543 research outputs found
Relationships Among Vision, Visual Attention, and Fitness to Drive in Adults With Multiple Sclerosis
No full textAbstract
Date Presented 4/1/2017
We quantified the relationships among visual abilities, visual attention, and fitness to drive in 30 adults with multiple sclerosis. Visual acuity and visual processing speed correlated with critical driving errors (predictive of crashes) may be useful to identify potential at-risk drivers.
Primary Author and Speaker: Sarah Krasniuk
Contributing Authors: Sherrilene Classen, Sarah A. Morrow</jats:p
Visual Attention Cut Points Predicting Fitness to Drive in People With Parkinson’s Disease
No full textAbstract
Date Presented 4/1/2017
People with Parkinson’s disease (PD) have impaired visual attention affecting driver fitness. This study presents cut points to demonstrate that visual attention is an early and persistent impairment in PD drivers and accurately predicts failing or passing an on-road assessment.
Primary Author and Speaker: Sherrilene Classen
Contributing Authors: Karla Crawford, Sarah Jenniex</jats:p
Driving Intervention for Returning Combat Veterans: Interim Analysis of a Randomized Controlled Trial
No full textAbstract
Date Presented 3/31/2017
Motor vehicle collisions are a leading cause of deaths for combat veterans, and effective occupational therapy driving interventions (OT–DIs) are needed. We conducted an analysis of an efficacy trial comparing an OT–DI with traffic safety education and demonstrated a reduction in driving errors for the OT–DI group.
Primary Author and Speaker: Sherrilene Classen
Additional Authors and Speakers: Sandra Winter
Contributing Authors: Charles Levy, Abraham Yarney, Miriam Monahan</jats:p
Grounded Theory Focus Group Findings in Combat Veterans With Driving Performance Issues
No full textAbstract
Date Presented 3/30/2017
Combat veterans (CVs) face an increased risk of motor vehicle crash and report driving difficulty that impacts community reintegration. Grounded theory methods were used to examine CVs’ driving perception and behaviors. Clinicians working with this population can use findings to tailor interventions.
Primary Author and Speaker: Sherrilene Classen
Additional Authors and Speakers: Sandra Winter
Contributing Authors: Cassie McGowan, Charles Levy, Miriam Monahan, Abraham Yarney</jats:p
[Photograph 2012.201.B1042.0454]
No full textPhotograph used for a story in the Oklahoma Times newspaper. Caption: "Eva Moesel and Tim Patty, both of Northwest Classen High School, will represent Oklahoma County youths at the 24th annual state 4-H Congress opening today in Oklahoma City.
Frontiers Of Science
No full textPhotograph used for a story in the Daily Oklahoman newspaper. Caption: "FRONTIERS OF SCIENCE award certificate is presented Tim K. Zinn, Northwest Classen High School student, by astronaut Gordon Cooper during space symposium in Shawnee Saturday.
The dysregulation of BRCA1, PTEN, or CHK1 influences therapy resistance of breast cancer cells by affecting DNA repair and DNA replication stress signaling
No full textBreast cancer is the most frequently diagnosed cancer worldwide. Despite good available therapeutic options, more than half a million women still die each year due to breast cancer. A major reason contributing to this high number is the development of therapy resistances. Thus, identification of proteins and associated pathways that are involved in resistance development are a focus of the cancer research field. A common mechanism by which tumor cells become resistant to therapy is their tolerance to genomic instability, which leads to accumulation of tumor-promoting mutations. DNA replication stress and defects in DNA repair pathways have been shown to contribute to genomic instability, thereby supporting the development of resistance to chemotherapeutics and radiotherapy. Since increased replication stress is a hallmark of cancer cells, it has been identified as a promising target for new therapeutic approaches. The aim of this thesis was to exploit how the replication stress response contributes to therapy resistance, depending on the dysregulation of the three selected candidate proteins BRCA1, PTEN, and CHK1. BRCA1 is a key protein of the DNA repair pathway homologous recombination and involved in DNA replication fork protection of stalled forks. An isogenic MCF7 BRCA1 mutated cell system with therapy resistant and sensitive clones was generated. The observed resistance to different DNA damaging sources correlated to low level of replication stress, efficient DNA repair and high CHK1 activation. CHK1, one of the main proteins of the replication stress response and highly expressed in chromosomal unstable tumors, counteracts exogenously induced replication stress by anti-cancer therapies. Similar