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Biomedical subjects

S C Hung

Publications and source records attributed to S C Hung.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effects of ultraviolet light irradiation in biotreatment of organophosphates.

Excess biomass accumulation in reactor biodegradation processes is undesirable: it increases the disposal cost and upsets the operation of biological reactors if not properly controlled. In this study, we investigated the feasibility of using ultraviolet (UV) light irradiation to reduce biomass accumulation and increase the specific biodegradation activity. UV irradiation has been widely used to introduce DNA damage in bacteria. Here we apply this technology to the biodegradation of organophosphates by recombinant Escherichia coli strains that contain a recA mutation and a cloned organophosphate hydrolase gene. We show that the recA negative strains after UV irradiation reduce the growth rate but increase the specific organophosphate hydrolase activity. This increase in specific enzyme activity is not owing to continued protein synthesis from the plasmid after the damage of chromosomal DNA by UV irradiation. Rather, it is likely to be caused by an increase in membrane permeability to the substrate. Kinetic analysis suggests that the membrane transport of paraoxon is the rate-limiting step in its biodegradation.

Biodegradation, Environmental↗
PubMed1996

Taiwan National Poison Center: epidemiologic data 1985-1993.

UNLABELLED: The Taiwan National Poison Center has received more than 30,000 telephone calls since its establishment in July 1985. OBJECTIVE: To obtain more information about poisoning exposures in Taiwan, a retrospective analysis was conducted of all telephone calls to the center concerning human poisoning exposures July 1985 through December 1993. METHODS: The following data were tabulated: age, sex, intent of exposure, route of exposure, substances ingested and clinical severity. RESULTS: During the eight years (1985-1993), 23,436 telephone calls concerning human poisoning exposure were recorded. Adults accounted for most cases (75.2%) and exposures involving males (54.2%) were somewhat more prevalent than female poisoning exposures (44.7%). Intentional poisonings (54.6%) were more common than unintentional poisonings (40.1%), with an inverse relationship in pediatric poisoning exposures. After amphetamines, the most frequently ingested poisons were pesticides, benzodiazepines, and cleaning products. Fatalities occurred most frequently following ingestion of pesticides. The mortality rate was 5.7% for all exposures. CONCLUSIONS: Human poisoning is a serious problem in Taiwan. The reduction of suicide attempts is a major objective. Childhood poisonings are underreported and of high mortality.

Adolescent↗
PubMed1996

Callus formation in femur and tibia during leg lengthening: 7 patients examined with DXA.

We examined the callus formation during leg lengthening in 7 achondroplastic patients who underwent 3 bilateral femoral and 4 bilateral tibial lengthenings. Bone mineral content and bone mineral density (BMD) in the lengthened callus space were evaluated every 1 or 2 weeks for 10 weeks after the start of distraction using dual energy X-ray absorptiometry. The mean rate of callus mineralization in femurs (0.64 g/wk) was higher than in tibias (0.22 g/wk). The mean BMD at 10 weeks after the start was 0.35 g/cm2 in the femur and 0.14 g/cm2 in the tibia. Different rates of callus formation in different kinds of long tubular bones have not been reported previously.

Achondroplasia↗
PubMed1996

Narrowing of the joint space of the hip after traumatic shortening of the femur.

Femoral lengthening has been associated with narrowing of the joint space at the hip. We have studied the joint space before lengthening in 20 patients with a short femur due to a femoral-shaft fracture (15) or distal femoral epiphyseal injury (5). Their mean age at injury was 16 years (3 to 27) and the mean shortening was 5.4 cm (1.1 to 14). We found that the hip joint space of the shortened femur was significantly narrower (p < 0.001) than that on the normal side, with a mean narrowing ratio of 15.5% (-5 to +43). The narrowing ratio was directly related to the period spent non-weight-bearing (p < 0.001), but not to the amount of femoral shortening. We have shown that the joint space of the hip in patients with post-traumatic femoral shortening was narrowed even before femoral lengthening had been started.

Adolescent↗
PubMed1995

Interaction between the phage HK022 Nun protein and the nut RNA of phage lambda.

