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Biomedical subjects

C H Hsu

Publications and source records attributed to C H Hsu.

At least 109 records · Page 6Linked to original sources
PubMed1993

Mechanism of decreased intestinal calcitriol receptor concentration in renal failure.

The biological actions of calcitriol and its receptor synthesis are believed to be mediated through the calcitriol-receptor complex interacting with nuclear chromatin of target cells. Thus inhibition of the receptor interaction with DNA could diminish the biological actions of calcitriol and upregulation of its receptor. We found that uremic ultrafiltrate reduced the receptor interaction with DNA in vitro. DNA-cellulose chromatography showed that the receptor from normal rats and rats infused with normal ultrafiltrate eluted as a single peak at 0.22 M KCl, whereas chronic renal failure rats and rats infused with uremic ultrafiltrate had two receptor peaks, i.e., one of normal activity at 0.22 M KCl and the other of weak activity at 0.12 M KCl. Furthermore, infusion of uremic ultrafiltrate to normal rats reduced the intestinal calcitriol receptor concentration (397 +/- 15.8 vs. 307 +/- 15.4 fmol/mg protein, both n = 4, P < 0.005). Uremic ultrafiltrate also suppressed the calcitriol-induced upregulation of the receptor (816 +/- 34.6 vs. 606 +/- 35.3 fmol/mg protein, P < 0.005). It appears that uremic toxins may reduce the biological action of calcitriol in renal failure by inhibiting receptor synthesis and the interaction of the hormone-receptor complex with nuclear chromatin.

Animals↗
PubMed1993

Effect of uric acid on plasma levels of 1,25(OH)2D in renal failure.

Previous studies from these laboratories have demonstrated that uremic biologic fluids contain substances that suppress 1,25(OH)2D metabolism. Among these substances, it was found that uric acid suppresses 1 alpha-hydroxylase activity and synthesis of 1,25(OH)2D in rats. In this study, the effect of uric acid on plasma concentrations of 1,25(OH)2D in patients with renal failure was examined. Nine patients with stable chronic renal failure (serum creatinine, 1.9 to 6.4 mg/dL) were studied. None of the patients received vitamin D supplementation. Plasma concentrations of Ca, P, parathyroid hormone, creatinine, uric acid, 1,25(OH)2D, and 25(OH)D were measured before and 1 wk after the patients received allopurinol, 300 mg daily. Plasma creatinine, Ca, P, parathyroid hormone, and 25(OH)D did not change before or after allopurinol treatment. However, plasma uric acid decreased significantly from 7.3 +/- 0.4 to 4.0 +/- 0.4 mg/dL (P < 0.01) and plasma concentration of 1,25(OH)2D rose from 30.8 +/- 2.7 to 38.2 +/- 4.8 pg/mL (P < 0.01) after the ingestion of allopurinol. Allopurinol itself did not appear to directly enhance 1 alpha-hydroxylase activity in rats. It was concluded that a short-term administration of allopurinol suppresses plasmic uric acid and increases plasma 1,25(OH)2D in patients with chronic mild to moderate renal failure.

Adult↗
PubMed1993

Duplex Doppler assessment of visceral and cerebral blood flow velocity in full-term newborns.

To assess postnatal visceral and cerebral blood flow velocity changes, transcutaneous duplex Doppler ultrasound was used to measure the superior mesenteric artery (SMA), celiac artery (CA) and anterior cerebral artery (ACA) blood flow velocity in 20 normal healthy newborns. Doppler indices of peak systolic velocity (PSV), time-averaged mean velocity, end-diastolic velocity and Pourcelot resistance index (PI) were measured immediately after delivery and consecutively for three days at 24-hour intervals. At 24 hours after delivery, PSV had risen significantly in the CA, SMA and ACA (p < 0.01). The PI had decreased significantly in all three vessels. We conclude that the most prominent hemodynamic changes in the splanchnic and cerebral artery circulation occur within 24 hours after delivery in normal healthy newborns. Possible mechanisms are discussed.

Blood Flow Velocity↗
PubMed1993

Liver transplantation for a hepatitis B-related cirrhotic patient.

