BACKGROUND: It has long been suggested that neutrophils and their products are implicated as the central mediators of the acute lung injuries. Contrary to the dominant role of neutrophils in ARDS, many cases of ARDS has occurred in the setting of severe neutropenia without pufrnonary neutrophil infiltration. Therefore it is certain that effector cell(s) other than neutrophil play an important role in the pathogenesis of ARDS. This experiment was performed to define the mechanism of ARDS in the setting of neutiopenia, 1) by comparing the severity of endotoxin-induced lung injury, 2) by measurement of hydrogen peroxide production and cytokine concentration in the bronchoalveolar lavage cells and fluids obtained from different rats with and without cyclophosphamide-pretreatment. METHOD: The male Sprague-Dawleys were divided into the normal control (NC)-, endotoxin (ETX)-, and cyclophosphamide (CPA)-group in which neutropenia was induced by injecting cyclophosphamide intraperitoneally. Acute lung injury was evoked by injecting lipopolysaccharide (LPS) into a tail vein. The bronchoalveolar lavage (BAL) was performed at 3 and 6 hour after administration of LPS to measure the change of cell counts and concentrations of protein and cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Hydrogen peroxide (HPO) production from BAL cel]s was measured at 6 hour after LPS administration by phenol red microassay with and without zymosan stimulation. RESULTS: The results were as follows. A change of leukocyte counts in the peripheral blood after treatment with CPA More than 95% of total leukocytes and neutrophils were reduced after CPA administration, resulting in severe neutropenia. A change of BAL cells In the ETX-group, the number of total cells (p<0.01) and of macrophage and neutrophll (p<0.05) were increased at 3 and 6 hour after LPS administration compared to those of NC- group. In the CPA-group, the number of total leukocyte and macrophage were not changed after LPS administration, but neutrophil counts were significantly reduced and jt took part in less than 0.1% of total BAL cells (p<0.01 vs NC-group). BAL cells in this group were almost all macrophages (99.7%). A change of protein concentration in the BALF In the ETX-group, protein concentration was increased at 3 hour and was more increased at 6 hour after LPS administration (p<0.05 and <0.01 vs NC-group, respectively). In the CPA-group, it was also significantly elevated at 3 hour after LPS administration (p<0.05 vs NC-group) , but the value was statistically not different from that of ETh-group. The value measured at 6 hour after LPS administration in the CPA-group became lower than that of ETX-group (p<0.05), but showed still a higher value compared to that of NC-group (p<0.05). A change of cytokine concentration in the BALF TNF-alpha and IL-6 were elevated in the ETX- and CPA-group compared to those of NC-group at both time intervals. There was no statistical difference in the values of both cytokines between the ETX- and CPA-groups. Measurement of hydrogen peroxide production from BAL cells There was no intergroup difference of HPO production from resting cells. HPO production after incubation with opsonized zymosan was significantly elevated in all groups. The percent increment of HPO production was highest in the ETX-group (89.0%, p<0.0008 vs NC-group ), and was 42.85 in the CPA-group (p = 0.003 vs NC-group ). Conclusion Acute lung injury in the setting of neutropenia might be caused by functional activation of resident alveola r macrophages.
Acute Lung Injury* ; Animals ; Bronchoalveolar Lavage ; Cell Count ; Cyclophosphamide ; Cytokines ; Humans ; Hydrogen Peroxide ; Interleukin-6 ; Leukocyte Count ; Leukocytes ; Lung Injury ; Macrophages* ; Male ; Neutropenia ; Neutrophil Infiltration ; Neutrophils ; Phenolsulfonphthalein ; Rats* ; Tumor Necrosis Factor-alpha ; Veins ; Zymosan

