Collective Hockey Against the Grit and Grind: Ice Hockey as a Reflection of Cold War Differences

Although the 1980 Miracle on Ice has been thoroughly examined from both the American and Soviet viewpoints, these studies set the game upon a pedestal of its own, a one-off incident that persists in American sports memory today because of its improbability and the subsequent public reaction. However, hockey played a role in Cold War tensions long before the Miracle and exemplified international dynamics and tensions on multiple levels. Through a review of existing literature, this thesis holistically examines the sport of ice hockey as a microcosm of the Cold War. Differences between communism and capitalism produced differences in the organization and play of hockey between the Soviet Union and North America. Moreover, Soviet propagandists took advantage of differing attitudes towards amateurism and capitalist exploitation of sport in order to denigrate the North American game and praise their own. Furthermore, smaller states such as Canada and Czechoslovakia were also able to leverage their substantial hockey programs in order to assert some modicum of independence from their respective superpowers. While many of these differences faded after the end of the Cold War allowed freer and easier exchange of ideas and practices, notably equalizing the playing field, the resumption of US-Russia tensions as well as increasing pressure for American athletes to use their platforms to voice political views mean that lessons learned during the Cold War regarding the politicization of sport are still relevant today

The Games Behind the Scenes: Newspaper Framing of Female African American Olympic Athletes

Competing in and representing their country in the Olympic games is considered one of the greatest achievements for an athlete. From heroes such as Michael Jordan and the “Dream Team,” to Michael Phelps setting world record after record in the pool, Olympians are remembered as legends to those watching at home. How their amazing achievements at these Olympic games have been framed by the media though is another story. Newspapers have facilitated a platform for a qualitative content analysis on the framing of three female African American Olympic gold medalists that showed statistical significance in terms of the amount of “Superhuman” athleticism attributes used as well as not used by four large well-known and respected newspapers

University Chronicle [November 2019]

St. Cloud State University student newspaper, volume 95, issue 3, November 2019https://repository.stcloudstate.edu/chron/1009/thumbnail.jp

The Chronicle [February 17, 2014]

The Chronicle, February 17, 2014https://repository.stcloudstate.edu/chron/4857/thumbnail.jp

Histone deacetylase controls adult stem cell aging by balancing the expression of polycomb genes and jumonji domain containing 3

Aging is linked to loss of the self-renewal capacity of adult stem cells. Here, we observed that human multipotent stem cells (MSCs) underwent cellular senescence in vitro. Decreased expression of histone deacetylases (HDACs), followed by downregulation of polycomb group genes (PcGs), such as BMI1, EZH2 and SUZ12, and by upregulation of jumonji domain containing 3 (JMJD3), was observed in senescent MSCs. Similarly, HDAC inhibitors induced cellular senescence through downregulation of PcGs and upregulation of JMJD3. Regulation of PcGs was associated with HDAC inhibitor-induced hypophosphorylation of RB, which causes RB to bind to and decrease the transcriptional activity of E2F. JMJD3 expression regulation was dependant on histone acetylation status at its promoter regions. A histone acetyltransferase (HAT) inhibitor prevented replicative senescence of MSCs. These results suggest that HDAC activity might be important for MSC self-renewal by balancing PcGs and JMJD3 expression, which govern cellular senescence by p16INK4A regulation

Volume 2, Chapter 17-2: Rodents - Muroidea: Non-Muridae

https://digitalcommons.mtu.edu/bryo-ecol-subchapters/1199/thumbnail.jp

The role and mechanism of action of BRK in breast cancer progression

Breast cancer is unanimously considered a highly heterogeneous disease due to its diverse molecular features. Breast tumor kinase (BRK), also known as protein tyrosine kinase 6 (PTK6), is a non-receptor tyrosine kinase that is highly expressed in over 80% of breast carcinomas. The role and mechanism of action of enzymatically activated BRK in breast pathology are unclear. The objectives of this project were to reveal the effect of BRK activation on cell migration, proliferation and tumorigenesis. We also aimed to determine the mechanism of action of BRK in the promotion of cell proliferation. We used BRK-negative cells (MCF10A, MDA-MB-231 and HEK293) to generate three sets of stable cell lines that stably expressed GFP alone, GFP-BRK-WT or GFP-BRK-Y447F (constitutively active) by retroviral infections. We also stably knocked down BRK from BRK-positive cells BT20 and SKBR3 by RNA interference using shRNAs against BRK. Western blotting, immunoprecipitation and qPCR studies were conducted to evaluate protein expression, protein-protein interaction and mRNA expression, respectively. Both sets of cell lines were used to determine the effect of BRK on cell proliferation (automated cell counter), cell migration (transwell and wound healing assay), transformation (colony formation assay) and tumor formation (mouse Xenograft assay). To investigate the mechanism of action of BRK, we validated downstream of tyrosine kinases 1 (Dok1), a tumor suppressor, as a BRK substrate. Deletion or site-directed mutagenesis was performed to map BRK-targeted tyrosines in Dok1 protein. Results obtained from this research project showed that stable expression of the constitutively active mutant of BRK (BRK-Y447F) in MDA-MB-231 cells led to a significant increase in the cell proliferation, migration rate and promoted colony formation and drastically enhanced tumor formation in athymic nude mice in comparison to control cells. Additionally, depletion of BRK abrogated the migration of BT20 and SKBR3 cells. Furthermore, we showed that BRK interacts with and phosphorylates Dok1, inducing Dok1 downregulation via a ubiquitin-proteasome-mediated mechanism. Together, our results show that the activation of BRK is essential for mammary gland tumorigenesis and suggest that targeting of Dok1 for degradation is a novel mechanism of action of BRK in the promotion of cell proliferation, migration and tumor formation