A patient with chronic end-stage liver cirrhosis resulting from a hepatitis B viral infection had a successful liver transplantation performed on 1 July 1991. Preoperative serology revealed that both HBsAg and HBeAg were positive, and the anti-HBs antibody was negative. Immunoprophylaxis included active immunization, as well as injections of large doses of hepatitis B immunoglobulin (HBIG) given perioperatively to reverse the antigen status. The patient has been anti-HBs antibody positive for more than 10 months since the transplantation. The immunoprophylaxis protocol used has been effective in the prevention of hepatitis B viral reinfection.

Adult↗
PubMed1993

Terbutaline-induced desensitization in rabbit aorta in vitro.

In vivo administration of terbutaline, a beta 2-adrenergic agonist, desensitizes beta-adrenergic agonist-induced responses in isolated rabbit aorta. Characteristics of the desensitization following in vitro application of terbutaline and prevention of such desensitization by certain agents were studied. Endothelium-denuded rabbit aorta rings were incubated with 10 or 50 microM terbutaline for 30 or 60 min, or with no drug as a control. Following contraction with 1 microM phenylephrine, relaxations to cumulative concentrations of isoproterenol were determined. Rings exposed to terbutaline relaxed less to isoproterenol, indicating desensitization of beta-adrenergic receptors. The desensitization was homologous, exposure time- and concentration-dependent, and at least partially reversible. It does not require extracellular calcium to develop and is not blocked by verapamil, ketotifen, prednisolone or nedocromil. Thus, terbutaline-induced desensitization occurs in vitro, is homologous, does not require calcium, and is not blocked by the four compounds tested.

Adenosine↗
PubMed1993

Progesterone facilitates thrust in female hamsters implanted with estradiol at the medial preoptic area.

Progesterone (P) facilitates male-like sexual behavior in female hamsters primed with estrogen. Since estrogen plus P activates lordosis in female hamsters and the site of the hormonal action is at the ventromedial hypothalamus (VMH), it is possible that the same hormones act at the same site to induce male-like sexual behavior. However, VMH lesion abolishes lordosis, but not thrust, in ovariectomized female hamsters treated with estrogen plus P. Therefore, we tried another brain site--the medial preoptic area (mPOA). We implanted cannula, 27 gauge and filled with estradiol at the tip, at the mPOA or the VMH bilaterally in ovariectomized female hamsters. The hamsters received subcutaneous injections of P (0.5 mg in 0.05 ml sesame oil) at noon every fourth day. Behavior tests were conducted the same night of the injection day and the day before. The procedure was repeated five times. During a test night, each experimental female hamster was paired with a male hamster first and then with another estrous female. Recorded behavioral events were duration of lordosis and frequency of thrust. Both mPOA and VMH groups displayed lordosis only on the day of P injection, without any significant group difference. As to the male-like sexual behavior, 9 out of 54 mPOA females displayed thrust at least once but none of 27 VMH females ever did. Furthermore, 7 of the 9 females displayed thrust only on the day of the P injection. We conclude that the mPOA was also the site for the activation of male sex behavior in female hamsters. However, the hormones acting at the mPOA to induce thrusts were estrogen plus P.

Animals↗
PubMed1993

Obturator hernia: a report of eight cases.

Obturator hernia is a rare problem that occurs predominantly in elderly, emaciated women. The diagnosis of obturator hernia is difficult to establish in most patients before an operation is performed. Both delayed diagnosis and delayed surgical intervention contribute to high mortality. From 1978 to 1992, eight cases of obturator hernia involved elderly females who had received operations at this hospital. Resection of the incarcerated bowel was required. The often debilitated condition of these patients and the frequent delay of diagnosis combined to produce significant operative mortality.

Aged↗
PubMed1992

Mechanism of decreased calcitriol degradation in renal failure.