OBJECTIVE: A number of soluble factors,which play important role in the pathophysiology of rheumatoid synovitis are also known to be involved in osteoclast differentiation and activation through RANKL (Receptor activator of NF-kB ligand). To investigate the importance of RANKL in the pathogenesis of bone erosion in rheumatoid arthritis (RA) patients, we analyzed the expression of RANKL and Osteoprotegerin (OPG) and examined the formation of osteoclasts in rheumatoid synovial fibroblasts under the influence of various osteotropic factors. METHODS: Primary culture synoviocytes or fibroblast-like synoviocytes isolated from synovial tissues of 8 RA patients were cultured and treated with IL-1beta (2 ng/ml), TNF-alpha (2 ng/ml), INF-gamma(1000 micro/ml), IL-15 (10 ng/ml), IL-12 (10 ng/ml), dexamethasone (10(-9) M), PMA (10 ng/ml) or 1,25 (OH)2D3 (10(-9) M) for 18 hours. Expression RANKL or OPG mRNA was measured by semiquantitative RT-PCR within linear amplification condition. TRAP (+) MNC (tartrate resistant acid phosphatase-positive multinucleated cell) formation was induced from primary culture synoviocytes or in coculture system of synovial fibroblasts with PBMCs in the presence of M-CSF and 1,25 (OH)2D3. RESULTS: 1. The intensity of base-line expression was different from patient to patient. Primary culture synoviocytes and synovial fibroblasts express RANKL and OPG mRNA with decreasing intensity when they are passaged. 2. Expresssion of RANKL mRNA was significantly increased by 1,25 (OH)2D3 and IL-1beta (158.8+/-21% and 197.2+/-17% of controls, p<0.05 and p<0.005, respectively), while decreased significantly by dexamethasone (25.6+/-4.6% of controls, p<0.005). Expression of RANKL mRNA was significantly increased by IL-1beta and decreased by dexamethasone, in a dose- and time-dependant manner. 3. TRAP (+) MNCs are formed from primary culture synoviocytes or in coculture system of synovial fibroblasts and PBMC in the presence of M-CSF and 1,25 (OH)2D3. Dexamethasone clearly inhibited TRAP (+) MNCs formation from synovial cells. CONCLUSION: The regulatory mechanism for the expression of RANKL or OPG in rheumatoid synoviocytes might be different from that in bone marrow cells. Modulating the expression of these molecules could have potential therapeutic implication targeting bone destruction in RA.
Arthritis, Rheumatoid ; Bone Marrow Cells ; Coculture Techniques ; Dexamethasone ; Fibroblasts* ; Humans ; Interleukin-12 ; Interleukin-15 ; Macrophage Colony-Stimulating Factor ; NF-kappa B* ; Osteoclasts* ; Osteoprotegerin ; RNA, Messenger ; Synovitis ; Tumor Necrosis Factor-alpha

Carcinoid is a neuroendocrine tumor and contains many peptide substances and biological active amines, so if it is released, it can cause carcinoid syndrome. However, most carcinoid tumors are unfortunately asymptomatic, and it is difficult to find one smaller than 1 cm because it doesn't have prominent mucosal elevation and change. We can reduce expenses and recovery period of the patient by using a relatively noninvasive endoscopic mucosal resection, unless it has distant organ and lymph node metastasis. Colonoscopy is an optimizing diagnostic tool for early detection of asymptomatic carcinoids. But according to colonoscopic guidelines of many institutes, they recommend to perform a screening colonoscopy in the asymptomatic fifties if there are no risk factors. However, a careful examination of colonoscopy is needed, because possibility of malignant tumor in aymptomatic young age. The authors report four cases of carcinoid tumor in asymptomatic thirties with review of several literatures.
Academies and Institutes ; Amines ; Carcinoid Tumor ; Colonoscopy ; Humans ; Lymph Nodes ; Mass Screening ; Neoplasm Metastasis ; Neuroendocrine Tumors ; Risk Factors

