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Survey researchers have long been concerned with the question of whether participation in preelection surveys increases voter turnout. This article presents findings from three large-scale field experiments conducted during the 2002 general election in Maryland, New York, and Pennsylvania. Unlike early studies, which found that participation in preelection surveys increased voter turnout, this study finds no significant effect. The author argues that the rigorous experimental methodology and large sample size in these three experiments should allay concern that survey participation affects turnout. Keywords: preelection surveys; voter turnout; experiments

The problems facing the development of klystrons for use at submillimeter wavelengths are reviewed. Analytical formulas for reentrant cavity resonance, starting conditions, output power, and oscillation buildup are presented. This paper describes methods of calculating cavity Q-factor, output coupling, focusing potentials, electron paths, and heating effects. The scaling of output power with frequency is derived. Examples of techniques that might be used to realize a working device are presented. Index Terms--Electron optics, klystrons, micromachining, submillimeter-wave devices.

As a target for gene therapy, Duchenne muscular dystrophy (DMD) presents many obstacles but also an unparalleled prospect for correction by alternative splicing. The majority of mutations in the dystrophin gene occur in the region encoding the spectrin-like central rod domain, which is largely dispensable. Thus, splicing around mutations can generate a shortened but in-frame transcript, permitting translation of a partially functional dystrophin protein. We have tested this idea in vivo in the mdx dystrophic mouse (carrying a mutation in exon 23 of the dystrophin gene) by combining a potent transfection protocol with a 2-O-methylated phosphorothioated antisense oligoribonucleotide (2OMeAO) designed to promote skipping of the mutated exon*. The treated mice show persistent production of dystrophin at normal levels in large numbers of muscle fibers and show functional improvement of the treated muscle. Repeated administration enhances dystrophin expression without eliciting immune responses. Our data establishes the realistic practicality of an approach that is applicable, in principle, to a majority of cases of severe dystrophinopathy. *NOTE:: In the version of this article initially published online, the following errors appeared: The fourth sentence of the abstract was incorrect. It has been changed to, "We have tested this idea in vivo in the mdx dystrophic mouse (carrying a mutation in exon 23 of the dystrophin gene) by combining...to promote skipping of the mutated exon." The sixth sentence of the first paragraph of the Results was incorrect and has been changed. It now reads, "...(C57Bl/10ScSn; designated C57)..." Figure 2 and its legend contained an error. The figure should be labeled with subpanels a and b. The legend should read, "Figure 2 Detection of dystrophin and dystrophin protein complexes. Exon mapping of 2OMeAO-induced dystrophin (a,b) and detection of dystrophin protein complexes (b) in serial sections..." These mistakes have been corrected for the HTML and print versions of the article., Author(s): Qi Long Lu (corresponding author) [1]; Christopher J Mann [2]; Fang Lou [3]; George Bou-Gharios [1]; Glenn E Morris [4]; Shao-an Xue [5]; Sue Fletcher [2]; Terence A Partridge [...]

This article attempts to explain the spread between government bonds and corporate bonds. Results show that premiums in corporate rates are affected by expected defaults to a small amount and by state taxes to a substantial extent, the rest being explained by risk premiums for common stocks.

Free fatty acids (FFA) are responsible for the direct induction of the binding of proteins released on the external surface of rat hepatocyte plasma membrane to lipoprotein. The affinity of lipolysis-stimulated receptor (LSR) for triglycerides suggests an inverse relation between postprandial plasma triglycerides and the number of LSRs in the liver. LSR activated by FFA acts as an intermediary in the binding of lipoproteins that have apoprotein B and apoprotein E and causes their degradation.

A study of oleate-activated receptor, present in LDL receptor-lacking cells, reveals that the receptor mediates intestinally derived triglyceride-rich lipoproteins clearance and is, consequently, designated the lipolysis-stimulated receptor (LSR). Free fatty acids generated by lipolytic enzyme action activate the LSR. LSR activity is seen in isolated liver membranes and is suppressed by lactoferrin action.

It's easy for many physicians in private practice to avoid an important professional priority: succession planning. While retirement or a reduced role in the practice might feel like a long [...]

Duchenne muscular dystrophy (DMD) is a severe muscle wasting disease arising from defects in the dystrophin gene, typically nonsense or frameshift mutations, that preclude the synthesis of a functional protein. A milder, allelic version of the disease, Becker muscular dystrophy, generally arises from in-frame deletions that allow synthesis of a shorter but still semifunctional protein. Therapies to introduce functional dystrophin into dystrophic tissue through either cell or gene replacement have not been successful to date. We report an alternative approach where 2'-O-methyl antisense oligoribonucleotides have been used to modify processing of the dystrophin pre-mRNA in the mdx mouse model of DMD. By targeting 2'-O-methyl antisense oligoribonucleotides to block motifs involved in normal dystrophin pre-mRNA splicing, we induced excision of exon 23, and the mdx nonsense mutation, without disrupting the reading frame. Exon 23 skipping was first optimized in vitro in transfected H-[2K.sup.b]-tsA58 mdx myoblasts and then induced in vivo. Immunohistochemical staining demonstrated the synthesis and correct subsarcolemmal localization of dystrophin and [Gamma]-sarcoglycan in the mdx mouse after intramuscular delivery of antisense oligoribonucleotide:liposome complexes. This approach should reduce the severity of DMD by allowing a dystrophic gene transcript to be modified, such that it can be translated into a Becker-dystrophin-like protein.