1,777,359 research outputs found
Rosemary Brown Award for Women.
Get PDFRosemary Brown Award for Women recognizes and honors a BC based woman or organization that promotes the values and ideals which Rosemary Brown championed during her lifetime
[News Clip: Rosemary]
No full textVideo footage from the WBAP-TV television station in Fort Worth, Texas, to accompany a news story about Rosemary O'Reilly organizing a teen fashion show in Dallas
Biography: Rosemary Avery
No full textBiography of
Rosemary Avery,
Professor,
Department of Policy Analysis and Managemen
An Investigation of Synaptic Dysfunction in Alzheimer’s Disease - Chapter 5 - Thresholding Macros
No full textAlzheimer’s disease (AD) is characterized by the presence of aggregates of amyloid beta (Aβ) in senile plaques and tau in neurofibrillary tangles, as well as marked neuron and synapse loss. Of these pathological changes, synapse loss correlates most strongly with cognitive decline. Understanding the contributions of different risk factors, toxic proteins, and protein networks to synaptic dysfunction is essential to understanding and one day curing this disease.
Oligomeric species of Aβ are implicated in synapse loss as is tau, however the interaction between them requires further exploration. The first aim of this thesis was to investigate the interaction of Aβ and tau in a novel mouse model AD. In this model APP/PS1 mice were crossed with mice expressing full length wild type human tau (hTau). Expression of hTau in APP/PS1 mice increased plaque size by~50% and increased plaque-associated dystrophic neurites. However, no increase in neurite curvature, neuron loss, or synapse loss was observed in the hTau APP/PS1 animals compared with APP/PS1 alone.
The underlying cause of most cases of AD is not known, however genetic risk factors have been identified, the strongest of which is the APOE ε4 allele. APOE ε4 is associated with increased risk of developing AD and increased rates of cognitive decline compared to the more common APOE ε3 allele. The second aim of this thesis was to detect differences in the AD synaptic proteome compared with controls and to also investigate the effect of an APOE ε4 allele on those changes. Unbiased label free LC-MS/MS based proteomics of synapses isolated from AD and control post-mortem brains of known APOE genotypes was used. Of the 1043 proteins detected in 20 synaptic preparations 17% (173) were found to differ significantly (p1.2) in AD compared with control. A significant sub-set of these proteins were affected by APOE ε4 allele genotype. One of these was Clusterin which was not only increased in the AD synapse but further increased in cases with an APOE ε4 allele. Clusterin is closely related to ApoE has also been genetically linked to AD in genome-wide association studies.
Aim three was to further investigate the involvement of Clusterin at the synapse and the interaction of ApoE with Clusterin using array tomography. Array tomography confirmed an increase in Clusterin co-localization with presynapses and postsynapses in AD cases compared with controls and found a further increase in cases with an APOE ε4 allele. Array tomography also found an increase in synapses which co-localized with Clusterin and Aβ together in cases with an APOE ε4 allele. This implies that Clusterin is important in Aβ mediated synapse loss in AD.
To further investigate the role of synapse loss in AD aim 4 of this thesis was to develop a novel human based model of Aβ mediated synapse loss. This model uses cortical neurons derived from induced pluripotent stem cells from a control individual that are challenged with Aβ extracted from brains from AD and control individuals. This model shows a significant and concentration dependent reduction in the number of synapses in response Aβ from AD brain but not to control brain extract or AD brain extract immunodepleted of Aβ.
