233 research outputs found
Part 2 of Age-related proteostatic imbalance exacerbates heart failure with preserved ejection fraction pathogenesis in old mice
No full text<p>Heart failure with preserved ejection fraction (HFpEF) is a leading cause of hospitalization and death in the elderly. While aging strongly increases the incidence of HFpEF, the specific influences of aging on HFpEF at molecular and pathophysiological levels remain unclear. Here, we show that aged mice, when subjected to chronic metabolic and hypertensive stress (2-hit stress), develop an aggravated cardiometabolic HFpEF phenotype compared to younger counterparts. Aged HFpEF mice also display unique pathological characteristics reminiscent of those found in HFpEF patients. We demonstrate that age-related dysfunction in protein quality control (PQC) exacerbates proteostatic stress in HFpEF. Specifically, we demonstrate that increased protein synthesis induced by 2-hit stress combines with age-related impairment in protein degradation in aged HFpEF hearts, culminating in the accumulation of protein aggregates. These findings underscore the importance of incorporating aging into preclinical HFpEF models and support the therapeutic potentials of targeting PQC mechanisms to ameliorate disease outcomes.</p>
<p>The deposited data are lc-ms data acquired on the Thermo QEx-Plus system. For any questions, please contact mike kinter mike-kinter at omrf.org</p>
<p>This upload contains the second part of the data. The majority of the data and a complete list of authors can be found in 10.5281/zenodo.10993216</p>
Age-related proteostatic imbalance exacerbates heart failure with preserved ejection fraction pathogenesis in old mice
No full text<p>Heart failure with preserved ejection fraction (HFpEF) is a leading cause of hospitalization and death in the elderly. While aging strongly increases the incidence of HFpEF, the specific influences of aging on HFpEF at molecular and pathophysiological levels remain unclear. Here, we show that aged mice, when subjected to chronic metabolic and hypertensive stress (2-hit stress), develop an aggravated cardiometabolic HFpEF phenotype compared to younger counterparts. Aged HFpEF mice also display unique pathological characteristics reminiscent of those found in HFpEF patients. We demonstrate that age-related dysfunction in protein quality control (PQC) exacerbates proteostatic stress in HFpEF. Specifically, we demonstrate that increased protein synthesis induced by 2-hit stress combines with age-related impairment in protein degradation in aged HFpEF hearts, culminating in the accumulation of protein aggregates. These findings underscore the importance of incorporating aging into preclinical HFpEF models and support the therapeutic potentials of targeting PQC mechanisms to ameliorate disease outcomes.</p>
<p>The deposited data are lc-ms data acquired on the Thermo QEx-Plus system. For any questions, please contact mike kinter mike-kinter at omrf.org</p>
<p>This upload contains the bulk of the LC-MS data. But, due to file sizes, and addition group of files can be found at doi 10.5281/zenodo.11094720</p>
The Idaho Forester - 1985 (Vol. 66)
No full textDedication 1 Needed: Wind and Sun for Fresh Ideas, an editorial, Lynn Kinter 2 Articles and Opinions 5 Why Idaho Needs a State River System, Murray D. Feldman 6 The Evolution of Point Springs Experimental Area, Lee Sharp 8 On Three Years of Teaching at the University of Idaho, Michael Frome 10 Secondary Forest Products from Dinderesso National Forest, Janet K. Miller 12 Reminiscing-Summer Camp 1984, Robin Naugler and Cathi Bailey 15 Natural Resources Week 1984, Claire Rausch 16 School Forest Update, Harold Osborne 18 Preserving Idaho's Natural Diversity in Research Natural Areas, Charles Wellner 20 Idaho's Endowments-An Investment in the Future, Stanley Hamilton 22 Faculty Changes, Pam Vaughn 24 Communicating Through a Magazine of Natural Resources, Joe Ulliman 45 Endless Pressure, Jim Tangen-Foster 48 The Next Seventy-five Years 25 State of the College at the Portal of Change, Jim Fazio 26 Funseekers Take Heart, the Future is Ours, Charlie Wells 28 Where Are We Headed in Fisheries, Christine Moffitt 30 A Look Into the Crystal Ball, Arland Hofstrand 32 Wildlifers and Landscape Architects Plan Nongame Future, Kerry P. Reese 37 The Range Revolution: A Study in High Tech, Dave Bryant 38 Forestry Revisited: Year 2017, John Dirks 39 Leaders or Followers: Our Future as Foresters, Joe Carbone 41 Clubs and Organizations 53 SAC-A Bridge for Better Communication, Robin McCoy 54 Range Club, Steve Jirik 55 American Fisheries Society, Palouse Unit, David B. Irving 56 The Wildlife Society, Brynna Evans 57 Wrec Club Capers, Lynn Kinter 58 Beyond Logging, Diana Hammer 59 Forest Products Club, Alan Prouty 60 Xi Sigma Pi, Bruce Romig 61 Alumni News 62 Index to Advertisers 6
