Effect of Oxygen Impurities on Positronium Formation in Voids of Vanadium

To clarify the effect of oxygen impurities on positronium (Ps) formed in irradiation-induced voids, measurements of the angular correlation of two photon annihilation radiation (ACAR) have been done on vanadium samples doped with oxygen impurities and subsequently irradiated with fast neutrons of doses up to 5.5x10^cm^ at about 400℃ in the Japan Materials Testing Reactor (JMTR). It has been shown that slight contamination of voids with oxygen impurity atoms, presumably submonolayer adsorption on the void surface, causes Ps formation. On the other hand, the considerable contamination leads suppression of Ps formation. Energy loss process of Ps in voids is found to be also influenced by the surface contamination

A novel reductive amino cyclization method and its application for the syntheses of pyrrolidine and piperidine nucleus

金沢大学大学院自然科学研究科生理活性物質科学金沢大学薬学

Relationship of Grade of Malignant Brain Tumor to Cancer Stem Cells and Survivin Expression

Glioblastoma (GBM) is difficult to completely cure by surgical treatment alone, and it is generally treated with a combination of surgery, radiotherapy, and chemotherapy. However, GBM is resistant to radiotherapy and chemotherapy, and complete cure cannot be achieved. Cancer stem cells (CSC) and survivin, which inhibit apoptosis, are considered as factors underlying tumor recurrence and the radiation- and drug-resistance of these tumors. We analyzed CSC and survivin expression in surgically excised specimens of malignant brain tumors to establish the relationships between the grades and CSC and survivin expression and between MIB-1 (Ki-67) expression and resistance. No relationship was noted between the grades and CSC or survivin expression, or between MIB-1 and CSC expression or between Grade 3 and 4 MIB-1 and survivin expression, although a correlation was noted between MIB-1 and survivin expression in Grade II tumors. These findings suggested that CSC are consistently contained in tumor tissue at a specific rate regardless of the histological grade, and the apoptosis of cells with low-level proliferative and cell cycling activities does not occur because these cells do not respond to chemotherapy or radiation, being resistant to treatment

The Chemistry of Indoles. XLIV. : Synthetic Study Directed toward 3, 4, 5, 6-Tetrahydro-1H-azepino[5, 4, 3-cd]indoles

[email protected] simple synthetic metho which can provide 3, 4, 5, 6-tetrahydro-1H-azepinol[5, 4, 3-cd]indole derivatives having a carbon side chain at any desired position of the nucleus was developed. The method was applied to the preparation of 4- and 5-alkyl-3, 4, 5, 6-tetrahydro-1H-azepino[5, 4, 3-cd]indoles

Combined Neuroprotective Effects of Propofol and Dexmedetomidine on Endoplasmic Reticulum Stress-mediated Apoptosis in SH-SY5Y Cells

Propofol is a short-acting intravenous anesthetic agent. Dexmedetomidine, a highly selective α2-adrenergic receptor agonist, has a well-known sedative effect. Both agents exhibit cytoprotective effects in the nervous system under ischemic conditions. Recently, the combination of propofol plus dexmedetomidine was used for the sedation of mechanically ventilated patients in an intensive care unit, but there are few experimental reports of the protective effects of the propofol plus dexmedetomidine combination in cells. Meanwhile, intraoperative brain ischemia–reperfusion induces endoplasmic reticulum (ER) stress-mediated apoptosis. The aim of the present study was to clarify molecular details underlying the neuroprotection afforded by the combination of propofol plus dexmedetomidine against thapsigargin (TG)-induced ER stress in human neuroblastoma SH-SY5Y cells, and whether the combination provided more efficient neuroprotection. TG was used to generate ER stress in SH-SY5Y cells. Cells were pretreated with propofol or dexmedetomidine, individually or in combination, for 1 h before cotreatment with TG for 20 h. There was a significant increase in [Ca2+]i, caspase activation, and the expression of ER stress biomarkers in TG-induced apoptotic cells. The increase in [Ca2+]i and the induction of ER stress by TG were suppressed by pretreatment with propofol, dexmedetomidine, and their combination. The dexmedetomidine-induced reduction in caspase activity and ER stress biomarkers was inhibited by pretreatment with an α2-adrenergic receptor antagonist, but was enhanced by pretreatment with a cAMP inhibitor. Treatment with the propofol plus dexmedetomidine combination exhibited the strongest protection against TG-induced apoptosis. These results demonstrate that the combination of propofol plus dexmedetomidine at clinically relevant concentrations suppresses ER stress-induced apoptosis in neuroblastoma SH-SY5Y cells. The findings suggest that the combination of propofol plus dexmedetomidine within a clinically relevant concentration range may be used safely in patients