BACKGROUNG AND OBJECTIVES: It was reported that low molecular weight heparin (LMWH) was more effective than unfractionated heparin in patients with acute coronary syndrome. Recent studies have shown that the pathophysiology of restenosis in stented lesions was different from those of nonstented lesions. Treatment strategies designed to limit cellular proliferation that were ineffective in nonstented lesions may be efficacious in reducing in-stent restenosis. This study was aimed to compare the clinical and angiographic results of LMWH (nadroparin) after coronary stenting with those of conventional ticlopidine regimen. MATERIALS AND METHODS: Patients were eligible for inclusion if they had angina and/or objective evidence of myocardial ischemia, and a significant (>50%) stenosis that was documented on a recent coronary angiogram. After stenting, prospective randomized comparison study was performed. Patients were randomly assigned to either nadroparin (200 IU/kg, sc, bid) or ticlopidine (250 mg bid) plus aspirin (200 mg qd) treatment groups. Repeat coronary angiography (KERN=*)was performed at 236+/-90days after stenting, and quantitative coronary angiographic analysis (QCA) was done. RESULTS: Intracoronary stent implantation was performed in eighty five lesions in eighty one patients (ticlopidine:40, nadroparin:41). There was no significant difference in any baseline clinical/angiographic variables between the two treatment groups. There were no subacute stent thrombosis, infarction and death in both groups. Six-month event-free survival was 36 (90%) in the ticlopidine group and 35 (85.4%) in the nadroparin group. Follow-up quantitative angiographic data such as late loss (1.35+/-0.70 vs 1.32+/-0.69), loss index (0.53+/-0.70 vs 0.56+/-0.23) and restenosis rate (36% vs 25.8%) were not different between ticlopidine and nadroparin groups. CONCLUSION: Effects of nadroparin were not different from those with ticlopidine therapy in the prevention of restenosis and subacute stent thorombosis after coronary stenting. Clinical outcomes between two strategies were similar. Low molecular weight heparin may be an alternative to ticlopidine in patients that ticlopidine cannot be administered because of severe adverse effects.
Acute Coronary Syndrome ; Aspirin ; Cell Proliferation ; Constriction, Pathologic ; Coronary Angiography ; Disease-Free Survival ; Follow-Up Studies ; Heparin ; Heparin, Low-Molecular-Weight ; Humans ; Infarction ; Myocardial Ischemia ; Nadroparin* ; Prospective Studies ; Stents* ; Thrombosis ; Ticlopidine*

Hemochromatosis is a disorder caused by excessive iron deposition in parenchymal cells that leads to cellular damage and organ dysfunction. The excessive iron overload of secondary hemochromatosis is associated with chronic disorders of erythropoiesis that are treated with prolonged repeated blood transfusions. We experienced two cases of transfusional hemochromatosis involving the pituitary gland, and we report the findings of the MR imaging.
Blood Transfusion ; Erythropoiesis ; Hemochromatosis* ; Humans ; Iron ; Iron Overload ; Magnetic Resonance Imaging* ; Pituitary Gland*

BACKGROUND: In pediatric anesthesia, a method using deliberate endobronchial intubation and auscultation has been used for proper endotracheal tube depth. Tube size, however, may influence on auscultation for air leak between the tube and main bronchus. We attempted to ascertain whether the uncuffed tracheal tube (TT) size affects verifying tube placement by auscultation in children. METHODS: In 23 children, we measured the distance from the carina to the tip of a tube when the first auscultatory sound could be detected on the left chest and when the breathing sound of both chests equalized during withdrawal from right main bronchus. Then, we compared them with those of either a one-size larger or a one-size smaller tube. RESULTS: The distance from the carina to the tip at the first sound was significantly longer in the smaller tracheal tube (1.8 cm vs 1.5 cm, P = 0.01). The tube tip at the equalized breath sounds was 0.6 cm below the carina in both tubes. CONCLUSIONS: These results suggest that detecting endobronchial intubation may be more difficult when using uncuffed tracheal tubes with one-size smaller tube and that auscultation with deliberate bronchial intubation can place the uncuffed TT deeper than an intended depth.
Anesthesia ; Auscultation* ; Bronchi ; Child* ; Humans ; Intubation ; Respiratory Sounds ; Thorax

