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Biomedical subjects

C H Hsu

Publications and source records attributed to C H Hsu.

At least 91 records · Page 5Linked to original sources
PubMed1995

Concurrent colon polyp with angiodysplasia causes lower gastrointestinal bleeding: a case report.

Angiodysplasia is an important cause of gastrointestinal bleeding which occurs mostly common in the right side of the colon, usually in the elderly but sometimes in younger adults. Herein, a case of rare clinical association-adenomatous colonic polyp with submucosal angiodysplasia in a forty year old man, who had repeated intestinal bleeding, is reported. We think colon polyps inducing intestinal blood loss may be caused by unidentified angiodysplasia. The diagnosis of these lesions is very difficult, so mesenteric angiography is recommended. Although various therapeutic methods were suggested, in patients who have repeated bleeding or are chronic anemics, resection of the involved segment of the bowel is the treatment of choices.

Adult↗
PubMed1994

Functional association of essential splicing factor(s) with PRP19 in a protein complex.

We have previously shown that the yeast PRP19 protein is a spliceosomal component, but is not tightly associated with small nuclear RNAs. It appears to associate with the spliceosome concomitant with or just after dissociation of the U4 small nuclear RNA during spliceosome assembly. We have found that PRP19 is associated with a protein complex in the splicing extract and that at least one of the associated components is essential for splicing. Taking advantage of the epitope tagging technique, we have isolated the PRP19-associated complex by affinity chromatography. The isolated complex is functional for complementation for the heat-inactivated prp19 mutant extract, and consists of at least seven polypeptides in addition to PRP19. At least three of these can interact directly with the PRP19 protein. We also show that the PRP19 protein itself is in an oligomeric form, which might be a prerequisite for its interaction with these proteins.

Base Sequence↗
PubMed1994

The effects of ricin on the sympathetic vascular neuroeffector system of the rabbit.

Ricin is a toxic lectin that inhibits protein synthesis. Because ricin decreases arterial pressure and causes cardiovascular collapse, its effects on the vascular neuroeffector system were investigated. Rabbits were given either of two doses of ricin, and then norepinephrine (NE) release from aorta to transmural stimulation, NE uptake into aorta, NE content of aorta, monoamine oxidase activity, and catechol-O-methyl transferase activity in aorta were determined 18 hours, 4 days or 7 days later. Norepinephrine uptake and enzyme activities in the aorta were not altered by ricin administration. Norepinephrine release and content of aorta were increased at most time periods following ricin administration, significantly so for NE content at 4 days and for release at 18 hours following the lower dose of ricin. We conclude that the mechanisms involved in the release of NE from sympathetic nerves in the vasculature are not impaired by ricin administration, but rather show changes that indicate increased compensatory activity.

Animals↗
PubMed1994

Effects of ricin administration to rabbits on the ability of their coronary arteries to contract and relax in vitro.

We have previously shown that ricin, a toxic lectin from the castor bean, increases cardiac output and blood flow to the heart in rabbits in the early stage of its intoxication and causes hemorrhage and necrosis in the heart following a lethal dose. To investigate possible alterations in coronary arteries following ricin administration, their responses to serotonin (5-HT), histamine, norepinephrine (NE), and acetylcholine (ACh) were determined. Rabbits were given 0.22 microgram/kg of ricin i.v. and euthanized 48 hr later. Cumulative contractions of rabbit coronary artery rings to 5-HT and histamine were measured. Cumulative relaxations to ACh and NE were measured in rings contracted with the histamine H1 receptor agonist 2-(2-aminoethyl)pyridine. Ricin significantly increased the EC50s of contractions of rabbit coronary artery rings to 5-HT and histamine. Maximal contractions to most agonists tested were increased. The EC50 of relaxation of rabbit coronary artery to NE was decreased, although the maximal relaxations to ACh and NE were not increased to a significant extent. It is likely that in the early stage of ricin intoxication in rabbits the sum of the effects of these vasoactive agents is to reduce the vascular tone of the coronary artery and thus reduce blood pressure and, in the late stage of ricin intoxication, vasospasm of coronary artery may cause micro- and macrocirculatory collapse.

