2,309 research outputs found
Complex and regional-specific changes in the morphological complexity of GFAP+ astrocytes in middle-aged mice.
During aging, alterations in astrocyte phenotype occur in areas associated with age-related cognitive decline, including hippocampus. Previous work also reported subregion-specific changes in surface, volume and soma size of hippocampal astrocytes during physiological aging. Herein we extensively analyzed, by morphometric analysis, fine morphological features of GFAP+ astrocytes in young (6-month-old) and middle-aged (14-month-old) male mice. We observed remarkable heterogeneity in the astrocytic response to aging in distinct subfields and along the dorso-ventral axis of the hippocampus and in the entorhinal cortex (EC). Specifically, in middle-aged mice dorsal granule cell and molecular layers, but not dorsal hilus, astrocytes underwent remarkable increase in their morphological complexity. These changes were absent in ventral Dentate Gyrus (vDG). In addition, in EC, the major input to dorsal DG (dDG), astrocytes underwent remarkable atrophic changes in middle-aged mice. Since dDG, and not vDG, is involved in cognitive functions, these findings appear worth of further evaluation. Our findings also suggest an additional level of complexity in the structural changes associated with brain aging
The Times, They Are Changing
In 2015, Rutgers became only the second accredited law school in the United States to select the open-source ILS, Koha. The merger of two unique catalogs at Rutgers Law School has presented unique challenges with respect to migration mapping, data recall for large records, and relevancy ranking, all of which affect search results and usability of the OPAC. System migrations always result in some data being lost or incorrectly transferred. The hope is to minimize just how much data is compromised while fixing errors that might not have come to light but for the migration.Peer reviewe
Heather McHugh, 4th Annual ODU Literary Festival
The author of Dangers, published in 1978 in Houghton Mifflin\u27s New Poetry Series, and A World of Difference, also a Houghton Mifflin publication (1981), Heather McHugh is a rare poet, known for her formal elegance, her piercing wit, and her supple use of rhyme and rhythm. The Denver Quarterly remarked on her interest in seeing doubly and double-talking and praised her passionate intelligence and affection for the tongue\u27s intimate intricacies. McHugh\u27s Thursday evening reading will conclude the 1981 Literary Festival. McHugh grew up in Williamsburg and now teaches at the State University of New York at Binghamton. She is a member of the board of directors of the Associated Writing Programs
Ep. #121 - Heather Paxson
This recording and transcript form part of a collection of podcasts conducted by the Cultures of Energy at Rice University. Cultures of Energy brings writers, artists and scholars together to talk, think and feel their way into the Anthropocene. We cover serious issues like climate change, species extinction and energy transition. But we also try to confront seemingly huge and insurmountable problems with insight, creativity and laughter.Dominic and Cymene plug Cultures of Energy 7—this year’s energy humanities symposium at Rice which begins today, details at culturesofenergy.org—and then they turn to cheese, why it’s funny, how it can be applied to cats, “cheddaring,” and much more. Is there an anthropologist who knows more about cheese than anyone? Yes of course there is, it’s MIT’s Heather Paxson, author of the award-winning The Life of Cheese: Crafting Food and Value in America (U California Press, 2012). She joins us (14:59) to talk about her research on the microbiopolitics of food and naturally we begin with what’s in her fridge. Heather tells us about her investigation of artisanal cheesemaking and what it tells us about the shift from Pasteurian to Post-Pasteurian regimes of microbiopower. We hear about goat ladies as revolutionaries, the truth about vegan cheese, and debate whether artisanal foodmaking is an elite project. Heather discusses the search for moral meaning in everyday life as a throughline in her work and we turn to her latest research on food safety inspections, the porosity of food borders and the synecdochic reasoning of the state when it comes to managing food flows. We close by discussing the impact of feminist analytics of labor in her research. What is “beef candy China”? Listen on and you might just find out
Systems biology analysis of the proteomic alterations induced by MPP+, a parkinson's disease-related mitochondrial toxin
