Extraction of the πNN\pi NN coupling constant from NN scattering data

We reexamine Chew's method for extracting the $\pi NN$ coupling constant from np differential cross section measurements. Values for this coupling are extracted below 350 MeV, in the potential model region, and up to 1 GeV. The analyses to 1~GeV have utilized 55 data sets. We compare these results to those obtained via $\chi^2$ mapping techniques. We find that these two methods give consistent results which are in agreement with previous Nijmegen determinations.Comment: 12 pages of text plus 2 figures. Revtex file and postscript figures available via anonymous FTP at ftp://clsaid.phys.vt.edu/pub/n

On the SigmaN cusp in the pp -> pK+Lambda reaction

Measurements of the $pp \to pK^+\Lambda$ reaction at $T_p$ = 2.28 GeV have been carried out at COSY-TOF. In addition to the $\Lambda p$ FSI and $N^*$ resonance excitation effects a pronounced narrow structure is observed in the Dalitz plot and in its projection on the $p\Lambda$-invariant mass. The structure appears at the $pp \to$N$K^+\Sigma$ threshold and is interpreted as $\Sigma$N cusp effect. The observed width of 20 MeV/$c^2$ is substantially broader than anticipated from previous inclusive measurements. Angular distributions of this cusp structure are shown to be dissimilar to those in the residual $pK^+\Lambda$ channel, but similar to those observed in the $pK^+\Sigma^0$ channel

Genetic predisposition to ductal carcinoma in situ of the breast

Background: Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer. It is often associated with invasive ductal carcinoma (IDC), and is considered to be a non-obligate precursor of IDC. It is not clear to what extent these two forms of cancer share low-risk susceptibility loci, or whether there are differences in the strength of association for shared loci. Methods: To identify genetic polymorphisms that predispose to DCIS, we pooled data from 38 studies comprising 5,067 cases of DCIS, 24,584 cases of IDC and 37,467 controls, all genotyped using the iCOGS chip. Results: Most (67 %) of the 76 known breast cancer predisposition loci showed an association with DCIS in the same direction as previously reported for invasive breast cancer. Case-only analysis showed no evidence for differences between associations for IDC and DCIS after considering multiple testing. Analysis by estrogen receptor (ER) status confirmed that loci associated with ER positive IDC were also associated with ER positive DCIS. Analysis of DCIS by grade suggested that two independent SNPs at 11q13.3 near CCND1 were specific to low/intermediate grade DCIS (rs75915166, rs554219). These associations with grade remained after adjusting for ER status and were also found in IDC. We found no novel DCIS-specific loci at a genome wide significance level of P < 5.0x10-8. Conclusion: In conclusion, this study provides the strongest evidence to date of a shared genetic susceptibility for IDC and DCIS. Studies with larger numbers of DCIS are needed to determine if IDC or DCIS specific loci exist