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19 results on '"Stem cells--Research"'

1. Use of stem cell-derived macrophages and gene editing to investigate viral pathology and innate immunity

Author

Vaughan-Jackson, Alun and James, William

Subjects
Immunology, Stem cells--Research, HIV (Viruses)
Abstract

Induced Pluripotent Stem Cell (iPSC)-derived macrophages are a rapidly emerging model of tissue resident macrophages for investigating human disease. As potentially infinitely replicating cells, iPSC lend themselves for genetic manipulation by CRISPR-Cas9 editing before terminal differentiation into a vast array of cell types. As such, long standing challenges in exploration of macrophage gene functions during inflammatory diseases and infections, such as HIV-1, caused by donor variability and immortalised cell line deficiencies can finally be overcome. With over 30 different protocols for macrophage differentiation from iPSC now described, culturing of these cells is gradually becoming more accessible to researchers, and essential processes for differentiation better understood. However, with this progress comes the ever-greater need for clear definition of culturing conditions of these cells, so that we can compare results between methodologies, and eliminate undesirable sources of variability. This thesis sought to capitalise on this new system to explore the complicated and often contradictory role of TRIM5α in HIV-1 infection, and to explore with a precision only achievable through CRISPR-Cas9 genome editing the function of the cyclophilin family of peptidyl-prolyl isomerases. I demonstrate protection of HIV-1 from TRIM5α restriction by cyclophilin A, as well as regulation of the innate immune inflammatory response more generally by the cyclophilin family. However, prior to exploring this, this thesis sets out to address some of current issues in iPSC-derived macrophage culture and the ill-defined components of growth media and cellular environment. I describe a new macrophage differentiation medium using serum free, defined, and open-sourced components to bring needed transparency into the field. I also address the variability in macrophage phenotype and function brought about by the fundamental, but largely overlooked, impact of cell crowding in ex vivo culture. This revealed evidence for a potential plating density-dependent anti-inflammatory feedback loop relevant for human diseases like Alzheimer's disease.

Published
2021

2. Modelling monogenic diabetes mutations using authentic human beta cell models

Author

Duff, Claire, Honoré, Christian, Hansson, Mattias, Gloyn, Anna, and Hastoy, Benoit

Subjects
616.4, Diabetes, Insulin, Stem cells--Research, Pancreatic beta cells
Abstract

Genome-wide association studies have identified over 400 loci associated with risk for type 2 diabetes (T2D), a large proportion are associated with pancreatic islet dysfunction. The parallel emergence of genome editing technology such as CRISPR/Cas9, alongside the ability to derive endocrine pancreatic cells from human stem cells, provides unprecedented opportunity to investigate and examine the mechanisms that underpin beta cell dysfunction. Given that several monogenic genes are also associated with T2D risk, investigating the mechanisms by which beta cell dysfunction occurs in monogenic diabetes also presents the opportunity to gain additional insight into T2D pathogenesis. The aim of my thesis was to model monogenic diabetes variants in INS and HNF1A in human beta cell models using both genome-edited human induced pluripotent stem cells (hiPSCs) and EndoC-βH1 cells. To investigate the role of INS mutations on beta cell function, I generated the first p.C43G INS hiPSC line, including a reporter line, using CRISPR/Cas9 editing and differentiated these cells along the pancreatic endocrine lineage. Gene expression analysis revealed no influence of the p.C43G mutation on either differentiation efficiency or ER stress, reflecting that differentiated hiPSCs may require further functional maturation in order to model INS-associated monogenic diabetes. Expression of the p.C43G INS mutant in the recently generated INS-KO EndoC-βH1 line was appropriately packaged into secretory vesicles. Subsequent gene expression and RNA-Seq analysis showed no significant differences between cells transfected with either the wildtype or p.C43G construct, echoing the findings from hiPSC differentiations. This would suggest that the negative effect of the mutation might translate through different cellular mechanisms. However, this study revealed various technical challenges, such as with transfection efficiency that considerably reduced the ability to fully characterise p.C43G expression in beta cells. Finally, I sought to investigate another gene involved in monogenic diabetes, HNF1A. As mouse models of HNF1A-diabetes do not fully recapitulate the human phenotype, I utilised a hiPSC line to characterise HNF1A knockout in parallel with a knockdown (KD) model of HNF1A within the EndoC-βH1 cell line. Loss of HNF1A led to decreased expression of insulin and glucagon at the final stage of differentiation. The HNF1A KO line, in comparison to the wildtype line, had an enrichment of differentially expressed genes involved in regulation of beta cell function, beta cell development and insulin secretion, recapitulating several features of the patient phenotype. Further comparisons with differentiated cells from a patient with an HNF1A-MODY causing variant and with my HNF1A KD EndoC-βH1 data, showed a significant overlap between the datasets demonstrating that many of the same gene signatures can be captured between different cellular models of HNF1A. My thesis illustrates the complementarity of utilising both iPSCs and EndoC-βH1 for disease modelling with each addressing different aspects of diabetes pathogenesis. This approach, although still being optimised, provides a better understanding of the cellular physiology that underlies genetic predisposition for diabetes.

