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C K Lin

Publications and source records attributed to C K Lin.

At least 73 records · Page 4Linked to original sources

Development and use of 16S rRNA gene targeted PCR primers for the identification of Escherichia coli cells in water.

The primary sequences of the V3 and V6 regions of the 16S rRNA gene of pathogenic and non-pathogenic strains of Escherichia coli were determined and compared with those obtained for a number of reference strains which belong to the family Enterobacteriaceae. Three oligonucleotide primers 16E1, 16E2 and 16E3 were designed and used in the polymerase chain reaction to identify specifically all E. coli isolates. When 16E1, 16E2 and 16E3 were used as primers for the identification of E. coli cells present in tap, underground and pond waters, as low as 1 cfu 100 ml-1 of water could be detected if an 8 h pre-culture step was performed prior to the PCR reaction.

DNA Primers↗

Dissolution difference between acidic and neutral media of acetaminophen tablets containing a super disintegrant and a soluble excipient. II.

The disintegration and dissolution of acetaminophen tablets containing sucrose and Ac-Di-Sol/Primojel was significantly different between acidic and neutral media. The purpose of this study was to investigate the mechanism of this phenomenon and to propose a way of reducing the dissolution difference between the two media. Tablets of different combinations of active ingredient, sucrose, and Ac-Di-Sol/Primojel were prepared and their dissolution in various media was evaluated. The dissolution differences were found to be largely related to the hydrophobicity of the active ingredient and pH difference of the two media. This difference was even more evident under the condition where acetaminophen, sucrose, and Primojel were combined. The dissolution difference was therefore attributed to the depressed function of Primojel in the acidic medium, the stronger binding of sucrose, the hydrophobicity of the active ingredient and pH difference of the two media. Increasing the concentration of Primojel or incorporating the surfactant in the tablet can thus greatly decrease the dissolution difference between acidic and neutral media.

Acetaminophen↗

The first case of the p phenotype in a Gurkha Nepalese.

A serum sample from a Gurkha Nepalese soldier, residing in Hong Kong, was found to cause hemolysis of reagent ABO red cells (RBCs) in the reverse blood grouping test. Subsequent follow-up studies revealed that he was of the p phenotype, with potent anti-PP1Pk that was strongly hemolytic both at room temperature and 37 degrees C. The anti-PP1Pk was composed of IgG and IgM, and its various components were separable.

Journal Article↗

Anti-IgM-induced growth inhibition and apoptosis are independent of ornithine decarboxylase in Ramos cells.

Ornithine decarboxylase (ODC) is a key enzyme involved in polyamine production and is thought to regulate growth and apoptosis in multiple cell systems. A potential link between ODC and growth may involve the action of an oncogene c-myc which is thought to transcriptionally regulate ODC. We have examined the involvement of ODC in anti-IgM-induced growth inhibition and apoptosis in Burkitt's lymphoma cells. Inhibitors of ODC such as difluoromethylornithine (DFMO) completely blocked ODC activity, resulting in growth inhibition but not apoptosis. Addition of putrescine, the product of ODC enzymatic action, to Ramos cells had only a minor effect on growth, did not cause apoptosis, did not augment or block anti-IgM-mediated growth inhibition and apoptosis, but did reverse DFMO-mediated growth inhibition. Anti-IgM treatment of Ramos cells, which markedly decreased c-myc mRNA and protein, caused a paradoxical increase in ODC mRNA level as well as ODC enzymatic activity and increased cellular levels of putrescine. DFMO and putrescine did not alter c-myc mRNA levels directly, nor did they have any affects on anti-IgM-mediated down-regulation of c-myc mRNA. TNF-alpha, which inhibited anti-IgM-mediated apoptosis, did not inhibit either anti-IgM or DFMO-mediated inhibition of growth. These agents were without effect on ODC activity itself or on the anti-IgM-mediated increase in ODC activity. From these studies we conclude that ODC inhibition affects growth but is unrelated to the induction of apoptosis. Both anti-IgM-mediated inhibition of growth and induction of apoptosis are independent of ODC. Thus two distinct pathways for growth regulation are present: one in which ODC and polyamines are important and the other cell surface receptor-mediated (sIg) which is independent of ODC and polyamines.

Apoptosis↗

Complete coding sequence of hepatitis C virus genotype 6a.

