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W C Ho

Publications and source records attributed to W C Ho.

At least 19 recordsLinked to original sources
PubMed2005

Threshold levels of ERK activation for chemotactic migration differ for NGF and EGF in rat pheochromocytoma PC12 cells.

In a previous study, we show that stimulation of chemotaxis in rat pheochromocytoma PC12 cells by nerve growth factor (NGF) and epidermal growth factor (EGF) requires activation of the RAS-ERK signaling pathway. In this study, we compared the threshold levels of ERK activation required for EGF and NGF-stimulated chemotaxis in PC12 cells. The threshold ERK activity required for NGF to stimulate chemotaxis was approximately 30% lower than that for EGF. PD98059 treatment inhibited EGF stimulation of growth and chemotaxis; however, stimulation of chemotaxis required an EGF concentration approximately 10 times higher than for stimulation of PC12 cell growth. Thus, ERK-dependent cellular functions can be differentially elicited by the concentration of EGF. Also, treatment of PC12 cells with the PI3-K inhibitor LY294002 reduced ERK activation by NGF; thus, higher NGF concentrations were required to initiate chemotaxis and to achieve the same maximal chemotactic response seen in untreated PC12 cells. Therefore, the threshold NGF concentration to stimulate chemotaxis could be adjusted by the crosstalk between the ERK and PI3-K pathways, and the contributions of PI3-K and ERK to signal chemotaxis varied with the concentrations of NGF used. In comparison, LY294002 treatment had no effect on ERK activation by EGF, but the chemotactic response was reduced at all the concentrations of EGF tested indicating that NGF and EGF differed in the utilization of ERK and PI3-K to signal chemotaxis in PC12 cells.

Adrenal Gland Neoplasms↗
PubMed2002

MRI of muscular hamartoma of the breast.

Muscular hamartoma is a well-demarcated tumour composed of smooth muscle and adipose tissue. We report the MRI findings of a patient with benign breast neoplasm. To the best of our knowledge, its appearance has not been previously reported.

Aged↗
PubMed2000

Transient removal of extracellular Mg(2+) elicits persistent suppression of LTP at hippocampal CA1 synapses via PKC activation.

Previous work has shown that seizure-like activity can disrupt the induction of long-term potentiation (LTP). However, how seizure-like event disrupts the LTP induction remains unknown. To understand the cellular and molecular mechanisms underlying this process better, a set of studies was implemented in area CA1 of rat hippocampal slices using extracellular recording methods. We showed here that prior transient seizure-like activity generated by perfused slices with Mg(2+)-free artificial cerebrospinal fluid (ACSF) exhibited a persistent suppression of LTP induction. This effect lasted between 2 and 3 h after normal ACSF replacement and was specifically inhibited by N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphovaleric acid (D-APV) and L-type voltage-operated Ca(2+) channel (VOCC) blocker nimodipine, but not by non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). In addition, this suppressive effect was specifically blocked by the selective protein kinase C (PKC) inhibitor NPC-15437. However, neither Ca(2+)/calmodulin-dependent protein kinase II inhibitor KN-62 nor cAMP-dependent protein kinase inhibitor Rp-adenosine 3', 5'-cyclic monophosphothioate (Rp-cAMPS) affected this suppressive effect. This persistent suppression of LTP was not secondary to the long-lasting changes in NMDA receptor activation, because the isolated NMDA receptor-mediated responses did not show a long-term enhancement in response to a 30-min Mg(2+)-free ACSF application. Additionally, in prior Mg(2+)-free ACSF-treated slices, the entire frequency-response curve of LTP and long-term depression (LTD) is shifted systematically to favor LTD. These results suggest that the increase of Ca(2+) influx through NMDA channels and L-type VOCCs in turn triggering a PKC-dependent signaling cascade is a possible cellular basis underlying this seizure-like activity-induced inhibition of LTP.

2-Amino-5-phosphonovalerate↗
PubMed1999

Solution structure of the aminoacyl-capped oligodeoxyribonucleotide duplex (W-TGCGCAC)(2).

