Solar neutrino interactions: Using charged currents at SNO to tell neutral currents at Super-Kamiokande

In the presence of flavor oscillations, muon and tau neutrinos can contribute to the Super-Kamiokande (SK) solar neutrino signal through the neutral current process \nu_{\mu,\tau} e^{-}\to \nu_{\mu,\tau} e^{-}. We show how to separate the \nu_e and \nu_{\mu,\tau} event rates in SK in a model independent way, by using the rate of the charged current process \nu_e d \to p p e^{-} from the Sudbury Neutrino Observatory (SNO) experiment, with an appropriate choice of the SK and SNO energy thresholds. Under the additional hypothesis of no oscillations into sterile states, we also show how to determine the absolute ^{8}B neutrino flux from the same data set, independently of the \nu_e survival probability.Comment: 14 pages (RevTeX), incl. 3 figures (epsf), submitted to Phys. ReV.

A sub-1 V, 26 μw, low-output-impedance CMOS bandgap reference with a low dropout or source follower mode

We present a low-power bandgap reference (BGR), functional from sub-1 V to 5 V supply voltage with either a low dropout (LDO) regulator or source follower (SF) output stage, denoted as the LDO or SF mode, in a 0.5-μm standard digital CMOS process with V tn≈ 0.6 V and |V tp| ≈ 0.7 V at 27 °C. Both modes operate at sub-1 V under zero load with a power consumption of around 26 μW. At 1 V (1.1 V) supply, the LDO (SF) mode provides an output current up to 1.1 mA (0.35 mA), a load regulation of ±8.5 mV/mA (±33 mV/mA) with approximately 10 μ s transient, a line regulation of ±4.2 mV/V (±50μV/V), and a temperature compensated reference voltage of 0.228 V (0.235 V) with a temperature coefficient around 34 ppm/° C from -20°C to 120 °C. At 1.5 V supply, the LDO (SF) mode can further drive up to 9.6 mA (3.2 mA) before the reference voltage falls to 90% of its nominal value. Such low-supply-voltage and high-current-driving BGR in standard digital CMOS processes is highly useful in portable and switching applications. © 2010 IEEE.published_or_final_versio

AAV-mediated and pharmacological induction of Hsp70 expression stimulates survival of retinal ganglion cells following axonal injury.

We evaluated the effect of AAV2- and 17-AAG (17-N-allylamino-17-demethoxygeldanamycin)-mediated upregulation of Hsp70 expression on the survival of retinal ganglion cells (RGCs) injured by optic nerve crush (ONC). AAV2-Hsp70 expression in the retina was primarily observed in the ganglion cell layer. Approximately 75% of all transfected cells were RGCs. RGC survival in AAV2-Hsp70-injected animals was increased by an average of 110% 2 weeks after the axonal injury compared with the control. The increase in cell numbers was not even across the retinas with a maximum effect of approximately 306% observed in the inferior quadrant. 17-AAG-mediated induction of Hsp70 expression has been associated with cell protection in various models of neurodegenerative diseases. We show here that a single intravitreal injection of 17-AAG (0.2 ug ul(-1)) results in an increased survival of ONC-injured RGCs by approximately 49% compared with the vehicle-treated animals. Expression of Hsp70 in retinas of 17-AAG-treated animals was upregulated approximately by twofold compared with control animals. Our data support the idea that the upregulation of Hsp70 has a beneficial effect on the survival of injured RGCs, and the induction of this protein could be viewed as a potential neuroprotective strategy for optic neuropathies