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2. Resolving Boardroom Conflicts

Author

Baldwin, Scott

Subjects
Corporate directors, Mediation, Boards of directors, Business, general, Business
Abstract

When we gather high-talent achievers around a board table to make crucial, strategic decisions, some degree of dissention is inevitable. When open debate turns into boardroom conflict, however, the danger [...]

Published
2021

3. Ras-association domain family 1C protein promotes breast cancer cell migration and attenuates apoptosis

Author

Reeves, Mark E, Baldwin, Scott W, Baldwin, Melissa L, Chen, Shin-Tai, Moretz, Jeremy M, Aragon, Robert J, Li, Xinmin, Strong, Donna D, Mohan, Subburaman, and Amaar, Yousef G

Abstract

Abstract Background The Ras association domain family 1 (RASSF1) gene is a Ras effector encoding two major mRNA forms, RASSF1A and RASSF1C, derived by alternative promoter selection and alternative mRNA splicing. RASSF1A is a tumor suppressor gene. However, very little is known about the function of RASSF1C both in normal and transformed cells. Methods Gene silencing and over-expression techniques were used to modulate RASSF1C expression in human breast cancer cells. Affymetrix-microarray analysis was performed using T47D cells over-expressing RASSF1C to identify RASSF1C target genes. RT-PCR and western blot techniques were used to validate target gene expression. Cell invasion and apoptosis assays were also performed. Results In this article, we report the effects of altering RASSF1C expression in human breast cancer cells. We found that silencing RASSF1C mRNA in breast cancer cell lines (MDA-MB231 and T47D) caused a small but significant decrease in cell proliferation. Conversely, inducible over-expression of RASSF1C in breast cancer cells (MDA-MB231 and T47D) resulted in a small increase in cell proliferation. We also report on the identification of novel RASSF1C target genes. RASSF1C down-regulates several pro-apoptotic and tumor suppressor genes and up-regulates several growth promoting genes in breast cancer cells. We further show that down-regulation of caspase 3 via overexpression of RASSF1C reduces breast cancer cells' sensitivity to the apoptosis inducing agent, etoposide. Furthermore, we found that RASSF1C over-expression enhances T47D cell invasion/migration in vitro. Conclusion Together, our findings suggest that RASSF1C, unlike RASSF1A, is not a tumor suppressor, but instead may play a role in stimulating metastasis and survival in breast cancer cells.

Published
2010

7. The Open Access Advantage for Studies of Human Electrophysiology: Impact on Citations and Altmetrics

Author

Clayson, Peter, Baldwin, Scott, and Larson, Michael

Subjects
PubMed, CrossRef, Internet privacy, Scientific literature, 050105 experimental psychology, Access to Information, 03 medical and health sciences, bepress|Life Sciences|Neuroscience and Neurobiology, 0302 clinical medicine, Physiology (medical), Political science, Openness to experience, Humans, 0501 psychology and cognitive sciences, bepress|Life Sciences|Neuroscience and Neurobiology|Cognitive Neuroscience, human electrophysiology (EEG), impact factor, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), open access, Altmetrics, Impact factor, business.industry, General Neuroscience, 05 social sciences, citation advantage, Popularity, Transparency (behavior), bepress|Social and Behavioral Sciences|Psychology|Cognitive Psychology, Electrophysiology, PsyArXiv|Neuroscience|Cognitive Neuroscience, PsyArXiv|Social and Behavioral Sciences, Neuropsychology and Physiological Psychology, PsyArXiv|Neuroscience, Publishing, preprints, event-related potentials (ERPs), bepress|Social and Behavioral Sciences, PsyArXiv|Social and Behavioral Sciences|Cognitive Psychology, Preprint, Journal Impact Factor, business, 030217 neurology & neurosurgery
Abstract

Barriers to accessing scientific findings contribute to knowledge inequalities based on financial resources and decrease the transparency and rigor of scientific research. Recent initiatives aim to improve access to research as well as methodological rigor via transparency and openness. We sought to determine the impact of such initiatives on open access publishing in the sub-area of human electrophysiology and the impact of open access on the attention articles received in the scholarly literature and other outlets. Data for 35,144 articles across 967 journals from the last 20 years were examined. Approximately 35% of articles were open access, and the rate of publication of open-access articles increased over time. Open access articles showed 9 to 21% more PubMed and CrossRef citations and 39% more Altmetric mentions than closed access articles. Green open access articles (i.e., author archived) did not differ from non-green open access articles (i.e., publisher archived) with respect to citations and were related to higher Altmetric mentions. These findings demonstrate that open-access publishing is increasing in popularity in the sub-area of human electrophysiology and that open-access articles enjoy the “open access advantage” in citations similar to the larger scientific literature. The benefit of the open access advantage may motivate researchers to make their publications open access and pursue publication outlets that support it. In consideration of the direct connection between citations and journal impact factor, journal editors may improve the accessibility and impact of published articles by encouraging authors to self-archive manuscripts on preprint servers.

Published
2020

8. Developmental basis for filamin-A-associated myxomatous mitral valve disease

Author

Sauls, Kimberly, de Vlaming, Annemarieke, Harris, Brett S., Williams, Katherine, Wessels, Andy, Levine, Robert A., Slaugenhaupt, Susan A., Goodwin, Richard L., Pavone, Luigi Michele, Merot, Jean, Schott, Jean-Jacques, Le Tourneau, Thierry, Dix, Thomas, Jesinkey, Sean, Feng, Yuanyi, Walsh, Christopher, Zhou, Bin, Baldwin, Scott, Markwald, Roger R., and Norris, Russell A.

