Identification of K-rich fragments in chondritic breccias using Imaging Plate (IP): an application to the planetary materials.

第2回極域科学シンポジウム/第34回南極隕石シンポジウム 11月17日（木） 国立国語研究所 2階講

The Subaru Coronagraphic Extreme Adaptive Optics system: enabling high-contrast imaging on solar-system scales

The Subaru Coronagraphic Extreme Adaptive Optics (SCExAO) instrument is a multipurpose high-contrast imaging platform designed for the discovery and detailed characterization of exoplanetary systems and serves as a testbed for high-contrast imaging technologies for ELTs. It is a multi-band instrument which makes use of light from 600 to 2500nm allowing for coronagraphic direct exoplanet imaging of the inner 3 lambda/D from the stellar host. Wavefront sensing and control are key to the operation of SCExAO. A partial correction of low-order modes is provided by Subaru's facility adaptive optics system with the final correction, including high-order modes, implemented downstream by a combination of a visible pyramid wavefront sensor and a 2000-element deformable mirror. The well corrected NIR (y-K bands) wavefronts can then be injected into any of the available coronagraphs, including but not limited to the phase induced amplitude apodization and the vector vortex coronagraphs, both of which offer an inner working angle as low as 1 lambda/D. Non-common path, low-order aberrations are sensed with a coronagraphic low-order wavefront sensor in the infrared (IR). Low noise, high frame rate, NIR detectors allow for active speckle nulling and coherent differential imaging, while the HAWAII 2RG detector in the HiCIAO imager and/or the CHARIS integral field spectrograph (from mid 2016) can take deeper exposures and/or perform angular, spectral and polarimetric differential imaging. Science in the visible is provided by two interferometric modules: VAMPIRES and FIRST, which enable sub-diffraction limited imaging in the visible region with polarimetric and spectroscopic capabilities respectively. We describe the instrument in detail and present preliminary results both on-sky and in the laboratory.Comment: Accepted for publication, 20 pages, 10 figure

Wide and deep near-UV (360nm) galaxy counts and the extragalactic background light with the Large Binocular Camera

Deep multicolour surveys are the main tool to explore the formation and evolution of the faint galaxies which are beyond the spectroscopic limit with the present technology. The photometric properties of these faint galaxies are usually compared with current renditions of semianalytical models to provide constraints on the fundamental physical processes involved in galaxy formation and evolution, namely the mass assembly and the star formation. Galaxy counts over large sky areas in the near-UV band are important because they are difficult to obtain given the low efficiency of near-UV instrumentation, even at 8m class telescopes. A large instrumental field of view helps in minimizing the biases due to the cosmic variance. We have obtained deep images in the 360nm U band provided by the blue channel of the Large Binocular Camera at the prime focus of the Large Binocular Telescope. We have derived over an area of ~0.4 sq. deg. the galaxy number counts down to U=27 in the Vega system (corresponding to U=27.86 in the AB system) at a completeness level of 30% reaching the faintest current limit for this wavelength and sky area. The shape of the galaxy counts in the U band can be described by a double power-law, the bright side being consistent with the shape of shallower surveys of comparable or greater areas. The slope bends over significantly at U>23.5 ensuring the convergence of the contribution by star forming galaxies to the EBL in the near-UV band to a value which is more than 70% of the most recent upper limits derived for this band. We have jointly compared our near-UV and K band counts collected from the literature with few selected hierarchical CDM models emphasizing critical issues in the physical description of the galaxy formation and evolution.Comment: Accepted for publication in A&A. Uses aa.cls, 9 pages, 4 figures. Citations update

Apoptosis of the fibrocytes type 1 in the spiral ligament and blood labyrinth barrier disturbance cause hearing impairment in murine cerebral malaria

