We present results from high-resolution, optical to near-IR imaging of host stars of Kepler Objects of Interest (KOIs), identified in the original Kepler field. Part of the data were obtained under ...the Kepler imaging follow-up observation program over six years (2009-2015). Almost 90% of stars that are hosts to planet candidates or confirmed planets were observed. We combine measurements of companions to KOI host stars from different bands to create a comprehensive catalog of projected separations, position angles, and magnitude differences for all detected companion stars (some of which may not be bound). Our compilation includes 2297 companions around 1903 primary stars. From high-resolution imaging, we find that ∼10% (∼30%) of the observed stars have at least one companion detected within 1″ (4″). The true fraction of systems with close ( 4″) companions is larger than the observed one due to the limited sensitivities of the imaging data. We derive correction factors for planet radii caused by the dilution of the transit depth: assuming that planets orbit the primary stars or the brightest companion stars, the average correction factors are 1.06 and 3.09, respectively. The true effect of transit dilution lies in between these two cases and varies with each system. Applying these factors to planet radii decreases the number of KOI planets with radii smaller than 2 by ∼2%-23% and thus affects planet occurrence rates. This effect will also be important for the yield of small planets from future transit missions such as TESS.
We present high-resolution near-infrared spectropolarimetric observations using the SPIRou instrument at Canada-France-Hawaii Telescope (CFHT) during a transit of the recently detected young planet ...AU Mic b, with supporting spectroscopic data from iSHELL at NASA InfraRed Telescope Facility. We detect Zeeman signatures in the Stokes
V
profiles and measure a mean longitudinal magnetic field of ¯
B
ℓ
= 46.3 ± 0.7 G. Rotationally modulated magnetic spots likely cause long-term variations of the field with a slope of d
B
ℓ
/d
t
= −108.7 ± 7.7 G d
−1
. We apply the cross-correlation technique to measure line profiles and obtain radial velocities through CCF template matching. We find an empirical linear relationship between radial velocity and
B
ℓ
, which allows us to estimate the radial-velocity induced by stellar activity through rotational modulation of spots for the five hours of continuous monitoring of AU Mic with SPIRou. We model the corrected radial velocities for the classical Rossiter-McLaughlin effect, using MCMC to sample the posterior distribution of the model parameters. This analysis shows that the orbit of AU Mic b is prograde and aligned with the stellar rotation axis with a sky-projected spin-orbit obliquity of
λ
= 0°
−15°
+18°
. The aligned orbit of AU Mic b indicates that it formed in the protoplanetary disk that evolved into the current debris disk around AU Mic.
An accumulating body of evidence shows that gut microbiota fulfill an important role in health and disease by modulating local and systemic immunity. The importance of the microbiome in the ...development of kidney disease, however, is largely unknown. To study this concept, we depleted gut microbiota with broad-spectrum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice. Depletion of the microbiota significantly attenuated renal damage, dysfunction, and remote organ injury and maintained tubular integrity after renal I/R injury. Gut flora-depleted mice expressed lower levels of F4/80 and chemokine receptors CX3CR1 and CCR2 in the F4/80
renal resident macrophage population and bone marrow (BM) monocytes than did control mice. Additionally, compared with control BM monocytes, BM monocytes from gut flora-depleted mice had decreased migratory capacity toward CX3CL1 and CCL2 ligands. To study whether these effects were driven by depletion of the microbiota, we performed fecal transplants in antibiotic-treated mice and found that transplant of fecal material from an untreated mouse abolished the protective effect of microbiota depletion upon renal I/R injury. In conclusion, we show that depletion of gut microbiota profoundly protects against renal I/R injury by reducing maturation status of F4/80
renal resident macrophages and BM monocytes. Therefore, dampening the inflammatory response by targeting microbiota-derived mediators might be a promising therapy against I/R injury.
The Solar Twin Planet Search Ramirez, I; Melendez, J; Bean, J ...
Astronomy and astrophysics (Berlin),
12/2014, Letnik:
572
Journal Article
Recenzirano
Odprti dostop
We are carrying out a search for planets around a sample of solar twin stars using the HARPS spectrograph. The goal of this project is to exploit the advantage offered by solar twins to obtain ...chemical abundances of unmatched precision. This survey will enable new studies of the stellar composition -- planet connection. We determine the fundamental parameters of the 88 solar twin stars that have been chosen as targets for our experiment. We present the largest sample of solar twins analyzed homogeneously using high quality spectra. The fundamental parameters derived from this work will be employed in subsequent work that aims to explore the connections between planet formation and stellar chemical composition.
DS Tuc Ab is a Neptune-sized planet that orbits around a G star in the 45 Myr old Tucana-Horologium moving group. Here, we report the measurement of the sky-projected angle between the stellar spin ...axis and the planet's orbital axis, based on the observation of the Rossiter-McLaughlin effect during three separate planetary transits. The orbit appears to be well aligned with the equator of the host star, with a projected obliquity of . In addition to the distortions in the stellar absorption lines due to the transiting planet, we observed variations that we attribute to large starspots, with angular sizes of tens of degrees. The technique that we have developed for simultaneous modeling of starspots and the planet-induced distortions may be useful in other observations of planets around active stars.
