Mechanism of anti-proliferation caused by YC-1, an indazole derivative, in cultured rat A10 vascular smooth-muscle cells.
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Retraction Notice↗
Biomedical subjects
F Y Lee
Publications and source records attributed to F Y Lee.
A prospective randomized comparative trial showing that omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful endoscopic therapy.
BACKGROUND: A blood clot in a peptic ulcer is unstable in a low pH environment. The use of omeprazole may prevent rebleeding by elevating intragastric pH in patients with bleeding peptic ulcer after hemostasis has been achieved. OBJECTIVES: To assess the influence of using omeprazole and cimetidine on 24-hour intragastric pH and to determine their ability to prevent rebleeding after having achieved initial hemostasis in patients with active bleeding or nonbleeding visible vessels. METHODS: One hundred patients with bleeding peptic ulcers who had obtained initial hemostasis were enrolled in this randomized comparative trial. In the cimetidine group (n = 50), a 300-mg intravenous bolus of cimetidine was given, followed by a 1200-mg continuous infusion daily for 3 days. Thereafter, 400 mg of cimetidine was given orally twice daily for 2 months. In the omeprazole group (n = 50), a 40-mg intravenous bolus of omeprazole was given, followed by 160 mg of continuous infusion daily for 3 days. Thereafter, 20 mg of omeprazole was given orally once daily for 2 months. A pH meter was inserted in each patient's fundus under fluoroscopic guidance after the intravenous bolus of cimetidine or omeprazole had been administered. RESULTS: The stigmata of recent hemorrhage before endoscopic therapy in the omeprazole and cimetidine groups were, respectively, spurting (9 vs 12), oozing (4 vs 9), and nonbleeding visible vessel (37 vs 29) (P > .05). The duration of intragastric pH higher than 6.0 was longer in the omeprazole group (mean [+/- SD], 84.4% +/- 22.9%) than that of the cimetidine group (mean [+/- SD], 53.5% +/- 32.3%) (P < .001). Rebleeding occurred in 2 patients (4%) in the omeprazole group and in 12 patients (24%) in the cimetidine group by day 14 after enrollment (P = .004). There was a tendency for patients in the omeprazole group to require less blood transfusion (median, 0 mL; range, 0-2500 mL) than those in the cimetidine group (median, 0 mL; range, 0-5000 mL) (P = .08). The hospital stay and number of operations and mortality rate were similar between both groups. CONCLUSIONS: The use of omeprazole is more effective than cimetidine in increasing intragastric pH and reducing rebleeding episodes in patients with bleeding peptic ulcers after successful endoscopic therapy. This suggests that omeprazole should be used routinely after successful endoscopic therapy.
Adolescent↗
Pathologic supracondylar fracture due to osteolytic pseudotumor of knee following cementless total knee replacement.
Wear debris of polyethylene, polymethylmethacrylate, and metal have been recognized to be associated with foreign body reactions, osteolysis, and aseptic prosthetic loosening after joint replacement arthroplasty. Further, foreign body reaction due to the presence of extensive wear debris can cause aggressive granulomatous lesions and pathologic fracture. To our knowledge, there has been no previous report of pathologic fracture of the femur due to an agressive pseudotumor. This report describes a case of pathologic supracondylar fracture of the femur 6 years and 5 months after cementless total knee replacement arthroplasty. The fracture occurred through an aggressive expanding soft tissue mass that was a tumorlike lesion secondary to polyethylene wear debris. The lesion was associated with massive osteolysis around the femoral component of the total knee prosthesis.
Arthroplasty, Replacement, Knee↗
Programmed removal of chondrocytes during endochondral fracture healing.