Parkinson's disease (PD) is a complex neurodegenerative disease whose etiology has not been completely characterized. Many cellular processes have been proposed to play a role in the neuronal damage and loss: defects in the proteosomal activity, altered protein processing, increased reactive oxygen species burden. Among them, the involvement of a decreased activity and an altered disposal of mitochondria is becoming more and more evident. The mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP(+)), an inhibitor of complex I, has been widely used to reproduce biochemical alterations linked to PD in vitro and its precursor, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP), to induce a Parkinson-like syndrome in vivo. Therefore, we performed a meta-analysis of the literature of all the proteomic investigations of neuronal alterations due to MPP(+) treatment and compared it with our results obtained with a mitochondrial proteomic analysis of SH-SY5Y cells treated with MPP(+). By using open-source bioinformatics tools, we identified the biochemical pathways and the molecular functions mostly affected by MPP(+), i.e., ATP production, the mitochondrial unfolded stress response, apoptosis, autophagy, and, most importantly, the synapse funcionality. Eventually, we generated protein networks, based on physical or functional interactions, to highlight the relationships among the molecular actors involved. In particular, we identified the mitochondrial protein HSP60 as the central hub in the protein-protein interaction network. As a whole, this analysis clarified the cellular responses to MPP(+), the specific mitochondrial proteome alterations induced and how this toxic model can recapitulate some pathogenetic events of PD.Parkinson's disease (PD) is a complex neurodegenerative disease whose etiology has not been completely characterized. Many cellular processes have been proposed to play a role in the neuronal damage and loss: defects in the proteosomal activity, altered protein processing, increased reactive oxygen species burden. Among them, the involvement of a decreased activity and an altered disposal of mitochondria is becoming more and more evident. The mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+), an inhibitor of complex I, has been widely used to reproduce biochemical alterations linked to PD in vitro and its precursor, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP), to induce a Parkinson-like syndrome in vivo. Therefore, we performed a meta-analysis of the literature of all the proteomic investigations of neuronal alterations due to MPP+ treatment and compared it with our results obtained with a mitochondrial proteomic analysis of SH-SY5Y cells treated with MPP+. By using open-source bioinformatics tools, we identified the biochemical pathways and the molecular functions mostly affected by MPP+, i.e., ATP production, the mitochondrial unfolded stress response, apoptosis, autophagy, and, most importantly, the synapse funcionality. Eventually, we generated protein networks, based on physical or functional interactions, to highlight the relationships among the molecular actors involved. In particular, we identified the mitochondrial protein HSP60 as the central hub in the protein-protein interaction network. As a whole, this analysis clarified the cellular responses to MPP+, the specific mitochondrial proteome alterations induced and how this toxic model can recapitulate some pathogenetic events of PD
HERStory Makers 2023: Heather Mcclelland
Heather Mcclelland is a chartered psychologist and researcher at the University of Glasgow studying mental health. She took part in HERStory Makers 2023.What is HERStory Makers?HERStory Makers is a social media competition for female-identifying early career researchers to share their research, their career journeys, and to inspire the next generation. Winners are selected by public vote. HERStory Makers is also part of EXPLORATHON, Scotland's contribution to European Researchers' Night.In 2022-23, EXPLORATHON was supported by the Engineering & Physical Sciences Research Council [grant number EP/X020762/1].Author contributions to contentHeather Mcclelland conceived, planned, and recorded the video content. Kirsty Ross edited the video content to insert HERStory Maker credits, add subtitles, and ensured the video length was below Twitter/X limit of 2 mins and 20 secs.</p
Creating and Scaling Innovative School Models Through Strategic Partnerships
· The Texas High School Project (THSP) was created in 2003 as a public-private alliance to support education reform across the state.
· This article focuses on the pivotal role of philanthropy within the THSP alliance to create early college high schools (ECHS).
· The model has been scaled at different levels to produce direct, affordable pathways for students to both attend college and attain skilled careers.
· The ECHS schools have higher test scores, greater credits earned, and reduced dropouts rates compared to traditional schools.
· Foundations with a track record for supporting successful work can increase the overall commitment to joint projects and attract additional members and support to an alliance.
