PURPOSE: This study was designed to compare the amount of polymerization shrinkage of dual-cure resin cements according to different polymerization modes and to determine the effect of light activation on the degree of polymerization. MATERIALS AND METHODS: Four kinds of dual-cure resin cements were investigated: Smartcem 2, Panavia F 2.0, Clearfil SA Luting and Zirconite. Each material was tested in three different polymerization modes: self-polymerization only, immediate light polymerization and 5 minutes-delayed light polymerization. The time-dependent polymerization shrinkage-strain was evaluated for 30 minutes by Bonded-disk method at 37degrees C. Five recordings of each material with three different modes were taken. Data were analyzed using one-way ANOVA and multiple comparison Scheffe'test (alpha=.05). RESULTS: All materials, except Panavia F 2.0, exhibited the highest polymerization shrinkage-strain through delayed light-activated polymerization. No significant difference between light activation modes was found with Panavia F 2.0. All materials exhibited more than 90% of polymerization rate in the immediate or delayed light activated group within 10 minutes. CONCLUSION: As a clinical implication of this study, the application of delayed light activation mode to dual-cure resin cements is advantageous in terms of degree of polymerization.
Polymerization* ; Polymers* ; Resin Cements*

The adverse effects of pain in post-surgery or trauma patients are well documented. A reliable, safe approach to achieving unilateral analgesia in multiple contiguous thoracic dermatomes would be of great benefit to anesthesiologists in acute pain setting following thoracic or upper abdominal surgery. The aim of this study of post-cholecystectomy pain was to compare two methods of postoperative analgesia with interpleural block and paravertebral block with bupivacaine. Thirty otherwise healthy patients who had undergone elective cholecystectomy through a subcostal incision were randomly allocated to two groups of fifteen patients each and given either interpleural block(group 1) or paravertebral block(group 2) with 20 ml 0.5% bupivacaine mixed with 1:200,000 epinephrine through a single catheter. The degree of analgesia was assessed by a verbal rating scale, Prince Henry pain score and a visual analogue scale(VAS 1-10 cm ; O=no pain, 10=worst pain). These pain scores and vital signs were assessed just before and 10, 20, 30, 60 and 120 minutes after injection of bupivacaine. The onset time of analgesia was similar in both groups(6.6+/-3.74 minutes in group 1 and 5.5+/-2.88 minutes in group 2), but the duration of analgesia was significantly longer in group 1(6.5+/-1.92 hours) than group 2(4.5+/-2.17 hours)(p<0.05). In both groups Prince Henry pain scores significantly decreased 10 minutes after injection of bupivacaine and VAS also significantly decreased 10 and 20 minutes after injection(p<0.05), but there was no significant difference between two groups. The systolic blood pressure decreased 10 minutes after the injection of bupivacaine in both groups(Group 1-3.7%, Group 2-6.5%) and the diastolic blood pressure decreased 10 minutes after the injection of bupivacaine only in group 1(2.5%), (p<0.05), however, these changes in arterial blood pressure were of minimal clinical significance. There is no complication in group 1, but 2 out of 15 patients in group 2 showed bilateral blockade without any serious hemodynamic derangement clinically. In conclusion, both techniques showed similarity in the onset and the degree of analgesia except the duration of analgesia, and presented only a few minor complications. Therefore, we feel that paravertebral block can be used in case that coexisting pulmonary or pleural pathology limits the use of interpleural block for post-cholecystectomy pain management. Furthermore, either of the two techniques may be used alternatively in management of thoracic or upper abdominal pain according to technical skill and preference of anesthesiologists.
Abdominal Pain ; Acute Pain ; Analgesia ; Arterial Pressure ; Blood Pressure ; Bupivacaine* ; Catheters ; Cholecystectomy* ; Epinephrine ; Hemodynamics ; Humans ; Pain Management ; Pathology ; Vital Signs