Reported here is the solution structure of the aminoacyl-DNA duplex (W-TGCGCAC)(2). This duplex forms a continuously pi-stacked helix consisting of both nucleobases and amino acid side chains. According to NMR and UV analyses, the duplex melts in a cooperative transition and with 1.3-1.8% greater hyperchromicity than the control duplex (TGCGCAC)(2). A van't Hoff analysis of UV melting points at different concentrations shows that the two tryptophan residues contribute 4.8 kcal/mol to the DeltaH degrees of complex formation at 10 mM salt concentration and less than 1 kcal/mol at 150 mM salt. The entropic cost for duplex association in the presence of the amino acid residues is 13 cal/molK greater than that for the control at 10 mM salt concentration, and 3 cal/molK lower than that of the control at 0.15 ionic strength. The conformation of W-TGCGCAC in duplex form, determined via restrained torsion angle molecular dynamics, shows an undisturbed B-form DNA duplex with dangling 3'-termini. The tryptophanyl residue at the 5'-terminus packs tightly against T2 and the proximal part of adenine, without engaging in hydrogen bonding. While not providing strong enthalpic net stabilization of the duplex, the tryptophan "cap" on the duplex does seem to reduce the fraying at the termini, indicating a subtle balance of entropic and enthalpic factors contributing to the molecular dynamics. The structure also shows that, at least in the present sequence context, stacking on the terminal base pair is more favorable than intercalation, probably because the enthalpic cost associated with breaking up the stacking between DNA base pairs cannot be paid for by favorable pi-stacking interactions with the indole ring of tryptophan. These results are of importance for understanding stacking interactions in protein-DNA complexes, particularly those in enzyme-substrate complexes involving exposed nucleobases.

Base Sequence↗
PubMed1999

Prior short-term synaptic disinhibition facilitates long-term potentiation and suppresses long-term depression at CA1 hippocampal synapses.

Long-term potentiation (LTP) and long-term depression (LTD) are two main forms of activity-dependent synaptic plasticity that have been extensively studied as the putative mechanisms underlying learning and memory. Current studies have demonstrated that prior synaptic activity can influence the subsequent induction of LTP and LTD at Schaffer collateral-CA1 synapses. Here, we show that prior short-term synaptic disinhibition induced by type A gamma-aminobutyric acid (GABA) receptor antagonist picrotoxin exhibited a facilitation of LTP induction and an inhibition of LTD induction. This effect lasted between 10 and 30 min after washout of picrotoxin and was specifically inhibited by the L-type voltage-operated Ca2+ channel (VOCC) blocker nimodipine, but not by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphopentanoic acid (D-APV). Moreover, this picrotoxin-induced priming effect was mimicked by forskolin, an activator of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA), and was blocked by the adenylyl cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22536) and the PKA inhibitor Rp-adenosine 3',5'-cyclic monophosphothioate (Rp-cAMPS). It was also found that following picrotoxin application, CA1 neurons have a higher probability of synchronous discharge in response to a population of excitatory postsynaptic potential (EPSP) of fixed slope (EPSP/spike potentiation). However, picrotoxin treatment did not significantly affect paired-pulse facilitation (PPF). These findings suggest that a brief of GABAergic disinhibition can act as a priming stimulus for the subsequent induction of LTP and LTD at Schaffer collateral-CA1 synapses. The increase in Ca2+ influx through L-type VOCCs in turn triggering a cAMP/PKA signalling pathway is a possible molecular mechanism underlying this priming effect.

Adenine↗
PubMed1999

Differences in phosphatase modulation of alpha4beta1 and alpha5beta1 integrin-mediated adhesion and migration of B16F1 cells.

It is well established that a biphasic relationship exists between the adhesive strength of beta1 integrins and their ability to mediate cell movement. Thus, cell movement increases progressively with adhesive strength, but beyond a certain point of optimal interaction, cell movement is reduced with further increases in adhesive function. The interplay between the various kinase and phosphatase activities provides the balance in beta1 integrin-mediated cell adhesion and migration. In the present study, the significance of protein tyrosine phosphatases (PTP) and ser/thr protein phosphatases (PP) in alpha4beta1 and alpha5beta1 integrin-mediated mouse melanoma B16F1 cell anchorage and migration on fibronectin was characterized using phosphatase inhibitors. At low fibronectin concentration, alpha5beta1 functioned as the predominant receptor for cell movement; a role for alpha4beta1 in B16F1 cell migration increased progressively with fibronectin concentration. Treatment of B16F1 cells with PTP inhibitors, sodium orthovanadate (Na3VO4) and phenylarsine oxide (PAO), or PP-1/2A inhibitor, okadaic acid (OA), abolished cell movement. Inhibition of cell movement by PAO and OA was associated by a reduction in the adhesive strength of alpha4beta1 and alpha5beta1. In contrast, treatment of B16F1 cells with Na3VO4 resulted in selective stimulation of the adhesive function of alpha5beta1, but not alpha4beta1. Therefore, our results demonstrate that (i) both PTP and PP-1/2A have roles in cell movement, (ii) modulation of cell movement by PTP and PP-1/2A may involve either a stimulation or reduction of beta1 integrin adhesive strength, and (iii) distinct phosphatase-mediated signaling pathways for differential regulation of the various beta1 integrins exist.

