The hyperfine transition in light muonic atoms of odd Z

The hyperfine (hf) transition rates for muonic atoms have been re-measured for select light nuclei, using neutron detectors to evaluate the time dependence of muon capture. For $^{19}$F $\Lambda$$_{h}$ = 5.6 (2) $\mu$s$^{-1}$ for the hf transition rate, a value which is considerably more accurate than previous measurements. Results are also reported for Na, Al, P, Cl, and K; that result for P is the first positive identification.Comment: 12 pages including 5 tables and 4 figures, RevTex, submitted to Phys. Rev.

Chemokine (C-C motif) receptor 7 (CCR7) associates with the tumour immune microenvironment but not progression in invasive breast carcinoma

Some previous studies have reported that the chemokine (C-C motif) receptor 7 (CCR7) plays a role in breast cancer, is associated with lymph node metastasis and drives the site of distant metastasis. However, the impact of its expression on patient outcome and its association with tumour infiltrating inflammatory cells remain to be validated. We evaluated CCR7 protein expression by immunohistochemistry in a large well characterized cohort (n = 866) of early invasive primary breast cancers. CCR7 was expressed in the cytoplasm and membrane of tumour cells. We observed a weak positive association of high CCR7 expression when in either cellular component, but not both together, with axillary lymph node stage 3 tumours (p = 0.043). Logistic regression analysis of lymph node stage revealed no independent predictive value for CCR7 expression. CCR7 expression was higher in HER2 positive tumours (p = 0.03) and associated with positive CD68+ FOXP3+ tumour infiltrating cells. CCR7 staining was negatively associated with CD3+ cells. There was no significant association of CCR7 expression with breast cancer recurrence or survival. We conclude that while CCR7 is not a useful biomarker for predicting lymph node metastasis, it may reflect altered intra- and inter-cellular signalling related to the immune microenvironment. The subcellular localization of CCR7 appears to affect the nature of these interactions

Measurement of Muon Capture on the Proton to 1% Precision and Determination of the Pseudoscalar Coupling g_P

The MuCap experiment at the Paul Scherrer Institute has measured the rate L_S of muon capture from the singlet state of the muonic hydrogen atom to a precision of 1%. A muon beam was stopped in a time projection chamber filled with 10-bar, ultra-pure hydrogen gas. Cylindrical wire chambers and a segmented scintillator barrel detected electrons from muon decay. L_S is determined from the difference between the mu- disappearance rate in hydrogen and the free muon decay rate. The result is based on the analysis of 1.2 10^10 mu- decays, from which we extract the capture rate L_S = (714.9 +- 5.4(stat) +- 5.1(syst)) s^-1 and derive the proton's pseudoscalar coupling g_P(q^2_0 = -0.88 m^2_mu) = 8.06 +- 0.55.Comment: Updated figure 1 and small changes in wording to match published versio

Mass splittings of nuclear isotopes in chiral soliton approach

The differences of the masses of nuclear isotopes with atomic numbers between \~10 and ~30 can be described within the chiral soliton approach in satisfactory agreement with data. Rescaling of the model is necessary for this purpose - decrease of the Skyrme constant by about 30%, providing the "nuclear variant" of the model. The asymmetric term in Weizsaecker-Bethe- Bacher mass formula for nuclei can be obtained as the isospin dependent quantum correction to the nucleus energy. Some predictions for the binding energies of neutron rich nuclides are made in this way, from, e.g. Be-16 and B-19 to Ne-31 and Na-32. Neutron rich nuclides with high values of isospin are unstable relative to strong interactions. The SK4 (Skyrme) variant of the model, as well as SK6 variant (6-th order term in chiral derivatives in the lagrangian as solitons stabilizer) are considered, and the rational map approximation is used to describe multiskyrmions.Comment: 16 pages, 10 tables, 2 figures. Figures are added and few misprints are removed. Submitted to Phys. Atom. Nucl. (Yad. Fiz.

