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Biomedical subjects

B H Cho

Publications and source records attributed to B H Cho.

At least 55 records · Page 3Linked to original sources

Esophageal strictures: treatment with a new design of modified Gianturco stent. Work in progress.

To overcome the drawbacks of the modified Gianturco stent tube with barbs, a new barbless stent tube was constructed. Twenty-two barbless stent tubes 4.5-14.0 cm long were placed with a new introducing tube in 21 patients: 10 stent tubes in 10 patients with recurrent dysphagia after radiation therapy or chemotherapy, 10 in 10 patients with esophageal cancer in whom surgical management was contraindicated, and two in one patient with postoperative benign stricture. No technical failure or procedural complications occurred. After the procedure, all but two patients could ingest most or all foods. In two patients with an esophagorespiratory fistula and one patient with esophageal rupture, the barbless stent tube successfully occluded the fistula and rupture site. The stent tube migrated in one patient. Fifteen patients are surviving, with the stent tubes patent for 3-35 weeks (mean patency, 13 weeks); the six other patients died 7-24 weeks (mean, 16 weeks) after stent placement. It is concluded that barbless stent tubes show promise in the management of dysphagia caused by esophageal strictures.

Aged↗

Percutaneous transhepatic biliary biopsy using gastrofiberscopic biopsy forceps.

To obtain a histopathologic diagnosis at the site of a biliary obstruction, we recently have performed 24 cases of biliary biopsy using gastrofiberscopic biopsy forceps (Olympus, Tokyo, Japan) via transhepatic tracts provided in the course of the procedure of percutaneous biliary drainage. Histopathologic diagnosis was successfully made at the first attempt of biopsy procedure but a second trial was made a week later in 6 cases who were negative for malignant cells on the first attempt. The histological results from the biopsy specimens were 18 adenocarcinomas, 5 chronic inflammations and one normal epithelium. Of 6 cases who were negative for malignant cells on forceps biopsy specimen, three cases were confirmed as adenocarcinoma of the ampulla of Vater, adenocarcinoma of the pancreas and chronic pancreatitis by surgical biopsy. The latter was a true negative result, which was diagnosed as chronic inflammation on forceps biopsy and verified as chronic pancreatitis by surgery. The remaining two cases were diagnosed as malignant obstructive jaundice by clinical and radiological follow-up findings. Major complications (bile peritonitis, bleeding, and hemopneumothorax) occurred in 3 patients, which mainly arose in the earlier period of study. This procedure can be performed at the same time as percutaneous transhepatic biliary drainage with low morbidity or mortality, and although the potential for perforation of bile ducts and injury to adjacent blood vessels is considered it is a useful addition to existing biopsy techniques for yielding material sufficient for histologic analysis.

Adult↗

Compositional changes and apoprotein A-I metabolism of plasma high density lipoprotein in estrogenized chicks.

The effect of estrogen on compositional changes, apolipoprotein (apo) A-I metabolism and the morphology of plasma high density lipoprotein (HDL) were investigated in chicks. The administration of 17 beta-estradiol (25 mg/kg body weight) to growing male chicks (8-week-old) markedly reduced the concentrations of plasma HDL components, except for triglyceride (TG). At the same time, levels of TG, total cholesterol (TC) and phospholipid (PL) in plasma were greatly elevated. The respective values for TG, TC, PL and protein in HDL were 13.9, 89.3, 154.1 and 231.7 (mg/dL) in the control, and 39.0, 35.1, 113.8 and 160.0 (mg/dL) in chicks upon estrogen treatment for one day. In vivo kinetic studies showed that the fractional catabolic rate of HDL apo A-I was significantly higher (p less than 0.05) in estrogen-treated chicks than in control birds, indicating an increased efficiency of HDL removal in the former. The production rate of HDL apo A-I also was significantly lower (p less than 0.05) in estrogen-treated chicks. Sodium dodecyl sulfate-acrylamide gel electrophoresis followed by laser scanning densitometry of HDL apolipoproteins in estrogen-treated chicks revealed a reduction of apo A-I and the occurrence of new apolipoproteins which had been absent in HDL of untreated birds. The HDL particles showed that the mean particle size of HDL became larger upon estrogen treatment. Particles with diameters between 70 and 123 A were predominant in HDL of control chicks, while particles with diameters between 97 and 143 A were most abundant in HDL of estrogen-treated chicks.

Animals↗

Esophagogastric neoplasms: palliation with a modified gianturco stent.