Acetylcholine↗
PubMed1994

Tissue distribution of 3H-terbutaline in rabbits.

Terbutaline is a widely used, selective beta 2-adrenergic agonist whose penetration into brain has not been demonstrated in laboratory animals. Although its tissue uptake has been reported in some animals, no uptake into brain has been demonstrated. A single dose of 20 microCi of 3H-terbutaline along with 10 mg/kg of unlabeled terbutaline was injected into a rabbit marginal ear vein. The distribution of 3H-terbutaline in several tissues was determined 0.5, 1, 3, or 6 hr later. Radioactivity in the brain was well-maintained over the 6 hr observation period. In most tissues, radioactivity peaked in less than 1 hr, then declined. Radioactivity in the urine was high at all time periods and was highest at 3 hr. Thus, terbutaline or a metabolite(s) does cross the blood-brain barrier in rabbits, and the radioactivity in the rabbit brain does not decrease during the 6 hours following terbutaline injection.

Animals↗
PubMed1994

Regulation of calcitriol receptor and its mRNA in normal and renal failure rats.

Homologous up-regulation of calcitriol receptor (VDR) by calcitriol is believed to be a transcriptional event. In this experiment, we studied the effect of calcitriol on VDR in normal and renal failure rats. The time course of the effect of calcitriol on VDR mRNA showed a biphasic change in VDR mRNA in response to calcitriol. The concentration of intestinal VDR mRNA increased at six hours and reached peak levels approximately 15 hours after calcitriol injection. Thereafter, the mRNA began to decrease and by 48 hours the level had declined to below the control values. The VDR levels also increased, though they lagged behind the VDR mRNA, and nearly plateaued at 24 hours after calcitriol treatment. In renal failure, the concentrations of VDR were lower and the levels of VDR mRNA were higher than the respective values of normal rats, suggesting that VDR synthesis was inhibited at post-transcriptional sites. Chronic administration of calcitriol increased the VDR but lowered the VDR mRNA levels in both normal and renal failure rats. Infusion of uremic ultrafiltrate to normal rats resulted in lower VDR and higher VDR mRNA levels similar to those found in rats with renal failure. The results indicate that uremic toxins are responsible for the low VDR and high VDR mRNA in renal failure.

Animals↗
PubMed1994

Inhibition of nuclear uptake of calcitriol receptor by uremic ultrafiltrate.

The biological action of calcitriol is mediated through a hormone-receptor complex interacting with nuclear chromatin. Interaction of the calcitriol receptor (VDR) with VDR response elements produces bioactive proteins which carry out the physiological actions of calcitriol. Since biological response to calcitriol appears to be diminished in renal failure, we studied the effect of uremic toxins on the interaction of VDR with nuclear chromatin using in vitro nuclear uptake of the 3H-calcitriol labeled VDR by intestinal nuclei. We found that nuclear uptake of the labeled intestinal VDR from renal failure rats was significantly lower than that from the control animals. HPLC fractionated uremic ultrafiltrate directly inhibited nuclear uptake of the labeled VDR when the labeled VDR was incubated with 50% of the ultrafiltrate for various time intervals ranging from 15 minutes to 6 hours. Infusion of uremic ultrafiltrate to normal rats for 20 hours also produced intestinal VDR with a lower binding affinity for intestinal nuclei when compared to the controls infused with normal ultrafiltrate. The latter study suggests that uremic toxins are responsible for the decreased nuclear uptake of VDR of rats with renal failure. Although it is difficult to extrapolate these results directly to the intact cells, our findings suggest that part of the calcitriol resistance in renal failure could be explained by decreased entry of receptor into the nucleus.

Animals↗
PubMed1994

Effect of vitamin D metabolites on calcitriol degradative enzymes in renal failure.

