314 research outputs found
Ruoff (ed.), Programming Film Festivals
No full textReview of Jeffrey Ruoff (ed.) Coming Soon To a Festival Near You:Programming Film Festivals.St. Andrews (St. Andrews Film Studies) 2012,274 p., isbn 978 1 908437 02
First Impressions of A. LaVonne Brown Ruoff as an Author
No full textIn January 1996 I enrolled in my first course in American Indian literatures. As a neophyte in the field, I searched for texts that could help me with the new concepts I was learning, ideas that would enhance my understanding of native authors and their works. One of the first books I purchased was American Indian Literatures: An Introduction, Bibliographic Review, and Selected Bibliography, by A. LaVonne Brown Ruoff (1990). A blurb on the back cover by SAIL summarizes my first impressions of the book, which I read from cover to cover, underlining, highlighting, and annotating: “The first thing likely to strike the reader upon opening LaVonne Ruoff’s new volume is the range, variety, and richness of American Indian Literatures. . . . Well conceived and well executed, [the book] will be welcomed by students and teachers who are approaching the subject for the first time.” As both student and teacher, I appreciated the comprehensive introduction that Ruoff provides in this work. For someone who was at the beginning of the learning curve, the book was a welcome resource. In fact, I kept hoping that she would eventually publish a new edition of this work, bringing it up to date with the wealth of publications that have followed since its first appearance
Telluride in the Film Festival Galaxy
No full textAbout the Book
For those who cherish art cinema, the Telluride Film Festival is America\u27s best known and most celebrated film festival. It is the quintessential cinephile film festival in the USA, and a destination festival prototype in the galaxy of festivals. It has been spoken and written about a lot in popular media, yet it has never been the subject of a monograph. This is the first study to explore Telluride\u27s multi-faceted contributions to the cultural life of the United States and beyond.
About the Author
Jeffrey Ruoff is a film historian, documentary filmmaker, and an associate professor of Film and Media Studies at Dartmouth College in New Hampshire, USA. In 2012, his anthology Coming Soon to a Festival Near You: Programming Film Festivals was published by St Andrews Film Studies. He produced and directed the documentary Still Moving: Pilobolus at Forty (2012) about the internationally renowned American dance company Pilobolus. In addition to writing academic articles and books Ruoff regularly publishes Op-Eds and reviews in popular newspapers and magazines.
About the Electronic Publication
This electronic publication of Telluride in the Film Festival Galaxy was made possible with the permission of the author. The University Press of New England created Kindle, EPUB and PDF files.
Rights Information
Creative Commons Attribution-NonCommercial License © Jeffrey Ruof
Model Development and Investigations on Ion Homeostasis
No full textThe environment surrounding an organism, a cell and an organelle is constantly changing. To keep organisms functioning there is an everlasting need to regulate and adapt in order to keep the internal environment relatively constant. Homeostasis is the term used to describe this ability of a system to regulate and stabilize its environment. Different processes and compensatory mechanisms are employed to do this. Homeostasis is also the overall theme binding this thesis together, spanning from iron regulation in plants to the regulation of calcium (Ca2+) in humans. Ever since the term emerged, scientists have been searching for answers on how biological control mechanisms function and how they are able to maintain homeostasis. The work presented in this thesis is based on a computational approach using systems biology and control mechanisms like negative feedback and integral control. Controller motifs based on negative feedback loops between a controlled and manipulated/compensatory variable was previously identified by the research group, and has been used as a basis for the computational calculations and models.
Plants need iron for their growth and development, and even though this essential nutrient is difficult to access through the soil due to its availability. In the soil iron is strongly bound as Fe2O3, and plants have developed different strategies for iron uptake. Iron is also of great importance for human nutrition. Iron deficiency is one of the major causes of anaemia. Anaemia is a world wide problem and is a condition with too few red bloods cells or where the haemoglobin level within these is lower than usual. Iron regulation and homeostasis was modeled for non-graminaceous plants, with Arabidopsis thaliana as a model species. Since iron is toxic for plants at high levels it needs to be under homeostatic control. A model in agreement with experimental observations was developed. Iron-dependent degradation of the high-affinity transporter IRT1 was included in agreement with experimental findings, as well as the importance of the transcription factor FIT for the regulation of cytosolic iron. Auxiliary feedback was also introduced and investigated in the model. The role of such feedback is to help improve adaptation kinetics without an influence to the set-point, resulting in a significant improvement of the system response time.
