37 research outputs found
Ariel - Volume 9 Number 5
Executive Editor
Seth B. Paul
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Warren J. Ventriglia
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Radio Interferometric Planet Search II: Constraints on sub-Jupiter-Mass Companions to GJ 896A
We present results from the Radio Interferometric Planet (RIPL) search for
compan- ions to the nearby star GJ 896A. We present 11 observations over 4.9
years. Fitting astrometric parameters to the data reveals a residual with
peak-to-peak amplitude of ~ 3 mas in right ascension. This residual is well-fit
by an acceleration term of 0.458 \pm 0.032 mas/y^2. The parallax is fit to an
accuracy of 0.2 mas and the proper motion terms are fit to accuracies of 0.01
mas/y. After fitting astrometric and acceleration terms residuals are 0.26 mas
in each coordinate, demonstrating that stellar jitter does not limit the
ability to carry out radio astrometric planet detection and characterization.
The acceleration term originates in part from the companion GJ 896B but the
amplitude of the acceleration in declination is not accurately predicted by the
orbital model. The acceleration sets a mass upper limit of 0.15 MJ at a
semi-major axis of 2 AU for a planetary companion to GJ 896A. For semi-major
axes between 0.3 and 2 AU upper limits are determined by the maximum angular
separation; the upper limits scale from the minimum value in proportion to the
inverse of the radius. Upper limits at larger radii are set by the acceleration
and scale as the radius squared. An improved solution for the stellar binary
system could improve the exoplanet mass sensitivity by an order of magnitude.Comment: Accepted for publication in Ap
Subcellular origin of mitochondrial DNA deletions in human skeletal muscle.
OBJECTIVE: In patients with mitochondrial DNA (mtDNA) maintenance disorders and with aging, mtDNA deletions sporadically form and clonally expand within individual muscle fibers, causing respiratory chain deficiency. This study aimed to identify the sub-cellular origin and potential mechanisms underlying this process.
METHODS: Serial skeletal muscle cryosections from patients with multiple mtDNA deletions were subjected to subcellular immunofluorescent, histochemical, and genetic analysis.
RESULTS: We report respiratory chain-deficient perinuclear foci containing mtDNA deletions, which show local elevations of both mitochondrial mass and mtDNA copy number. These subcellular foci of respiratory chain deficiency are associated with a local increase in mitochondrial biogenesis and unfolded protein response signaling pathways. We also find that the commonly reported segmental pattern of mitochondrial deficiency is consistent with the three-dimensional organization of the human skeletal muscle mitochondrial network.
INTERPRETATION: We propose that mtDNA deletions first exceed the biochemical threshold causing biochemical deficiency in focal regions adjacent to the myonuclei, and induce mitochondrial biogenesis before spreading across the muscle fiber. These subcellular resolution data provide new insights into the possible origin of mitochondrial respiratory chain deficiency in mitochondrial myopathy
Mitochondrial physiology
As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery