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Biomedical subjects

S H Woo

Publications and source records attributed to S H Woo.

At least 19 recordsLinked to original sources
PubMed2006

Cloning and characterization of six highly similar endo-1,3-beta-glucanase genes in hexaploid wheat.

Pathogenesis-related (PR) proteins are often used as a marker of plant defense reactions. Some endo-1,3-beta-glucanase (Gns) genes encode proteins that belong to the PR protein family 2 (PR-2). Although the number of homologous family member genes is significantly greater in hexaploid wheat (Triticum aestivum L.) compared to other model plants, earlier studies did not evaluate the possible contribution of their homologs to hybridization signals in Northern blot analysis. In this study, we have examined whether routine transcriptional analyses of a PR gene is of high reliability or not by isolating six highly similar Gns genes (TaGlb2a, TaGlb2b, TaGlb2c, TaGlb2d, TaGlb2e, and TaGlb2f) and characterizing their expression patterns in detail. While TaGlb2b was shown to be a PR-2 gene, transcription of TaGlb2c and TaGlb2d was not induced upon infection with either powdery mildew (Erysiphe graminis) or head blight (Fusarium graminearum) pathogens; their transcripts were most abundant in healthy spikes (lemmas and in particular paleae). Therefore, in some cases, the conventional analyses do not necessarily provide accurate information on expression pattern of a PR gene in hexaploid wheat. This is also the first report of wheat genes that are specifically expressed in lemma/palea tissues of flowering spikelets.

Base Sequence↗
PubMed2006

Salvage of the lower extremity free flap using cross-leg venous repair.

This retrospective study was designed to evaluate a salvage technique for free flaps suffering venous congestion by using a cross-leg vein repair in patients with venous-impaired lower extremities. Four free flap reconstructions were performed using the latissimus dorsi muscle to reconstruct soft tissue defects in the lower extremity. The recipient artery was confined to the ipsilateral leg and the venous anastomosis was performed with a long saphenous vein from the contralateral side. The legs were immobilised together by means of an external fixator. All patients were males with a mean age of 31 years. The mean time of pedicle division was 8.8 days (7-10). The mean size of the free flap was 186.5 cm(2). All flaps survived after pedicle division without venous congestion. There were no complications such as joint stiffness or donor site morbidity except for a linear scar. The cross-leg venous repair is a refinement of a salvage procedure for compromised free flaps used in the reconstruction of severe soft tissue defects in vascularly compromised lower extremities.

Accidents, Traffic↗
PubMed2001

Design and synthesis of a novel class of histone deacetylase inhibitors.

Histone deacetylase inhibitors (HDACs) have emerged as a novel class of antiproliferative agents. Utilizing structure-based design, the synthesis of a series of sulfonamide hydroxamic acids is described. Further optimization of this series by substitution of the terminal aromatic ring yielded HDAC inhibitors with good in vitro and in vivo activities.

Cell Division↗
PubMed2001

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis is dependent on activation of cysteine and serine proteases.

We examined the role of caspases and serine protease(s) in cell death induced by tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). After incubation of adenocarcinoma cells with TRAIL, caspase-3, -8 were activated and the cleavage of Bid induced the release of cytochrome c, from the mitochondria to the cytosol. Tetrapeptide inhibitors of caspase-1, -2, -3, and -8 suppressed DNA fragmentation and attenuated the release of cytochrome c, whereas inhibitors of caspase-5 did not. Interestingly, the general serine protease(s) inhibitor 4-(2-aminoethyl)benzylsulfonyl fluoride (AEBSF) resulted in the arrest of apoptosis. However, the AEBSF did not prevent the release of mitochondrial cytochrome c during TRAIL-induced apoptosis. From these results, we postulate that serine protease(s) may be involved in post-mitochondrial apoptotic events, that lead to the activation of the initiator, caspase-9.

Apoptosis↗
PubMed2001

Evaluation of the interaction between biodegradation and sorption of phenanthrene in soil-slurry systems.

This work develops and utilizes a non-steady-state model for evaluating the interactions between sorption and biodegradation of hydrophobic organic compounds in soil-slurry systems. The model includes sorption/desorption of a target compound, its utilization by microorganisms as a primary substrate existing in the dissolved phase, and/or the sorbed phase in biomass and soil, oxygen transfer, and oxygen utilization as an electron acceptor. Biodegradation tests with phenanthrene were conducted in liquid and soil-slurry systems. The soil-slurry tests were performed with very different mass transfer rates: fast mass transfer in a flask test at 150 rpm, and slow mass transfer in a roller-bottle test at 2 rpm. The results of liquid tests indicate that biodegradation of the soil-soluble organic fraction did not significantly enhance the biodegradation rate. In the slurry tests, phenanthrene was degraded more rapidly than in liquid tests, but at a similar rate in both slurry systems. Modeling analyses with several hypotheses indicate that a model without biodegradation of compound sorbed to the soil was not able to account for the rapid degradation of phenanthrene, particularly in the roller-bottle slurry test. The model with sorbed-phase biodegradation and the same biokinetic parameters, but unique mass transfer coefficients, simulated the experimental data in both slurry tests most successfully. Reduced mass transfer resistance to bacteria attached to the soil is the most likely phenomenon accounting for rapid sorbed-phase biodegradation.