Homeostasis was also explored in order to see whether oscillatory conditions, which are common in biological systems, could show robust homeostasis. Homeostatic oscillators were identified, where compensatory frequency or amplitude levels lead to the average level corresponding to the set-point. This indicates that even during sustained oscillatory conditions homeostasis can be observed, suggesting an extension of the concept. Frequency control with the frequency being homeostatically regulated have also been described by us. Cytosolic calcium (Ca2+) is a biological example of one of these conditions where oscillations, transients etc. take place even though Ca2+ is under strict homeostatic control. Dysregulation of cytosolic Ca2+ is critical as it will affect cellular signaling and promote apoptosis at high levels. A simple initial model of oscillating Ca2+ regulation was used as an example of oscillatory homeostats, which spiked the interest to investigate Ca2+ homeostasis on a cellular level.
Thus started the approach on building a model on cytosolic Ca2+ homeostasis and regulatory mechanisms in non-excitable cells. The work was started from an initial simple model based on erythrocytes with few organelles by studying the inflow and outflow mechanisms through the plasma membrane. Hysteretic properties in the plasma membrane Ca2+ ATPase (PMCA) was studied and identified, and compared well with experimental results. We also suggest that the inflow of Ca2+ could be inhibited by carboxyeosin which was used as an inhibitor in experimental research based on model calculations fitting well with these. For the Ca2+ induced Ca2+ release mechanism through the inositol 1,4,5-trisphosphate receptor (IP3R) a dicalcic model has been presented. Comparing theoretical calculations with experimental bell-shaped curves of the Ca2+ dependency of the IP3R channel at different IP3 levels, a cooperativity of 2 has been suggested in the inhibition by Ca2+. Cooperativity in the capacitative Ca2+ entry was also investigated and compared to experiments. Finally, even though oscillations was not the focus of this latest project, the cellular model can show sustained Ca2+ oscillations with period length ranging from a few seconds up to 30 hours
Suppl_Table_2_17.04.2019 – Supplemental material for Fatigue in primary Sjögren’s syndrome: A proteomic pilot study of cerebrospinal fluid
No full textSupplemental material, Suppl_Table_2_17.04.2019 for Fatigue in primary Sjögren’s syndrome: A proteomic pilot study of cerebrospinal fluid by Eivind Larssen, Cato Brede, Anne Hjelle, Anne Bolette Tjensvoll, Katrine Brække Norheim, Kjetil Bårdsen, Kristin Jonsdottir, Peter Ruoff, Roald Omdal and Mari Mæland Nilsen in SAGE Open Medicine</p
Supplementary_table_1_fVAS_09.11-2018_(1) – Supplemental material for Fatigue in primary Sjögren’s syndrome: A proteomic pilot study of cerebrospinal fluid
No full textSupplemental material, Supplementary_table_1_fVAS_09.11-2018_(1) for Fatigue in primary Sjögren’s syndrome: A proteomic pilot study of cerebrospinal fluid by Eivind Larssen, Cato Brede, Anne Hjelle, Anne Bolette Tjensvoll, Katrine Brække Norheim, Kjetil Bårdsen, Kristin Jonsdottir, Peter Ruoff, Roald Omdal and Mari Mæland Nilsen in SAGE Open Medicine</p
Supplementary_Table_3_09.12.2018 – Supplemental material for Fatigue in primary Sjögren’s syndrome: A proteomic pilot study of cerebrospinal fluid
No full textSupplemental material, Supplementary_Table_3_09.12.2018 for Fatigue in primary Sjögren’s syndrome: A proteomic pilot study of cerebrospinal fluid by Eivind Larssen, Cato Brede, Anne Hjelle, Anne Bolette Tjensvoll, Katrine Brække Norheim, Kjetil Bårdsen, Kristin Jonsdottir, Peter Ruoff, Roald Omdal and Mari Mæland Nilsen in SAGE Open Medicine</p
Interleukin-1β, heat shock protein 90α, and hypocretin-1 in chronic fatigue
No full textBackground: Fatigue, defined as an overwhelming sense of tiredness, lack of energy, and feeling of exhaustion, is a phenomenon many people have experienced in connection with infections such as influenza, Epstein-Barr virus, etc. Fatigue is also common in cancer, neurological conditions like multiple sclerosis, Parkinson’s disease, and in chronic inflammatory and autoimmune diseases such as rheumatoid arthritis, psoriasis, and others.
