The New Politics of Sports Franchise Policy Innovation in Chicago

The urban regime in Chicago was an integral player in the determination of sports policy during the 1980s and early 1 990s. As the mediator of every major sports issue, the regime orchestrated the policy response in innovative ways. Regulatory powers were used to control night baseball in Wrigleyville, ultimately appeasing the team owners and most neighborhood residents. Economic development policies were adapted to keep the White Sox, but these were adopted with a major regulatory component and the progressive regime also wove a major social benefit into the redevelopment of the ballpark neighborhood. Although an accommodation to appease the football Bears has yet to be achieved, the regime has worked tirelessly to develop unique solutions. All of this represents a departure from the way in which the Democratic Party machine made policy for Chicago and demonstrates the effectiveness of a working progressive regime in Chicago in recent years

Exercise-Induced Cardiac Remodeling: Lessons from Humans, Horses, and Dogs

Physical activity is dependent upon the cardiovascular system adequately delivering blood to meet the metabolic and thermoregulatory demands of exercise. Animals who regularly exercise therefore require a well-adapted heart to support this delivery. The purpose of this review is to examine cardiac structure, and the potential for exercise-induced cardiac remodeling, in animals that regularly engage in strenuous activity. Specifically, we draw upon the literature that has studied the “athlete’s heart” in humans, horses, and dogs, to enable the reader to compare and contrast cardiac remodeling in these three athletic species. The available literature provides compelling evidence for exercise-induced cardiac remodeling in all three species. However, more work is required to understand the influence of species/breed specific genetics and exercise-related hemodynamics, in order to fully understand the impact of exercise on cardiac structure

The cytotoxin of Pseudomonas aeruginosa:Cytotoxicity requires proteolytic activation

The primary structure of a cytotoxin from Pseudomonas aeruginosa was determined by sequencing of the structural gene. The cytotoxin (31,700 Mr) lacks an N-terminal signal sequence for bacterial secretion but contains a pentapeptide consensus sequence commonly found in prokaryotic proteins which function in a TonB-dependent manner. The cytotoxin gene has a [G + C]-content of 53.8% which is considerably lower than generally observed for genes from Pseudomonas aeruginosa. The cytotoxin gene was exclusively detected in strain 158 but not in three other clinical isolates, as determined by Southern and Northern hybridization. The latter technique revealed that the toxin is translated from monocistronic mRNA. The promoter of the cytotoxin is inactive in Escherichia coli. Upon site-directed modification of the 5'-noncoding region by the polymerase chain reaction the gene was expressed under control of the trc-promoter. The gene product obtained in Escherichia coli was nontoxic. Toxicity was induced by subsequent treatment with trypsin. [35S]methionine-labeled cytotoxin with high specific radioactivity was obtained by in vitro transcription/translation. Like [125I] labeled material from Pseudomonas aeruginosa this polypeptide bound to membrane preparations from Ehrlich ascites cells, as evidenced by sedimentation through a sucrose gradient at neutral pH

Abrupt transition to heightened poliomyelitis epidemicity in England and Wales, 1947–1957, associated with a pronounced increase in the geographical rate of disease propagation

The abrupt transition to heightened poliomyelitis epidemicity in England and Wales, 1947–1957, was associated with a profound change in the spatial dynamics of the disease. Drawing on the complete record of poliomyelitis notifications in England and Wales, we use a robust method of spatial epidemiological analysis (swash-backwash model) to evaluate the geographical rate of disease propagation in successive poliomyelitis seasons, 1940–1964. Comparisons with earlier and later time periods show that the period of heightened poliomyelitis epidemicity corresponded with a sudden and pronounced increase in the spatial rate of disease propagation. This change was observed for both urban and rural areas and points to an abrupt enhancement in the propensity for the geographical spread of polioviruses. Competing theories of the epidemic emergence of poliomyelitis in England and Wales should be assessed in the light of this evidence