The work presented in this thesis has investigated two novel models of AD to assess the effect of known toxic proteins in AD related synapse degeneration. This work also shows that profound protein changes occur at the synapse in AD and that many of these are affected by APOE genotype. Many of these changes potentially cause or contribute to synaptic dysfunction in AD and therefore could be important for therapeutic interventions
No. 664 Rosemary Gray
No full textTranscript (26 pages) of an interview by Anne Peterson with Rosemary Gray on 7 September 2011. Part of the University Oral History Project, Everett Cooley Collection tape no. U-3076Rosemary Gray was born in Tynemouth on the northeast corner of England. Her parents, who were avid bird watchers, spent a lot of time gardening and taking her and her brother out into the nature of northern England. This is where she developed a passion for science and nature. Rosemary´s family then moved to Cincinnati, Ohio when she was nine, then moved back to England for two years, then back to Cincinnati for two years, and then to Mexico City. She attended high school in Cincinnati and Mexico City. In Ohio she had a great biology teacher who facilitated her skills as a blossoming biologist.She earned her Masters in biology at Texas A and M and went to the University of North Carolina to finish her PhD. She worked as a researcher and taught in a minority advancement program. After she had her first child, Rosemary decided she would be able to raise her daughter more easily if she were a teacher because research takes up so much time. She took a job at the University of Utah, and her family moved to Utah. She was hired to be the director of the Bioscience Undergraduate Research Program, but because of another teacher´s accident she was asked to teach biology for the ACCESS Program.The ACCESS Program is a seven week program during the summer designed to help gifted high school girls transition from high school to university. Rosemary loves being able to watch these students develop from high school through their first year of college. She´s able to give them advice about classes, careers, and help them decide what path they want to take.It´s important for Rosemary to help young women have access to scientific study because she believes there is less opportunity for women than for men. This has changed since she started, but there is still work to be done to allow young women more opportunity to have careers in the sciences. She feels she is doing her part to bring about that equality for women. Rosemary describes the details of the ACCESS Program - what the students do, the benefits it creates for their future, the networking and job opportunities it presents young women. It guides students through university and beyond: students learn to apply for jobs and how to write personal statements and resumes, etc. She provides examples of what students have researched and what they´ve gone on to do after taking part in the ACCESS Program. Project: University Oral History Project. Interviewer: Anne Peterson
An Investigation of Synaptic Dysfunction in Alzheimer’s Disease - Chapter 5 - Matlab Scripts
No full textAlzheimer’s disease (AD) is characterized by the presence of aggregates of amyloid beta (Aβ) in senile plaques and tau in neurofibrillary tangles, as well as marked neuron and synapse loss. Of these pathological changes, synapse loss correlates most strongly with cognitive decline. Understanding the contributions of different risk factors, toxic proteins, and protein networks to synaptic dysfunction is essential to understanding and one day curing this disease.
Oligomeric species of Aβ are implicated in synapse loss as is tau, however the interaction between them requires further exploration. The first aim of this thesis was to investigate the interaction of Aβ and tau in a novel mouse model AD. In this model APP/PS1 mice were crossed with mice expressing full length wild type human tau (hTau). Expression of hTau in APP/PS1 mice increased plaque size by~50% and increased plaque-associated dystrophic neurites. However, no increase in neurite curvature, neuron loss, or synapse loss was observed in the hTau APP/PS1 animals compared with APP/PS1 alone.
The underlying cause of most cases of AD is not known, however genetic risk factors have been identified, the strongest of which is the APOE ε4 allele. APOE ε4 is associated with increased risk of developing AD and increased rates of cognitive decline compared to the more common APOE ε3 allele. The second aim of this thesis was to detect differences in the AD synaptic proteome compared with controls and to also investigate the effect of an APOE ε4 allele on those changes. Unbiased label free LC-MS/MS based proteomics of synapses isolated from AD and control post-mortem brains of known APOE genotypes was used. Of the 1043 proteins detected in 20 synaptic preparations 17% (173) were found to differ significantly (p1.2) in AD compared with control. A significant sub-set of these proteins were affected by APOE ε4 allele genotype. One of these was Clusterin which was not only increased in the AD synapse but further increased in cases with an APOE ε4 allele. Clusterin is closely related to ApoE has also been genetically linked to AD in genome-wide association studies.
Aim three was to further investigate the involvement of Clusterin at the synapse and the interaction of ApoE with Clusterin using array tomography. Array tomography confirmed an increase in Clusterin co-localization with presynapses and postsynapses in AD cases compared with controls and found a further increase in cases with an APOE ε4 allele. Array tomography also found an increase in synapses which co-localized with Clusterin and Aβ together in cases with an APOE ε4 allele. This implies that Clusterin is important in Aβ mediated synapse loss in AD.
To further investigate the role of synapse loss in AD aim 4 of this thesis was to develop a novel human based model of Aβ mediated synapse loss. This model uses cortical neurons derived from induced pluripotent stem cells from a control individual that are challenged with Aβ extracted from brains from AD and control individuals. This model shows a significant and concentration dependent reduction in the number of synapses in response Aβ from AD brain but not to control brain extract or AD brain extract immunodepleted of Aβ.
