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1.
Asian J Endosc Surg ; 5(3): 126-30, 2012 Aug.
Article in English | MEDLINE | ID: mdl-22776684

ABSTRACT

INTRODUCTION: Myomectomy for cervical myoma is problematic because cervical myomas are very close to neighboring structures, such as the ureters, uterine artery, bladder and rectum. There are a few reports on laparoscopic myomectomy for cervical myomas to avoid blood loss, such as occlusion of iliac arteries and clipping of the uterine artery. We evaluated the efficacy and safety of bipolar electrode grasping forceps for laparoscopic myomectomy in uterine cervical myoma. METHODS: From November 2006 to May 2009, eight women with uterine cervical myoma underwent laparoscopic myomectomy. We employed electrode grasping forceps with a combination of two tenaculums for separating and securing hemostatsis. RESULTS: Seven of eight cases were successfully treated by laparoscopic myomectomy, but one patient, with a large 900-g myoma was converted to the laparotomy as a result of blood loss (1800 mL). Among the other seven cases, the average weight of the myoma was 132 g (range, 16-310 g) and the operating time was 176 min. (range, 125-255 min). No complications occurred. Of the four cases who wanted to become pregnant postoperatively, two became pregnant and delivered by Caesarean section. CONCLUSION: These findings indicate that bipolar electrode grasping forceps using two tenaculums for traction of the myoma are useful for laparoscopic myomectomy in cervical myomas.


Subject(s)
Blood Loss, Surgical/prevention & control , Catheter Ablation/instrumentation , Laparoscopy/methods , Myoma/surgery , Uterine Neoplasms/surgery , Adult , Equipment Design , Female , Follow-Up Studies , Humans , Magnetic Resonance Imaging , Myoma/diagnosis , Retrospective Studies , Uterine Neoplasms/diagnosis
2.
Oncogene ; 27(19): 2737-45, 2008 Apr 24.
Article in English | MEDLINE | ID: mdl-18193094

ABSTRACT

Although there is growing evidence that estrogens promote tumor progression in epithelial ovarian cancer, the molecular mechanisms accounting for this are still unclear. Selective estrogen receptor modulators (SERMs) mimic estrogen action in certain tissues while opposing it in others. The molecular mechanisms of the effects of SERMs such as raloxifene on the tumor progression of epithelial ovarian cancer are also still unclear. Here, we show that various genomic actions of estrogen differ from those of raloxifene in human ovarian cancer cell lines expressing estrogen receptor alpha (ERalpha). 17beta-Estradiol (E2) induced the gene expression of c-Myc and IGF-1 and increased the binding of ERalpha to the AP1 site of the promoters of c-Myc and IGF-1. ERalpha silencing abolished the E2-stimulated c-Myc expression. E2 induced the recruitment of co-activators such as SRC-1, SRC-3 and CBP to the promoters of c-Myc and IGF-1, and SRC-1 silencing abolished both the E2-stimulated c-Myc expression and cell-cycle progression. In contrast, although raloxifene increased the binding of ERalpha to the AP1 site of the promoters of c-Myc and IGF-1, raloxifene had no effect on the gene expression of c-Myc or IGF-1. Raloxifene induced the recruitment of co-repressors such as HDAC2, N-CoR and SMRT to the promoter of IGF-1. Thus, the difference between the genomic actions exerted by estrogen and raloxifene in human ovarian cancer cell lines expressing ERalpha appear to be dependent on the recruitment of co-regulators.


Subject(s)
Estrogens/physiology , Genome, Human/drug effects , Ovarian Neoplasms/drug therapy , Raloxifene Hydrochloride/pharmacology , Selective Estrogen Receptor Modulators/pharmacology , Cell Line, Tumor , Estrogen Receptor alpha/biosynthesis , Estrogen Receptor alpha/genetics , Female , Humans , Insulin-Like Growth Factor I/biosynthesis , Insulin-Like Growth Factor I/genetics , Ovarian Neoplasms/metabolism , Proto-Oncogene Proteins c-myc/biosynthesis , Proto-Oncogene Proteins c-myc/genetics
3.
Pediatr Res ; 39(1): 117-9, 1996 Jan.
Article in English | MEDLINE | ID: mdl-8825395

ABSTRACT

We measured the plasma concentration of allantoin, an oxidation product of uric acid and an "in vivo" marker of free radical generation, within 24-48 h after birth in 10 premature infants who subsequently developed chronic lung disease (CLD) and 9 infants without CLD (non-CLD). The plasma allantoin level (mean +/- SD, 25.9 +/- 9.8 microM for CLD versus 11.0 +/- 5.7 microM for non-CLD, p < 0.01) and the allantoin/urate ratio (5.8 +/- 2.0% for CLD infants versus 2.4 +/- 0.9% for non-CLD infants, p < 0.01) were significantly higher in the CLD group than those in the non-CLD group. These observations suggest the possible involvement of oxygen radicals in triggering CLD. In addition, the plasma allantoin concentration and the allantoin/urate ratio may be useful early predictors of the development of CLD.


Subject(s)
Allantoin/blood , Lung Diseases/etiology , Uric Acid/blood , Chronic Disease , Female , Free Radicals , Humans , Infant, Newborn , Male , Oxygen
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