Self-expanding metallic stents of a modified Gianturco design were used for palliative treatment of malignant esophagogastric strictures. Over a 10-month period, 10 stents were placed in nine patients. All patients with severe dysphagia due to malignant strictures in whom all other treatment options had failed were candidates for these stents. Neither extensive length of esophageal involvement nor complete esophageal obstruction was a contraindication. All stents were placed with fluoroscopic guidance without any technical failures or procedural morbidity or mortality. Mild reflux occurred in three patients in whom the stent tubes straddled the distal esophageal sphincter. Five patients were still alive after 1-8 months. The remaining four patients died 6-28 weeks after stent placement; all stents were patent at the time of death. These stents are easy to insert, safe, and reasonably effective for short-term palliative treatment of esophagogastric neoplasms.

Adenocarcinoma↗

Effects of estrogen on very-low-density lipoprotein triacylglycerol metabolism in chicks.

Estrogen administration (25 mg/kg body weight) in chicks resulted in a marked elevation of plasma very-low-density lipoprotein (VLDL) triacylglycerol (TG). To determine whether the VLDL produced from estrogen (E)-treated birds is catabolized differently from VLDL of control birds, VLDL-TG kinetic studies were conducted. The [14C]TG-labeled VLDL was prepared by intravenous injection of [14C]palmitate into control and E-treated chicks. The [14C]TG-labeled VLDL prepared from the control (C-VLDL-TG) and E-treated chicks (E-VLDL-TG) were then reinjected into fed and fasted chicks with or without E-treatment. The metabolism of VLDL-TG was found to be different, depending upon whether its donor was the control of E-treated chick. The fractional catabolic rate (FCR) of E-VLDL-TG was significantly (P less than 0.05) lower than that of C-VLDL-TG in both fed and fasted chicks. Compared to the fed state, fasting resulted in significantly (P less than 0.05) increased FCRs of both C-VLDL-TG and E-VLDL-TG. The turnover rate of VLDL-TG was significantly higher in E-treated chicks than in their respective controls. In addition, the endogenously produced VLDL-TG differed in their affinity for lipoprotein lipase in which E-VLDL-TG had a higher Km value for the enzyme than C-VLDL-TG. On agarose gel electrophoresis, the VLDL of E-treated chicks showed beta-mobility and it eluted into two peaks on agarose gel filtration, whereas VLDL of control chicks had a pre-beta-mobility on the former and it eluted into a single peak on the latter. SDS-gel electrophoresis also revealed that the apolipoprotein composition of VLDL from control and E-treated chicks was notably different from each other. Present findings suggest that estrogen treatment results not only in an increased secretion of VLDL but also in the production of different VLDL particles, thereby affecting their clearance from the plasma.

Animals↗

Effects of a dietary magnesium deficiency and excess vitamin D3 on swine coronary arteries.

The effect of a moderate magnesium (Mg) deficiency on coronary arteries of 61 swine, fed various levels of vitamin D3, was studied by light and electron microscopy. The effect of subnormal Mg intake on vitamin D3-induced intimal lesions of the arteries showed a trend towards increased damage. The degree of cell degeneration and intimal thickening, which was induced by high vitamin D intakes, was as great in swine whose diet was low in Mg and moderately high in vitamin D as it was in those on twice as much vitamin D. Also, the degree of arterial calcification was intensified by inadequate Mg intake at the two higher vitamin D intakes. Present findings indicate that suboptimal dietary Mg, in combination with an excess of vitamin D, has an additive effect in the initiation of ultrastructural changes in the coronary arteries. Extension of the study is indicated to ascertain the extent to which further reduction of Mg intake can potentiate vitamin-D-induced coronary lesions.

Animals↗

Estrogen induces hyperlipidemia in fasted chicks.

