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C W Chung

Publications and source records attributed to C W Chung.

At least 19 recordsLinked to original sources
PubMed2005

Feasibility study of nitrogen removal with the mecellulose wasted liquor as an external carbon source in the two-stage denitrification process.

The utilization of mecellulose wasted liquor (MWL) as an external carbon source was investigated to find an alternative for methanol in the two-stage denitrification pilot process. The pilot plant was supplied with the raw water from the J-Municipal Sewage Treatment Plant (J-MSTP) in Korea. The raw water of J-Municipal Sewage Treatment Plant contains low and high concentration of biodegradable organics and nitrogen source, respectively, due to the inflow of industrial wastewater and landfill leachate. Methanol was fed to provide external carbon source for high concentration of nitrogen source removal by denitrification in this J-Municipal Sewage Treatment Plant, and thus this study was performed to test effects to the effluent quality and efficiencies of nitrogen source removal with an alternative carbon source for the cost reduction. The 6.5mg 1(-1) and 5.7mg l(-1) of total nitrogen (TN) concentration in the effluent were achieved with mecellulose and methanol, whereas mecellulose and methanol were fed to give the same ratio of gCODgNO,-N(-1), respectively. The 60% of COD in mecellulose wasted liquor was used as a carbon source for denitrification and the stable denitrification rate was earned when one half of the required total carbon source for denitrification was fed to pre-anoxic tank in the pilot plant. The required gCODgNO,-N(-1) ratio with mecellulose wasted liquor was 1.4 times higher than with methanol. Mecellulose wasted liquor is feasible to be used as external carbon source for organic loading, nitrogen and phosphorus removal. If mecellulose wasted liquor is considered as an alternative external carbon source to substitute methanol 26-28m3 mecellulose wasted liquor per 1 m3 methanol will be required. However, to meet with the effluent standard (10 mg BOD l(-1)) for J-Municipal Sewage Treatment Plant, the feed concentration of mecellulose wasted liquor should be recommended to be lower than 200 mgl(-1).

Carbon↗
PubMed2001

FLASH coordinates NF-kappa B activity via TRAF2.

FLASH is a protein recently shown to interact with the death effector domain of caspase-8 and is likely to be a component of the death-inducing signaling complex in receptor-mediated apoptosis. Here we show that antisense oligonucleotide-induced inhibition of FLASH expression abolished TNF-alpha-induced activation of NF-kappaB in HEK293 cells, as determined by luciferase reporter gene expression driven by a NF-kappaB responsive promoter. Conversely, overexpression of FLASH dose-dependently activated NF-kappaB, an effect suppressed by dominant negative mutants of TRAF2, NIK, and IKKalpha, and partially by those of TRAF5 and TRAF6. TRAF2 was co-immunoprecipitated with FLASH from the cell extracts of HEK293 cells or HeLa cells stably expressing exogenous FLASH (HeLa/HA-FLASH). Furthermore, serial deletion mapping demonstrated that a domain spanning the residues 856-1191 of FLASH activated NF-kappaB as efficiently as the full-length and could directly bind to TRAF2 in vitro and in the transfected cells. Taken together, these results suggest that FLASH coordinates downstream NF-kappaB activity via a TRAF2-dependent pathway in the TNF-alpha signaling.

Animals↗
PubMed2001

An anti-apoptotic protein human survivin is a direct inhibitor of caspase-3 and -7.

Survivin, an apoptosis inhibitor/cell-cycle regulator, is critically required for suppression of apoptosis and ensuring normal cell division in the G2/M phase of the cell cycle. It is highly expressed in a cell cycle-regulated manner and localizes together with caspase-3 on microtubules within centrosomes. Whether survivin is a physiologically relevant caspase inhibitor has been unclear due to the difficulties with obtaining correctly folded survivin and finding the right conditions for inhibition assay. In this study, recombinant, active human survivin was expressed in Escherichia coli and purified to homogeneity. The protein, existing as a homodimer in solution, binds caspase-3 and -7 tightly with dissociation constants of 20.9 and 11.5 nM, respectively, when evaluated by surface plasmon resonance spectroscopy. Consistently, survivin potently inhibits the cleavage of a physiological substrate poly(ADP-ribose) polymerase and an artificial tetrapeptide by caspase-3 and -7 in vitro with apparent inhibition constants of 36.0 and 16.5 nM, respectively. The data suggest that sequestering caspase-3 and -7 in inhibited states on microtubules is at least one mechanism of survivin in the suppression of default apoptosis in the G2/M phase. The localization of survivin on microtubules, which is essential for its function, should increase the protective activity at the action site.