Lung cancer has high mortality and incidence rates. The leading causes of lung cancer are smoking and radon exposure. Indeed, the World Health Organization (WHO) has categorized radon as a carcinogenic substance causing lung cancer. Radon is a natural, radioactive substance; it is an inert gas that mainly exists in soil or rock. The gas decays into radioactive particles called radon progeny that can enter the human body through breathing. Upon entering the body, these radioactive elements release α-rays that affect lung tissue, causing lung cancer upon long-term exposure thereto. Epidemiological studies first outlined a high correlation between the incidence rate of lung cancer and exposure to radon progeny among miners in Europe. Thereafter, data and research on radon exposure and lung cancer incidence in homes have continued to accumulate. Many international studies have reported increases in the risk ratio of lung cancer when indoor radon concentrations inside the home are high. Although research into indoor radon concentrations and lung cancer incidence is actively conducted throughout North America and Europe, similar research is lacking in Korea. Recently, however, studies have begun to accumulate and report important data on indoor radon concentrations across the nation. In this study, we aimed to review domestic and foreign research into indoor radon concentrations and to outline correlations between indoor radon concentrations in homes and lung cancer incidence, as reported in ecological studies thereof. Herein, we noted large differences in radon concentrations between and within individual countries. For Korea, we observed tremendous differences in indoor radon concentrations according to region and year of study, even within the same region. In correlation analysis, lung cancer incidence was not found to be higher in areas with high indoor radon concentrations in Korea. Through our review, we identified a need to implement a greater variety of statistical analyses in research on indoor radon concentrations and lung cancer incidence. Also, we suggest that cohort research or patient-control group research into radon exposure and lung cancer incidence that considers smoking and other factors is warranted.
Cohort Studies ; Elements, Radioactive ; Epidemiologic Studies ; Europe ; Human Body ; Incidence ; Korea ; Lung Neoplasms* ; Lung* ; Miners ; Mortality ; North America ; Odds Ratio ; Radon* ; Respiration ; Smoke ; Smoking ; Soil ; World Health Organization

Peutz-Jeghers syndrome is a genetic disorder consisting of mucocutaneous pigmentation and gastrointestinal polyposis. Although the polyp may be found in a solitary fashion in this syndrome, such a case is exceedingly rare and would result in a case report even in other countries. A solitary Peutz-Jeghers polyp had not been reported domestically until now, and thereby, the authors here present a case of a clinical experience of Peutz-Jeghers syndrome with a solitary hamartomatous polyp in the duodenum.
Diagnosis* ; Duodenum* ; Hemorrhage* ; Peutz-Jeghers Syndrome ; Pigmentation ; Polyps*

Atrial fibrillation occurs in 10 to 25% of patients with thyrotoxicosis. Several recent studies have found a high frequency of cerebral thromboembolism in such patients. Thus anticoagulation has been recommended for patients with thyrotoxic atrial fibrillation to prevent embolic complications especially when associated with predictors of an increased risk of arterial thromboembolism in nonrheumatic atrial fibrillation such as recent congestive heart failure, history of hypertension, previous thromboembolism, left atrial enlargement, and global left ventricular dysfunction. Most reported cases of embolic events involving central nervous system in thyrotoxic atrial fibrillation affected cerebrum, and cerebellar embolic infarction from the heart was rarely seen. We herein report our experience of a case of cerebellar embolism in thyrotoxic atrial fibrillation.
Atrial Fibrillation* ; Central Nervous System ; Cerebrum ; Embolism ; Heart ; Heart Failure ; Hepatitis ; Humans ; Hypersensitivity ; Hypertension ; Infarction* ; Thromboembolism ; Thyrotoxicosis ; Ventricular Dysfunction, Left

OBJECTIVE: Diverse glomerular disorders leadsing to progressive glomerulosclerosis share the common features of increased mRNA expression for extra- cellular matrix protein and growth factors. The precise role of angiotensin II in contributing to these disturbances is currently unknown. ACE inhibitors have been proved to be beneficial in protecting against glomerular injury in animal models and many of human glomerular diseases. Type IV collagen is a main component of extracellular matrix in the mesangium : its increased accumulation is a common pathologic finding in the glomerulosclerosis. There are some evidences that the beneficial effect of ACE inhibitor does not solely depend on the hemodynamic effect, but may be mediated by other effect. The purpose of this study is to evaluate the effects of high glucose, angiotensin II and angiotensin converting enzyme inhibitor on the expression of PC alpha1(lV) in mesansial cells(MCs). METHODS: Human mesangial cells were cultured with standard method. To investigate the effect of each drug and high glucose condition, MCs were cultured in the normal-glucose medium(100mg/dl) and high-glucose medium(450mg/dl), respectively. An- giotensin II and angiotensin converting enzyme inhibitor(captopril) were added to culture medium at final concentration of 10 M which is the physiologic dose in vivo. MCs were cultured in each condition for 3days, when the maximal effect of high glucose on MCs, and harvested for mesurement of the expression of PC alpha1(IV) mRNA. To quantitate the PC alpha(1V) mRNA levels in each condition, semiquantitatine RT-PCR was done with co-amplification of house keeping gene. RESULTS: PCa1(IV) mRNA expression was significantly increased in high-glucose medium(30mM) compared to normal-glucose medium(5.5mM)(2.28+/-0.34 vs 0.96+/-0.08, p<0.05). Administration of angiotensin ll(10(-6)M) in culture media induced a further increment in the PC a >(IV) mRNA expression to 4.64+/-0.28(p<0.05). Angiotensin II in the normal-glucose medium increased the PC alpha1(lV) mHNA expression as 2.69+/-0.23 control(p<0.05). Addition of angiotensin converting enzyme inhibitor(Capopril, 10(-6)M) in high- glucose culture medium significantly suppressed the PC alpha1(IV) mRNA expression as 0.690.11(p<0.05). CONCLUSION: High glucose concentration in culture medium significantly increases the mRNA expression of procollagen alphal(IV) than normal glucose concentration. Angiotensin II increases the collagen mRNA expression directly and this effect was significantly prevented by ACE inhibitor. This result suggests that hyperglycemia in diabetic millieu can directly increase collagen production, and ACE inhibitor may inhibit progressive glomerulosclerosis by decreasing collagen production as well as reducing intraglomerular pressure.
Angiotensin II ; Angiotensin-Converting Enzyme Inhibitors ; Angiotensins* ; Collagen ; Collagen Type IV ; Culture Media ; Extracellular Matrix ; Glucose* ; Hemodynamics ; Humans* ; Hyperglycemia ; Intercellular Signaling Peptides and Proteins ; Mesangial Cells* ; Models, Animal ; Peptidyl-Dipeptidase A ; Procollagen ; RNA, Messenger*

