Laparoendoscopic Single Site Surgery for the Treatment of Huge Ovarian Cysts Using an Angiocatheter Needle

PURPOSE: The aim of this study was to evaluate the feasibility and safety of laparoendoscopic single site (LESS) surgery using an angiocatheter needle in patients with huge ovarian cysts (diameter ≥15 cm). MATERIALS AND METHODS: Thirty-one patients with huge ovarian cysts underwent LESS surgery using an angiocatheter needle between March 2011 and August 2016. An intra-umbilical vertical incision (1.5–2.0 cm) was made in the midline. After the cyst wall was punctured using an angiocatheter needle, the fluid contents were aspirated with a connected vacuum aspirator. After placing a Glove port in the umbilical incision, LESS surgery was performed using a rigid 0-degree, 5-mm laparoscope and conventional, rigid, straight laparoscopic instruments. Knife-in-bag morcellation was instituted for specimen collection. RESULTS: The median maximal diameter of ovarian cysts was 18 cm (range, 15–30 cm), the median operation time was 150 minutes (range, 80–520 minutes), and the median volume of blood loss was 100 mL (range, 20–800 mL). Three patients (9.7%) were diagnosed with malignant ovarian cancer using intraoperative frozen examination, and 1 patient was converted to laparotomy due to advanced disease. Thirty patients underwent LESS, and there was no need for an additional laparoscopic port. CONCLUSION: LESS surgery using an angiocatheter needle, with leaving only a small postoperative scar, was deemed feasible for the management of huge ovarian cysts.

Electrophysiological and Behavioral Changes by Phosphodiesterase 4 Inhibitor in a Rat Model of Alcoholic Neuropathy

OBJECTIVE: Alcoholic neuropathy is characterized by allodynia (a discomfort evoked by normally innocuous stimuli), hyperalgesia (an exaggerated pain in response to painful stimuli) and spontaneous burning pain. The aim of the present study is to investigate the effect of rolipram, a phosphodiesterase 4 inhibitor, against alcohol-induced neuropathy in rats. METHODS: Allodynia was induced by administering 35% v/v ethanol (10 g/kg; oral gavage) to Spraue-Dawley rats for 8 weeks. Rolipram and saline (vehicle) were administered intraperitoneally. Mechanical allodynia was measured by using von Frey filaments. Somatosensory evoked potential (SEP) was proposed as complementary measure to assess the integrity of nerve pathway. RESULTS: The ethanol-induced mechanical allodynia began to manifest from 3 week, and then peaked within 1 week. Beginning from 3 week, latency significantly started to increased in control group. In rolipram treated rats, the shorter latency was sustained until 8 weeks (p<0.05). The mechanical allodynia, which began to manifest on the 3 weeks, intraperitoneal injections of rolipram sustained statistical difference until 8 weeks, the final week of the study (p<0.05). CONCLUSION: This study suggests that rolipram might alleviate mechanical allodynia induced by alcohol in rats, which clearly has clinical implication.

Regulation of leptin gene expression by insulin and growth hormone in mouse adipocytes

The role of leptin in the control of obesity, insulin resistance and type II diabetes has been reported, however, the regulatory mechanism of leptin in animals affected by hormones is not clearly understood. In this study, the effects of insulin, epinephrine, growth hormone or dexamethasone on the expression of leptin was examined in mouse primary adipocytes. The leptin expression was also studied in the adipose tissue of the mouse treated with insulin or growth hormone (0.3 or 0.6 units/animal). Insulin (100 nM) or dexamethasone (100 nM) stimulated leptin mRNA transcription while epinephrine (100 nM) alleviated its transcription in mouse primary adipocytes. The level of leptin protein in cultured media of adipocytes treated with insulin or dexamethasone was higher than that of the control group but growth hormone or epinephrine treatment had no effect on them. Insulin administration (0.6 units/mouse) enhanced leptin mRNA as well as leptin protein in mouse adipose tissue but growth hormone administration (0.3 or 0.6 units/mouse) had no effect on them. Leptin protein level in sera of mice injected with insulin or growth hormone was not significantly different from that of control group. These results indicate that both insulin and dexamethasone stimulate leptin gene expression and secretion of its product, whereas, growth hormone has no effect on the expression of leptin gene in mouse adipocytes.