This investigation tested the hypothesis that the removal of chondrocytes during endochondral fracture healing involves an ordered process of programmed cell death. To accomplish this, unilateral closed fractures were created in the femora of 36 Sprague-Dawley rats. The rats were killed in groups of four on days 1, 3, 7, 14, 21, 28, 42, 49, and 56 after fracture. The femora were embedded in paraffin and tested for expression of specific markers of fragmented DNA with use of a terminal deoxyuridyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) technique. To determine the potential for transdifferentiation of chondrocytes to osteoblasts, calluses were also hybridized to detect expression of osteocalcin mRNA. Cell proliferation was assessed by an immunohistochemical detection method for proliferating cell nuclear antigen. A separate group of four rats was killed on day 28 to represent the later stage of the endochondral ossification, and the calluses were examined for cellular morphology with transmission electron microscopy. The results showed a coordination in both time and space of the activities of cellular proliferation and programmed cell death. Cell proliferation was most active in the earlier phases of fracture healing (days 1 through 14), although TUNEL expression was apparent in hypertrophic chondrocytes on day 14 after fracture and persisted until day 28. In the later stages of fracture healing (days 14 through 28), proliferating cell nuclear antigen was no longer synthesized in hard callus (intramembranous bone) and cell removal was the dominant activity in soft callus chondrocytes. Expression of osteocalcin mRNA was detected in osteoblasts but not in hypertrophic chondrocytes or in any other nonosteoblastic cell type. These findings support the hypothesis that the removal of chondrocytes during endochondral fracture healing is part of an ordered transition of tissue types in which the cellular mechanisms are genetically programmed to involve proliferation, maturation, and apoptotic cell death.
Animals↗
Colocalization of iron and ceroid in human atherosclerotic lesions.
The presence of ceroid, a complex of protein associated with oxidized lipids, is commonly observed in human atherosclerotic lesions. When the human aortic walls were examined by Perls' staining, it was found that the iron deposits were evident in aortas with atherosclerosis. The extent of iron deposition was associated with the severity of the lesion. Furthermore, the iron deposits appeared to be colocalized with ceroids either extracellularly or intracellularly in foam cell-like macrophages or smooth muscle cells. Electron microscopy and X-ray microanalysis revealed that some of the extracellular iron aggregates were present within the ceroids. Likewise, some of the subcellular iron aggregates were found to be located near the lipid droplets or within the ceroids of foam cells. Collectively, these observations support the theory that the lipid oxidation occurring in lipid-laden cells of aortic lesions is facilitated by iron-overload in these cells.
Adult↗
Sequential variceal pressure measurement by endoscopic needle puncture during maintenance sclerotherapy: the correlation between variceal pressure and variceal rebleeding.
BACKGROUND/AIMS: The risk factors for esophageal variceal rebleeding are little known. Variceal pressure is one of the major determinants of variceal rupture, but the relationship between variceal pressure and variceal rebleeding during maintenance sclerotherapy has not been determined. This study was undertaken to evaluate the relationship between variceal pressure/gradient change and variceal rebleeding during maintenance sclerotherapy. METHODS: Patients with liver cirrhosis and recent esophageal variceal hemorrhage underwent consecutive variceal pressure measurements by direct puncture of the varices before each elective sclerotherapy. RESULTS: In 46 patients, the initial variceal pressure was no different regardless of age, sex, underlying etiology or hepatic reserve. Variceal pressure was higher in large varices, varices with more severe red wale markings, and varices with slower reduction in size during maintenance sclerotherapy. A larger volume of sclerosant was required to eradicate large varices, varices with more severe red wale markings, and varices with slower reduction in size during maintenance sclerotherapy. There was a positive correlation between initial variceal pressure and total amount of sclerosant (r=0.485, p=0.001). Initial variceal pressure was not related to rebleeding. Variceal pressure increased more in patients with rebleeding from varices per se (n=7) than in those without rebleeding (n= 24). There was no difference in pressure change between patients without rebleeding (n=24) and those with rebleeding from variceal ulcers (n=7). CONCLUSIONS: Large varices, severe red color signs and slow reduction in variceal size were associated with higher initial variceal pressure, and more sclerosant was required to eradicate the varices. An increase in variceal pressure during maintenance sclerotherapy indicates a higher risk of variceal rebleeding, but not of variceal ulcer rebleeding.
