Blending in Future Space-based Microlensing Surveys

We investigate the effect of blending in future gravitational microlensing surveys by carrying out simulation of Galactic bulge microlensing events to be detected from a proposed space-based lensing survey. From this simulation, we find that the contribution of the flux from background stars to the total blended flux will be equivalent to that from the lens itself despite the greatly improved resolution from space observations, implying that characterizing lenses from the analysis of the blended flux would not be easy. As a method to isolate events for which most of the blended flux is attributable to the lens, we propose to use astrometric information of source star image centroid motion. For the sample of events obtained by imposing a criterion that the centroid shift should be less than three times of the astrometric uncertainty among the events for which blending is noticed with blended light fractions $f_{\rm B}>0.2$, we estimate that the contamination of the blended flux by background stars will be less than 20% for most ($\sim 90$) of the sample events. The expected rate of these events is $\gtrsim 700$ events/yr, which is large enough for the statistical analysis of the lens populations.Comment: total 6 pages, including 5 figures, ApJ, in pres

Charge-spin correlation in van der Waals antiferromagenet NiPS3

Strong charge-spin coupling is found in a layered transition-metal trichalcogenide NiPS3, a van derWaals antiferromagnet, from our study of the electronic structure using several experimental and theoretical tools: spectroscopic ellipsometry, x-ray absorption and photoemission spectroscopy, and density-functional calculations. NiPS3 displays an anomalous shift in the optical spectral weight at the magnetic ordering temperature, reflecting a strong coupling between the electronic and magnetic structures. X-ray absorption, photoemission and optical spectra support a self-doped ground state in NiPS3. Our work demonstrates that layered transition-metal trichalcogenide magnets are a useful candidate for the study of correlated-electron physics in two-dimensional magnetic material.Comment: 6 pages, 3 figur

The role of melatonin in the onset and progression of type 3 diabetes

Abstract Alzheimer’s disease (AD) is defined by the excessive accumulation of toxic peptides, such as beta amyloid (Aβ) plaques and intracellular neurofibrillary tangles (NFT). The risk factors associated with AD include genetic mutations, aging, insulin resistance, and oxidative stress. To date, several studies that have demonstrated an association between AD and diabetes have revealed that the common risk factors include insulin resistance, sleep disturbances, blood brain barrier (BBB) disruption, and altered glucose homeostasis. Many researchers have discovered that there are mechanisms common to both diabetes and AD. AD that results from insulin resistance in the brain is termed “type 3 diabetes”. Melatonin synthesized by the pineal gland is known to contribute to circadian rhythms, insulin resistance, protection of the BBB, and cell survival mechanisms. Here, we review the relationship between melatonin and type 3 diabetes, and suggest that melatonin might regulate the risk factors for type 3 diabetes. We suggest that melatonin is crucial for attenuating the onset of type 3 diabetes by intervening in Aβ accumulation, insulin resistance, glucose metabolism, and BBB permeability

Identification and Characterization of mRNA and lncRNA Expression Profiles in Age-Related Hearing Loss

Objectives Age-related hearing loss (ARHL), or presbycusis, is caused by disorders of sensory hair cells and auditory neurons. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, noise, inflammation, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Long non-coding RNA (lncRNA) has been reported to play important roles in various diseases. However, the function of lncRNA in ARHL remains unclear. In this study, we analyzed the common expression profiles of messenger RNA (mRNA) and lncRNA through ARHL-related RNA-sequencing datasets. Methods We selected and downloaded three different sets of RNA-sequencing data for ARHL. We performed differential expression analysis to find common mRNA and lncRNA profiles in the cochleae of aged mice compared to young mice. Gene Ontology (GO) analysis was used for functional exploration. Real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was performed to validate mRNAs and lncRNAs. In addition, we performed trans target prediction analysis with differentially expressed mRNAs and lncRNAs to understand the function of these mRNAs and lncRNAs in ARHL. Results We identified 112 common mRNAs and 10 common lncRNAs in the cochleae of aged mice compared to young mice. GO analysis showed that the 112 upregulated mRNAs were enriched in the defense response pathway. When we performed qRT-PCR with 1 mM H2O2-treated House Ear Institute-Organ of Corti 1 (HEI-OC1) cells, the qRT-PCR results were consistent with the RNA-sequencing analysis data. lncRNA-mRNA networks were constructed using the 10 common lncRNAs and 112 common mRNAs in ARHL. Conclusion Our study provides a comprehensive understanding of the common mRNA and lncRNA expression profiles in ARHL. Knowledge of ARHL-associated mRNAs and lncRNAs could be useful for better understanding ARHL and these mRNAs and lncRNAs might be a potential therapeutic target for preventing ARHL

A case of Creutzfeldt–Jakob disease in a patient on hemodialysis

abstractWe report an unusual case of probable Creutzfeldt–Jakob disease (CJD) in hemodialysis patient. A woman 59 years of age with a past history of hypertension and end-stage renal disease presented with a stuporous state preceded by rapidly progressive cognitive dysfunction, myoclonus, and akinetic mutism. At first, the cause of the altered mental status was assumed to be uremic or hypertensive encephalopathy combined with fever. Proper managements, however, did not improve the neurologic symptoms. Diffusion-weighted magnetic resonance imaging revealed bilaterally asymmetric high signal intensity in both basal ganglia and cerebral cortices. Electroencephalography showed diffuse generalized theta-to-delta range slow wave and intermittent medium-to-high voltage complexes with a characteristic triphasic pattern on both hemispheres. Cerebrospinal fluid assay for the 14-3-3 protein was positive and diagnostic of CJD

