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Biomedical subjects

K K Liu

Publications and source records attributed to K K Liu.

At least 19 recordsLinked to original sources
PubMed2003

An update on avian influenza in Hong Kong 2002.

An outbreak of highly pathogenic avian influenza caused by multiple genotypes of H5N1 virus occurred in Hong Kong, commencing in January 2002. Infection in local chicken farms was preceded by the detection of virus in multiple retail markets and the main poultry wholesale market. The first case of this disease on a local farm was detected on February 1, 2002. By February 9, 2002, 15 farms were infected, and by late March a total of 22 infected farms had been identified. Three main clusters of infected farms were seen, suggesting multiple incursions of virus, and subsequent limited lateral spread to neighboring firms. Control of this disease has been effected through a combination of quarantine, tightening of biosecurity measures, and depopulation of infected and contact farms. About 950,000 birds have been destroyed. Vaccination using a killed H5 vaccine was introduced in April 2002 to farms in one zone where infection has persisted. None of the viruses isolated contained the internal genes found in the 1997 H5N1 virus.

Animals↗
PubMed2003

Avian influenza in Hong Kong 1997-2002.

In 1997, a high-pathogenicity H5N1 avian influenza virus caused serious disease in both man and poultry in Hong Kong, China. Eighteen human cases of disease were recorded, six of which were fatal. This unique virus was eliminated through total depopulation of all poultry markets and chicken farms in December 1997. Other outbreaks of high-pathogenicity avian influenza (HPAI) caused by H5N1 viruses occurred in poultry in 2001 and 2002. These H5N1 viruses isolated had different internal gene constellations to those isolated in 1997. No new cases of infection or disease in man due to these or other H5N1 viruses have been reported. This paper provides an overview and chronology of the events in Hong Kong relating to avian influenza, covering the period from March 1997 to March 2002.

Animals↗
PubMed2002

Capsule-substrate contact deformation: determination of adhesion energy.

A study is reported of a cellular entity (liquid-filled microcapsule) adhered on a flat glass substrate in response to changes in osmotic pressure and temperature. High-resolution reflection interference contrast microscopy (HR-RICM) and phase-contrast microscopy were developed for probing the adhesion contact area, capsule-substrate separation profile and adhesion energy of the adhering microcapsule. The new technique increased the detection limit of the measured capsule wall-substrate separation in the cohesive zone from 1 to 4.5 microm and improved the spatial resolution of the heterogeneous contact zones. A theoretical model was applied to correlate quantitatively the adhesion energy to the area of the contact zone. The work demonstrated the possibility of ascertaining the quantitative interfacial adhesion energy of a liquid-filled microcapsule using the present technique and represents the first step in extending this novel approach to study more complicated systems, such as cell-substrate interactions, in the future.

Animals↗
PubMed2001

Contact mechanics of a thin-walled capsule adhered onto a rigid planar substrate.

A thin-walled capsule, modelled as an incompressible liquid droplet contained in a thin flexible membrane, was allowed to adhere onto a rigid substrate. The contact mechanics were formulated, based on linear elasticity, to portray quantitatively the relationships between osmotic inflation, contact area and angle, membrane stretching and adhesion strength. The predicted results shed light on fundamental adhesive contact mechanics in a cell-substrate system.

Biomechanical Phenomena↗
PubMed2000

New model to characterise cell-substrate adhesion in the presence of osmosis.

A simple model of cell-substrate adhesion, in response to osmosis change, is derived to describe quantitatively the interrelationships between osmotic inflation, contact area and angle, membrane stretching and adhesion strength. As the cell inflates, the contact area shrinks in dimension, until the cell is eventually lifted off the substrate. The theoretical prediction is consistent with other published data.

Biomechanical Phenomena↗
PubMed2000

The use of laparoscopy in the management of adnexal pathologies in children.