BACKGROUND: The p38 mitogen-activated protein kinases (p38Map kinases) are a family of prolinedirected serine/threonine kinases. At least four isoforms of p38Map kinases have been identified; however, their physiological significances remain to be understood. Recently, the role of p38Map kinase in insulin-stimulated glucose uptake has been suggested. The present study aimed to investigate which isoform(s) were responsive to insulin stimulation. In addition, the activities of p38 Map kinase isoforms that may participate in the insulin's antiapoptotic function in CHO-IR cells were also determined. METHODS: Chinese hamster ovary cells, expressing wild- or mutated human insulin receptors (CHO-IR cells), were used to investigate whether insulin can stimulate any of the isoform(s) of the p38Map kinases. The p38Map kinase activity was determined by measuring the degree of 32P-labelling of ATF-2 protein, a specific substrate of p38Map kinase. A DNA laddering assay was performed to examine the degree of apoptosis and a RT-PCR analysis to determine which isoform(s) of the p38Map kinases were expressed in response to insulin. RESULTS: p38Map kinase activation by insulin was sharply suppressed in only the CHO-IR/A1018K cells, which lack the intrinsic tyrosine kinase activity of insulin receptors. Insulin stimulation of p38Map kinase was insensitive to SB203580, an inhibitor of the alpha(alpha)-and beta(beta)-isoforms of p38Map kinases. Moreover, orthovanadate, known as a specific stimulator of the gamma(gamma)-and delta(delta-) isoforms, stimulated the p38Map kinase activity in CHO-IR cells. Insulin increased the degree of mRNA expression of the delta-isoform, but not that of the alpha-isoform p38Map kinase. Interestingly, PD98059, an inhibitor of ERK, suppressed p38Map kinase stimulation, as well as the antiapoptotic protection of cells by insulin. As insulin was found to still protect ERK-lacking cells (CHO-IR/ SOS) from apoptosis, any substantial role(s) of ERK might be excluded. CONCLUSION: Our data suggest that insulin may stimulate the activity and expression of the-isoform of p38Map kinase in a MEK1/2-dependent manner. The involvement of the delta-isoform of p38Map kinase in insulin's antiapoptotic protection was also suggested, but remains to be investigated further to clarify the nature of its mechanism of action
Animals ; Apoptosis ; Cricetinae ; Cricetulus ; DNA ; Female ; Glucose ; Humans ; Insulin ; Ovary ; p38 Mitogen-Activated Protein Kinases ; Phosphotransferases* ; Protein Isoforms ; Protein-Tyrosine Kinases ; Receptor, Insulin ; RNA, Messenger ; Vanadates