Adiponectin controls the apoptosis and the expression of tight junction proteins in brain endothelial cells through AdipoR1 under beta amyloid toxicity

AbstractAlzheimer’s disease (AD) is the most common neurodegenerative disease, characterized by excessive beta amyloid (Aβ) deposition in brain, leading to blood–brain barrier (BBB) disruption. The mechanisms of BBB disruption in AD are still unclear, despite considerable research. The adipokine adiponectin is known to regulate various metabolic functions and reduce inflammation. Though adiponectin receptors have been reported in the brain, its role in the central nervous system has not been fully characterized. In the present study, we investigate whether adiponectin contributes to the tight junction integrity and cell death of brain endothelial cells under Aβ-induced toxicity conditions. We measured the expression of adiponectin receptors (AdipoR1 and AdipoR2) and the alteration of tight junction proteins in in vivo 5xFAD mouse brain. Moreover, we examined the production of reactive oxygen species (ROS) and the loss of tight junction proteins such as Claudin 5, ZO-1, and inflammatory signaling in in vitro brain endothelial cells (bEnd.3 cells) under Aβ toxicity. Our results showed that Acrp30 (a globular form of adiponectin) reduces the expression of proinflammatory cytokines and the expression of RAGE as Aβ transporters into brain. Moreover, we found that Acrp 30 attenuated the apoptosis and the tight junction disruption through AdipoR1-mediated NF-κB pathway in Aβ-exposed bEnd.3 cells. Thus, we suggest that adiponectin is an attractive therapeutic target for treating BBB breakdown in AD brain.</jats:p

KMT-2016-BLG-1107: A New Hollywood-Planet Close/Wide Degeneracy

We show that microlensing event KMT-2016-BLG-1107 displays a new type of degeneracy between wide-binary and close-binary Hollywood events in which a giant-star source envelops the planetary caustic. The planetary anomaly takes the form of a smooth, two-day "bump" far out on the falling wing of the light curve, which can be interpreted either as the source completely enveloping a minor-image caustic due to a close companion with mass ratio $q=0.036$, or partially enveloping a major-image caustic due to a wide companion with $q=0.004$. The best estimates of the companion masses are both in the planetary regime ($3.3^{+3.5}_{-1.8}\,M_{\rm jup}$ and $0.090^{+0.096}_{-0.037}\,M_{\rm jup}$) but differ by an even larger factor than the mass ratios due to different inferred host masses. We show that the two solutions can be distinguished by high-resolution imaging at first light on next-generation ("30m") telescopes. We provide analytic guidance to understand the conditions under which this new type of degeneracy can appear.Comment: 23 pages, 7 figures, accepted for publication in A

KMT-2018-BLG-1990Lb: A Nearby Jovian Planet From A Low-Cadence Microlensing Field

We report the discovery and characterization of KMT-2018-BLG-1990Lb, a Jovian planet $(m_p=0.57_{-0.25}^{+0.79}\,M_J)$ orbiting a late M dwarf $(M=0.14_{-0.06}^{+0.20}\,M_\odot)$, at a distance (D_L=1.23_{-0.43}^{+1.06}\,\kpc), and projected at $2.6\pm 0.6$ times the snow line distance, i.e., a_{\rm snow}\equiv 2.7\,\au (M/M_\odot), This is the second Jovian planet discovered by KMTNet in its low cadence ($0.4\,{\rm hr}^{-1}$) fields, demonstrating that this population will be well characterized based on survey-only microlensing data.Comment: 24 pages, 7 figures, 4 table

The reemergence of long-term potentiation in aged Alzheimer's disease mouse model

Mouse models of Alzheimer’s disease (AD) have been developed to study the pathophysiology of amyloid β protein (Aβ) toxicity, which is thought to cause severe clinical symptoms such as memory impairment in AD patients. However, inconsistencies exist between studies using these animal models, specifically in terms of the effects on synaptic plasticity, a major cellular model of learning and memory. Whereas some studies find impairments in plasticity in these models, others do not. We show that long-term potentiation (LTP), in the CA1 region of hippocampal slices from this mouse, is impared at Tg2576 adult 6–7 months old. However, LTP is inducible again in slices taken from Tg2576 aged 14–19 months old. In the aged Tg2576, we found that the percentage of parvalbumin (PV)-expressing interneurons in hippocampal CA1-3 region is significantly decreased, and LTP inhibition or reversal mediated by NRG1/ErbB signaling, which requires ErbB4 receptors in PV interneurons, is impaired. Inhibition of ErbB receptor kinase in adult Tg2576 restores LTP but impairs depotentiation as shown in aged Tg2576. Our study suggests that hippocampal LTP reemerges in aged Tg2576. However, this reemerged LTP is an insuppressible form due to impaired NRG1/ErbB signaling, possibly through the loss of PV interneurons