Reconstruction of the East Antarctic ice sheet variability during the last 3 Ma: A perspective for future JARE expeditions at the central & eastern Droning Maud Land

第6回極域科学シンポジウム分野横断セッション：[IG] 全球環境変動を駆動する南大洋・南極氷床11月17日（火）　国立極地研究所１階交流アトリウ

East Antarctic deglaciation and the link to global cooling during the Quaternary: evidence from glacial geomorphology and 10Be surface exposure dating of the Sør Rondane Mountains, Dronning Maud Land

AbstractReconstructing past variability of the Antarctic ice sheets is essential to understand their stability and to anticipate their contribution to sea level change as a result of future climate change. Recent studies have reported a significant decrease in thickness of the East Antarctic Ice Sheet (EAIS) during the last several million years. However, the geographical extent of this decrease and subsequent isostatic rebound remain uncertain. In this study, we reconstruct the magnitude and timing of ice sheet retreat at the Sør Rondane Mountains in Dronning Maud Land, East Antarctica, based on detailed geomorphological survey, cosmogenic exposure dating, and glacial isostatic adjustment modeling. Three distinct deglaciation phases are identified for this sector during the Quaternary, based on rock weathering and 10Be surface exposure data. We estimate that the ice sheet thinned by at least 500 m during the Pleistocene. This thinning is attributed to the reorganization of Southern Ocean circulation associated with global cooling into the Pleistocene, which reduced the transport of moisture from the Southern Ocean to the interior of EAIS. The data also show that since the Last Glacial Maximum the ice surface has lowered less than ca 50 m and that this lowering probably started after ca 14 ka. This suggests that the EAIS in Dronning Maud Land is unlikely to have been a major contributor to postglacial sea-level rise and Meltwater pulse 1A

Glacial melting and uplift estimations around the Sør-Rondane Mountains of the East Antarctica since the Pliocene

第2回極域科学シンポジウム/第31回極域地学シンポジウム 11月16日（水） 国立国語研究

ヒョウメン ショウシャ ネンダイホウ ニオケル ケイタイガタ デンドウ カッター ヲ モチイタ アラタナ シリョウ サイシュ ホウホウ

宇宙線生成核種を用いた表面露出年代測定法は,地球表層における様々な現象を理解するために非常に重要な年代測定法である.この年代測定法には,年代決定精度が試料形状に依存するという特徴があり,試料採取の際に試料の厚さと形を高精度で測定することが必要となる.しかし,ハンマーやタガネを用いた従来の手法では,このような要求を満たす試料採取は時として困難であった.そこで本研究では,新たに携帯型電動カッターを用いた試料採取手法を提案する.この手法は,迅速かつ精密な試料採取および形状測定を可能とすることから,結果として年代測定精度の向上につながるものである.簡単な理論計算に基づき不完全な試料形状に起因する年代差を求めたところ,試料の採取深度が大きくなるにしたがって年代差が大きくなることが分かり,表面露出年代測定法における精密な試料形状測定の重要性が示された.Surface exposure dating using in situ cosmogenic nuclides has contributed to our understanding of Earth-surface processes. The precision of the ages estimated by this method is affected by the sample geometry; therefore, high accuracy measurements of the thickness and shape of the rock sample (thickness and shape) is crucial. However, it is sometimes diffi cult to meet these requirements by conventional sampling methods with a hammer and chisel. Here, we propose a new sampling technique using a portable electric rock cutter. This sampling technique is faster, produces more precisely shaped samples, and allows for a more precise age interpretation. A simple theoretical modeldemonstrates that the age error due to defective sample geometry increases as the total sample thickness increases, indicating the importance of precise sampling for surface exposure dating

Ultraviolet Action Spectrum and Effect of EPC-K1 on Ultraviolet Radiation-induced Injury in Cultured Normal Human Epidermal Keratinocytes

This study was aimed to determine the ultraviolet (UV: 235-310nm) action spectrum for killing normal human epidermal keratinocytes (NHEK) and to investigate the preventive effect of EPC-K1, a phosphate diester of vitamin C and vitamin E on UV radiation-induced NHEK injury. NHEK were cultured in EpiLife medium supplemented with Human Keratinocyte Growth Supplement Kit. NHEK viability was determined by crystal violet (CV) staining 48 h after the UV irradiation. The mRNA expressions of the C/EBP homologous protein (Chop) transcription factor and endoplasmic reticulum-resident molecular chaperone, Bip, were determined by RT-PCR analyses. UV was especially effective in killing NHEK when applied in the wavelength region of 250-280nm. The minimum exposure dose required to kill 50% of cells (LD50) was 1.64mJ/cm2 at 269nm. At 235 and 310nm, the LD50 for NHEK was 6.62 and 293mJ/cm2, respectively. Irradiation of 660-mJ/cm2 at 310nm significantly decreased the cell viability to 30% of control (without irradiation). The addition of 0.1mM EPC-K1 after irradiation returned the cell viability to 118%. Six hours after the 660-mJ/cm2 irradiation at 310nm, Chop and Bip mRNA levels in NHEK were increased to 487% and 283%, respectively, and were not significantly affected by EPC-K1. Chop and Bip are responsive to ER stress. These results suggested that EPC-K1 exerts a protective effect against UV-induced NHEK injury, and further studies should investigate the molecular mechanism underlying this effect