Published
2012
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10. Provider Contributions to Disparities in Mental Health Care

Author

Merced, Kritzia, primary, Imel, Zac E., additional, Baldwin, Scott A., additional, Fischer, Heidi, additional, Yoon, Tae, additional, Stewart, Christine, additional, Simon, Greg, additional, Ahmedani, Brian, additional, Beck, Arne, additional, Daida, Yihe, additional, Hubley, Sam, additional, Rossom, Rebecca, additional, Waitzfelder, Beth, additional, Zeber, John E., additional, and Coleman, Karen J., additional

Published
2020
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11. Methodological Reporting Behavior, Sample Sizes, and Statistical Power in Studies of Event- Related Potentials: Barriers to Reproducibility and Replicability

Author

Baldwin , Scott, Larson , Michael, Clayson , Peter, and Carbine , Kaylie

Subjects
PsyArXiv|Social and Behavioral Sciences, bepress|Social and Behavioral Sciences, PsyArXiv|Social and Behavioral Sciences|Cognitive Psychology, bepress|Social and Behavioral Sciences|Psychology|Cognitive Psychology
Abstract

Methodological reporting guidelines for studies of event-related potentials (ERPs) were updated in Psychophysiology in 2014. These guidelines facilitate the communication of key methodological parameters (e.g., preprocessing steps). Failing to report key parameters represents a barrier to replication efforts, and difficultly with replicability increases in the presence of small sample sizes and low statistical power. We assessed whether guidelines are followed and estimated the average sample size and power in recent research. Reporting behavior, sample sizes, and statistical designs were coded for 150 randomly-sampled articles from five high-impact journals that frequently publish ERP research from 2011 to 2017. An average of 63% of guidelines were reported, and reporting behavior was similar across journals, suggesting that gaps in reporting is a shortcoming of the field rather than any specific journal. Publication of the guidelines paper had no impact on reporting behavior, suggesting that editors and peer reviewers are not enforcing these recommendations. The average sample size per group was 21. Statistical power was conservatively estimated as .72-.98 for a large effect size, .35-.73 for a medium effect, and .10-.18 for a small effect. These findings indicate that failing to report key guidelines is ubiquitous and that ERP studies are primarily powered to detect large effects. Such low power and insufficient following of reporting guidelines represent substantial barriers to replication efforts. The methodological transparency and replicability of studies can be improved by the open sharing of processing code and experimental tasks and by a priori sample size calculations to ensure adequately powered studies.

Published
2019

14. RASSF1C modulates the expression of a stem cell renewal gene, PIWIL1

Author

Reeves Mark E, Baldwin Melissa L, Aragon Robert, Baldwin Scott, Chen Shin-Tai, Li Xinmin, Mohan Subburaman, and Amaar Yousef G

Subjects
RASSF1C, PIWIL1, Gene expression, RASSF1C target genes, ERK1/2, Medicine, Biology (General), QH301-705.5, Science (General), Q1-390
Abstract

Abstract Background RASSF1A and RASSF1C are two major isoforms encoded by the Ras association domain family 1 (RASSF1) gene through alternative promoter selection and mRNA splicing. RASSF1A is a well established tumor suppressor gene. Unlike RASSF1A, RASSF1C appears to have growth promoting actions in lung cancer. In this article, we report on the identification of novel RASSF1C target genes in non small cell lung cancer (NSCLC). Methods Over-expression and siRNA techniques were used to alter RASSF1C expression in human lung cancer cells, and Affymetrix-microarray study was conducted using NCI-H1299 cells over-expressing RASSF1C to identify RASSF1C target genes. Results The microarray study intriguingly shows that RASSF1C modulates the expression of a number of genes that are involved in cancer development, cell growth and proliferation, cell death, and cell cycle. We have validated the expression of some target genes using qRT-PCR. We demonstrate that RASSF1C over-expression increases, and silencing of RASSF1C decreases, the expression of PIWIL1 gene in NSCLC cells using qRT-PCR, immunostaining, and Western blot analysis. We also show that RASSF1C over-expression induces phosphorylation of ERK1/2 in lung cancer cells, and inhibition of the MEK-ERK1/2 pathway suppresses the expression of PIWIL1 gene expression, suggesting that RASSF1C may exert its activities on some target genes such as PIWIL1 through the activation of the MEK-ERK1/2 pathway. Also, PIWIL1 expression is elevated in lung cancer cell lines compared to normal lung epithelial cells. Conclusions Taken together, our findings provide significant data to propose a model for investigating the role of RASSF1C/PIWIL1 proteins in initiation and progression of lung cancer.

Published
2012
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15. Registered replication report: Dijksterhuis and van Knippenberg (1998)

Author

O'Donnell, Michael, Nelson, Leif D, Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A, Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Białobrzeska, Olga, Birt, Angie R, Boot, Walter R, Braithwaite, Scott R, Briggs, Jessie C, Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L, Cannon, Peter R, Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P, Coulthard, Jacob, Cramwinckel, Florien M, Denson, Thomas F, Díaz-Lago, Marcos, DiDonato, Theresa E, Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E, Finnigan, Katherine M, Fisher, Justin, Frankowska, Natalia, García-Sánchez, Efraín, Golom, Frank D, Graves, Andrew J, Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A, Harder, Jenna A, Harrell, Erin R, Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N, Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J, Légal, Jean-Baptiste, Lucas, Richard E, Lynott, Dermot, Magaldino, Corey M, Massar, Karlijn, McBee, Matthew T, McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C, Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R, Noordewier, Marret K, Özdogğru, Asil Ali, Pantazi, Myrto, Parzuchowski, Michał, Peters, Kim, Philipp, Michael C, Pollmann, Monique M H, Rentzelas, Panagiotis, Rodríguez-Bailón, Rosa, Röer, Jan Philipp, Ropovik, Ivan, Roque, Nelson A, Rueda, Carolina, Rutjens, Bastiaan T, Sackett, Katey, Salamon, Janos, Sánchez-Rodríguez, Ángel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R, Sherman, Martin F, Steele, Kenneth M, Steffens, Niklas K., Sun, Jessie, Susa, Kyle J, Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M, Tinghög, Gustav, Tong, Yuk-Yue, Tweten, Carol, Vadillo, Miguel A, Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N, Willis, Guillermo B, Wood, Sarah E, Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, Zrubka, Mark, Leerstoel Finkenauer, Youth in Changing Cultural Contexts, Section Applied Social Psychology, RS: FPN WSP II, Leerstoel Finkenauer, Youth in Changing Cultural Contexts, and Language, Communication and Cognition

Subjects
Psychologie sociale expérimentale, Male, replication, CATEGORY ACCESSIBILITY, Psychologie sociale, 05 social sciences, 050109 social psychology, intelligence, 050105 experimental psychology, Test (assessment), ACTIVATION, 5. Gender equality, Social Perception, Replication (statistics), Humans, 0501 psychology and cognitive sciences, Female, Psychology, priming, PRIMES, General Psychology, BEHAVIOR, Prejudice, Clinical psychology
Abstract