Animals↗
PubMed1999

Use of intravenous immunoglobulin in a patient with refractory myasthenia gravis associated with malignant thymoma.

We report on a case of refractory myasthenia gravis that was managed by using intravenous immunoglobulin. A 35-year-old Chinese woman with malignant thymoma-associated myasthenia gravis was treated by total thymectomy, followed by chemotherapy. Thirty months later, she developed respiratory failure and required mechanical ventilation for 2 months. A course of intravenous immunoglobulin was given and her condition improved significantly. Two weeks later, the patient became ambulatory, was prescribed oral pyridostigmine, and was discharged home.

Journal Article↗
PubMed1997

The presence of RNA splicing signals in the cDNA construct of the E2 gene of classical swine fever virus affected its expression.

E2 is the major neutralizing antigen for classical swine fever virus (CSFV) infection. Previously, we have cloned and sequenced the E2 cDNA of Taiwan strain p97 by the reverse transcription-polymerase chain reaction (RT-PCR) method from CSFV-infected tissue. The presence of RNA splicing donor and acceptor sites were found in the cDNA sequence. In this study, transfection of E2 cDNA into mammalian cells resulted in the production of a spliced RNA. Site-directed mutagenesis of the donor and acceptor sites prevented the RNA splicing event and generated a full length transcript in COS7 cells. Although the spliced E2 transcript has not been reported in natural infection of CSFV, this study suggested that the potential splicing sites affected the E2 gene expression when the plasmid-based E2 gene was introduced into mammalian cells.

Amino Acid Sequence↗
PubMed1997

Modulation of in vivo migratory function of alpha 2 beta 1 integrin in mouse liver.

We report herein that expression of alpha 2 beta 1 integrin increased human erythroleukemia K562 transfectant (KX2C2) cell movement after extravasation into liver parenchyma. In contrast, a previous study demonstrated that alpha 2 beta 1 expression conferred a stationary phenotype to human rhabdomyosarcoma RD transfectant (RDX2C2) cells after extravasation into the liver. We therefore assessed the adhesive and migratory function of alpha 2 beta 1 on KX2C2 and RDX2C2 cells using a alpha 2 beta 1-specific stimulatory monoclonal antibody (mAb), JBS2, and a blocking mAb, BHA2.1. In comparison with RDX2C2 cells, KX2C2 were only weakly adherent to collagen and laminin. JBS2 stimulated alpha 2 beta 1-mediated interaction of KX2C2 cells with both collagen and laminin resulting in increases in cell movement on both matrix proteins. In the presence of Mn2+, JBS2-stimulated adhesion on collagen beyond an optimal level for cell movement. In comparison, an increase in RDX2C2 cell movement on collagen required a reduction in its adhesive strength provided by the blocking mAb BHA2.1. Consistent with these in vitro findings, in vivo videomicroscopy revealed that alpha 2 beta 1-mediated postextravasation cell movement of KX2C2 cells in the liver tissue could also be stimulated by JBS2. Thus, results demonstrate that alpha 2 beta 1 expression can modulate postextravasation cell movement by conferring either a stationary or motile phenotype to different cell types. These findings may be related to the differing metastatic activities of different tumor cell types.

Animals↗
PubMed1997

Vanidilol: a vanilloid-type vasorelaxant and ocular hypotensive beta-adrenoceptor blocker with partial beta-2-agonist activity.