Adsorption↗
PubMed2001

Bimodal regulation of Na(+)--Ca(2+) exchanger by beta-adrenergic signaling pathway in shark ventricular myocytes.

In shark heart, the Na(+)--Ca(2+) exchanger serves as a major pathway for both Ca(2+) influx and efflux, as there is only rudimentary sarcoplasmic reticulum in these hearts. The modulation of the exchanger by a beta-adrenergic agonist in whole-cell clamped ventricular myocytes was compared with that of the Na(+)--Ca(2+) exchanger blocker KB-R7943. Application of 5 microM isoproterenol and 10 microM KB-R7943 suppressed both the inward and the outward Na(+)--Ca(2+) exchanger current (I(Na--Ca)). The isoproterenol effect was mimicked by 10 microM forskolin. Isoproterenol and forskolin shifted the reversal potential (E(rev)) of I(Na--Ca) by approximately -23 mV and -30 mV, respectively. An equivalent suppression of outward I(Na--Ca) by KB-R7943 to that by isoproterenol produced a significantly smaller shift in E(rev) of about --4 mV. The ratio of inward to outward exchanger currents was also significantly larger in isoproterenol- than in control- and KB-R7943-treated myocytes. Our data suggest that the larger ratio of inward to outward exchanger currents as well as the larger shift in E(rev) with isoproterenol results from the enhanced efficacy of Ca(2+) efflux via the exchanger. The protein kinase A-mediated bimodal regulation of the exchanger in parallel with phosphorylation of the Ca(2+) channel and enhancement of its current may have evolved to satisfy the evolutionary needs for accelerated contraction and relaxation in hearts of animals with vestigial sarcoplasmic Ca(2+) release stores.

Adrenergic beta-Agonists↗
PubMed2001

Inhibition of baclofen on morphine-induced hyperactivity, reverse tolerance and postsynaptic dopamine receptor supersensitivity.

The effects of baclofen on the development of reverse tolerance and postsynaptic dopamine receptor supersensitivity induced by morphine were examined in mice. A single administration of morphine induced hyperactivity and the morphine-induced hyperactivity was inhibited dose dependently by the administration of a GABA(B)receptor agonist, baclofen (1.25, 2.5 and 5 mg kg(-1), i.p.). Daily repeated administration of morphine developed reverse tolerance to the hyperactivity of morphine. The concomitant administration of baclofen inhibited the morphine-induced hyperactivity and the baclofen administration prior to and during the chronic administration of morphine in mice inhibited the development of reverse tolerance to the hyperactivity of morphine (10 mg kg(-1), s.c.). Postsynaptic dopamine receptor supersensitivity was also developed in reverse-tolerant mice that had received the same morphine. The development of postsynaptic dopamine receptor supersensitivity was evidenced by the enhanced ambulatory activity of apomorphine (2 mg kg(-1), s.c.). Baclofen also inhibited the development of postsynaptic dopamine receptor supersensitivity induced by the chronic administration of morphine. These results suggest that the hyperactivity, reverse tolerance and postsynaptic dopamine receptor supersensitivity induced by morphine may be modulated via the activation of GABA(B)receptors induced by baclofen.

Animals↗
PubMed2001

Inhibition of diazepam on morphine-induced hyperactivity, reverse tolerance and postsynaptic dopamine receptor supersensitivity.

The effects of diazepam on the development of reverse tolerance and postsynaptic dopamine receptor supersensitivity induced by morphine were examined in mice. A single administration of morphine induced hyperactivity and the morphine-induced hyperactivity was inhibited dose-dependently by the administration of diazepam (1, 2 and 4 mg x kg(-1), i.p.), an agonist for benzodiazepine receptor linked to the GABA(A) receptor. Daily repeated administration of morphine developed reverse tolerance to the hyperactivity of morphine. The concomitant administration of diazepam inhibited the morphine-induced hyperactivity and the diazepam administration prior to and during the chronic administration of morphine in mice inhibited the development of reverse tolerance to the hyperactivity of morphine (10 mg x kg(-1), s.c.). Postsynaptic dopamine receptor supersensitivity was also developed in reverse tolerant mice that had received the same morphine. The development of postsynaptic dopamine receptor supersensitivity was evidenced by the enhanced ambulatory activity of apomorphine (2 mg x kg(-1), s.c.). Diazepam also inhibited the development of postsynaptic dopamine receptor supersensitivity induced by the chronic administration of morphine. These results suggest that the hyperactivity, reverse tolerance and postsynaptic dopamine receptor supersensitivity induced by morphine may be modulated via the activation of the GABA(A) receptor induced by diazepam.