BACKGROUND: Restenosis remains as the major limitation of percutaneous translumainal coronary balloon angioplasty (PTCA). Although its mechanism remains incompletely understood, proliferative action of arterial smooth muscle cells has been found to play an important role on restenosis by neointimal formation after PTCA. Glycosaminoglycan-containing compounds, including Sulodexide (Vessel Due , ALFA, Wasserman, S.p.A, Italy), inhibit the proliferation and maigration of vascular smooth muscle cells in vitro. OBJECTIVES: This study was performed to assess the efficacy of Sulodexide, a glycosaminoglycan compound with antithrombotic and antiproliferative properties, in preventing restenosis after PTCA. METHOD: Two hundred eighty-four patients with ischemic heart disease were randomized to receive either the standard PTCA without Sulodexide in 144 patients (control group, M : F = 99 : 45, Age = 58 +9 or -9), 160 lesions or the standard PTCA with Sulodexide in 140 patients (treated group, M : F = 89 : 51, age = 58 +10 or -10), 158 lesions. Successful angioplasties were performed in 258 atheromatous coronary lesions in 224 patients for whom follow-up angiographic data were obtained 6 month later. Quantitative coronary angiographic analysis (QCA) was performed before , immediate after PTCA and 6-month later. Angiographic restenosis (>50% diameter stenosis at follow-up) was the primary end point : miniamal luminal diameter at follow-up angiogram was the secondary end point. RESULT: Successful PTCA was 97.6% and 97.5% in the standard PTCA with Sulodexide and the standard PTCA without Sulodexide, respectively. Although reference vessel size and minimal luminal diamater after PTCA were larger in the control group than in the Sulodexide group(2.94+0.11 or-0.11 vs 2.83+0.13 or -0.13 mm and 2.26+0.12 or -0.12 vs 2.18+0.08 or -0.08 mm, respectively, p=NS), there was a increased tendency of minimal lumen diameter at 6 months angiogram in the Sulidexide group than in the control group (1.12+0.50 or -0.50 vs 1.07 + 0.53 or -0.53 mm, respectively, p=NS). Angiographic restenosis occured in 42% of lesions in the Sulodexide group and 52% of the control group (p=NS). CONCLUSIONS: Sulodexide treatment had a tendency to reduce restenosis rate in 6 months after coronary angioplasty. However, further study is necessary to verify the antiproliferative effect of Sulodexide with much larger number of patients.
Angioplasty ; Angioplasty, Balloon, Coronary* ; Constriction, Pathologic ; Follow-Up Studies ; Humans ; Muscle, Smooth, Vascular ; Myocardial Ischemia ; Myocytes, Smooth Muscle ; Phenobarbital ; Prospective Studies*

BACKGROUND: The clinical use of intracoronary stents is impeded by the risk of subacute stent thrombosis and complications associated with the anticoagulant regimen. The use of high pressure balloon dilatations and confirmation of adequate stent expansion by intravascular ultrasound provide assurance that anticoagulation therapy can be safely omitted. Therefore, we evaluated the effect of anticoagulation of subacute thrombosis sfter stenting retrospectively on a consecutive series of patients who received palmaz-Schatz coronary stents with high pressure balloon dilatation. METHOD: From March 1995 to August 1995, 62 patients underwent Palmaz-Schatz coronary stent implantation. After deploying stents successfully, high pressure overdilatation of the stents was performed in all patients. According to post-stent anticoagulation, 32 patients received aspirin 200 mg/day, ticlopidine 500 mg/day and warfarin for two months, 30 patients received aspirin and ticlopidine. RESULTS: The clinical or angiographic variables were not significantly different between the two groups. There was no acute or subacute thrombosis in the two groups. The hospital stay after stenting was significantly shorter in the patients without antcoagulation than in patients with anticoagulation. CONCLUSION: The Palmaz-Schatz stent can be safely implanted without anticoagulation provided that stent expansion is daequate by the use high pressure balloon dilatation This technique significantly reduces hospital time and vascular complications and has a low stent thrombosis rate.
Aspirin ; Dilatation* ; Humans ; Length of Stay ; Retrospective Studies ; Stents* ; Thrombosis ; Ticlopidine ; Ultrasonography ; Warfarin

BACKGROUND: Restenosis is a major limitation of balloon angioplasty. Recently, new angioplasty devices have been used in an attempt to reduce the restenosis compared with coronary balloon angioplasty. Directional coronary atherectomy effectively dilated the lesion by removal of the atherosclerotic plaque. Therefore, we tried to evaluate immediate and late clinical outcomes after directional coronary atherectomy in the 57 patients with coronary artery disease. METHODS: From October 1991 to March 1997, fifty seven consecutive patients with 69 lesions were treated with directional coronary atherectomy. The patients underwent coronary angiography at pre-intervention, immediately after intervention and at 6 months post-intervention. Restenosis was assessed clinically and by computer-assissted quantitative measurements of luminal dimensions. Patients were requested to undergo coronary angiography at 6 months after directional coronary atherectomy. Angiographic restenosis was defined as more than 50% diameter stenosis by quantitative coronary angiographic analysis. RESULTS: Successful results were achieved in 61 of the 69 lesions(88%) and mean stenosis was reduced from 78.0+/-13.0% to 10.0+/-5.0%. Atherectomy resulted in an increase in minimal lumen diameter from 0.8+/-0.3mm to 3.0+/-0.6mm. Six months follow-up angiogram was obtained in 68% of 50 eligible lesions. The overall angiographic restenosis rate was 32%. Six month clinical follow-up was obtained in 94% of the eligible lesions. The clinical recurrence occured in 38% of the patients. The target lesion revascularization rate was 17%. CONCLUSIONS: Removal of coronary artery plaque with directional atherectomy led to large luminal diameter and six months follow-up angiography shows an overall restenosis rate of 32% However, further clinical study is warranted to evaluate the efficacy of atherectomy with larger numbers of patients.
Angiography ; Angioplasty ; Angioplasty, Balloon ; Angioplasty, Balloon, Coronary ; Atherectomy ; Atherectomy, Coronary* ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease ; Coronary Vessels ; Follow-Up Studies ; Humans ; Phenobarbital ; Plaque, Atherosclerotic ; Recurrence

