BACKGROUND: AVP (arginine vasopressin) shows unique hemodynamic characteristics, as a vasopressor. AVP has been tried in many cathecholamine refractory vasodilatory situations, and sometimes resulted in effective hemodynamic improvement. In this study, we hypothesized that low dose AVP infusion could recover the decreased SVR (systemic vascular resistance) induced by milrinone infusion with minimal effect on PVR (pulmonary vascular resistance). METHODS: Sixteen patients undergoing OPCAB participated in this study. After a loading dose milrinone was infused, low dose vasopressin infusion was started and titrated until the systemic blood pressure increased by 20%. During the study, hemodynamic factors including pulmonary capillary wedge pressure and cardiac output were measured using a continuous thermodilution technique with a Swan-Ganz catheter. RESULTS: Milrinone infusion reduced both SVR and PVR. And vasopression infusion increased SVR, but show relatively less effect on PVR. CONCLUSIONS: Low-dose vasopressin infusion could be used to recover the SVR decrease caused by milirinone infusion with little effect on PVR.
Blood Pressure ; Cardiac Output ; Catheters ; Hemodynamics* ; Humans ; Milrinone* ; Pulmonary Wedge Pressure ; Thermodilution ; Vasopressins*

Although the association of genetic polymorphisms in glutathione S-transferase(GST) and N-acetyltransferase(NAT) with bladder cancer has been reported, limited numbers of studies have been indicated the association of CYP2E1 with bladder cancer, particularly in Asian population. A hospital based case-control study was conducted in South Korean, consisting of 232 histologically confirmed prevalent bladder cancer cases and 165 controls to evaluate the association between genetic polymorphisms of CYP2E1(RsaI) and development of bladder cancer. The frequency of CYP2E1(RsaI) c1/c1 genotype in bladder cancer cases was higher than in controls; 114 of 201(56.7%) vs. 62 of 146(42.5%). Men with CYP2E1(RsaI) c1/c1 genotype had increased risk of development of bladder cancer compared to men with at least one c2 allele(OR=1.7, 95% CI=1.1-2.7). The bladder cancer risk increased as the number of c1 allele increased(p for trend=0.005). The risk increased as the amount of smoking increased(p for trend=0.009). When data were analyzed for the interaction between smoking and CYP2E1 genetic polymorphisms, smokers with c1/c1 genotype have 2.5 greater risk in development of bladder cancer(95% CI=1.0-6.2) compared to nonsmokers with c2 allele(p for interaction=0.008). Our findings suggest that the interaction between genetic polymorphisms of CYP 2E1 (RsaI, c1/c1) and smoking may play an important role for development of bladder cancer among Koreans.
Alleles ; Asian Continental Ancestry Group ; Case-Control Studies ; Cytochrome P-450 CYP2E1* ; Cytochrome P-450 Enzyme System* ; Cytochromes* ; Genotype ; Glutathione ; Humans ; Korea* ; Male ; Polymorphism, Genetic* ; Smoke ; Smoking ; Urinary Bladder Neoplasms* ; Urinary Bladder*

