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Biomedical subjects

H R Lee

Publications and source records attributed to H R Lee.

At least 55 records · Page 3Linked to original sources
PubMed1993

Prevalence of Helicobacter pylori infection in patients with peptic ulcer diseases and non-ulcer dyspepsia.

BACKGROUND: Helicobacter pylori is known to be a cause of active chronic gastritis and has been proposed as an etiologic factor in the development of peptic ulcer disease, but controversy continues regarding the pathogenic importance and mechanism. We examined the prevalence of H. pylori infection in patients with peptic ulcers and non-ulcer dyspepsia. METHOD: 749 patients (373 with duodenal ulcer, 303 with gastric ulcer, 73 with non-ulcer dyspepsia) were included. Endoscopic mucosal biopsies were done at antrum, duodenum, and, if present, ulcer margin. The specimens were tested by Gram staining, Giemsa staining, culture, urease testing for identification of H. pylori. Antibody to H. pylori was examined in 83 patient of these patients by ELISA, and the result was compared with the results of bacteriologic studies. RESULT: Prevalence of H. pylori in antral mucosa was higher in patients with duodenal ulcers (81.5%) than in patients with gastric ulcer and non-ulcer dyspepsia (56% and 52.8%) (P < 0.05). Also in the duodenal mucosa of non-ulcer sites, and the ulcer margin of patients with duodenal ulcers, the detection rates (12% and 40.7%) were higher than those in the duodenal mucosa of patients with gastric ulcer and non-ulcer dyspepsia (7% and 8%)(p < 0.005). Antibody to H. pylori was detected in all patients with duodenal and gastric ulcers and non-ulcer dyspepsia who were tested for antibody. In contrast, the detection rates of antibody in adult control and child control were 33.3% and 27%. Among patients with antibody to H. pylori, H. pylori was detected in 85.7% of patients with duodenal ulcer, 62.5% of patients with gastric ulcers and 22.2% of patients with non-ulcer dyspepsia (p < 0.05). CONCLUSION: These data suggest that H. pylori is a possible pathogen for duodenal ulcer by duodenal colonization probably via gastric metaplasia. Also the past or present infection of H. pylori in antral mucosa may play a role at least partially in generation of upper gastrointestinal symptoms.

Adolescent↗
PubMed1992

Morphological changes in the respiratory system of mice after inhalation of mosquito-coil smoke.

Male ICR mice were exposed to mosquito-coil smoke with d-allethrin or without d-allethrin at airborne particles concentration of 1.27 mg/m3, 7 h/day, 7 days/week for 1, 3, 6, and 12 months. Additional groups of air exposure animals served as controls. At 1 month after exposure, the histopathological lesions included the loss of cilia, and the alteration of the alveolar pattern in the treated and the sham mice. Volume fractions of the type I and II cells were smaller (0.028 +/- 0.006, 0.044 +/- 0.002) in the treated group than those of the controls (0.049 +/- 0.008, 0.059 +/- 0.003). Fractions of the lumina of vessels and the vessel wall decreased in both the treated and the sham groups as compared to the control group. However, the volume fraction of alveolar air space increased significantly in both treated and sham groups as compared to the controls (0.619 +/- 0.022, 0.685 +/- 0.018 vs. 0.507 +/- 0.025). After 3- and 6-months exposure, the lesions observed in the trachea persisted. The intercellular fibrosis in the lung was increased in both the treated and sham groups at 6 months and became more severe at the later stages. At 12-months exposure, an increase in vascularity of the alveolar wall was observed and fine granular debris was frequently present in the alveolar space. The fraction volumes of the type II cells in the treated group and the type I cells in the sham group were significantly increased (0.059 +/- 0.010, 0.042 +/- 0.003) compared with those of the controls (0.038 +/- 0.008, 0.033 +/- 0.003). However, the fraction volume of air space and vessel lumen were not different among the three groups. Finally, there were no differences in the morphologic appearance of the airways and the lung periphery between the treated and the sham-exposed animals.