The nun gene product of prophage HK022 excludes phage lambda infection by blocking the expression of genes downstream from the lambda nut sequence. The Nun protein functions both by competing with lambda N transcription-antitermination protein and by actively inducing transcription termination on the lambda chromosome. We demonstrate that Nun binds directly to a stem-loop structure within nut RNA, boxB, which is also the target for the N antiterminator. The two proteins show comparable affinities for boxB and they compete with each other. Their interactions with boxB are similar, as shown by RNase protection experiments, NMR spectroscopy, and analysis of boxB mutants. Each protein binds the 5' strand of the boxB stem and the adjacent loop. The stem does not melt upon the binding of Nun or N, as the 3' strand remains sensitive to a double-strand-specific RNase. The binding of RNA partially protects Nun from proteolysis and changes its NMR spectra. Evidently, although Nun and N bind to the same surface of boxB RNA, their respective complexes interact differently with RNA polymerase, inducing transcription termination or antitermination, respectively.

Bacteriophage lambda↗
PubMed1995

Phage HK022 Nun protein arrests transcription on phage lambda DNA in vitro and competes with the phage lambda N antitermination protein.

Phage HK022 Nun protein excludes phage lambda by terminating transcription near the lambda nut sites. We have established a purified in vitro system that reproduces the in vivo sequence and factor requirements of Nun. Nun arrests transcription by E. coli RNA polymerase at or near elongation pause sites distal to the nut sites. The boxB sequence of nut is required for optimal Nun activity; boxA plays a lesser role. The efficiency of transcription arrest is strongly enhanced by the four E. coli Nus factors. The factors increase the specific activity of Nun, and allow it to act at higher ribonucleoside triphosphate concentrations. A wild-type boxA is required for stimulation by Nus factors. Nun and the lambda N antitermination protein compete for their opposing reactions. This competition may be at the level of binding of boxB RNA.

Bacterial Proteins↗
PubMed1994

Successive action of Escherichia coli chaperones in vivo.

Escherichia coli DnaK, DnaJ and GrpE are required for renaturation of heat-inactivated lambda Cl857 repressor (Gaitanaris et al., 1990). Here we demonstrate that in addition to the above three proteins, GroEL and GroES are necessary for the Cl857 repressor to acquire full activity at the permissive temperature. Although full-length soluble repressor is present at normal amounts, the protein has reduced specific activity and migrates abnormally on native gels. To determine where the different chaperones act in protein folding, we identified their cellular locations. DnaK and DnaJ are associated with nascent polypeptide chains in translating ribosomes. In contrast, GroEL, although it is transiently associated with newly synthesized proteins, is absent from the ribosomes. This suggests that DnaK and DnaJ play an early role in protein maturation, whereas GroEL acts at a later stage.

Bacterial Proteins↗
PubMed1984

2-(6-carboxyhexyl)cyclopentanone hexylhydrazone: a potent inhibitor of the blood platelet cyclo-oxygenase.

Previous studies have demonstrated that 13-azaprostanoic acid (13-APA) is a potent and specific antagonist of thromboxane A2/prostaglandin H2 (TXA2/PGH2) at the platelet receptor level. In the present study we evaluated the effects of a new azaprostanoid , 2-(6- carboxyhexyl ) cyclopentanone hexylhydrazone (CPH), on human platelet function. This hydrazone was found to completely inhibit arachidonic acid (AA)-induced platelet aggregation at 1 microM CPH. On the other hand, CPH was not an effective inhibitor of PGH2-induced aggregation. Furthermore, 100 microM CPH was completely ineffective in blocking platelet aggregation stimulated by adenosine diphosphate (ADP) or the stable prostaglandin endoperoxide analog U46619 (which presumably acts at the TXA2/PGH2 receptor). Measurement of platelet thromboxane B2 (TXB2) production demonstrated tha the primary site-of-action of CPH is at the cyclo-oxygenase level. Thus, CP inhibited TXB2 formation from AA in a dose-dependent manner (0.1 microM-100 microM CPH)2. In contrast, CPH blocked TXB2 production from PGH2 only at the highest CPH concentration tested, i.e., 100 microM. These results indicate that relative to 13-APA, addition of a second nitrogen at C14 and a double bond between the 12- and 13- positions results in a loss of receptor activity but produces a high affinity for the platelet cyclo-oxygenase.

Arachidonic Acid↗
PubMed1984

Synthesis of [17,18-3H] trans-13-azaprostanoic acid. A labeled probe for the PGH2/TXA2 receptor.