BACKGROUND: The authors' experience of using laparoscopy in the management of 23 girls (mean age: 8.9 years; range: 3 months-15 years) with various adnexal pathologies over a 3-year period is reviewed. METHODS: Of the 23 patients, seven were evaluated for congenital gonadal pathologies, 15 presented with abdominal pain and one patient had an antenatally diagnosed adnexal mass. Detailed laparoscopic examination of the pelvic cavity and laparoscopic gonadectomy were successfully performed in all seven patients with congenital gonadal pathologies: mosaic Turner's syndrome (n = 2), gonadal dysgenesis (n = 3) and testicular feminization syndrome (n = 2). Of 15 patients presenting with abdominal pain, 11 had an adnexal mass, two had acute appendicitis and two had pelvic inflammatory disease. RESULTS: Laparoscopic excision of the adnexal masses were successfully performed in 10 of 11 patients. Conversion to open surgery was required in one patient with a huge teratoma. Laparoscopic appendicectomy was successfully performed in both patients with acute appendicitis while diagnostic laparoscopy was the only procedure required in the two patients with pelvic inflammatory disease. Laparoscopy in the infant with an antenatally diagnosed adnexal mass confirmed this to be an omental cyst, which was successfully excised. All patients recovered without complications and good cosmetic result was universally achieved. CONCLUSION: Laparoscopy is safe and effective in both diagnosis and treatment of adnexal pathologies in children.

Adnexa Uteri↗
PubMed1999

Picrotoxin blockade of invertebrate glutamate-gated chloride channels: subunit dependence and evidence for binding within the pore.

Glutamate-gated chloride channels have been described in nematodes, insects, crustaceans, and mollusks. Subunits from the nematode and insect channels have been cloned and are phylogenetically related to the GABA and glycine ligand-gated chloride channels. Ligand-gated chloride channels are blocked with variable potency by the nonselective blocker picrotoxin. The first two subunits of the glutamate-gated chloride channel family, GluClalpha and GluClbeta, were cloned from the free living nematode Caenorhabditis elegans. In this study, we analyze the blockade of these novel channels by picrotoxin. In vitro synthesized GluClalpha and GluClbeta RNAs were injected individually or coinjected into Xenopus oocytes. The EC50 values for picrotoxin block of homomeric GluClalpha and GluClbeta were 59 microM and 77 nM, respectively. Picrotoxin block of homomeric GluClbeta channels was promoted during activation of membrane current with glutamate. In addition, recovery from picrotoxin block was faster during current activation by glutamate. A chimeric channel between the N-terminal extracellular domain of GluClalpha and the C-terminal membrane-spanning domain of GluClbeta localized the higher affinity picrotoxin binding site to the membrane-spanning domains of GluClbeta. A point mutation within the M2 membrane-spanning domain of GluClbeta reduced picrotoxin sensitivity >10,000-fold. We conclude that picrotoxin blocks GluCl channels by binding to a site accessible when the channel is open.

Amino Acid Sequence↗
PubMed1996

Identification of a Drosophila melanogaster glutamate-gated chloride channel sensitive to the antiparasitic agent avermectin.

Glutamate-gated chloride channels, members of the ligand-gated ion channel superfamily, have been shown in nematodes and in insects to be a target of the antiparasitic agent avermectin. Two subunits of the Caenorhabditis elegans glutamate-gated chloride channel have been cloned: GluCl-alpha and GluCl-beta. We report the cloning of a Drosophila melanogaster glutamate-gated chloride channel, DrosGluCl-alpha, which shares 48% amino acid and 60% nucleotide identity with the C. elegans GluCl channels. Expression of DrosGluCl-alpha in Xenopus oocytes produces a homomeric chloride channel that is gated by both glutamate and avermectin. The DrosGluCl-alpha channel has several unique characteristics not observed in C. elegans GluCl: dual gating by avermectin and glutamate, a rapidly desensitizing glutamate response, and a lack of potentiation of the glutamate response by avermectin. The pharmacological data support the hypothesis that the DrosGluCl-alpha channel represents the arthropod H-receptor and an important target for the avermectin class of insecticides.

