Charmless hadronic B decays at BABAR

Using 22.7M BBbar events collected with the BABAR detector at SLAC, we present preliminary measurements of the branching fractions for charmless hadronic decays of B mesons into two-body, quasi two-body and three-body final states with pions, kaons, and rho and a0 resonances. In the search for exclusive $B^0 \to \pi^+\pi^-\pi^0$, we measure ${\cal B}(B^0 \to \rho^{\pm}(770)\pi^{\mp})=(28.9\pm5.4\pm4.3) \times 10^{-6}$, together with the relative asymmetry ${\cal A}_{\rm phys} = -0.04 \pm 0.18 \pm 0.02$. We also set the upper limits on $B^0 \to \rho^0(770)\pi^0$, non-resonant $B^0 \to \pi^+\pi^-\pi^0$, $B^0 \to a_0^{\pm}(\to \eta\pi^{\pm})\pi^{\mp}$ and $B^0 \to K^0\bar K^0$.Comment: 6 pages, 4 postscript figures, submitted to EPS HEP 200

Mechanism of regulation of Raf-1 by Ca2+/Calmodulin-dependent kinase II

The calcium-calmodulin dependent kinase II (CaMKII) is an ubiquitous serine/threonine protein kinase involved in multiple signalings and biological functions. It has been demonstrated that in epithelial and mesenchimal cells CaMKII participates with Ras to Raf-1 activation and that it is necessary for ERK activation by diverse factors. Raf-1 activation is complex. Maximal Raf-1 activation is reached by phosphorylation at Y341 by Src and at S338. Although early data proposed the involvement of p21-activated kinase 3 (Pak3), the kinase phosphorylating S338 is not definitively identified. Aim of my thesis is to go more insight into the molecular mechanisms of CaMKII/Raf-1 interaction and to verify the hypothesis that CaMKII phosphorylates Raf-1 at Ser338. To this purpose, I investigated the role of CaMKII in Raf-1 and ERK activation by oncogenic Ras and other factors, in COS-7 and NIH3T3 cells. Serum, SrcY527 and RasV12 activated CaMKII. CaMKII was necessary for Raf-1 and ERK activation by all these factors. CaMKII was necessary to the phosphorylation of S338 Raf-1 by serum, fibronectin or oncogenic Ras. Conversely, the inhibition of phosphatidylinositol 3-kinase, which in turn activates Pak3, was ineffective. The direct kinase activity of CaMKII on the serine 338 residue, was demonstrated in vitro by interaction of purified kinases. These results demonstrate that CaMKII phosphorylates Raf-1 at S338 and partecipates to ERK activation upon different physiologic and pathologic stimuli in the MAPK cascade. This kinase, might have a role in cancers harbouring oncogenic Ras and could represent a new therapeutic target for pharmacological intervention in these tumors

Magicity of the 52^{52}Ca and 54^{54}Ca isotopes and tensor contribution within a mean--field approach

We investigate the magicity of the isotopes $^{52}$Ca and $^{54}$Ca, that was recently confirmed by two experimental measurements, and relate it to like--particle and neutron--proton tensor effects within a mean--field description. By analyzing Ca isotopes, we show that the like--particle tensor contribution induces shell effects that render these nuclei more magic than they would be predicted by neglecting it. In particular, such induced shell effects are stronger in the nucleus $^{52}$Ca and the single--particle gaps are increased in both isotopes due to the tensor force. By studying $N=32$ and $N=34$ isotones, neutron--proton tensor effects may be isolated and their role analyzed. It is shown that neutron--proton tensor effects lead to increasing $N=32$ and $N=34$ gaps, when going along isotonic chains, from $^{58}$Fe to $^{52}$Ca, and from $^{60}$Fe to $^{54}$Ca, respectively. The mean--field calculations are perfomed by employing one Skyrme parameter set, that was introduced in a previous work by fitting the tensor parameters together with the spin--orbit strength. The signs and the values of the tensor strengths are thus checked within this specific application. The obtained results indicate that the employed parameter set, even if generated with a partial adjustment of the parameters of the force, leads to the correct shell behavior and provides, in particular, a description of the magicity of $^{52}$Ca and $^{54}$Ca within a pure mean--field picture with the effective two--body Skyrme interaction.Comment: 7 figure

The Racial Oppression in America’s Mass Incarceration

This paper seeks to expose the racial oppression embedded within the United States\u27 practice of mass incarceration and will provide recommendations to ameliorate this discriminatory practice that harshly and inequitably impacts people of color. Many minority communities are stuck in a continuous cycle of poverty and incarceration, in part because they are targeted and oppressed by the criminal justice system more frequently than middle class white communities. Consequently, incarcerated people of color exhibit high rates of recidivism because of being stripped of resources and being sent back to impoverished, drug-ridden neighborhoods. The War on Drugs in the 1980s and the continuance of poor relations between law enforcement and minority communities are significant contributing factors that have led to the mass incarceration of racial minority groups. The economic, political, and societal oppression of minority communities that unquestionably contributes to mass incarceration will be highlighted throughout this paper. Creating policies that involve transforming the U.S. legal system and providing communal support will be crucial in eradicating this systemic racial oppression