Hepatitis C virus (HCV) genotype 6a is found in a restricted part of South East Asia, including Hong Kong, Macau and Vietnam. We determined the full length coding sequence of a type 6a isolate (EUHK2) obtained from a Hong Kong blood donor. The sequence of EUHK2 contained a single open reading frame coding for a polyprotein of 3018 amino acids, within the range of 3008 to 3037 for other HCV genotypes. The full length sequence of EUHK2 showed 30.3%-32.9% nucleotide (24.3%-29.4% amino acid) sequence divergence from genotypes 1-4, but only 27.7% (20.7% amino acid) divergence from JK046 ("type 11a"). These similarity values were intermediate between those of other HCV genotypes (minimum 28.4%) and between subtypes (maximum 25%). The close evolutionary relationship of EUHK2 with JK046 was further indicated by their grouping together by phylogenetic analysis.

Cloning, Molecular↗

Emergency banding ligation versus sclerotherapy for the control of active bleeding from esophageal varices.

Active bleeding varices are a great challenge to endoscopists. In this study, we compared the short-term efficacy and safety of banding ligation with injection sclerotherapy in the arresting of active bleeding from esophageal varices. Seventy-one cirrhotic patients with active variceal bleeding were randomized to receive banding ligation (37 patients) or sclerotherapy (34 patients) immediately after endoscopic examinations. Primary success rate (bleeding stopped for 72 hours) was 97% in the ligation group and 76% in the sclerotherapy group (P = .009). The efficacy of ligation was similar to sclerotherapy in the control of oozing varices (100% vs. 89%, P = .23), whereas ligation was superior to sclerotherapy in the control of spurting varices (94% vs. 62%, P = .012). The requirement of vasoconstrictors after emergency endoscopic treatment was lower in the ligation group than in the sclerotherapy group (11% vs. 41%, P = .007). Treatment failure within 1 month was 8% in the ligation group vs. 30% in the sclerotherapy group (P = .02). Blood transfusion requirements were significantly lower in the ligation group than in the sclerotherapy group (3.2 +/- 1.2 vs. 4.5 +/- 1.8 units, P < .01). Rebleeding rate within 1 month was 17% in the ligation group and 33% in the sclerotherapy group (P = .19). Significant complications were encountered in 5% of the ligation group and 29% of the sclerotherapy group (P = .007). Mortality rates within 1 month were 19% in the ligation group and 35% in the sclerotherapy group (P = .19). Banding ligation and sclerotherapy were comparable in the arresting of oozing varices, whereas ligation was superior to sclerotherapy in the control of spurting varices. Patients treated with ligation required fewer vasoconstrictors and fewer transfusion units than patients treated with sclerotherapy. Furthermore, banding ligation was associated with a lower complication rate than sclerotherapy.

Adult↗

Correlation of serum immunoglobulin G Helicobacter pylori antibody titers with histologic and endoscopic findings in patients with dyspepsia.

Serum immunoglobulin G (IgG) antibody tests are used extensively. We attempted to find out whether the titers of anti-Helicobacter pylori IgG antibody correlated with the degree of macroscopic gastrointestinal damage, the severity of antral gastritis, and the density of antral H. pylori colonization in symptomatic patients. Peripyloric antral biopsy specimens were obtained from 50 consecutive patients with dyspepsia undergoing upper gastrointestinal endoscopy. The macroscopic gastrointestinal damage and the histologic grades of antral gastritis were scored by a modified Lanza scale and Sydney system, respectively. In addition, the densities of antral H. pylori colonization were graded semiquantitatively. Serum IgG antibodies to H. pylori were measured by enzyme-linked immunosorbent assay. Thirty-six (M/F = 29/7) of the 50 patients had H. pylori infection documented by histologic examination or rapid urease test or both. Among the subjects, the IgG antibody titers to H. pylori correlated significantly with the grades of antral polymorphonuclear cell infiltration (p = 0.002) and antral bacterial density (p = 0.01) but not with endoscopic scores, the grades of mononuclear cell infiltration, mucosal atrophy, or intestinal metaplasia (p > 0.05). In addition, endoscopic scores also were found to be significantly correlated with antral bacterial density (p = 0.049) and the grade of polymorphonuclear cell infiltration (p = 0.012). We therefore conclude that high titers of IgG antibody to H. pylori in patients with dyspepsia indicate dense H. pylori colonization and severe antral polymorphonuclear cell infiltration. However, it cannot replace endoscopic examination to evaluate the degree of macroscopic gastrointestinal damage.