Allethrins↗
PubMed1992

Distribution of prostaglandin E2 in gastric and duodenal mucosa: possible role in the pathogenesis of peptic ulcer.

BACKGROUND: Prostaglandin E which is present abundantly in the gastric mucosa is a powerful inhibitor of gastric acid secretion and a stimulus to gastric mucus production. In addition, prostaglandin E2 inhibits ulcer formation in animals, and the synthetic analogues of prostaglandin E have successfully been used in the treatment of patients with gastric and duodenal ulcer disease. To evaluate the role of endogenous prostaglandin E2 in the pathogenesis of the peptic ulcer disease, we measured mucosal prostaglandin E2 levels in patients with gastric and duodenal ulcer disease and compared with that of non-ulcer control persons. METHODS: The study population was made up of 44 non-ulcer persons, 36 patients with a benign gastric ulcer, and 48 with a duodenal ulcer. Every mucosal specimen, taken from the antrum and from the duodenal bulb, were homogenized, mixed with 1 M HCl, and centrifuged. After removal of the supernatant, precipitate was eluted with ethyl acetate in the Amprep C18 minicolumn. Then the extracted prostaglandin E2 in the ethyl acetate fractions was converted into its methyl oximate derivatives, and the prostaglandin E2 level was measured by radioimmunoassay. During the procedure any homogenized specimen which was looking grossly bloody was removed from the assay in order to avoid any possible contamination or prostaglandin E2 in blood. RESULTS: In non-ulcer persons, the mean values was 258.17 +/- 127.03 pg/mg. tissue in antrum and 121.07 +/- 67.46 pg/mg. tissue in duodenal bulb. The corresponding values were 186.42 +/- 70.51 pg/mg. tissue, 79.44 +/- 39.04 pg/mg. tissue in gastric ulcer patients and 204. 94 92.03 pg/mg. tissue, 99.66 +/- 56.10 pg/mgl. tissue in duodenal ulcer patients respectively. Gastric ulcer patients have the significantly lower level of the antral and duodenal prostaglandin E2 (p < 0.005). Those levels of duodenal ulcer patients were also significantly lower than those of non-ulcer persons (p < 0.025 & 0.05). Antral prostaglandin E2 level increased to 305.21 +/- 104.91 pg/mg. tissue in the gastric ulcer patients (p < 0.005) and to 271.02 +/- 93. 23 pg/mg. tissue in the duodenal ulcer (p < 0.005) when the ulcer crater was healed. The duodenal bulb prostaglandin E2 level was also increased in the healed stage of ulcer, e. g., 128.84 +/- 57.62 (p < 0.005) and 112.60 +/- 42.25 pg/mg. tissue, respectively. CONCLUSION: These results suggest that prostaglandin deficiency in the antral and duodenal bulb mucosa may have an important role in the pathogenesis of peptic ulcer disease.

Adult↗
PubMed1992

Prevalence of antibodies to hepatitis C virus in patients with various types of liver diseases.

BACKGROUND: Hepatitis C virus (HCV) is known to be a major cause of non-A, non-B hepatitis (NANBH) and is thought to be an important causative agent of serious liver disease. Recently the role of HCV in the development of various liver disease is suggested. METHODS: Sera from 222 patients with various liver diseases had been kept frozen at -20 degrees C until the test. Anti-HCV was detected using the ABBOTT HCV EIA Test System (ABBOTT Co., America) following the manufacturer's instructions. The assay uses a recombinant HCV antigen (C 100-3) synthesized in yeast. RESULTS: HCV antibodies (anti-HCV) were detected in 35 (31.5%) of 111 HBsAg-negative patients. The prevalence rate of anti-HCV was 61.9% (13 out of 21 patients) in chronic hepatitis, 29.1% (14 out of 48) in liver cirrhosis, 26.3% (5 out of 19) in hepatocellular carcinoma and 13% (3 out of 23) in acute hepatitis was far less (3 out of 111 patients, 2. 7%) than that of HBsAg-negative patients (p < 0.01). In this group, anti-HCV was detected in 2 (5.1%) out of 39 liver cirrhosis, 1 (1.9%) out of 52 chronic hepatitis, among them 47 were biopsy-proven chronic active hepatitis, and none of 20 hepatocellular carcinoma. CONCLUSIONS: These data suggest that, in Korea, 1) coinfection of HCV and HBV is infrequent, 2) HCV might be an important cause of HBsAg-negative chronic hepatitis, 3) HCV is seemed to be a less likely important factor associated with liver cirrhosis or hepatocellular carcinoma in HBsAg-negative patients, but further prospective study with a large population is necessary.