To determine whether the estrogen-induced hyperlipidemia is affected by fasting, male growing chicks were administered subcutaneously a single dose of 17 beta-estradiol (25 mg/kg body wt), and the hormone treatment lasted for 2 days with or without feed (Experiment 1). In the second experiment, chicks were initially fasted for 1 or 3 days, and then treated with the same dosage of 17 beta-estradiol as in Experiment 1 for 2 days without feed. Plasma and liver lipids, and the activities of hepatic malic enzyme, glucose-6-phosphate dehydrogenase, and hormone-sensitive lipase in the adipose tissue were determined. Compared with fed control chicks, estrogen treatment in fed birds resulted in a marked elevation of plasma lipids, especially triglyceride during the 2-day period (137 vs 2263 mg/dl). In fasted chicks, the present finding that estrogen also induced a marked hyperlipidemia is noteworthy. Upon estrogen treatment (Experiment 1), the level of plasma triglyceride in fasted birds increased about 16 times over that of the fasted control group (133 vs 2093 mg/dl). Even in chicks fasted for 5 days (Experiment 2), estrogen treatment resulted in a persistent hypertriglyceridemia (75 vs 1369 mg/dl). In fed chicks, estrogen treatment also induced a fatty liver with massive accumulation of triglyceride, but the liver of estrogen-treated/fasted chicks appeared to be normal. In both fed and fasted chicks, malic enzyme was found to be the major NADPH producing enzyme in the liver. Upon fasting, both malic enzyme and glucose-6-phosphate dehydrogenase activities decreased significantly (P less than 0.05). In fed chicks, the total activities of both enzymes increased with estrogen treatment, whereas the effect of hormone on these enzymes was less obvious in fasted chicks. The hormone-sensitive lipase activity in the adipose tissue was much lower in fed chicks compared with that of fasted birds (0.15 vs 0.33 nmol of oleic acid released/min/mg protein). Estrogen treatment in fed chicks had no effect on the hormone-sensitive lipase activity, but its activity was enhanced by the hormone treatment in fasted chicks. The present finding that hyperlipidemia persisted in estrogenized chicks during the fasting seems to indicate the complex nature of this hormonal influence on lipid metabolism.

Adipose Tissue↗

Dual effects of pertussis toxin on murine neutrophils in vivo. I. Pertussis toxin inhibits extravasation potential of mature neutrophils while simultaneously stimulating granulopoiesis.

Pertussis toxin (Ptx) has been employed as an adjuvant by many investigators to augment various types of cell-mediated and humoral immune responses. Recent work from our laboratory indicates that the exacerbation of delayed-type hypersensitivity (DTH) and contact hypersensitivity (CH) responses observed in Ptx-treated mice may be mediated by an absolute increase in the number of circulating neutrophils capable of migrating into tissue sites of antigen challenge. The purpose of the present study was to analyze the effects of Ptx on neutrophils and neutrophil function in vivo. Evidence is presented here suggesting that Ptx has both direct and indirect effects on neutrophils following its in vivo administration to normal mice. Mature neutrophils that are directly exposed to the actions of Ptx in vivo exhibit a marked reduction in their ability to extravasate into tissue sites of inflammation. These findings are consistent with those that have been reported following the exposure of isolated neutrophils to the effects of Ptx in vitro (i.e., that Ptx has an inhibitory effect on many of the functional capabilities of isolated neutrophils). Moreover, we have also determined that Ptx can affect the kinetics of neutrophil production indirectly through its ability to stimulate granulopoiesis. Ptx-exposed mice develop a protracted peripheral blood neutrophilia following toxin administration. Although the mechanism(s) involved in stimulating increased neutrophil production is presently unclear, both dexamethasone and indomethacin (cyclooxygenase pathway inhibitors) are able to function synergistically with Ptx to produce a markedly enhanced neutrophilia in exposed mice. We propose that the capacity of Ptx to augment CH and DTH responses and act as a potent adjuvant may relate, in part, to its ability to alter the rate of neutrophil production in vivo.

Animals↗

Effects of estrogen-induced hyperlipidemia on the erythrocyte membrane in chicks.

The effects of estrogen-induced hyperlipidemia on plasma lipid peroxidation, fatty acid composition and osmotic fragility of erythrocytes in chickens were studied. Young male chickens implanted with estrogen for three wk developed a marked hyperlipidemia. Plasma levels of triglyceride, cholesterol and phospholipid were elevated 68-, four- and 24-fold, respectively, over controls. There was also a two-fold increase in plasma lipid peroxidation measured by the thiobarbituric acid test. Vitamin E supplement (1,000 IU/kg diet) reduced the plasma lipid peroxidation to the control level, but had no effect on the plasma lipid content. Estrogen-induced hyperlipidemia resulted in changes in the fatty acid composition of membrane lipids of erythrocytes. The major changes were an increase in oleic acid from 10.0% to 14.2% and a decrease in linoleic acid from 31.3% to 26.0%. The erythrocytes with an altered membrane fatty acid composition were found to have an increased osmotic fragility. It was apparent that there was a direct correlation between the oleic acid content and the osmotic fragility of erythrocytes.

Animals↗

Changes in plasma lipids, lipoproteins, triglyceride secretion and removal in chicks with estrogen implants.

