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Undergraduate research programs have been used as a tool to attract and retain student interest in science careers. This study evaluates the short and long-term benefits of a Summer Science Internship (SSI) at the University of Texas Health Science Center at Houston– School of Public Health – in Brownsville, Texas, by analyzing survey data from alumni. Questions assessing short-term program impact were aimed at three main topics, student: satisfaction with program, self-efficacy for science after completing the program, and perceived benefits. Long-term program impact was assessed by looking at student school attendance and college majors along with perceived links between SSI and future college plans. Students reported high program satisfaction, a significant increase in science self-efficacy and high perceived benefits. At the time data were collected for the study, one-hundred percent of alumni were enrolled in school (high school or college). The majority of students indicated they were interested in completing a science major/career, heavily influenced by their participation in the program.^

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During the 82nd Texas legislature, state leaders passed a provision stating that healthcare providers, who perform, promote, or affiliate with providers who perform or promote elective abortion services may not be eligible to participate in the Texas Medicaid Women's Health Program (WHP). The federal government reacted to this new provision by vowing to eliminate its 90% share of program support on the grounds that the provision violated a patient's freedom to choose a provider; a right protected by the Social Security Act. Texas leaders stated that the Women's Health Program would continue without federal support, financed exclusively with state funds.^ The following policy analysis compares the projected impact of the current Medicaid Women's Health Program to the proposed state-run program using the criteria-alternative matrix framework. The criteria used to evaluate the program alternatives include population affected, unintended pregnancy and abortion impact, impact on cervical cancer rate, and state-level government expenditures. Each criterion was defined by selected measures. The population affected was measured by the number of women served in the programs. Government expenditures were measured in terms of payments for program costs, Medicaid delivery costs, and cervical cancer diagnostic costs. Unintended pregnancy impact was measured by the number of projected unplanned pregnancies and abortions under each alternative. The impact on cervical cancer was projected in terms of the number of new cervical cancer cases under each alternative. Differences in the projections with respect to each criterion were compared to assess the impact of shifting to the state-only policy.^ After examining program alternatives, it is highly recommended that Texas retain the Medicaid WHP. If the state does decide to move forward with the state-run WHP, it is recommended that the program run at its previous capacity. Furthermore, for the purpose of addressing the relatively high cervical cancer incidence rate in Texas, incorporating HPV vaccination coverage for women ages 18-26 as part of the Women's Health Program is recommended.^

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The p53 tumor suppressor gene product is negatively regulated by the product of its downstream target, mdm2. The mdm2 oncogene abrogates p53 transactivation function. Amplification of mdm2 occurs in 36% of human sarcomas, which often retain p53 in wild type form, suggesting that overexpression of mdm2 in tumors results in p53 inactivation. Thus, the relationship of p53 to mdm2 is important in tumorigenesis. The deletion of mdm2 in the mouse results in embryonic lethality by 5.5 days post coitum. Embryonic lethality of the mdm2 null embryos was overcome by simultaneous loss of the p53 tumor suppressor, which substantiates the importance of the negative regulatory function of MDM2 on p53 function in vivo. These data suggest that the loss of MDM2 function allowed the constitutively active p53 protein to induce either a complete G1 arrest or the p53-dependent apoptotic pathway, resulting in the death of the mdm2−/− embryos.^ The present study examines the hypothesis that the absence of mdm2 induces apoptosis due to p53 activation. Viability of the p53−/−mdm2−/− mice has allowed establishment of mouse embryo fibroblasts (MEFs) and a detailed examination of the properties of these cells. To introduce p53 into this system, and essentially recreate a mdm2 null cell, a temperature sensitive p53 (tsp53) point mutant (A135V) was used, which exhibits a nonfunctional, mutant conformation at 39°C and wild type, functional conformation at 32°C. Infected pools of p53−/− and p53−/−mdm2−/− MEFs with the tsp53 gene were established and single-cell clonal populations expressing tsp53 were selected. Shifting the cells from 39°C to 32°C caused p53−/−mdm2 −/− lines expressing tsp53 to undergo up to 80% apoptosis, which did not occur in the p53−/− lines expressing tsp53 nor the parental lines lacking p53 expression. Furthermore, the amount of p53 present in the clonal population determined the extent of apoptosis. Tsp53 is transcriptionally active in this system, however, it discriminates among different target promoters and does not induce the apoptosis effector targets bax or Fas/Apo1. ^ In summary, this study indicates that the presence or absence of mdm2 is the determining factor for the ability of p53 to trigger apoptosis in this system. The loss of mdm2 promotes p53-dependent apoptosis in MEFs in a cell cycle and dose-dependent manner. p53 is differentially phosphorylated in the presence and absence of mdm2, but does not induce the apoptosis effectors, bax or Fas/ Apo1. ^