Aged↗

Prediction of recurrent choledocholithiasis by quantitative cholescintigraphy in patients after endoscopic sphincterotomy.

BACKGROUND: Endoscopic sphincterotomy (EST) is widely used for the removal of stones from the bile duct, but stones recur in about one fifth of patients. AIMS: To investigate hepatic clearance by quantitative cholescintigraphy (QC) in patients after EST and to discern the relationship between biliary emptying and stone recurrence. METHODS: One hundred and forty nine patients who had EST and clearance of the bile duct for choledocholithiasis were selected. All patients were confirmed to have complete EST by sphincter of Oddi manometry and underwent QC soon after normalisation of liver function. Regular clinical follow up was performed for each patient. RESULTS: During a mean 36 month follow up, 22 (14.8%) patients developed recurrent stones in the bile duct. Irrespective of the status of the gall bladder, patients with recurrent stones had a slower hepatic clearance of radioisotope during QC compared with patients without stone recurrence, but only the differences in cholecystectomised patients had statistical significance. After carrying out multivariate analysis, one parameter of QC, percentage clearance of maximal count at 45 minutes, was found to be the only significant factor for stone recurrence. All recurrent stones in the common bile duct were successfully removed at endoscopy. CONCLUSION: Slower hepatic clearance as shown by QC is an important factor responsible for stone recurrence after sphincter ablation.

Adult↗

Report on anti-Dib encountered in two Hong Kong Chinese.

Two cases of anti-Dib, a rarely encountered antibody, were identified in serum samples referred by hospital blood banks during the past 13 months. Case 1 is a 41-year-old female who required blood for elective surgery. Case 2 is a premature infant suffering from mild neonatal jaundice on day 2 after birth. The anti-Dib in both cases exhibited marked dosage effect. The titer/score against Di(a+b+) and Di(a-b+) red blood cells (RBCs) in case 1 was 8/10 and 32/32, respectively, and in case 2, 4/18 and 32/46. The monocyte monolayer assay (MMA) also gave a similar pattern of results, being l5 percent and 100 percent reactive when tested with Di(a+b+) and Di(a-b+) RBCs in case 1, and 0.4 percent (within normal range) and l4.4 percent in case 2. The patient in case 1 underwent her operation without blood transfusion. The infant in case 2 was treated by phototherapy and subsequently recovered without the need for exchange transfusion.

Journal Article↗

Expression of DNA topoisomerase II alpha and multidrug resistance p-glycoprotein in acute leukemia.

BACKGROUND: Drug resistance is a major cause of treatment failure in acute leukemia. Overexpression of multidrug resistance gene and decreased activity of topoisomerase II alpha are suggested as two important mechanisms for this resistance. METHODS: We used immunohistochemical method to determine the expressions of both topoisomerase II alpha (topo II alpha) and p-glycoprotein (gp-170) in bone marrow biopsy specimens from 68 cases of acute leukemia. Patients were divided into four groups: (1) leukemia cells with high score for topo II alpha and negative for gp-170; (2) leukemia cells with high score for topo II alpha and positive for gp-170; (3) leukemia cells with low score for topo II alpha and negative for gp-170; and (4) leukemia cells with low score for topo II alpha and positive for gp-170. The clinical responses were then followed as routine, and the clinical correlation was evaluated by analysis of variance and Pearson Chi-Square test. RESULTS: The measure of the single parameter (either topo II alpha or gp-170 alone) did not show a significant difference in the overall survival. However, the complete response rate was much higher in the first group patients whose bone marrow reading score was high in topo II alpha and negative for gp-170 expression. Survival duration increased with the increase in the complete response rate. CONCLUSIONS: Combined parameters of topo II alpha and gp-170 are more useful than any individual parameter for the prognosis of acute leukemia.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Anti-IgM-mediated regulation of c-myc and its possible relationship to apoptosis.