<p>Abstract</p> <p>Background</p> <p>Experimental murine malaria has been shown to result in significant hearing impairment. Microscopic evaluation of the temporal bones of these animals has revealed regular morphology of the cochlea duct. Furthermore, the known vascular pathologic changes being associated with malaria could not be found. Immunohistochemistry for ICAM1 showed a strong marking in the <it>stria vascularis</it>, indicating a disturbance of the endocochlear potential. The aim of this study was to evaluate the role of apoptosis and the disturbance of the blood labyrinth barrier in the murine malaria associated hearing impairment.</p> <p>Methods</p> <p>The temporal bones of seven mice with cerebral malaria-four with hearing impairment, three without hearing impairment-were evaluated with immunohistochemistry for cleaved caspase 3 to detect apoptosis and connexin 26, a gap junction protein being a cornerstone in the endocochlear potassium recirculation. Furthermore five animals with cerebral malaria were treated with Evans blue prior to sacrification to detect disturbances of the blood labyrinth barrier.</p> <p>Results</p> <p>Cleaved caspase 3 could clearly be detected by immunohistochemistry in the fibrocytes of the spiral ligament, more intensively in animals with hearing impairment, less intensively in those without. Apoptosis signal was equally distributed in the spiral ligament as was the connexin 26 gap junction protein. The Evans blue testing revealed a strong signal in the malaria animals and no signal in the healthy control animals.</p> <p>Conclusion</p> <p>Malfunction of the fibrocytes type 1 in the spiral ligament and disruption of the blood labyrinth barrier, resulting in a breakdown of the endocochlear potential, are major causes for hearing impairment in murine cerebral malaria.</p

Clinical practice: The bleeding child. Part II: Disorders of secondary hemostasis and fibrinolysis

Bleeding complications in children may be caused by disorders of secondary hemostasis or fibrinolysis. Characteristic features in medical history and physical examination, especially of hemophilia, are palpable deep hematomas, bleeding in joints and muscles, and recurrent bleedings. A detailed medical and family history combined with a thorough physical examination is essential to distinguish abnormal from normal bleeding and to decide whether it is necessary to perform diagnostic laboratory evaluation. Initial laboratory tests include prothrombin time and activated partial thromboplastin time. Knowledge of the classical coagulation cascade with its intrinsic, extrinsic, and common pathways, is useful to identify potential defects in the coagulation in order to decide which additional coagulation tests should be performed

Rapid method for determination of DNA repair capacity in human peripheral blood lymphocytes amongst smokers

<p>Abstract</p> <p>Background</p> <p>DNA repair capacity is an important determinant of susceptibility to cancer. The hOGG1 enzyme is crucial for repairing the 8-oxoguanine lesion that occurs either as a byproduct of oxidative metabolism or as a result of exogenous sources such as exposure to cigarette smoke. It has been previously reported that smokers with low hOGG1 activity had significantly higher risk of developing lung cancer as compared to smokers with high hOGG1 activity.</p> <p>Methods</p> <p>In the current study we elucidate the association between plasma levels of 8-OHdG and the OGG1 repair capacity. We used the commercially available 8-OHdG ELISA (enzyme-linked immunosorbent assay), the Comet assay/FLARE hOGG1 (Fragment Length Analysis by Repair Enzymes) assay for quantification of the levels of 8-OHdG and measured the constitutive, induced and unrepaired residual damage, respectively. We compared the DNA repair capacity in peripheral blood lymphocytes following H₂O₂exposure in 30 lung cancer patients, 30 non-, 30 former and 30 current smoker controls matched by age and gender.</p> <p>Results</p> <p>Our results show that lung cancer cases and current smoker controls have similar levels of 8-OHdG lesions that are significantly higher compared to the non-smokers controls. However, lung cancer cases showed significantly poorer repair capacity compared to all controls tested, including the current smokers controls. After adjustment for age, gender and family history of smoking-related cancer using linear regression, we observed a 5-fold increase in risk of lung cancer associated with high levels of residual damage/reduced repair capacity. Reduced OGG1 activity could be expected to be a risk factor in other smoking-related cancers.</p> <p>Conclusion</p> <p>Our study shows that the Comet/FLARE assay is a relatively rapid and useful method for determination of DNA repair capacity. Using this assay we could identify individuals with high levels of residual damage and hence poor repair capacity who would be good candidates for intensive follow-up and screening.</p

Decreased surfactant phosphatidylcholine synthesis in neonates with congenital diaphragmatic hernia during extracorporeal membrane oxygenation

