Homothetic Self-Similar Solutions of the Three-Dimensional Brans-Dicke Gravity

All homothetic self-similar solutions of the Brans-Dicke scalar field in three-dimensional spacetime with circular symmetry are found in closed form.Comment: latex, five pages, without figur

Charge conservation and time-varying speed of light

It has been recently claimed that cosmologies with time dependent speed of light might solve some of the problems of the standard cosmological scenario, as well as inflationary scenarios. In this letter we show that most of these models, when analyzed in a consistent way, lead to large violations of charge conservation. Thus, they are severly constrained by experiment, including those where $c$ is a power of the scale factor and those whose source term is the trace of the energy-momentum tensor. In addition, early Universe scenarios with a sudden change of $c$ related to baryogenesis are discarded.Comment: 4 page

Bounds from Primordial Black Holes with a Near Critical Collapse Initial Mass Function

Recent numerical evidence suggests that a mass spectrum of primordial black holes (PBHs) is produced as a consequence of near critical gravitational collapse. Assuming that these holes formed from the initial density perturbations seeded by inflation, we calculate model independent upper bounds on the mass variance at the reheating temperature by requiring the mass density not exceed the critical density and the photon emission not exceed current diffuse gamma-ray measurements. We then translate these results into bounds on the spectral index n by utilizing the COBE data to normalize the mass variance at large scales, assuming a constant power law, then scaling this result to the reheating temperature. We find that our bounds on n differ substantially (\delta n > 0.05) from those calculated using initial mass functions derived under the assumption that the black hole mass is proportional to the horizon mass at the collapse epoch. We also find a change in the shape of the diffuse gamma-ray spectrum which results from the Hawking radiation. Finally, we study the impact of a nonzero cosmological constant and find that the bounds on n are strengthened considerably if the universe is indeed vacuum-energy dominated today.Comment: 24 pages, REVTeX, 5 figures; minor typos fixed, two refs added, version to be published in PR

Equation of state for Universe from similarity symmetries

In this paper we proposed to use the group of analysis of symmetries of the dynamical system to describe the evolution of the Universe. This methods is used in searching for the unknown equation of state. It is shown that group of symmetries enforce the form of the equation of state for noninteracting scaling multifluids. We showed that symmetries give rise the equation of state in the form $p=-\Lambda+w_{1}\rho(a)+w_{2}a^{\beta}+0$ and energy density $\rho=\Lambda+\rho_{01}a^{-3(1+w)}+\rho_{02}a^{\beta}+\rho_{03}a^{-3}$, which is commonly used in cosmology. The FRW model filled with scaling fluid (called homological) is confronted with the observations of distant type Ia supernovae. We found the class of model parameters admissible by the statistical analysis of SNIa data. We showed that the model with scaling fluid fits well to supernovae data. We found that $\Omega_{\text{m},0} \simeq 0.4$ and $n \simeq -1$ ($\beta = -3n$), which can correspond to (hyper) phantom fluid, and to a high density universe. However if we assume prior that $\Omega_{\text{m},0}=0.3$ then the favoured model is close to concordance $\Lambda$CDM model. Our results predict that in the considered model with scaling fluids distant type Ia supernovae should be brighter than in $\Lambda$CDM model, while intermediate distant SNIa should be fainter than in $\Lambda$CDM model. We also investigate whether the model with scaling fluid is actually preferred by data over $\Lambda$CDM model. As a result we find from the Akaike model selection criterion prefers the model with noninteracting scaling fluid.Comment: accepted for publication versio

String Cosmology: The Pre-Big Bang Scenario

A review is attempted of physical motivations, theoretical and phenomenological aspects, as well as outstanding problems, of the pre-big bang scenario in string cosmology.Comment: 46 pages, 8 Figures, Latex, Lectures delivered in Les Houches, July 199