Female↗
PubMed1991

Molecular cloning of the ecotin gene in Escherichia coli.

The nucleotide sequence of a 876 bp region in E. coli chromosome that encodes Ecotin was determined. The proposed coding sequence for Ecotin is 486 nucleotides long, which would encode a protein consisting of 162 amino acids with a calculated molecular weight of 18,192 Da. The deduced primary sequence of Ecotin includes a 20-residue signal sequence, cleavage of which would give rise to a mature protein with a molecular weight of 16,099 Da. Ecotin does not contain any consensus reactive site sequences of known serine protease inhibitor families, suggesting that Ecotin is a novel inhibitor.

Amino Acid Sequence↗
PubMed1991

Low-dose enoximone in subjects awaiting cardiac transplantation. Clinical results and effects on beta-adrenergic receptors.

During a 3-year period we administered enoximone, a phosphodiesterase inhibitor with positive inotropic and vasodilator properties, to 73 pretransplantation patients with end-stage heart failure who exhibited a clinical requirement for additional inotropic support. The clinical course and myocardial beta-adrenergic receptor status in the explanted hearts of these 73 patients was compared with results in 113 concurrently listed pretransplantation patients not requiring additional inotropic support. Only three patients required cessation of enoximone because of adverse effects, all from exacerbation of ventricular arrhythmias. Sixty-six of 73 (90.4%) enoximone-treated patients ultimately underwent cardiac transplantation a mean of 39.2 +/- 6.6 days (range 1 to 221 days) after starting enoximone, whereas seven patients (9.6%) died awaiting cardiac transplantation. The respective 1-, 3-, and 6-month pretransplantation survival rates of patients treated with enoximone calculated from their time on the waiting list for transplantation were 88.0%, 82.5%, and 82.5% compared with 92.1%, 83.8%, and 76.2% in control patients not receiving enoximone (all p = not significant). In 25 patients who received enoximone, ventricular myocardial beta-adrenergic receptors were measured at the time of transplantation and compared with values in failing ventricles from 52 pretransplantation patients not exposed to enoximone. Compared with ventricular myocardium of patients not given enoximone or intravenous beta-adrenergic agonists, total beta-adrenergic receptor (beta 1 plus beta 2) density was not decreased in patients treated with enoximone or enoximone plus intravenous beta-adrenergic agonists, but was decreased by 31% (p less than 0.05) in patients given intravenous beta-adrenergic agonists alone. Additionally, patients treated with enoximone had higher myocardial beta 2-adrenergic receptor densities than respective subgroups treated without (28% higher, p less than 0.01) or with (65% higher, p less than 0.01) intravenous beta-adrenergic agonists. Finally, isoproterenol- or calcium-mediated contractile responses in isolated right ventricular preparations from 14 patients treated with enoximone were similar to values in control patients not exposed to enoximone or intravenous beta-adrenergic agonists, suggesting that enoximone-related beta-adrenergic subsensitivity or damage to the contractile apparatus does not occur.

Adult↗
PubMed1990

A case of adrenal lymphangiectatic cyst associated with severe hypertension.

