating its association according to several clinicopathological characteristics in CRC, and by relating it to CRC-specific survival in CRC patients. A hospital-based series of samples including cancer, adenoma and adjacent histologically normal tissue from primary CRC patients (n = 56) and recurrent CRC (n = 16) was studied as well as colon mucosa samples from healthy subjects (n = 76). Furthermore, mtDNA copy number was assessed in carcinomas of 693 CRC cases identified from the population-based Netherlands Cohort Study (NLCS). MtDNA copy number was significantly lower in carcinoma tissue (P = 0.011) and adjacent tissue (P <0.001) compared to earlier resected adenoma tissue and in primary CRC tissue compared to recurrent CRC tissue (P = 0.011). Within both study populations, mtDNA copy number was significantly lower in mutated BRAF (P = 0.027 and P = 0.006) and in microsatellite unstable (MSI) tumors (P = 0.033 and P <0.001) and higher in KRAS mutated tumors (P = 0.004). Furthermore, the association between mtDNA and survival seemed to follow an inverse U-shape with the highest HR observed in the second quintile of mtDNA copy number (HR = 1.70, 95% CI = 1.18, 2.44) compared to the first quintile. These results might reflect an association of mtDNA copy number with various malignant processes in cancer cells and warrants further research on tumor energy metabolism in CRC prognosis