130 research outputs found
Interview with Morgan Callen Rogers, Bath native and author of the novel Red Rub
No full textInterview with Morgan Callen Rogers, Bath native and author of the novel Red Ruby Heart in a Cold Blue Sea
Rowell, Archer and Callen
No full textActress and author Victoria Rowell spoke to students, staff and faculty on her memoir, *The Women Who Raised Me.* She also announced a fundraising program she\u27s beginning, Loose Change for Change, for the Charleston, MS, SonEdna Foundation. Rowell poses here with Glenna Callen (l) and Pattye Archer
Molecular and functional analyses of the human and the murine genes coding for AFG3L1p, a metalloprotease homologous to the human spastic paraplegia protein
No full textLove Don't Need a Reason
No full text"From a stage erected in front of the US Capitol, on April 25, 1993, Michael Callen surveyed the throng: an estimated one million people stretched across the National Mall in the largest public demonstration of queer political solidarity in history. “What a sight,” he told the crowd, his earnest Midwestern twang reverberating through loudspeakers. “You’re a sight for sore eyes. Being gay is the greatest gift I have ever been given, and I don’t care who knows about it.” He then launched into a gorgeous rendition of “Love Don’t Need a Reason,” the AIDS anthem he composed with Marsha Malamet and the late Peter Allen. As Callen finished singing, people stood cheering and flashing the familiar American Sign Language symbol for “I Love You.” For they knew the song’s sentiment rang true for Callen, who had recently announced his retirement from music and activism after a living for more than a decade with what was then called “full-blown AIDS.” After the March on Washington, Callen returned to his recently adopted West Coast home, Los Angeles. In the ensuing months, his health rapidly declined, and on 27 December 1993, Callen died of AIDS-related pulmonary Kaposi’s sarcoma.
Love Don’t Need a Reason focuses on Callen’s most important and lasting legacy: his music. A witness to the overlooked last years of Gay Liberation and a major figure in the early years of the AIDS crisis, Michael Callen chronicled these experiences in song. A community organizer, activist, author, and architect of the AIDS self-empowerment movement, he literally changed the way we have sex in an epidemic when he co-authored one of the first safe-sex guides in 1983. A gifted singer, songwriter, and performer, he also made gay music for gay people and used music to educate and empower people with AIDS. Listening again to his music allows us to hear the shifting dynamics of American families, changing notions of masculinity, gay migration to urban areas, the sexual politics of Gay Liberation, and HIV/AIDS activism. Using extensive archival materials and newly-conducted oral history interviews with Callen’s friends, family, and fellow musicians, Matthew J. Jones reintroduces Callen to the history of LGBTQIA+ music and places Callen’s music at the center of his important activist work.
A familial cryptic subtelomeric deletion 12p with variable phenotypic effect
No full textThe definitive version is available at www.blackwell-synergy.comA 15-year-old-boy and his mother, both carrying a cryptic deletion within 12p13.33, are described. The proband has a mild phenotype with moderate mental retardation and severe behavioural problems. The mother had some learning difficulties at school. Conventional GTL-banded high-resolution chromosome analysis showed normal karyotypes. Subsequent analysis by fluorescence in situ hybridization using a set of probes specific for the subtelomeric regions of all chromosomes, plus a series of probes at 12p13.33 extending from the 12p telomere, showed that both mother and son carry a 1.65 Mb terminal deletion in this region. There are 10 predicted genes within the deleted region. The unanticipated familial nature of the deletion emphasizes the value of family studies in all cases with subtelomeric abnormalities. It also demonstrates the difficulty in making a clinical diagnosis of individuals with this deletion. To the best of the present authors' knowledge, the proband and his mother are the first patients described with a submicroscopic deletion at 12p13.33.E Baker, L Hinton, DF Callen, EA Haan, A Dobbie and GR Sutherlan
Potential trisomy 21 misdiagnosis by amniocentesis due to a resorbed twin [1]
No full text[No abstract available]CALLEN DF, 1991, PRENATAL DIAG, V11, P437, DOI 10.1002-pd.1970110705; Lloveras E, 2001, PRENATAL DIAG, V21, P896, DOI 10.1002-pd.174; REDDY KS, 1991, PRENATAL DIAG, V11, P679, DOI 10.1002-pd.1970110903; THARAPEL AT, 1989, PRENATAL DIAG, V9, P467, DOI 10.1002-pd.197009070311
Targeting the p53 pathway in Ewing Sarcoma
No full textExtent: 17p.The p53 tumour suppressor plays a pivotal role in the prevention of oncogenic transformation. Cancers frequently evade the potent antitumour surveillance mechanisms of p53 through mutation of the TP53 gene, with approximately 50% of all human malignancies expressing dysfunctional, mutated p53 proteins. Interestingly, genetic lesions in the TP53 gene are only observed in 10% of Ewing Sarcomas, with the majority of these sarcomas expressing a functional wild-type p53. In addition, the p53 downstream signaling pathways and DNA-damage cell cycle checkpoints remain functionally intact in these sarcomas. This paper summarizes recent insights into the functional capabilities and regulation of p53 in Ewing Sarcoma, with a particular focus on the cross-talk between p53 and the EWS-FLI1 gene rearrangement frequently associated with this disease. The development of several activators of p53 is discussed, with recent evidence demonstrating the potential of small molecule p53 activators as a promising systemic therapeutic approach for the treatment of Ewing Sarcomas with wild-type p53.Paul M. Neilsen, Kathleen I. Pishas, David F. Callen and David M. Thoma