Vanidilol, [4'-(2-hydroxy-3-(tert-butylamino)propoxy)-3'-methoxyphenyl] -benzaldehyde, newly synthesized from vanillin, is a vanilloid-type beta-adrenoceptor blocker. The beta-adrenoceptor-blocking properties of vanidilol were studied both in vivo and in vitro. Intravenous injection of vanidilol (1.0, 3.0, 5.0 mg/kg) in anesthetized Wistar rats produced a decrease in blood pressure and a dose-dependent bradycardia response. Vanidilol inhibited the tachycardia effects induced by (-)isoproterenol, but had no blocking effect on the arterial pressor responses induced by phenylephrine. In isolated guinea-pig tissues, vanidilol attenuated the (-)isoproterenol-induced positive chronotropic and inotropic effects of the atria and trachea relaxation responses in a concentration-dependent manner. The parallel shift to the right of the concentration-response curve of (-)isoproterenol suggested that the agent was a beta-adrenoceptor competitive antagonist. The apparent pA2 values for vanidilol on the right atria, left atria and trachea were 7.67 +/- 0.03, 7.89 +/- 1.02 and 7.66 +/- 0.15, respectively, denoting that vanidilol was a nonselective beta-blocker. The intrinsic sympathomimetic activity of vanidilol and propranolol was determined on isolated atria and trachea from reserpinized guinea pigs. Propranolol caused significantly negative inotropic and chronotropic effects at 10(-6) mol/l or above, whereas vanidilol possessed less cardiodepressant activities than propranolol. In reserpinized tracheal strips, vanidilol produced dose-dependent relaxant responses, but propranolol was ineffective. Preincubating the preparations with ICI 118,551 (0.1-10 nmol/l), a beta 2-adrenoceptor antagonist, significantly shifted the concentration-relaxation curves of vanidilol to a region of higher concentrations. In isolated guinea-pig thoracic aorta, vanidilol (0.1-10 mumol/l) inhibited the phenylephrine (10(-5) mol/l)-induced tonic contraction in vascular smooth muscle which was related to the block of calcium influx. In 20% saline-perfused rabbits, vanidilol showed a marked delay in intraocular pressure recovery, demonstrating an ocular hypotensive action. Binding characteristics of vanidilol and propranolol were evaluated in [3H]dihydroalprenolol binding to porcine ventricular membranes. Vanidilol was less potent than propranolol in competing for the beta-adrenoceptor-binding sites. On the other hand, vanidilol had a high hydrophilicity in comparison with propranolol. In conclusion, vanidilol exhibited nonselective beta-adrenoceptor blocking, vasorelaxant and ocular hypotensive activities, but was devoid of alpha-adrenoceptor blocking and beta 1-agonist activity. Partial beta 2-adrenoceptor agonist activity and inhibitory activity on calcium influx may share in the vasorelaxant activity.

Adrenergic beta-2 Receptor Agonists↗
PubMed1996

Molecular cloning and nucleotide sequence determination of three envelope genes of classical swine fever virus Taiwan isolate p97.

A strain of classical swine fever virus (CSFV) has been isolated in Taiwan. The cDNA coding for three envelope glycoproteins E1, E2 and E3 were molecularly cloned from purified viral particles using the reverse transcription-polymerase chain reaction (RT-PCR) method and sequence-specific primers. The resulting PCR products (1113 bp for E1. 699 bp for E2 and 567 bp for E3) were cloned into the SmaI site of pUC19 and then subjected to DNA sequence analysis. Data showed that nucleotide sequence of the three envelope genes shared a 82-83% homology with the corresponding genes of three other strains (Alfort, Brescia and Weybridge). However, the homology of the deduced amino acid sequence was greater than 90% among the four strains. The potential asparagine-linked glycosylation sites for E1 (5 sites), E2 (7 sites) and E3 (2 sites) were conserved. This suggests that the Taiwan p97 strain is distinct from other three strains described. The variations may have implications for future vaccine development. The sequence has been submitted to GenBank. The accession numbers are U43924 and U03290.

Amino Acid Sequence↗
PubMed1996

The imaging diagnosis of hepatic schistosomiasis japonicum sequelae.

