3,288 research outputs found
Parameterizing probabilities for estimating age-composition distributions for mixture models
When estimating parameters that constitute a discrete probability distribution {pj}, it is difficult to determine how constraints should be made to guarantee that the estimated parameters { pˆj} constitute a probability distribution (i.e., pˆj>0, Σ pˆj =1). For age distributions estimated from mixtures of length-at-age distributions, the EM (expectationmaximization) algorithm (Hasselblad, 1966; Hoenig and Heisey, 1987; Kimura and Chikuni, 1987), restricted least squares (Clark, 1981), and weak quasisolutions (Troynikov, 2004) have all been used. Each of these methods appears to guarantee that the estimated distribution will be a true probability distribution with all categories greater than or equal to zero and with individual probabilities that sum to one. In addition, all these methods appear to provide a theoretical basis for solutions that will be either maximum-likelihood estimates or at least convergent to a probability distribu
Annualized cost of an irrigation system
Presented at the Central Plains irrigation short course and exposition on February 5-6, 2001 at the Holiday Inn in Kearney, Nebraska
Technology Transfer at the Department of Energy Laboratories -Selected Case Studies from the Lawrence Livermore Laboratory
The U.S. Department of Energy has, by transfer from the U.S. Energy and Research Development Administration, continued the policy of programs for dissemination of information. By the language of the charter, this extends to scientific, technical and practical information. Thus, DOE has a statutory responsibility to ensure full and widespread transfer of its technology.
Each Laboratory conducts its own Technology Transfer Program as an integral part of the National Program, and the activities of the Laboratories are directed towards the National Goals. Because of specific and sometimes different needs in the various geographical regions and the different styles of technology transfer, the methods used by each DOE Laboratory to achieve technology transfer vary. This paper describes the DOE Laboratory Technology Transfer Programs and, in general terms, some of the activities of the various participants. In addition, a discussion of some of Lawrence Livermore Laboratory\u27s accomplishments in technology transfer is presented
Multi-frequency imaging of perfectly conducting cracks via boundary measurements
Imaging of perfectly conducting crack(s) in a 2-D homogeneous medium using
boundary data is studied. Based on the singular structure of the Multi-Static
Response (MSR) matrix whose elements are normalized by an adequate test
function at several frequencies, an imaging functional is introduced and
analyzed. A non-iterative imaging procedure is proposed. Numerical experiments
from noisy synthetic data show that acceptable images of single and multiple
cracks are obtained.Comment: 4 pages, 3 figure
Mechanisms of non-apoptotic programmed cell death in diabetes and heart failure
Programmed cell elimination is an important pathological mediator of disease. Multiple pathways to programmed cell death have been delineated, including apoptosis, autophagy and programmed necrosis. Cross-talk between the signaling pathways mediating each process has made it difficult to define specific mechanisms of in vivo programmed cell death. For this reason, many “apoptotic” diseases may involve other death signaling pathways. Recent advances in genetic complementation using mouse knockout models are helping to dissect apoptotic and necrotic cell death in different pathological states. The current state of research in this area is reviewed, focusing upon new findings describing the role of programmed necrosis induced by the mitochondrial permeability transition in mouse models of heart failure and diabetes
Mitochondrial dynamism and heart disease: Changing shape and shaping change
Mitochondria of adult cardiomyocytes appear hypo-dynamic, lacking interconnected reticular networks and the continual fission and fusion observed in many other cell types. Nevertheless, proteins essential to mitochondrial network remodeling are abundant in adult hearts. Recent findings from cardiac-specific ablation of mitochondrial fission and fusion protein genes have revealed unexpected roles for mitochondrial dynamics factors in mitophagic mitochondrial quality control. This overview examines the clinical and experimental evidence for and against a meaningful role for the mitochondrial dynamism–quality control interactome in normal and diseased hearts. Newly discovered functions of mitochondrial dynamics factors in maintaining optimal cardiac mitochondrial fitness suggest that deep interrogation of clinical cardiomyopathy is likely to reveal genetic variants that cause or modify cardiac disease through their effects on mitochondrial fission, fusion, and mitophagy
Reversing dysdynamism to interrupt mitochondrial degeneration in amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis is one of several chronic neurodegenerative conditions in which mitochondrial abnormalities are posited to contribute to disease progression. Therapeutic options targeting mitochondria include enhancing metabolism, suppressing reactive oxygen production and disrupting mitochondria-mediated programmed cell death pathways. Herein is reviewed mechanistic evidence supporting a meaningful pathophysiological role for the constellation of abnormal mitochondrial fusion, fission and transport, collectively designated mitochondrial dysdynamism, in ALS. Following this is a discussion on preclinical studies in ALS mice that seemingly validate the idea that normalizing mitochondrial dynamism can delay ALS by interrupting a vicious cycle of mitochondrial degeneration, leading to neuronal die-back and death. Finally, the relative benefits of suppressing mitochondrial fusion vs. enhancing mitochondrial fusion in ALS are speculated upon, and the paper concludes with the prediction that the two approaches could be additive or synergistic, although a side-by-side comparative trial may be challenging to perform
Mitofusin 2 dysfunction and disease in mice and men
A causal relationship between Mitofusin (MFN) 2 gene mutations and the hereditary axonal neuropathy Charcot-Marie-Tooth disease type 2A (CMT2A) was described over 15 years ago. During the intervening period much has been learned about MFN2 functioning in mitochondrial fusion, calcium signaling, and quality control, and the consequences of these MFN2 activities on cell metabolism, fitness, and development. Nevertheless, the challenge of defining the central underlying mechanism(s) linking mitochondrial abnormalities to progressive dying-back of peripheral arm and leg nerves in CMT2A is largely unmet. Here, a different perspective of why, in humans, MFN2 dysfunction preferentially impacts peripheral nerves is provided based on recent insights into its role in determining whether individual mitochondria will be fusion-competent and retained within the cell, or are fusion-impaired, sequestered, and eliminated by mitophagy. Evidence for and against a regulatory role of mitofusins in mitochondrial transport is reviewed, nagging questions defined, and implications on mitochondrial fusion, quality control, and neuronal degeneration discussed. Finally, in the context of recently described mitofusin activating peptides and small molecules, an overview is provided of potential therapeutic applications for pharmacological enhancement of mitochondrial fusion and motility in CMT2A and other neurodegenerative conditions
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