Aged↗
Effects of high dose octreotide on retrograde bile salt-induced pancreatitis in rats.
The effects of somatostatin and octreotide (a long acting somatostatin analogue) in acute pancreatitis are inconclusive. This study examined the prophylactic and therapeutic effects of different doses of octreotide on retrograde sodium taurodeoxycholate-induced acute necrotizing pancreatitis in rats. The rats were divided into 4 groups receiving subcutaneous injection of saline, octreotide 10 microg/kg, 20 microg/kg at 0, 8 and 16 h and octreotide 20 microg/kg at 5, 13 and 21 h, separately. The serum levels of amylase and lipase, pancreatic histopathology, mortality and hemodynamics were examined. Octreotide significantly reduced serum levels of amylase and lipase at 12 h and the degree of pancreatic edema, necrosis and hemorrhage at 18-24 h as compared to the control group. Prophylactic octreotide 10 microg/kg significantly decreased the 24-h mortality from 100% to 44.4% (p < 0.05). The 24-h mortality further reduced to 12.5% and 10% with prophylactic and therapeutic octreotide 20 microg/kg, respectively. The decrease of mean arterial pressure at 12 h was significantly lower in octreotide groups than in the control group. We conclude that octreotide improves pancreatic histopathology and survival in acute necrotizing pancreatitis in rats.
Amylases↗
Chronic administration of octreotide ameliorates portal hypertension and portal hypertensive gastropathy in rats with cirrhosis.
1. Portal hypertension and hyperdynamic circulation have been postulated to play a role in the pathogenesis of portal hypertensive gastropathy. Administration of octreotide to portal hypertensive rats has been shown to reduce portal pressure and ameliorate hyperdynamic circulation. 2. This study investigated the effects of chronic administration of octreotide on systemic and portal haemodynamics and the development of portal hypertensive gastropathy in carbon tetrachloride-induced cirrhotic rats. 3. After 12 weeks of carbon tetrachloride induction, cirrhotic rats were randomly assigned to receive either placebo (5% dextrose in water) or octreotide (65 micrograms/kg in 5% dextrose in water) subcutaneously twice daily for 10 days. Haemodynamic studies with a thermodilution technique and gastric morphometric analyses were performed at 10 days after treatment. 4. In cirrhotic rats, octreotide treatment induced a significant increase in systemic vascular resistance (2.7 +/- 0.2 versus 3.4 +/- 0.2 mmHg/ml.min-1.100 g-1, P < 0.05) and decrease in portal pressure (12.5 +/- 1.2 versus 9.9 +/- 0.5 mmHg, P < 0.05) compared with placebo-treated rats. In addition, octreotide treatment significantly reduced the mean cross-sectional area of gastric mucosal vessels (2290 +/- 145 versus 1810 +/- 101 micron 2, P < 0.05). 5. This study shows that chronic octreotide treatment ameliorates the development of portal hypertensive gastropathy in cirrhotic rats. The effect of octreotide on portal hypertensive gastropathy may, at least partly, be due to the alleviation of portal hypertension and hyperdynamic circulation.
Animals↗
Effect of long-term octreotide and isosorbide dinitrate on haemodynamics in rats with portal vein stenosis.
