Irisin is a myokine caused by exercise that improves insulin resistance and weight loss. However, under unfavorable conditions such as air pollution, and during the pandemic, outdoor activities are uncomfortable. Therefore, in this study, the effect of heat therapy (half bath 42 ± 0.5°C for 30 min) on irisin circulation levels as an exercise alternative for middle-aged obese women after menopause was investigated. Subjects were 33 women aged 49.54 ± 6.04 years, with parameters of height, 160.12 ± 4.33 cm, weight, 69.71 ± 7.52 kg, body surface area 1.73 ± 0.13 m2 , body mass index, 27.19 ± 3.40 kg/m2 . The results suggest that circulating irisin levels showed a significant increase after one-time thermotherapy (TH-1). However, the increase in circulating irisin levels after 15 treatments (TH-15, 5 days/week, 3 weeks) was significantly varied. The level of adiponectin, which increases fatty oxidation to reduce fatty deposition, increased significantly at TH-1, but further increased at TH-15, which was significantly different from the level of TH-1. In addition, the basic serum free fatty acid (FFA) level was significantly increased at TH-15 compared to TH-1. Significant differences were also found in the lipid profile (body mass index, waist circumference, and % body fat). Thermotherapy can significantly increase the tympanic temperature and induce changes in circulating irisin and adiponectin levels. Thus, it resulted in positive changes in FFA and lipid profiles. Therefore, repeated thermotherapy is effective in increasing circulating irisin levels in postmenopausal obese women.

< 0.001); the Hb was > 10.0 g/dl in group B (minimum Hb 10.4 g/dl). The rate of bloodless OPCAB increased from 2% to 57%. There was a similar number of blood restorations and wastage, incidence of wound infections, bleeding, arrhythmias, myocardial infarctions, sudden death, length of the ICU stay and postoperative admissions in the two groups. CONCLUSIONS: With the new transfusion guideline, number of P-RBC preparations and transfusions was decreased significantly without an increase in the incidence of complications.
Arrhythmias, Cardiac ; Blood Transfusion ; Coronary Artery Bypass, Off-Pump* ; Death, Sudden ; Erythrocytes* ; Hemorrhage ; Incidence ; Myocardial Infarction ; Prognosis* ; Transplants* ; Wound Infection

OBJECTIVE: Arsenic trioxide (As2O3) is known to have potent anti-vascular activity and significantly suppress solid tumor growth. The present study was conducted to investigate the vascular shutdown effects of a novel arsenic compound, tetraasrsenic oxide (As4O6), in comparison with As2O3 using cervical cancer animal model. METHODS: Mice tumor challenge model was used C57BL/6 mice transplanted with TC-1 cells. After the growth of tumors was reached up 200~250 mm3, mice were divided into 3 groups randomly for control and treatment of either As2O3 or As4O6. As2O3 and As4O6 was treated by i.p. injection. The tumor size was caliperated in twice for weeks and anti-vascular effect were assessed by Evans blue extraction assay and Hoechst 33342 staining. In tumor tissue, histopathological feaure was obserevd by hematoxylin and eosin (H&E) staining. RESULTS: In mice treated with either As2O3 and As4O6 (i.p.), both of As2O3 and As4O6 was significantly suppressed the tumor growth compared with control group. Moreover, effect of As4O6 is more pronounced. These tumor growth inhibition is led to the massive necrosis and vacular shutdown in tumor tissue. CONCLUSION: This study suggests that As4O6 may have potential anticancer activity via vascular shutdown in C57BL/6 mice transplanted with TC-1 cells.
Animals ; Arsenic ; Arsenicals ; Benzimidazoles ; Eosine Yellowish-(YS) ; Evans Blue ; Hematoxylin ; Mice ; Models, Animal ; Necrosis ; Oxides ; Transplants ; Uterine Cervical Neoplasms

BACKGROUND AND OBJECTIVES: Heavy metal ions released from a stainless steel stent can induce an inflammatory reaction that might be associated with in-stent restenosis. A carbon ion implantation technique, which physically integrates carbon ions into the surface of the stainless steel lattice, can block heavy metal ion diffusion, and improve the biocompatibility. This study was designed to evaluate the efficacy of a carbon ion implanted Arthosinert stent on the reduction of in-stent restenosis and the improvement in the clinical outcomes. SUBJECTS AND METHODS: 193 de novo coronary lesions in 191 anginal patients at 14 centers, with reference diameters from 2.75 to 4.5 mm, were randomly assigned to either an Arthosinert (100 patients, 102 lesions) or an Arthos (91 patients, 91 lesions) stent. The lesion length was 14.1+/-5.7 mm. The ACC/AHA (American College of Cardiology/American Heart Association) lesion classifications were A:15.0%, B1:36.8%, B2:35.8% and C:12.4%. The study end points are angiographic restenosis, during a six-month follow-up, and Major adverse cardiac event. In-stent restenosis was defined as a diameter of stenosis > or =50%. RESULTS: A six-month angiographic follow-up was obtained for 72.3% (138/191) of the subjects. There were no significant differences between the Arthosinert and Arthos groups in the rates of restenosis (17.8% vs. 31.8%, p=0.055) and Target vessel revascularization (7.0% vs. 11.0%, p=0.476). There were no deaths or non-fatal myocardial infarction in either group. CONCLUSION: The treatment of de novo coronary stenosis, with carbon ion implanted stents, showed a tendency for lower six-month angiographic restenosis rates than the conventional 316L stainless steel stents. A larger trial will be needed to confirm the efficacy of the carbon ion implanted stent.
Carbon* ; Classification ; Constriction, Pathologic ; Coronary Restenosis ; Coronary Stenosis ; Diffusion ; Follow-Up Studies ; Heart ; Humans ; Ions ; Myocardial Infarction ; Stainless Steel ; Stents

OBJECTIVE: The aim of this study was to investigate the gene expression profiles using GeneFishing(TM) DEG kit in Korean women with cervical squamous cell carcinoma. METHODS: Cervical cancer biopsies were obtained from patients at the Department of Obstetrics and Gynecology, St. Mary's hodpital. In this study, we used a common reference that was mixed with an equal amount of RNA extracted from non-cervical cancer patients. The profiles of expression genes between cervical normal and squamous cell carcinoma tissue were identified using GeneFishing(TM) DEG Kit and screened by BLAST search. RESULTS: Almost 100 differential expressed genes were identified in universal control and cervical squamous cell carcinoma, 53 of differential expressed genes, up-regulated expression of 32 and 21 down-regulated expression was sequenced. Up-regulated genes were calcylin, calgranulin A, TRK oncogene, HLC5, fibrillarin, collagene type I alpha1 etc. and down-regulated genes were galectin 1, PRP8 pre-mRNA precessing factor 8 homology, clusterin etc. CONCLUSION: We identified gene expression profile in cervical squamous cell carcinoma using GeneFishing(TM) Kit in Korean women. The functional genomics of these genes should be further studied.
Biopsy ; Calgranulin A ; Carcinoma, Squamous Cell* ; Clusterin ; Collagen ; Female ; Galectin 1 ; Gene Expression* ; Genomics ; Gynecology ; Humans ; Obstetrics ; Oncogenes ; Polymerase Chain Reaction* ; RNA ; RNA Precursors ; Transcriptome ; Uterine Cervical Neoplasms

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.