Purpose: Congenital diaphragmatic hernia (CDH) may result in severe respiratory insufficiency with a high morbidity. The role of a disturbed surfactant metabolism in the pathogenesis of CDH is unclear. We therefore studied endogenous surfactant metabolism in the most severe CDH patients who required extracorporeal membrane oxygenation (ECMO). Methods: Eleven neonates with CDH who required ECMO and ten ventilated neonates without significant lung disease received a 24-h infusion of the stable isotope [U-13C] glucose. The13C-incorporation into palmitic acid in surfactant phosphatidylcholine (PC) isolated from serial tracheal aspirates was measured. Mean PC concentration in epithelial lining fluid (ELF) was measured during the first 4 days of the study. Results: Fractional surfactant PC synthesis was decreased in CDH-ECMO patients compared to controls (2.4 ± 0.33 vs. 8.0 ± 2.4%/day, p = 0.04). The control group had a higher maximal enrichment (0.18 ± 0.03 vs. 0.09 ± 0.02 APE, p = 0.04) and reached this maximal enrichment earlier (46.7 ± 3.0 vs. 69.4 ± 6.6 h, p = 0.004) compared to the CDH-ECMO group, which reflects higher and faster precursor incorporation in the control group. Surfactant PC concentration in ELF was similar in both groups. Conclusion: These results show that CDH patients who require ECMO have a decreased surfactant PC synthesis, which may be part of the pathogenesis of severe pulmonary insufficiency and has a negative impact on weaning from ECMO

Decreased surfactant phosphatidylcholine synthesis in neonates with congenital diaphragmatic hernia during extracorporeal membrane oxygenation

Purpose: Congenital diaphragmatic hernia (CDH) may result in severe respiratory insufficiency with a high morbidity. The role of a disturbed surfactant metabolism in the pathogenesis of CDH is unclear. We therefore studied endogenous surfactant metabolism in the most severe CDH patients who required extracorporeal membrane oxygenation (ECMO). Methods: Eleven neonates with CDH who required ECMO and ten ventilated neonates without significant lung disease received a 24-h infusion of the stable isotope [U-13C] glucose. The13C-incorporation into palmitic acid in surfactant phosphatidylcholine (PC) isolated from serial tracheal aspirates was measured. Mean PC concentration in epithelial lining fluid (ELF) was measured during the first 4 days of the study. Results: Fractional surfactant PC synthesis was decreased in CDH-ECMO patients compared to controls (2.4 ± 0.33 vs. 8.0 ± 2.4%/day, p = 0.04). The control group had a higher maximal enrichment (0.18 ± 0.03 vs. 0.09 ± 0.02 APE, p = 0.04) and reached this maximal enrichment earlier (46.7 ± 3.0 vs. 69.4 ± 6.6 h, p = 0.004) compared to the CDH-ECMO group, which reflects higher and faster precursor incorporation in the control group. Surfactant PC concentration in ELF was similar in both groups. Conclusion: These results show that CDH patients who require ECMO have a decreased surfactant PC synthesis, which may be part of the pathogenesis of severe pulmonary insufficiency and has a negative impact on weaning from ECMO

Common Molecular Etiologies Are Rare in Nonsyndromic Tibetan Chinese Patients with Hearing Impairment

Background: Thirty thousand infants are born every year with congenital hearing impairment in mainland China. Racial and regional factors are important in clinical diagnosis of genetic deafness. However, molecular etiology of hearing impairment in the Tibetan Chinese population living in the Tibetan Plateau has not been investigated. To provide appropriate genetic testing and counseling to Tibetan families, we investigated molecular etiology of nonsyndromic deafness in this population. Methods: A total of 114 unrelated deaf Tibetan children from the Tibet Autonomous Region were enrolled. Five prominent deafness-related genes, GJB2, SLC26A4, GJB6, POU3F4, and mtDNA 12S rRNA, were analyzed. Inner ear development was evaluated by temporal CT. A total of 106 Tibetan hearing normal individuals were included as genetic controls. For radiological comparison, 120 patients, mainly of Han ethnicity, with sensorineural hearing loss were analyzed by temporal CT. Results: None of the Tibetan patients carried diallelic GJB2 or SLC26A4 mutations. Two patients with a history of aminoglycoside usage carried homogeneous mtDNA 12S rRNA A1555G mutation. Two controls were homozygous for 12S rRNA A1555G. There were no mutations in GJB6 or POU3F4. A diagnosis of inner ear malformation was made in 20.18 % of the Tibetan patients and 21.67 % of the Han deaf group. Enlarged vestibular aqueduct, the most common inner ear deformity, was not found in theTibetan patients, but was seen in 18.33 % of the Han patients. Common molecular etiologies