Adrenal lymphangiectatic cyst is a very rare pathological and clinical disease entity, and its clinical silence and lack of characteristic symptoms and signs makes it difficult to diagnose preoperatively. We experienced a case of adrenal lymphangiectatic cyst, accompanied by severe refractory hypertension, which was corrected by surgical removal of the cyst. We report it with a review of the literature.

Adrenal Gland Diseases↗
PubMed1989

Immunosuppression and beta-blockade in heart failure.

Two potential treatments, immunosuppression for myocarditis and beta-adrenergic blockade for heart failure, have been advocated. However, definitive conclusions await the result of ongoing large, multicenter, randomized clinical trials. There is circumstantial evidence that myocarditis may be a common precursor of dilated cardiomyopathy. Animal studies of myocarditis suggest that critically timed immunosuppression may be an effective therapy. Although promising, clinical studies to date are small and mostly uncontrolled. Clinical studies have demonstrated that beta-blockers are generally well tolerated in heart failure, and long-term treatment may result in improved symptomatic and functional status. These effects may be due to antagonism of direct and indirect effects of chronic reflex sympathetic stimulation on the cardiovascular system, including down-regulation of the myocardial beta-adrenergic receptor. However, prolongation of survival has not been documented by any studies. Initiation of beta-blockade requires careful patient selection and titration with small initial doses of metoprolol.

Adrenergic beta-Antagonists↗
PubMed1988

Alpha 1-adrenergic stimulation of cardiac gene transcription in neonatal rat myocardial cells. Effects on myosin light chain-2 gene expression.

Previous studies have demonstrated that alpha-adrenergic stimulation of cultured, neonatal rat myocardial cells results in an increase in intracellular volume and protein content of cultured neonatal rat myocardial cells. Utilizing this model of cardiac hypertrophy, we have examined the effects of alpha-adrenergic stimulation on the accumulation of sarcomeres and the expression of a rat cardiac myofibrillar gene, myosin light chain-2 (MLC-2). Following alpha-adrenergic stimulation, cultured myocardial cells displayed a severalfold increase in the number of sarcomeric units, as assessed by electron microscopy, an increase in cellular MLC-2 content, and a 2-3 fold increase in the steady state levels of MLC-2 mRNA. This effect of alpha-adrenergic stimulation was accompanied by a 2-3-fold increase in total transcriptional activity, which was dependent on the concentration and duration of exposure to the agonist, and displayed alpha 1-adrenergic receptor specificity. The transcriptional response was not immediate, with a lag period of at least 1 h, and a maximal effect required continuous occupancy of the receptor. The increase in steady state levels of MLC-2 mRNA is regulated, in part, at the level of transcription of the cardiac MLC-2 gene. These results suggest that alpha 1-adrenergic stimulation may be important in the growth of the neonatal heart through the activation of total transcriptional activity. In addition, increases in the levels of myofibrillar proteins during myocardial cell growth and hypertrophy, may be mediated in part by the stimulation of transcription of myofibrillar genes.

Animals↗
PubMed1988

Effect of increasing heart rate on left ventricular performance in patients with normal cardiac function.

The influence of an increase in heart rate on left ventricular (LV) contractile performance was assessed in patients with normal LV function. In 19 patients (3 men, 16 women) ages 55 +/- 9 years (mean +/- standard deviation) with normal global and segmental LV function and normal coronary arteries, LV dP/dt max was measured at baseline heart rate and during atrial pacing at baseline +5, baseline +25 and baseline +45 beats/min. In 10 of the patients, intravascular volume was not altered during pacing and, as a result, echocardiographically measured LV end-diastolic dimension decreased (5.4 +/- 0.4 at baseline vs 4.9 +/- 0.5 cm at baseline +45 beats/min, p less than 0.05). In these patients, LV dP/dt max increased modestly (1,571 +/- 237 at baseline vs 1,760 +/- 199 mm Hg/s at baseline +45 beats/min, p less than 0.05). In the other 9 patients, intravascular volume was expanded rapidly (by saline infusion) during pacing and, as a result, LV end-diastolic dimension was held constant (5.2 +/- 0.6 at baseline vs 5.1 +/- 0.6 cm at baseline +45 beats/min, difference not significant). In these patients, LV dP/dt max increased substantially with pacing (1,505 +/- 228 at baseline vs 2,050 +/- 258 mm Hg/s at baseline +45 beats/min, p less than 0.05). Thus, an increase in heart rate induces a modest increase in LV dP/dt max in patients in whom LV preload (as reflected by end-diastolic dimension) is allowed to decrease; in contrast, it causes a marked increase in LV dP/dt max in those in whom LV preload is maintained constant.

