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Biomedical subjects

T C Chu

Publications and source records attributed to T C Chu.

At least 37 records · Page 2Linked to original sources

Possible mechanisms of salt-induced hypertension in Dahl salt-sensitive rats.

Genetic factors, diet, and salt sensitivity have all been implicated in hypertension. To further understand the mechanisms involved in salt-induced hypertension, cardiovascular, hemodynamics, and biochemical parameters in Dahl salt-sensitive rats were evaluated in animals on high- and low-sodium diets. During a 4-week treatment period, blood pressure was significantly elevated in the high (8.0%) salt group compared to the low (0.3%) salt group (p< or =0.05 for weeks 2 and 4, respectively). No significant changes were observed in heart rate. The increase in blood pressure was associated with significant increases in lower abdominal aortic and renal vascular resistance, along with a reduction in blood flow. A fourfold increase in arginine vasopressin was observed in animals on the high-salt diet. In contrast, there was no effect on plasma sodium, potassium, or aldosterone levels during the treatment period. As measured in isolated aortic rings, the high-salt diet also caused a significant elevation in stimulated norepinephrine release and a reduction in cyclic GMP levels. These data suggest that salt-induced elevation in blood pressure is due to activation of both the sympathetic and arginine vasopressin systems via mechanisms involving decreased cyclic GMP generation in vascular smooth muscle.

Aldosterone↗

Radiostrontium analytical method using crown-ether compound and Cerenkov counting and its applications in environmental monitoring.

The radiostrontium content in environmental samples was determined by chemical analysis by means of the fuming nitric acid method and ion exchange method with low-level beta counting and the newly developed method using crown-ether compound. Counting was performed with a low-background counter and a liquid scintillation counter together; the latter was the Cerenkov counting method. All results obtained by these three methods were in good agreement. The time for chemical separation of radiostrontium, using crown-ether compound, is much faster than fuming nitric acid and ion exchange methods. However, due to the high background of the liquid scintillation counter, the detection limit for Cerenkov counting is about two times higher than that for low-background counting.

Chromatography, Ion Exchange↗

Lisuride acts at multiple sites to induce ocular hypotension and mydriasis.

Topically unilaterally applied lisuride caused dose-related lowering of intraocular pressure in ipsilateral (treated) but not in contralateral eyes of normal rabbits. The ocular hypotensive response induced by lisuride was antagonized by pretreatment with metoclopramide, a dopamine receptor antagonist, and was partially reduced by local sympathetic denervation. In contrast to the unilateral effect on intraocular pressure, lisuride caused mydriasis in both eyes. Mydriasis was of greater magnitude and more sustained in normal eyes compared to sympathetically denervated eyes. Additional in vivo experiments demonstrated that lisuride caused dose-related suppression of neuronally initiated contractions of cat nictitating membrane. In in vitro experiments lisuride caused dose-related inhibition of norepinephrine release from isolated rabbit iris-ciliary bodies. Pretreatment with Bay K 8644, a calcium channel activator, did not attenuate lisuride-induced inhibition of norepinephrine release in isolated rabbit iris-ciliary bodies. Because lisuride pretreatment caused no change in isoproterenol-stimulated cAMP accumulation in isolated iris-ciliary bodies, suppression of adenylate cyclase was unlikely. It is concluded that the ocular hypotensive effect of lisuride results, in part, from activation of prejunctional dopaminergic receptors on peripheral sympathetic nerves in the anterior segment of the eye but may also involve antagonism on peripheral postjunctional alpha1 adrenoceptors as well. Bilateral increases in pupil diameter antagonized by metoclopramide suggest a stimulatory action of lisuride on dopamine receptors in the central nervous system.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Efficacy of fenbendazole in the treatment of experimental Giardia infection in dogs.