Because of its highly unstable nature, TXA2, produced by platelet metabolism of arachidonic acid, does not lend itself to use as a receptor probe for its own receptor. As such, the stable TXA2/PGH2 antagonist, trans-13-azaprostanoic acid (trans-13-APA, 12b), was prepared as the [17, 18 3H] derivative [( 3H] trans-13-APA, 12c) to study this receptor and to better evaluate the mechanism of action of these azaprostanoids. Tritiated trans-13-APA, 12c, was prepared in nearly theoretical specific activity (57 Ci/mmole) from (17Z)-trans-13-azaprost-17-enoic acid (11b) by catalytic tritiation. The unsaturated 11b was prepared by condensation of cis-7-amino-3-heptene (8) with 2-(6-carboxyhexyl) cyclopentanone (9), NaBH4 reduction, chromatography, and hydrolysis of the trans isomer so isolated. The olefins 11a and b were also of biochemical interest because of the unsaturation in the lower side chain. The presence of similar unsaturation in PGH3(4) and TXA3 (3) renders these prostaglandins inactive as proaggregatory agents. Evaluation of the antiaggregatory activity of 11a and b indicated it to be about the same potency in inhibiting human platelet aggregation as the parent cis and trans-13-APAs, suggesting that introduction of a double bond at the 17 position in platelet prostaglandin antagonists is unlikely to result in enhanced antiplatelet activity.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1983

Specific binding of the thromboxane A2 antagonist 13-azaprostanoic acid to human platelet membranes.

In the present study we characterized the interaction between the thromboxane A2/prostaglandin H2 antagonist, trans-13-azaprostanoic acid (13-APA), and isolated human platelet membranes. In these studies, we developed a binding assay using trans [3H] 13-APA as the ligand. It was found that trans [3H] 13-APA specific binding was rapid, reversible, saturable and temperature dependent. Scatchard analysis of the binding data yielded a curvilinear plot which indicated the existence of two classes of binding sites: a high-affinity binding site with an estimated dissociation constant (Kd) of 100 nM; and a low-affinity binding site with an estimated Kd of 3.5 microM. At saturation, approximately 1 pmol/mg protein of [3H] 13-APA was bound to the high affinity site. In order to further characterize the nature of the [3H] 13-APA binding site, we evaluated competitive binding by cis 13-APA, cis 15-APA, prostaglandin F2 alpha, U46619, 6-ketoprostaglandin F1 alpha and thromboxane B2. It was found that the [3H] 13-APA binding site was stereospecific and structurally specific. Thus, the cis isomer of 13-APA exhibited substantially reduced affinity for binding. Furthermore, the prostaglandin derivatives, thromboxane B2 and 6-ketoprostaglandin F1 alpha, which do not possess biological activity, also did not compete for [3H] 13-APA binding. On the other hand, U46619 which acts as a thromboxane A2/prostaglandin H2 mimetic, and prostaglandin F2 alpha which acts as a thromboxane A2/prostaglandin H2 antagonist, both effectively competed for [3H] 13-APA binding. These findings indicate that trans 13-APA binds to a specific site on the platelet membrane which presumably represents the thromboxane A2/prostaglandin H2 receptor.

Binding Sites↗
PubMed1983

2-(6-carboxyhexyl)cyclopentanone hexylhydrazone. A potent and time-dependent inhibitor of platelet aggregation.

Two new azaprostanoids, a hydrazone (3) and hydrazide (4), have been prepared by the condensation of 2-(6-carboxyhexyl)cyclopentanone with n-hexylhydrazine and caproic acid hydrazide. Preliminary results with the stable hydrazide 4 indicate that it inhibits arachidonic acid (AA) induced human platelet aggregation and that, unlike 13-azaprostanoic acid (1), its site of action is at the cyclooxygenase level. Results with the unstable hydrazone derivative 3 indicate it to be a potent and time-dependent inhibitor of AA-induced human platelet aggregation, with its site of action also at the cyclooxygenase level.

Arachidonic Acid↗
PubMed1982

Prostaglandin F2 alpha antagonizes thromboxane A2-induced human platelet aggregation.