Published
2020

3. Use of stem cell-derived macrophages and gene editing to investigate viral pathology and innate immunity

Author

Vaughan-Jackson, A and James, W

Subjects
HIV (Viruses), Immunology, Stem cells--Research
Abstract

Induced Pluripotent Stem Cell (iPSC)-derived macrophages are a rapidly emerging model of tissue resident macrophages for investigating human disease. As potentially infinitely replicating cells, iPSC lend themselves for genetic manipulation by CRISPR-Cas9 editing before terminal differentiation into a vast array of cell types. As such, long standing challenges in exploration of macrophage gene functions during inflammatory diseases and infections, such as HIV-1, caused by donor variability and immortalised cell line deficiencies can finally be overcome. With over 30 different protocols for macrophage differentiation from iPSC now described, culturing of these cells is gradually becoming more accessible to researchers, and essential processes for differentiation better understood. However, with this progress comes the ever-greater need for clear definition of culturing conditions of these cells, so that we can compare results between methodologies, and eliminate undesirable sources of variability. This thesis sought to capitalise on this new system to explore the complicated and often contradictory role of TRIM5α in HIV-1 infection, and to explore with a precision only achievable through CRISPR-Cas9 genome editing the function of the cyclophilin family of peptidyl-prolyl isomerases. I demonstrate protection of HIV-1 from TRIM5α restriction by cyclophilin A, as well as regulation of the innate immune inflammatory response more generally by the cyclophilin family. However, prior to exploring this, this thesis sets out to address some of current issues in iPSC-derived macrophage culture and the ill-defined components of growth media and cellular environment. I describe a new macrophage differentiation medium using serum free, defined, and open-sourced components to bring needed transparency into the field. I also address the variability in macrophage phenotype and function brought about by the fundamental, but largely overlooked, impact of cell crowding in ex vivo culture. This revealed evidence for a potential plating density-dependent anti-inflammatory feedback loop relevant for human diseases like Alzheimer’s disease.