BACKGROUND: In elective intervention, the implantation of an intracoronary stent is an established treatment modality to reduce restenosis in comparison with balloon angioplasty. However, stenting was empirically thought to be contraindicated for acute myocardial infarction because of the propensity for thrombosis, althought the percutaneous transluminal coronary balloon angioplasty(PTCA) on infarct-related artery is associated with a high incidence of restenosis. To knowlege, there is no report comparing the longterm efficacy of coronary stenting with PTCA in patients with acute myocardial infarction. Accordingly, we investigated the effect of stent implantation on restenosis of infarct-related artery in acute myocardial infarction, comparing with conventional balloon angioplasty. METHOD: From January 1994 to December 1995, 97 patients (stenting in 45 patients : PTCA in 52 patients) underwent intracoronary stenting or PTCA on infarct-related artery successfully at 7-10 days after onset of infarction. The coronary stents were Palmaz-Schatz stent in 35 patients and Cordis stent in 10 patients. Follow-up coronary angiography was performed in all patients 6 months later after intervention. RESULTS: No death, emergency coronary artery bypass surgery or reinfarction occurred during hospitalization in 97 patients. In 45 patients with stent implantation, no stent thrombosisoccurred. The 6-months angiographic restenosis rate was 13 percent in patients assigne to stent implantation and 52 percent in patients assigned to PTCA(p<0.05). CONCLUSION: We conclude that the intracoronary stent implantation on infarct-related artery at 7-10 days after acute myocardial infarction is safe, feasible and significantly reduces the restenosis rate.
Angioplasty, Balloon ; Arteries ; Coronary Angiography ; Coronary Artery Bypass ; Emergencies ; Follow-Up Studies ; Hospitalization ; Humans ; Incidence ; Infarction ; Myocardial Infarction* ; Stents* ; Thrombosis

BACKGROUND: The signal pathways and their precise roles for acute respiratory distress syndrome caused by endotoxin (ETX) has not been established. Since there has been several in vitro experiments suggesting that activation of protein kinase C (PKC) pathway may be responsible for endotoxin-induced inflammatory reaction, we performed in vivo experiments in the rats with the hypothesis that PKC-inhibition can effectively prevent endotoxin-induced acute lung injury. METHODS: We studied the role of PKC in ETX-induced ALl using PKC inhibitor (staurosporine, 5Th) in the rat. Specific pathogen free male Sprague-Dawley weighted from 165 to 270g were used for the study. Animals were divided into the normal control (NC)-, vehicle control (VC)-, ETX-, PMA (phorbolmyristateacetate)-, STP+PMA-, and STP+ETX-group. PMA (50mg/kg) or ETX (7mg/kg) was instilled through polyethylen catheter after aseptic tracheostomy with and without STP (0.2mg/kg) pretreatment. STP was injected via tail vein 30mm before intratracheal injection (IT) of PMA or ETX. Bronchoalveolar lavage (BAL) was done 3- or 6-hrs after IT of PMA or FTX respectively, to measure protein concentration, total and differential cell counts. RESULTS The results were as follows. The protein concentrations in BALF in the PMA- and ETX-group were very higher than that of VC-group (p<0.001). When animals were pretreated with STP, the %reduction of the protein concentration in BALF was 64.8 8.5 and 30.4 2.5% in the STP+PMA- and STP+ETX-group, respectively (p=0.028). There was no difference in the total cell counts between the PMA-and VC-group (p = 0.26). However the ETX-group showed markedly increased total cell counts as compared to the VC- (p=0.003) and PMA group (p=0.0027), respectively. The total cell counts in BALF were not changed after pretreatment with STP compared to the PMA- (p=0.22) and ETX-group (p=0.46). The percentage of PMN, but not alveolar macrophage, was significantly elevated in the PMA-, and ETX-group. Especially in the ETX-group, the percentage of PMN was 17 times higher than that of PMA (p<0.001). The differential cell counts was not different between the PMA and STP+PMA. On the contrary the STP+ETX-group showed decreased percentage of PMN (p = 0.016). There was no significant relationship between the protein concentration and the total or differential cell counts in each group. CONCLUSION: Pretreatment with PKC-inhibitor (staurosporine) partially but significantly inhibited ETX-in-duced ALI.
Acute Lung Injury* ; Animals ; Bronchoalveolar Lavage ; Catheters ; Cell Count ; Humans ; Macrophages, Alveolar ; Male ; Protein Kinase C* ; Protein Kinases* ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; Signal Transduction ; Specific Pathogen-Free Organisms ; Staurosporine ; Tracheostomy ; Veins