OBJECTIVE: To evaluate the efficacy of fenbendazole as a treatment for Giardia sp. ANIMALS: 10 male and 10 female commercial-source Beagles. PROCEDURE: The experiment was conducted in 2 replicates. Dogs considered free of Giardia infection on the basis of results of 3 consecutive negative fecal examinations were experimentally infected with approximately 1,000 Giardia cysts isolated from dog feces. After verification of infection, the dogs were allocated to 2 groups (treated and untreated) and were housed in separate rooms. Treated dogs received 50 mg of fenbendazole/kg of body weight, p.o., daily, for 3 days. After treatment on the third day, treated dogs were removed from their runs, shampooed, rinsed with disinfectant, and returned to disinfected runs. Fecal samples were collected from all dogs 12 times during the next 25 days. RESULTS: Giardia cysts were found in the feces of every untreated dog during all or part of the test period. Nine of 10 treated dogs did not have Giardia cysts in any fecal sample examined; the other dog had a positive result on a single sample in the third week after treatment. CONCLUSION AND CLINICAL RELEVANCE: Fenbendazole, at the nematocidal label dosage, is an effective drug for treatment of Giardia infection in dogs.

Animals↗

Potential mechanisms of moxonidine-induced ocular hypotension: role of norepinephrine.

In rabbit's aqueous humor, norepinephrine, epinephrine, dopamine and serotonin were detected simultaneously by a high performance liquid chromatography with electrochemical detection. Furthermore, the changes in catecholamine levels in aqueous humor were evaluated after topical application of moxonidine, an imidazoline1/alpha 2 receptor agonist, in the presence and absence of efaroxan. The level of norepinephrine in aqueous humor was reduced by moxonidine treatment. However, under the same set of conditions, there were no significant changes in the levels of dopamine, epinephrine or serotonin. Pretreatment with efaroxan antagonized moxonidine-induced suppression of norepinephrine levels. In other in vivo experiments, moxonidine caused a decrease in intraocular pressure which was antagonized by pretreatment with efaroxan. In the superior cervical ganglion preparation, norepinephrine release was increased 5-fold by the presence of a high K+ medium. The K(+)-evoked norepinephrine secretion was reduced by 55% by moxonidine. Pretreatment with efaroxan blocked the moxonidine-induced inhibition of norepinephrine release. It is concluded that inhibition of norepinephrine release from the superior cervical ganglion and suppression of aqueous norepinephrine levels contribute to the moxonidine-induced lowering of intraocular pressure. Moreover, the antagonism of moxonidine's in vivo and in vitro effects by efaroxan suggests the involvement of imidazoline1 receptors, but does not preclude activity on alpha 2 adrenoceptors.

Administration, Topical↗

Moxonidine-induced inhibition of norepinephrine release in monkey and rabbit ciliary bodies: role of cGMP.

This study was designed to determine whether in isolated rabbits iris-ciliary bodies and monkey ciliary bodies, cGMP plays a role in the action of moxonidine, an alpha 2- and imidazoline (I1) receptor agonist. In field-stimulated rabbit iris-ciliary bodies, dose-related inhibition of norepinephrine release was induced by 8-Br-cGMP, moxonidine or sodium nitroprusside; 8-Br-cGMP in combination with moxonidine did not enhance inhibition of norepinephrine release. Sodium nitroprusside at intermediate and high concentrations stimulated cGMP production in rabbit iris-ciliary bodies, whereas moxonidine stimulated cGMP production modestly only at a high concentration. When iris-ciliary bodies were pretreated with a low concentration of moxonidine, sodium nitroprusside-stimulated cGMP production was enhanced from 1.6 to 2.2 pmol/mg protein. In field-stimulated monkey ciliary bodies, both sodium nitroprusside and moxonidine inhibited norepinephrine release. Pretreatment of electrically stimulated monkey ciliary bodies with sodium nitroprusside enhanced the suppressive effect of moxonidine on norepinephrine release. In monkey ciliary bodies, moxonidine raised cGMP production more than sodium nitroprusside did, but there was no synergism in cGMP production by combined treatment with moxonidine and sodium nitroprusside. These results suggest that cGMP could play a role in the ocular action(s) of moxonidine in ciliary bodies; however, involvement of cGMP in the action of moxonidine in monkey ciliary bodies seems to be more pronounced than in rabbit iris-ciliary bodies.

