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Tin Tin Su

Bio: Tin Tin Su is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Cell cycle & Mitosis. The author has an hindex of 31, co-authored 80 publications receiving 3601 citations. Previous affiliations of Tin Tin Su include University of California, San Francisco & Anschutz Medical Campus.


Papers
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Journal ArticleDOI
02 Jan 2009-Science
TL;DR: It is shown that peer discussion enhances understanding, even when none of the students in a discussion group originally knows the correct answer, when students answer individually and then revote on the same question.
Abstract: When students answer an in-class conceptual question individually using clickers, discuss it with their neighbors, and then revote on the same question, the percentage of correct answers typically increases. This outcome could result from gains in understanding during discussion, or simply from peer influence of knowledgeable students on their neighbors. To distinguish between these alternatives in an undergraduate genetics course, we followed the above exercise with a second, similar (isomorphic) question on the same concept that students answered individually. Our results indicate that peer discussion enhances understanding, even when none of the students in a discussion group originally knows the correct answer.

786 citations

Journal ArticleDOI
TL;DR: The authors found that when students answer an in-class conceptual question individually using clickers, discuss it with their neighbors, and then revote on the same question, the percentage of correct answers typically increases.

233 citations

Journal ArticleDOI
TL;DR: This work reviews recent data on cellular responses to DNA double-strand breaks and investigates whether a cell may arrest division via checkpoint activation to fix DSBs or commit suicide by apoptosis.
Abstract: DNA double-strand breaks (DSBs) produce a number of cellular responses, some mutually exclusive. Depending on where on the chromosome it occurs, a DSB may become preserved inside a telomere or eliminated by repair. A cell may arrest division via checkpoint activation to fix DSBs or commit suicide by apoptosis. What determines the outcome: to bury, fix, or succumb to DNA DSBs? With this question in mind, we review recent data on cellular responses to DSBs.

227 citations

Journal ArticleDOI
TL;DR: It is proposed that comparison to the rapid peri-gastrulation cycles is more appropriate and suggested that these cycles are related by evolutionary descent to the early cleavage stages of embryos such as those of frog and fly.

204 citations

Journal ArticleDOI
23 Apr 2007-Fly
TL;DR: Drosophila researchers met in sunny San Diego for the 49th annual meeting of The Genetics Society of America and searched out and covered talks and posters in ‘Cell Division and Growth Control’, ‘Gametogenesis’.
Abstract: Drosophila researchers met in sunny San Diego for the 49th annual meeting of The Genetics Society of America. It was cold outside and even colder inside. Like last year, ‘Mitosis, Meiosis and Cell Division’ was no longer a session. Instead, we searched out and covered talks and posters in ‘Cell Division and Growth Control’, ‘Gametogenesis’, ‘Cytoskeleton and Cell Biology’ and ‘Genome and Chromosome Structure’. We split up for maximal coverage and re-grouped later for the Workshop on Cell Cycle and Checkpoints. We apologize in advance for the brevity or omission of some reports.

170 citations


Cited by
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Journal ArticleDOI
20 Nov 1998-Science
TL;DR: After DNA damage, many cells appear to enter a sustained arrest in the G2 phase of the cell cycle but this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21.
Abstract: After DNA damage, many cells appear to enter a sustained arrest in the G 2 phase of the cell cycle. It is shown here that this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21. After disruption of either the p53 or the p21 gene, γ radiated cells progressed into mitosis and exhibited a G 2 DNA content only because of a failure of cytokinesis. Thus, p53 and p21 appear to be essential for maintaining the G 2 checkpoint in human cells.

2,882 citations

Journal Article
TL;DR: Research data show that more resistant stem cells than common cancer cells exist in cancer patients, and to identify unrecognized differences between cancer stem cells and cancer cells might be able to develop effective classification, diagnose and treat for cancer.
Abstract: Stem cells are defined as cells able to both extensively self-renew and differentiate into progenitors. Research data show that more resistant stem cells than common cancer cells exist in cancer patients.To identify unrecognized differences between cancer stem cells and cancer cells might be able to develope effective classification,diagnose and treat ment for cancer.

