Keith T. Poole

A Spatial Model for Legislative Roll Call Analysis

A general nonlinear logit model is used to analyze political choice data. The model assumes probabilistic voting based on a spatial utility function. The parameters of the utility function and the spatial coordinates of the choices and the choosers can all be estimated on the basis of observed choices. Ordinary Guttman scaling is a degenerate case of this model. Estimation of the model is implemented in the NOMINATE program for one dimensional analysis of two alternative choices with no nonvoting. The robustness and face validity of the program outputs are evaluated on the basis of roll call voting data for the U.S. House and Senate.

PATTERNS OF CONGRESSIONAL VOTING

Congressional roll call voting has been highly structured for most of U.S. history. The structure is revealed by a dynamic, spatial analysis of the entire roll call voting record from 1789 to 1985. The space is characterized by a predominant major dimension with, at times, a significant, but less important second dimension. In the modern era, spatial positions are very stable. This stability is such that, under certain conditions, short run forecasting of roll call votes is possible. Since the end of World War II, changes in congressional voting patterns have occurred almost entirely through the process of replacement of retiring or defeated legislators with new members. Politically, selection is far more important than adaptation.

Overexpression of the mexC-mexD-oprJ efflux operon in nfxB-type multidrug-resistant strains of Pseudomonas aeruginosa.

OprJ, overproduced in nfxB multidrug‐resistant strains of Pseudomonas aeruginosa, and OprK, overproduced in the multidrug‐resistant strain K385, were demonstrated to be immunologically cross‐reactive using an OprJ‐specific monoclonal antibody. Treatment of the purified proteins with trypsin or chymotrypsin yielded virtually indistinguishable digestion patterns, and the N‐terminal sequence of two trypsin fragments was identical for both proteins, indicating that OprJ and OprK share identity. The N‐terminal amino acid sequences were used to facilitate cloning of the oprJ gene on a 5kbp KpnI fragment and a 10kbp BamHI fragment. Nucleotide sequencing of portions of these fragments revealed that oprJ was the terminal gene in a putative three‐gene operon, The predicted mexC–mexD–oprJ gene products exhibit homology to the MexA–MexB–OprM components of the multidrug‐resistance efflux pump of P. aeruginosa (43–46% identity). Consistent with an implied role for mexC–mexD–oprJ in drug efflux, the mexC–mexD–oprJ‐hyperexpressing strain K385 showed reduced accumulation of a variety of antibiotics as compared with its parent strain, and this drug ‘exclusion’ was abrogated by energy inhibitors. The mexC and oprJ products are putative lipoproteins of a molecular mass of 40707 and 51742Da, respectively, while mexD was predicted to encode a protein of 111936Da. Sequencing upstream of mexC revealed the presence of the nfxB gene transcribed divergently from the efflux genes. Overproduction of OprJ and the attendant multiple‐antibiotic resistance of strain K385 was shown to result from a point mutation in nfxB, resulting in a H87→R change in the predicted NfxB polypeptide. OprJ overproduction and multidrug resistance in K385 was reversed by the cloned nfxB gene, suggesting that nfxB encodes a repressor of mexC–mexD–oprJ expression. Consistent with this, the cloned nfxB gene repressed synthesis of a mexC–lacZ fusion in Escherichia coli. nfxB also repressed expression of a nfxB–lacZ fusion, indicating that NfxB negatively regulates its own expression. These data indicate that the multidrug resistance of nfxB strains is due to overexpression of an efflux operon, mexC–mexD–oprJ, encoding components of a second efflux pump in P. aeruginosa.

RECOVERING A BASIC SPACE FROM A SET OF ISSUE SCALES

This paper develops a scaling procedure for estimating the latent/unobservable dimensions underlying a set of manifest/observable variables. The scaling procedure performs, in effect, a singular value decomposition of a rectangular matrix of real elements with missing entries. In contrast to existing techniques such as factor analysis which work with a correlation or covariance matrix computed from the data matrix, the scaling procedure shown here analyzes the data matrix directly. The scaling procedure is a general-purpose tool that can be used not only to estimate latent/unobservable dimensions but also to estimate an Eckart-Young lower-rank approximation matrix of a matrix with missing entries. Monte Carlo tests show that the procedure reliably estimates the latent dimensions and reproduces the missing elements of a matrix even at high levels of error and missing data. A number of applications to political data are shown and discussed.