Animals↗

Elevation of intracellular Ca2+ concentration in rabbit nonpigmented ciliary epithelial cells by allicin.

A previous study has shown that allicin produces changes in aqueous humor dynamics, and this study was conducted to examine possible cellular mechanisms. In rabbit nonpigmented ciliary epithelial cells, basal levels of [Ca2+]i were determined to be 164 +/- 34 nM. Allicin, a sulfhydryl-reactive agent, induced Ca2+ transients at 0.01 mM and at 0.2 mM, the Ca2+ transient peaked at 732 +/- 35 nM. Allicin-induced Ca2+ transients were prevented by pretreatment with dithiothreitol which did not affect the basal Ca2+ levels. Allicin had only a slight, insignificant, effect on L-type Ca2+ currents, and allicin-induced Ca2+ transients were also present under extracellular Ca(2+)-free conditions. These data suggest that intracellular Ca2+ stores are the most probable source of allicin's effect. Pretreatment of cells with ryanodine, an inhibitor of Ca(2+)-induced-Ca(2+)-release, inhibited allicin-induced Ca2+ transients, but the basal Ca2+ levels were unaffected by ryanodine. Thus, allicin-induced Ca2+ transients are most likely mediated through ryanodine-sensitive intracellular Ca2+ stores.

Animals↗

Comparison of nucleoside transport binding sites in rabbit iris-ciliary body and cultured rabbit nonpigmented ciliary epithelial cells.

The iris-ciliary body (ICB) is a site of action for topically applied antiglaucoma drugs. Moreover, adenosine has been implicated as a modulator of aqueous humor dynamics. The present study compares the binding of the nucleoside transporter probe, [3H]nitrobenzylthioinosine ([3H]NBMPR), to homogenates prepared from rabbit ICB and a cultured rabbit nonpigmented ciliary epithelial cell line (NPE) to determine whether NPE can be used as an experimental model to study the nucleoside transporter. Linear transformation of the saturation binding data revealed that [3H]NBMPR binds to a homogeneous population of binding sites with similar binding affinities (Kd = 0.3 +/- 0.1 and 0.6 +/- 0.1 nM in NPE and ICB, respectively). However, the maximal binding capacity in NPE (Bmax = 288 +/- 54 fmol/mg protein) was significantly higher than that in ICB (Bmax = 154 +/- 17 fmol/mg protein). Selected inhibitors of the nucleoside transport system and structural analogs of adenosine inhibited the binding in both homogenate preparations with a similar rank order of potency: NBMPR > DPY > CV-1808 > CHA > R-PIA > S-PIA > 2-CADO > NECA. The results suggest that NPE is a useful model which could be used for characterizing the nucleoside transporter in ICB and for the screening of nucleoside transport inhibitors as potential antiglaucoma drugs.

Adenosine↗

Oxymetazoline: potential mechanisms of inhibitory effects on aqueous humor dynamics.

Oxymetazoline, an alpha 2 agonist, was active in lowering intraocular pressure in normal and sympathetically denervated rabbit eyes. Ocular hypotension was accompanied by decreased aqueous humor inflow. Topical pretreatment with rauwolscine, an alpha 2 antagonist, reduced the oxymetazoline-induced hypotensive effect more in contralateral than in ipsilateral eyes indicating the possible involvement of central alpha 2 adrenoceptors. Efaroxan, a relatively selective imidazoline antagonist, and diclofenac, a cyclooxygenase inhibitor, failed to inhibit the oxymetazoline-induced ocular hypotensive response. Oxymetazoline induced mydriasis in treated eyes at all doses. In in vitro studies, oxymetazoline inhibited isoproterenol-stimulated cAMP production in rabbit iris-ciliary bodies and cultured rabbit nonpigmented ciliary epithelial cells. The inhibition of cAMP accumulation induced by oxymetazoline was antagonized by rauwolscine or by BRL-44408, a relatively selective alpha 2A-adrenoceptor antagonist. These data indicate that oxymetazoline lowered intraocular pressure by activating alpha 2A receptors (ciliary epithelium) and that the ocular hypotensive effect was not totally dependent on intact sympathetic nerves. Results suggest that mechanisms involving centrally mediated effects of oxymetazoline are probable and this possibility is currently under investigation.

