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Biomedical subjects

P K Wong

Publications and source records attributed to P K Wong.

At least 19 recordsLinked to original sources
PubMed2002

Mathematical relationships between vapor pressure, water solubility, Henry's law constant, n-octanol/water partition coefficent and gas chromatographic retention index of polychlorinated-dibenzo-dioxins.

Mathematical relationships between vapor pressures (P), water solubilities (S), Henry's law constants (Hc). noctanol/water partition coefficients (Kow) and gas chromatograph retention indices (GC-RIs) of polychlorinated-dibenzo-dioxins (PCDDs) were established. A model equation was established between GC-RIs (= RI) and other physico-chemical parameters (K) of PCDDs in the form of log K = aRI2 + bRI + c with correlation coefficients (R2) greater than 0.97, except Hc. These equations were derived from 56 experimental data of PCDDs reported previously. The values of P, S, Hc and Kow of PCDDs predicted by these equations based on their GC-RIs in the present study deviated from those calculated by the SOFA method in a previous study by only 0.19, 0.13, 0.18 and 0.096 log units, respectively.

Chromatography, Gas↗
PubMed2002

Degradation of azo dye Procion Red MX-5B by photocatalytic oxidation.

The photocatalytic oxidation (PCO) of a monoazo dye Procion Red MX-5B under various physico-chemical conditions was investigated. Degradation of the dye by PCO was enhanced by augmentation in UV intensity, titanium dioxide and hydrogen peroxide concentrations but was inhibited by increase in initial dye concentration. The PCO process was affected by pH in a peculiar way. In the presence of 100 mg/l of TiO2 and the absence of H2O2, the highest reaction rate was observed when the initial pH was 10. With 500 mg/l of TiO2 and 10 mM of H2O2, the reaction was the fastest at initial pH of 3-5. The optimal conditions for the degradation of the dye, at an UV intensity of 17 mW/cm2, were determined to be: TiO2 concentration, 500 mg/l; initial H2O2 concentration, 10 mM; initial pH, 5.0. Monitoring of TOC loss showed that the dye was mineralized by 90% within 80 min under these conditions. Nevertheless, the persistence of a low level of TOC indicated that mineralization was not complete and dead-end product(s) which was (were) resistant to PCO might have accumulated.

Azo Compounds↗
PubMed2001

A single Glu(62)-to-Lys(62) mutation in the Mos residues of the R7Delta447Gag-tMos protein causes the mutant virus to induce brain lesions.

We previously reported that R7Delta447, a 2954-base-pair (bp) laboratory-generated Moloney murine sarcoma virus, induced subcutaneous tumors in about 14% of infected mice but did not induce brain lesions. We now report that R7Delta447K, a spontaneous mutant of R7Delta447, induced brain lesions as well as subcutaneous tumors in all injected mice. The genomes of the two viruses differ in a single base pair: the deduced Glu(62) of the Mos residue of the R7Delta447 Gag-tMos protein is changed to Lys(62). More R7Delta447 than R7Delta447K focus-forming units were detected in both NIH3T3 and mouse cerebral vascular endothelial (MCVE) cells. However, R7Delta447K transformed NIH3T3 and MCVE cells more acutely than did R7Delta447. A distinctive feature that distinguished the morphologic transformation of R7Delta447- and R7Delta447K-infected MCVE cells is the markedly prolonged spindle-shaped phase exhibited by R7Delta447-infected MCVE cells. In addition, R7Delta447K was more efficient in inducing the phosphorylation of ERK1/2 than R7Delta447 in both MCVE and NIH3T3 cells. Moreover morphologic transformation was inhibited, and levels of phosphorylated ERK1/2 were reduced when R7Delta447- or R7Delta447K-infected NIH3T3 or MCVE cells were grown in the presence of the MEK1/2-specific inhibitor PD98095. Thus, we have identified a key residue in the Gag-tMos protein that profoundly affects activation of the Mos/MEK/ERK pathway, virus and cell replication, morphologic transformation in vitro and pathogenicity in vivo.

3T3 Cells↗
PubMed2001

The accumulation of polycyclic aromatic hydrocarbons in lubricating oil over time--a comparison of supercritical fluid and liquid-liquid extraction methods.