We have demonstrated that in renal failure calcitriol degradation is decreased and that administration of vitamin D metabolites increases the degradation. In this study, we measured intestinal 24- and 26-hydroxylase activities and the effects of chronic infusion (7 days) of vitamin D metabolites on these enzymes' activities in rats with experimental renal failure. The enzymatic activity of intestinal 24-hydroxylase, but not 26-hydroxylase, was significantly lower in renal failure rats compared to control sham operated rats. Replacement of calcitriol (3 ng/day) significantly increased 24-hydroxylase activity by 17% in rats with renal failure (P < 0.01), although the activity remained 15% lower than the controls (P < 0.01). Intestinal 26-hydroxylase activity was not lower in renal failure; however, calcitriol treatment increased the activity beyond that of normal controls. In contrast, administration of 25(OH)D3 (600 ng/day) and 24,25(OH)2D3 (1 microgram/day) reduced the conversion of calcitriol to 1,24,25(OH)3D3 by more than 50% and to 1,25,26(OH)3D3 by more than 38%, respectively. We conclude that calcitriol increased its own degradation in renal failure by increasing the enzymatic activities of both 24- and 26-hydroxylase. However, the mechanisms of increased calcitriol degradation by 25(OH)D3 and 24,25(OH)2D3 in renal failure remain unknown.

24,25-Dihydroxyvitamin D 3↗
PubMed1994

Acute segmental obstructing enteritis in children.

We studied a group of 15 children with acute segmental enteritis associated with intestinal obstruction. The disease is characterized by fever, leukocytosis, copious bilious vomiting, and severe abdominal pain with signs of intestinal obstruction. Exploration revealed varying degrees of segmental ischemic change in the small bowel, but surgery seemed to be unnecessary in most cases. Antibiotics were effective in nonoperative cases. The clinical illness lasted 10-14 days. The disease was self-limited, and no mortality was found in our series. To our knowledge, this is the first report of this disease entity in Chinese children.

Abdominal Pain↗
PubMed1994

Prospective evaluation of insulin resistance and lipid metabolism in women receiving oral contraceptives.

OBJECTIVES: It has been suggested that normal women receiving oral contraceptives (OC) may develop a series of metabolic side-effects which relate to the risk of cardiovascular disease. These metabolic disturbances include changes in glucose and insulin metabolism, raised serum lipid and lipoprotein concentrations and elevated blood pressure. All these changes indicate that OC might cause insulin resistance. We have prospectively examined the effect of OC on insulin resistance and lipid metabolism including Lp(a) values. PATIENTS: The study group comprised 13 normally menstruating Chinese women. DESIGN: The study subjects were given a combined triphasic oral contraceptive which was administered on a 21-day on, 7-day off medication cyclic regimen, the first pill being administered on day 5 from the beginning of menses. The metabolic investigations were carried out during luteal phase before OC and again the third week of the third month of OC administration. MEASUREMENTS: Metabolic evaluation including insulin secretion and insulin-mediated glucose uptake were evaluated by oral glucose tolerance test and the modification of insulin suppression test. Fasting triglyceride, cholesterol, HDL-cholesterol and Lp(a) concentrations were also measured. RESULTS: The plasma glucose and insulin responses during a 75-g oral glucose challenge increased significantly (P < 0.05 and P < 0.03, respectively). The steady-state plasma glucose (SSPG) concentrations achieved during constant infusion of glucose, insulin and somatostatin increased significantly after 3 cycles of OC administration (glucose 7.5 +/- 0.8 vs 12.4 +/- 0.7 mmol/l, P < 0.001) while the steady-state plasma insulin (SSPI) concentrations were relatively similar (410 +/- 14 vs 391 +/- 7 pmol/l, NS). Plasma triglyceride levels increased significantly (0.81 +/- 0.12 vs 1.09 +/- 0.19 mmol/l, P < 0.03) following OC administration. Fasting plasma cholesterol, HDL cholesterol and calculated LDL cholesterol concentrations did not change as compared with baseline values, nor did the ratio of total cholesterol to HDL cholesterol. The Lp(a) concentrations did not change during the administration of OC (81 +/- 25 vs 71 +/- 21 mg/l, NS). CONCLUSIONS: These data indicated that intake of OC for 3 cycles induced glucose intolerance, hyperinsulinaemia and insulin resistance in normal menstruating Chinese women. These changes occurred in association with elevated plasma triglyceride concentrations and no alteration in Lp(a) or other lipid values.