Adrenergic alpha-Agonists↗

Rilmenidine-induced ocular hypotension: role of imidazoline1 and alpha 2 receptors.

PURPOSE: To examine ocular actions by rilmenidine, an imidazoline1 and alpha 2 adrenoceptor agonist. METHODS: Intraocular pressure was measured in normal and sympathetically denervated rabbits by pneumatonometry. Electrically stimulated 3H-norepinephrine release from sympathetic nerves was determined in isolated, perfused rabbit iris-ciliary bodies. cAMP levels were evaluated in rabbit iris-ciliary bodies by radioimmunoassay. Ca2+ concentrations were measured in rabbit transformed nonpigmented ciliary epithelial cells by fluorescence ratio microscopy. RESULTS: Topical, unilateral administration of rilmenidine produced hypotensive responses in normal rabbits which were antagonized by either bilaterally administered efaroxan, an imidazoline receptor antagonist or rauwolscine, an alpha 2 receptor antagonist. Sympathectomy also eliminated the ocular hypotensive response. Rilmenidine (0.001, 0.01, 0.1, 1 microM) caused 5 +/- 1%, 18 +/- 5%, 35 +/- 10%, and 48 +/- 9% inhibition, respectively, of 3H-norepinephrine overflow whereas 10 microM efaroxan or rauwolscine caused enhancement of norepinephrine release by 102 +/- 23% or 86 +/- 25%, respectively. Furthermore, pretreatment with efaroxan or rauwolscine partially antagonized the inhibition of norepinephrine release induced by rilmenidine. In other experiments, rilmenidine (1 microM) inhibited isoproterenol-stimulated cAMP accumulation in rabbit iris-ciliary bodies by 43 +/- 9% which was antagonized by 10 microM efaroxan or rauwolscine. Rilmenidine induced large increases in [Ca2+]i in rabbit nonpigmented ciliary epithelial cells which were effectively antagonized by efaroxan or rauwolscine. CONCLUSIONS: These in vivo and in vitro data suggest that the ocular hypotensive activity induced by rilmenidine is due, in part, to suppression of sympathetic neuroeffector function in the rabbit ciliary body and that alpha 2 adrenergic receptors and/or imidazoline1 receptors are involved.

Adrenergic alpha-Agonists↗

Alpha-2 adrenoceptor mediated changes in aqueous dynamics: effect of pertussis toxin.

Because alpha-2 (alpha 2) adrenoceptor-mediated inhibition of signal transduction mechanisms is regulated, in part, by inhibitory G (Gi) protein, we studied the effects of pertussis toxin (PTX) pretreatment on alpha 2 adrenergic agonist, UK 14,304-18 (UK; brimonidine)-induced: (1) changes in intraocular pressure (IOP) and aqueous flow rate of rabbits; (2) modulation of 3H-norepinephrine (NE) overflow of rabbit iris-ciliary bodies (ICBs) and (3) accumulation of cyclic AMP in rabbit ICBs and cultured non-pigmented ciliary epithelial (NPE) cells. Results showed that UK (50 micrograms) lowered the IOP of normal rabbits by 8 +/- 1 mmHg (n = 8) at 3 hr when treated topically and that the reduction of IOP was accompanied by a decrease in aqueous humor inflow (35%, n = 5). Therefore, it was postulated that these UK-induced effects involve activation of a Gi protein linked to alpha 2 adrenoceptors. In PTX-pretreated (2.5 micrograms kg-1, i.a.) rabbits, hypotensive responses to UK were reduced by 50% and 70% (n = 8) at days 4 and 7 post PTX treatment, respectively. The suppression of aqueous humor inflow induced by UK was also prevented by the PTX treatment. In isolated, perfused rabbit ICBs, UK (1 microM) caused 50% inhibition of 3H-NE overflow from electrical field stimulation. Pretreatment with PTX (150 ng ml-1, 4 hr) partially prevented UK-induced inhibition of NE overflow. In in vitro assays of postjunctional alpha 2 adrenoceptor activity, UK (1 microM) inhibited isoproterenol (ISO, 1 microM)-stimulated cAMP accumulation by 45% and 48% in ICBs and NPE cells, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

Discrimination of airborne radioactivity from radon progeny.

