Methods for a quantitative evaluation of odd-even staggering effects

Odd-even effects, also known as "staggering" effects, are a common feature observed in the yield distributions of fragments produced in different types of nuclear reactions. We review old methods, and we propose new ones, for a quantitative estimation of these effects as a function of proton or neutron number of the reaction products. All methods are compared on the basis of Monte Carlo simulations. We find that some are not well suited for the task, the most reliable ones being those based either on a non-linear fit with a properly oscillating function or on a third (or fourth) finite difference approach. In any case, high statistic is of paramount importance to avoid that spurious structures appear just because of statistical fluctuations in the data and of strong correlations among the yields of neighboring fragments.Comment: 16 pages, 9 figures - Revised version, mainly with an expanded sect. 2 about smoothing methods (three more methods are presented and an appendix on relevant aspects of the finite-differences formalism is added); results are shown also for the simulations with the three additional methods. Some more references are added. Conclusions are unchange

Vav1 is ectopically expressed in breast tumors in which reduces the efficiency of the metastatic process

Vav1, normally restricted to hematopoietic cells, results ectopically expressed in solid tumors, including breast cancer (Sebban et al., 2013) in which, contrarily to other neoplasias, seems to be higher in tumors from patients who remained diseasefree than in patients who developed recurrence (Lane et al., 2008). The significance of Vav1 expression in breast tumors was evaluated by immunohistochemical analysis on TMAs containing invasive breast tumors from patients without lymph node involvement. Our findings indicate that Vav1 is expressed in almost all investigated cancers and shows a peculiar localization inside the nucleus of tumor cells. High amounts of nuclear Vav1 positively correlates with low incidence of relapse, regardless phenotype and molecular subtype of the neoplasia. Experiments performed with breast tumor-derived cells showing different morphology, immunoprofile and invasive properties indicated that Vav1 negatively modulates their invasiveness in vitro and their metastatic efficiency in vivo, possibly by affecting the expression of genes involved in invasion and/or metastasis of breast cancer. Since the high heterogeneity of breast tumors makes difficult to predict the evolution of early neoplasias, the evaluation of nuclear Vav1 levels may help in profiling and management of early breast cancer patients. In addition, Vav1 may serve as a target for new therapies designed to prevent breast cancer progression

New investigations on the 32S(3He,d)33Cl reaction at 9.6 MeV bombarding energy

The 32S(3He,d)33Cl one-proton transfer reaction is a powerful tool to investigate the spectroscopy of low-lying states in the proton-rich 33Cl nucleus. However, the extraction of firm differential cross-section data at various angles to benchmark and constrain theoretical models is made challenging by the presence of competitive reactions on target contaminants. In this paper we report on arecent measurement using a new generation hodoscope of silicon detectors, capable to detect and identify emitted deuterons down to energies of the order of 2 MeV. The high angular segmentation of our hodoscope combined with a suitable target to control possible contaminants, allowed to unambiguously disentangle the contribution of various states in 33Cl, in particular the 2.352 MeV state lying just few tens of keV above the proton separation energy

Study of the 32S(3He,d)33Cl one-proton transfer reaction with a new generation hodoscope

Abstract The 32S(3He,d)33Cl one-proton transfer reaction is a powerful tool to investigate the spectroscopy of low-lying states in the proton-rich 33Cl nucleus. However, the extraction of firm differential cross-section data at various angles, against which benchmarking theoretical models to correctly constrain the spectroscopy of 33Cl, is made challenging by the presence of competitive reaction products contaminating the detected energy spectra. We have recently measured the 32S(3He,d)33Cl reaction at 9.8 MeV incident energy by using a new generation hodoscope of silicon detectors, capable to detect and identify emitted deuterons down to energies of the order of 2 MeV. The high angular segmentation of our hodoscope allowed to unambiguously disentangle the contribution of one-proton transfer reactions in the ground state of 33Cl and in its 0.810 MeV, 2.352 MeV, 2.685 MeV, 2.846 MeV excited states from contaminant deuteron-emitting reactions. These data will be crucial to help to constrain Jπ and spectroscopic factor C 2 Sp values of low-lying 33Cl states, still ambiguous in the literature. The present status of the analysis is discussed in the paper

The Loss of the p53 Activator HIPK2 Is Responsible for Galectin-3 Overexpression in Well Differentiated Thyroid Carcinomas