Metabolic clearance rate (MCR) of calcitriol is decreased in renal failure, and uremic toxins play a major role in the suppression of calcitriol degradation. In this experiment, we studied the effect of uremic toxins on renal 24- and 26-hydroxylase (HX) activities. Normal rats were infused for 20 h with 30 ml of normal or uremic plasma ultrafiltrates. At the end of infusion, renal enzymes activities were measured by the generations of 1,24,25- and 1,25,26-trihydroxyvitamin D3 10 min after the addition of 25 nM or 1 microM calcitriol. Renal 24-HX activity decreased approximately 50%, whereas 26-HX activity did not decrease in rats infused with uremic plasma ultrafiltrate. The induction of 24-HX activity by 100 ng calcitriol also decreased in rats infused with uremic ultrafiltrate. To examine whether uremic ultrafiltrate could directly inhibit the degradation enzymes, 24- and 26-HX activities were measured in kidney homogenates preincubated for 3 h with either normal or uremic ultrafiltrate. Uremic ultrafiltrate did not directly suppress 24- and 26-HX activities. Furthermore, the disappearance rate of calcitriol was similar for 90 min in kidney homogenates after they were preincubated for 3 h with uremic and normal ultrafiltrates. Because 24-HX synthesis is induced by the calcitriol-receptor complex binding to nuclear chromatin and activating genes coding for the enzyme, we studied the effect of uremic toxins on the binding affinity of calcitriol-receptor complex for DNA-cellulose. Uremic ultrafiltrate significantly reduced the binding affinity of the hormone receptor complex for DNA when the receptor was preincubated with the ultrafiltrate for 3 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Uremic plasma contains factors inhibiting 1 alpha-hydroxylase activity.

The effect of uremic plasma ultrafiltrate on calcitriol synthesis was investigated. Renal 1 alpha-hydroxylase activity was measured in normal rats infused for 20 h with 20 mL of normal or uremic plasma ultrafiltrate. Renal 1 alpha-hydroxylase activity was determined by the generation of calcitriol measured 5, 10, 20, and 30 min after the reaction was initiated by the addition of cold 25(OH)D3. The activity was significantly lower in rats infused with uremic plasma ultrafiltrate. Kidney homogenates preincubated for 3 h with uremic plasma ultrafiltrate also had significantly lower renal 1 alpha-hydroxylase activity than did those preincubated with normal plasma ultrafiltrate. In addition, the effect of the putative uremic toxin, guanidinosuccinic acid (GSA), on renal 1 alpha-hydroxylase activity was studied. Normal rats infused for 20 h with 20 mL of saline solution containing 1.5 mg/dL of GSA had significantly lower renal 1 alpha-hydroxylase activity than did rats infused with normal saline. The enzyme activity was also lower in kidney homogenates preincubated for 3 h with 4 mg/dL of GSA. Enzyme kinetic analysis revealed that the inhibition of renal 1 alpha-hydroxylase by GSA was noncompetitive. It was concluded that uremic plasma contains substances that directly inhibit renal 1 alpha-hydroxylase activity.

Animals↗
PubMed1992

Isolation and partial purification of cytochrome oxidases from Bacillus thuringiensis subsp. israelensis HD-567.

Analyses of the cell membrane fractions by spectral absorbance revealed the presence of cytochrome c and three cytochrome oxidases in Bacillus thuringiensis subsp. israelensis HD-567-cytochromes a+a3, d, and o. A modified procedure was used to purify the cytochrome c:o complex from this organism. The oxidase complex was first solubilized from a sonic-disrupted cell membrane fraction (R3 fraction) using deoxycholate and KCl. The resulting soluble fraction was further purified by Sephadex G-50 gel filtration and DEAE ionexchange chromatography. TMPD oxidase specific activity and cytochrome concentration were assayed to monitor the purification procedures. The F7 fraction (obtained after G-50 chromatography) contained cytochrome c (0.44 nmole/mg protein), cytochrome a+a3 (0.26 nmole/mg protein), and cytochrome o (0.38 nmole/mg protein), which had 6-fold, 3.4-fold and 18.9-fold increase, respectively, by comparison with the original R3 fraction. The TMPD oxidase specific activity of the F7 fraction also increased 4.8 fold. The F8 fraction (obtained after the final DEAE chromatography) contained a cytochrome c:o complex only (cytochrome c, 0.46 nmole/mg protein; cytochrome o, 0.16 nmole/mg protein), but no cytochrome a+a3 was found. Both the TMPD oxidase specific activity and the cytochrome o were attenuated greatly in comparison with the F7 fraction. SDS-PAGE analysis revealed that the F7 fraction contained numerous protein components, while the F8 fraction contained only a prominent major protein of 113.5 kD thought to be the cytochrome c:o complex, and a minor polypeptide (MW = 65.8 kD). Although the final DEAE procedure removed many undesired polypeptides, TMPD oxidase activity and cytochrome o component were also lost greatly. Kinetic studies of this cytochrome c:o complex is in progress in our laboratory.