Naturally occurring radon and thoron progeny are the most interfering nuclides in the aerosol monitoring system. The high background and fluctuation of natural radioactivity on the filter can cause an error message to the aerosol monitor. A theoretical model was applied in the simulation of radon and thoron progeny behavior in the environment and on the filter. Results show that even a small amount of airborne nuclides on the filter could be discriminated by using the beta:alpha activity ratio instead of gross beta or alpha counting. This method can increase the sensitivity and reliability of real-time aerosol monitoring.

Air Pollutants, Radioactive↗

Ocular actions of moxonidine: a possible role for imidazoline receptors.

Moxonidine (MOX, 4-chloro-N-[4,5 dihydro-1H-imidazol-2-yl]-6-methoxy-2- methyl-5-pyridinamine), a relatively selective alpha-2 agonist, was investigated for effects on: 1) aqueous humor dynamics in normal and unilaterally sympathectomized rabbits; 2) noradrenergic functions in cat nictitating membrane (CNM); 3) [3H]norepinephrine overflow in rabbit iris-ciliary bodies (ICBs) and 4) cyclic AMP (cAMP) accumulation in rabbit ICBs and nonpigmented ciliary epithelial (NPE) cells. Unilateral, topical administration of MOX to the normal rabbit eyes produced decreases in intraocular pressure, aqueous humor flow rate and ipsilateral increases in pupil diameter. Ocular hypotensive response to MOX was inhibited by bilateral, topical pretreatment with idazoxan, an alpha-2/imidazoline antagonist, and efaroxan, an imidazoline antagonist. In sympathectically denervated rabbit eyes, MOX did not lower intraocular pressure or decrease aqueous humor flow rate. MOX suppressed, dose dependently, contractions of the CNM elicited by electrically stimulating the preganglionic sympathetic trunk, an effect antagonized by rauwolscine, an alpha-2 antagonist. In other experiments, MOX caused a dose-related inhibition of [3H]norepinephrine release from field-stimulated ICBs, an effect antagonized by efaroxan. MOX antagonized isoproterenol-induced cAMP accumulation in rabbit ICBs and NPE cells, an effect inhibited by rauwolscine. These results demonstrate that MOX: 1) produces ocular hypotension in rabbits by suppressing aqueous humor flow; 2) antagonizes electrically induced contractions of the CNM by inhibiting sympathetic neuronal function; 3) suppresses norepinephrine release of rabbit ICBs, an effect that was inhibited by efaroxan and 4) prevents isoproterenol-induced cAMP accumulation in the rabbit ICBs and NPE cells via action on alpha-2 adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

Thermodontic stimulator--a new technology for assessment of thermal dentinal hypersensitivity.

A clinical investigation of the reproducibility of threshold and pain temperature scores obtained from use of the Thermodontic Stimulator (TDS) is reported. The TDS is designed for accurate clinical testing of thermal dentinal hypersensitivity. This instrument employs a variable stimulus/fixed response approach to clinical testing of thermal dentinal hypersensitivity. The TDS consists of a probe in a handpiece, a patient signaling device (joystick), a computer, and interface electronics. The TDS provides a precise means of assessing and recording the temperature which elicits a response to thermal stimulation from the subject being evaluated. Two temperatures are recorded. The threshold temperature is recorded when the patient is first able to sense that a cold stimulus has been applied to the tooth. The second score, pain temperature, is recorded when the subject first notices discomfort. Twenty-two subjects participated in this study. Results obtained from the 21 subjects who completed this study (one subject dropped out for non-compliance) demonstrated a reproducibility standard deviation of 1.1 degrees C for the threshold temperature, and 2.8 degrees C for the pain temperature for the duration of the study. There was a good degree of correlation between the measurements of any two test days (Pearson's correlation coefficient). There was no significant difference between the mean pain temperature scores of any two testing days.