Regulation of leptin gene expression by insulin and growth hormone in mouse adipocytes

The role of leptin in the control of obesity, insulin resistance and type II diabetes has been reported, however, the regulatory mechanism of leptin in animals affected by hormones is not clearly understood. In this study, the effects of insulin, epinephrine, growth hormone or dexamethasone on the expression of leptin was examined in mouse primary adipocytes. The leptin expression was also studied in the adipose tissue of the mouse treated with insulin or growth hormone (0.3 or 0.6 units/animal). Insulin (100 nM) or dexamethasone (100 nM) stimulated leptin mRNA transcription while epinephrine (100 nM) alleviated its transcription in mouse primary adipocytes. The level of leptin protein in cultured media of adipocytes treated with insulin or dexamethasone was higher than that of the control group but growth hormone or epinephrine treatment had no effect on them. Insulin administration (0.6 units/mouse) enhanced leptin mRNA as well as leptin protein in mouse adipose tissue but growth hormone administration (0.3 or 0.6 units/mouse) had no effect on them. Leptin protein level in sera of mice injected with insulin or growth hormone was not significantly different from that of control group. These results indicate that both insulin and dexamethasone stimulate leptin gene expression and secretion of its product, whereas, growth hormone has no effect on the expression of leptin gene in mouse adipocytes.

Retroviral - mediated Transduction of Leptin Gene in Genetically Obese Mice / 대한내분비학회지

BACKGROUND: Leptin gene is known to be related to obesity in human and animals and complete genetic defect of the gene in ob/ob mouse has been identified. Therefore, ob/ob mouse is widely used as an animal model for the study of etiology and therapy of obesity. The main biological function of leptin was thought to involve in the regulation of food intake and weight gain, however, the regulatory mechanisms by which leptin functions in the weight reduction and lowering the blood glucose level are uncertain. In the present study, retroviral-mediated leptin gene transduction into ob/ob mouse was attempted for the correction of biochemical parameters of obesity. METHODS: Leptin cDNA was inserted into pLXSN retroviral vector (pLXSN-lep) and recombinant leptin expressing retrovirus particles (3 X10 CFU/mL) were produced in psi2 ecotropic packaging cells and subsequent transfection into PA317 amphotropic packaging cells. The leptin expressing recombinant viruses (LER) were transduced into NIH3T3 mouse fibroblasts and insertion of leptin cDNA into chromosomal DNA of PA317 and MH3T3 mouse fibroblasts was confirmed by Southern blot hybridizations. Leptin mRNA and its protein expressed in the cells were identified by Northern blot hybridization and Western blot immunodetection method, respectively. LER were injected I. P. into ob/ob mice, and body weight, food intake, serum leptin level and blood glucose level were measured. RESULTS: Expression of leptin was identified in PA317 and NIH3T3 mouse fibroblasts transduced with LER. Leptin content in sera of mice transfused with LER was drastically increased after 1 week and decreased to the almost basal level at 3 weeks after the transfusion. The body weight as well as food intake of ob/ob mouse transduced by LER decreased for the first 3 weeks and slightly increased thereafter. The reduction of both body weight and food intake in ob/ob mice transduced with LER was observed with the concomitant increase of serum leptin level, indicating that retroviral-mediated transduction of leptin gene in ob/ob mouse in vivo produced a biologically active leptin protein and released it into blood circulation. CONCLUSION: A transient expression of leptin cDNA in ob/ob mice by a retroviral-mediated transduction was performed and further studies are required for long term expression of the gene in vivo.