Published
2021

4. Modelling monogenic diabetes mutations using authentic human beta cell models

Author

Duff, C, Hastoy, B, Gloyn, A, Honoré, C, and Hansson, M

Subjects
Diabetes, Stem cells--Research, Insulin, Pancreatic beta cells
Abstract

Genome-wide association studies have identified over 400 loci associated with risk for type 2 diabetes (T2D), a large proportion are associated with pancreatic islet dysfunction. The parallel emergence of genome editing technology such as CRISPR/Cas9, alongside the ability to derive endocrine pancreatic cells from human stem cells, provides unprecedented opportunity to investigate and examine the mechanisms that underpin beta cell dysfunction. Given that several monogenic genes are also associated with T2D risk, investigating the mechanisms by which beta cell dysfunction occurs in monogenic diabetes also presents the opportunity to gain additional insight into T2D pathogenesis. The aim of my thesis was to model monogenic diabetes variants in INS and HNF1A in human beta cell models using both genome-edited human induced pluripotent stem cells (hiPSCs) and EndoC-βH1 cells. To investigate the role of INS mutations on beta cell function, I generated the first p.C43G INS hiPSC line, including a reporter line, using CRISPR/Cas9 editing and differentiated these cells along the pancreatic endocrine lineage. Gene expression analysis revealed no influence of the p.C43G mutation on either differentiation efficiency or ER stress, reflecting that differentiated hiPSCs may require further functional maturation in order to model INS-associated monogenic diabetes. Expression of the p.C43G INS mutant in the recently generated INS-KO EndoC-βH1 line was appropriately packaged into secretory vesicles. Subsequent gene expression and RNA-Seq analysis showed no significant differences between cells transfected with either the wildtype or p.C43G construct, echoing the findings from hiPSC differentiations. This would suggest that the negative effect of the mutation might translate through different cellular mechanisms. However, this study revealed various technical challenges, such as with transfection efficiency that considerably reduced the ability to fully characterise p.C43G expression in beta cells. Finally, I sought to investigate another gene involved in monogenic diabetes, HNF1A. As mouse models of HNF1A-diabetes do not fully recapitulate the human phenotype, I utilised a hiPSC line to characterise HNF1A knockout in parallel with a knockdown (KD) model of HNF1A within the EndoC-βH1 cell line. Loss of HNF1A led to decreased expression of insulin and glucagon at the final stage of differentiation. The HNF1A KO line, in comparison to the wildtype line, had an enrichment of differentially expressed genes involved in regulation of beta cell function, beta cell development and insulin secretion, recapitulating several features of the patient phenotype. Further comparisons with differentiated cells from a patient with an HNF1A-MODY causing variant and with my HNF1A KD EndoC-βH1 data, showed a significant overlap between the datasets demonstrating that many of the same gene signatures can be captured between different cellular models of HNF1A. My thesis illustrates the complementarity of utilising both iPSCs and EndoC-βH1 for disease modelling with each addressing different aspects of diabetes pathogenesis. This approach, although still being optimised, provides a better understanding of the cellular physiology that underlies genetic predisposition for diabetes.

Published
2021

6. A qualitative study to identify an appropriate regulatory framework for human stem cell research in Malaysia

Author

Bin Abdul Aziz, M, Kaye, J, and Morrison, M

Subjects
Embryonic stem cells--Research, Stem cells--Research--Law and legislation, Stem cells--Research, Stem cells--Research--Moral and ethical aspects
Abstract

Human stem cell research (hSCR) is known as the future of medical intervention of the 21st century. It is one of the most rapidly progressing emerging technologies in the areas of science, with promising and potential benefits to develop therapy to cure many degenerative diseases that are incurable by the conventional medical procedures. Notwithstanding its importance, this field is rather controversial and ethically contentious as well as legally challenging. Malaysia is among the countries that recognise the importance of this technology. However, its current regulatory system does not seem adequate to ensure ethical compliance. In the light of this situation, one would question as to what would be the appropriate and suitable regulatory approach to this matter? What ought to be done to ensure this area progresses in an ethical fashion? This thesis was carried out with an aim to examine the regulatory landscape of this area, by looking at the roles and techniques of regulation and its application in hSCR arena across the globe, with a focus on Commonwealth countries. An empirical study was also undertaken, using qualitative interview methods, to find out more about Malaysia's system. The empirical findings obtained, supported by the comparative analysis between Malaysia's system and of other jurisdictions, suggest that Malaysia's framework is lacking of important regulatory measures that are necessary to secure compliance. This thesis concluded that to achieve an optimal regulatory outcome, the framework would require some improvements by adopting a combination of different regulatory techniques and strengthening its rules enforcement strategies. In addition, there are regulatory options have been identified to improve the current framework including legal transplants, however, there are challenges that need to be recognised.

Published
2016

7. Characterization of cancer stem cells in hepatocellular carcinoma

Author

Abdüsselamoğlu, Merve Deniz, Gürsel, İhsan, Öztürk, Mehmet, and Moleküler Biyoloji ve Genetik Anabilim Dalı

Subjects
cancer stem cells, Moleküler Tıp, Stem cells--Research, FGFR, Liver--Cancer, WI735 .A23 2014, hepatocellular carcinoma, digestive system diseases, Wnt, TGF- B, EpCAM, Cancer cells, Molecular Medicine, CD133, Biology, Carcinoma, Hepatocellular, Biyoloji
Abstract