Metabolic and Stress Response Changes Precede Disease Onset in the Spinal Cord of Mutant SOD1 ALS Mice
No full text<p>Many Amyotrophic Lateral Sclerosis (ALS) patients experience hypermetabolism, or an increase in measured versus calculated metabolic rate. The cause of hypermetabolism and the effects on neuronal metabolism in ALS are currently unknown, but the efficacy of dietary interventions shows promise for metabolism as an ALS therapeutic target. The goal of this study is to measure changes in metabolic pathways as a function of disease progression in spinal cords of the SOD1G93A mouse model of ALS. We conducted a comprehensive assessment of protein expression for metabolic pathways, antioxidants, chaperones, and proteases in lumbar spinal cord from male SOD1G93A mice at pre-onset, onset, and end-stages of the disease using targeted proteomic analysis. These results reveal that protein content of metabolic proteins including proteins involved in glycolysis, β‐oxidation, and mitochondrial metabolism is altered in SOD1G93A mouse spinal cord well before disease onset. The changes in mitochondrial metabolism proteins are associated with decreased maximal respiration and glycolytic flux in SOD1G93A dermal fibroblasts and increased hydrogen peroxide and lipid hydroperoxide production in mitochondria from sciatic nerve and gastrocnemius muscle fibers at end stage of disease. Consistent with redox dysregulation, expression of the glutathione antioxidant system is decreased, and peroxiredoxins and catalase expression are increased. In addition, stress response proteases and chaperones, including those involved in the mitochondrial unfolded protein response, are induced before disease onset. In summary, we report that metabolic and stress response changes occur in SOD1G93A lumbar spinal cord before motor symptom onset, and are primarily caused by SOD1G93A expression and do not vary greatly as a function of disease course.</p>These files can be opened using the program Skyline. The program is free to download at: https://skyline.ms/project/home/software/Skyline/begin.view
The general experimental design was two genotypes (WT and G93A) with three groups of mice within each genotype (preonset, onset, and endstage). The samples were analyzed by three different targeted protein quantification panels (1antioxidant and glycolysis, 2beta oxidation, and 3krebs cycle). For each panel, the name is a general description of most, but not all, of the proteins measured in the panel
Current Trends in Income of Communications Enterprises
No full text Communications income shows more stability than national income, but costs appear to increase more rapidly than revenue in a boom and fall less in a depression. Author of several earlier articles * on this subject, Dr. Kinter is economist with a Chicago investment firm and lecturer on economics at Northwestern. </jats:p
El Niño and the Southern Oscillation in Parameterized and Super-Parameterized Coupled General Circulation Models
No full textThe explicit treatment of cloud-scale processes in a super-parameterized coupled general circulation model (SP-CGCM) is known to produce improved total heating and low-level wind variability on interannual time scales relative to a model with conventional parameterization of convection. In this study, a novel linear statistical adjustment method has been explored to introduce a state-dependent adjustment such that the dominant modes of variability in the model with the explicit treatment of clouds are captured in the conventional model. This method was applied to isolate and quantify the impact of the horizontal gradients and time evolution of the surface stress forcing of the ocean due to the interannual surface stress variability of the SP-CGCM. The usefulness of this approach in isolating the effects of equatorial and off-equatorial oceanic wave response to the interannual surface stress forcing is demonstrated.This work is embargoed by the author and will not be available until June 2014
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