Adult↗
PubMed1994

Effects of terbutaline on alpha-adrenergic responses and Ca2+ influx in isolated rabbit aorta.

Effects of terbutaline applied in vivo or in vitro on alpha-adrenergic receptors in the rabbit aorta in normal and Ca(2+)-free solution, and on basal, high potassium-, and phenylephrine-stimulated Ca2+ uptake into aorta were investigated. Three day terbutaline administration (25 mg/kg, subcutaneously three times daily) to rabbits increased the pKB for phentolamine in aorta rings (control 7.3 +/- 0.2, n = 9; terbutaline 7.8 +/- 0.2, n = 15). It also depressed phenylephrine-stimulated contractions of aorta rings in Ca(2+)-free but not those in normal Krebs solution. It did not significantly depress the basal, or phenylephrine-evoked Ca2+ influx into aorta rings, but decreased high potassium-induced Ca(2+)-influx (control 0.58 +/- 0.05 mumoles/g aorta; n = 3, terbutaline 0.41 +/- 0.06 mumoles/g aorta, n = 3). In vitro application of 50 microM terbutaline did not significantly alter phenylephrine-stimulated contractions of aorta rings in Ca(2+)-free Krebs solution or significantly depress basal or phenylephrine-induced Ca2+ influx into aortas, but did decrease high potassium-stimulated Ca(2+)-influx. Thus, 3-day terbutaline administration increased the affinity of alpha-adrenergic receptors for phentolamine and had a tendency to increase contractions of aorta rings to phenylephrine. It also decreased high potassium-stimulated Ca2+ influx, and depressed phenylephrine-induced contractions in Ca(2+)-free Krebs solution, while in vitro terbutaline application also decreased potassium-induced Ca2+ influx.

Animals↗
PubMed1994

The cardiovascular effects of ricin in rabbits.

Ricin is a toxic lectin from the castor bean. The time course of its toxic effects on the cardiovascular system of rabbits was investigated after determining its LD50 and minimum lethal dose in rabbits by the Up and Down method, as a basis for dosing. Systolic and diastolic arterial pressures, electrocardiogram and heart rate were recorded for 48 hr following administration of either a toxic sublethal (0.22 microgram/kg) or minimum lethal dose (0.44 microgram/kg) of ricin. After a delayed onset of about 20 hr, the minimum lethal dose (0.44 microgram/kg) of ricin caused a significant decrease in both systolic and diastolic pressures (P < 0.05). The systolic and diastolic pressures decreased 0.47 and 0.39 mmHg/hr more so than control groups, respectively. A toxic sublethal dose (0.22 microgram/kg) of ricin did not significantly alter either systolic or diastolic pressure. Neither dose of ricin caused cardiac arrhythmias or significantly increased heart rate. We conclude that the lethal hypotensive sequelae of ricin toxicity in the rabbit were peripheral in origin and not cardiogenic at these two doses.

Animals↗
PubMed1994

Duplex ultrasonographic assessment of gut blood flow velocity: effect of meal composition in normal full-term newborns after first feed.

We used transcutaneous duplex Doppler ultrasound to measure superior mesenteric artery and celiac artery blood flow velocity in 45 normal healthy newborn infants. Doppler indices of PSV, TAMV, EDV, and PI were measured immediately before and after feeding at 15 minute intervals up to 75 minutes. Maximal changes were compared with preprandial baseline values. There were no significant differences between the preprandial and postprandial blood pressures and heart rates. In the superior mesenteric artery the PSV, TAMV, and EDV rose progressively and peaked 30 minutes after feeding in both the milk-fed group and the 5% glucose, water-fed group over baseline (73 versus 41% and 110 versus 63%, 130 versus 100%) (P < 0.05). The PI decreased significantly in the milk-fed group only. There were no significant changes in any blood flow velocity parameters derived from the celiac artery. We conclude that duplex ultrasonography provides a noninvasive means of studying the reactivity of the splanchnic arterial circulation to different stimuli. The chemical composition of the meal is a significant factor determining postprandial mesenteric hyperemia.