Magnetic Field Amplification in Galaxy Clusters and its Simulation

We review the present theoretical and numerical understanding of magnetic field amplification in cosmic large-scale structure, on length scales of galaxy clusters and beyond. Structure formation drives compression and turbulence, which amplify tiny magnetic seed fields to the microGauss values that are observed in the intracluster medium. This process is intimately connected to the properties of turbulence and the microphysics of the intra-cluster medium. Additional roles are played by merger induced shocks that sweep through the intra-cluster medium and motions induced by sloshing cool cores. The accurate simulation of magnetic field amplification in clusters still poses a serious challenge for simulations of cosmological structure formation. We review the current literature on cosmological simulations that include magnetic fields and outline theoretical as well as numerical challenges.Comment: 60 pages, 19 Figure

The global burden of cancer attributable to risk factors, 2010–19: a systematic analysis for the Global Burden of Disease Study 2019

BACKGROUND: Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. METHODS: The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk–outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. FINDINGS: Globally, in 2019, the risk factors included in this analysis accounted for 4·45 million (95% uncertainty interval 4·01–4·94) deaths and 105 million (95·0–116) DALYs for both sexes combined, representing 44·4% (41·3–48·4) of all cancer deaths and 42·0% (39·1–45·6) of all DALYs. There were 2·88 million (2·60–3·18) risk-attributable cancer deaths in males (50·6% [47·8–54·1] of all male cancer deaths) and 1·58 million (1·36–1·84) risk-attributable cancer deaths in females (36·3% [32·5–41·3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20·4% (12·6–28·4) and DALYs by 16·8% (8·8–25·0), with the greatest percentage increase in metabolic risks (34·7% [27·9–42·8] and 33·3% [25·8–42·0]). INTERPRETATION: The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden

Insulin-like growth factor-1 receptor signalling and acquired resistance to gefitinib (ZD1839; IRESSATM) in DU145 human prostate cancer cells

Introduction: Although gefitinib (ZD1839; IRESSATM), a specific EGF-R tyrosine kinase inhibitor (TKI), has been shown to possess anti-tumour activity in a range of cancer types including androgen refractory prostate cancer, de novo and acquired resistance to the inhibitor has been reported clinically (Ranson, The Oncologist 2001; 58 (suppl 2A):114-22). In this study, we examined the involvement of the IGF1-R in the acquisition of resistance to gefitinib in the DU145 model of prostate cancer. Methods: The DU145 human prostate cancer cell line was continuously exposed to 1mM gefitinib. Alterations in signalling pathways were assessed using immunocytochemical, Western blotting and/or RTPCR techniques. Matrigel invasion assays were performed and cell proliferation was assessed by evaluating anchorage dependent growth. Cell sensitivity to the specific IGF1-R TKI, AG1024, (1-10mg/ml) was also measured. Results: Continuous exposure of the DU145 cells to 1mM gefitinib resulted in an approximate 60% initial growth inhibition after 10 days treatment. The surviving cells however, showed slow but steady increases in growth over the following 2 months, reaching a stable growth rate which far exceeded that of the parental cell line after a total of 3 months. This gefitinib-resistant subline designated DU145/TKI-R, demonstrated reduced EGF-R expression and negligible basal phosphorylated EGF-R activity. Compared with the parental DU145 cells, the DU145/TKI-R cells showed i) an increased production of IGFII mRNA, ii) elevated levels of both total and phosphorylated IGF1-R and PKCd, and iii) a marked increased sensitivity to growth inhibition by the IGF1-R inhibitor AG1024. Significantly, while 1mM gefitinib initially reduced the invasion of the DU145 cells through matrigel by 40%, the DU145/TKI-R cells overcame this inhibition. Furthermore, the migratory activity of the DU145/TKI-R cells was substantially reduced (45%) by treatment with AG1024 (10mM). Conclusion: In prostate cancer cells, acquired resistance to gefitinib is associated with increased signalling through the IGF1-R, which also plays a role in the invasive capacity of the gefitinib-resistant phenotype. Thus, therapeutic strategies that target the IGF1-R may increase the efficacy and duration of response to gefitinib