Oscillations of solar and atmospheric neutrinos

Motivated by recent results from SuperKamiokande, we study both solar and atmospheric neutrino fluxes in the context of oscillations of the three known neutrinos. We aim at a global view which identifies the various possibilities, rather than attempting the most accurate determination of the parameters of each scenario. For solar neutrinos we emphasise the importance of performing a general analysis, independent of any particular solar model and we consider the possibility that any one of the techniques --- chlorine, gallium or water Cerenkov --- has a large unknown systematic error, so that its results should be discarded. The atmospheric neutrino anomaly is studied by paying special attention to the ratios of upward and downward going nu_e and nu_mu fluxes. Both anomalies can be described in a minimal scheme where the respective oscillation frequencies are widely separated or in non-minimal schemes with two comparable oscillation frequencies. We discuss explicit forms of neutrino mass matrices in which both atmospheric and solar neutrino fluxes are explained. In the minimal scheme we identify only two `zeroth order' textures that can result from unbroken symmetries. Finally we discuss experimental strategies for the determination of the various oscillation parameters.Comment: 20 pages, 7 figures. Final version: one reference added; fit of atmospheric neutrinos improve

Transform-limited pulses are not optimal for resonant multiphoton transitions

Maximizing nonlinear light-matter interactions is a primary motive for compressing laser pulses to achieve ultrashort transform limited pulses. Here we show how, by appropriately shaping the pulses, resonant multiphoton transitions can be enhanced significantly beyond the level achieved by maximizing the pulse's peak intensity. We demonstrate the counterintuitive nature of this effect with an experiment in a resonant two-photon absorption, in which, by selectively removing certain spectral bands, the peak intensity of the pulse is reduced by a factor of 40, yet the absorption rate is doubled. Furthermore, by suitably designing the spectral phase of the pulse, we increase the absorption rate by a factor of 7.Comment: 4 pages, 3 figure

CSF protein biomarkers predicting longitudinal reduction of CSF β-amyloid42 in cognitively healthy elders.

β-amyloid (Aβ) plaque accumulation is a hallmark of Alzheimer's disease (AD). It is believed to start many years prior to symptoms and is reflected by reduced cerebrospinal fluid (CSF) levels of the peptide Aβ1-42 (Aβ42). Here we tested the hypothesis that baseline levels of CSF proteins involved in microglia activity, synaptic function and Aβ metabolism predict the development of Aβ plaques, assessed by longitudinal CSF Aβ42 decrease in cognitively healthy people. Forty-six healthy people with three to four serial CSF samples were included (mean follow-up 3 years, range 2-4 years). There was an overall reduction in Aβ42 from a mean concentration of 211-195 pg ml(-1) after 4 years. Linear mixed-effects models using longitudinal Aβ42 as the response variable, and baseline proteins as explanatory variables (n=69 proteins potentially relevant for Aβ metabolism, microglia or synaptic/neuronal function), identified 10 proteins with significant effects on longitudinal Aβ42. The most significant proteins were angiotensin-converting enzyme (ACE, P=0.009), Chromogranin A (CgA, P=0.009) and Axl receptor tyrosine kinase (AXL, P=0.009). Receiver-operating characteristic analysis identified 11 proteins with significant effects on longitudinal Aβ42 (largely overlapping with the proteins identified by linear mixed-effects models). Several proteins (including ACE, CgA and AXL) were associated with Aβ42 reduction only in subjects with normal baseline Aβ42, and not in subjects with reduced baseline Aβ42. We conclude that baseline CSF proteins related to Aβ metabolism, microglia activity or synapses predict longitudinal Aβ42 reduction in cognitively healthy elders. The finding that some proteins only predict Aβ42 reduction in subjects with normal baseline Aβ42 suggest that they predict future development of the brain Aβ pathology at the earliest stages of AD, prior to widespread development of Aβ plaques