“Sickness behavior” observed in animals is a conceptual model for understanding fatigue. In this model, infection or tissue damage is followed by behavioral changes like social withdrawal, inactivity, sleepiness, fatigue, and reduced food and water intake. The proinflammatory cytokine interleukin (IL)-1β produced during activation of innate immune cells has a prominent role in mediating this behavior. IL-1β crosses the blood-brain barrier and in the brain IL-1β amplifies its own signaling by inducing microglia to produce IL-1β. In cerebral neurons IL-1β signals through a receptor complex including interleukin-1 receptor I (IL-1RI) and an alternative IL-1 receptor accessory protein that does not mediate inflammation but induce neuronal activation and sickness behavior.
The inflammatory response needs to be controlled and is therefore downregulated in a timely manner not to run rampant. In addition, cellular protection mechanisms are activated during inflammation and tissue damage to preserve cellular life from reactive molecules that kill pathogens. Some variants of heat shock proteins (HSPs) released into the extracellular space could represent a defense mechanism of cellular life that also influence fatigue mechanisms.
In addition, sleepiness and weariness are closely related to fatigue and part of the sickness behavior response. Inflammation can alter sleep patterns. The master regulator of sleep- and wakefulness, neuropeptide hypocretin-1 (Hcrt1), could therefore have a role in fatigue generation.
Objectives:
I) Investigate if mechanisms that protect cellular life and homeostasis are involved in the generation of fatigue.
II) Develop a non-radioactive, sensitive and selective method for measurement of Hcrt1 in cerebrospinal fluid (CSF).
III) Explore how IL-1β and other selected molecules interact in generation of fatigue, and to investigate a possible link between the neuropeptide Hcrt1 and fatigue.
Methods: To explore mechanism of fatigue, a cohort of 71 patients with primary Sjögren’s syndrome were investigated. CSF samples where available from 49 patients. A method based on liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) was developed for measurements of Hcrt1. Hcrt1 was measured in CSF samples from 22 healthy subjects and 9 patients with narcolepsy type 1.
The clinical variables fatigue, depression and pain were scored using the fatigue Visual Analogue Scale (fVAS), Beck Depression Inventory, and the pain item of the Medical Outcome Survey short form 36, respectively. ELISAs were used to measure HSP32, -60, -72, and -90α in plasma, and in CSF to measure concentrations of IL-1Ra, IL-1RII, IL-6, and the calcium binding protein S100B. Hcrt1 in CSF was measured using a radioimmunoassay (RIA) method, in addition to a non-radioactive method based on liquid chromatography coupled with tandem mass spectrometry. Results were analyzed by non-parametric group comparisons, logistic regression, univariate- and multiple regression, and principal component analysis (PCA).
Results: Measures of HSP32, -60, -72, and -90α in plasma revealed that the concentrations of HSP90α were significantly higher in pSS patients with high fatigue versus low fatigue. A tendency toward higher concentrations of HSP72 was observed in patients with high fatigue compared to patients with low fatigue.
The LC-MS/MS method for Hcrt1 in CSF revealed much lower
concentrations in healthy subjects than what has previously been published. Patients with narcolepsy type 1, a sleep disorder characterized by low levels of Hcrt1 in CSF, also had lower levels of Hcrt1 in CSF compared to previous published studies. The LC-MS/MS method was compared to the commonly used RIA method. A Bland-Altman plot showed agreement between the two methods.