Hepatosellüler karsinom (HSK) teşhis ve tedavi sürecindeki sıkıntılardan dolayı, dünyada, kansere bağlı ölümlerde ilk üç sırada yer almaktadır. Yapılan son çalışmalara göre, HSK tümörleri, diğer birçok solid tümör gibi, `kanser kök hücreleri (KKH)` ya da ` kanser başlatan hücreler (KBH)` olarak adlandırılan hücreler tarafından başlatılır ve tümörün devamlılığı bu hücrelere bağlıdır. HSK kök hücreleri bazı CD markörlerinin ifadesi ile tanınabilir, CD133 (Prominin-1) ve EpCAM de bu markörlerden biridir. Bu çalışma genel olarak, HSK kök hücrelerinin oluşmasında yer alan mekanizmaları, 15 adet HSK hücre hattından oluşan bir panelde incelemeye odaklanmıştır. Ön çalışmalarımız, akış sitometresi deneylerinde, sadece dört hücre hattının (27%), 8-90% olarak değişen oranlarda CD133+ kök hücre topluluğuna sahip olduğunu göstermiştir. Bu CD133 pozitif hücre hatları arasında iki izojenik hücre hattı, farklı pozitivite seviyeleri nedeniyle odaklanılmıştır,, i) parental hücre hattı HepG2 ve hepatit B virüsünün (HBV) dört kopyasıyla transfekte edilmiş olan klonu, ii) HepG2-2215. Atymic çıplak farelerde yapılan tümör gelişimini deneyi ile yüksek CD133+ hücre oranına sahip HepG2-2215, daha az CD133+ hücre sayısına sahip HepG2'den daha hızlı ve çabuk tümör oluşumu göstermiştir. Mikro-dizi analizi yapılarak bu hücre hatlarının CD133 + hücre sayıları farkı altında yatan mekanizmalarını keşfetmek amaçlanmıştır. İlk bulgularımız FGFR sinyal yolağının role sahip olabileceğini düşündürmektedir. Bu bulguları test etmek için FGFR yolağı güçlü bir inhibitör ve siRNA muamelesi ile susturulmuştur. Ancak, ilk veriler bu düşüncelerimizi desteklememiştir. Bu yüzden HSK'da FGRF yolağı ve KKH oluşumu arasındaki ilişkiyi netleştirmek için başka çalışmalara ihtiyaç vardır. Ayrıca, DNA güdümlü immün uyarıcı etkileri susturan, baskılayıcı oligodeoxynucleotide (ODN) rolü DNA çalışılmıştır. Bulgular baskılayıcı ODN muamelesinin CD133 oranlarını düşürdüğünü göstermiş. Sonuçlar, bu iki hücre hattının farklı CD133 positivite oranlarına sahip olmasının sebebinin HepG2-2215 hücre hattının HBV transfekte olup, HBV partikül oluşturmasından dolayı olabileceğine işaret etmiştir. Ancak, HSK'daki KKH nüfusu ile HBV ilişkisini anlamak için daha fazla araştırma gereklidir. Hepatocellular carcinoma (HCC) is the third most common cause of death from cancer worldwide due to the challenges in both its diagnosis and treatment. According to recent studies, HCC tumors, like many other solid tumors are initiated and maintained by a subpopulation of cells called `cancer stem cells (CSCs)` or `tumor-initiating cells (TICs)`. HCC stem cells can be identified by the expression of cardinal CD markers such as CD133 (Prominin-1) and epithelial cell adhesion molecule (EpCAM). This study primarily focuses on the investigation of mechanisms involved in the generation of HCC stem cell sub-population using a panel of 15 HCC cell lines. Preliminary data indicates that four cell lines (27%) display CD133+ stem cell populations at frequencies ranging from 8 to 90% when tested by flow cytometry. Among these CD133 positive cell lines, two isogenic cell line with different positivity levels prompted us to focus on two specific cell lines;, i) parental HepG2 cell line and its clone, which was transfected with four copies of hepatitis B virus (HBV), namely ii) HepG2-2215. With tumorigenicity assay induced in atymic nude mice, data revealed that HepG2-2215 that had higher CD133+ ratio, showed higher and rapid tumor formation than parental HepG2 that had much lower CD133+ sub-cellular proportion. Microarray analyses were performed to underpin the mechanisms of in CD133+ cell number variations of these two cell lines. Our initial findings suggested that FGFR signaling pathway might have played a role. To investigate these findings, FGFR signaling pathway was inhibited via potent inhibitor as well as knock down with siRNA. However, preliminary data did not indicate these presumptions and further studies are needed to clarify the relationship between FGFR signaling and CSC formation in HCC. Also, role of suppressive oligodeoxynucleotide (ODN) was studied to see the effects of suppression of DNA-driven immunostimulation. Findings showed that suppressive ODN decreased CD133 levels, which indicates the difference between these two cell lines may arise from the HBV transfection of HepG2-2215 cell line which can produce HBV particles. However, further investigation is needed to understand the relationship between HBV infection and CSC population in HCC. 111