Animals↗
PubMed2001

Pre-expanded arterialised venous free flaps for burn contracture of the cervicofacial region.

Despite the fact that arterialised venous flaps provide thin good-quality tissue to repair defects of the face and neck, their clinical applications have been limited by an unstable postoperative course and variable flap necrosis. In an effort to resolve these problems, a tissue-expansion technique has been applied to the arterialised venous flap before flap transfer. Three pre-expanded arterialised venous free flaps have been used to treat post-burn scar contracture of the cervicofacial region. The donor site was confined to the forearm in each case. A rectangular expander was usually placed over the fascia of the flexor muscles in the proximal two-thirds of the forearm. The mean expansion period, volume and flap size were 44 days, 420 cm(3)and 147 cm(2), respectively. There were no complications caused by insertion and expansion. The cervicofacial region was successfully reconstructed, after excision of the post-burn contractures, with pre-expanded arterialised venous flaps, with no marginal necrosis or postoperative instability. Large thin arterialised venous flaps are well matched with the recipient defect in the cervicofacial area and the colour and texture match obtained with forearm tissue produced an aesthetically favourable result. Pre-expanded arterialised venous flaps are another new option for free flap reconstruction of the face and neck.

Adult↗
PubMed2001

Optimizing the correction of severe postburn hand deformities by using aggressive contracture releases and fasciocutaneous free-tissue transfers.

Severe postburn hand deformities were classified into three major patterns: hyperextension deformity of the metacarpophalangeal joint of the fingers with dorsal contracture of the hand, adduction contracture of the thumb with hyperextension deformity of the interphalangeal joint, and flexion contracture of the palm. Over the past 6 years, 18 cases of severe postburn hand deformities were corrected with extensor tenotomy, joint capsulotomy, and release of volar plate and collateral ligament. The soft-tissue defects were reconstructed with various fasciocutaneous free flaps, including the arterialized venous flap (n = 4), dorsalis pedis flap (n = 3), posterior interosseous flap (n = 3), first web space free flap (n = 3), and radial forearm flap (n = 1). Early active physical therapy was applied. All flaps survived. Functional return of pinch and grip strength was possible in 16 cases. In 11 cases of reconstruction of the dorsum of the hand, the total active range of motion in all joints of the fingers averaged 140 degrees. The mean grip strength was 16.5 kg and key pinch was 3.5 kg. In palm reconstruction, the wider contact area facilitated the grasping of larger objects. In thumb reconstruction, key-pinch increased to 5.5 kg and the angle of the first web space increased to 45 degrees. Jebsen's hand function test was not possible before surgery; postoperatively, it showed more functional recovery in gross motion and in the dominant hand. Aggressive contracture release of the bone,joints, tendons, and soft tissue is required for optimal results in the correction of severe postburn hand deformities. Various fasciocutaneous free flaps used to reconstruct the defect provide early motion, appropriate thinness, and excellent cosmesis of the hand.

Adolescent↗
PubMed2001

Cdc5 interacts with the Wee1 kinase in budding yeast.

Development of a multicellular organism requires that mitosis and morphogenesis be coordinated. These processes must also be synchronized during the growth of unicellular organisms. In the yeast Saccharomyces cerevisiae, mitosis is dependent on the prior growth of a daughter cell in the form of a bud. Overexpression of wild-type Polo-like kinase Cdc5 or a catalytically inactive form resulted in the formation of multinucleate cells in budding yeast. Immunofluorescence analysis of these multinulceate cells showed that mitosis and bud formation were no longer linked. Others have shown that Swe1 is required for coupling mitosis to bud formation during a perturbed cell cycle. When the normal pathway of bud formation is perturbed, Swe1 functions to delay mitosis through negative regulation of Clb/Cdk. In cells lacking Swe1, multinucleate cells are formed in response to delays in bud formation. Affinity purification, two-hybrid analysis, and mutant characterization results suggested that Cdc5 and Swe1 interact. From these results, we conclude that multinucleate formation in response to Cdc5 overexpression is linked to titration of Swe1 function. These results also suggest that Cdc5 may be a negative regulator of Swe1.