Cold Temperature↗

Allicin-induced hypotension in rabbit eyes.

The intent of this work was to examine the actions of allicin on 1) intraocular pressure (IOP) in normal and unilaterally sympathectomized (SX) rabbits; 2) cAMP accumulation in the rabbit iris-ciliary body (ICB) and cultured nonpigmented epithelial (NPE) ciliary body cells; and 3) 3H-norepinephrine (NE) release by calculating fractional tritium overflow in response to electrical field stimulation (EFS, 5 Hz, 12 V/cm) in isolated, perfused rabbit ICBs. Allicin, one of the active compounds produced by garlic, was evaluated on IOP and it was determined that allicin (1, 2.5, or 10 micrograms), topically, but not the precursor, alliin (10 micrograms), lowered the IOP unilaterally in normal rabbits. Allicin (10 micrograms) reduced the IOP by 6 +/- 1 mmHg (n = 4) in normal rabbits at 2 hrs (maximum response) whereas no change occurred in sympathectomized rabbit eyes. Moreover, allicin (0.01, 0.1, or 1 microM) caused 40, 40, or 52% inhibition, respectively, of 3H-NE overflow in response to EFS. Isoproterenol (ISO, 1 microM) stimulated cAMP accumulation by 3.6 and 9 fold in isolated rabbit ICB and cultured NPE cells, respectively. Allicin (1 microM) had no effect on basal cAMP level while it inhibited ISO-stimulated cAMP accumulation by 40% and 23% in ICB and NPE cells, respectively. This study suggests that allicin lowered IOP, in part, by dual actions at the neuroeffector junction.

Animals↗

Evaluation of natural radiation in houses built with black schist.

Natural radiation in houses built with black schist slabs located at an altitude of 1,000 m in the mountainous southern part of Taiwan were investigated by studying the naturally occurring radionuclides present in the black schist. Both indoor and outdoor radon concentrations were monitored. The cosmic-ray contribution to the dose received by the inhabitants was also estimated. Gamma-ray spectroscopy was performed for radionuclide analyses. In situ measurements were carried out using a survey meter coupled to a sodium iodide detector. Cellulose nitrate films, ZnS (Ag) scintillation cells, and alpha spectroscopy were used to study radon and radon daughters. Radiation doses due to all natural sources were calculated and compared with that incurred in common concrete dwellings at lower altitudes.

Air Pollution, Indoor↗

Radon exhalation rate from various building materials.

Solid-state alpha-track detectors using cellulose nitrate films were used to measure the radon exhalation rates from building materials. The radon flux emitted from the surface of the building material was measured by placing an inverted cup on the top of the building material. Cellulose nitrate film was placed within the cup. Tracks due to alpha particles from radon that migrate from the building material into the air space in the cup were registered on the cellulose nitrate film. The films were etched in a solution consisting of 10(-3) m3 2.5 N NaOH solution. A spark counter or microscope was used to record the tracks appearing on the cellulose nitrate film. The average exhalation rate of radon was obtained by means of a simple mathematical approach that can be used to estimate the maximum possible radon concentration in a closed room due to building materials alone. Infiltration and ventilation effects were excluded in this work. This new technique and simple approach can be used to establish the data base for average radon exhalation rates from all available building materials and walls or floors. The maximum indoor radon concentration can be estimated from the measured average radon exhalation rate by using this simplified model.

Air Pollution, Indoor↗

Allopurinol-induced toxic pustuloderma.

We report the case of a 67-year-old man who developed a pustular eruption, fever, neutrophilia and eosinophilia, following a short course of allopurinol. Toxic pustuloderma is an uncommon form of generalized pustular eruption with several characteristic clinical and pathological features. A number of drugs have been incriminated, but to our knowledge this is the first reported case of toxic pustuloderma occurring after the administration of allopurinol.

Aged↗