Published
2014

8. Religion, Partisanship, and Attitudes Toward Science Policy

Author

Jelen, Ted G., Lockett, Linda A., Jelen, Ted G., and Lockett, Linda A.

Abstract

We examine issues involving science which have been contested in recent public debate. These “contested science” issues include human evolution, stem-cell research, and climate change. We find that few respondents evince consistently skeptical attitudes toward science issues, and that religious variables are generally strong predictors of attitudes toward individual issues. Furthermore, and contrary to analyses of elite discourse, partisan identification is not generally predictive of attitudes toward contested scientific issues.

Published
2014

9. The developmental potential of adult mouse hair bulge stem cells.

Author

Wong, Wai Chung., Chinese University of Hong Kong Graduate School. Division of Anatomy., Wong, Wai Chung., and Chinese University of Hong Kong Graduate School. Division of Anatomy.

Abstract

Wong, Wai Chung., Thesis (M.Phil.)--Chinese University of Hong Kong, 2008., Includes bibliographical references (leaves 113-130)., s in English and Chinese., Thesis/Assessment Committee --- p.i, p.ii, 中文摘要 --- p.iv, Acknowledgements --- p.vi, List of Figures --- p.vii, List of Tables --- p.ix, Table of Abbreviations --- p.x, Contents --- p.xv, Chapter Chapter I --- Introduction, Chapter 1.1 --- Stem cells --- p.1, Chapter 1.1.1 --- Embryonic stem cells --- p.2, Chapter 1.1.2 --- Adult stem cells --- p.2, Chapter 1.1.3 --- Artificial stem cells --- p.5, Chapter 1.2 --- Hair bulge stem cells (HBSC) --- p.7, Chapter 1.2.1 --- Hair follicle --- p.7, Chapter 1.2.2 --- The discovery of hair bulge stem cells --- p.9, Chapter 1.2.3 --- The hair bulge niche --- p.10, Chapter 1.2.4 --- Molecular markers --- p.12, Chapter 1.2.5 --- Physiological roles of bulge stem cells --- p.13, Chapter 1.2.6 --- Pathological roles of bulge stem cells --- p.15, Chapter 1.2.7 --- Developmental plasticity of bulge stem cells --- p.16, Chapter 1.3 --- "Regulation of adipogenic, osteogenic and cardiogenic differentiation" --- p.17, Chapter 1.3.1 --- Regulation of adipogenic differentiation --- p.17, Chapter 1.3.2 --- Regulation of osteogenic differentiation --- p.18, Chapter 1.3.3 --- Regulation of cardiogenic differentiation --- p.19, Chapter 1.4 --- Proteomics --- p.23, Chapter 1.4.1 --- Definition of proteomics --- p.23, Chapter 1.4.2 --- Two-dimensional gel electrophoresis (2DGE) --- p.25, Chapter 1.4.3 --- Mass spectrometry and protein identification --- p.29, Chapter 1.4.4 --- Other techniques associated with proteomics --- p.34, Chapter 1.4.5 --- Proteomics and stem cells --- p.36, Chapter 1.5 --- General summary --- p.37, Chapter 1.6 --- Aims of my study --- p.38, Chapter Chapter II --- Materials and Methods, Chapter 2.1 --- Animals --- p.39, Chapter 2.2 --- Immunohistochemistry --- p.39, Chapter 2.2.1 --- Histology --- p.39, Chapter 2.2.2 --- Immunohistochemistry --- p.40, Chapter 2.3 --- Establishment of hair bulge CD34+ stem cell line --- p.41, Chapter 2.3.1 --- Isolation of hair bulge explants --- p.41, Chapter 2.3.2 --- Establishing hair bulge primary cultured cells --- p.42, Chapter 2.3.3 --- Purification of hair bulge stem cells --- p.43, Chapter 2.4 --- Karyotyping --- p.45, Chapter 2.5 --- In vitro