Adult↗
PubMed1987

In vivo induction and reversal of nitroglycerin tolerance in human coronary arteries.

The mechanism by which tolerance to the clinical effects of organic nitrates develops has not been elucidated. This study was done to determine whether an intravenous infusion of nitroglycerin induces tolerance in the coronary vascular bed and whether such tolerance is reversed by the sulfhydryl-group donor N-acetylcysteine. We studied 19 subjects--17 with coronary artery disease and 2 without it--who had a mean age (+/- SD) of 54 +/- 9 years. Coronary sinus blood flow, which approximates blood flow to the left ventricle, was measured before and during intracoronary injections of nitroglycerin (10, 25, 50, and 100 micrograms). The patients then received a 24-hour intravenous infusion of saline (n = 7) or of nitroglycerin, 45 +/- 13 micrograms per minute (n = 12), after which the responses of coronary sinus flow to the same doses of intracoronary nitroglycerin used earlier were measured. In the seven patients given saline, the four doses of intracoronary nitroglycerin caused similar percentage increases in coronary sinus flow before and after the saline infusion. In the 12 patients given intravenous nitroglycerin, the four intracoronary doses caused percentage increases in coronary flow before the infusion of 30 +/- 9, 35 +/- 14, 41 +/- 12, and 52 +/- 15, respectively. After the infusion, the same doses of nitroglycerin caused smaller (P less than 0.05) percentage increases (16 +/- 6, 21 +/- 11, 23 +/- 12, and 27 +/- 11, respectively), indicating the development of partial tolerance. Subsequently, 7 of the 12 patients received N-acetylcysteine, after which intracoronary nitroglycerin caused percentage increases in coronary sinus flow similar to the values measured before the intravenous nitroglycerin was given (34 +/- 13, 32 +/- 8, 38 +/- 11, and 44 +/- 16, respectively). We conclude that the coronary vasodilator effect of nitroglycerin is attenuated by an intravenous infusion of nitroglycerin (that is, partial tolerance develops) and that tolerance to the agent can be reversed by administration of the sulfhydryl-group donor N-acetylcysteine. The mechanism by which N-acetylcysteine reverses tolerance will require further investigation.

Acetylcysteine↗
PubMed1985

Decreased [3H]nitrendipine binding in the brainstem of deoxycorticosterone-NaCl hypertensive rats.

Binding studies with the 1,4-dihydropyridine calcium channel antagonist [3H]nitrendipine [( 3H]NTD) were performed in uninephrectomized, deoxycorticosterone (DOCA)-NaCl hypertensive rats and vehicle treated normotensive control littermates. After 6 weeks of treatment, hypertensive (199 mmHg, systolic arterial pressure) DOCA rats showed significantly increased heart, left ventricle, and kidney weight in contrast to normotensive (135 mmHg) controls. [3H]NTD binding in the brainstem was significantly reduced (51 +/- 5 fmol/mg protein) in DOCA-NaCl rats, as compared to controls (116 +/- 24 fmol/mg protein). However, no significant differences were found in the [3H]NTD dissociation constants for DOCA-NaCl (0.43 +/- 0.03 nM) or control rats (0.62 +/- 0.06 nM). Cerebral cortical and left ventricular tissue showed no significant alterations in receptor binding density or affinity. Specific [3H]NTD binding was not significantly altered in other selected brain regions or the atria. These data suggest that alterations in the dihydropyridine binding sites associated with calcium channels in the brainstem may be involved in the etiology of DOCA-NaCl-induced hypertension.