Optimal extraction conditions including extraction temperature, fluid density of carbon dioxide and concentration of modifier for supercritical fluid extraction (SFE) to extract of 16 2-6-ring polycyclic aromatic hydrocarbons (PAHs) spiked into used lubricating oil collected from a gasoline-driven automobile were determined. A comparison of extraction efficiency 2-6-ring PAHs spiked into the used lubricating oil extracted by SFE and liquid-liquid extraction (LLE) methods was made. Results indicated that recoveries of PAHs extracted by SFE from the used lubricating oil were higher than those by LLE. PAH profiles of lubricating oil samples collected at various driving distances from an old and a new gasoline-driven automobiles were determined by combining SFE, gel permeation chromatography clean up and gas chromatography-mass spectrometry analysis. Results showed that the concentrations of total PAH in lubricating oils collected from both automobiles increased rapidly after oil change. Two- and three-ring PAHs dominated the PAH profiles of oil samples collected from both automobiles. High concentrations of the more toxic 4-6-ring PAHs, were found in the oil samples collected from both automobiles even at a short driving distance after oil change. The concentrations of total PAH in lubricating oil collected from two automobiles driven for a longer distance after oil change were very similar.

Chromatography, Gel↗
PubMed2001

Enhanced proteolysis of IkappaBalpha and IkappaBbeta proteins in astrocytes by Moloney murine leukemia virus (MoMuLV)-ts1 infection: a potential mechanism of NF-kappaB activation.

Moloney murine leukemia virus (MoMuLV)-ts1-mediated neuronal degeneration in mice is likely due to loss of glial support and release of inflammatory cytokines and neurotoxins from surrounding ts1-infected glial cells including astrocytes. NF-kappaB is a transcription factor that participates in the transcriptional activation of a variety of immune and inflammatory genes. We investigated whether ts1 activates NF-kappaB in astrocytes and examined the mechanism(s) responsible for the activation of NF-kappaB by ts1 infection in vitro. Here we present evidence that ts1 infection of astrocytes in vitro activates NF-kappaB by enhanced proteolysis of the NF-kappaB inhibitors, IkappaBalpha and IkappaBbeta. In in vitro studies using protease inhibitors, IkappaBalpha proteolysis in ts1-infected astrocytes was significantly blocked by a specific calpain inhibitor calpeptin but not by MG-132, a specific proteasome inhibitor, whereas rapid IkappaBbeta proteolysis was blocked by MG-132. Furthermore, treatment with MG-132 increased levels of multiubiquitinated IkappaBbeta protein in ts1-infected astrocytes. These results indicate that the calpain proteolysis is a major mechanism of IkappaBalpha proteolysis in ts1-infected astrocytes. Additionally, ts1 infection of astrocytes in vitro increased expression of inducible nitric oxide synthase (iNOS), a NF-kappaB-dependent gene product. Our results suggest that NF-kappaB activation in ts1-infected astrocytes is mediated by enhanced proteolysis of IkappaBalpha and IkappaBbeta through two different proteolytic pathways, the calpain and ubiquitin-proteasome pathways, resulting in increased expression of iNOS, a NF-kappaB-dependent gene.

Active Transport, Cell Nucleus↗
PubMed2001

The ataxia-telangiectasia gene product may modulate DNA turnover and control cell fate by regulating cellular redox in lymphocytes.

The ATM kinase, when activated postnatally, exerts multiple functions to prevent the onset of ataxia-telangiectasia (AT). Using freshly isolated thymocytes from Atm-/- mice that were under stress during postnatal differentiation, we noted that thiol redox activity, as indicated by reduction of the tetrazolium MTS, and DNA turnover activity, as indicated by incorporation of [(3)H]thymidine into DNA, were both greatly increased compared with activities in thymocytes from Atm+/+ mice. This increased thymidine incorporation could be suppressed by the thiol N-acetylcysteine. In primary noncycling splenocytes, mitogens proportionally increased both the rate of [(3)H]thymidine incorporation and the rate of reduction of MTS. The mitogen-induced activities in splenocytes were not affected by ATM but were suppressed by the calcineurin-dependent inhibitor FK-506, which has no effect on these activities in thymocytes. These findings suggest that increased [(3)H]thymidine incorporation and reducing power indicate increased cell cycling in mitogenically stimulated splenocytes, whereas these two indicators represent increased FK-506-independent DNA turnover activities in thymocytes. Thus, a primary function of ATM is to activate the redox-sensitive checkpoint required for down-regulation of DNA turnover activities in developing lymphocytes. Cell-cycling checkpoints in undamaged quiescent lymphocytes are not activated by ATM with mitogenic stimulation. ATM may suppress abnormal DNA turnover and the resultant oncogenesis by regulating cellular thiol redox pathways.

