Treating Solar Model Uncertainties: A Consistent Statistical Analysis of Solar Neutrino Models and Data

We describe how to consistently incorporate solar model uncertainties, along with experimental errors and correlations, when analyzing solar neutrino data to derive confidence limits on parameter space for proposed solutions of the solar neutrino problem. Our work resolves ambiguities and inconsistencies in the previous literature. As an application of our methods we calculate the masses and mixing angles allowed by the current data for the proposed MSW solution using both Bayesian and frequentist methods, allowing purely for solar model flux variations, to compare with previous work. We consider the effects of including metal diffusion in the solar models and also discuss implications for future experiments.Comment: 29 pages (incl figs), latex, 6 figures (appended as separate uuencoded file. To embed figures in text, uncomment 6 \epsfysize lines which appear before bibliography), CWRU-P5-94, CfPA-94-TTH-29, Fermilab-Pub-94/176-

Role of Basal Ganglia Circuits in Resisting Interference by Distracters: A swLORETA Study

BACKGROUND: The selection of task-relevant information requires both the focalization of attention on the task and resistance to interference from irrelevant stimuli. Both mechanisms rely on a dorsal frontoparietal network, while focalization additionally involves a ventral frontoparietal network. The role of subcortical structures in attention is less clear, despite the fact that the striatum interacts significantly with the frontal cortex via frontostriatal loops. One means of investigating the basal ganglia's contributions to attention is to examine the features of P300 components (i.e. amplitude, latency, and generators) in patients with basal ganglia damage (such as in Parkinson's disease (PD), in which attention is often impaired). Three-stimulus oddball paradigms can be used to study distracter-elicited and target-elicited P300 subcomponents. METHODOLOGY/PRINCIPAL FINDINGS: In order to compare distracter- and target-elicited P300 components, high-density (128-channel) electroencephalograms were recorded during a three-stimulus visual oddball paradigm in 15 patients with early PD and 15 matched healthy controls. For each subject, the P300 sources were localized using standardized weighted low-resolution electromagnetic tomography (swLORETA). Comparative analyses (one-sample and two-sample t-tests) were performed using SPM5® software. The swLORETA analyses showed that PD patients displayed fewer dorsolateral prefrontal (DLPF) distracter-P300 generators but no significant differences in target-elicited P300 sources; this suggests dysfunction of the DLPF cortex when the executive frontostriatal loop is disrupted by basal ganglia damage. CONCLUSIONS/SIGNIFICANCE: Our results suggest that the cortical attention frontoparietal networks (mainly the dorsal one) are modulated by the basal ganglia. Disruption of this network in PD impairs resistance to distracters, which results in attention disorders

Detection and Quantitation of Simian Virus 40 Genetic Material in Abortively Transformed BALB/3T3 Clones

Infection with simian virus 40 is known to induce many cells to synthesize DNA and to divide in a medium lacking serum protein growth factor(s) that is essential for growth of uninfected cells (factor-free medium). Cells infected under these conditions then go through several rounds of division, since colonies containing more than 100 cells are formed. Many of these colonies are abortively transformed since, upon subsequent passage of the cells in standard medium, they can no longer grow in factor-free medium and show no other properties of viral transformation. We have examined these abortively transformed cells for the presence of simian virus 40 DNA sequences. Of the three clones tested, two were found to contain viral genetic material despite the fact that they were phenotypically normal. The number of simian virus 40 genome equivalents present was determined by measurement of DNA reassociation kinetics on hydroxyapatite. Two of the abortively transformed lines contained approximately five viral genome equivalents per diploid cell, while the DNA from a third abortive transformant was indistinguishable from that of uninfected BALB/3T3 cells. A standard simian virus 40 transformant, isolated under similar conditions, contained two copies of the viral genome per cell. The abortive transformants also appear to contain the entire viral genome rather than multiple partial copies. Subclones of one abortively transformed line containing five copies per cell had 2.7-10 copies of viral genetic material per diploid cell

Extended lamivudine retreatment for chronic hepatitis B: Maintenance of viral suppression after discontinuation of therapy

In patients with chronic hepatitis B, brief lamivudine therapy suppresses hepatitis B virus (HBV) DNA but results infrequently in sustained losses of virus replication posttreatment. We evaluated treatment response and its posttreatment durability during up to 18 months of lamivudine therapy (100 mg/d) in 24 patients who had hepatitis B e antigen (HBeAg) despite 1 to 3 months of prior therapy. Therapy was to be stopped after HBeAg loss or seroconversion (acquisition of antibody to HBeAg); posttreatment monitoring continued for 6 months. During therapy, which was well tolerated, HBV DNA became undetectable in all evaluable patients, accompanied by reduced alanine transaminase (ALT) activity. The cumulative 18‐month confirmed loss of HBeAg during therapy was 9 of 24 (38%) and seroconversion was 5 of 24 (21%). Therapy was discontinued after HBeAg loss/seroconversion in 7 patients, and HBeAg status was maintained in all. Four of the patients with HBeAg responses lost HBsAg at least once. In 10 (43%) of 23 patients tested, we identified HBV polymerase YMDD mutations, 3 with detectable HBV DNA (2 with ALT elevations) and 7 without virological/biochemical breakthrough. In conclusion, up to 18 months of lamivudine therapy was well tolerated, suppressed HBV replication consistently, and tripled the frequency of HBeAg losses observed during brief‐duration therapy; HBeAg loss/seroconversion remained durable posttreatment. The emergence of YMDD‐variant HBV was relatively common but occurred typically without reappearance of detectable HBV DNA or ALT elevation. Our observations suggest that lamivudine can be stopped after confirmed HBeAg loss or seroconversion