Background: Galectin-3 (Gal-3) is an anti-apoptotic molecule involved in thyroid cells transformation. It is specifically overexpressed in thyroid tumour cells and is currently used as a preoperative diagnostic marker of thyroid malignancy. Gal-3 expression is downregulated by wt-p53 at the transcriptional level. In well-differentiated thyroid carcinomas (WDTCs) there is an unexplained paradoxical concomitant expression of Gal-3 and wt-p53. HIPK2 is a co-regulator of different transcription factors, and modulates basic cellular processes mainly through the activation of wt-p53. Since we demonstrated that HIPK2 is involved in p53-mediated Gal-3 downregulation, we asked whether HIPK2 deficiency might be responsible for such paradoxical Gal-3 overexpression in WDTC. Methodology/Principal Findings: We analyzed HIPK2 protein and mRNA levels, as well as loss of heterozygosity (LOH) at the HIPK2 locus (7q32-34), in thyroid tissue samples. HIPK2 protein levels were high in all follicular hyperplasias (FHs) analyzed. Conversely, HIPK2 was undetectable in 91.7% of papillary thyroid carcinomas (PTCs) and in 60.0% of follicular thyroid carcinomas (FTCs). HIPK2 mRNA levels were upregulated in FH compared to normal thyroid tissue (NTT), while PTC showed mean HIPK2 mRNA levels lower than FH and, in 61.5% of cases, also lower than NTT. We found LOH at HIPK-2 gene locus in 37.5% of PTCs, 14.3% of FTCs and 18.2% of follicular adenomas. To causally link these data with Gal-3 upregulation, we performed in vitro experiments, using the PTC-derived K1 cells, in which HIPK2 expression was manipulated by RNA interference (RNAi) or plasmid-mediated overexpression. HIPK2 RNAi was associated with Gal-3 upregulation, while HIPK2 overexpression with Gal-3 downregulation. Conclusions/Significance: Our results indicate that HIPK2 expression and function are impaired in WDTCs, in particular in PTCs, and that this event explains Gal-3 overexpression typically observed in these types of tumours. Therefore, HIPK2 can be considered as a new tumour suppressor gene for thyroid cancers

Vav1 downmodulates Akt in different breast cancer subtypes: A new promising chance to improve breast cancer outcome

Targeting different members of the Akt pathways is a promising therapeutic chance in solid tumors including breast cancer. The variable expression levels of Akt isoforms with opposite effects on tumor growth and metastasis, however, make it difficult to select the inhibitors to be used for specific breast tumor subtypes. Using in vitro and in vivo models, we demonstrated here that Vav1, ectopically expressed in invasive breast tumors derived cells, downmodulates Akt acting at expression and/or activation levels depending on tumor subtype. The decreased p-Akt1 (Ser473) levels are a common effect of Vav1 upmodulation, suggesting that, in breast tumor-derived cells and independently of their phenotype, Vav1 interferes with signaling pathways ended to specifically recruit Akt1. Only in ER-negative cell lines, the silencing of Vav1 induced the expression but not the activation of Akt2. A retrospective analysis of early invasive breast tumors allowed to establish the prognostic significance of the p-Akt/Vav1 relationship. In particular, low Vav1 levels negatively influence the follow-up of patients with low p-Akt in their primary tumors and subjected to adjuvant chemotherapy. As the use of specific or pan Akt inhibitors may not be sufficient or may even be detrimental, increasing the levels of Vav1 could be a new approach to improve breast cancer outcomes. This might be particularly relevant for tumors with a triple-negative phenotype, for which target-based therapies are not currently available

High nuclear level of Vav1 is a positive prognostic factor in early invasive breast tumors: a role in modulating genes related to the efficiency of metastatic process.

Vav1 is one of the signalling proteins normally restricted to hematopoietic cells that results ectopically expressed in solid tumors, including breast cancer. By immunohistochemical analysis on TMAs containing invasive breast tumor from patients without lymph node involvement, we have found that Vav1 is expressed in almost all investigated cancers and shows a peculiar localization inside the nucleus of tumor cells. High amounts of nuclear Vav1 are positively correlated with low incidence of relapse, regardless phenotype and molecular subtype of breast neoplasia. In particular, Kaplan-Meier plots showed an elevated risk of distant metastasis in patients with low Vav1 expression compared with patients with high Vav1 expression in their tumors. Experiments performed with breast tumor-derived cells indicated that Vav1 negatively modulates their invasiveness in vitro and their metastatic efficiency in vivo, possibly by affecting the expression of genes involved in invasion and/or metastasis of breast tumors. Since the high heterogeneity of breast tumors makes difficult to predict the evolution of early breast neoplasias, the evaluation of nuclear Vav1 levels may help in the characterization and management of early breast cancer patients. In particular, Vav1 may serve as a prognostic biomarker and a target for new therapies aimed to prevent breast cancer progression

Lights and (some) shadows in the comparison among experimental data of heavy ion collisionat Fermi energies and the dynamical model AMD

The simulation of heavy ion collisions in the Fermi energy region is a challenge for the theoretical models; in particular it is difficult to obtain a coherent description in all the impact parameter range and to reproduce all the experimental observables. In this contribution we will show the very good job done by the dynamical model AMD [1] followed by the statistical code GEMINI [2, 3] as an afterburner. The model is able to reproduce the main characteristics of peripheral and semiperipheral collisions, although some discrepancies still persist