Acetylcysteine↗
PubMed2001

Effects of pulse methylprednisolone on macrophage chemotactic protein-1 and macrophage inflammatory protein-1alpha in rheumatoid synovium.

OBJECTIVE: To determine the effect of pulse methyprednisolone (PMP; 1000 mg) on the expression of monocyte chemoattractant protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha in rheumatoid synovial membrane. METHODS: Seven patients with rheumatoid arthritis (RA) were studied. Arthroscopically-directed synovial biopsies were taken before and 24 hours after treatment with intravenous PMP. Synovial membranes were stained by immunohistochemical techniques with monoclonal antibodies against MCP-1, MIP-1alpha and CD68 (a macrophage marker). Quantitation of staining was performed by computer-assisted color video image analysis. RESULTS: PMP therapy was associated with a rapid (within 24 hours) and substantial decrease in the expression of MCP-1 and MIP-1alpha expression by a mean of 55% (p = 0.05) and 45% (p = 0.03), respectively, with no effect on CD68 expression in the synovial lining layer. There was no significant change in MCP-1, MIP-1alpha or CD68 expression in the synovial sublining. CONCLUSION: PMP therapy rapidly reduces MCP-1 and MIP-1alpha levels in the synovial lining layer without a fall in macrophage numbers. It thus appears that the initial effect of PMP is that of reducing macrophage activation.

Aged↗
PubMed2001

[Determination of Henry's law constants for dimethyl sulfide in seawater].

The article presents the method of determination of Henry's Law Constant(K) for dimethyl sulfide (DMS) in seawater using multiple phase equilibration/headspace gas chromatography. The method is based on the demonstration that analysis of only one phase after multiple phase equilibration give all necessary data. The values of K of DMS in seawater determined by this method was 0.089 with relative standard deviation(RSD) of 5.50% at 22 degrees C. The linear relationship between log K and w (NaCl) was log K = 0.0688.w (NaCl) - 1.3568 with correlation coefficient(r) of 0.997. The regression equation of log K against reciprocal of absolute temperature(T) was log K = -1,544.8/T + 4.2112 with r of 0.996.

Chromatography, Gas↗
PubMed2000

Modulation of G-protein linked cAMP accumulation in immortalized murine cortical astrocytes by retroviral infection.

The present study characterized beta-adrenergic receptors (beta-AR) in a clonal cell line (C1) immortalized from cerebral cortical astroglial cells of FVB/N mice. We also determined whether the wild type Moloney murine leukemia virus (wt-MoMuLV) and one of its neuropathogenic mutants, ts1-MoMuLV, modulated the beta-AR system in these cells. We observed that C1 cells possess a functional beta-AR system coupled to cAMP accumulation and capable of normal agonist-induced regulation (desensitization). Significant increases were observed in forskolin stimulated cAMP accumulation in C1 cells infected by wt MoMuLV and by ts1-MoMuLV. In contrast, the cAMP response to beta-AR stimulated by isoproterenol was relatively spared after viral exposure.

Adenylyl Cyclases↗
PubMed2000

Motor neuronal loss and neurofilament-ubiquitin alteration in MoMuLV-ts1 encephalopathy.

A temperature-sensitive mutant of Moloney murine leukemia virus (MoMuLV-ts1) induces immunosuppression and spongiform encephalopathy in susceptible newborn mice. The associated neuronal degeneration primarily involves the motor neurons in specific target areas of the central nervous system (CNS). Neuronal loss occurs in the absence of direct viral infection of neurons and is the most dramatic pathological change in the CNS of infected mice. To quantitatively demonstrate neuronal loss, an unbiased morphometric stereological study was undertaken using the optical disector method. Using highly susceptible FVB/N mice, neuronal loss was quantitated in the tissue sections of brain stem from infected and noninfected mice at 20 and 35 days post inoculation (dpi). Results indicated that there was no significant neuronal loss at 20 dpi, but significant (P < 0.05) at 35 dpi. In addition, histology, transmission electron microscopy and immunohistochemistry revealed Lewy body-like inclusions consisting of aggregates of neurofilaments and cellular organelles. Degenerated neurons and glial cells were heavily ubiquitinated. Together, these results suggest that significant neuronal loss occurs at the end of the disease process and that Lewy body-like formation and protein ubiquitination are part of the pathogenic process in ts1-induced encephalopathy.

