Effects of topography and sea surface temperature anomalies on heavy rainfall induced by Typhoon Chaba in 2016

Typhoon Chaba made landfall on the Korean Peninsula in the fall of 2016, resulting in record-breaking rainfall in southeastern Korea. In particular, the Ulsan metropolitan region experienced the most severe floods due to heavy rainfall of 319 mm for just 3 h. The heavy rainfall was possibly associated with the mountainous southeastern Korea topography and the warm sea surface temperature (SST) anomaly in the East China Sea. In this study, the Weather Research and Forecasting (WRF) model was used to investigate the effects of topography and SST anomalies through high-resolution numerical experiments. Simulation using original topography showed more rainfall on the windward and less on the leeward slope compared to the experiment with reduced topography around Ulsan. The moist flow in the typhoon was raised by orographic uplift, enhancing precipitation on the windward side and summits of the mountains. The orographically induced updraft extended to the mid-troposphere and contributed to the upward vertical moisture flux associated with rainfall. Therefore, the mountainous topography around Ulsan affected the local change in rainfall induced by the simulated typhoon. In addition, SST on the track of the typhoon controlled storm intensity and caused extreme precipitation changes. The experiment using the original SST in the East China Sea simulated less decayed typhoons and produced more precipitation compared to the experiment wherein the positive SST anomaly in the East China Sea was removed. The warm SST anomaly hindered the weakening of the typhoon moving northward to the mid-latitudes. At landfall, the stronger typhoon contained more water vapor, transported more moisture inland, and generated increased precipitation

Improving the Accuracy of a Heliocentric Potential (HCP) Prediction Model for the Aviation Radiation Dose

The space radiation dose over air routes including polar routes should be carefully considered, especially when space weather shows sudden disturbances such as coronal mass ejections (CMEs), flares, and accompanying solar energetic particle events. We recently established a heliocentric potential (HCP) prediction model for real-time operation of the CARI-6 and CARI-6M programs. Specifically, the HCP value is used as a critical input value in the CARI-6/6M programs, which estimate the aviation route dose based on the effective dose rate. The CARI-6/6M approach is the most widely used technique, and the programs can be obtained from the U.S. Federal Aviation Administration (FAA). However, HCP values are given at a one month delay on the FAA official webpage, which makes it difficult to obtain real-time information on the aviation route dose. In order to overcome this critical limitation regarding the time delay for space weather customers, we developed a HCP prediction model based on sunspot number variations (Hwang et al. 2015). In this paper, we focus on improvements to our HCP prediction model and update it with neutron monitoring data. We found that the most accurate method to derive the HCP value involves (1) real-time daily sunspot assessments, (2) predictions of the daily HCP by our prediction algorithm, and (3) calculations of the resultant daily effective dose rate. Additionally, we also derived the HCP prediction algorithm in this paper by using ground neutron counts. With the compensation stemming from the use of ground neutron count data, the newly developed HCP prediction model was improved

FDG PET/CT to Predict Recurrence of Early Breast Invasive Ductal Carcinoma

This study investigated the prognostic value of FDG PET/CT radiomic features for predicting recurrence in patients with early breast invasive ductal carcinoma (IDC). The medical records of consecutive patients who were newly diagnosed with primary breast IDC after curative surgery were reviewed. Patients who received any neoadjuvant treatment before surgery were not included. FDG PET/CT radiomic features, such as a maximum standardized uptake value (SUVmax), metabolic tumor volume (MTV), total lesion glycolysis (TLG), skewness, kurtosis, entropy, and uniformity, were measured for the primary breast tumor using LIFEx software to evaluate recurrence-free survival (RFS). A total of 124 patients with early breast IDC were evaluated. Eleven patients had a recurrence (8.9%). Univariate survival analysis identified large tumor size (>2 cm, p = 0.045), high Ki-67 expression (≥30%, p = 0.017), high AJCC prognostic stage (≥II, p = 0.044), high SUVmax (≥5.0, p = 0.002), high MTV (≥3.25 mL, p = 0.044), high TLG (≥10.5, p = 0.004), and high entropy (≥3.15, p = 0.003) as significant predictors of poor RFS. After multivariate survival analysis, only high MTV (p = 0.045) was an independent prognostic predictor. Evaluation of the MTV of the primary tumor by FDG PET/CT in patients with early breast IDC provides useful prognostic information regarding recurrence