1. Both octreotide and isosorbide dinitrate have been shown to have portal hypotensive effects in animals with portal hypertension. Moreover, in both animals and humans with portal hypertension, the reduction of portal pressure was enhanced when nitrovasodilators were combined with propranolol or vasopressin. The present study was undertaken to evaluate the effect of long-term administration of octreotide and isosorbide dinitrate on haemodynamics in rats with portal vein stenosis. 2. Portal hypertension was induced by portal vein stenosis. Portal hypertensive rats were allocated into one of four groups (eight rats in each group): vehicle group, octreotide group (100 micrograms/kg via subcutaneous injection every 12 h), isosorbide dinitrate group (5 mg/kg via gastric gavage every 12 h) and combined treatment group. Drug was given for eight consecutive days, starting 1 day before surgery. Haemodynamic values were measured using a radioactive microsphere technique. 3. Long-term octreotide treatment decreased portal pressure and improved the hyperdynamic circulation. In contrast, long-term administration of isosorbide dinitrate reduced portal pressure but did not ameliorate vasodilatation. A combination of octreotide and isosorbide dinitrate improved the hyperdynamic circulation with a reduction of portal pressure. In addition, the mean value of portal pressure after combination treatment was significantly lower than in rats receiving octreotide alone. 4. These results showed that, in rats with portal hypertension, long-term combined administration of octreotide and isosorbide dinitrate improved the hyperdynamic circulation together with a more profound reduction of portal pressure than rats receiving octreotide alone.
Animals↗
Aminoguanidine ameliorates splanchnic hyposensitivity to glypressin in a haemorrhage-transfused rat model of portal hypertension.
1. Hyposensitivity to vasopressin is a well-documented phenomenon in animals with portal hypertension and patients with cirrhosis subjected to haemorrhage. Excessive formation of nitric oxide is at least partly responsible for the vascular hyporesponsiveness to vasoconstrictors observed in experimental portal hypertension or in rats with haemorrhagic shock. This study investigated whether addition of aminoguanidine, a preferential inducible nitric oxide synthase inhibitor, to glypressin (a long-acting vasopressin analogue) could enhance its portal hypotensive effect in portal-hypertensive rats with bleeding.2. Portal hypertension was induced by partial portal vein ligation. Fourteen days after operation, systemic and portal haemodynamics were measured in stable or bleeding portal vein-ligated rats receiving intravenous glypressin (0.07 mg/kg) or aminoguanidine (70 mg/kg) followed by glypressin infusion. In rats with a hypotensive haemorrhage, 4.5 ml of blood was withdrawn and 50% of the withdrawn blood was reinfused before the administration of glypressin or aminoguanidine.3. Glypressin resulted in a significantly greater decrease in portal pressure in portal vein-ligated rats without bleeding than in those with bleeding (P<0.001). In contrast, glypressin induced similar changes in mean arterial pressure between the two groups (P>0.05). The addition of aminoguanidine significantly potentiated the portal-hypotensive effect of glypressin in bleeding portal vein-ligated rats (P<0.005) without an effect on the changes in mean arterial pressure induced by glypressin infusion (P>0.05).4. Splanchnic hyposensitivity to glypressin exists in a haemorrhage-transfused rat model of portal hypertension. This hyposensitivity can be ameliorated by the administration of aminoguanidine.
Animals↗
Clonal disease of natural killer large granular lymphocytes in Taiwan.
Lymphoproliferative diseases of large granular lymphocytes (LDGL) may arise from either CD3+ T cells or CD3- natural killer (NK) cells. LDGL with clonal proliferation of large granular lymphocytes (LGL) is defined as LGL leukaemia. The number of patients with NK-LGL leukaemia reported is limited and the pathogenesis of the disease is not yet clear. From 1991 to 1998 six patients with cytogenetically proved clonal disease of NK-LGL were identified in our institute. All were seropositive for Epstein-Barr virus (EBV). EBV RNA or DNA could be detected in LGL from four patients by EBV in situ hybridization or Southern blot analysis. Most patients ran an aggressive clinical course and five died of the disease. Nonrandom clonal chromosomal abnormalities, including duplication of 1q, rearrangement at 3q and loss of chromosomes Y, 13 or 10, were noted in the six patients from this study and in eight from the literature. The implications of these recurrent cytogenetic aberrations in the development and progression of the disease deserve further studies.
Adolescent↗
Reconstruction of the shoulder joint using an acetabular allograft. A report of two cases.
