EFFICACY OF THREE BACKWARD MASKING SIGNALS

Increased backward masking has been correlated with Auditory Processing Disorders (APD). An efficacious test of the backward masking function that is compatible with naïve listeners could have clinical utility in diagnosing APDs. In order to determine an appropriate probe for such a test, three 20-ms signal-types were compared for ease-of-task. Response times (RT) were taken as a proxy for ease-of-task. Seven participants used a method-of-adjustment to track threshold in the presence of a 50-ms broadband-Gausian-noise backward-masker. The signal-types yielded two comparisons: Linear rise-fall on a 1000Hz sine-wave versus a “chirp” (750 Hz-4000Hz); Linear rise-fall vs Blackman gating function on a 1000Hz sine-wave. The results suggest that signal-type is a significant factor in participant response time and hence, confidence. Moreover, the contribution of signal-type to RT is not confounded by any potential interaction terms, such as inter-stimulus interval (ISI). The signal-type that yielded the quickest RTs across all participants, ISIs, and intensity levels was the 20-ms, 1000 Hz sine-wave fitted with a trapezoidal gating function. This may be the most efficacious signal-type to serve as a probe in a clinical test of backward masking

The Ursinus Weekly, May 29, 1969

S.F.A.R.C. blocked on rules proposals • William F. Buckley featured at June 9th Commencement for 304 graduating seniors • 316 freshmen admitted for Fall \u2769 semester • New Vice-Presidents: Pettit, Richter named • IF wrap-up • New members of Sigma Xi Club; 11 students, 4 faculty selected • Editorials: Proper emphasis; Goodbye, and all that • Focus: T.W. Rhody • It\u27s all over • Polemic finale • One-acts reviewed • A story • Eulogy to Dr. Courtney Smith and the one dead in the ghetto • Velikovsky: The outcast • Board meeting • Outing Club ends diversified year • Tacconelli, Maurer finish with highest batting marks • UC netmen hammer way to best log since \u2756 • Final examination schedulehttps://digitalcommons.ursinus.edu/weekly/1176/thumbnail.jp

Reduction of Murine Colon Tumorigenesis Driven by Enterotoxigenic Bacteroides fragilis Using Cefoxitin Treatment

BACKGROUND: Chronic inflammation and composition of the colon microbiota have been associated with colorectal cancer in humans. The human commensal enterotoxigenic Bacteroides fragilis (ETBF) is linked to both inflammatory bowel disease and colorectal cancer and, in our murine model, causes interleukin 17A (IL-17A)-dependent colon tumors. In these studies, we hypothesized that persistent colonization by ETBF is required for tumorigenesis. METHODS: We established a method for clearing ETBF in mice, using the antibiotic cefoxitin. Multiple intestinal neoplasia mice were colonized with ETBF for the experiment duration or were cleared of infection after 5 or 14 days. Gross tumors and/or microadenomas were then evaluated. In parallel, IL-17A expression was evaluated in wild-type littermates. RESULTS: Cefoxitin treatment resulted in complete and durable clearance of ETBF colonization. We observed a stepwise increase in median colon tumor numbers as the duration of ETBF colonization increased before cefoxitin treatment. ETBF eradication also significantly decreased mucosal IL-17A expression. CONCLUSIONS: The timing of ETBF clearance profoundly influences colon adenoma formation, defining a period during which the colon is susceptible to IL-17A-dependent tumorigenesis in this murine model. This model system can be used to study the microbiota-dependent and molecular mechanisms contributing to IL-17A-dependent colon tumor initiation

The Ursinus Weekly, March 6, 1970

Light show, Ben Hair Campus Chest events • USGA elects President: Novak, Emig meet press • Haas, Karpinski selected Woodrow Wilson scholars • Student Union to occupy Memorial Library building • Editorial: Student election, Ursinus style • Focus: John Fioravanti • Faculty self-portrait: Dr. Allan Lake Rice • Survey surveyed • Lantern in the limelight • Letters to the editor: Mr. Swarr; Dr. Helfferich; Sorority slander; Michener Forum • Perspectives: Drug forum • First semester Dean\u27s List • Kings and Queens crowned • Contemplations: Tom Rush • Matmen trim PMC for first win • Hoopmen sink Drexel • Badminton netgals prolong streak • Rams syndrome snaps Bearettes Boston-bound • 1970 Ursinus Festival of Artshttps://digitalcommons.ursinus.edu/weekly/1156/thumbnail.jp

