Preparation of ultracold atom clouds at the shot noise level

We prepare number stabilized ultracold clouds through the real-time analysis of non-destructive images and the application of feedback. In our experiments, the atom number ${N\sim10^6}$ is determined by high precision Faraday imaging with uncertainty $\Delta_N$ below the shot noise level, i.e., $\Delta_N <\sqrt{N}$. Based on this measurement, feedback is applied to reduce the atom number to a user-defined target, whereupon a second imaging series probes the number stabilized cloud. By this method, we show that the atom number in ultracold clouds can be prepared below the shot noise level.Comment: Main text: 4 Figures, 4 pages. Supplemental Information: 4 figures, 5 page

Spin dynamics in a two dimensional quantum gas

We have investigated spin dynamics in a 2D quantum gas. Through spin-changing collisions, two clouds with opposite spin orientations are spontaneously created in a Bose-Einstein condensate. After ballistic expansion, both clouds acquire ring-shaped density distributions with superimposed angular density modulations. The density distributions depend on the applied magnetic field and are well explained by a simple Bogoliubov model. We show that the two clouds are anti-correlated in momentum space. The observed momentum correlations pave the way towards the creation of an atom source with non-local Einstein-Podolsky-Rosen entanglement.Comment: 5 pages, 4 figure

Counting atoms in a deep optical microtrap

We demonstrate a method to count small numbers of atoms held in a deep, microscopic optical dipole trap by collecting fluorescence from atoms exposed to a standing wave of light that is blue detuned from resonance. While scattering photons, the atoms are also cooled by a Sisyphus mechanism that results from the spatial variation in light intensity. The use of a small blue detuning limits the losses due to light assisted collisions, thereby making the method suitable for counting several atoms in a microscopic volume

Planning and delivery of intensity modulated bolus electron conformal therapy

PURPOSE: Bolus electron conformal therapy (BECT) is a clinically useful, well-documented, and available technology. The addition of intensity modulation (IM) to BECT reduces volumes of high dose and dose spread in the planning target volume (PTV). This paper demonstrates new techniques for a process that should be suitable for planning and delivering IM-BECT using passive radiotherapy intensity modulation for electrons (PRIME) devices. METHODS: The IM-BECT planning and delivery process is an addition to the BECT process that includes intensity modulator design, fabrication, and quality assurance. The intensity modulator (PRIME device) is a hexagonal matrix of small island blocks (tungsten pins of varying diameter) placed inside the patient beam-defining collimator (cutout). Its design process determines a desirable intensity-modulated electron beam during the planning process, then determines the island block configuration to deliver that intensity distribution (segmentation). The intensity modulator is fabricated and quality assurance performed at the factory (.decimal, LLC, Sanford, FL). Clinical quality assurance consists of measuring a fluence distribution in a plane perpendicular to the beam in a water or water-equivalent phantom. This IM-BECT process is described and demonstrated for two sites, postmastectomy chest wall and temple. Dose plans, intensity distributions, fabricated intensity modulators, and quality assurance results are presented. RESULTS: IM-BECT plans showed improved D CONCLUSION: These results demonstrated the feasibility of translating IM-BECT to the clinic using the techniques presented for treatment planning, intensity modulator design and fabrication, and quality assurance processes

Have Anglo-Catholics lost their vision for mission agencies? : an empirical enquiry among newly ordained clergy in Britain

Attitude toward Christian mission agencies was investigated in a sample of 827 Anglican clergy ordained in the UK from 2002 to 2006. The Scale of Attitude Toward Mission Agencies (SATMA) consisted of six items related to the work that agencies do, and whether clergy wished to engage with this work. It had a high internal consistency reliability (Cronbach's alpha = 0.80). After controlling for theological liberalism or conservatism, attitudes were most positive among evangelicals and least positive among Anglo-Catholics. Both liberal and conservative Anglo-Catholic clergy showed less positive attitudes toward mission agencies than did other clergy

Genetic Variants of VEGFA and FLT4 Are Determinants of Survival in Renal Cell Carcinoma Patients Treated with Sorafenib