Wide resection of tumors involving the glenoid region of the scapula compromises a center of motion in the shoulder joint and can cause significant loss of function. Two patients with aggressive tumor of the scapula were treated with wide resection and reconstruction using an osteoarticular acetabular allograft. The ball and socket geometry of the newly reconstructed joint and secure reattachment of soft tissues in the allograft provided a stable shoulder joint. The functional results of the two patients were 87% and 93%, respectively according to the Musculoskeletal Tumor Society system. In a select group of patients with locally aggressive lesions of the scapula, a surgical reconstruction with an osteoarticular allograft would yield satisfactory functional and cosmetic results.
Acetabulum↗
A discrete soft tissue mass in the distal thigh of a 29-year-old man.
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Adult↗
Predictive factors for rebleeding in patients with peptic ulcer bleeding after multipolar electrocoagulation: a retrospective analysis.
The role of endoscopic therapy for peptic ulcer bleeding is well-documented. Nevertheless, rebleeding occurs in 10% to 30% of patients, and such patients are at high risk for death without early retreatment or definitive surgery. The aim of our study was to predict which patients would rebleed within 1 month after successful multipolar electrocoagulation of 100 patients with active peptic ulcer bleeding (spurting, oozing, or nonbleeding visible vessel). We had achieved initial hemostasis in 97 patients and carried out univariate and multivariate analyses to predict which patients would rebleed. Rebleeding occurred within 1 month in 17 (17.5%) patients. we correlated 20 clinical and endoscopic factors with rebleeding episodes. With univariate analysis, blood transfusion of 500 ml or more at entry (p < 0.0001) and use of cimetidine (p = 0.01) were statistically significant for rebleeding. With multivariate analysis, use of omeprazole was an independent factor for preventing rebleeding (odds ratio, 7.68; 95% confidence interval, 1.642-35.929). We suggest that omeprazole may help to prevent rebleeding in patients who have had hemostasis with multipolar electrocoagulation.
Anti-Ulcer Agents↗
Effect of sucralfate granules in suspension on endoscopic variceal sclerotherapy induced ulcer: analysis of the factors determining ulcer healing.
Oesophageal ulcers commonly occur after endoscopic variceal sclerotherapy and usually cause complications and a delay in further sclerotherapy. The aims of this study are to investigate the effect of sucralfate granules in suspension on the treatment of endoscopic variceal sclerotherapy induced ulcer and analyse the factors determining the ulcer healing. Fifty-two patients with oesophageal variceal bleeding received elective endoscopic variceal sclerotherapy. After endoscopically proved oesophageal ulcers, they were randomized to receive either sucralfate granules in suspension (n = 22) or antacid (n = 23). Follow-up endoscopy was performed weekly. Ulcer healing rates were compared between the groups using the log-rank test. Forty-one ulcers receiving sucralfate and 48 ulcers receiving antacid treatment were evaluated. The clinical characteristics of the ulcers were similar in both groups. The ulcers in patients receiving sucralfate healed faster than those receiving antacid (P<0.02). On analysis of factors affecting ulcer healing, ulcers smaller than 1 cm2 (n = 59) appeared to heal faster than those larger than 1 cm2 (n = 30; P= 0.059) and shallow ulcers (n = 46) healed faster than deep ulcers (n = 43; P<0.001). On multifactorial analysis, ulcer depth was the only factor determining ulcer healing. The ulcer healing effects of sucralfate became more prominent when the ulcer was larger than 1.0cm2 (1.7+/-0.6 weeks vs 2.3+/-0.6 weeks, P= 0.011) and deep (1.7+/-0.7 weeks vs 2.5+/-1.0 weeks, P= 0.013) when compared with those receiving antacid. Sucralfate granules in suspension speed the healing of endoscopic variceal sclerotherapy induced ulcer, especially deep and large ulcers.
Adult↗
The effect of ciprofloxacin in the prevention of bacterial infection in patients with cirrhosis after upper gastrointestinal bleeding.