Dijksterhuis and van Knippenberg (1998) reported that participants primed with an intelligentcategory (“professor”) subsequently performed 13.1% better on a trivia test than participantsprimed with an unintelligent category (“soccer hooligans”). Two unpublished replications of thisstudy by the original authors, designed to verify the appropriate testing procedures, observed asmaller difference between conditions (2-3%) as well as a gender difference: men showed theeffect (9.3% and 7.6%) but women did not (0.3% and -0.3%). The procedure used in thosereplications served as the basis for this multi-lab Registered Replication Report (RRR). A total of40 laboratories collected data for this project, with 23 laboratories meeting all inclusion criteria.Here we report the meta-analytic result of those 23 direct replications (total N = 4,493) of theupdated version of the original study, examining the difference between priming with professorand hooligan on a 30-item general knowledge trivia task (a supplementary analysis reportsresults with all 40 labs, N = 6,454). We observed no overall difference in trivia performancebetween participants primed with professor and those primed with hooligan (0.14%) and nomoderation by gender., 0, info:eu-repo/semantics/published

Published
2018

16. Self-control, implicit alcohol associations, and the (lack of) prediction of consumption in an alcohol taste test with college student heavy episodic drinkers

Author

Lindgren, Kristen P., primary, Baldwin, Scott A., additional, Ramirez, Jason J., additional, Olin, Cecilia C., additional, Peterson, Kirsten P., additional, Wiers, Reinout W., additional, Teachman, Bethany A., additional, Norris, Jeanette, additional, Kaysen, Debra, additional, and Neighbors, Clayton, additional

Published
2019
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17. Ras-association domain family 1C protein promotes breast cancer cell migration and attenuates apoptosis

Author

Aragon Robert J, Moretz Jeremy M, Chen Shin-Tai, Baldwin Melissa L, Baldwin Scott W, Reeves Mark E, Li Xinmin, Strong Donna D, Mohan Subburaman, and Amaar Yousef G

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The Ras association domain family 1 (RASSF1) gene is a Ras effector encoding two major mRNA forms, RASSF1A and RASSF1C, derived by alternative promoter selection and alternative mRNA splicing. RASSF1A is a tumor suppressor gene. However, very little is known about the function of RASSF1C both in normal and transformed cells. Methods Gene silencing and over-expression techniques were used to modulate RASSF1C expression in human breast cancer cells. Affymetrix-microarray analysis was performed using T47D cells over-expressing RASSF1C to identify RASSF1C target genes. RT-PCR and western blot techniques were used to validate target gene expression. Cell invasion and apoptosis assays were also performed. Results In this article, we report the effects of altering RASSF1C expression in human breast cancer cells. We found that silencing RASSF1C mRNA in breast cancer cell lines (MDA-MB231 and T47D) caused a small but significant decrease in cell proliferation. Conversely, inducible over-expression of RASSF1C in breast cancer cells (MDA-MB231 and T47D) resulted in a small increase in cell proliferation. We also report on the identification of novel RASSF1C target genes. RASSF1C down-regulates several pro-apoptotic and tumor suppressor genes and up-regulates several growth promoting genes in breast cancer cells. We further show that down-regulation of caspase 3 via overexpression of RASSF1C reduces breast cancer cells' sensitivity to the apoptosis inducing agent, etoposide. Furthermore, we found that RASSF1C over-expression enhances T47D cell invasion/migration in vitro. Conclusion Together, our findings suggest that RASSF1C, unlike RASSF1A, is not a tumor suppressor, but instead may play a role in stimulating metastasis and survival in breast cancer cells.

Published
2010
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19. Registered Replication Report: Dijksterhuis and van Knippenberg (1998)

Author

Leerstoel Finkenauer, Youth in Changing Cultural Contexts, O'Donnell, Michael, Nelson, Leif D, Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A, Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Białobrzeska, Olga, Birt, Angie R, Boot, Walter R, Braithwaite, Scott R, Briggs, Jessie C, Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L, Cannon, Peter R, Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P, Coulthard, Jacob, Cramwinckel, Florien M, Denson, Thomas F, Díaz-Lago, Marcos, DiDonato, Theresa E, Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E, Finnigan, Katherine M, Fisher, Justin, Frankowska, Natalia, García-Sánchez, Efraín, Golom, Frank D, Graves, Andrew J, Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A, Harder, Jenna A, Harrell, Erin R, Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N, Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J, Légal, Jean-Baptiste, Lucas, Richard E, Lynott, Dermot, Magaldino, Corey M, Massar, Karlijn, McBee, Matthew T, McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C, Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R, Noordewier, Marret K, Özdogğru, Asil Ali, Pantazi, Myrto, Parzuchowski, Michał, Peters, Kim, Philipp, Michael C, Pollmann, Monique M H, Rentzelas, Panagiotis, Rodríguez-Bailón, Rosa, Röer, Jan Philipp, Ropovik, Ivan, Roque, Nelson A, Rueda, Carolina, Rutjens, Bastiaan T, Sackett, Katey, Salamon, Janos, Sánchez-Rodríguez, Ángel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R, Sherman, Martin F, Steele, Kenneth M, Steffens, Niklas K., Sun, Jessie, Susa, Kyle J, Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M, Tinghög, Gustav, Tong, Yuk-Yue, Tweten, Carol, Vadillo, Miguel A, Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N, Willis, Guillermo B, Wood, Sarah E, Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, Zrubka, Mark, Leerstoel Finkenauer, Youth in Changing Cultural Contexts, O'Donnell, Michael, Nelson, Leif D, Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A, Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Białobrzeska, Olga, Birt, Angie R, Boot, Walter R, Braithwaite, Scott R, Briggs, Jessie C, Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L, Cannon, Peter R, Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P, Coulthard, Jacob, Cramwinckel, Florien M, Denson, Thomas F, Díaz-Lago, Marcos, DiDonato, Theresa E, Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E, Finnigan, Katherine M, Fisher, Justin, Frankowska, Natalia, García-Sánchez, Efraín, Golom, Frank D, Graves, Andrew J, Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A, Harder, Jenna A, Harrell, Erin R, Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N, Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J, Légal, Jean-Baptiste, Lucas, Richard E, Lynott, Dermot, Magaldino, Corey M, Massar, Karlijn, McBee, Matthew T, McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C, Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R, Noordewier, Marret K, Özdogğru, Asil Ali, Pantazi, Myrto, Parzuchowski, Michał, Peters, Kim, Philipp, Michael C, Pollmann, Monique M H, Rentzelas, Panagiotis, Rodríguez-Bailón, Rosa, Röer, Jan Philipp, Ropovik, Ivan, Roque, Nelson A, Rueda, Carolina, Rutjens, Bastiaan T, Sackett, Katey, Salamon, Janos, Sánchez-Rodríguez, Ángel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R, Sherman, Martin F, Steele, Kenneth M, Steffens, Niklas K., Sun, Jessie, Susa, Kyle J, Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M, Tinghög, Gustav, Tong, Yuk-Yue, Tweten, Carol, Vadillo, Miguel A, Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N, Willis, Guillermo B, Wood, Sarah E, Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, and Zrubka, Mark