Bacillus thuringiensis↗
PubMed1992

Purification of radioiodinated human insulin by high performance liquid chromatography for a sensitive radioimmunoassay.

The optimal sensitivity of a radioimmunoassay depends on the purity of the radiolabeled antigen. The conventional purification methods are not complete and are time consuming. The combination of a Sep-pak C18 cartridge and high performance liquid chromatography (HPLC) for the purification of 125I-labeled insulin in our study revealed that the Sep-pak cartridge can serve as the preliminary step to remove unreacted radioactive iodide, the reactants, and labeled but presumably damaged materials unadsorbed to the cartridge. The fractions eluted from the Sep-pak containing high radioactivity and high immunoreactivity to the antibody were chosen for further purification by HPLC to eliminate undesirable radiolabeled substances with a lesser immunoreactivity. The purified radiolabeled insulin was used to develop a sensitive radioimmunoassay with detecting limits of 0.03 microU/mL per tube.

Chromatography, High Pressure Liquid↗
PubMed1991

Stimulation of 22Na+ efflux from rat forebrain membrane vesicles by L-glutamic acid, L-aspartic acid and kainic acid.

A glass fiber filter assay method is described for measuring 22Na+ efflux stimulated by L-glutamic acid, L-aspartic acid and kainic acid from osmotically sensitive membrane vesicles prepared from rat brain. L-Glutamic acid and L-aspartic acid showed the greatest efficacy for the stimulation of 22Na+ efflux with EC50 values of 3 microM. Kainic acid produced 28% of the maximal efflux seen with L-glutamic acid or L-aspartic acid with an EC50 value of 1.5 microM. Quisqualic acid never showed statistically significant increases in 22Na+ efflux over control experiments. N-Methyl-D-aspartic acid showed no detectable efflux activity in this preparation. DL-2-Amino-4-phosphonobutyric acid (APB) inhibited up to 40% of the 50 microM L-glutamic acid-stimulated or 50 microM L-aspartic acid-stimulated 22Na+ efflux with an IC50 value of 1.5 nM. Calcium was required for the inhibitory action of APB, but not for the stimulatory actions of L-glutamic, L-aspartic, or kainic acids. L-Glutamic, L-aspartic, and kainic acids at concentrations above 100 microM were found to inhibit rather than to stimulate 22Na+ efflux. Veratridine (1 microM) had no influence on the 22Na+ efflux component which was produced by L-glutamic or kainic acids. We are unable to firmly establish the mechanism for the stimulated 22Na+ efflux.

Animals↗
PubMed1991

Effects of soman on calcium uptake in microsomes and mitochondria from rabbit aorta.

Daily administration of soman for several days results in several alterations in the vascular neuroeffector system. To determine whether or not soman alters intracellular Ca2+ uptake, the effects of acute exposure to soman or 7-day administration of 5 micrograms kg-1 of soman on the capacity of microsomes and mitochondria from rabbit aortic vascular smooth muscle to take up 45Ca2+ were determined. Acute exposure to soman concentrations of 1-100 microM did not alter significantly (P greater than 0.05) 45Ca2+ uptake by either microsomes or mitochondria. On the other hand, 7-day soman administration markedly reduced (P less than 0.05) 45Ca2+ uptake by both microsomes and mitochondria. Thus, calcium uptake and intracellular calcium uptake-dependent responses will be affected by repeated soman administration.

Adenosine Triphosphate↗
PubMed1991

Preparation of radioiodinated secretin for radioimmunoassay.