Apoptosis↗
PubMed2001

Pro-apoptotic function of calsenilin/DREAM/KChIP3.

Apoptotic cell death and increased production of amyloid b peptide (Ab) are pathological features of Alzheimer's disease (AD), although the exact contribution of apoptosis to the pathogenesis of the disease remains unclear. Here we describe a novel pro-apoptotic function of calsenilin/DREAM/KChIP3. By antisense oligonucleotide-induced inhibition of calsenilin/DREAM/KChIP3 synthesis, apoptosis induced by Fas, Ca2+-ionophore, or thapsigargin is attenuated. Conversely, calsenilin/DREAM/KChIP3 expression induced the morphological and biochemical features of apoptosis, including cell shrinkage, DNA laddering, and caspase activation. Calsenilin/DREAM/KChIP3-induced apoptosis was suppressed by caspase inhibitor Z-VAD and by Bcl-XL, and was potentiated by increasing cytosolic Ca2+, expression of Swedish amyloid precursor protein mutant (APPSW) or presenilin 2 (PS2), but not by a PS2 deletion lacking its C-terminus (PS2/411stop). In addition, calsenilin/DREAM/KChIP3 expression increased Ab42 production in cells expressing APPsw, which was potentiated by PS2, but not by PS2/411stop, which suggests a role for apoptosis-associated Ab42 production of calsenilin/DREAM/KChIP3.

Amino Acid Chloromethyl Ketones↗
PubMed2001

Inactivation of farnesyltransferase and geranylgeranyltransferase I by caspase-3: cleavage of the common alpha subunit during apoptosis.

Caspase plays an important role in apoptosis. We report here that farnesyltransferase/geranylgeranyltransferase (FTase/GGTase)-alpha, a common subunit of FTase (alpha/beta(FTase)) and GGTase I (alpha/beta(GGTase)), was cleaved by caspase-3 during apoptosis. FTase/GGTase-alpha (49 kDa) was cleaved to 35 kDa (p35) in the Rat-2/H-ras, W4 and Rat-1 cells treated with FTase inhibitor (LB42708), anti-Fas antibody and etoposide, respectively. This cleavage was inhibited by caspase-inhibitors (YVAD-cmk, DEVD-cho). Serial N-terminal deletions and site-directed mutagenesis showed that Asp59 of FTase/GGTase-alpha was cleaved by caspase-3. The common FTase/GGTase-alpha subunit, but not the beta subunits, of the FTase or GGTase I protein complexes purified from baculovirus-infected SF-9 cells was cleaved to be inactivated by purified caspase-3. In contrast, FTase mutant protein complex [(D(59)A)alpha/beta(FTase)] was resistant to caspase-3. Expression of either the cleavage product (60-379) or anti-sense of FTase/GGTase-alpha induced cell death in Rat-2/H-ras cells. Furthermore, expression of (D(59)A)FTase/GGTase-alpha mutant significantly desensitized cells to etoposide-induced death. Taken together, we suggest that cleavage of prenyltransferase by caspase contributes to the progression of apoptosis.

Alkyl and Aryl Transferases↗
PubMed2001

Proapoptotic effects of tau cleavage product generated by caspase-3.

Using an in vitro translation assay to screen a human brain cDNA library, we isolated the microtubule-associated protein Tau and determined it to be a caspase-3 substrate whose C-terminal cleavage occurred during neuronal apoptosis. DeltaTau, the 50-kDa cleavage product, was detected by Western blot in apoptotic cortical cells probed with anti-PHF-1 and anti-Tau-5 antibodies, but not anti-T-46 antibody which recognizes the C-terminus. Overexpression of DeltaTau in SK-N-BE2(C) cells significantly increased the incidence of cell death. Staurosporine-induced Tau cleavage was blocked by 20 microM z-Asp-Glu-Val-Asp-chloromethylketone, a caspase-3 inhibitor, and in vitro, Tau was selectively cleaved by caspase-3 or calpain, a calcium-activated protease, but not by caspases-1, -8, or -9. (D421E)-Tau, a mutant in which Asp421 was replaced with a Glu, was resistant to cleavage by caspase-3 and tended to suppress staurosporine-induced cell death more efficiently than did wild-type Tau in both transient and stable expression systems. Finally, the incidence of DeltaTau-induced cell death was augmented by expression of Abeta precursor protein (APP) or Swedish APP mutant. Taken together, these results suggest that the caspase-3 cleavage product of Tau may contribute to the progression of neuronal cell death in Alzheimer's disease.