BACKGROUND: Tetrabromobisphenol A (TBBPA), one of the most widely used brominated flame-retardants, is a representative persistent organic pollutants group. Studies on TBBPA toxicity have been conducted using various target cells; however, few studies have investigated TBBPA toxicity in bone cells. Therefore, this study investigated the in vitro effects of TBBPA on osteoclasts, a cell type involved in bone metabolism. METHODS: RAW264.7 cells were cultured in medium containing 50 ng/mL receptor activator of nuclear factor kappa B ligand (RANKL) and varying concentrations of TBBPA. To evaluate the effects of TBBPA on the differentiation and function of osteoclasts, osteoclast-specific gene expression, tartrate-resistant acid phosphatase (TRAP) activity, bone resorbing activity, mitochondrial membrane potential (MMP) and mitochondrial superoxide were measured. RESULTS: The presence of 20 μM TBBPA significantly increased TRAP activity in RANKL-stimulated RAW264.7 cells, the bone resorbing activity of osteoclasts, and the gene expression of Akt2, nuclear factor of activated T-cells cytoplasmic 1, and chloride channel voltage-sensitive 7. However, TBBPA treatment caused no change in the expression of carbonic anhydrase II, cathepsin K, osteopetrosis-associated transmembrane protein 1, Src, extracellular signal-related kinase, GAB2, c-Fos, or matrix metalloproteinase 9. Furthermore, 20 μM TBBPA caused a significant decrease in MMP and a significant increase in mitochondrial superoxide production. CONCLUSION: This study suggests that TBBPA promotes osteoclast differentiation and activity. The mechanism of TBBPA-stimulated osteoclastogenesis might include increased expression of several genes involved in osteoclast differentiation and reactive oxygen species production.
Acid Phosphatase ; Carbonic Anhydrase II ; Cathepsin K ; Chloride Channels ; Cytoplasm ; Gene Expression ; In Vitro Techniques ; Matrix Metalloproteinase 9 ; Membrane Potential, Mitochondrial ; Metabolism ; Osteoclasts ; Phosphotransferases ; RANK Ligand ; Reactive Oxygen Species ; Receptor Activator of Nuclear Factor-kappa B ; Superoxides ; T-Lymphocytes

The Korean Endocrine Society (KES) published clinical practice guidelines for the treatment of acromegaly in 2011. Since then, the number of acromegaly cases, publications on studies addressing medical treatment of acromegaly, and demands for improvements in insurance coverage have been dramatically increasing. In 2017, the KES Committee of Health Insurance decided to publish a position statement regarding the use of somatostatin analogues in acromegaly. Accordingly, consensus opinions for the position statement were collected after intensive review of the relevant literature and discussions among experts affiliated with the KES, and the Korean Neuroendocrine Study Group. This position statement includes the characteristics, indications, dose, interval (including extended dose interval in case of lanreotide autogel), switching and preoperative use of somatostatin analogues in medical treatment of acromegaly. The recommended approach is based on the expert opinions in case of insufficient clinical evidence, and where discrepancies among the expert opinions were found, the experts voted to determine the recommended approach.
Acromegaly ; Consensus ; Expert Testimony ; Insurance Coverage ; Insurance, Health ; Octreotide ; Somatostatin

Acromegaly is a chronic disorder caused by excessive growth hormone (GH) secretion. In most cases, the excess GH originates from GH-producing pituitary adenomas. Surgery is the preferred first-line treatment for patients with acromegaly, but medical management is considered when the disease persists after surgery or in cases where patients refuse surgery or are poor candidates for surgery. Somatostatin analogues are commonly used to treat acromegaly. The Korean Endocrine Society and the Korean Neuroendocrine Study Group have developed a position statement for the use of somatostatin analogues in the medical treatment of acromegaly. This position statement is based on evidence from the current literature and expert opinions. In the case of discrepancies among expert opinions, the experts voted to determine the recommended approach.
Acromegaly ; Expert Testimony ; Growth Hormone ; Humans ; Octreotide ; Pituitary Neoplasms ; Somatostatin

Acromegaly is a chronic disorder caused by excessive growth hormone (GH) secretion. In most cases, the excess GH originates from GH-producing pituitary adenomas. Surgery is the preferred first-line treatment for patients with acromegaly, but medical management is considered when the disease persists after surgery or in cases where patients refuse surgery or are poor candidates for surgery. Somatostatin analogues are commonly used to treat acromegaly. The Korean Endocrine Society and the Korean Neuroendocrine Study Group have developed a position statement for the use of somatostatin analogues in the medical treatment of acromegaly. This position statement is based on evidence from the current literature and expert opinions. In the case of discrepancies among expert opinions, the experts voted to determine the recommended approach.