Animals↗
PubMed2000

Effects of 2,4-D, glyphosate and paraquat on growth, photosynthesis and chlorophyll-a synthesis of Scenedesmus quadricauda Berb 614.

The effects of 2,4-D, glyphosate and paraquat on growth, photosynthesis and chlorophyll-a synthesis by a freshwater green alga, Scenedesmus quadricauda Berb 614, were determined. These herbicides are the most often used in Hong Kong. Within the concentration range 0.02-200 mg/l, paraquat was more toxic than glyphosate and 2,4-D to the growth, photosynthesis and chlorophyll-a synthesis. The presence of 0.02, 0.2 or 2 mg/l of 2,4-D was not toxic to the alga. Algal growth, photosynthesis and chlorophyll-a synthesis were stimulated by the presence of low concentrations (0.02 or 0.2 and 0.02 mg/l, respectively) of 2,4-D and glyphosate. The presence of 0.02 or 0.2 mg/l of paraquat, 2 mg/l of glyphosate or 20 mg/l of 2,4-D was significantly inhibitory to the three test parameters, whereas the presence of 2 or more mg/l of paraquat, 20 or more mg/l of glyphosate or 200 mg/l of 2,4-D completely inhibited algal growth, photosynthesis and chlorophyll-a synthesis. The use of the alga as a bio-indicator of herbicide contamination in freshwater environment was discussed.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2000

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Aged↗
PubMed2000

A novel magnetite-immobilized cell process for heavy metal removal from industrial effluent.

The sorption and desorption of copper (II) (Cu[II]) ions from the wastewater by magnetite-immobilized cells of Pseudomonas putida 5-x with acidic pretreatment were studied. Pretreating cells with 0.6 N HCl was found to enhance greatly the adsorption capacity of biomass up to 85.6 mg/g and had no significant effect on the loss of P. putida 5-x cells during biosorbent pretreatment. The biosorption capacity to Cu2+ of magnetite-immobilized cells of P. putida 5-x harvested during various growth phases was also investigated. The experimental results illustrated that the adsorption capacity to Cu2+ of P. putida 5-x cultured in sulfate-limiting medium reached maximum during the late stationary growth phase or early death phase, and reached minimum during the log growth phase. The mechanism of copper sequestering by this type of biomass was studied via transmission electron microscopy. A degradation of the peptidoglycan layer of the cell wall was observed in the acidic pretreatment, but no further degradation appeared after the adsorption-desorption cycle. Cu(II) accumulated mostly on the surface of the cell walls and was effectively desorbed by the acidic treatment during the desorption process.

Adsorption↗
PubMed2000

Studies on the pathology, especially brain hemorrhage and angioendotheliomas, induced by two new mos-containing viruses.

Recombinant virus 7 (R7), a spontaneous deletion mutant of SV7, which is itself a molecular clone of Moloney murine sarcoma virus 124 (MoMuSV 124), induces brain lesions and tumors of the subcutaneous tissue and spleen in all infected mice. In contrast, SV7 only induces tumors of the spleen and subcutaneous tissues. One of the genetic differences between R7 and SV7 is that R7 encodes a Gag-Mos protein whereas SV7 encodes an Env-Mos protein. To investigate whether the novel R7 gag-mos oncogene is required for brain lesion induction, two viruses (SV7d1 and SVM1) were constructed in which the R7 gag-mos sequences and the adjacent 53 bp of the 5' noncoding sequence were replaced by either the SV7 or myeloproliferative sarcoma virus (MPSV) env-mos oncogenes, respectively. Like R7, SV7d1 and SVM1 induced brain lesions and tumors in the spleen and subcutaneous tissues. A prominent component of R7-, SV7d1-, and SVM1-induced tumors of the brain, subcutaneous tissues, and spleen was the presence of abnormally enlarged cells with eccentric nuclei lining vessels, scattered singly or in small clusters. Their size, localization to the luminal surface of distended vessels, and binding to Bandeiraea simplicifolia (BS-1) lectin, an endothelial cell (EC) marker, suggest that they are most likely transformed ECs. Our findings therefore indicate that the induction of brain lesions is not limited to the expression of the R7 Gag-Mos protein. However, our findings also indicate that expression of the different forms of the Mos protein results in differences in the relative abundance of ECs in brain angioendotheliomas and subcutaneous and spleen tumors induced by these viruses.

3T3 Cells↗
PubMed2000

Changes in the N- and C-terminal sequences of the murine R7 Gag-tMos protein affect brain lesion induction.