Published
2018

20. Registered Replication Report: Dijksterhuis and van Knippenberg (1998)

Author

O’Donnell, Michael, Nelson, Leif D., Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A., Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Białobrzeska, Olga, Birt, Angie R., Boot, Walter R., Braithwaite, Scott R., Briggs, Jessie C., Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L., Cannon, Peter R., Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P., Coulthard, Jacob, Cramwinckel, Florien M., Denson, Thomas F., Díaz-Lago, Marcos, DiDonato, Theresa E., Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E., Finnigan, Katherine M., Fisher, Justin, Frankowska, Natalia, García-Sánchez, Efraín, Golom, Frank D., Graves, Andrew J., Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A., Harder, Jenna A., Harrell, Erin R., Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N., Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J., Légal, Jean-Baptiste, Lucas, Richard E., Lynott, Dermot, Magaldino, Corey M., Massar, Karlijn, McBee, Matthew T., McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C., Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R., Noordewier, Marret K., Ali Özdoğru, Asil, Pantazi, Myrto, Parzuchowski, Michał, Peters, Kim, Philipp, Michael C., Pollmann, Monique M. H., Rentzelas, Panagiotis, Rodríguez-Bailón, Rosa, Philipp Röer, Jan, Ropovik, Ivan, Roque, Nelson A., Rueda, Carolina, Rutjens, Bastiaan T., Sackett, Katey, Salamon, Janos, Sánchez-Rodríguez, Ángel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R., Sherman, Martin F., Steele, Kenneth M., Steffens, Niklas K., Sun, Jessie, Susa, Kyle J., Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M., Tinghög, Gustav, Tong, Yuk-yue, Tweten, Carol, Vadillo, Miguel A., Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N., Willis, Guillermo B., Wood, Sarah E., Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, Zrubka, Mark, O’Donnell, Michael, Nelson, Leif D., Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A., Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Białobrzeska, Olga, Birt, Angie R., Boot, Walter R., Braithwaite, Scott R., Briggs, Jessie C., Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L., Cannon, Peter R., Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P., Coulthard, Jacob, Cramwinckel, Florien M., Denson, Thomas F., Díaz-Lago, Marcos, DiDonato, Theresa E., Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E., Finnigan, Katherine M., Fisher, Justin, Frankowska, Natalia, García-Sánchez, Efraín, Golom, Frank D., Graves, Andrew J., Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A., Harder, Jenna A., Harrell, Erin R., Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N., Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J., Légal, Jean-Baptiste, Lucas, Richard E., Lynott, Dermot, Magaldino, Corey M., Massar, Karlijn, McBee, Matthew T., McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C., Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R., Noordewier, Marret K., Ali Özdoğru, Asil, Pantazi, Myrto, Parzuchowski, Michał, Peters, Kim, Philipp, Michael C., Pollmann, Monique M. H., Rentzelas, Panagiotis, Rodríguez-Bailón, Rosa, Philipp Röer, Jan, Ropovik, Ivan, Roque, Nelson A., Rueda, Carolina, Rutjens, Bastiaan T., Sackett, Katey, Salamon, Janos, Sánchez-Rodríguez, Ángel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R., Sherman, Martin F., Steele, Kenneth M., Steffens, Niklas K., Sun, Jessie, Susa, Kyle J., Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M., Tinghög, Gustav, Tong, Yuk-yue, Tweten, Carol, Vadillo, Miguel A., Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N., Willis, Guillermo B., Wood, Sarah E., Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, and Zrubka, Mark

Abstract

Dijksterhuis and van Knippenberg (1998) reported that participants primed with a category associated with intelligence (“professor”) subsequently performed 13% better on a trivia test than participants primed with a category associated with a lack of intelligence (“soccer hooligans”). In two unpublished replications of this study designed to verify the appropriate testing procedures, Dijksterhuis, van Knippenberg, and Holland observed a smaller difference between conditions (2%–3%) as well as a gender difference: Men showed the effect (9.3% and 7.6%), but women did not (0.3% and −0.3%). The procedure used in those replications served as the basis for this multilab Registered Replication Report. A total of 40 laboratories collected data for this project, and 23 of these laboratories met all inclusion criteria. Here we report the meta-analytic results for those 23 direct replications (total N = 4,493), which tested whether performance on a 30-item general-knowledge trivia task differed between these two priming conditions (results of supplementary analyses of the data from all 40 labs, N = 6,454, are also reported). We observed no overall difference in trivia performance between participants primed with the “professor” category and those primed with the “hooligan” category (0.14%) and no moderation by gender.