Cell Cycle Proteins↗
PubMed2000

Implication of a small GTPase Rac1 in the activation of c-Jun N-terminal kinase and heat shock factor in response to heat shock.

Heat shock induces c-Jun N-terminal kinase (JNK) activation as well as heat shock protein (HSP) expression through activation of the heat shock factor (HSF), but its signal pathway is not clearly understood. Since a small GTPase Rac1 has been suggested to participate in the cellular response to stresses, we examined whether Rac1 is involved in the heat shock response. Here we show that moderate heat shock (39-41 degrees C) induces membrane translocation of Rac1 and membrane ruffling in a Rac1-dependent manner. In addition, Rac1N17, a dominant negative mutant of Rac1, significantly inhibited JNK activation by heat shock. Since Rac1V12 was able to activate JNK, it is suggested that heat shock may activate JNK via Rac1. Similar inhibition by Rac1N17 of HSF activation in response to heat shock was observed. However, inhibitory effects of Rac1N17 on heat shock-induced JNK and HSF activation were reduced as the heat shock temperature increased. Rac1N17 also inhibited HSF activation by l-azetidine-2-carboxylic acid, a proline analog, and heavy metals (CdCl)), suggesting that Rac1 may be linked to HSF activation by denaturation of polypeptides in response to various proteotoxic stresses. However, Rac1N17 did not prevent phosphorylation of HSF1 in response to these proteotoxic stresses. Interestingly, a constitutively active mutant Rac1V12 did not activate the HSF. Therefore, Rac1 activation may be necessary, but not sufficient, for heat shock-inducible HSF activation and HSP expression, or otherwise a signal pathway(s) involving Rac1 may be indirectly involved in the HSF activation. In sum, we suggest that Rac1 may play a critical role(s) in several aspects of the heat shock response.

Animals↗
PubMed2000

Microbial energetics and stoichiometry for biodegradation of aromatic compounds involving oxygenation reactions.

Oxygenation reactions significantly alter the energy and electron flows and, consequently, the overall stoichiometry for the microbial utilization of aromatic compounds. Oxygenation reactions do not yield a net release of electrons, but require an input of electrons to reduce oxygen molecules. The biodegradation pathway of phenanthrene as a model compound was analyzed to determine the impact of oxygenation reactions on overall stoichiometry using the half-reaction method. For individual oxygenation reactions, the half-reaction method for analyzing the electron and energy flows must be modified, because the reactions do not release electrons for synthesis or energy generation. Coupling the oxygenation reaction to subsequent reaction steps provides a net electron release for the coupled reactions. Modeling results indicate that oxygenation reactions increase the oxygen requirement and reduce the cell yield, compared to the conventional mineralization represented by hydroxylation reactions in place of oxygenations. The computed yields considering oxygenation reactions conform better to empirical yields reported in the literature than do yields computed by the hydroxylation single-step methods. The coupled-reaction model also is consistent with information about the ways in which micro-organisms that degrade aromatics accumulate intermediates, regulate degradation genes, and organize enzyme clusters.

Bacteria↗
PubMed1999

Antimalarial, antiproliferative, and antitumor activities of artemisinin-derived, chemically robust, trioxane dimers.

Nine C-10 non-acetal derivatives of the natural trioxane artemisinin (1) were prepared as dimers using some novel chemistry. As designed, each dimer was stable chemically. C-10 Olefinic dimers 7 and C-10 saturated dimers 8-13 all showed good to excellent antimalarial and antiproliferative activities in vitro. Dimers 8, 10, and 12 were especially potent and selective at inhibiting growth of some human cancer cell lines in the NCI in vitro 60-cell line assay.

Animals↗
PubMed1999

Topoisomerase II inhibition by aporphine alkaloids.

The aporphine alkaloids (+)-dicentrine and (+)-bulbocapnine are non-planar molecules lacking features normally associated with DNA binding by intercalation or minor groove binding. Surprisingly, dicentrine showed significant activity as a topoisomerase II (EC 5.99.1.3) inhibitor and also was active in a DNA unwinding assay. The DNA unwinding suggests DNA intercalation, which could explain the inhibition of topoisomerase II. Bulbocapnine, which differs from dicentrine only by the presence of a hydroxyl group at position 11 and the absence of a methoxyl group at position 9, was inactive in all assays. Molecular modeling showed that dicentrine can attain a relatively planar conformation, whereas bulbocapnine cannot, due to steric interaction between the 11-hydroxyl group and an oxygen of the methylenedioxy ring. These observations suggest that dicentrine is an "adaptive" DNA intercalator, which can bind DNA only by adopting a somewhat strained planar conformation. The requirement of a suboptimal conformation to achieve DNA binding appears to make dicentrine a weaker topoisomerase II inhibitor than the very planar oxoaporphine alkaloid liriodenine. These results suggest that it may be possible to modulate DNA binding and biologic activity of drugs by modifications affecting their ability to adopt planar conformations.