The effects of prostaglandin F2 alpha on human blood platelet function were investigated. PGF2 alpha at 15 muM completely blocked platelet aggregation induced by 500 muM arachidonic acid or 3 muM U46619 but had no effect on aggregation induced by 7.5 muM ADP. A similar specificity of action was not obtained with either PGI2 or PGE2. Thus concentrations of PGI2 (3 nM) or PGE2 (20 muM) which inhibited U46619- induced aggregation by 100% also blocked ADP-stimulated aggregation. The inhibitory properties of PGF2 alpha were not related to increases in platelet cAMP, since direct measurement of intracellular cAMP revealed that 15 muM PGF2 alpha produced no substantial change in cAMP levels. This finding was in direct contrast to results obtained using induced significant increases in platelet cAMP levels. The possibility that PGF2 alpha directly interacts at the platelet TXA2/PGH2 receptor was investigated by measuring [3H]PGF2 alpha binding to isolated platelet membranes. It was found that [3H] PGF2 alpha binding reached equilibrium within 30 min at room temperature and could be 90% displaced by addition of 1000 fold excess of unlabelled PGF2 alpha. Furthermore, when 1000 fold excess of either the TXA2/PGH2 "mimetic' U46619 or the TXA2/PGH2 antagonist displaced by 95% and 85% respectively. In contrast, the same molar excess of 6-keto-PFG1 alpha, azo analog 2, or TXB2, caused displacement of only 15%, 20% or 25% of the [3H] PHF2 alpha binding. Scatchard analysis indicated that [3H] PGF2 alpha has two binding sites; i.e., a high affinity binding site with an apparent Kd of 50 nM and a low affinity binding site with apparent Kd of 320 nM. These results suggest that the selective inhibition by PGF2 alpha of AA or U46619- induced aggregation may be mediated through interaction at the platelet TXA2/PGH2 receptor.

Adenosine Diphosphate↗
PubMed1977

Increase in activity of partially purified alkaline phosphatase after treatment with Mg2+, Zn2+ and lysolecithin.

When lysolecithin predispersed in 0.15 mol/l KCl was sonicated with partially purified alkaline phosphatase, the enzyme activity was increased. Lysolecithin moderately modified the kinetic parameters by increasing the apparent Vmax and decreasing the apparent Km. The pH profile of the enzyme was shifted slightly from a peak at pH 9.5 for the soluble enzyme to a plateau between pH 9.5 and 10.2 for the lysolecithin enzyme mixture. In addition, lysolecithin enhanced the thermostability and resistance of the soluble enzyme preparation to chemical denaturants.

Alkaline Phosphatase↗
PubMed1976

Alkaline phosphatase in HeLa cells. Stimulation by phospholipase A2 and lysophosphatidylcholine.

Treatment of homogenates and plasma membrane preparations from HeLa cells with phospholipase A2 (EC 3.1.1.4) caused a 50% increase in activity of membrane-associated alkaline phosphatase. Lysophosphatidylcholine, dispersed in 0.15 M KCl, affected alkaline phosphatase in a similar fashion by releasing the enzyme from particulate fractions into the incubation medium and by elevating its specific activity. Higher concentrations of lysophosphatidylcholine solubilized additional protein from particulate fractions but did not further increase the specific activity of the released alkaline phosphatase. Particulate fractions from HeLa cells were exposed to the effects of liposomes prepared from lysophosphatidylcholine and cholesterol. The ratio of particulate protein/lysophosphatidylcholine (by weight) required for optimal activation of alkaline phosphatase was one. Kinetic studies indicated that phospholipase A2 and lysophosphatidylcholine enhanced the apparent V of the enzyme but did not significantly alter its apparent Km. The increased release of alkaline phosphatase from the particulate matrix by lysophosphatidylcholine was confirmed by disc electrophoresis. The release of the enzyme by either phospholipase A2 or by lysophosphatidylcholine appeared to be followed by the formation of micelles that contained lysophosphatidylcholine. The new complexes had relatively less cholesterol and more lysophosphatidylcholine than the native membranes. The possibility that lysophosphatidylcholine formed a lipoprotein complex with the solubilized alkaline phosphatase was indicated by a break point in the Arrhenius plot which was evident only in the lysophosphatidylcholine-solubilized enzyme but could not be demonstrated in alkaline phosphatase that had been released with 0.15 M KCl alone.

Alkaline Phosphatase↗
PubMed1975

Epidemic hemorrhagic keratoconjunctivitis.

A new type of acute keratoconjunctivitis developed throughout Southeast Asia, beginning in Singapore in the summer of 1970. It was highly contagious and probably was transmitted from person to person by the hand to eye route. Sixteen cases, diagnosed by viral isolation or serologic study, or both, were subjected to detailed clinical observation. The characteristic features included a short incubation period of one or two days, watery or serous discharge, subconjunctival hemorrhage, and pinpoint superficial keratopathy. The disease usually resolved rapidly within one to two weeks without sequelae.

Adolescent↗