BACKGROUND: The p38 mitogen-activated protein kinases (p38Map kinases) are a family of prolinedirected serine/threonine kinases. At least four isoforms of p38Map kinases have been identified; however, their physiological significances remain to be understood. Recently, the role of p38Map kinase in insulin-stimulated glucose uptake has been suggested. The present study aimed to investigate which isoform(s) were responsive to insulin stimulation. In addition, the activities of p38 Map kinase isoforms that may participate in the insulin's antiapoptotic function in CHO-IR cells were also determined. METHODS: Chinese hamster ovary cells, expressing wild- or mutated human insulin receptors (CHO-IR cells), were used to investigate whether insulin can stimulate any of the isoform(s) of the p38Map kinases. The p38Map kinase activity was determined by measuring the degree of 32P-labelling of ATF-2 protein, a specific substrate of p38Map kinase. A DNA laddering assay was performed to examine the degree of apoptosis and a RT-PCR analysis to determine which isoform(s) of the p38Map kinases were expressed in response to insulin. RESULTS: p38Map kinase activation by insulin was sharply suppressed in only the CHO-IR/A1018K cells, which lack the intrinsic tyrosine kinase activity of insulin receptors. Insulin stimulation of p38Map kinase was insensitive to SB203580, an inhibitor of the alpha(alpha)-and beta(beta)-isoforms of p38Map kinases. Moreover, orthovanadate, known as a specific stimulator of the gamma(gamma)-and delta(delta-) isoforms, stimulated the p38Map kinase activity in CHO-IR cells. Insulin increased the degree of mRNA expression of the delta-isoform, but not that of the alpha-isoform p38Map kinase. Interestingly, PD98059, an inhibitor of ERK, suppressed p38Map kinase stimulation, as well as the antiapoptotic protection of cells by insulin. As insulin was found to still protect ERK-lacking cells (CHO-IR/ SOS) from apoptosis, any substantial role(s) of ERK might be excluded. CONCLUSION: Our data suggest that insulin may stimulate the activity and expression of the-isoform of p38Map kinase in a MEK1/2-dependent manner. The involvement of the delta-isoform of p38Map kinase in insulin's antiapoptotic protection was also suggested, but remains to be investigated further to clarify the nature of its mechanism of action
Animals ; Apoptosis ; Cricetinae ; Cricetulus ; DNA ; Female ; Glucose ; Humans ; Insulin ; Ovary ; p38 Mitogen-Activated Protein Kinases ; Phosphotransferases* ; Protein Isoforms ; Protein-Tyrosine Kinases ; Receptor, Insulin ; RNA, Messenger ; Vanadates

Patients with traumatic aortic rupture rarely reach the hospital alive. Even among those who arrive at the hospital alive, traumatic aortic rupture after high-speed motor vehicle accidents leads to a high in-hospital mortality rate and is associated with other major injuries. Here, we report a rare case of descending midthoracic aortic rupture with blunt diaphragmatic rupture. Successful management with emergency laparotomy after an immediate endovascular procedure resulted in a favorable prognosis in this case.

Peutz-Jeghers syndrome is an autosomal dominant inherited disease that manifests as a combination of mucocutaneous pigmentation and gastrointestinal hamartomatous polyps that usually cause intussusception and intestinal hemorrhage. We report the case of a 40-year-old male patient who was diagnosed 20 years ago and had previously undergone 3 intestinal resection surgeries. This time, with the use of combined operative and endoscopic polypectomy, more than 100 polyps were removed. This technique is useful for providing a "clean" small intestine that allows the patient a long interval between laparotomies and reduces the complications associated with multiple laparotomies and resections.
Adult ; Endoscopy ; Hemorrhage ; Humans ; Intestine, Small ; Intussusception ; Laparotomy ; Male ; Peutz-Jeghers Syndrome* ; Pigmentation ; Polyps*

