Investigation of the Coefficient of Earth Pressure for Improved Ground by Compaction Grouting in the Full-Scale Field Liquefaction Experiment

This paper describes the effect of countermeasures for liquefaction by compaction grouting, which was investigated by the experiment of full-scale field liquefaction by controlled blast technique. The experiment was conducted to assess the performance of airport facilities subjected to liquefaction, to investigate damage mechanism, and to estimate the effect of countermeasures for liquefaction by compaction grouting applied to liquefiable sand layer under runway pavement. In this study, before and after grouting and after artificial liquefaction caused by in-situ blasting, self boring pressure-meter tests at the center and the edge of a grouted area were carried out to investigate the coefficient of earth pressure, K, for evaluation of the improved ground because it is generally known that compaction grouting makes K-value increase in and around the grouted area. Additionally, to estimate the continuation of improving effect after liquefaction, K-values after blast were also investigated at same points. As the results of investigation, it was found that post-liquefaction K-value was higher than that of untreated ground before improvement and compaction grouting with cost-reduction design examined in this study, that is, the cost-reduction design is effective

ガンマデルタT細胞を介したミノドロン酸の非小細胞肺癌細胞株に対するアポトーシス誘導効果の検討

Background/aim: Non-small cell lung carcinoma (NSCLC) is one of the leading causes of cancer-related death worldwide. Recent studies showed that nitrogen-containing bisphosphonates (N-BPs) directly and indirectly prevent proliferation, induce apoptosis, and inhibit metastasis of various types of cancer cell. In order to investigate the effect of combining minodronic acid (MDA) with γδ T-cells, NSCLC cells were treated with five concentrations of MDA. Materials and methods: NSCLC cells were cultured with different concentrations of MDA alone or in combination with γδ T-cells for 24 h. Results: MDA with γδ T-cells had differential apoptotic effects on the NSCLC cell lines. The cells showed significant apoptotic effects in the presence of MDA in a dose-dependent manner. Conclusion: This study is the first to report an indirect effect of MDA against NSCLC. We report the induction of apoptosis by MDA in combination with γδ T-cells.博士（医学）・乙第1446号・令和元年12月5日Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.発行元の規定により、本文の登録不可。本文は以下のURLを参照 "http://dx.doi.org/10.21873/anticanres.11174"（※全文閲覧は学内限定

Pathways Involving Beta-3 Adrenergic Receptors Modulate Cold Stress-Induced Detrusor Overactivity in Conscious Rats

ObjectiveTo investigate pathways involving beta-3 adrenergic receptors (ARs) in detrusor overactivity induced by cold stress, we determined if the beta-3 AR agonist CL316243 could modulate the cold stress-induced detrusor overactivity in normal rats. MethodsTwodays prior to cystometric investigations, the bladders of 10-week-old female Sprague-Dawley rats were cannulated. Cystometric measurements of the unanesthetized, unrestricted rats were taken to estimate baseline values at room temperature (RT, 272 degrees C) for 20min. They were then intravenously administered vehicle, 0.1, or 1.0mg/kg CL316243 (n=6 in each group). Fiveminutes after the treatments, they were gently and quickly transferred to the low temperature (LT, 42 degrees C) room for 40min where the cystometric measurements were again made. Afterward, the rats were returned to RT for final cystometric measurements. The cystometric effects of CL316243 were also measured at RT (n=6 in each group). ResultsAt RT, both low and high dose of CL316243 decreased basal and micturition pressure while the high dose (1.0mg/kg) significantly increased voiding interval and bladder capacity. During LT exposure, the high dose of CL316243 partially reduced cold stress-induced detrusor overactivity characterized by increased basal pressure and urinary frequency. The high drug dose also significantly inhibited the decreases of both voiding interval and bladder capacity compared to the vehicle- and low dose (0.1mg/kg)-treated rats. ConclusionA high dose of the beta-3 agonist CL316243 could modulate cold stress-induced detrusor overactivity. Therefore, one of the mechanisms in cold stress-induced detrusor overactivity includes a pathway involving beta-3 ARs.ArticleLUTS-LOWER URINARY TRACT SYMPTOMS.7(1):50-55(2014)journal articl

Pseudocyst in the Pancreatic Tail Associated with Chronic Pancreatitis Successfully Treated by Transpapillary Cyst Drainage

We report a 50-year-old male with pseudocysts in the pancreatic tail associated with chronic pancreatitis successfully treated by transpapillary cyst drainage. He had previously undergone ultrasonography-guided percutaneous cyst drainage for a pancreatic pseudocyst in our hospital. He was readmitted due to abdominal pain and fever. Computed tomography showed recurrence of a pseudocyst in the pancreatic tail measuring 5 cm in diameter. Since conservative treatment failed, endoscopic retrograde pancreatography was performed. There was communication between the pseudocyst and the main pancreatic duct, and pancreatic duct stenosis proximal to the pseudocyst. First, transpapillary pancreatic duct drainage was performed using a plastic stent, but the pseudocyst did not decrease in size and became infected. After removal of the stent, a pigtail type nasocystic catheter was placed in the pseudocyst via the pancreatic duct. The pseudocyst infection immediately disappeared, and the pseudocyst gradually decreased and disappeared. After removal of the nasocystic catheter, no recurrence was observed. As transpapillary drainage of pancreatic pseudocyst, cyst drainage and pancreatic duct drainage have been reported. In our patient with pseudocyst in the pancreatic tail, duct drainage was ineffective and the pseudocyst was infected, whereas cyst drainage was very effective. We considered that cyst drainage by a nasocystic catheter was the first-line therapy as the transpapillary drainage of the pancreatic pseudocyst