differentiation --- p.46, Chapter 2.5.1 --- Adipogenic differentiation --- p.46, Chapter 2.5.2 --- Osteogenic differentiation --- p.47, Chapter 2.5.3 --- Cardiogenic differentiation --- p.48, Chapter 2.6 --- Proteomic analysis --- p.48, Chapter 2.6.1 --- Sample preparation --- p.48, Chapter 2.6.2 --- Quantification of proteins --- p.49, Chapter 2.6.3 --- First-dimensional separation of proteins 226}0ؤ isoelectric focusing (IEF) --- p.50, Chapter 2.6.4 --- Second-dimensional separation - sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) --- p.51, Chapter 2.6.5 --- "Silver staining, imaging and destaining" --- p.52, Chapter 2.6.6 --- In-gel digestion and matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry analysis --- p.53, Chapter 2.7 --- Histochemistry --- p.54, Chapter 2.7.1 --- Oil Red O staining --- p.54, Chapter 2.7.2 --- Alizarin Red S staining --- p.55, Chapter 2.8 --- Immunocytochemistry --- p.56, Chapter 2.9 --- Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) --- p.57, Chapter 2.9.1 --- Isolation of total cellular RNA --- p.57, Chapter 2.9.2 --- Complementary DNA (cDNA) synthesis --- p.58, Chapter 2.9.3 --- Polymerase chain reaction and agarose gel electrophoresis --- p.59, Chapter 2.10 --- Western blot analysis --- p.62, Chapter 2.10.1 --- Sample preparation and quantification of proteins --- p.62, Chapter 2.10.2 --- SDS-PAGE --- p.63, Chapter 2.10.3 --- Protein transfer --- p.64, Chapter 2.10.4 --- Immunodetection --- p.65, Chapter 2.11 --- Cell proliferation assay --- p.66, Chapter 2.11.1 --- Determination of growth pattern --- p.66, Chapter 2.11.2 --- MTT assay --- p.66, Chapter 2.12 --- Ultrastructural analysis --- p.67, Chapter 2.12.1 --- Scanning electron microscopy (SEM) --- p.67, Chapter 2.12.2 --- Transmission electron microscopy (TEM) --- p.68, Chapter 2.13 --- Statistical analysis --- p.68, Chapter Chapter III --- Results, Chapter 3.1 --- Isolation and characterization hair bulge stem cells --- p.69, Chapter 3.2 --- Directed adipogenic differentiation --- p.70, Chapter 3.3 --- Directed osteogenic differentiation --- p.71, Chapter 3.4 --- Ability of cardiogenol C to induce cardiogenesis in HBSCs --- p.71, Chapter 3.5 --- Comparative proteomic analysis of HBSC cardiogenic differentiation induced by cardiogenol C --- p.72, Chapter 3.6 --- Role of Wnt signaling pathway in cardiogenol C-induced cardiogenesis --- p.74, Chapter 3.7 --- Role of chromatin remodeling in cardiogenol C-induced cardiogenesis --- p.75, Chapter 3.8 --- Legends and tables --- p.76, Chapter Chapter IV --- Discussion --- p.98, References --- p.113, Appendices --- p.131, Publication --- p.134, http://library.cuhk.edu.hk/record=b5896804, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Published
2008

10. Empire State Stem Cell Board Archived Websites B2100

Subjects
Hematopoietic stem cells, Stem cells--Research, Embryonic stem cells--Research
Abstract

This series consists of archival copies of the publicly accessible websites of the Empire State Stem Cell Board, which was established in 2007 to support stem cell research in New York State and is headed by the Commissioner of the State Department of Health.

Published
2008

14. Stem Cell Press Conference

Author

Darden, Tom and Darden, Tom

Abstract

Photograph from the Stem Cell Press Conference on July 6, 2006.