Published
2018

21. Registered Replication Report: Dijksterhuis and van Knippenberg (1998)

Author

ODonnell, Michael, Nelson, Leif D., Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A., Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Bialobrzeska, Olga, Birt, Angie R., Boot, Walter R., Braithwaite, Scott R., Briggs, Jessie C., Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L., Cannon, Peter R., Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P., Coulthard, Jacob, Cramwinckel, Florien M., Denson, Thomas F., Diaz-Lago, Marcos, DiDonato, Theresa E., Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E., Finnigan, Katherine M., Fisher, Justin, Frankowska, Natalia, Garcia-Sanchez, Efrain, Golom, Frank D., Graves, Andrew J., Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A., Harder, Jenna A., Harrell, Erin R., Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N., Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J., Legal, Jean-Baptiste, Lucas, Richard E., Lynott, Dermot, Magaldino, Corey M., Massar, Karlijn, McBee, Matthew T., McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C., Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R., Noordewier, Marret K., Ozdogru, Asil Ali, Pantazi, Myrto, Parzuchowski, Michal, Peters, Kim, Philipp, Michael C., Pollmann, Monique M. H., Rentzelas, Panagiotis, Rodriguez-Bailon, Rosa, Roeer, Jan Philipp, Ropovik, Ivan, Roque, Nelson A., Rueda, Carolina, Rutjens, Bastiaan T., Sackett, Katey, Salamon, Janos, Sanchez-Rodriguez, Angel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R., Sherman, Martin F., Steele, Kenneth M., Steffens, Niklas K., Sun, Jessie, Susa, Kyle J., Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M., Tinghög, Gustav, Tong, Yuk-yue, Tweten, Carol, Vadillo, Miguel A., Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N., Willis, Guillermo B., Wood, Sarah E., Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, Zrubka, Mark, ODonnell, Michael, Nelson, Leif D., Ackermann, Evi, Aczel, Balazs, Akhtar, Athfah, Aldrovandi, Silvio, Alshaif, Nasseem, Andringa, Ronald, Aveyard, Mark, Babincak, Peter, Balatekin, Nursena, Baldwin, Scott A., Banik, Gabriel, Baskin, Ernest, Bell, Raoul, Bialobrzeska, Olga, Birt, Angie R., Boot, Walter R., Braithwaite, Scott R., Briggs, Jessie C., Buchner, Axel, Budd, Desiree, Budzik, Kathryn, Bullens, Lottie, Bulley, Richard L., Cannon, Peter R., Cantarero, Katarzyna, Cesario, Joseph, Chambers, Stephanie, Chartier, Christopher R., Chekroun, Peggy, Chong, Clara, Cleeremans, Axel, Coary, Sean P., Coulthard, Jacob, Cramwinckel, Florien M., Denson, Thomas F., Diaz-Lago, Marcos, DiDonato, Theresa E., Drummond, Aaron, Eberlen, Julia, Ebersbach, Titus, Edlund, John E., Finnigan, Katherine M., Fisher, Justin, Frankowska, Natalia, Garcia-Sanchez, Efrain, Golom, Frank D., Graves, Andrew J., Greenberg, Kevin, Hanioti, Mando, Hansen, Heather A., Harder, Jenna A., Harrell, Erin R., Hartanto, Andree, Inzlicht, Michael, Johnson, David J., Karpinski, Andrew, Keller, Victor N., Klein, Olivier, Koppel, Lina, Krahmer, Emiel, Lantian, Anthony, Larson, Michael J., Legal, Jean-Baptiste, Lucas, Richard E., Lynott, Dermot, Magaldino, Corey M., Massar, Karlijn, McBee, Matthew T., McLatchie, Neil, Melia, Nadhilla, Mensink, Michael C., Mieth, Laura, Moore-Berg, Samantha, Neeser, Geraldine, Newell, Ben R., Noordewier, Marret K., Ozdogru, Asil Ali, Pantazi, Myrto, Parzuchowski, Michal, Peters, Kim, Philipp, Michael C., Pollmann, Monique M. H., Rentzelas, Panagiotis, Rodriguez-Bailon, Rosa, Roeer, Jan Philipp, Ropovik, Ivan, Roque, Nelson A., Rueda, Carolina, Rutjens, Bastiaan T., Sackett, Katey, Salamon, Janos, Sanchez-Rodriguez, Angel, Saunders, Blair, Schaafsma, Juliette, Schulte-Mecklenbeck, Michael, Shanks, David R., Sherman, Martin F., Steele, Kenneth M., Steffens, Niklas K., Sun, Jessie, Susa, Kyle J., Szaszi, Barnabas, Szollosi, Aba, Tamayo, Ricardo M., Tinghög, Gustav, Tong, Yuk-yue, Tweten, Carol, Vadillo, Miguel A., Valcarcel, Deisy, Van der Linden, Nicolas, van Elk, Michiel, van Harreveld, Frenk, Västfjäll, Daniel, Vazire, Simine, Verduyn, Philippe, Williams, Matt N., Willis, Guillermo B., Wood, Sarah E., Yang, Chunliang, Zerhouni, Oulmann, Zheng, Robert, and Zrubka, Mark

Abstract

Dijksterhuis and van Knippenberg (1998) reported that participants primed with a category associated with intelligence (professor) subsequently performed 13% better on a trivia test than participants primed with a category associated with a lack of intelligence (soccer hooligans). In two unpublished replications of this study designed to verify the appropriate testing procedures, Dijksterhuis, van Knippenberg, and Holland observed a smaller difference between conditions (2%-3%) as well as a gender difference: Men showed the effect (9.3% and 7.6%), but women did not (0.3% and -0.3%). The procedure used in those replications served as the basis for this multilab Registered Replication Report. A total of 40 laboratories collected data for this project, and 23 of these laboratories met all inclusion criteria. Here we report the meta-analytic results for those 23 direct replications (total N = 4,493), which tested whether performance on a 30-item general-knowledge trivia task differed between these two priming conditions (results of supplementary analyses of the data from all 40 labs, N = 6,454, are also reported). We observed no overall difference in trivia performance between participants primed with the professor category and those primed with the hooligan category (0.14%) and no moderation by gender., Funding Agencies|Association for Psychological Science; Arnold Foundation

Published
2018
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24. Comment.

Author

Baldwin, Scott

Subjects
Complex litigation -- Analysis, Products liability -- Asbestos
Published
1990

25. Closed-loop bias voltage control for plasma etching

Author

Patrick, Roger, Baldwin, Scott, and Williams, Norman

Subjects
Plasma etching -- Design and construction -- Product information, Metal products industry -- Product information, Engraving -- Product information
Abstract

The stated goal for high-density etchers of completely decoupling plasma generation from ion energy control cannot be achieved with conventional methods of monitoring RF power delivery. By using a closed-loop […]

Published
2000

26. Intraclass correlation associated with therapists : estimates and applications in planning psychotherapy research

Author

Baldwin, Scott A., Murray, David M., Shadish, William R., Pals, Sherri L., Holland, Jason M., Abramowitz, Jonathan S., Andersson, Gerhard, Atkins, David C., Carlbring, Per, Carroll, Kathleen M., Christensen, Andrew, Eddington, M., Ehlers, Anke, Feaster, Daniel J., Keijesers, Ger P. J., Koch, Ellen, Kuyken, Willem, Lange, Alfred, Lincoln, Tania, Stephens, Robert S., Taylor, Steven, Trepka, Chris, Watson, Jeanne, Baldwin, Scott A., Murray, David M., Shadish, William R., Pals, Sherri L., Holland, Jason M., Abramowitz, Jonathan S., Andersson, Gerhard, Atkins, David C., Carlbring, Per, Carroll, Kathleen M., Christensen, Andrew, Eddington, M., Ehlers, Anke, Feaster, Daniel J., Keijesers, Ger P. J., Koch, Ellen, Kuyken, Willem, Lange, Alfred, Lincoln, Tania, Stephens, Robert S., Taylor, Steven, Trepka, Chris, and Watson, Jeanne

