A novel transcutaneous CO2 therapy significantly enhanced the antitumor effectiveness of X-ray irradiation in human MFH xenografts The results strongly suggest that transcutaneous CO2 therapy could be a novel therapeutic tool for overcoming radioresistance in human malignancies. Hypoxia contributes to tumor radioresistance. In the presence of oxygen, reactive oxygen species (ROS) play crucial roles in cellular apoptosis to irradiation. We previously showed that a novel transcutaneous application of CO2 can improve hypoxia and that it induces apoptosis and decreases the expression of HIF-1α in sarcoma. Therefore, we hypothesised that a transcutaneous application of CO2 may increase radiosensitivity in sarcoma by improvement of hypoxic condition and increasing ROS production in tumors. The purpose of this study is to examine the effect of transcutaneous application of CO2 on radiosensitivity in human malignant fibrous histiocytoma (MFH) cells.Summary Statement
Introduction
Survivin is a member of the inhibitor of apoptosis family, which may contribute to the progression of human MFH via inhibiting the mitochondrial apoptosis, and may be considered as a potent therapeutic target for the treatment of human MFH. Survivin is a member of the inhibitor of apoptosis (IAP) family, which usually expresses in the embryonic lung and fetal organs in the developmental stages, but is undetectable in normal adult tissues other than thymus, placenta, CD34+ stem cells, and basal colonic epitherial cells. However, several studies reported that survivin is highly expressed in various human malignancies, including sarcomas, and increased expression of survivin is an unfavorable prognostic marker correlating with decreased overall survival in cancer patients. We have previously reported that survivin was strongly expressed in human malignant fibrous histiocyoma (MFH), however, the roles of survivin in human MFH have not been studied. The aim of this study was to evaluate the effect of survivin inhibition on apoptotic activity in human MFH cells.Summary Statement
Introduction
The most considerable cause of nerve root damage are compression force and stretch force. Many researchers had reported about experimental study of the compression force, but it is difficult to find the report describing the stretch force to the nerve roots. The purpose of this study is to evaluate the physiological reaction of nerve roots of rats nuder stretch force. The nerve roots were prepared from the cauda equina of 8 Wister rats (weight: 300 – 400g). We investigated the changes in threshold and action potential of the nerve roots under stretch force and compression force. The threshold of the nerve roots increased and action potential decreased in parallel with stretch force. Also, the threshold and action potential recovered after releasing the stretch force. On the other hand, by compression force, the action potential decreased parallel with compression force, but the threshold did not change with compression force. Ten minutes after releasing compression force, the action potential did not recover as much as before, and the threshold increased rather than control. The different physiological reactions that occurred between compression force and stretch force are hard to explain by circulation insufficiency, as previously reported (hypoxemia and lack of nutrition). We considered that the etiology of the stretch force might be a change in internal pressure of nerve roots and a structural change in nerve cells. The physiological reaction of the nerve root under stretch force differed from that under compression force and recovered from the damage after release from stretch force.