2,194 citations

Journal ArticleDOI
TL;DR: It is shown that in human cells, Chk1 is phosphorylated on serine 345 (S345) in response to UV, IR, and hydroxyurea (HU).
Abstract: Chk1, an evolutionarily conserved protein kinase, has been implicated in cell cycle checkpoint control in lower eukaryotes. By gene disruption, we show that CHK1 deficiency results in a severe proliferation defect and death in embryonic stem (ES) cells, and peri-implantation embryonic lethality in mice. Through analysis of a conditional CHK1-deficient cell line, we demonstrate that ES cells lacking Chk1 have a defective G(2)/M DNA damage checkpoint in response to gamma-irradiation (IR). CHK1 heterozygosity modestly enhances the tumorigenesis phenotype of WNT-1 transgenic mice. We show that in human cells, Chk1 is phosphorylated on serine 345 (S345) in response to UV, IR, and hydroxyurea (HU). Overexpression of wild-type Atr enhances, whereas overexpression of the kinase-defective mutant Atr inhibits S345 phosphorylation of Chk1 induced by UV treatment. Taken together, these data indicate that Chk1 plays an essential role in the mammalian DNA damage checkpoint, embryonic development, and tumor suppression, and that Atr regulates Chk1.

1,707 citations

Journal ArticleDOI
TL;DR: The hypothesis is that the function of reasoning is argumentative: It is to devise and evaluate arguments intended to persuade and is adaptive given the exceptional dependence of humans on communication and their vulnerability to misinformation.
Abstract: Reasoning is generally seen as a means to improve knowledge and make better decisions. However, much evidence shows that reasoning often leads to epistemic distortions and poor decisions. This suggests that the function of reasoning should be rethought. Our hypothesis is that the function of reasoning is argumentative. It is to devise and evaluate arguments intended to persuade. Reasoning so conceived is adaptive given the exceptional dependence of humans on communication and their vulnerability to misinformation. A wide range of evidence in the psychology of reasoning and decision making can be reinterpreted and better explained in the light of this hypothesis. Poor performance in standard reasoning tasks is explained by the lack of argumentative context. When the same problems are placed in a proper argumentative setting, people turn out to be skilled arguers. Skilled arguers, however, are not after the truth but after arguments supporting their views. This explains the notorious confirmation bias. This bias is apparent not only when people are actually arguing, but also when they are reasoning proactively from the perspective of having to defend their opinions. Reasoning so motivated can distort evaluations and attitudes and allow erroneous beliefs to persist. Proactively used reasoning also favors decisions that are easy to justify but not necessarily better. In all these instances traditionally described as failures or flaws, reasoning does exactly what can be expected of an argumentative device: Look for arguments that support a given conclusion, and, ceteris paribus, favor conclusions for which arguments can be found.

1,442 citations

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TL;DR: This text is a general introduction to radiation biology and a complete, self-contained course especially for residents in diagnostic radiology and nuclear medicine that follows the Syllabus in Radiation Biology of the RSNA.
Abstract: The text consists of two sections, one for those studying or practicing diagnostic radiology, nuclear medicine and radiation oncology; the other for those engaged in the study or clinical practice of radiation oncology--a new chapter, on radiologic terrorism, is specifically for those in the radiation sciences who would manage exposed individuals in the event of a terrorist event. The 17 chapters in Section I represent a general introduction to radiation biology and a complete, self-contained course especially for residents in diagnostic radiology and nuclear medicine that follows the Syllabus in Radiation Biology of the RSNA. The 11 chapters in Section II address more in-depth topics in radiation oncology, such as cancer biology, retreatment after radiotherapy, chemotherapeutic agents and hyperthermia.

1,359 citations