Nimbus-7 Earth Radiation Budjet compact solar data set user's guide

Nimbus-7 Earth Radiation Budget (ERB) solar measurements extend from November 16, 1978, to December 13, 1993, but with data gaps in 1992 and 1993. The measurements include the total solar irradiance plus six broadband spectral components. The Channel 10c total irradiance data appears very stable, and the calibration, well done. A number of characterization problems remain in the spectral measurements. In the original program, the solar and Earth flux measurements were intermixed and spread over about 170 computer tapes. For easier access, the solar data have been collected into two compact data sets. All of the data are collected into 14 Summary Solar Tapes (SST's). In addition, two Channel 10c Solar Tapes (CST's) give a separate listing of the stable total solar irradiance measurements. Channel 10c calibration and orbital irradiance values are given on separate PC disks. This document gives data descriptions and formats, together with quality control and calibration procedures

Dynamics in a supercooled molecular liquid: Theory and Simulations

We report extensive simulations of liquid supercooled states for a simple three-sites molecular model, introduced by Lewis and Wahnstr"om [L. J. Lewis and G. Wahnstr"om, Phys. Rev. E 50, 3865 (1994)] to mimic the behavior of ortho-terphenyl. The large system size and the long simulation length allow to calculate very precisely --- in a large q-vector range --- self and collective correlation functions, providing a clean and simple reference model for theoretical descriptions of molecular liquids in supercooled states. The time and wavevector dependence of the site-site correlation functions are compared with detailed predictions based on ideal mode-coupling theory, neglecting the molecular constraints. Except for the wavevector region where the dynamics is controlled by the center of mass (around 9 nm-1), the theoretical predictions compare very well with the simulation data.

Nanomaterial-based Sensors for the Study of DNA Interaction with Drugs

The interaction of drugs with DNA has been searched thoroughly giving rise to an endless number of findings of undoubted importance, such as a prompt alert to harmful substances, ability to explain most of the biological mechanisms, or provision of important clues in targeted development of novel chemotherapeutics. The existence of some drugs that induce oxidative damage is an increasing point of concern as they can cause cellular death, aging, and are closely related to the development of many diseases. Because of a direct correlation between the response, strength/ nature of the interaction and the pharmaceutical action of DNA-targeted drugs, the electrochemical analysis is based on the signals of DNA before and after the interaction with the DNA-targeted drug. Nowadays, nanoscale materials are used extensively for offering fascinating characteristics that can be used in designing new strategies for drug-DNA interaction detection. This work presents a review of nanomaterials (NMs) for the study of drug-nucleic acid interaction. We summarize types of drug-DNA interactions, electroanalytical techniques for evidencing these interactions and quantification of drug and/or DNA monitoring

PP2A inactivation is a crucial step in triggering apoptin-induced tumor-selective cell killing

Apoptin (apoptosis-inducing protein) harbors tumor-selective characteristics making it a potential safe and effective anticancer agent. Apoptin becomes phosphorylated and induces apoptosis in a large panel of human tumor but not normal cells. Here, we used an in vitro oncogenic transformation assay to explore minimal cellular factors required for the activation of apoptin. Flag-apoptin was introduced into normal fibroblasts together with the transforming SV40 large T antigen (SV40 LT) and SV40 small t antigen (SV40 ST) antigens. We found that nuclear expression of SV40 ST in normal cells was sufficient to induce phosphorylation of apoptin. Mutational analysis showed that mutations disrupting the binding of ST to protein phosphatase 2A (PP2A) counteracted this effect. Knockdown of the ST-interacting PP2A–B56γ subunit in normal fibroblasts mimicked the effect of nuclear ST expression, resulting in induction of apoptin phosphorylation. The same effect was observed upon downregulation of the PP2A–B56δ subunit, which is targeted by protein kinase A (PKA). Apoptin interacts with the PKA-associating protein BCA3/AKIP1, and inhibition of PKA in tumor cells by treatment with H89 increased the phosphorylation of apoptin, whereas the PKA activator cAMP partially reduced it. We infer that inactivation of PP2A, in particular, of the B56γ and B56δ subunits is a crucial step in triggering apoptin-induced tumor-selective cell death