The president, committees, and the legislative agenda.

I make three major theoretical moves in this project. I begin by treating the administration and Congress as two parts of a single U.S. legislative system rather than as adversaries competing in a zero-sum game. Congress and the administration share power, and they share control of the legislative agenda. Presidential obstruction is as important a feature of the U.S. legislative system as presidential activism. Second, I emphasize the role of congressional committees as agenda setters. Committees are treated as censors--they report only a small, biased subset of all the bills they are assigned. Consequently, analyses based on floor outcomes alone will produce biased statistical estimates. Finally, I focus on the administration as an organization rather than on the president as an individual. Many players besides the president affect the fate of the administration's legislative program, and one key group of players I focus on is the Cabinet secretaries. These three departures lay the foundation for a new approach to the study of presidential success in Congress. I model Congress as a two-stage process in which committees decide whether a bill will be reported and the floor decides whether a reported bill will pass or fail. I estimate this model using a two-stage Maximum Likelihood Estimator that corrects for the selection bias introduced by the committee censoring process. Data are taken from the Education and Labor Committee in the U.S. House of Representatives for the 95th and 101st Congress. This project generates several important findings. First, selection bias is shown to introduce a large degree of bias in analyses of roll call votes. The results of roll call analyses cannot be trusted. Second, the administration is found to be an important player in committee deliberations. Administration support makes a bill much more likely to be reported by the Education and Labor committee. Third, the effect of the administration on committee outcomes is related to the president's political capital. The administration is more likely to succeed in committee when the president's party controls Congress and when the president's popularity is high.Ph.D.Political ScienceUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/104298/1/9513355.pdfDescription of 9513355.pdf : Restricted to UM users only

Breast Cancer Incidence in Black and White Women Stratified by Estrogen and Progesterone Receptor Statuses

BACKGROUND: There is increasing evidence that breast cancer is a heterogeneous disease presented by different phenotypes and that white women have a higher breast cancer incidence rate, whereas black women have a higher mortality rate. It is also well known that white women have lower incidence rates than black women until approximately age 40, when rate curves cross over and white women have higher rates. The goal of this study was to validate the risk of white and black women to breast cancer phenotypes, stratified by statuses of the estrogen (ER) and progesterone (PR) receptors. METHODOLOGY/PRINCIPAL FINDINGS: SEER17 data were fractioned by receptor status into [ER+, PR+], [ER−, PR−], [ER+, PR−], and [ER−, PR+] phenotypes. It was shown that in black women compared to white women, cumulative age-specific incidence rates are: (i) smaller for the [ER+, PR+] phenotype; (ii) larger for the [ER−, PR−] and [ER−, PR+] phenotypes; and (iii) almost equal for the [ER+, PR−] phenotype. Clemmesen's Hook, an undulation unique to women's breast cancer age-specific incidence rate curves, is shown here to exist in both races only for the [ER+, PR+] phenotype. It was also shown that for all phenotypes, rate curves have additional undulations and that age-specific incidence rates are nearly proportional in all age intervals. CONCLUSIONS/SIGNIFICANCE: For black and white women, risk for the [ER+, PR+], [ER−, PR−] and [ER−, PR+] phenotypes are race dependent, while risk for the [ER+, PR−] phenotype is almost independent of race. The processes of carcinogenesis in aging, leading to the development of each of the considered breast cancer phenotypes, are similar in these racial groups. Undulations exhibited on the curves of age-specific incidence rates of the considered breast cancer phenotypes point to the presence of several subtypes (to be determined) of each of these phenotypes

Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes?

We propose that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup. First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessive fructose induces features of metabolic syndrome in both laboratory animals and humans. Third, fructose appears to mediate the metabolic syndrome in part by raising uric acid, and there are now extensive experimental and clinical data supporting uric acid in the pathogenesis of metabolic syndrome. Fourth, environmental and genetic considerations provide a potential explanation of why certain groups might be more susceptible to developing diabetes. Finally, we discuss the counterarguments associated with the hypothesis and a potential explanation for these findings. If diabetes might result from excessive intake of fructose, then simple public health measures could have a major impact on improving the overall health of our populace