BACKGROUND: Balloon angioplasty of ostial left anterior descending coronary artery lesions has been associated with high rate of acute complications and late restenosis. Recently, coronary stenting has been proposed as one of effective treatment modalites of ostial left anterior descending artery lesions. METHODS: To evaluate the effects of stent design on the development of late restenosis, we retrospectively analyzed the efficacy of slotted tube stent implantation (40 patients, Palmaz-Schatz stent) and coil stent implantation (15 patients, tantalum Cordis stent) of ostial left anterior descending artery stenosis. Six-month angiographic follow-up data were obtained in 31 patients (82%) with slotted tube stent implantation and 12 patients (86%) with coil stent implantation. Angiographic restenosis was defined as > or = 50% diameter stenosis. RESULTS: Angiographic resten-osis rate was significantly lower in slotted tube stent implantation (32%) than in coil stent implantation (67%) (p<0.05). Target lesion revascularization rate of slotted tube stent implantation was significantly lower (26%) than that of coil stent implantation (57%) (p<0.05). CONCLUSIONS: Coil stent implantation of ostial left anterior descending artery lesions was associated with higher late restenosis compared with slotted tube stent impla-ntation. In conclusion, slotted tube stent implantation might be considered for ostial left anterior descending artery lesions to improve late clinical outcomes.
Angioplasty, Balloon ; Arteries ; Constriction, Pathologic ; Coronary Artery Disease ; Coronary Stenosis* ; Coronary Vessels* ; Follow-Up Studies ; Humans ; Retrospective Studies ; Stents* ; Tantalum

BACKGROUND: The results of new devices for long coronary stenotic lesion is disappointing. We evaluate the feasibility and efficacy of single long coronary stenting for long coronary stenosis, we implanted two types of long stents, newly developed less shortening Wall stent and Gianturco-Roubin II stent. METHODS: This study reports on the use of stents in 106 patients with 109 lesions with long lesion. Long coronary disease was defined as a lesion length longer than 20 mm. After the implantation of the stent, the stented coronary segment was dilated further with high pressure balloon inflation to achieve angiographic optimization. RESULTS: The mean age was 59+/-9 years. Mean stent length was 35+/-11 mm. Vessel distribution was 2 (2%) left main, 66 (61%) LAD, 10 (9%) LCX and 31 (28%) RCA. Implanted stents were 57 (52%) Gianturco-Roubin II stents and 52 (48%) Wall stents. Procedural success was achieved in 109 (100%) lesions. The MLD at lesion site increased from 0.8+/-0.4 mm to 3.2+/-0.5 mm. Procedure associated complications included 4 non-Q myocardial infarction. Angiographic follow up at 6 months was performed on 78 (72%) eligible lesions. There was one myocardial infarction and no death during follow up period. Restenosis by 50% diameter stenosis criteria was present in 39 (50%) of lesions. The target lesion revascularization was performed in 21 (19%) lesions. CONCLUSIONS: Stent implantation for long coronary disease is associated with excellent procedural success rates and low complication rates in the majority of patients. However, the restenosis rate is high regardless of the stent used. Further study needs to be done to improve the long-term clinical outcome.
Constriction, Pathologic ; Coronary Disease ; Coronary Stenosis ; Follow-Up Studies* ; Humans ; Inflation, Economic ; Myocardial Infarction ; Stents*