Effects of Bepridil on Spiral Reentry

Bepridil is effective for conversion of atrial fibrillation to sinus rhythm and in the treatment of drug-refractory ventricular tachyarrhythmias. We investigated the effects of bepridil on electrophysiological properties and spiral-wave (SW) reentry in a 2-dimensional ventricular muscle layer of isolated rabbit hearts by optical mapping. Ventricular tachycardia (VT) induced in the presence of bepridil (1 μM) terminated earlier than in the control. Bepridil increased action potential duration (APD) by 5% – 8% under constant pacing and significantly increased the space constant. There was a linear relationship between the wavefront curvature (κ) and local conduction velocity: LCV = LCV0 − D·κ (D, diffusion coefficient; LCV0, LCV at κ = 0). Bepridil significantly increased D and LCV0. The regression lines with and without bepridil crossed at κ = 20 – 40 cm−1, resulting in a paradoxical decrease of LCV at κ > 40 cm−1. Dye transfer assay in cultured rat cardiomyocytes confirmed that bepridil increased intercellular coupling. SW reentry in the presence of bepridil was characterized by decremental conduction near the rotation center, prominent drift, and self-termination by collision with boundaries. These results indicate that bepridil causes an increase of intercellular coupling and a moderate APD prolongation, and this combination compromises wavefront propagation near the rotation center of SW reentry, leading to its drift and early termination

IKs Block and Spiral-Wave Reentry

We tested a hypothesis that an enhancement of IKs may play a pivotal role in ventricular proarrhythmia under high sympathetic activity. A 2-dimensional ventricular muscle layer was prepared in rabbit hearts, and action potential signals were analyzed by optical mapping. During constant stimulation, isoproterenol (ISP, 0.1 μM) significantly shortened action potential duration (APD); chromanol 293B (30 μM), a selective IKs-blocker, reversed the APD shortening. VTs induced in the presence of ISP lasted longer than in the control, and this was reversed by 293B. E-4031 (0.1 μM), a selective IKr-blocker, did not cause such reversal. Spiral-wave (SW) reentry with ISP was characterized by more stable rotation around a shorter functional block line (FBL) than in the control. After application of 293B, SW reentry was destabilized, and rotation around a longer FBL with prominent drift reappeared. The APD abbreviation by ISP close to the rotation center was more pronounced than in the periphery, leading to an opposite APD gradient (center < periphery) compared with controls. This effect was also reversed by 293B. In conclusion, β-adrenergic stimulation stabilizes SW reentry most likely though an enhancement of IKs. Blockade of IKs may be a promising therapeutic modality in prevention of ventricular tachyarrhythmias under high sympathetic activity

Integrated genetic and epigenetic analysis defines novel molecular subgroups in rhabdomyosarcoma.

横紋筋肉腫におけるゲノム・エピゲノム異常の全体図を解明 -横紋筋肉腫を4群に分類-. 京都大学プレスリリース. 2015-07-03.Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma in childhood. Here we studied 60 RMSs using whole-exome/-transcriptome sequencing, copy number (CN) and DNA methylome analyses to unravel the genetic/epigenetic basis of RMS. On the basis of methylation patterns, RMS is clustered into four distinct subtypes, which exhibits remarkable correlation with mutation/CN profiles, histological phenotypes and clinical behaviours. A1 and A2 subtypes, especially A1, largely correspond to alveolar histology with frequent PAX3/7 fusions and alterations in cell cycle regulators. In contrast, mostly showing embryonal histology, both E1 and E2 subtypes are characterized by high frequency of CN alterations and/or allelic imbalances, FGFR4/RAS/AKT pathway mutations and PTEN mutations/methylation and in E2, also by p53 inactivation. Despite the better prognosis of embryonal RMS, patients in the E2 are likely to have a poor prognosis. Our results highlight the close relationships of the methylation status and gene mutations with the biological behaviour in RMS