Animals↗
PubMed1985

Identification of calcium-channel receptors in intact animals.

In this study, we demonstrate the in vivo labeling by [3H]nitrendipine ([3H]NTD) of peripheral tissues and the brain in Sprague-Dawley rats. Specific binding is decreased in a dose-dependent manner by nifedipine, with a mean inhibitory dose of 2-10 mg/kg (i.p.). Thin-layer chromatography of the particulate-bound radioactivity reveals that the predominant tritiated drug bound in the left ventricle and the cerebral cortex is [3H]NTD, whereas metabolites constitute the main species in the liver. Peak radioactivity is seen at 15 min following an intravenous injection of [3H]NTD. Highly perfused tissues such as the heart, brain, and lung have significant [3H]NTD binding. In contrast to previously reported in vitro studies, [3H]NTD binding is low in the aorta, skeletal muscle, and ileum. This in vivo animal model is suitable for pharmacokinetic and physiological studies of the calcium channel in intact animals.

Animals↗
PubMed1985

Potent enhancement of [3H]nitrendipine binding in rat cerebral cortical and cardiac homogenates: a putative mechanism for the action of MDL 12,330A.

[3H]Nitrendipine [( 3H]NTD), a specific high-affinity calcium channel antagonist, was used to label dihydropyridine binding sites associated with calcium channels in rat cerebral cortical and cardiac homogenates. A novel lactamimide compound, MDL 12,330A, has been shown previously to have negative inotropic and chronotropic effects in isolated working guinea-pig hearts and these effects are reversed by the administration of calcium. MDL 12,330A is potent in enhancing [3H]NTD binding in membranes prepared from the cerebral cortex and the heart, with EC50 values of 6.1 X 10(-8) and 3.4 X 10(-8) M, respectively, at 37 degrees C. This allosteric effect by MDL 12,330A is similar to that produced by a known calcium channel antagonist, d-cis diltiazem, which has been shown previously to enhance [3H]NTD binding at 37 degrees C. The extent of enhancement by MDL 12,330A depends on incubation temperature (37 degrees C greater than 25 degrees C greater than 0 degrees C). The mechanism of this enhancement by MDL 12,330A is due to a decrease in the dissociation rate constant of the dihydropyridine-calcium channel supramolecular complex. MDL 12,330A is the most potent drug thus far examined which demonstrates the enhancement of [3H]NTD binding.

Animals↗
PubMed1984

High affinity specific [3H](+)PN 200-110 binding to dihydropyridine receptors associated with calcium channels in rat cerebral cortex and heart.

The binding properties of the 1,4-dihydropyridine calcium channel antagonist, [3H](+)PN 200-110, were studied in rat cerebral cortical and cardiac homogenates (37 degrees C, Krebs phosphate buffer). Specific binding of [3H](+)PN 200-110 was saturable, reversible, and of high affinity (Kd values are 35 and 64 pM for the cerebral cortex and heart, respectively). In parallel studies with [3H](+)PN 200-110, the dissociation constant of [3H]nitrendipine was 10-12 times higher. Substituted dihydropyridine calcium channel antagonists and agonists competitively inhibited specific [3H](+)PN 200-110 binding, but d-cis diltiazem enhanced and verapamil incompletely inhibited [3H](+)PN 200-110 binding in both the cerebral cortex and the heart. The effects of diltiazem and verapamil on [3H](+)PN 200-110 binding were due mainly to alterations in the dissociation constant (Kd), without alterations in the binding density (Bmax). The new [3H](+)PN 200-110 receptor binding assay is remarkable for its low degree of nonspecific binding as compared to [3H]nitrendipine at physiological temperatures. [3H](+)PN 200-110 is a useful ligand for the further analysis of the dihydropyridine binding sites associated with calcium channels.

Animals↗