BACKGROUND: Glomerular diseases of diverse origins are characterized by heavy proteinuria and tubulointerstitial changes in pathology. Numerous studies have recently demonstrated that interstitial fibrosis and tubular atrophy are better predictors of renal disease progression compared with glomerular pathology. One of the important mechanisms of these tubulointerstitial injury is tubulointerstitial damage due to increased protein trafficking across the proximal tubular epithelial cells. We tested the hypothesis that tubular cells exposed to high concentration of protein express TGF-beta, which can be related to tubulointerstitial fibrosis, and Fas antigen, which can be associated with tubular cell apoptosis. METHODS: Cultured human proximal tubular cells were incubated with varying concentrations of BSA (1, 10 mg/mL) and nephrotic range proteinuria, due to diabetic nephropathy (1, 10 mg/mL), with or without inactivation of complement. After 24 hr-incubation period, the expressions of TGF-beta and Fas mRNA were examined by RT-PCR. RESULTS: The amount of expression of TGF-beta was increased in BSA 10 mg/mL group (0.78+/-0.12, p=0.016) and in diabetic proteinuria 10 mg/mL group (0.7+/-0.08, p=0.012) compared to control group which was incubated in medium alone (0.48+/-0.02), and the amount of expression of Fas was increased in BSA 10 mg/mL group (0.97+/-0.09, p=0.021) and showed increased tendency in diabetic proteinuria 10 mg/mL group (0.94+/-0.14, p=0.067) also. Furthermore, the anti TGF-beta antibody ameliorated the increased albumin-induced expression of Fas. CONCLUSION: Collectively, our results showed that protein overload increased the expression of TGF-beta & Fas, which can play an important role in tubulointerstitial atrophy by inducing apoptosis of renal tubular cells.
Antigens, CD95 ; Apoptosis ; Atrophy ; Complement System Proteins ; Diabetic Nephropathies ; Disease Progression ; Epithelial Cells ; Fibrosis ; Humans* ; Pathology ; Protein Transport ; Proteinuria* ; RNA, Messenger ; Transforming Growth Factor beta*

BACKGROUND: Glomerular diseases of diverse origins are characterized by heavy proteinuria and tubulointerstitial changes in pathology. Numerous studies have recently demonstrated that interstitial fibrosis and tubular atrophy are better predictors of renal disease progression compared with glomerular pathology. One of the important mechanisms of these tubulointerstitial injury is tubulointerstitial damage due to increased protein trafficking across the proximal tubular epithelial cells. We tested the hypothesis that tubular cells exposed to high concentration of protein express TGF-beta, which can be related to tubulointerstitial fibrosis, and Fas antigen, which can be associated with tubular cell apoptosis. METHODS: Cultured human proximal tubular cells were incubated with varying concentrations of BSA (1, 10 mg/mL) and nephrotic range proteinuria, due to diabetic nephropathy (1, 10 mg/mL), with or without inactivation of complement. After 24 hr-incubation period, the expressions of TGF-beta and Fas mRNA were examined by RT-PCR. RESULTS: The amount of expression of TGF-beta was increased in BSA 10 mg/mL group (0.78+/-0.12, p=0.016) and in diabetic proteinuria 10 mg/mL group (0.7+/-0.08, p=0.012) compared to control group which was incubated in medium alone (0.48+/-0.02), and the amount of expression of Fas was increased in BSA 10 mg/mL group (0.97+/-0.09, p=0.021) and showed increased tendency in diabetic proteinuria 10 mg/mL group (0.94+/-0.14, p=0.067) also. Furthermore, the anti TGF-beta antibody ameliorated the increased albumin-induced expression of Fas. CONCLUSION: Collectively, our results showed that protein overload increased the expression of TGF-beta & Fas, which can play an important role in tubulointerstitial atrophy by inducing apoptosis of renal tubular cells.
Antigens, CD95 ; Apoptosis ; Atrophy ; Complement System Proteins ; Diabetic Nephropathies ; Disease Progression ; Epithelial Cells ; Fibrosis ; Humans* ; Pathology ; Protein Transport ; Proteinuria* ; RNA, Messenger ; Transforming Growth Factor beta*