Amyloid beta-Protein Precursor↗
PubMed2001

Cometabolic biosynthesis of copolyesters consisting of 3-hydroxyvalerate and medium-chain-length 3-hydroxyalkanoates by Pseudomonas sp. DSY-82.

A newly isolated strain, designated as Pseudomonas sp. DSY-82, synthesized medium-chain-length polyhydroxyalkanoate (MCL-PHA) copolyesters when grown on alkanoates from hexanoate to undecanoate as the sole carbon source. When used alone, butyrate and valerate supported the growth of the isolate but not PHA production. However, unusual polyesters containing 3-hydroxyvalerate, as well as various MCL 3-hydroxyalkanoate monomeric units, were synthesized when valerate was cofed with either nonanoate or 10-undecenoate, suggesting the formation of monomer units from both substrates. Concentrations of 3-hydroxyvalerate, 3-hydroxyoctanoate, and 3-hydroxydecanoate in the PHAs produced were significantly elevated by the addition of valerate, indicating that the incorporation of these monomer units to PHA occurred primarily through cometabolism. The total amount of these monomer units in the PHAs reached up to 30%. The PHAs produced in this study were most likely random copolyesters as determined by differential scanning calorimetric analysis. This is the first case of microbial synthesis of copolyesters consisting of 3-hydroxyvalerate and MCL 3-hydroxyalkanoate monomer units through cometabolism.

Aerobiosis↗
PubMed2001

Cleavage of Bax is mediated by caspase-dependent or -independent calpain activation in dopaminergic neuronal cells: protective role of Bcl-2.

Two cysteine protease families, caspase and calpain, are known to participate in cell death. We investigated whether a stress-specific protease activation pathway exists, and to what extent Bcl-2 plays a role in preventing drug-induced protease activity and cell death in a dopaminergic neuronal cell line, MN9D. Staurosporine (STS) induced caspase-dependent apoptosis while a dopaminergic neurotoxin, MPP(+) largely induced caspase-independent necrotic cell death as determined by morphological and biochemical criteria including cytochrome c release and fluorogenic caspase cleavage assay. At the late stage of both STS- and MPP(+)-induced cell death, Bax was cleaved into an 18-kDa fragment. This 18-kDa fragment appeared only in the mitochondria-enriched heavy membrane fraction of STS-treated cells, whereas it was detected exclusively in the cytosolic fraction of MPP(+)-treated cells. This proteolytic cleavage of Bax appeared to be mediated by calpain as determined by incubation with [(35)S]methionine-labelled Bax. Thus, cotreatment of cells with calpain inhibitor blocked both MPP(+)- and STS-induced Bax cleavage. Intriguingly, overexpression of baculovirus-derived inhibiting protein of caspase, p35 or cotreatment of cells with caspase inhibitor blocked STS- but not MPP(+)-induced Bax cleavage. This appears to indicate that calpain activation may be either dependent or independent of caspase activation within the same cells. However, cotreatment with calpain inhibitor rescued cells from MPP(+)-induced but not from STS-induced neuronal cell death. In these paradigms of dopaminergic cell death, overexpression of Bcl-2 prevented both STS- and MPP(+)-induced cell death and its associated cleavage of Bax. Thus, our results suggest that Bcl-2 may play a protective role by primarily blocking drug-induced caspase or calpain activity in dopaminergic neuronal cells.

1-Methyl-4-phenylpyridinium↗
PubMed2001

Comparison of balloon dacryocystoplasty to probing as the primary treatment of congenital nasolacrimal duct obstruction.