results were observed in BRCA1 proficient MDA-MB-231 cells with resistant and sensitive sublines. An inhibition of the ATR-CHK1 axis led to sensitization of the resistant cell lines. PTEN prevents genomic instability through association with replication forks. Analysis of the TCGA dataset revealed that a low PTEN expression correlated with a high chromosomal instability score and significantly worse overall survival in breast cancer patients. Low PTEN expression was associated with increased replication stress, manifested by increased origin firing in several breast cancer cell lines. Additionally, PTEN expression correlated with the fork stability upon replication stress induction. The elevated replication stress led to increased sensitivity against PARP1 inhibition. The observed results show that the replication stress response is a suitable target to sensitize resistant cancer cells to radio- and chemotherapy, which was independent of the analyzed breast cancer subtype and BRCA status. This suggests that a wide range of breast cancer patients could benefit from combination therapies that target the replication stress response.Brustkrebs ist weltweit die am häufigsten diagnostizierte Krebsart. Trotz guter Behandlungsmöglichkeiten sterben mehr als eine halbe Million Frauen jedes Jahr daran. Ein Grund für diese hohe Zahl ist die Entstehung von Therapieresistenzen. Die Identifizierung von Proteinen und damit verbundenen Signalwegen, die an der Resistenzentwicklung beteiligt sind, ist daher ein Schwerpunkt der Krebsforschung. Genomische Instabilität von Tumorzellen begünstigt das Auftreten weiterer tumorfördernder Mutationen und daraus resultierende Resistenzen. DNA-Replikationsstress und Defekte in der Reparatur von DNA-Schäden tragen zur genomischen Instabilität bei und begünstigen die Entwicklung von Chemo- und Strahlenresistenz. Da erhöhter Replikationsstress ein Merkmal von Krebszellen ist, ist es ein vielversprechendes Ziel für neue therapeutische Ansätze. Das Ziel dieser Arbeit war es, den Beitrag der Replikationsstressreaktion für die Therapieresistenz, in Abhängigkeit von der Deregulierung der drei Kandidatenproteine BRCA1, PTEN und CHK1 zu untersuchen. BRCA1 ist ein Schlüsselprotein des DNA-Reparaturweges homologe Rekombination und beteiligt am Schutz vom angehaltenen DNA-Replikationsgabeln. Es wurde ein isogenes MCF7 BRCA1-mutiertes Zellsystem mit therapieresistenten und -empfindlichen Klonen erzeugt. Die beobachtete Resistenz korrelierte mit geringem Replikationsstress, effizienter DNA-Reparatur und erhöhter CHK1-Aktivierung. CHK1, eines der wichtigsten Proteine der Replikationsstressreaktion, wirkt durch hohe Expression dem durch Krebstherapien induziertem Replikationsstress entgegen. Diese Beobachtungen konnten in BRCA1-kompetenten MDAMB-231-Zellen mit resistenten und empfindlichen Sublinien bestätigt werden. Eine Inhibition der ATR-CHK1-Achse führte zur Sensibilisierung der resistenten Zelllinien. PTEN verhindert eine genomische Instabilität durch Assoziation mit Replikationsgabeln. Eine Analyse des TCGA-Datensatzes ergab, dass eine niedrige PTEN-Expression mit hoher chromosomalen Instabilität und einer signifikant schlechteren Gesamtüberlebensrate bei Brustkrebspatientinnen korreliert. Verschiedene Zelllinien mit niedriger PTEN-Expression wiesen erhöhten Replikationsstress auf, der sich durch die vermehrte Aktivierung von ruhenden Replikationsursprüngen äußerte. Darüber hinaus wurde eine Korrelation von PTENExpression und Stabilität der Replikationsgabel nach Induktion von Replikationsstress beobachtet. Erhöhter Replikationsstress führte zu einer höheren Empfindlichkeit gegenüber PARP1-Inhibition. Diese Ergebnisse zeigen, dass die Replikationsstressreaktion ein geeignetes Ziel ist, um resistente Krebszellen gegenüber Radio- und Chemotherapie zu sensibilisieren, unabhängig vom Brustkrebs-Subtyp und BRCA Status. Dies deutet darauf hin, dass ein breites Spektrum von Brustkrebspatientinnen von Kombinationstherapien profitieren könnte, die auf die Replikationsstressreaktion abzielen
05-11-2012 SWOSU Biology Students Win Awards 3/9
No full text(from left): John Bradshaw, Cherokee, Jerry and Shawn Grizzle Foundation Scholarship; Zella Classen, Fairview, Otis King Memorial Foundation Scholarship; and Tim Stein, Enid, Tri-Beta Initiate, Arthur Shuck (Outstanding Freshman) Award and Otis King Memorial Foundation Scholarship.https://dc.swosu.edu/barkpic12/1213/thumbnail.jp
[Photograph 2012.201.B0136.0350]
No full textPhotograph used for a story in the Oklahoma Times newspaper. Caption: "Classen High School student Tim Bailey, 17, looking like a modern day Uncle Sam, was whooping it up today as the school staged a political-type convention to attract members into campus clubs.
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