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*

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

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: 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*

Arsenic trioxide (As2O3) has been found to be remarkably effective in the treatment of patients with acute promyelocytic leukemia (APL). Although evidences for the proapoptotic activity of As2O3 have been suggested in leukemic and other solid cancer cells, the nature of intracellular mechanisms is far from clear. In the present study, we investigated As2O3 affect on the stress-responsive signaling pathways and pretreatment with antioxidants using HepG2 cells. When treated with micromolar concentrations of As2O3, HepG2 cells became highly apoptotic paralleled with activation of caspase-3 and members of mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) but not p38 MAP kinase. However, inhibition of each kinase activity failed to inhibit apoptosis by As2O3. Addition of n-acetyl cysteine (NAC) or diphenyleneiodonium (DPI) effectively protected cells from apoptosis and significantly lowered As2O3-induced activation of caspase-3. However, neither NAC nor DPI was able to effect ERK or JNK activation induced by As2O3. Guanidinoethyldisulfide dihydrochloride (GED) and 2-ethyl- 2-thiopseudourea (ETU), known inhibitors of the inducible nitric oxide synthase (iNOS), also suppressed the apoptotic activity of As2O3. These results suggest that As2O3 induces caspase-mediated apoptosis involving a mechanism generating oxidative stress. However, activation of some stress- responsive signaling pathways by As2O3 may not be the major determinant in the course of apoptotic processes.
Antioxidants/administration & dosage/pharmacology ; Apoptosis/*drug effects ; Arsenicals/administration & dosage/*pharmacology ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Enzyme Activation/drug effects ; Enzyme Inhibitors/*pharmacology ; Human ; Nitric-Oxide Synthase/*antagonists & inhibitors/metabolism ; *Oxidative Stress/drug effects ; Oxides/administration & dosage/*pharmacology ; *Signal Transduction/drug effects

Hemangioma is one of the most common tumor in the region of the head and neck. There are many methods were tried for the treatment of hemangioma, however no single satisfactory method was introduced. The hemangioma which arised from the external ear are rare. Authors report three cases of the hemangioma which involved the external ear. The hemangioma was aesthetically treated with surgical reduction and ligation
Ear, External* ; Head ; Hemangioma* ; Ligation* ; Neck

Spontaneous internal biliary fistulas are not an uncommon complication of primary biliary disease. Almost 90% of the abnormal biliary-enteric communications between the gallbladder and the duodenum are caused by perforation via gallstones into an otherwise normal duodenum. However, biliary-enteric communications that are caused by primary duodenal ulcer disease are much less common. We experienced a case of duodenal peptic ulcer disease that perforated into the common bile duct in a 45-year-old woman.
Biliary Fistula ; Common Bile Duct ; Duodenal Ulcer* ; Duodenum ; Female ; Fistula* ; Gallbladder ; Gallstones ; Humans ; Middle Aged ; Peptic Ulcer