Published
2006

16. Fresh Air with Terry Gross, April 13, 2005: Interview with Gareth Cook; Interview with Musa Mayer.

Author

Cook, Gareth, 1969, Mayer, Musa, WHYY Public Media, Miller, Danny (Radio producer), Gross, Terry, Cook, Gareth, 1969, Mayer, Musa, WHYY Public Media, Miller, Danny (Radio producer), and Gross, Terry

Abstract

Since its national debut in 1987, Fresh Air with Terry Gross has been a highly acclaimed and much adored weekday magazine among public radio listeners. Each week, nearly 4.8 million people turn to Peabody Award-winning host Terry Gross for insightful conversations with the leading voices in contemporary arts and issues. The renowned program reaches a global audience, with over 620 public radio stations broadcasting Fresh Air, and 3 million podcast downloads each week. Fresh Air has broken the mold of 'talk show' by weaving together superior journalism and intimate storytelling from modern-day intellectuals, politicians and artists alike. Through probing questions and careful research, Gross's interviews are lauded for revealing a fresh perspective on cultural icons and trends. Her thorough conversations are often complemented by commentary from well-known contributors. Fresh Air is produced at WHYY-FM in Philadelphia and broadcast nationally by NPR., (1.) Journalist GARETH COOK covers science for the Boston Globe. Last week he won the 2005 Pulitzer Prize for explanatory journalism for his yearlong series of stories on stem cell research. The judges praised COOK's work for 'explaining, with clarity and humanity, the complex scientific and ethical dimensions of stem cell research.' (2.) Writer and patient advocate MUSA MAYER (MOO-sa MAY-er). She is a breast cancer survivor and is the author of several books about breast cancer, including: 'Advanced Breast Cancer: A Guide to Living with Metastatic Disease' (2nd edition, O'Reilly, 1998-this book is easier to get now than the others); 'After Breast Cancer: Answers to the Questions You're Afraid to Ask' (O'Reilly, 2003); 'Examining Myself: One Woman's Story of Breast Cancer Treatment and Recovery' (Faber & Faber). MAYER also has a website where some of the books may be available: advancedbc.org. (THIS INTERVIEW CONTINES THRU THE END OF THE SHOW).

Published
2005

17. Fresh Air with Terry Gross, July 22, 2004: Interview with Ro Reagan Jr.; Review of HBO television programs.

Author

Reagan, Ron, 1958, Powers, John, 1951, WHYY Public Media, Miller, Danny, Gross, Terry, Reagan, Ron, 1958, Powers, John, 1951, WHYY Public Media, Miller, Danny, and Gross, Terry

Abstract

Since its national debut in 1987, Fresh Air with Terry Gross has been a highly acclaimed and much adored weekday magazine among public radio listeners. Each week, nearly 4.8 million people turn to Peabody Award-winning host Terry Gross for insightful conversations with the leading voices in contemporary arts and issues. The renowned program reaches a global audience, with over 620 public radio stations broadcasting Fresh Air, and 3 million podcast downloads each week. Fresh Air has broken the mold of 'talk show' by weaving together superior journalism and intimate storytelling from modern-day intellectuals, politicians and artists alike. Through probing questions and careful research, Gross's interviews are lauded for revealing a fresh perspective on cultural icons and trends. Her thorough conversations are often complemented by commentary from well-known contributors. Fresh Air is produced at WHYY-FM in Philadelphia and broadcast nationally by NPR., (1.) RON REAGAN JR. the son of the late president Ronald Reagan. He's been invited to speak at the Democratic convention next week. He and his mother have become outspoken proponents of stem cell research, which puts them at odds with President Bush and much of the Republican party. REAGAN has edited the book, 'If You Had Five Minutes with the President.' (HarperCollins). (THIS INTERVIEW CONTINUES INTO THE SECOND HALF OF THE SHOW) (2.) Critic at large JOHN POWERS considers the programming on HBO.