Adaptive Change of AP DNA Endonuclease Against Genotoxic Agents in Normal and Transformed Cells / 대한암학회지

PURPOSE: AP DNA endonuclease (APE), an enzyme responsible for the repair of damaged DNAs, is essential for the maintenance of genetic information of cells. Deficiency of APE in certain hereditary skin tumor and senescent cells has been implicated but the regulation of APE activity as well as the expression of APE gene in response to DNA damage has not been well documented. Genotoxic agents including ultimate carcinogens that can damage DNA were treated to cultured normal and transformed human cells and adaptive response of APE gene expression to these treatments was measured in order to evaluate the role of APE in chemical carcinogenesis. MATERIALS AND METHODS: Hydroxyl radical ('OH) generated from H2O2 (60 uM) through Fenton reaction, each 100 uM of N-nitrosomethylurea (NMU), 3-methyl-4-monomethyl- aminoazobenzene (3'-MeMAB) and N-acetoxy-2-acetaminofluorene (AAAF) were treated to umbilical cord blood cells (UCBC), HepG2 cells and HL-60 cells. APEX mRNA and APEX protein contents expressed in these cells exposed to each of these agents were measured by Northern blot hybridization and Western blot immunodetection analysis. The changes of APE activity in cells exposed to these genetoxic agents were measured. RESULTS: Treatment of H2O2 (60 uM) to UCBC, HepG2, and HL-60 cells increased APE activity significantly and pretreatment of a catalytic agent for OH, FeSO4 (60 pM) to the cells prior to H2O2 exposure did not further increase the APE activity in cells. Adaptive response to H2O2 in HL-60 cells increased in proportion to the concentration of H2O2 up to 60 pM. However, further increase in H2O2 concentration had no effect on the enzyme activity. Treatment of NMU (100 pM), 3-MeMAB (100 pM) and AAAF (100 pM) to these cells brought about a slight increase in the APE activity. APEX mRNA expression in UCBC and HepG2 cells exposed to H2O2, NMU, 3-MeMAB was markedly increased in APEX mRNA expression. APEX mRNA expression was also increased in HL-60 cells exposed to H2O2 (60 pM) and 3-MeMAB (100 uM) but NMU (100 pM) exposure to the cells resulted in a slight increase of it (Fig. 2). APEX protein expression was increased in all UCBC, HepG2 and HL-60 cells exposed to these genotoxic agents (Fig. 3). CONCLUSION: These results implicate that exposure of genotoxic agents to the cultured cells may cause DNA damage and lead to adaptive increase in APE activity as well as APE gene expression. It is probable that APE gene is transcriptionally regulated in response to the exposure of H2O2 or 3-MeMAB in cultured human cells as a consequence of activation of DNA repair system for the adaptation to the crisis.

c-erb B2 and p53 Overexpression in Presence of Human Papilloma Virus Type 16/18 Infection in Carcinomas of the Uterine Cervix: Genesis and Clinicopathologic Analysis / 대한산부인과학회잡지

The 43 cases of the primary uterine cervical carcinoma were analyzed for HPV type 16/18 infection and also analyzed for overexpression of p53 and c-erb B2 oncoprotein to evaluate theirs oncogenic and clinicopathologic relationships. HPV type 16/18 infection was examined by polymerase chain reaction(PCR) and the overexpression of p53 and c-erb B2 protein by using immunohistochemical method. The results were as follow: 1. The HPV infection rate in primary uterine cervical carcinomas was 83.7% respectively.The standard clinicopathologic characteristics(age, histologic type, koilocytosis, mitosis, clinical stage, tumor size, cervical invasion depth, lymph node metastasis, parametrial invasion) were nat significantly correlated with HPV type 16/18 infectivity. 2. The overexpression rate of p53 protein was 72.1% and there was no Significant correlation between expression of p53 protein and the Clinicopathologic characteristics. 3. The overexpression of c-erb B2 oncoprotein was 44.2% and there was no significant correlation between the overexpression of c-erb B2 oncoprotein and the clinicopathologic characteristics. 4. There was no significant correlation between HPV type 16/18 infection and overexpression of p53 and c-erb B2 oncoprotein.