PURPOSE: In children older than 18 months, primary probing procedures for congenital nasolacrimal duct obstruction (CNLDO) are thought to have lower rates of success. This study compares the results of primary probing to balloon dacryocystoplasty (DCP) in children stratified by age category. METHODS: In a retrospective chart review, 29 eyes with CNLDO that underwent balloon DCP in children older than 18 months were identified and age-matched to 29 eyes that underwent probing. The eyes were divided into 3 age categories: category 1 (18-24 months), category 2 (24-36 months), and category 3 (>36 months). RESULTS: Of the 29 eyes treated with balloon DCP (mean age, 37.1 months), 26 were successfully treated. Twenty-five of the 29 matched probed eyes (mean age, 31.1 months) were successfully treated, resulting in an overall success rate of 90% for balloon DCP and 86% for primary probing. Within each age category, the success rate varied but did not show an advantage to balloon DCP. The presence of crusting and expressible discharge from the puncta during preoperative evaluation predicted a successful probing (OR, 16; 95% CI, 1.3-192). CONCLUSION: Overall, balloon DCP did not appear to present an advantage as compared with primary probing as the initial treatment in these children. Primary probing has an impressive overall success rate that did not diminish in the children older than 36 months.

Catheterization↗
PubMed2001

Penetrating keratoplasty in iridocorneal endothelial syndrome.

PURPOSE: To evaluate the clinical outcome of penetrating keratoplasty (PK) in iridocorneal endothelial (ICE) syndrome. METHODS: Clinical charts of patients who underwent penetrating keratoplasty for ICE syndrome between 1985 and 1999 were reviewed retrospectively. Glaucoma control, best corrected visual acuity pre- and post-PK, graft clarity, graft rejection episodes, improvement in pain, and additional procedures were analyzed. RESULTS: Fourteen cases were reviewed with an average follow-up of 58 months after PK. Initial grafts failed in seven patients (50%), in six cases because of rejection, and one owing to endothelial failure without signs of rejection. Repeat PKs were performed in six patients. At final follow-up, 12 grafts were clear. Glaucoma was controlled pre- and post-PK (average intraocular pressure, 16 mmHg for both eyes). Pre-PK, eight patients were using glaucoma medicines and nine had had glaucoma surgery. At the end of the follow-up, seven patients were using glaucoma medicines; six patients required glaucoma surgery after their initial PK. At the final follow-up visit, visual acuity in three patients (21%) was 20/40 or better, it ranged from 20/50 to 20/100 in four patients (29%) and 20/200 to 20/400 in five patients (36%), and in two patients with failed grafts (14%) it was counting fingers or worse. CONCLUSION: Clear grafts were achieved in 12 cases, although six patients (43%) underwent repeat PKs. All patients had glaucoma, which was controlled before and after PK by medical treatment and surgical procedures. Favorable outcomes can be achieved in patients with ICE syndrome but may require multiple corneal and glaucoma procedures.

Adult↗
PubMed2001

Human immunodeficiency virus p24 antigen testing in cornea donors.

PURPOSE: Testing for the p24 antigen of the human immunodeficiency virus (HIV) may detect early HIV infection in the seronegative window; however, falsely reactive results may occur in cadaver specimens. Although neither the Food and Drug Administration (FDA) nor the Eye Bank Association of America requires p24 testing of cornea donors, many tissue banks using other organs from cornea donors do perform this assay, and the FDA requires that eye banks reject corneal tissue if a reactive p24 assay is reported. We investigated the impact of p24 testing on eye banking and corneal transplantation. METHODS: Two clinical cases and records from the Lions Eye Bank of Delaware Valley (LEBDV) were reviewed retrospectively. RESULTS: Two corneas from the LEBDV were transplanted before the reporting of p24 reactivity by other tissue banks. In one case, because of the young age of the recipient, the surgeon elected to replace the cornea with new tissue hours after the original transplant, and later polymerase chain reaction (PCR) testing was negative. In the other case, there was not enough specimen to perform Western blot or PCR confirmatory testing. The patient was followed with periodic serologic testing for HIV and has remained seronegative. To avoid such problems in the future, the LEBDV initiated testing of all donors with p24 and other nonrequired screening tests. Over a 2-month period, 22 corneas (from 11 donors) were discarded because of these tests: 4 donors had reactive p24 tests, 6 were reactive for antibody to hepatitis B core antigen, and 1 had a reactive syphilis test. CONCLUSIONS: Results from p24 assays by other tissue banks may cause difficult clinical situations when the results are received after transplantation of the tissue, but the use of the p24 assay in the screening of cornea donors may result in excessive waste of donor tissue. Further guidance is needed regarding the management of positive results from this and other nonrequired screening tests.