Lung function declines as people age and their lungs become stiffer. With an increasing elderly population, understanding mechanisms that contribute to these structural and functional changes in the ...aging lung is important. Part of the aging process is characterized by thicker, more fibrotic airways, and senile emphysema caused by changes in lung parenchyma. There is also senescence, which occurs throughout the body with aging. Here, using human airway smooth muscle (ASM) cells from patients in different age groups, we explored senescence pathways and changes in intracellular calcium signaling and extracellular matrix (ECM) deposition to elucidate potential mechanisms by which aging leads to thicker and stiffer lungs. Senescent markers p21, gammaH2AX, and beta-gal, and some senescence-associated secretory proteins (SASP) increased with aging, as shown by staining and biochemical analyses. Agonist-induced intracellular Ca.sup.2+ responses, measured using fura-2 loaded cells and fluorescence imaging, increased with age. However, biochemical analysis showed that expression of the following markers decreased with age: M.sub.3 muscarinic receptor, TRPC3, Orai1, STIM1, SERCA2, MMP2 and MMP9. In contrast, collagen III, and fibronectin deposition increased with age. These data show that senescence increases in the aging airways that is associated with a stiffer but surprisingly greater intracellular calcium signaling as a marker for contractility. ASM senescence may enhance fibrosis in a feed forward loop promoting remodeling and altered calcium storage and buffering.
Dying cells are capable of activating the innate immune system and inducing a sterile inflammatory response. Here, we show that necrotic cells are sensed by the Nlrp3 inflammasome resulting in the ...subsequent release of the proinflammatory cytokine IL-1β. Necrotic cells produced by pressure disruption, hypoxic injury, or complement-mediated damage were capable of activating the Nlrp3 inflammasome. Nlrp3 inflammasome activation was triggered in part through ATP produced by mitochondria released from damaged cells. Neutrophilic influx into the peritoneum in response to necrotic cells in vivo was also markedly diminished in the absence of Nlrp3. Nlrp3-deficiency moreover protected animals against mortality, renal dysfunction, and neutrophil influx in an in vivo renal ischemic acute tubular necrosis model. These findings suggest that the inhibition of Nlrp3 inflammasome activity can diminish the acute inflammation and damage associated with tissue injury.
Tissue fibrosis and chronic inflammation are common causes of progressive organ damage, including progressive renal disease, leading to loss of physiological functions. Recently, it was shown that ...Toll-like receptor 2 (TLR2) is expressed in the kidney and activated by endogenous danger signals. The expression and function of TLR2 during renal fibrosis and chronic inflammation has however not yet been elucidated. Therefore, we studied TLR2 expression in human and murine progressive renal diseases and explored its role by inducing obstructive nephropathy in TLR2(-/-) or TLR2(+/+) mice. We found that TLR2 is markedly upregulated on tubular and tubulointerstitial cells in patients with chronic renal injury. In mice with obstructive nephropathy, renal injury was associated with a marked upregulation and change in distribution of TLR2 and upregulation of murine TLR2 danger ligands Gp96, biglycan, and HMGB1. Notably, TLR2 enhanced inflammation as reflected by a significantly reduced influx of neutrophils and production of chemokines and TGF-beta in kidneys of TLR2(-/-) mice compared with TLR2(+/+) animals. Although, the obstructed kidneys of TLR2(-/-) mice had less interstitial myofibroblasts in the later phase of obstructive nephropathy, tubular injury and renal matrix accumulation was similar in both mouse strains. Together, these data demonstrate that TLR2 can initiate renal inflammation during progressive renal injury and that the absence of TLR2 does not affect the development of chronic renal injury and fibrosis.
Ischemia reperfusion injury is a common cause of acute kidney injury and is characterized by tubular damage. Mitochondrial DNA is released upon severe tissue injury and can act as a damage-associated ...molecular pattern via the innate immune receptor TLR9. Here, we investigated the role of TLR9 in the context of moderate or severe renal ischemia reperfusion injury using wild-type C57BL/6 mice or TLR9KO mice. Moderate renal ischemia induced renal dysfunction but did not decrease animal well-being and was not regulated by TLR9. In contrast, severe renal ischemia decreased animal well-being and survival in wild-type mice after respectively one or five days of reperfusion. TLR9 deficiency improved animal well-being and survival. TLR9 deficiency did not reduce renal inflammation or tubular necrosis. Rather, severe renal ischemia induced hepatic injury as seen by increased plasma ALAT and ASAT levels and focal hepatic necrosis which was prevented by TLR9 deficiency and correlated with reduced circulating mitochondrial DNA levels and plasma LDH. We conclude that TLR9 does not mediate renal dysfunction following either moderate or severe renal ischemia. In contrast, our data indicates that TLR9 is an important mediator of hepatic injury secondary to ischemic acute kidney injury.
The dynorphin peptides are the endogenous ligands for the kappa opioid receptor (KOR) and regulate food intake. Administration of dynorphin-A1-13 (DYN) in the paraventricular hypothalamic nucleus ...(PVN) increases palatable food intake, and this effect is blocked by co-administration of the orexin-A neuropeptide, which is co-released with DYN in PVN from neurons located in the lateral hypothalamus. While PVN administration of DYN increases palatable food intake, whether it increases food-seeking behaviors has yet to be examined. We tested the effects of DYN and norBNI (a KOR antagonist) on the seeking and consumption of sucrose using a progressive ratio (PR) and demand curve (DC) tasks. In PVN, DYN did not alter the sucrose breaking point (BP) in the PR task nor the elasticity or intensity of demand for sucrose in the DC task. Still, DYN reduced the delay in obtaining sucrose and increased licks during sucrose intake in the PR task, irrespective of the co-administration of orexin-A. In PVN, norBNI increased the delay in obtaining sucrose and reduced licks during sucrose intake in the PR task while increasing elasticity without altering intensity of demand in the DC task. However, subcutaneous norBNI reduced the BP for sucrose and increased the delay in obtaining sucrose in the PR task while reducing the elasticity of demand. Together, these data show different effects of systemic and PVN blockade of KOR on food-seeking, consummatory behaviors, and incentive motivation for sucrose and suggest that KOR activity in PVN is necessary but not sufficient to drive seeking behaviors for palatable food.
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