· Lessons for successful partnerships include investing in time together, managing the partnership through one organization, and using data for decision-making
Institutional Racism and the Dynamics of Privilege in Public Health
Institutional racism, a pattern of differential access to material resources and power determined by race, advantages one sector of the population while disadvantaging another. Such racism is not only about conspicuous acts of violence but can be carried in the hold of mono-cultural perspectives. Overt state violation of principles contributes to the backdrop against which much less overt yet insidious violations occur. New Zealand health policy is one such mono-cultural domain. It is dominated by western bio-medical discourses that preclude and under-value Māori, the indigenous peoples of this land, in the conceptualisation, structure, content, and processes of health policies, despite Te Tiriti o Waitangi guarantees to protect Māori interests.
Since the 1980s, the Department of Health has committed to honouring the Treaty of Waitangi as the founding document of Māori-settler relationships and governance arrangements. Subsequent Waitangi Tribunal reports, produced by an independent Commission of Inquiry have documented the often-illegal actions of successive governments advancing the interests of Pākehā at the expense of Māori. Institutional controls have not prevented inequities between Māori and non-Māori across a plethora of social and economic indicators.
Activist scholars work to expose and transform perceived inequities. My research interest lies in how Crown Ministers and officials within the public health sector practice institutional racism and privilege and how it can be transformed. Through dialogue with Māori working within the health sector, fuelled by critical analysis and strategic advice from a research whānau (family) of Māori health leaders and a Pākehā Tiriti worker, and embracing the traditions of feminist and critical race theory I provide evidence of racism that can invoke strong emotional reactions. More disturbing is its normalisation to nigh imperceptibility within ones personal and professional life. The exposure of racism as a socially created phenomenon is a strength of the research presented here.
My action orientation is my ethical response. Honouring Te Tiriti o Waitangi is a pathway to transforming racism. Such change is likely to be resisted by the Pākehā majority. This anticipated resistance is not a credible reason to weaken responsibility for such necessary change. Transforming institutional racism needs to be driven by senior managers, professional bodies, unions, and by communities. Policies, practices and leadership that enable institutional racism need to be systematically eliminated from the health sector. Crown officials must be supported to strengthen their professional accountabilities and to embrace ethical bicultural practice. Greater transparency could enable more effective monitoring of Crown behaviour and support transformed practice
Why Look at Animals in Landscapes?
This book was published on the occasion of the two-person exhibition Reflexive Animals with work by Heather Passmore and Carrie Walker. The exhibition was held at SFU Gallery from September 8 to October 20, 2012. It includes written contributions by artist Julie Andreyev, poet Peter Culley and Bill Jeffries.final article publishe
Systems biology analysis of the proteomic alterations in Parkinson's disease: Common and disease-specific pathways
Objectives: Many biochemical mechanisms have been proposed to play a role in different neurodegenerative disorders. To distinguish what is disease-specific from what is generically linked to a neurodegenerative state is essential to better describe Parkinson's disease (PD) pathogenesis. PD and Amyotrophic Lateral Sclerosis (ALS) share some common mechanisms. Moreover, a high incidence of comorbidity may be explained by common biochemical altered pathways.
Methods: We performed a bioinformatics meta-analysis of all the proteomic investigations of neuronal alterations in PD, ALS and Alzheimer's disease (AD), used as control (non-motor neurodegenerative disease). We combined these data with genes found in a curated disease-gene database (DisGeNET). Moreover, we are currently going to analyze Peripheral Blood Mononuclear Cells samples coming from 20 ALS patients, 20 PD patients and 20 comorbid ALS/PD patients by two-dimensional electrophoresis.
Results: From our bioinformatics analysis some proteins were associated uniquely to PD, whereas others were associated to both diseases. Biological processes mostly associated to PD turned out to be chromatin organization, mitochondrion organization and protein folding. In addition, we found common dysregulated pathways, i.e., translation, SRP-dependent protein targeting to membrane and protein transport.
Conclusions: PD and ALS pathogenesis have some common mechanisms, due to the fact that they are both neurodegenerative diseases. The combination of bioinformatics tools and proteomic analysis of samples coming from comorbid patients will allow u also to highlight the disease-specific pathways, which may justify the degeneration of different neuron populations
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