Abstract

It is essential that outcome research permit clear conclusions to be drawn about the efficacy of interventions. The common practice of nesting therapists within conditions can pose important methodological challenges that affect interpretation, particularly if the study is not powered to account for the nested design. An obstacle to the optimal design of these studies is the lack of data about the intraclass correlation coefficient (ICC), which measures the statistical dependencies introduced by nesting. To begin the development of a public database of ICC estimates, the authors investigated ICCs for a variety outcomes reported in 20 psychotherapy outcome studies. The magnitude of the 495 ICC estimates varied widely across measures and studies. The authors provide recommendations regarding how to select and aggregate ICC estimates for power calculations and show how researchers can use ICC estimates to choose the number of patients and therapists that will optimize power. Attention to these recommendations will strengthen the validity of inferences drawn from psychotherapy studies that nest therapists within conditions.

Published
2011
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31. Antibody-Mediated p53 Protein Therapy Prevents Liver MetastasisIn vivo

Author

Hansen, James E., primary, Fischer, Laurice K., additional, Chan, Grace, additional, Chang, Sophia S., additional, Baldwin, Scott W., additional, Aragon, Robert J., additional, Carter, Jacqueline J., additional, Lilly, Michael, additional, Nishimura, Robert N., additional, Weisbart, Richard H., additional, and Reeves, Mark E., additional

Published
2007
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35. Cell-Autonomous and Non-Cell-Autonomous Roles for Irf6 during Development of the Tongue.

Author

Goudy, Steven, Angel, Peggi, Jacobs, Britni, Hill, Cynthia, Mainini, Veronica, Smith, Arianna L., Kousa, Youssef A., Caprioli, Richard, Prince, Lawrence S., Baldwin, Scott, and Schutte, Brian C.

Subjects
INTERFERON regulatory factors, VAN der Woude syndrome, EPITHELIAL cells, CELL growth, TRANSCRIPTION factors, DNA, DNA-binding proteins, DEVELOPMENTAL biology
Abstract

Interferon regulatory factor 6 (IRF6) encodes a highly conserved helix-turn-helix DNA binding protein and is a member of the interferon regulatory family of DNA transcription factors. Mutations in IRF6 lead to isolated and syndromic forms of cleft lip and palate, most notably Van der Woude syndrome (VWS) and Popliteal Ptyerigium Syndrome (PPS). Mice lacking both copies of Irf6 have severe limb, skin, palatal and esophageal abnormalities, due to significantly altered and delayed epithelial development. However, a recent report showed that MCS9.7, an enhancer near Irf6, is active in the tongue, suggesting that Irf6 may also be expressed in the tongue. Indeed, we detected Irf6 staining in the mesoderm-derived muscle during development of the tongue. Dual labeling experiments demonstrated that Irf6 was expressed only in the Myf5+ cell lineage, which originates from the segmental paraxial mesoderm and gives rise to the muscles of the tongue. Fate mapping of the segmental paraxial mesoderm cells revealed a cell-autonomous Irf6 function with reduced and poorly organized Myf5+ cell lineage in the tongue. Molecular analyses showed that the Irf6−/− embryos had aberrant cytoskeletal formation of the segmental paraxial mesoderm in the tongue. Fate mapping of the cranial neural crest cells revealed non-cell-autonomous Irf6 function with the loss of the inter-molar eminence. Loss of Irf6 function altered Bmp2, Bmp4, Shh, and Fgf10 signaling suggesting that these genes are involved in Irf6 signaling. Based on these data, Irf6 plays important cell-autonomous and non-cell-autonomous roles in muscular differentiation and cytoskeletal formation in the tongue. [ABSTRACT FROM AUTHOR]

Published
2013
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36. BUSINESS FORUM; DON'T DEBASE A 200-YEAR-OLD TRADITION

Author

Baldwin, Scott

Abstract

A RECENT New Yorker cartoon characterizes for me the sentiment of those who would drastically change the historic way we legally compensate victims of dangerous and defective products. The cartoon […]

Published
1985

37. 'Malpractice and state reform': replies

Author

Lister, Betty and Baldwin, Scott

Subjects
Medical personnel -- Malpractice, Medical malpractice insurance -- Laws, regulations and rules, Physicians -- Malpractice
Published
1985

39. Response to Ridgeway, Dunston, & Qian: On methodological rigor: Has rigor mortis set in?

Author

Baldwin, Scott and Vaughn, Sharon

Subjects
SECONDARY education research, META-analysis, READING exercises, EDUCATION, LEARNING strategies, STUDENTS, LITERACY, SCHOOLS, TEACHERS
Abstract

The article comments on the quality of research concerning secondary reading practices conducted by researchers Victoria G. Ridgeway, Pamela J. Dunston, Gaoyin Qian. According to the author, Ridgeway and colleagues calculated the percentages of design flaws and violations of various assumptions across the 98 studies. The researchers provide a microanalysis of the methodology of teaching and learning strategy research by examining the extent to which a body of research, as a whole, conforms to the conventions of a particular paradigm. From the author's viewpoint, better research is empiricism that solves real problems or broadens ones collective knowledge base. The best of educational research influences students, teachers and policy makers in ways that are constructive with respect to societal goals.

Published
1993
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40. Abnormal embryonic lymphatic vessel development in Tie1 hypomorphic mice.