Animals↗
PubMed1999

Effects of endothelin-1 on Ca2+ signaling in guinea-pig ventricular myocytes: role of protein kinase C.

The effects of ET-1 on contraction, Ca2+ transient and L-type Ca2+ current (ICa.L) were studied in single cells isolated from ventricles of guinea-pig hearts. The aim of our study was to elucidate the mechanism of the positive inotropic effect during endothelin receptor stimulation by focusing on the role of PKC. ET-1 at concentrations of 5 and 10 nM produced a biphasic pattern of inotropism: a first decrease in contraction by 34.4 +/- 2.5% of the control followed by a sustained increase in contraction by 66.6 +/- 8.4% (mean +/- SEM, n = 9). The Ca2+ transient decreased by 13.5 +/- 1.0% during the negative inotropic phase, while it increased by 58.1 +/- 8.4% (n = 10) during the positive inotropic phase. Using the whole-cell voltage-clamp technique with conventional microelectrodes, the application of ET-1 (5 nM) increased the ICa.L by 32.6 +/- 5.1% (n = 10), which was preceded by a short-lived decrease in ICa.L. Incubation of myocytes with pertussis toxin (PTX, at 2 micrograms/ml for > 3 h at 35 degrees C) failed to block the ET-1-induced enhancement of ICa.L. The increases in contraction, Ca2+ transient, and ICa.L by ET-1 were inhibited by pretreatment with 5-N-methyl-N-isobutyl amiloride (MIA; 10 microM), an amiloride analog, and a novel selective Na+/H+ exchange inhibitor HOE694 (10 microM). To determine whether activation of protein kinase C (PKC) is responsible for the enhancement of ICa.L by ET-1, we tested a PKC inhibitor, GF109203X, and found that it does exert an inhibitory effect on the ET-1-induced ICa.L increase. Our study suggests that during ET receptor stimulation an increase in ICa.L due to stimulation of Na+/H+ exchange via PKC activation causes an increase in Ca2+ transients and thereby in the contractile force of the ventricular myocytes.

Amiloride↗
PubMed1999

Role of PKC in the effects of alpha1-adrenergic stimulation on Ca2+ transients, contraction and Ca2+ current in guinea-pig ventricular myocytes.

The effects of alpha1-adrenoceptor stimulation on intracellular Ca2+ transients, contractility and L-type Ca2+ current (ICa,L) were studied in single cells isolated from ventricles of guinea-pig hearts. The aim of our study was to elucidate the mechanisms of the positive inotropic effect of alpha1-adrenergic stimulation by focussing on the role of protein kinase C (PKC). Phenylephrine, an alpha1-adrenergic agonist, at concentrations of 50-100 microM elicited a biphasic inotropic response: a transient negative inotropic response (22.9+/-6.0% of control) followed by a sustained positive inotropic response (61.0+/-8.4%, mean+/-SE, n=12). The Ca2+ transient decreased by 10.2+/-3.9% during the negative inotropic phase, while it increased by 67.7+/-10% (n=12) during the positive inotropic phase. These effects were inhibited by prazosin (1 microM), a alpha1-adrenergic antagonist. Phenylephrine increased the ICa,L by 60.8+/-21% (n=5) during the positive inotropic phase. To determine whether activation of PKC is responsible for the increases in Ca2+ transients, contractile amplitude and ICa,L during alpha1-adrenoceptor stimulation, we tested the effects of 4beta-phorbol 12-myristate 13-acetate (PMA), a PKC activator, and of bisindolylmaleimide I (GF109203X) and staurosporine, both of which are PKC inhibitors. PMA mimicked phenylephrine's effects on Ca2+ transients, contractile amplitude and ICa,L. PMA (100 nM) increased the Ca2+ transient, contractile amplitude and ICa,L by 131+/-17%, 137+/-25% (n=8), and 81.1+/-26% (n=5), respectively. Prior exposure to GF109203X (1 microM) or staurosporine (10 nM) prevented the phenylephrine-induced increases in Ca2+ transients, contractile amplitude and ICa,L. Our study suggests that during alpha1-adrenoceptor stimulation increase in ICa,L via PKC causes an increase in Ca2+ transients and thereby in the contractile force of the ventricular myocytes.

Action Potentials↗