Adolescent↗
PubMed2001

Use of SoftPerm contact lenses when rigid gas permeable lenses fail.

PURPOSE: We evaluated the performance of the SoftPerm contact lens (Wesley Jessen) in patients with irregular astigmatism, usually due to keratoconus or after penetrating keratoplasty (PK), who were unable to befitwith, or intolerant of, rigid gas permeable (RGP) contact lenses. METHODS: A retrospective study of patients fit with SoftPerm lenses in the Cornea Department at Wills Eye Hospital between March 1985 and March 2000 was performed. RESULTS: Thirty-five cases were reviewed, with follow-up available in 33 cases. Most of the eyes had irregular astigmatism secondary to keratoconus (22/35,62.9%) or PK (10/35,28.6%) and had failed a trial of RGP lenses. The mean logMAR visual acuity with SoftPerm lenses was 0.13+/-0.18 (range -0.12 to 0.6). In 25 cases in which comparison with glasses or RGP lenses was possible, SoftPerm lenses provided better visual acuity than glasses in 17/25 cases (68%) with a mean difference of -0.24 (P = 0.001, paired t-test); visual acuity with SoftPerm lenses was better than RGP visual acuity in 13/25 cases (52%), with a mean difference of -0.06 (P = 0.07, paired t-test). Complications included broken lenses (16/33,48.5%), giant papillary conjunctivitis (GPC) (9/33, 27.3%), and peripheral corneal neovascularization (9/33, 27.3%). The GPC and peripheral corneal neovascularization were often delayed in presentation. The major subjective complaint was discomfort (13/33, 39.4%). At the last follow-up, the SoftPerm lens was still in use in 22/33 cases (66.7%). Discomfort was the most common reason for discontinuation. The mean duration of lens wear was 52.5+/-31.7 months, range 3 to 110 months. CONCLUSIONS: The SoftPerm lens can provide satisfactory visual correction in many cases of irregular astigmatism with RGP failure. However, problems such as frequent breakage, GPC, peripheral corneal neovascularization, and discomfort necessitate close follow-up.

Adolescent↗
PubMed2000

Reconstitution of caspase-8 sensitizes JB6 cells to TRAIL.

TRAIL induces apoptosis in various tumor cells. We report here that caspase-8 is required in TRAIL-induced cell death. Western blot analyses and enzyme assays showed that exposing Jurkat cells to TRAIL resulted in activation of caspases-8 followed by caspase-3 and -9. Acetyl-IETD-fluoromethylketone, a caspase-8 inhibitor, potently suppressed TRAIL-induced cell death compared to acetyl-DEVD-fluoromethylketone and acetyl-LEHD-fluoromethylketone, inhibitors of caspase-3 and caspase-9, respectively. JB6 cells, a caspase-8-deficient Jurkat variant, were completely resistant to TRAIL. However, reconstitution with a caspase-8, but not with caspase-2 or -3, sensitized JB6 cells to subsequent exposure to TRAIL. These results are indicative of the crucial function of caspase-8 in TRAIL-induced apoptosis in Jurkat cells.

Apoptosis↗
PubMed2000

Effect of dietary linoleate/alpha-linolenate balance on the brain lipid composition, reproductive outcome and behavior of rats during their prenatal and postnatal development.

The effect of the dietary linoleate (LA)/alpha-linolenate (LNA) balance during development on the brain lipid composition, reproductive outcome and behavior of rats was studied. Female rats were fed on experimental diets during pregnancy and the resulting pups for 16 weeks. The dietary LA/LNA ratios were 1.07 (LA1), 2.64 (LA2), 4.45 (LA3), 7.68 (LA4) and 10.35 (LA5). The relative content of docosahexaenoate (DHA) in the brain of pups tended to increase with decreasing LA/LNA ratio at 0 and 3 weeks, while the level of DHA was maintained constant at 16 weeks regardless of the dietary LA/LNA ratio. The learning ability was measured at 12 weeks of age, and there was no difference among the groups. In an open field test, the exploratory index was significantly lower in the LA1 group than in the LA2 group. The LA1 group had a smaller litter size and lower survival rate than the other groups. We conclude that if the diet contained appropriate amounts and balance of LA and LNA, it was possible for rats to synthesize an appropriate amount of DHA and have normal behavioral activity without DHA supplementation.