The Polarization of American Politics

Elected officials in the United States appear to represent relatively extreme support coalitions rather than the interests of middle-of-the-road voters. This contention is supported by analysis of variance of liberal-conservative positions in the United States Senate from 1959 to 1980. Within both the Democratic and the Republican parties, there is considerable variation in liberal-conservative positions, but two senators from the same state and party tend to be very similar. In contrast, senators from the same state but from different parties are highly dissimilar, suggesting that each party represents an extreme support coalition in the state. Moreover, the distribution of senators is now consistent with the hypothesis that, in the long run, both parties have an equal chance of winning any seat in the Senate. This result suggests that there is now competition between equally balanced but extreme support coalitions throughout most of the United States.

Efflux-mediated resistance to fluoroquinolones in gram-negative bacteria

The introduction of the fluoroquinolones (FQs) in the 1980s provided clinicians with a class of broad-spectrum agents applicable to a range of gram-negative infections including urinary tract infections, gastrointestinal infections, respiratory tract infections, sexually transmitted diseases, bone

Aminoglycoside Resistance in Pseudomonas aeruginosa

Aminoglycosides ([35][1]) are a vital component of antipseudomonal chemotherapy implicated in the treatment of a variety of infections ([9][2], [45][3]), particularly pulmonary infections in cystic fibrosis (CF) patients ([22][4]). These agents are bactericidal and exhibit synergy with other

The Relationship Between Information, Ideology, and Voting Behavior

The question of voter sophistication is important for understanding voter and candidate behavior in mass elections. We develop an index of voter information - based on perceptual data - and find that it is significantly related to ideological extremism and voting behavior. Individuals with a high level of information tend to be more extreme than those with low levels and are much more likely to vote.

Multidrug Efflux Systems Play an Important Role in the Invasiveness of Pseudomonas aeruginosa

Pseudomonas aeruginosa is an important opportunistic human pathogen. Certain strains can transmigrate across epithelial cells, and their invasive phenotype is correlated with capacity to cause invasive human disease and fatal septicemia in mice. Four multidrug efflux systems have been described in P. aeruginosa, however, their contribution to virulence is unclear. To clarify the role of efflux systems in invasiveness, P. aeruginosa PAO1 wild-type (WT) and its efflux mutants were evaluated in a Madin-Darby canine kidney (MDCK) epithelial cell monolayer system and in a murine model of endogenous septicemia. All efflux mutants except a ΔmexCD-oprJ deletion demonstrated significantly reduced invasiveness compared with WT. In particular, a ΔmexAB-oprM deletion strain was compromised in its capacity to invade or transmigrate across MDCK cells, and could not kill mice, in contrast to WT which was highly invasive (P < 0.0006) and caused fatal infection (P < 0.0001). The other mutants, including ΔmexB and ΔmexXY mutants, were intermediate between WT and the ΔmexAB-oprM mutant in invasiveness and murine virulence. Invasiveness was restored to the ΔmexAB-oprM mutant by complementation with mexAB-oprM or by addition of culture supernatant from MDCK cells infected with WT. We conclude that the P. aeruginosa MexAB-OprM efflux system exports virulence determinants that contribute to bacterial virulence.

Contribution of the MexXY Multidrug Transporter to Aminoglycoside Resistance in Pseudomonas aeruginosa Clinical Isolates

ABSTRACT MexXY is an aminoglycoside-inducible multidrug transporter shown to contribute to intrinsic and acquired aminoglycoside resistance in laboratory isolates of Pseudomonas aeruginosa. To assess its contribution to aminoglycoside resistance in 14 clinical isolates demonstrating a panaminoglycoside resistance phenotype unlikely to be explained solely by aminoglycoside modification, expression of mexXY by these isolates was examined by reverse transcription-PCR. Elevated levels of mexXY expression were evident for most strains compared with those detected for an aminoglycoside-susceptible control strain, although there was no correlation between mexXY levels and the aminoglycoside MICs for the resistant strains, indicating that if MexXY was playing a role, other factors were also contributing. Deletion of mexXY from 9 of the 14 isolates resulted in enhanced susceptibilities to multiple aminoglycosides, confirming the contribution of this efflux system to the aminoglycoside resistance of these clinical isolates. Still, the impact of MexXY loss varied, with some strains clearly more or less dependent on MexXY for aminoglycoside resistance. Expression of mexXY also varied in these strains, with some showing high-level expression of the efflux genes independent of aminoglycoside exposure (aminoglycoside-independent hyperexpression) and others showing hyperexpression of the efflux genes that was to a greater or lesser degree aminoglycoside dependent. None of these strains carried mutations in mexZ, which encodes a negative regulator of mexXY expression, or in the mexZ-mexXY intergenic region. Thus, mexXY hyperexpression in aminoglycoside-resistant clinical isolates occurs via mutation in one or more as yet unidentified genes.