Dasatinib Accelerates Valproic Acid-Induced Acute Myeloid Leukemia Cell Death by Regulation of Differentiation Capacity

<div><p>Dasatinib is a compound developed for chronic myeloid leukemia as a multi-targeted kinase inhibitor against wild-type BCR-ABL and SRC family kinases. Valproic acid (VPA) is an anti-epileptic drug that also acts as a class I histone deacetylase inhibitor. The aim of this research was to determine the anti-leukemic effects of dasatinib and VPA in combination and to identify their mechanism of action in acute myeloid leukemia (AML) cells. Dasatinib was found to exert potent synergistic inhibitory effects on VPA-treated AML cells in association with G₁ phase cell cycle arrest and apoptosis induction involving the cleavage of poly (ADP-ribose) polymerase and caspase-3, -7 and -9. Dasatinib/VPA-induced cell death thus occurred via caspase-dependent apoptosis. Moreover, MEK/ERK and p38 MAPK inhibitors efficiently inhibited dasatinib/VPA-induced apoptosis. The combined effect of dasatinib and VPA on the differentiation capacity of AML cells was more powerful than the effect of each drug alone, being sufficiently strong to promote AML cell death through G₁ cell cycle arrest and caspase-dependent apoptosis. MEK/ERK and p38 MAPK were found to control dasatinib/VPA-induced apoptosis as upstream regulators, and co-treatment with dasatinib and VPA to contribute to AML cell death through the regulation of differentiation capacity. Taken together, these results indicate that combined dasatinib and VPA treatment has a potential role in anti-leukemic therapy.</p></div

Dasatinib/VPA-induced apoptosis is via a caspase-dependent pathway and depends on MEK/ERK and p38 MAPK.

<p>Cells were preincubated with caspase-3 inhibitor (10 µM Z-DEVD-FMK), caspase-9 inhibitor (10 µM LEHD-CHO), MEK/ERK inhibitor (5 µM U0126 and 10 µM PD98059), p38 MAPK inhibitor (10 µM SB203580) and JNK inhibitor (10 µM SP600125) for 1 hr prior to treatment with 0.5 mM of VPA and 5 µM of dasatinib for 72 hr. (A, D) Caspase-9 activity; (B, E) caspase-3 activity (C, F); apoptotic cells. These data represent the means ± SEM. Significantly different from the control (*) or combination of VPA and dasatinib (#); ***, ###: <i>P</i><0.001. Cas3i, caspase-3 inhibitor; cas9i, caspase-9 inhibitor; U, U0126; PD, PD98059; SB, SB203580; SP, SP600125.</p

Mechanism by which dasatinib potentiates VPA-treated AML cell death.

<p>The combination of dasatinib and VPA on AML cell differentiation capacity is more potent than that of each drug alone. The combination is enough to promote intensive AML cell death through G₁ cell cycle arrest and caspase-dependent apoptosis. In addition, MEK/ERK and p38 MAPK control dasatinib/VPA-evoked apoptosis as upstream regulators. Eventually, the regulation of cell differentiation capacity contributes to AML cell death.</p

Effects of VPA and dasatinib on the cell viability.

<p>These data represent the means ± SEM. Significantly different from control (*) or combination of VPA and D (#); ***, ###: <i>P</i><0.001. *: <i>P</i><0.05. VPA, Valproic acid; D, dasatinib.</p

Effects of VPA and dasatinib on the apoptotic cells.

<p>These data represent the means ± SEM. Significantly different from control (*) or combination of VPA and D (#); ***, ###: <i>P</i><0.001. **: <i>P</i><0.01. *, #: <i>P</i><0.05. VPA, Valproic acid; D, dasatinib.</p

Combination of dasatinib and VPA inhibits HL60 cell proliferation.

<p>Cells were stimulated with various concentrations of 0, 0.5, 1, 1.5 and 2 µM dasatinib for 72 hr. The cytotoxicity was then evaluated by an MTS assay. (A) Dose-dependent responses of VPA on cell viability. (B) Dose-dependent responses of dasatinib on cell viability. (C) Treatment of VPA and/or dasatinib at 72 hr. Representative data are shown for at least three independent experiments. These data represent the means ± SEM. Significantly different from the control (*) or combination of VPA and dasatinib (#); *: <i>P</i><0.05; ***, ###: <i>P</i><0.001.</p