Measurement of the CP-Violating Asymmetry Amplitude sin2β\beta

We present results on time-dependent CP-violating asymmetries in neutral B decays to several CP eigenstates. The measurements use a data sample of about 88 million Y(4S) --> B Bbar decays collected between 1999 and 2002 with the BABAR detector at the PEP-II asymmetric-energy B Factory at SLAC. We study events in which one neutral B meson is fully reconstructed in a final state containing a charmonium meson and the other B meson is determined to be either a B0 or B0bar from its decay products. The amplitude of the CP-violating asymmetry, which in the Standard Model is proportional to sin2beta, is derived from the decay-time distributions in such events. We measure sin2beta = 0.741 +/- 0.067 (stat) +/- 0.033 (syst) and |lambda| = 0.948 +/- 0.051 (stat) +/- 0.017 (syst). The magnitude of lambda is consistent with unity, in agreement with the Standard Model expectation of no direct CP violation in these modes

EuFe2_2As2_2 under high pressure: an antiferromagnetic bulk superconductor

We report the ac magnetic susceptibility $\chi_{ac}$ and resistivity $\rho$ measurements of EuFe$_2$As$_2$ under high pressure $P$. By observing nearly 100% superconducting shielding and zero resistivity at $P$ = 28 kbar, we establish that $P$-induced superconductivity occurs at $T_c \sim$~30 K in EuFe$_2$As$_2$. $\rho$ shows an anomalous nearly linear temperature dependence from room temperature down to $T_c$ at the same $P$. $\chi_{ac}$ indicates that an antiferromagnetic order of Eu$^{2+}$ moments with $T_N \sim$~20 K persists in the superconducting phase. The temperature dependence of the upper critical field is also determined.Comment: To appear in J. Phys. Soc. Jpn., Vol. 78 No.

Dalitz plot analysis of the decay B±→K±K±K∓

We analyze the three-body charmless decay B-+/-->(KKK -/+)-K-+/--K-+/- using a sample of 226.0 +/- 2.5 million B (B) over bar pairs collected by the BABAR detector. We measure the total branching fraction and CP asymmetry to be B=(35.2 +/- 0.9 +/- 1.6)x10(-6) and A(CP)=(-1.7 +/- 2.6 +/- 1.5)%. We fit the Dalitz plot distribution using an isobar model and measure the magnitudes and phases of the decay coefficients. We find no evidence of CP violation for the individual components of the isobar model. The decay dynamics is dominated by the K+K- S-wave, for which we perform a partial-wave analysis in the region m(K+K-)< 2 GeV/c(2). Significant production of the f(0)(980) resonance, and of a spin zero state near 1.55 GeV/c(2) are required in the isobar model description of the data. The partial-wave analysis supports this observation.This work is supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF and DFG (Germany), INFN (Italy), FOM (The Netherlands), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from CONACyT (Mexico), Marie Curie EIF (European Union), the A. P. Sloan Foundation, the Research Corporation, and the Alexander von Humboldt Foundation

Subpial Thorn-shaped Astrocytes Are Prevalent In Guam ALS/PDC

Guam amyotrophic lateral sclerosis/parkinsonism-dementia complex is a progressive neurodegenerative disorder characterized by neuronal and glial tau pathologies. With the aim to evaluate aging-related tau astrogliopathy (ARTAG) we examined the collection at the University of Pennsylvania, consisting of blocks of the frontal parietal, temporal, and occipital cortices. Formalin fixed, paraffin-embedded tissue blocks were evaluated using anti-tau antibodies PHF-1 and AT8. In addition to neuronal and oligodendroglial tau pathology, granular/fuzzy astrocytes in the gray matter and thorn-shaped astrocytes (TSAs) in subpial location were also observed. Twenty-one out of 33 cases (63%) showed subpial TSAs diffusely along the cortical surface in one or more cortical regions. Accumulation of TSAs in the depth of the sulci were seen in 41% in the temporal, 7% in the frontal and 14% in parietal cortex. This was not associated with perivascular neuronal tau pathology in the depth of the sulci. Accumulation of TSAs in the depth of cortical sulci in this cohort is approximately 20 times more frequent than reported in a European aging cohort. The presence of subpial TSAs in the depth of cortical sulci in CTE and Guam PDC, and less frequently in aging brains, might suggest common mechanisms.Learning ObjectivesDescribe the spectrum of neuropathology in Guam ALS/PDCDescribe the frequency of tau positive cortical subpial thorn-shaped astrocytes</jats:sec

Progressive degeneration of nonphosphorylated neurofilament protein-enriched pyramidal neurons predicts cognitive impairment in Alzheimer's disease: stereologic analysis of prefrontal cortex area 9.

We performed a stereologic analysis of a subset of pyramidal neurons known to be vulnerable in Alzheimer's disease (AD) and characterized by particularly high somatodendritic levels of nonphosphorylated neurofilament protein. In the neocortex, these large pyramidal neurons reside in the deep part of layer III (layer IIIc) and the superficial part of layer V (layer Va). We focused on prefrontal cortex area 9 in elderly control cases in comparison to cases with different degrees of cognitive dysfunction. The results confirmed that these neurons are preferentially vulnerable in AD, as their numbers decrease dramatically in cases with definite dementia, correlating strongly with the severity of the disease, to a nearly complete loss (&gt;90%) in the endstages of AD. Furthermore, a triple-labeling experimental paradigm revealed that these particular neurons are far more likely to develop neurofibrillary tangles (NFT) and do so at a faster rate than other pyramidal cells. Nonphosphorylated neurofilament protein-rich neurons also shrink considerably during formation of NFT and the largest among them are preferentially affected. Laminar differences in the severity of these effects were observed, layer Va being more severely affected, possibly correlating with the involvement of specific cortical projections. These data reveal that different populations of neurons prone to NFT formation are lost at different rates in AD, and that nonphosphorylated neurofilament protein-enriched neurons emerge as a strikingly vulnerable subpopulation of neurons. Their preferential involvement suggests that neurons providing specific corticocortical connections between association areas are at high risk for degeneration in AD