Published
2004

18. Fresh Air with Terry Gross, October 11, 2004: Interview with Philip Roth; Obituary for Christopher Reeve.

Author

Roth, Philip, 1933, Reeve, Christopher, 1952-2004, WHYY Public Media, Miller, Danny (Radio producer), Gross, Terry, Roth, Philip, 1933, Reeve, Christopher, 1952-2004, WHYY Public Media, Miller, Danny (Radio producer), and Gross, Terry

Abstract

Since its national debut in 1987, Fresh Air with Terry Gross has been a highly acclaimed and much adored weekday magazine among public radio listeners. Each week, nearly 4.8 million people turn to Peabody Award-winning host Terry Gross for insightful conversations with the leading voices in contemporary arts and issues. The renowned program reaches a global audience, with over 620 public radio stations broadcasting Fresh Air, and 3 million podcast downloads each week. Fresh Air has broken the mold of 'talk show' by weaving together superior journalism and intimate storytelling from modern-day intellectuals, politicians and artists alike. Through probing questions and careful research, Gross's interviews are lauded for revealing a fresh perspective on cultural icons and trends. Her thorough conversations are often complemented by commentary from well-known contributors. Fresh Air is produced at WHYY-FM in Philadelphia and broadcast nationally by NPR., (1.) Pulitzer prize winning novelist PHILIP ROTH. His new book "The Plot Against America" (Houghton Mifflin) imagines a world in which Franklin D. Roosevelt loses the presidency to America's biggest hero and celebrity Charles Lindberg who forms alliances with Germany and Japan. His book "The Human Stain" won the PENN/Faulkner Award for Fiction and was made into a film. It was the third of a trilogy which includes his "American Pastoral" and "I Married a Communist". (2.) We remember actor CHRISTOPHER REEVE. He died yesterday of heart failure at the age of 52. Reeve is known for starring in the "Superman" film series (I,II,III and IV). A 1995 horseback riding accident left him paralyzed from the neck down. After the accident, he became a worldwide advocate for spinal cord research. In 2000, Reeve was able to move his index finger, and a specialized workout regimen made his legs and arms stronger. He also regained sensation in other parts of his body. His books include, "Nothing is Impossible: Reflections on a New Life," and "Still Me." (ORIGINAL BROADCAST: 9/30/02)

Published
2004

19. Fresh Air with Terry Gross, July 17, 2001; Interview with Arthur Caplan; Review of the new edition of Grove’s Dictionary of Music and Musicians.

Author

Caplan, Arthur L, Schwartz, Lloyd, 1941, WHYY Public Media, Miller, Danny (Radio producer), Gross, Terry, Caplan, Arthur L, Schwartz, Lloyd, 1941, WHYY Public Media, Miller, Danny (Radio producer), and Gross, Terry

Abstract

Since its national debut in 1987, Fresh Air with Terry Gross has been a highly acclaimed and much adored weekday magazine among public radio listeners. Each week, nearly 4.8 million people turn to Peabody Award-winning host Terry Gross for insightful conversations with the leading voices in contemporary arts and issues. The renowned program reaches a global audience, with over 620 public radio stations broadcasting Fresh Air, and 3 million podcast downloads each week. Fresh Air has broken the mold of 'talk show' by weaving together superior journalism and intimate storytelling from modern-day intellectuals, politicians and artists alike. Through probing questions and careful research, Gross's interviews are lauded for revealing a fresh perspective on cultural icons and trends. Her thorough conversations are often complemented by commentary from well-known contributors. Fresh Air is produced at WHYY-FM in Philadelphia and broadcast nationally by NPR., (1.) Biomedical ethicist ARTHUR CAPLAN, Ph.D. We talk about the news that human embryos are being grown by researchers doing stem cell research. Previously, the cells were harvested from aborted fetuses. The idea of fetal farming is quite controversial. Proponents cite the enormous potential for finding cures to cancer, Alzheimer's and diabetes. Opponents are aghast at the notion of using and destroying human life for the sole purpose of research. Caplan is the Director of the Center for Bioethics and Trustee Professor of Bioethics at the University of Pennsylvania. He is also a Professor of Molecular and Cellular Engineering and Professor of Philosophy. Caplan has written seven books on bioethical topics, including 'Ethics and Organ Transplants' and 'Am I My Brother's Keeper? The Ethical Frontiers of Biomedicine.' He's consulted for numerous government offices and is a frequent commentator in the national media.(2.) Classical music critic LLOYD SCHWARTZ reviews the New edition of Grove's Dictionary of Music and Musicians.

Published
2001

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