Estradiol implants in chicks resulted in marked elevation of all major plasma lipids with greatest increase in triglyceride (TG) followed by phospholipid (PL) and cholesterol (C). During the two-wk period, plasma TG level in estrogen (E)-treated chicks increased to about 45 times that of controls (139.6 vs 6,368.3 mg/dl). The level of cholesterol also increased steadily during the same period, attaining nearly a six-fold increase in comparison with the control (150.7 vs 871.8 mg/dl), and the level of PL was markedly elevated from 209 to 2,861 mg/dl. Besides the induction of hyperlipidemia, E treatment also resulted in a notable alteration in the fatty acid composition of plasma lipids; there was an increase in oleic acid concomitant with a decrease in polyunsaturated fatty acids, particularly, linoleic acid. One day after implantation, the percentage of oleic acid in TG fraction increased from 39.2 to 43.7%, reaching 55.4% of the total fatty acids at day 14. In contrast, the levels of linoleic and arachidonic acid decreased significantly from 16.1 to 8.3% and 4.3 to 0.6%, respectively, during the same period. In cholesteryl ester (CE) and PL, the oleic acid level also increased from 25.2 to 47.3% in the former and from 11.9 to 29.6% in the latter, reflecting enhanced hepatic lipogenesis. Analysis of plasma lipoproteins in E-treated chicks revealed dramatic alterations in the concentrations of lipids and protein in individual lipoprotein fractions, especially very low density lipoprotein (VLDL) fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Parallel recovery of epidermal antigen-presenting cell activity and contact hypersensitivity responses in mice exposed to ultraviolet irradiation: the role of a prostaglandin-dependent mechanism.

Contact hypersensitivity (CH) responsiveness to 2-4-dinitro-1-fluorobenzene (DNFB) is depressed in mice that are sensitized through skin sites exposed to ultraviolet radiation (UVR). This is partially due to a reduction in antigen-presenting cell (APC) activity within UVR-exposed skin, a condition marked by a decrease in the density of ATPase/Ia-positive epidermal cells. The purpose of this study was to correlate the histological and functional recovery of APC activity in the skin of C3H mice exposed to low-dose (4 X 450 J/m2) or high-dose (1 X 15 kJ/m2) UVR with the normalization of CH responsiveness. Skin biopsy specimens taken at various intervals after UVR exposure revealed a rapid recovery in the density of ATPase/Ia positive cells: about 70% of normal by 3 days, and normal after 5 days. Functional analyses showed that lymph node cells obtained from donors that were sensitized with DNFB 3 days after UVR treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus indicating that APC activity in UVR-exposed skin paralleled the recovery of ATPase/Ia-positive epidermal cells. This suggested that an alternative mechanism causes the persistent depression of CH in mice exposed to UVR. Mice pretreated with indomethacin prior to UVR exposure demonstrated a capacity to elicit CH responses to DNFB, which paralleled the histological and functional recovery of APC in the skin (i.e., normal CH responses were elicited 3 days after exposure to UVR). We conclude from this study that APC activity in the skin recovers rapidly after exposure to UVR, and that a PG-dependent mechanism is responsible for many of the persistent and systemic effects that cause a depression in the CH responsiveness of mice treated with UVR.

Adenosine Triphosphatases↗

Alpha-melanocyte-stimulating hormone exhibits target cell selectivity in its capacity to affect interleukin 1-inducible responses in vivo and in vitro.

The ability of i.v.-administered recombinant human interleukin 1 (IL 1 beta) to increase core body temperature, stimulate an increased production of serum amyloid P substance, and augment blood levels of circulating neutrophils in mice was inhibited in a dosage-dependent manner by administration of the neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH). alpha-MSH administration was also capable of inhibiting the capacity of i.v.-administered IL 1 beta to enhance plasma levels of corticosterone and to depress the generation and/or elicitation of contact hypersensitivity responses to skin-reactive chemicals. An analog of alpha-MSH (Nle4, D-Phe7 alpha-MSH), known to be more potent than native alpha-MSH in a number of melanotropin-sensitive systems, was determined to be more active than alpha-MSH in the modification of these same in vivo responses. Neither alpha-MSH nor its analog were capable of altering the capacity of IL 1 to stimulate increased plasma levels in prostaglandin E2 (PGE2). In vitro, neither alpha-MSH nor its analog were capable of reducing the capacity of IL 1 to stimulate fibroblast production of PGE2 or to augment the proliferation of murine thymocytes exposed to phytohemagglutinin. The apparent selectivity associated with the regulatory influences of alpha-MSH on IL 1-induced responses in vivo suggests that this neuropeptide may function as an endogenous inhibitor of certain immunomodulatory and inflammatory activities of the cytokine IL 1.