A 15q25-qter partial trisomy characterized by pre or postnatal overgrowth, tall stature, macrocephaly and craniosynostosis has rarely been reported. The cause of overgrowth has been thought to be the triplication of the insulin-like growth factor 1 receptor (IGF1R) gene located on the 15q26.3. We report a patient with partial trisomy 15q25.3-qter showing mental retardation, developmental delay, macrocephaly, long narrow face, ptosis, high palate arch, scoliosis, clinodactyly and overgrowth. Additional material located on terminal 2q was found in karyotyping analysis. In bacterial artificial chromosome (BAC) clone-based-array comparative genomic hybridization (aCGH) analysis, a gain of 31 clones on 15q25.3-qter and a loss of 2 clones on 2q37.3 were observed. An extra copy of IGF1R gene was observed on derivative chromosome 2 in FISH analysis. In conclusion, the patient was diagnosed to have de novo 46,XX,der(2)t(2;15)(q37.3;q25.3) chromosome complement. Adequate genetic counseling and regular follow-ups would be needed for the patient.
Abnormalities, Multiple/genetics ; Child, Preschool ; *Chromosomes, Human, Pair 15 ; Comparative Genomic Hybridization ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Receptor, IGF Type 1/*genetics ; Translocation, Genetic ; *Trisomy

OBJECTIVE: Diabetic nephropathy is an important cause of end stage renal disease in Korea and associated with major morbidity and mortality. The precise pathogenic mechanism of this disease is still controversial, but it has been considered that multiple factors are contribute to the development and progression of diabetic nephropathy. One of these factors, renin-angiotensin system has been proven to be a major mediator of this disease via activation of angiotensin II, which has multiple functions such as induction of production of extracellular matrix protein and various intraglomerular cells, tubulointerstital component and increment of intraglomerular pressure. Transforming growth factor(TGFbeta) is a multifunctional cytokine with major profibrotic character, which stimulates the production of extracellular matrx(ECM) protein, inhibit the degradation of ECM and induce the interaction of mesangial cells with ECM via integrin receptors. This study was done to evaluate the role of angiotensin II and angiotensin converting enzyme inhibitor in expression of TGFbeta mRNA which is a main mediator in the pathogenesis of diabetic nephropathy. METHODS: Human mesangial cells(MCs) were cultured by standard culture techniqne. For this study, cells in the 5th to 7th passage were used. To make a different glucose concentration in culture medium, normal(100mg/dl) or high glucose(450mg/dl) concentrations of D-glucose were added, and cultured in 17% heat inactivated fetal bovine serum. Angiotensin II and ACE inhibitor(captopril) were administered to the culture medium at final concentration of 10-6M. After 72 hours, MCs were harvested to measure the expression of TGFbeta mRNA. To measure the mRNA expression of TGFbeta in each condition, semi quantitative PCR was done and all results were corrected by beta-actin gene. RESULTS: mRNA expression of TGFbeta was significantly increased in the high glucose medium(30 mM) compared to normal glucose medium(5.5mM) (3.82+/-0.465 vs 2.27+/-0.13, p<0.05). Administration of angiotensinII(10-6M) in high glucose medium induced a further increase in the TGFbeta expression to 4.29+/-0.476(p<0.05). AngiotensinII(10-6M) in normal glucose medium also showed a significant increase in TGFbeta expression as 3.40+/-1.88(p<0.05). Administration of ACE inhibitor(Captopril, 10-6M) in high glucose medium prevented the increse of TGFbeta expression(1.20+/-0.18 vs 3.82+/-0.465, p<0.05). CONCLUSION: From these findings, it suggest that angiotensinII is an important mediator in the pathogenesis of diabetic nephropathy. ACE inhibitor may have a role in the progress of this disease via direct suppression of TGFbeta system as well as beneficial intraglomerular hemodynamic effect.
Actins ; Angiotensin II* ; Angiotensins* ; Diabetic Nephropathies ; Extracellular Matrix ; Glucose* ; Hemodynamics ; Hot Temperature ; Humans* ; Kidney Failure, Chronic ; Korea ; Mesangial Cells* ; Mortality ; Peptidyl-Dipeptidase A ; Polymerase Chain Reaction ; Renin-Angiotensin System ; RNA, Messenger* ; Transforming Growth Factor beta*