OBJECTIVES: Cirrhotic patients with upper gastrointestinal bleeding are prone to bacterial infection. The aim of this study was to investigate the efficacy of prophylactic intestinal decontamination with oral ciprofloxacin for the prevention of bacterial infections in cirrhotic patients with upper gastrointestinal bleeding. METHODS: A total of 120 cirrhotic patients with acute upper gastrointestinal bleeding were enrolled. Sixty patients received ciprofloxacin 500 mg twice daily given orally or through nasogastric tube immediately after upper gastrointestinal endoscopic examination; drug administration continued for 7 days. The remaining 60 patients, who received placebo, served as controls. RESULTS: The incidence of proven bacterial infection in the ciprofloxacin-treated group was significantly lower than that of placebo group (10% vs 45%, p < 0.001). The incidences of bacteremia, spontaneous bacterial peritonitis, and urinary tract infection in the ciprofloxacin-treated group were significantly lower than those in the placebo group (0% vs 23%, 3.3% vs 13%, and 5% vs 18%, respectively; p < 0.05, respectively). Multivariate logistic regression analysis showed that a lack of prophylactic treatment with ciprofloxacin and severity of cirrhosis were the independent significant predictors for cirrhotic patients with acute gastrointestinal bleeding with infection. CONCLUSIONS: Prophylactic intestinal decontamination with oral ciprofloxacin is effective in the prevention of bacterial infections in patients with cirrhosis who were suffering from acute upper gastrointestinal hemorrhage.
Acute Disease↗
A vanishing liver abscess complicated with Klebsiella pneumoniae chest wall abscess: a case report.
Septic metastasis is a unique feature of Klebsiella pneumoniae liver abscess in Taiwan. The case we report is a vanishing K. pneumoniae liver abscess with septic metastasis of the chest wall. The initial finding of a 36 year-old male with no previous medical history, was a huge hepatic mass presented on the sonography during a physical checkup. Hepatitis B, C serology, tumor markers and evidence of metastatic diseases were all negative. A computerized tomography examination was also inconclusive about its nature. Due to the patient's refusal of a liver biopsy, only oral antibiotics were medicated at the outpatient department. Unexpectedly, the follow-up computerized tomography, taken 4 weeks later, demonstrated that the liver mass was nearly absent, while a protruding painful lesion developed over the right chest wall. Under sono-guided aspiration, the chest wall mass was proved to be a pyogenic abscess. The Gram stain revealed gram-negative bacilli and the bacterial culture yielded K. pneumoniae. Under the impression of K. pneumoniae liver abscess with chest wall septic metastasis, after performing percutaneous drainage of the chest wall abscess, the patient was only given parenteral antibiotics for treatment. Both the liver and the chest wall abscesses were at last completely eradicated.
Adult↗
Expression of heme oxygenase-1 in atherosclerotic lesions.
Heme oxygenase-1 (HO-1) is a heme-degradation enzyme induced under various oxidative stress conditions. To elucidate the potential involvement of HO-1 in atherogenesis, the expression of this enzyme in atherosclerotic lesions of apolipoprotein E-deficient mice and humans were examined. Both immunostaining and in situ hybridization clearly demonstrated that the expression of HO-1 was prominent in endothelium and foam cells/macrophages of thickened intima in lesions from both humans and experimental animals. The expression of this enzyme was also detected in medial smooth muscle cells of advanced lesions. The induction of HO-1 mRNA was observed in murine peritoneal macrophages after treatment with oxidized low density lipoprotein (LDL) but not with native LDL in a dose-dependent manner. Time course study demonstrated that the induction was prominent at 3 hours, reached a maximal induction at 6 hours, and remained evident up to 24 hours after oxidized LDL treatment. The degree of induction was in concordant with the extent of oxidation in the LDL preparation. Lysophosphatidylcholine, one of the major components present in oxidized LDL, was ineffective to induce the gene expression, suggesting that other lipophilic substances derived from LDL oxidation are responsible for the induction of HO-1. These results clearly demonstrate that HO-1 is one of the stress proteins expressed in atherosclerotic lesions.
Aged↗