We reviewed the ultrasound (US) and computed tomography (CT) examinations of the liver in 21 patients with hepatic schistosomiasis japonicum (HSJ), to assess the role of imaging in its diagnosis. Thirteen patients had histopathological evidence of hepatic ova deposition. A 'network' pattern was present in 14 of 17 (82%) patients on US, and 'turtle-back' calcification in 11 of 13 (85%) patients on non-contrast CT (NCCT). The combination of US and NCCT was positive for HSJ in all nine patients subjected to both investigations. These findings are specific for HSJ and we discuss how they differ from the imaging findings reported in hepatic Schistosoma mansoni (HSM). We conclude that the sequelae of HSJ infection create an imaging diagnosis. Although an uncommon incidental finding at liver imaging, the combined US and CT appearances are so characteristic that in the majority of patients biopsy can potentially be avoided.

Aged↗
PubMed1990

What's new in cytoskeleton-organelle interactions? Relationship between microtubules and the Golgi-apparatus.

Several biochemical processes in animal cells are confined to distinct membrane-bounded compartments. Segregation of specialized functions into different compartments necessitates intercompartment transfer of material. This transfer is mediated by carrier vesicles which, by precise sorting and transport mechanisms, are targetted to their correct destinations. Microtubules, major constituents of the cytoskeleton, are involved both in these intracellular transport processes and in the spatial organization of cytoplasmic organelles. Accumulating evidence suggests that various classes of membranous organelles interact with microtubules. The positioning of several organelles, including the Golgi apparatus and lysosomes, depends on an intact interphase microtubule network. Furthermore, it has been shown that many of these organelles, for example Golgi elements, tubules of the endoplasmic reticulum, exocytic or secretory vesicles and lysosomes move along microtubules. In this article we will discuss the role of microtubules in the movement and positioning of elements of the Golgi complex. The first part will summarize structural and functional aspects of microtubules and the Golgi apparatus and review evidence for their interaction. In the second part, the possible physiological relevance of this interaction will be discussed and correlated with other membrane-microtubule interactions. Finally, emerging questions and perspectives in this field are outlined.

Animals↗
PubMed1990

One-stage closure of the entire primary palate.

Timing of the closure of the anterior palate and alveolus is a subject of debate. Late repair of this defect is complicated by high fistula formation and subjects the patient to the problems of palate fistula for extended periods of time. We have utilized a single procedure performed when the child is 3 months of age that completely closes the anterior hard palate and alveolus along with the cleft lip. Our series consisted of 61 consecutive patients with unilateral clefts of the primary and secondary palate. Mucosal turnover flaps from the vomer along with lateral nasal mucosal flaps provide the nasal lining. A buccal sulcus flap with a Veau flap completes the oral repair. Ninety-five percent (58 of 61) of the patients had complete and stable closure of their anterior palate and alveolus after 1 year. The incidence of fistula formation in our series (3 of 61) is much lower than that reported with the utilization of other protocols. Excellent exposure of the anterior palate and alveolar defect during lip repair, early restoration of anatomic relationships, establishment of a good nostril floor and sill, and very low fistula formation are among the benefits of this procedure. The increase in operative time is considered minimal in light of aforementioned advantages.

Cleft Lip↗
PubMed1990

Movement of interphase Golgi apparatus in fused mammalian cells and its relationship to cytoskeletal elements and rearrangement of nuclei.

Virus-induced Vero cell fusion was used to analyze the rearrangement of Golgi apparatus during the development of syncytia. Individual Golgi apparatus, associated initially with the separate microtubule-organizing centers in the perinuclear area of fused cells, congregated in the center of the syncytia and formed an extended Golgi complex within 3 to 5 h. The relocation of the Golgi apparatus, but not of nuclei, depended on the presence of an intact microtubule network, since both the microtubule depolymerizing drug nocodazole and the microtubule-stabilizing drug taxol interfered with the formation of an extended Golgi complex. Depolymerization of microfilaments with cytochalasin D and the complete collapse of intermediate filaments induced by microinjected monoclonal antibodies against vimentin had no effect on these processes. Cooling cells to 20 degrees C inhibited both congregation of Golgi apparatus and relocation of nuclei. Visualization of the movement of Golgi apparatus labeled in living cells with fluorescent metabolites of C6-NBD-ceramide showed that relocation of the Golgi apparatus was a process in which congregation and coalescence of the intact organelles was seen, rather than dispersal and reassembly of smaller Golgi elements in the center of the polykaryons. Thus, movement of intact Golgi apparatus in fused interphase cells depends on an undisturbed microtubule network and occurs independently of the relocation of nuclei.

Actin Cytoskeleton↗