Analysis of IL-1β related proteins (IL-1Ra, IL-1RII, and S100B), IL-6, and Hcrt1 in CSF demonstrated that IL-1Ra showed significant association with fVAS scores together with the clinical variables BDI scores and pain scores. The relationship of the biochemical variables was explored in PCA, and two significant components appeared: Variables related to IL-1β activity dominated the first component while in the second component there was a negative association between IL-6 and Hcrt1. Fatigue was introduced as an additional variable in a second model. In this PCA, fVAS scores were associated with the first component as was the IL-1β related variables. In addition, the second PCA model revealed a third component that showed a negative relationship between Hcrt1 and fatigue.
Conclusions:
I) HSP90α and to a lesser degree HSP72 in blood may possibly be parts of a fatigue inducing mechanism.
II) The LC-MS/MS method with high selectivity and accuracy revealed considerably lower levels of Hcrt1 in CSF than previously reported.
III) IL-1β signaling is a primary driver in fatigue. Several other proteins and molecules interact with IL-1β in a complex network, in which several cell types (neurons, microglia, and astrocytes) probably participate.
IV) Hcrt1 also influences fatigue, but probably through another pathway than the IL-1 route
CHARGE REARRANGEMENT IN (HCN)2 AND (HCN)3***
No full text Work supported by NSF and PRF. R. S. Ruoff, T. Emilsson, C. Chuang, T. D. Kiots, and H. S. Gutowsky. Chem. Phys. Letters 138, 553 (1987). R.S. Ruoff, T. Emlisson. T. D. Kiots, C. Chuang, and H. S. Gutowsky, J. Chem. Phys., submitted. E. J. Campbell and S. G. Kukolich, Chem. Phys. 76, 225 (1983).Author Institution: Noyes Chemical Laboratory, University of IllinoisCharge rearrangement during cluster formation may be determined from its effects upon the dipole moments u and the electric field gradients of the monomeric units,provided that corrections can be made for their vibrational averaging. An isotopic substitution method has enabled us to obtain vibrational amplitudes in the linear and A dipole moment of 6.552(35) D has been reported for the dimer3 and we have found 10.6(2) D for the These lead to induced dipole moments Au of 0.703(3) D for the dimer and 1.75(10) D for the trimer. A similar analysis was made of . A mutual polarization model was used to predict the induced dipole moments from the four known electrical multipole moments of HCN and its bond polarizabilities. The results are 0.703 D for the dimer and 1.68 D for the trimer. The calculations give ratios of the dipoles induced in the C-N bonds which are essentially identical with the ratios of the experimental . Equations are derived for calculation of Au of an infinite H-bonded chain and are applied to HCN. The convergence of multipale expansions for the electric field due to a molecular charge distribution will be discussed. The mutual polarization model works so well on HCN dimer and trimer that any charge transfer between the HCN monomers seems likely to be very small or negligible
Computational evaluation of different arrangements for the circadian clock in Arabidopsis thaliana.
No full textThe circadian clock is an endogenous timekeeper that enables individuals to predict and adjust to their environment's regular differences between light and dark and high and low temperatures. This biological timing mechanism enables the organism coordinate evolutionary and metabolic occurrences to the best time of the day. Such a system is of significant value to plants as they cannot alter their place when the climate becomes detrimental as opposed to animals. The plant clock is a sophisticated system of interwoven feedback loops. Mathematical modeling methods have been used over the past few decades to comprehend the clock's internal functioning in the Arabidopsis thaliana model plant. These attempts have generated a range of increasingly complex designs. Here, a review of the research is presented which is done in order to find out the molecular machinery responsible for circadian rhythms. Along with this, a simple model and alterations in this model are conducted to check out the impact of such changes on phases as well as period of rhythms. An effort is also done to show comparison of model in relation to the findings presented in previous research. We are proposing an applicant model centered on LSODE optimization sub-routine calculation
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