A Centre-Stable Manifold for the Focussing Cubic NLS in R1+3R^{1+3}

Consider the focussing cubic nonlinear Schr\"odinger equation in $R^3$: $$i\psi_t+\Delta\psi = -|\psi|^2 \psi.$$ It admits special solutions of the form $e^{it\alpha}\phi$, where $\phi$ is a Schwartz function and a positive ($\phi>0$) solution of $$-\Delta \phi + \alpha\phi = \phi^3.$$ The space of all such solutions, together with those obtained from them by rescaling and applying phase and Galilean coordinate changes, called standing waves, is the eight-dimensional manifold that consists of functions of the form $e^{i(v \cdot + \Gamma)} \phi(\cdot - y, \alpha)$. We prove that any solution starting sufficiently close to a standing wave in the $\Sigma = W^{1, 2}(R^3) \cap |x|^{-1}L^2(R^3)$ norm and situated on a certain codimension-one local Lipschitz manifold exists globally in time and converges to a point on the manifold of standing waves. Furthermore, we show that \mc N is invariant under the Hamiltonian flow, locally in time, and is a centre-stable manifold in the sense of Bates, Jones. The proof is based on the modulation method introduced by Soffer and Weinstein for the $L^2$-subcritical case and adapted by Schlag to the $L^2$-supercritical case. An important part of the proof is the Keel-Tao endpoint Strichartz estimate in $R^3$ for the nonselfadjoint Schr\"odinger operator obtained by linearizing around a standing wave solution.Comment: 56 page

Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk

BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat

Macrosocial determinants of population health in the context of globalization

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/55738/1/florey_globalization_2007.pd

Open data from the third observing run of LIGO, Virgo, KAGRA, and GEO

The global network of gravitational-wave observatories now includes five detectors, namely LIGO Hanford, LIGO Livingston, Virgo, KAGRA, and GEO 600. These detectors collected data during their third observing run, O3, composed of three phases: O3a starting in 2019 April and lasting six months, O3b starting in 2019 November and lasting five months, and O3GK starting in 2020 April and lasting two weeks. In this paper we describe these data and various other science products that can be freely accessed through the Gravitational Wave Open Science Center at https://gwosc.org. The main data set, consisting of the gravitational-wave strain time series that contains the astrophysical signals, is released together with supporting data useful for their analysis and documentation, tutorials, as well as analysis software packages

A paradoxical severe decrease in serum HDL-cholesterol after treatment with a fibrate

There have been a handful of reports in the literature of a paradoxical decrease in serum high density lipoprotein (HDL)-cholesterol in patients on fibrate drugs. The reason for this decline in cardioprotective HDL-cholesterol is not known and may have potential deleterious effects on the patient. This report describes a decrease in serum HDL-cholesterol in a patient on both simvastatin and bezafibrate. This patient also developed abnormal renal function, probably interstitial nephritis. In addition, the literature of fibrate induced serum HDL-cholesterol decline is reviewed and possible mechanisms for this phenomenon discussed. Key Words: fibrate • high density lipoprotein-cholesterol • renal functio