Animals↗

Murine responses to immunization with pertussis toxin and bovine serum albumin: I. Mortality observed after bovine albumin challenge is due to an anaphylactic reaction.

It has been suggested that pertussis toxin (Ptx) is involved in the pathogenesis of the adverse neurologic reactions that can occur in infants and children after pertussis immunization. One group of investigators has recently reported that a clinical syndrome with pathological features very similar to post-pertussis vaccination encephalopathy can be induced in specific strains of mice after their immunization with bovine serum albumin (BSA) and Ptx. The aim of this investigation was to further characterize the immunologic mechanisms operative in this murine model. Studies were undertaken to determine whether the role played by Ptx in this condition required the A-protomer of the toxin to enter a cell and ADP-ribosylate a nucleotide binding protein (a Class I activity) or was dependent upon the binding of the B-oligomer of the toxin to the surface of target cells (a Class II activity). The results of our experiments have established that the disease induced by coimmunizing mice with Ptx and BSA is due to an immediate type hypersensitivity reaction rather than an encephalopathy and that the mechanism of action of Ptx in this system seems to be dependent upon a Class II activity of the toxin and independent of its ADP-ribosyl transferase activity.

Adenosine Diphosphate Ribose↗

Fecal steroid excretion in chickens with hereditary hyperlipidemia.

Plasma lipids (cholesterol, triglycerides, and phospholipids; mg/dl) and the fecal excretion (mg/day) of neutral steroids and bile acids were studied in layers (L), hereditary nonlayer hens (NL), and roosters (R) fed a basal cholesterol-free grain diet ad libitum. Each group had significantly (P less than 0.05) different levels of plasma cholesterol, triglycerides, and phospholipids when compared to the other groups. The highest lipid values were found in the NL group (cholesterol, 798 +/- 89; triglycerides, 8914 +/- 679; phospholipids, 2458 +/- 112). There was no difference in the fecal excretion of neutral steroids between L and NL; however, fecal bile acid excretion by these two groups was significantly different (P less than 0.05) (L, 13.1 +/- 1.7 vs NL, 26.9 +/- 3.4). Fecal neutral steroid excretion by R was significantly greater (P less than 0.05) than that by either L or NL (L, 6.4 +/- 1.3; NL, 6.0 +/- 1.4; R, 14.4 +/- 1.2). While fecal excretion of bile acids by R (36.1 +/- 4.0) was also greater than that by either L or NL, only the difference between R and L was statistically significant (P less than 0.05). Since, in the steady state, fecal bile acid excretion is equal to its synthesis, these results suggest that bile acid metabolism in these animals can be affected by both sex and egg-laying status.

Animals↗

Effects of postnatal protein undernutrition on myelination in rat brain.

Pups were subjected, from birth, to protein undernutrition by feeding the lactating dams 8% casein (CS) or 8% soy protein (SP) diet up to weaning; the weanlings were fed the same diets until 6 weeks of age. At 3 and 6 weeks of age, myelin was isolated from the brains and characterized. The quantities of myelin and its content of cholesterol, galactolipids and phospholipids, were significantly depressed in the 8% CS and 8% SP groups but not when soy protein was fed at the same level as casein (25%) in the control. Furthermore, the severity of the deficits in myelination showed a differential pattern depending on the type of dietary protein fed. At weaning, the deficits with the 8% SP diet were 1.5-2.0-times greater than with the corresponding casein diet. A more pronounced retardation in the initiation, progression and capacity of myelination in postnatal soy protein undernutrition was indicated.

Animals↗

Effects of pure and auto-oxidized forms of cholesterol on plasma, liver lipids and hepatic lipogenesis in chicks.

Pure cholesterol (PC), oxidized cholesterol (OC) and cholestane-3 beta,5 alpha,6 beta-triol (CT) were fed to male Hubbard chicks for 3 weeks in a basal grain diet. Feed consumption and weight gain of chicks fed OC (1.0%) or CT (0.1%) were not significantly different from that of chicks fed PC (0.85%) or the basal diet alone. Plasma cholesterol level was significantly (P less than 0.05) higher in chicks fed PC compared to controls; however, compared to other dietary groups, differences were not significant. Measurement of hepatic lipogenesis, in vivo, from labeled substrates showed that [14C]acetate was primarily utilized for fatty acid synthesis in all dietary groups. The relative order was PC greater than PC + CT greater than OC greater than CT greater than basal. Conversely, [3H]mevalonate was preferentially used for cholesterogenesis and the relative effectiveness was basal greater than CT greater than OC greater than PC + CT greater than PC.

Animals↗