Modeling the effects of aircraft flight track variability on community noise exposure
No full textThesis: S.M., Massachusetts Institute of Technology, Department of Aeronautics and Astronautics, 2017.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.Cataloged from student-submitted PDF version of thesis.Includes bibliographical references (pages 119-121).The implementation of Performance Based Navigation (PBN) routes across the National Airspace System (NAS) has caused a significant concentration of flight tracks. This flight track concentration also creates a concentration of noise impacts on the communities surrounding airports, which has led to an increase in noise complaints at many airports that have implemented these routes. In order to understand these changes in noise, and to design procedures that could help mitigate any negative effects, it is important to have modeling tools capable of capturing the noise impacts of flight track variability. This thesis develops a model for this purpose. First, twenty days of radar flight trajectory data from 2015 and 2016 at Boston Logan International Airport (KBOS) is used to quantify the observed distributions of variability in speed, altitude, and lateral track position. It is shown that altitude and speed variability have relatively small impacts on noise, but that the impacts of observed lateral variability are significant. Using this information, a physics-based model is developed to capture the noise impacts of lateral flight track variability. This tool is then used to model several example scenarios. First, the changes in noise due to pre- and post-PBN procedures are examined for KBOS Runway 33L departures. Next, a hypothetical procedure is designed to intentionally introduce lateral dispersion to KBOS Runway 33L departures. Finally, the tool is used to rapidly model noise impacts on due to both arrival and departure operations on all runways at KBOS. The model is shown to reduce computational expense by 1-2 order of magnitude relative to traditional methods. The results of these example analyses show that increased lateral dispersion causes a significant noise reduction at higher noise levels directly below the flight track at the cost of wider contours at lower noise levels. Because of this, any decision to add or remove flight track lateral dispersion has highly localized impacts that depend on the geometry of the route and the population of the surrounding area, and thus must be closely analyzed on an individual basis.This work was sponsored by the FAA under ASCENT Center of Excellence Project 23, Cooperative Agreement 13-C-AJFE-MIT-008.by Callen T. Brooks.S.M
A template-based approach to inhibitors of calpain 2, 20S proteasome, and HIV-1 protease
No full textArticle first published online: 15 OCT 2013Specificity counts: A template-based approach to protease inhibitors is presented using a core macrocycle that presents a generic β-strand template for binding to protease active sites. This is then specifically functionalized at P2 , and the C and N termini to give inhibitors of calpain 2, 20S proteasome, and HIV-1 protease.Seth A. Jones, Paul M. Neilsen, Limei Siew, David F. Callen, Nathan E. Goldfarb, Ben M. Dunn, and Andrew D. Abel
Abstract P4-05-02: Conditional inactivation of the 25-hydroxyvitamin D-24-hydroxylase (Cyp24a1) in the mouse mammary epithelium alters mammary gland development
No full textAbstract
The biologically active form of vitamin D (1,25(OH)2D) regulates proliferation, differentiation, and apoptosis in diverse cell types. We have previously identified anti-proliferative activities of 1,25(OH)2D in human breast tissue, as well as 1,25(OH)2D target gene expression consistent with reports that elevated vitamin D levels may protect against cancer. In mouse studies, vitamin D signaling modulates normal mammary gland development, including ductal outgrowth and branching, and protects against tumorigenesis. Degradation of 1,25(OH)2D is initiated by the enzyme Cyp24a1 in target tissues, providing critical local control of 1,25(OH)2D bioactivity. In vitro, blockade of Cyp24a1 activity potentiates the anti-proliferative effects of 1,25(OH)2D. However, the extent to which endogenous Cyp24a1 activity within the mammary epithelium regulates local 1,25(OH)2D levels to modulate normal mammary gland development, with possible implications for cancer, has not been investigated. We generated a novel mouse model with conditional knockout of the Cyp24a1 gene specifically in the mammary epithelium (MMTV-Cre x Cyp24a1lox/lox). Ablation of Cyp24a1 activity in the mammary epithelium does not alter either gland or body weight at 4, 6 or 10 weeks of age. Preliminary analyses of mammary gland whole mounts indicate that virgin knockout mice form fewer terminal end buds compared to glands from wild-type littermates at 4 and 6 weeks of age (P<0.05). Moreover, the width of the ducts proximal to the central lymph node of knockout mice was less than that of wild-type mice at 4 and 10 weeks of age (P<0.05 and P<0.01, respectively). In addition, the number of secondary and tertiary branching points is reduced in mammary glands from knockout mice at 6 weeks of age (P<0.05 and P<0.01, respectively). In summary, our findings suggest that Cyp24a1 activity within epithelial cells plays a crucial role to modulate postnatal mammary gland development, presumably by limiting the local accumulation of 1,25(OH)2D.
Citation Format: Sheng L, Turner AG, Tarulli GA, Barratt K, Kremer R, Morris HA, Callen DF, Anderson PH. Conditional inactivation of the 25-hydroxyvitamin D-24-hydroxylase (Cyp24a1) in the mouse mammary epithelium alters mammary gland development [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-05-02.</jats:p
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