The work presented in this thesis has investigated two novel models of AD to assess the effect of known toxic proteins in AD related synapse degeneration. This work also shows that profound protein changes occur at the synapse in AD and that many of these are affected by APOE genotype. Many of these changes potentially cause or contribute to synaptic dysfunction in AD and therefore could be important for therapeutic interventions
Rosemary Stanton on ethical eating
No full textThere once was a time when what to have for dinner was a simple choice, decided by cost and availability. But no longer. In a world with increasingly diminishing resources, eating is now complicated by a range of social, environmental and agricultural concerns. Choosing our food is getting confusing, but here, talking at UTS in Sydney, nutritionist Rosemary Stanton gives some practical advice on ethical eating. She is joined by researcher Dana Cordell, who\u27s been studying the environmental implications of the decreasing supply of phosperous in Australia and the world. The event is chaired by Prof. Stuart White from UTS\u27s Institute for Sustainable Futures, and presented as part of the UTSpeaks Series.
Professor Stuart White has been researching sustainability for the last twenty years. In 1998 he was a member of the NSW Task Force on Water Conservation.
Dr Rosemary Stanton is a nutritionist and author of numerous books on the topic of healthy eating. She is also a member of the NSW Health Department\u27s Food Advisory Committee.
Dana Cordell is a senior researcher and doctoral student at the Institute for Sustainable Futures (ISF) at the University of Technology, Sydney. She is also co-founder of the Global Phosphorus Research Initiative.
 
An Investigation of Synaptic Dysfunction in Alzheimer’s Disease - Chapter 3 - Matlab Scripts
No full textAlzheimer’s disease (AD) is characterized by the presence of aggregates of amyloid beta (Aβ) in senile plaques and tau in neurofibrillary tangles, as well as marked neuron and synapse loss. Of these pathological changes, synapse loss correlates most strongly with cognitive decline. Understanding the contributions of different risk factors, toxic proteins, and protein networks to synaptic dysfunction is essential to understanding and one day curing this disease.
Oligomeric species of Aβ are implicated in synapse loss as is tau, however the interaction between them requires further exploration. The first aim of this thesis was to investigate the interaction of Aβ and tau in a novel mouse model AD. In this model APP/PS1 mice were crossed with mice expressing full length wild type human tau (hTau). Expression of hTau in APP/PS1 mice increased plaque size by~50% and increased plaque-associated dystrophic neurites. However, no increase in neurite curvature, neuron loss, or synapse loss was observed in the hTau APP/PS1 animals compared with APP/PS1 alone.
The underlying cause of most cases of AD is not known, however genetic risk factors have been identified, the strongest of which is the APOE ε4 allele. APOE ε4 is associated with increased risk of developing AD and increased rates of cognitive decline compared to the more common APOE ε3 allele. The second aim of this thesis was to detect differences in the AD synaptic proteome compared with controls and to also investigate the effect of an APOE ε4 allele on those changes. Unbiased label free LC-MS/MS based proteomics of synapses isolated from AD and control post-mortem brains of known APOE genotypes was used. Of the 1043 proteins detected in 20 synaptic preparations 17% (173) were found to differ significantly (p1.2) in AD compared with control. A significant sub-set of these proteins were affected by APOE ε4 allele genotype. One of these was Clusterin which was not only increased in the AD synapse but further increased in cases with an APOE ε4 allele. Clusterin is closely related to ApoE has also been genetically linked to AD in genome-wide association studies.
Aim three was to further investigate the involvement of Clusterin at the synapse and the interaction of ApoE with Clusterin using array tomography. Array tomography confirmed an increase in Clusterin co-localization with presynapses and postsynapses in AD cases compared with controls and found a further increase in cases with an APOE ε4 allele. Array tomography also found an increase in synapses which co-localized with Clusterin and Aβ together in cases with an APOE ε4 allele. This implies that Clusterin is important in Aβ mediated synapse loss in AD.
To further investigate the role of synapse loss in AD aim 4 of this thesis was to develop a novel human based model of Aβ mediated synapse loss. This model uses cortical neurons derived from induced pluripotent stem cells from a control individual that are challenged with Aβ extracted from brains from AD and control individuals. This model shows a significant and concentration dependent reduction in the number of synapses in response Aβ from AD brain but not to control brain extract or AD brain extract immunodepleted of Aβ.
The work presented in this thesis has investigated two novel models of AD to assess the effect of known toxic proteins in AD related synapse degeneration. This work also shows that profound protein changes occur at the synapse in AD and that many of these are affected by APOE genotype. Many of these changes potentially cause or contribute to synaptic dysfunction in AD and therefore could be important for therapeutic interventions
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