BACKGROUND/AIMS: Adefovir dipivoxil (ADV) resistance in patients with lamivudine-resistant chronic hepatitis B is not well understood. This study examined the initial virologic response (IVR) to ADV, the rate of ADV resistance and the factors associated with ADV resistance. METHODS: Eighty one lamivudine-resistant HBeAg-positive patients were enrolled in this study. IVR was defined as HBV DNA < 4 log10 copies/mL after 6 months of therapy. RESULTS: IVR was observed in 37/81(45.7%) patients and it was associated with higher pretreatment ALT (P=0.002), and low pretreatment HBV DNA level (P=0.015). The HBV DNA levels were significantly higher in the non-IVR patients than the IVR patients at 12, 18 and 24 months (4.73 vs 2.59, 4.53 vs 2.31, 4.39 vs 2.40 log10 copies/mL, respectively; P<0.01). During the follow-up period, 17(21.0%) patients showed phenotypic resistance to ADV and 9 (11.1%) patients had ADV-resistant mutations. The cumulative probabilities of the phenotypic resistance to ADV at 12 and 24 months were 8.7% and 32.5%, respectively. The cumulative probabilities of the genotypic resistance to ADV at 12 and 24 months were 0% and 14.6%, respectively. Resistance to ADV was associated with a higher pretreatment HBV DNA (P=0.019), and non-IVR (P<0.001). CONCLUSIONS: The cumulative probabilities of the phenotypic and genotypic resistance to ADV at 24 months were 32.5% and 14.6%. The high pretreatment HBV DNA and non-IVR (HBV DNA > or = 4 log10 copies/mL after 6 months of therapy) were associated with ADV resistance.
Adenine/*analogs & derivatives/therapeutic use ; Adult ; Alanine Transaminase/blood ; Antiviral Agents/*therapeutic use ; DNA, Viral/blood ; Drug Resistance, Viral ; Female ; Hepatitis B e Antigens/blood ; Hepatitis B virus/drug effects/genetics ; Hepatitis B, Chronic/*drug therapy/virology ; Humans ; Lamivudine/*therapeutic use ; Male ; Middle Aged ; Phosphonic Acids/*therapeutic use ; Predictive Value of Tests ; Retrospective Studies

OBJECTIVE: The relationship was studied between expression of c-erbB-2 oncoprotein and topoisomerase II-alpha as proliferating marker in precancerous lesions and invasive squamous carcinomas of the uterine cervix. METHODS: Total 81 formalin-fixed, paraffin-embedded sections of low-grade intrasquamous lesion (22 cases), high-grade intraepithelial lesions (42 cases) and invasive squamous cell carcinomas (17 cases) in the uterine cervix were stained by immunohistochemistry for expression of the c-erbB-2 oncoprotein and topoisomerase II-alpha. RESULTS: The expression of c-erbB-2 oncoprotein and staining index (mean+/-S.D) of topoisomerase II-alpha were statistically significant between precancerous lesions and invasive carcinoma. The expression of c-erbB-2 oncoprotein has correlation with staining index (mean+/-S.D) of topoisomerase II-alpha. CONCLUSION: There results suggest that the expression of c-erbB-2 protein has relationship with progression of squamous lesions and topoisomerase II-alpha is an useful proliferating marker in the uterine cervix. And, the expression of c-erbB-2 protein has correlation with expression of topoisomerase II-alpha.
Carcinoma, Squamous Cell* ; Cervix Uteri* ; DNA Topoisomerases, Type I* ; DNA* ; Female ; Immunohistochemistry ; Receptor, erbB-2

This paper described a collaborative exercise intended to see what kinds of short tandem repeat (STR) loci are used in different DNA typing laboratories in Korea and to compare their results for the demonstration whether uniformity of DNA profiling results from different laboratory could be achieved in Korea. Laboratories were asked to test five tissue DNAs using methods routinely used in each laboratory and to report the results to the coordinating laboratory. The exercise demonstrated that each laboratory was using different STR loci for the typing with different STR numbers, 2 VNTRs, 36 STRs and amelogenin in total, and the direct comparison of the results from all the laboratory for the 18 loci could not be done as only one laboratory submitted typing results. Among 21 loci for which several laboratories submitted typing results, results for 14 loci were the same and results for the other 7 loci were different depending on the participating laboratory. D1S80, F13A01, D16S539, D21S11, D18S51, D3S1744 were the loci with different typing results. Even in the cases where commercial kits were used, the results were not the same depending on the machines used, that is the capillary electrophoresis or the gel based electrophoresis. The reason for the different results, points about the standardization of the methods and the profiling data were described.
Amelogenin ; DNA ; DNA Fingerprinting ; Electrophoresis ; Electrophoresis, Capillary ; Korea ; Microsatellite Repeats