Animals↗
PubMed1999

Magnesium fluoride-dependent binding of small G proteins to their GTPase-activating proteins.

GTPase-activating proteins (GAPs) enhance the intrinsic GTPase activity of small G proteins, such as Ras and Rho, by contributing a catalytic arginine to the active site. An intramolecular arginine plays a similar role in heterotrimeric G proteins. Aluminum fluoride activates the GDP form of heterotrimeric G proteins, and enhances binding of the GDP form of small G proteins to their GAPs. The resultant complexes have been interpreted as analogues of the transition state of the hydrolytic reaction. Here, equilibrium binding has been measured using scintillation proximity assays to provide quantitative information on the fluoride-mediated interaction of Ras and Rho proteins with their respective GAPs, neurofibromin (NF1) and RhoGAP. High-affinity fluoride-mediated complex formation between Rho.GDP and RhoGAP occurred in the absence of aluminum; however, under these conditions, magnesium was required. Additionally, the novel observation was made of magnesium-dependent, fluoride-mediated binding of Ras.GDP to NF1 in the absence of aluminum. Aluminum was required for complex formation when the concentration of magnesium was low. Thus, either aluminum fluoride or magnesium fluoride can mediate the high-affinity binding of Rho. GDP or Ras.GDP to GAPs. It has been reported that magnesium fluoride can activate heterotrimeric G proteins. Thus, magnesium-dependent fluoride effects might be a general phenomenon with G proteins. Moreover, these data suggest that some protein.nucleotide complexes previously reported to contain aluminum fluoride may in fact contain magnesium fluoride.

Aluminum↗
PubMed1999

Cisatracurium neuromuscular block at the adductor pollicis and the laryngeal adductor muscles in humans.

We have compared the dose-response relationship (n = 30) and time course of neuromuscular block (n = 20) of cisatracurium at the laryngeal adductor and the adductor pollicis muscles. ED95 values for cisatracurium were 66.8 (95% confidence interval 61.3-72.3) micrograms kg-1 at the larynx and 45.2 (42.1-48.3) micrograms kg-1 at the adductor pollicis muscle (P < 0.0001). After administration of cisatracurium 0.1 mg kg-1, onset time was 2.7 (2.2-3.2) min at the larynx and 3.9 (3.0-4.8) min at the adductor pollicis (P < 0.0001). Time to 95% recovery of the first twitch of the TOF was 26.9 (20.1-33.7) min and 45.6 (39.7-51.5) min, respectively (P < 0.0001). We found that the laryngeal adductors were more resistant to the action of cisatracurium than the adductor pollicis muscle, but onset and recovery were faster at the larynx.

Atracurium↗
PubMed1999

Rabbits treated with chronic isepamicin are resistant to mivacurium and rocuronium.

UNLABELLED: We compared the dose-response relationships and the neuromuscular blocking effects of mivacurium and rocuronium after chronic isepamicin therapy for 7 days in 56 anesthetized rabbits. Train-of-four stimuli were applied every 10 s to the common peroneal nerve, and the force of contraction of the tibialis anterior muscle was measured. Chronic isepamicin therapy is associated with a rightward shift of the mivacurium and rocuronium dose-response curves. The effective dose for 50% twitch depression of mivacurium and rocuronium increased significantly, from 16.9 +/- 4.8 and 56.5 +/- 5.3 microg/kg, respectively, with placebo to 30.6 +/- 5.3 and 75.6 +/- 4.7 microg/kg, respectively, during isepamicin therapy. The isepamicin rabbits receiving mivacurium 0.18 mg/kg or rocuronium 0.6 mg/kg had an accelerated recovery from neuromuscular blockade compared with those receiving placebo. The results of this study show that mivacurium and rocuronium have both a decreased effect and a shorter duration of action in rabbits when used during concurrent isepamicin therapy. IMPLICATIONS: We studied the dose-response relationships and the neuromuscular blocking effects of mivacurium and rocuronium during chronic isepamicin therapy in rabbits. Mivacurium and rocuronium have both a decreased effect and a shorter duration of action during chronic aminoglycoside antibiotic therapy in rabbits.

Androstanols↗