Radioiodination of synthetic human secretin on its N-terminal histidyl residue was not difficult when a greater amount of Chloramine T and a longer reaction time were employed to achieve better incorporation of 125I. The radioiodinated tracer for an optimal radioimmunoassay required purification. The combination of Sep-pak C18 Cartridge and high performance liquid chromatography for the purification of 125I-secretin in our study revealed that the Sep-pak cartridge was a preliminary step in removing unlabeled radioactive iodide, the reactant, and labeled materials unadsorbed to the cartridge. The eluate eluted from the Sep-pak containing high radioactivity and high immunoreactivity to the antibody were selected for further purification by HPLC which eliminated undesirable radiolabeled substances with lower immunoreactivity. The purified radiolabeled secretin was used in developing a sensitive radioimmunoassay.

Humans↗
PubMed1991

Calcitriol metabolism in patients with chronic renal failure.

We studied calcitriol metabolism in white patients with chronic renal failure and in age- and sex-matched normal subjects. The plasma levels of calcitriol (21.9 +/- 1.6 pg/mL, n = 7, v control, 37.4 +/- 2.9 pg/mL, P less than 0.001), metabolic clearance rate (MCR) of calcitriol (0.45 +/- .01 mL/min/kg v control, 0.58 +/- .02 mL/min/kg, P less than 0.001), and production rate (PR) of calcitriol (14.2 +/- 1.0 ng/kg/d v control, 31.8 +/- 3.2 ng/kg/d, P less than 0.001) were significantly lower in patients with moderate renal failure (average creatinine clearance, 0.59 +/- 0.01 mL/s [35.1 +/- 6.1 mL/min]) when compared with the respective values of normal control subjects. The MCR of calcitriol was determined again in patients with renal failure after they received calcitriol, 1 microgram/d, for 1 week. The MCR remained unchanged (0.46 +/- .04 mL/min/kg, n = 7) and plasma levels of calcitriol were increased to 34.6 +/- 2.77 pg/mL. The mechanism by which the MCR of calcitriol decreases in renal failure is partly due to the presence of inhibitory factors of degradation enzymes in uremic plasma. When the ultrafiltrates of uremic plasma obtained from hemodialysis patients were infused to normal Sprague-Dawley rats, the MCRs of calcitriol (0.20 +/- .01 mL/min/kg, n = 6) were markedly suppressed in comparison to those of rats infused with the ultrafiltrates of normal plasma (0.37 +/- .01 mL/min/kg, n = 6, P less than 0.001). The uremic plasma also contained factors that inhibit the synthesis of calcitriol. We conclude that metabolic degradation of calcitriol is decreased in patients with renal failure, and uremic plasma contains inhibitory factors that suppress the synthesis and degradation of calcitriol.

Adult↗
PubMed1991

Subfractions in uremic plasma ultrafiltrate inhibit calcitriol metabolism.

Previous study from our laboratory has demonstrated that uremic plasma ultrafiltrate suppresses both the production rate (PR) and metabolic clearance rate (MCR) of calcitriol in normal rats. To characterize the the substances responsible for the suppression of the synthesis and degradation of calcitriol, we fractionated 20 ml uremic plasma ultrafiltrates into 13 fractions using high-performance liquid chromatography (HPLC) and studied the effect of each fraction on calcitriol metabolism. We measured the MCR and PR of calcitriol in normal rats after they were infused for 20 hours with each fraction dissolved in 20 ml normal saline. Using a UV absorption and fluorescence emission technique, several known uremic compounds were identified as individual peaks corresponding to the fractions. We found that fractions 4, and 6 to 13 markedly reduced the MCR of calcitriol. The patterns of the MCR suppression by the HPLC fractions suggest that there were at least two groups of chemically distinguishable compounds. Infusion of a solution containing all 13 fractions of the uremic ultrafiltrate also inhibited the calcitriol synthesis. One of the 13 fractions (fraction 4, containing uric acid, xanthine, and hypoxanthine) was further fractionated into eight subfractions. Infusion of subfractions 4 to 7 markedly reduced both the PR and MCR of calcitriol. We conclude that uremic plasma ultrafiltrate contains factors that inhibit calcitriol synthesis and degradation. These substances have molecular weight less than 2,000 Daltons.

Animals↗