The Ursinus Weekly, October 10, 1969

Seven join, six leave Ursinus faculty • UC and 500 colleges schedule Vietnam moratorium Wednesday; Classes not officially cancelled • William D. Reimert dies, Ursinus Board President • Dr. E. Lewis\u27 math textbook aids Ursinus blind students • Pre-Med convention • Dean Harris weds Bryn Mawr man • Editorial: A very good year • Focus: Mike Stoner in exile • Compulsory convocation: Its validity and purpose • New view of Ursinus • Dr. Rice endorses Vietnam moratorium • Kitchen cynic: Suppose U.C. had mandatory convocations • Perspectives • To eat or not to eat • Board names new members • Spotlight: Mr. Jones, cook • Centennial plans • Opinion: Suggestions for revision of the school calendar • Weaver raps • Faculty portrait: Mrs. Lucas • Woodstock vs. Ursinus • Essay on the new age • Building plans • Freshman class • Harriers extend streak to 26 • Shuman, Mangan potential greats • Flying Dutchmen edge Bears on late T.D. • Ursinus drops grid opener to Diplomats • Registration system analyzed • Lack of needed funds signals impending collapse of agency • Astronaut Scott Carpenter opens Fall Forum series • Ursinus accounting students rank first twice, and secondhttps://digitalcommons.ursinus.edu/weekly/1149/thumbnail.jp

1967: Abilene Christian College Bible Lectures - Full Text

LIFTING UP THE CHRIST” Being the Abilene Christian College Annual Bible Lectures 1967 $3.95 Published by ABILENE CHRISTIAN COLLEGE STUDENTS EXCHANGE ACC Station Abilene, Texa

G-protein coupled receptor 35 (GPR35) regulates the colonic epithelial cell response to enterotoxigenic Bacteroides fragilis

G protein-coupled receptor (GPR)35 is highly expressed in the gastro-intestinal tract, predominantly in colon epithelial cells (CEC), and has been associated with inflammatory bowel diseases (IBD), suggesting a role in gastrointestinal inflammation. The enterotoxigenic Bacteroides fragilis (ETBF) toxin (BFT) is an important virulence factor causing gut inflammation in humans and animal models. We identified that BFT signals through GPR35. Blocking GPR35 function in CECs using the GPR35 antagonist ML145, in conjunction with shRNA knock-down and CRISPRcas-mediated knock-out, resulted in reduced CEC-response to BFT as measured by E-cadherin cleavage, beta-arrestin recruitment and IL-8 secretion. Importantly, GPR35 is required for the rapid onset of ETBF-induced colitis in mouse models. GPR35-deficient mice showed reduced death and disease severity compared to wild-type C57Bl6 mice. Our data support a role for GPR35 in the CEC and mucosal response to BFT and underscore the importance of this molecule for sensing ETBF in the colon

Here Versus There: Creating British Sexual Politics Elsewhere

This reflection draws upon two recent ‘moments’ in British sexuality politics—a series of Parliamentary debates on Global LGBT rights and Brighton Pride’s campaign to ‘Highlight Global LGBT Communities’. It contrasts these two moments in order to demonstrate how, at a time when LGBT rights have ostensibly been ‘won’ in the UK, there is an increasing tendency to shift focus to the persecution of SOGI minorities elsewhere in the world. This shift in focus sets up a binary of here versus there that is politically persuasive but ultimately limited and limiting. By reflecting on the way that this growing trend of creating sexual politics elsewhere occurs in two very different locations in British politics and activism, we seek to begin a conversation about the relational affects of placing sexual politics ‘elsewhere’

AMBRA1 regulates cyclin D to guard S-phase entry and genomic integrity

Mammalian development, adult tissue homeostasis and the avoidance of severe diseases including cancer require a properly orchestrated cell cycle, as well as error-free genome maintenance. The key cell-fate decision to replicate the genome is controlled by two major signalling pathways that act in parallel-the MYC pathway and the cyclin D-cyclin-dependent kinase (CDK)-retinoblastoma protein (RB) pathway(1,2). Both MYC and the cyclin D-CDK-RB axis are commonly deregulated in cancer, and this is associated with increased genomic instability. The autophagic tumour-suppressor protein AMBRA1 has been linked to the control of cell proliferation, but the underlying molecular mechanisms remain poorly understood. Here we show that AMBRA1 is an upstream master regulator of the transition from G1 to S phase and thereby prevents replication stress. Using a combination of cell and molecular approaches and in vivo models, we reveal that AMBRA1 regulates the abundance of D-type cyclins by mediating their degradation. Furthermore, by controlling the transition from G1 to S phase, AMBRA1 helps to maintain genomic integrity during DNA replication, which counteracts developmental abnormalities and tumour growth. Finally, we identify the CHK1 kinase as a potential therapeutic target in AMBRA1-deficient tumours. These results advance our understanding of the control of replication-phase entry and genomic integrity, and identify the AMBRA1-cyclin D pathway as a crucial cell-cycle-regulatory mechanism that is deeply interconnected with genomic stability in embryonic development and tumorigenesis