Animals↗
PubMed1996

A receptor in pituitary and hypothalamus that functions in growth hormone release.

Small synthetic molecules termed growth hormone secretagogues (GHSs) act on the pituitary gland and the hypothalamus to stimulate and amplify pulsatile growth hormone (GH) release. A heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPC-R) of the pituitary and arcuate ventro-medial and infundibular hypothalamus of swine and humans was cloned and was shown to be the target of the GHSs. On the basis of its pharmacological and molecular characterization, this GPC-R defines a neuroendocrine pathway for the control of pulsatile GH release and supports the notion that the GHSs mimic an undiscovered hormone.

Amino Acid Sequence↗
PubMed1996

An amino acid substitution in the pore region of a glutamate-gated chloride channel enables the coupling of ligand binding to channel gating.

Many of the subunits of ligand-gated ion channels respond poorly, if at all, when expressed as homomeric channels in Xenopus oocytes. This lack of a ligand response has been thought to result from poor surface expression, poor assembly, or lack of an agonist binding domain. The Caenorhabditis elegans glutamate-gated chloride channel subunit GluClbeta responds to glutamate as a homomeric channel while the GluClalpha subunit is insensitive. A chimera between GluClalpha and GluClbeta was used to suggest that major determinants for glutamate binding are present on the GluClalpha N terminus. Amino acid substitutions in the presumed pore of GluClalpha conferred direct glutamate gating indicating that GluClalpha is deficient in coupling of ligand binding to channel gating. Heteromeric channels of GluClalpha+beta may differ from the prototypic muscle nicotinic acetylcholine receptor in that they have the potential to bind ligand to all of the subunits forming the channel.

Amino Acid Sequence↗
PubMed1996

Ectopic ureter as a cause of wetting: the role of laparoscopy in its management.

A diagnosis of wetting caused by an ectopic ureter usually can be made from the history because of the characteristic pattern of wetting. Localization of the origin of the ectopic ureter is important in guiding the surgical approach. This is usually not a problem for cases of ectopic ureter arising from a duplex system. However, the single ectopic ureter arising from a small dysplastic and often ectopic kidney may defy a long search. Videolaparoscopy, with its magnifying effect, can confirm the diagnosis, localize the dysplastic kidney and allow its removal using endoscopic equipment.

Child↗
PubMed1996

Detection of intracellular calcium elevations in Xenopus laevis oocytes: aequorin luminescence versus electrophysiology.

Detection of receptor expression in Xenopus oocytes often relies upon functional coupling to second messengers such as Ca2+ or cyclic adenosine monophosphate. To detect intracellular Ca2+, electrophysiological measurement of the endogenous Ca(2+)-activated chloride current (ICl(Ca)) is often used (Dascal, 1987). An alternative utilizes the Ca2+ sensing, bioluminescent protein aequorin (Parker and Miledi(1986) Proc. R. Soc. Lond. B, 228: 307-315; Giladi and Spindel (1991) BioTechniques, 10: 744-747). In the present study the sensitivities of aequorin and electrophysiology for detecting receptor-mediated Ca2+ transients were compared. Assays were performed on the same batches of oocytes using either animal serum or ligands of exogenous receptors to generate inositol 1,4,5-trisphosphate (InsP3) and ultimately elevate intracellular Ca2+. Signal amplitudes were controlled by titrating the concentration of animal serum, or titrating the amount of receptor mRNA injected. Both assays detected signals with high concentrations of animal serum, or with high receptor density. However, aequorin signals were not detected in experiments with average ICl(Ca) current amplitudes below 200 nA. To further evaluate the differences between these two techniques, membrane current and bioluminescence were measured simultaneously. Results of these studies suggest that the signals differ due to the spatial distribution of aequorin, the chloride channels, and the calcium release sites.

Animals↗