Author

Xianghu Qu, Tompkins, Kevin, Batts, Lorene E., Puri, Mira, and Baldwin, Scott

Subjects
PROTEIN-tyrosine kinases, BLOOD vessels, LYMPHATICS, EMBRYOLOGY, MICE, PROTEIN kinases
Abstract

Tie1 is an endothelial receptor tyrosine kinase that is essential for development and maintenance of the vascular system; however, the role of Tie1 in development of the lymphatic vasculature is unknown. To address this question, we first documented that Tie1 is expressed at the earliest stages of lymphangiogenesis in Prox1-positive venous lymphatic endothelial cell (LEC) progenitors. LEC Tie1 expression is maintained throughout embryonic development and persists in postnatal mice. We then generated two lines of Tie1 mutant mice: a hypomorphic allele, which has reduced expression of Tie1, and a conditional allele. Reduction of Tie1 levels resulted in abnormal lymphatic patterning and in dilated and disorganized lymphatic vessels in all tissues examined and in impaired lymphatic drainage in embryonic skin. Homozygous hypomorphic mice also exhibited abnormally dilated jugular lymphatic vessels due to increased production of Prox1-positive LECs during initial lymphangiogenesis, indicating that Tie1 is required for the early stages of normal lymphangiogenesis. During later stages of lymphatic development, we observed an increase in LEC apoptosis in the hypomorphic embryos after mid-gestation that was associated with abnormal regression of the lymphatic vasculature. Therefore, Tie1 is required for early LEC proliferation and subsequent survival of developing LECs. The severity of the phenotypes observed correlated with the expression levels of Tie1, confirming a dosage dependence for Tie1 in LEC integrity and survival. No defects were observed in the arterial or venous vasculature. These results suggest that the developing lymphatic vasculature is particularly sensitive to alterations in Tie1 expression. [ABSTRACT FROM AUTHOR]

Published
2010

41. Down Syndrome Critical Region-1 Is a Transcriptional Target of Nuclear Factor of Activated T Cells-c1 within the Endocardium during Heart Development.

Author

Hai Wu, Shih-Chu Kao, Barrientos, Tomasa, Baldwin, Scott H., Olson, Eric N., Crabtree, Gerald R., Zhou, Bin, and Ching-Pin Chang

Subjects
*ENDOTHELIUM, *PROTEINS, *T cells, *CHEMICAL reactions, *BIOMOLECULES, *LIFE sciences, *BIOCHEMISTRY
Abstract

Patients with Down syndrome have characteristic heart valve lesions resulting from endocardial cushion defects. The Down syndrome critical region 1 (DSCR1) gene, identified at the conserved trisomic 21 region in those patients, encodes a calcineurin inhibitor that inactivates nuclear factor of activated T cells (NFATc) activity. Here, we identify a regulatory sequence in the promoter region of human DSCR1 that dictates specific expression of a reporter gene in the endocardium, defined by the temporal and spatial expression of Nfatcl during heart valve development. Activation of this evolutionally conserved DSCR1 regulatory sequence requires calcineurin and NFATcl signaling in the endocardium. NFATcl proteins bind to the regulatory sequence and trigger its enhancer activity. NFATcl is sufficient to induce the expression of Dscrl in cells that normally have undetectable or minimal NFATcl or DSCR1. Pharmacologic inhibition of calcineurin or genetic Nfatcl null mutation in mice abolishes the endocardial activity of this DSCR1 enhancer. Furthermore, in mice lacking endocardial NFATc1, the endogenous Dscrl expression is specifically inhibited in the endocardium but not in the myocardium. Thus, our studies indicate that the DSCR1 gene is a direct transcriptional target of NFATcl proteins within the endocardium during a critical window of heart valve formation. [ABSTRACT FROM AUTHOR]

Published
2007
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42. Congenital heart disease-causing Gata4 mutation displays functional deficits in vivo

Author

Sara N. Koenig, William T. Pu, Vidu Garg, Chaitali Misra, Caryn Rothrock McNally, Pamela A. Lucchesi, Nita Sachan, Deepak Srivastava, Haley A. Nichols, Anuradha Guggilam, and Baldwin, Scott

Subjects
Cancer Research, Heart disease, Mutant, medicine.disease_cause, Cardiovascular, Pediatrics, Mice, Congenital, 0302 clinical medicine, Pediatric Cardiology, Missense mutation, Cyclin D2, 2.1 Biological and endogenous factors, Heart looping, Myocytes, Cardiac, Developmental, Aetiology, Genetics (clinical), reproductive and urinary physiology, Heart Defects, Genetics, Pediatric, 0303 health sciences, Mutation, GATA4, Gene Expression Regulation, Developmental, respiratory system, Null allele, 3. Good health, Mutant Strains, Heart Disease, embryonic structures, cardiovascular system, Medicine, Cardiac, Research Article, Biotechnology, Heart Defects, Congenital, endocrine system, lcsh:QH426-470, Heart Ventricles, 1.1 Normal biological development and functioning, Embryonic Development, Biology, 03 medical and health sciences, Model Organisms, Underpinning research, medicine, Animals, Humans, Molecular Biology, Ecology, Evolution, Behavior and Systematics, 030304 developmental biology, Cell Proliferation, Myocytes, Atrial Septum, Business and Management, medicine.disease, Molecular biology, Mice, Mutant Strains, GATA4 Transcription Factor, lcsh:Genetics, Gene Expression Regulation, T-Box Domain Proteins, 030217 neurology & neurosurgery, Developmental Biology
Abstract

Defects of atrial and ventricular septation are the most frequent form of congenital heart disease, accounting for almost 50% of all cases. We previously reported that a heterozygous G296S missense mutation of GATA4 caused atrial and ventricular septal defects and pulmonary valve stenosis in humans. GATA4 encodes a cardiac transcription factor, and when deleted in mice it results in cardiac bifida and lethality by embryonic day (E)9.5. In vitro, the mutant GATA4 protein has a reduced DNA binding affinity and transcriptional activity and abolishes a physical interaction with TBX5, a transcription factor critical for normal heart formation. To characterize the mutation in vivo, we generated mice harboring the same mutation, Gata4 G295S. Mice homozygous for the Gata4 G295S mutant allele have normal ventral body patterning and heart looping, but have a thin ventricular myocardium, single ventricular chamber, and lethality by E11.5. While heterozygous Gata4 G295S mutant mice are viable, a subset of these mice have semilunar valve stenosis and small defects of the atrial septum. Gene expression studies of homozygous mutant mice suggest the G295S protein can sufficiently activate downstream targets of Gata4 in the endoderm but not in the developing heart. Cardiomyocyte proliferation deficits and decreased cardiac expression of CCND2, a member of the cyclin family and a direct target of Gata4, were found in embryos both homozygous and heterozygous for the Gata4 G295S allele. To further define functions of the Gata4 G295S mutation in vivo, compound mutant mice were generated in which specific cell lineages harbored both the Gata4 G295S mutant and Gata4 null alleles. Examination of these mice demonstrated that the Gata4 G295S protein has functional deficits in early myocardial development. In summary, the Gata4 G295S mutation functions as a hypomorph in vivo and leads to defects in cardiomyocyte proliferation during embryogenesis, which may contribute to the development of congenital heart defects in humans., Author Summary Cardiac malformations occur due to abnormal heart development and are the most prevalent human birth defect. Defects of atrial and ventricular septation are the most common type of congenital heart defect and are the result of incomplete closure of the atrial and ventricular septa, a process required for formation of a four-chambered heart. The molecular mechanisms that underlie atrial and ventricular septal defects are unknown. We previously published a highly penetrant autosomal dominant mutation (G296S) in GATA4, which was associated with atrial and ventricular septal defects in a large kindred. The disease-causing mutation has a spectrum of biochemical deficits affecting both DNA binding and protein–protein interactions. Here, we report the generation and phenotypic characterization of mice harboring the orthologous mutation in Gata4 (G295S). While homozygous mutant mice display embryonic lethality and cardiac defects, the phenotype is less severe than Gata4-null mice. A subset of Gata4 G295S heterozygote mice display a persistent interatrial communication (patent foramen ovale) and stenosis of the semilunar valves. Molecular characterization of the mutant mice suggests that the Gata4 G295S mutant protein results in diminished expression of Gata4 target genes in the heart and functional deficits in cardiomyocyte proliferation. Thus, cardiomyocyte proliferation defects may contribute to defects of cardiac septation found in humans with GATA4 mutations.