Molecular markers of sorafenib efficacy in patients with metastatic renal cell carcinoma (mRCC) are not available. The purpose of this study was to discover genetic markers of survival in patients with mRCC treated with sorafenib. Germline variants from 56 genes were genotyped in 295 patients with mRCC. Variant-overall survival (OS) associations were tested in multivariate regression models. Mechanistic studies were conducted to validate clinical associations. VEGFA rs1885657, ITGAV rs3816375, and WWOX rs8047917 (sorafenib arm), and FLT4 rs307826 and VEGFA rs3024987 (sorafenib and placebo arms combined) were associated with shorter OS. FLT4 rs307826 increased VEGFR-3 phosphorylation, membrane trafficking, and receptor activation. VEGFA rs1885657 and rs58159269 increased transcriptional activity of the constructs containing these variants in endothelial and RCC cell lines, and VEGFA rs58159269 increased endothelial cell proliferation and tube formation. FLT4 rs307826 and VEGFA rs58159269 led to reduced sorafenib cytotoxicity. Genetic variation in VEGFA and FLT4 could affect survival in sorafenib-treated patients with mRCC. These markers should be examined in additional malignancies treated with sorafenib and in other angiogenesis inhibitors used in mRCC. Significance: Clinical and mechanistic data identify germline genetic variants in VEGFA and FLT4 as markers of survival in patients with metastatic renal cell carcinoma.Peer reviewe

Challenges facing early career academic cardiologists

Early career academic cardiologists currently face unprecedented challenges that threaten a highly valued career path. A team consisting of early career professionals and senior leadership members of American College of Cardiology completed this white paper to inform the cardiovascular medicine profession regarding the plight of early career cardiologists and to suggest possible solutions. This paper includes: 1) definition of categories of early career academic cardiologists; 2) general challenges to all categories and specific challenges to each category; 3) obstacles as identified by a survey of current early career members of the American College of Cardiology; 4) major reasons for the failure of physician-scientists to receive funding from National Institute of Health/National Heart Lung and Blood Institute career development grants; 5) potential solutions; and 6) a call to action with specific recommendations

The Role of Calcineurin/NFAT in SFRP2 Induced Angiogenesis—A Rationale for Breast Cancer Treatment with the Calcineurin Inhibitor Tacrolimus

Tacrolimus (FK506) is an immunosuppressive drug that binds to the immunophilin FKBPB12. The FK506-FKBP12 complex associates with calcineurin and inhibits its phosphatase activity, resulting in inhibition of nuclear translocation of nuclear factor of activated T-cells (NFAT). There is increasing data supporting a critical role of NFAT in mediating angiogenic responses stimulated by both vascular endothelial growth factor (VEGF) and a novel angiogenesis factor, secreted frizzled-related protein 2 (SFRP2). Since both VEGF and SFRP2 are expressed in breast carcinomas, we hypothesized that tacrolimus would inhibit breast carcinoma growth. Using IHC (IHC) with antibodies to FKBP12 on breast carcinomas we found that FKBP12 localizes to breast tumor vasculature. Treatment of MMTV-neu transgenic mice with tacrolimus (3 mg/kg i.p. daily) (n = 19) resulted in a 73% reduction in the growth rate for tacrolimus treated mice compared to control (n = 15), p = 0.003; which was associated with an 82% reduction in tumor microvascular density (p<0.001) by IHC. Tacrolimus (1 µM) inhibited SFRP2 induced endothelial tube formation by 71% (p = 0.005) and inhibited VEGF induced endothelial tube formation by 67% (p = 0.004). To show that NFATc3 is required for SFRP2 stimulated angiogenesis, NFATc3 was silenced with shRNA in endothelial cells. Sham transfected cells responded to SFRP2 stimulation in a tube formation assay with an increase in the number of branch points (p<0.003), however, cells transfected with shRNA to NFATc3 showed no increase in tube formation in response to SFRP2. This demonstrates that NFATc3 is required for SFRP2 induced tube formation, and tacrolimus inhibits angiogenesis in vitro and breast carcinoma growth in vivo. This provides a rationale for examining the therapeutic potential of tacrolimus at inhibiting breast carcinoma growth in humans