Blood Flow Velocity↗
PubMed1994

Hormonal change in an adult with Prader-Willi syndrome: report of a case.

We report a classical case of Prader-Willi syndrome (PWS) in an adult with typical interstitial deletion of chromosome 15, and emphasize the study of hormonal change. This 21-year-old female had PWS face characteristics, small hands and feet, marked obesity, mental retardation, growth retardation, absence of puberty and amenorrhea. She also had the characteristic history of infantile hypotonia, poor feeding, failure to thrive and then improved appetite, followed by obesity from the age of four years. She had compulsive hyperphagia, to the extent of stealing and lying to take food. Chromosome study with high resolution banding technique revealed a small interstitial deletion at band q12 of chromosome 15, which is characteristically found in a majority of patients with PWS. Hormonal study revealed hypogonadism and growth hormone deficiency of supposed hypothalamic origin. She also had non-insulin-dependent diabetes mellitus with decreased pancreatic insulin reserve.

Adult↗
PubMed1993

Monocyte 1 alpha-hydroxylase regulation: induction by inflammatory cytokines and suppression by dexamethasone and uremia toxin.

Alveolar macrophages acquire 1 alpha-hydroxylase activity in inflammation, and thereby metabolize 25 hydroxyvitamin D3 (25 D3) to the active metabolite, 1 alpha,25-dihydroxyvitamin D3 (1,25 D3, calcitriol). Calcitriol is a potent differentiation agent that modulates mononuclear phagocyte activation and effector functions. The mediators that induce macrophage 1 alpha-hydroxylase activity are not well delineated. Furthermore, it is unclear whether calcitriol is a product only of terminally differentiated macrophages or whether less mature mononuclear phagocytes can produce it as well. The ability of newly recruited monocytes to produce calcitriol as an autocrine differentiation agent is particularly important in inflammation, as it may substantially expand the functional repertoire of these cells. To assess the effects of cytokines on 1 alpha-hydroxylase activity, blood monocytes were cultured in the presence and absence of human recombinant tumor necrosis factor alpha (TNF-alpha), interferon-gamma (IFN-gamma), and interleukins 1 and 2 and then incubated with 25 D3 substrate. The conditioned media were assayed for calcitriol by high-performance liquid chromatography and competitive receptor binding assay. No detectable calcitriol was produced by unstimulated monocytes. However, all the cytokines markedly increased monocyte calcitriol production (range 133-151 pg/mg protein; in all cases P < .001). We then determined whether calcitriol production was suppressed by preincubation with either dexamethasone or the putative uremia toxin guanidinosuccinic acid (GSA). Dexamethasone pretreatment significantly inhibited subsequent cytokine-induced calcitriol production by monocytes, as did GSA (average 69 and 63% of control, respectively).

Calcitriol↗
PubMed1993

Efficacy of plasmin-treated intravenous gamma-globulin for therapy of Kawasaki syndrome.

In order to delineate the efficacy of plasmin-treated intravenous gamma-globulin (IVGG) in the treatment of Kawasaki syndrome, we compared the frequency of coronary artery abnormalities in children treated or not with IVGG for Kawasaki syndrome. Among 291 cases of Kawasaki syndrome diagnosed during the period of 1987 to 1991 without coronary abnormalities within 10 days of the onset of illness, 128 were treated with IVGG and aspirin and were compared with 163 treated with aspirin alone. IVGG was given in a dosage of 400 mg/kg/day for 4 consecutive days. The detection of coronary abnormalities was monitored by two dimensional echocardiography. Two weeks after enrollment coronary artery abnormalities were present in 37 (22.7%) of 163 children in the aspirin group and in 9 (9%) of 128 in the gamma-globulin group (P < 0.05). Seven weeks after enrollment, abnormalities were present in 20 (12.3%) of 163 children in the aspirin group and in 6 (4.6%) of 128 in the IVGG group (P < 0.05). We conclude that plasmin-treated IVGG is effective in reducing the prevalence of coronary artery abnormalities in Kawasaki syndrome and suggest a predominant role of the Fc gamma fragment of IgG in the therapeutic effect.

Aspirin↗