Our preliminary studies suggested that the novel gag-truncated mos (tmos) open reading frame (ORF) of R7, a spontaneous deletion mutant of Moloney murine sarcoma virus 124 (MoMuSV124), may be responsible for R7's unique ability to induce brain lesions in all R7-injected mice. However, when we replaced the gag-tmos ORF with either the MoMuSV124 or the homologous myeloproliferative sarcoma virus env-mos gene, we found that both recombinant viruses also induced brain lesions in all injected mice. Although these studies suggested that the critical determinants for brain lesion induction may reside in the tmos sequence common to all three viruses, they did not demonstrate if the N-terminus of Mos was dispensable for this activity. By inserting the FLAG sequence at the 3' end of the R7 gag-tmos ORF, we demonstrated that R7 does synthesize a Gag-tMos fusion protein. Using R7 gag deletion mutants with and without the FLAG sequence, we further demonstrated that (i) deletion of the entire gag sequence abolished R7's transforming activity; (ii) the ability of the virus to transform cultured NIH/3T3 cells was significantly reduced only when most of gag was deleted; (iii) the ability of the virus to induce brain lesions was inversely proportional to the extent of its gag deletions; and (iv) the insertion of FLAG at the Mos C-terminus did not reduce the in vitro transforming activity of the FLAG-tagged viruses but did reduce their ability to induce brain lesions. Thus, we have demonstrated that altering the N- or C-terminus of the R7 Gag-tMos fusion protein can affect disease manifestation.

3T3 Cells↗
PubMed1999

Retinopathy of prematurity in very low birth weight infants.

This study aims to determine the prevalence of and risk factors associated with retinopathy of prematurity (ROP) in very low birth weight (VLBW) infants. All premature VLBW infants, admitted into the neonatal intensive care unit of the University Hospital Kuala Lumpur, were screened from 4 weeks of life. Perinatal and neonatal data were retrieved from the infants' medical notes. Between August 1994 and July 1996, 100 infants had their eyes examined serially. Of the 15 (15%) infants with ROP, all were less than 31 weeks gestation, and only 1 infant had birth weight above 1250 g. Five (5%) infants had severe ROP; 4 infants underwent cryotherapy for stage 3 threshold disease. Infants with ROP, as compared to infants without ROP, had lower birth weight [mean (SEM) 993 (50) g versus 1205 (22) g, P < 0.001], lower gestational age [mean (SEM) 28.0 (0.4) weeks versus 30.1 (0.2) weeks, P < 0.001], higher rates of patent ductus arteriosus and chronic lung disease, greater number of radiographic examinations and episodes of late-onset suspected/confirmed sepsis, and required longer duration of supplemental oxygen, ventilation, xanthine, antibiotics and intralipid use, but were slower to establish full enteral feeds. On multivariate logistic regression analysis, birth weight < or = 1000 g [OR 2.38, 95% CI 1.25, 4.55, P = 0.009] and gestational age < or = 28 weeks [OR 2.86, 95% CI 1.47, 5.56, P = 0.002] were significant predictors of increased risk of this disease. In conclusion, ROP is strongly associated with smaller, more immature and sicker neonates. Prevention of prematurity would help reduce the incidence of this disease.

Anti-Bacterial Agents↗
PubMed1998

Neurodegeneration induced by MoMuLV-ts1 and increased expression of Fas and TNF-alpha in the central nervous system.

Infection of neonatal mice with ts1, the neuropathogenic mutant of the Moloney murine leukemia virus, results in motor neuronal death in the brainstem and the spinal cord, with gliosis and demyelination, but no inflammatory cell infiltration into the CNS. To evaluate the possible mechanism(s) of ts1-induced neuropathogenesis, we measured CNS expression of cytokines and cell death-related genes in ts1-infected mice with neurological signs and compared with control uninfected mice. In the brainstem, the expression of Fas and tumor necrosis factor alpha (TNF-alpha) was increased in the ts1-infected mice. Both TNF-alpha and Fas were detected in astrocytes, and Fas was also detected in neurons in the brainstem. Some TNF-alpha-immunolabeled cells also appeared to be microglial cells. Most Fas-positive cells, including astrocytes and neurons, showed cytoplasmic vacuolization and other degenerative changes. In addition, Fas ligand-immunolabeled cells were also detected in sites where spongiform degeneration occurred. This study suggests that neural cell death in ts1-induced neurodegeneration is likely due to Fas- and TNF-alpha-mediated cell death mechanisms.

Animals↗