Ariel - Volume 9 Number 5

Executive Editor Seth B. Paul Associate Editor Warren J. Ventriglia Business Manager Fredric Jay Matlin University News John Patrick Welch World News George Robert Coar Editorials Editor Steve Levine Features Mark Rubin Brad Feldstein Sports Editor Eli Saleeby Photo Editor Ken Buckwalter Circulation Victor Onufreiczuk Lee Wugofski Graphics and Art Steve Hulkower Commons Editor Brenda Peterso

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 complex I activity in microglia sustains neuroinflammation

Sustained smouldering, or low-grade activation, of myeloid cells is a common hallmark of several chronic neurological diseases, including multiple sclerosis1. Distinct metabolic and mitochondrial features guide the activation and the diverse functional states of myeloid cells2. However, how these metabolic features act to perpetuate inflammation of the central nervous system is unclear. Here, using a multiomics approach, we identify a molecular signature that sustains the activation of microglia through mitochondrial complex I activity driving reverse electron transport and the production of reactive oxygen species. Mechanistically, blocking complex I in pro-inflammatory microglia protects the central nervous system against neurotoxic damage and improves functional outcomes in an animal disease model in vivo. Complex I activity in microglia is a potential therapeutic target to foster neuroprotection in chronic inflammatory disorders of the central nervous system3