Legumain is an independent predictor for invasive recurrence in breast ductal carcinoma in situ

© 2018, United States & Canadian Academy of Pathology. Legumain is a proteolytic enzyme that plays a role in the regulation of cell proliferation in invasive breast cancer. Studies evaluating its role in ductal carcinoma in situ (DCIS) are lacking. Here, we aimed to characterize legumain protein expression in DCIS and evaluate its prognostic significance. Legumain was assessed immunohistochemically in a tissue microarray of a well-characterized cohort of DCIS (n = 776 pure DCIS and n = 239 DCIS associated with invasive breast cancer (DCIS-mixed)). Legumain immunoreactivity was scored in tumor cells and surrounding stroma and related to clinicopathological parameters and patient outcome. High legumain expression was observed in 23% of pure DCIS and was associated with features of high-risk DCIS including higher nuclear grade, comedo necrosis, hormone receptor negativity, HER2 positivity, and higher proliferation index. Legumain expression was higher in DCIS associated with invasive breast cancer than in pure DCIS (p < 0.0001). In the DCIS-mixed cohort, the invasive component showed higher legumain expression than the DCIS component (p < 0.0001). Legumain was an independent predictor of shorter local recurrencefree interval for all recurrences (p = 0.0003) and for invasive recurrences (p = 0.002). When incorporated with other risk factors, legumain provided better patient risk stratification. High legumain expression is associated with poor prognosis in DCIS and could be a potential marker to predict DCIS progression to invasive disease

The prognostic significance of lysosomal protective protein (Cathepsin A) in breast ductal carcinoma in situ

Background: Cathepsin A (CTSA) is a key regulatory enzyme for galactoside metabolism. Additionally, it has a distinct proteolytic activity and plays a role in tumour progression. CTSA is differentially expressed at the mRNA level between breast ductal carcinoma in situ (DCIS) and invasive breast carcinoma (IBC). In this study, we aimed to characterise CTSA protein expression in DCIS and evaluate its prognostic significance. Methods: A large cohort of DCIS (n=776 for pure DCIS and n=239 for DCIS associated with IBC (DCIS/IBC)) prepared as tissue microarray was immunohistochemically stained for CTSA. Results: High CTSA expression was observed in 48% of pure DCIS. High expression was associated with features of poor DCIS prognosis including younger age at diagnosis (less than 50 years), higher nuclear grade, hormone receptor negativity, HER2 positivity, high proliferative index and high hypoxia inducible factor 1 alpha expression. High CTSA expression was associated with shorter recurrence free interval (RFI) (p=0.0001). In multivariate survival analysis for patients treated with breast conserving surgery, CTSA was an independent predictor of shorter RFI (p=0.015). DCIS associated with IBC showed higher CTSA expression than pure DCIS (p=0.04). In the DCIS/IBC cohort, CTSA expression was higher in the invasive component than DCIS component (p less than 0.0001). Conclusion: CTSA is not only associated with aggressive behaviour and poor outcome in DCIS but also a potential marker to predict co-existing invasion in DCIS

Amplicon-Dependent CCNE1 Expression Is Critical for Clonogenic Survival after Cisplatin Treatment and Is Correlated with 20q11 Gain in Ovarian Cancer

Genomic amplification of 19q12 occurs in several cancer types including ovarian cancer where it is associated with primary treatment failure. We systematically attenuated expression of genes within the minimally defined 19q12 region in ovarian cell lines using short-interfering RNAs (siRNA) to identify driver oncogene(s) within the amplicon. Knockdown of CCNE1 resulted in G1/S phase arrest, reduced cell viability and apoptosis only in amplification-carrying cells. Although CCNE1 knockdown increased cisplatin resistance in short-term assays, clonogenic survival was inhibited after treatment. Gain of 20q11 was highly correlated with 19q12 amplification and spanned a 2.5 Mb region including TPX2, a centromeric protein required for mitotic spindle function. Expression of TPX2 was highly correlated with gene amplification and with CCNE1 expression in primary tumors. siRNA inhibition of TPX2 reduced cell viability but this effect was not amplicon-dependent. These findings demonstrate that CCNE1 is a key driver in the 19q12 amplicon required for survival and clonogenicity in cells with locus amplification. Co-amplification at 19q12 and 20q11 implies the presence of a cooperative mutational network. These observations have implications for the application of targeted therapies in CCNE1 dependent ovarian cancers