Published
2012

43. Abnormal embryonic lymphatic vessel development in Tie1 hypomorphic mice.

Author

Qu X, Tompkins K, Batts LE, Puri M, and Baldwin HS

Subjects
Animals, Apoptosis, Blood Vessels embryology, Blood Vessels physiology, DNA Primers, DNA Probes, Gene Expression Regulation, Developmental, In Situ Hybridization, Lymphangiogenesis physiology, Lymphatic System physiology, Mice, Mice, Knockout, Mice, Mutant Strains, Phenotype, Polymerase Chain Reaction, Receptor Protein-Tyrosine Kinases deficiency, Receptor Protein-Tyrosine Kinases genetics, Receptors, TIE deficiency, Receptors, TIE genetics, Reverse Transcriptase Polymerase Chain Reaction, Embryonic Development genetics, Lymphangiogenesis genetics, Lymphatic System embryology, Receptors, TIE physiology
Abstract

Tie1 is an endothelial receptor tyrosine kinase that is essential for development and maintenance of the vascular system; however, the role of Tie1 in development of the lymphatic vasculature is unknown. To address this question, we first documented that Tie1 is expressed at the earliest stages of lymphangiogenesis in Prox1-positive venous lymphatic endothelial cell (LEC) progenitors. LEC Tie1 expression is maintained throughout embryonic development and persists in postnatal mice. We then generated two lines of Tie1 mutant mice: a hypomorphic allele, which has reduced expression of Tie1, and a conditional allele. Reduction of Tie1 levels resulted in abnormal lymphatic patterning and in dilated and disorganized lymphatic vessels in all tissues examined and in impaired lymphatic drainage in embryonic skin. Homozygous hypomorphic mice also exhibited abnormally dilated jugular lymphatic vessels due to increased production of Prox1-positive LECs during initial lymphangiogenesis, indicating that Tie1 is required for the early stages of normal lymphangiogenesis. During later stages of lymphatic development, we observed an increase in LEC apoptosis in the hypomorphic embryos after mid-gestation that was associated with abnormal regression of the lymphatic vasculature. Therefore, Tie1 is required for early LEC proliferation and subsequent survival of developing LECs. The severity of the phenotypes observed correlated with the expression levels of Tie1, confirming a dosage dependence for Tie1 in LEC integrity and survival. No defects were observed in the arterial or venous vasculature. These results suggest that the developing lymphatic vasculature is particularly sensitive to alterations in Tie1 expression.

Published
2010
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44. Antibody-mediated p53 protein therapy prevents liver metastasis in vivo.

Author

Hansen JE, Fischer LK, Chan G, Chang SS, Baldwin SW, Aragon RJ, Carter JJ, Lilly M, Nishimura RN, Weisbart RH, and Reeves ME

Subjects
Animals, Antibodies, Monoclonal genetics, Antibodies, Monoclonal immunology, Antibodies, Monoclonal pharmacology, Cell Line, Tumor, Colonic Neoplasms immunology, Colonic Neoplasms therapy, Female, Humans, Immunoglobulin Fragments genetics, Liver Neoplasms, Experimental immunology, Mice, Mice, Inbred BALB C, Ovarian Neoplasms immunology, Ovarian Neoplasms therapy, Recombinant Fusion Proteins genetics, Recombinant Fusion Proteins immunology, Recombinant Fusion Proteins pharmacology, Tumor Suppressor Protein p53 genetics, Immunoglobulin Fragments immunology, Immunoglobulin Fragments pharmacology, Liver Neoplasms, Experimental prevention & control, Liver Neoplasms, Experimental secondary, Tumor Suppressor Protein p53 immunology, Tumor Suppressor Protein p53 pharmacology
Abstract

To evaluate the clinical efficacy of monoclonal antibody (mAb) 3E10 Fv antibody-mediated p53 protein therapy, an Fv-p53 fusion protein produced in Pichia pastoris was tested on CT26.CL25 colon cancer cells in vitro and in vivo in a mouse model of colon cancer metastasis to the liver. In vitro experiments showed killing of CT26.CL25 cells by Fv-p53 but not Fv or p53 alone, and immunohistochemical staining confirmed that Fv was required for transport of p53 into cells. Prevention of liver metastasis in vivo was tested by splenic injection of 100 nmol/L Fv-p53 10 min and 1 week after injection of CT26.CL25 cancer cells into the portal vein of BALB/c mice. Mice were sacrificed 1 week after the second injection of Fv-p53 and assigned a quantitative metastasis score. Control mice had an average metastasis score of 3.3 +/- 1.3, whereas mice treated with Fv-p53 had an average metastasis score of 0.8 +/- 0.4 (P = 0.004). These results indicate that Fv-p53 treatment had a profound effect on liver metastasis and represent the first demonstration of effective full-length p53 protein therapy in vivo. mAb 3E10 Fv has significant clinical potential as a mediator of intracellular and intranuclear delivery of p53 for prevention and treatment of cancer metastasis.

Published
2007
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