A Photometric and Spectroscopic Study of the Short-Period Algol EW Bo\"{o}tis with a δ\delta Sct Pulsator

In this paper, we present TESS photometry and high-resolution spectra of the short-period Algol EW Boo. We obtained double-lined radial velocities (RVs) from the time-series spectra and measured the effective temperature of the primary star as $T_{\rm{eff,1}}$ = 8560 $\pm$ 118 K. For the orbital period study, we collected all times of minima available for over the last 30 years. It was found that the eclipse timing variation of the system could be represented by a periodic oscillation of 17.6 $\pm$ 0.3 years with a semi-amplitude of 0.0041 $\pm$ 0.0001 d. The orbital and physical parameters were derived by simultaneously analyzing the TESS light and RV curves using the Wilson-Devinney (WD) binary star modeling code. The component masses and radii were showed over 3% precision: $M_{1}$ = 2.67 $\pm$ 0.08 M$_{\odot}$, $M_{2}$ = 0.43 $\pm$ 0.01 M$_{\odot}$, $R_{1}$ = 2.01 $\pm$ 0.02 R$_{\odot}$, and $R_{2}$ = 1.35 $\pm$ 0.01 R$_{\odot}$. Furthermore, multiple frequency analyses were performed for the light-curve residuals from the WD model. As a result, we detected 17 pressure-mode pulsations in the region of 40.15 - 52.37 d$^{-1}$. The absolute dimensions and pulsation characteristics showed that the $\delta$ Sct pulsator was the more massive and hotter primary star of the EW Boo.Comment: 27 pages, 8 figures, Accepted for publication in A

Long-term outcome of vertebral artery origin stenosis in patients with acute ischemic stroke

BACKGROUND: Vertebral artery origin (VAO) stenosis is occasionally observed in patients who have acute ischemic stroke. We investigated the long-term outcomes and clinical significance of VAO stenosis in patients with acute ischemic stroke. METHODS: We performed a prospective observational study using a single stroke center registry to investigate the risk of recurrent stroke and vascular outcomes in patients with acute ischemic stroke and VAO stenosis. To relate the clinical significance of VAO stenosis to the vascular territory of the index stroke, patients were classified into an asymptomatic VAO stenosis group and a symptomatic VAO stenosis group. RESULTS: Of the 774 patients who had acute ischemic stroke, 149 (19.3%) of them had more than 50% stenosis of the VAO. During 309 patient-years of follow-up (mean, 2.3 years), there were 7 ischemic strokes, 6 hemorrhagic strokes, and 2 unknown strokes. The annual event rates were 0.97% for posterior circulation ischemic stroke, 4.86% for all stroke, and 6.80% for the composite cardiovascular outcome. The annual event rate for ischemic stroke in the posterior circulation was significantly higher in patients who had symptomatic VAO stenosis than in patients who had asymptomatic stenosis (1.88% vs. 0%, p = 0.046). In a multivariate analysis, the hazard ratio, per one point increase of the Essen Stroke Risk Score (ESRS) for the composite cardiovascular outcome, was 1.46 (95% CI, 1.02-2.08, p = 0.036). CONCLUSIONS: Long-term outcomes of more than 50% stenosis of the VAO in patients with acute ischemic stroke were generally favorable. Additionally, ESRS was a predictor for the composite cardiovascular outcome. Asymptomatic VAO stenosis may not be a specific risk factor for recurrent ischemic stroke in the posterior circulation. However, VAO stenosis may require more clinical attention as a potential source of recurrent stroke when VAO stenosis is observed in patients who have concurrent ischemic stroke in the posterior circulation

Catheter Ablation of a Left Free-Wall Accessory Pathway via the Radial Artery Approach

Catheter ablation of the left free-wall accessory pathways (APs) is normally performed by the retrograde transaortic approach via a femoral artery or the transseptal approach. Here we report a case of an overt left free-wall AP, which was successfully ablated with a retrograde transaortic approach via the radial artery without any vascular complications. The patient has remained free of any symptoms or pre-excitation observed on the ECG during a 10-month post-ablation follow-up

Enhancement of radiation response in human cervical cancer cells in vitro and in vivo by arsenic trioxide (As2O3)

AbstractArsenic trioxide (As2O3) inhibits cell growth and induces apoptosis in certain types of cancer cells including acute promyelocytic leukemia, prostate and ovarian carcinomas, but its effect on response of tumor cells to ionizing radiation has never been explored before. Here we demonstrate that As2O3 can sensitize human cervical cancer cells to ionizing radiation both in vitro and in vivo. As2O3 in combination with ionizing radiation have a synergistic effect in decreasing clonogenic survival and in the regression of established human cervical tumor xenografts. Pretreatment of the cells with As2O3 also synergistically enhanced radiation-induced apoptosis. Apoptosis of the cells by combined treatment of As2O3 and radiation was associated with reactive oxygen species generation and loss of mitochondrial membrane potential, resulting in the activation of caspase-9 and caspase-3. The combined treatment also resulted in an increased G2/M cell cycle distribution at the concentration of As2O3 which did not alter cell cycle when applied alone. These results indicate that As2O3 can synergistically enhance radiosensitivity of human cervix carcinoma cells in vitro and in vivo, suggesting a potential clinical applicability of combination treatment of As2O3 and ionizing radiation in cancer therapies

Cordycepin induces apoptosis of human ovarian cancer cells by inhibiting CCL5-mediated Akt/NF-κB signaling pathway

The chemokine, CCL5, is a key mediator for the recruitment of immune cells into tumors and tissues. Akt/NF-κB signaling is significantly activated by CCL5. However, the role of NF-κB inactivation in apoptosis induced by negative regulation of CCL5 remains unclear. Here, we analyzed the effect of cordycepin on NF-κB activity in SKOV-3 cells and found that cordycepin-mediated inhibition of NF-κB signaling induced apoptosis in SKOV-3 cells via the serial activation of caspases. In addition, immune-blotting analysis showed that CCL5 is highly expressed in SKOV-3 cells. In addition to activating caspases, we show that, cordycepin prevents TNF-α-induced increase in CCL5, Akt, NF-κB, and c-FLIPL activation and that CCL5 siRNA could inhibit Akt/NF-κB signaling. Moreover, cordycepin negatively regulated the TNF-α-mediated IκB/NF-κB pathway and c-FLIPL activation to promote JNK phosphorylation, resulting in caspase-3 activation and apoptosis. Also, we show that c-FLIPL is rapidly lost in NF-κB activation-deficient. siRNA mediated c-FLIP inhibition increased JNK. SP600125, a selective JNK inhibitor, downregulated p-JNK expression in cordycepin-treated SKOV-3 cells, leading to suppression of cordycepin-induced apoptosis. Thus, these results indicate that cordycepin inhibits CCL5-mediated Akt/NF-κB signaling, which upregulates caspase-3 activation in SKOV-3 cells, supporting the potential of cordycepin as a therapeutic agent for ovarian cancer