Anti-IgM treatment of Burkitt's lymphoma cells is followed by either growth arrest or induction of apoptosis. In this study we have explored the role of c-myc in these events. Our results in Ramos cells indicate the following. (a) The decline in c-myc mRNA occurs at about 4 h; inhibition of about 80% being observed. (b) The stability of c-myc message is involved since the half-life of c-myc mRNA is decreased from about 30 min in untreated cells to about 15 min following treatment with anti-IgM. In the presence of cycloheximide, a protein synthesis inhibitor, the half-life is increased to about 50 min and was unaltered by treatment with anti-IgM. (c) By contrast, nuclear run-on experiments indicated no change in transcription rates for c-myc message due to treatment with anti-IgM. (d) A decrease in c-myc causes apoptosis since specific repression of c-myc with antisense oligonucleotides decreases the levels of c-Myc, inhibits growth rate, decreases viability, and induces apoptosis. (e) Anti-CD40 inhibition of apoptosis occurs without alteration in anti-IgM-induced down-regulation of c-myc mRNA, suggesting that it acts distally to c-myc down-regulation. Other cell lines were also investigated. In Epstein-Barr virus (EBV)-positive cell lines (Daudi, Raji, and Namalwa), anti-IgM treatment for 24 h results in growth inhibition without induction of apoptosis. In EBV-negative cell lines (ST486 and CA46, as well as Ramos), a more heterogeneous pattern of responses to anti-IgM are observed. Ramos and ST486 cells both show growth inhibition and apoptosis upon anti-IgM treatment; CA46 cells shown only growth inhibition but not apoptosis. Anti-IgM causes a decline in c-myc mRNA levels in all of these lines, as well as in c-Myc protein level in the two lines investigated, Daudi and Ramos, regardless of apoptosis. Addition of antisense c-myc oligonucleotides to the cells reduced growth in both Daudi and Ramos cells lines, however it resulted in substantial apoptosis only in Ramos cells. These results suggest that anti-IgM destabilizes c-myc mRNA by a process that involves mRNA turnover, rather than transcription rates. However anti-IgM exerts differential effects in EBV-positive and EBV-negative cell lines. EBV-positive cells are uniformly resistant to apoptosis, while EBV-negative cell lines show a tendency to apoptosis but with exceptions. Growth inhibition can be uncoupled from apoptosis in EBV-positive cell lines, but not in those EBV-negative cell lines prone to apoptosis. Furthermore, down-regulation of c-myc message correlates with growth inhibition in these cells, but is an insufficient link to apoptosis. By contrast inhibition of apoptosis by anti-CD40 occurs even though c-myc mRNA is decreased.

Antibodies, Anti-Idiotypic↗

TNF-alpha inhibits anti-IgM-mediated apoptosis in Ramos cells.

We have examined the effects of tumor necrosis factor-alpha (TNF-alpha) as an inducer or modulator of necrosis and/or apoptosis in B cell lines. TNF-alpha does not induce either necrosis or apoptosis in EBV-positive or -negative cell lines, regardless of the culture conditions of the cells or the presence or absence of cytokines. By contrast anti-IgM induces apoptosis in two EBV-negative cell lines (Ramos and ST486) but not in EBV-positive cell lines. Since TNF receptor and CD40 belong to the TNF receptor superfamily and anti-CD40 is a known inhibitor of apoptosis, we tested for TNF-alpha's effects on the inhibition of apoptosis induced by anti-IgM. Our results indicate that TNF-alpha inhibits apoptosis induced by anti-IgM in Ramos cells but not in ST486. The effects are dose and time dependent; the degree of apoptosis achieved and the selectivity of the effect among cell lines are strikingly similar for both TNF-alpha and anti-CD40. Furthermore when both agents are tested together no additivity in the inhibition is observed. The inhibition of apoptosis is a direct effect of TNF-alpha and not a permissive effect of another cytokine, since it is observed in defined medium. Although anti-IgM induces both TNF-alpha secretion and TNF receptors in Ramos cells, the concentration of secreted TNF-alpha is too low to affect apoptosis. Inhibition does not involve perturbation of the cell cycle distribution of Ramos cells. Furthermore rapid induction of c-fos and the decrease in c-myc observed after anti-IgM treatment are both unaltered by TNF-alpha. Our results suggest that TNF-alpha is an inhibitor of apoptosis in Ramos cells, that its overall pattern of inhibition is similar to that of anti-CD40, and that both agents act at some point distal to the alteration of c-fos and c-myc by anti-IgM.

Apoptosis↗

Detection and clinical features of hepatitis C virus type 6 infections in blood donors from Hong Kong.

The genotype distribution of hepatitis C virus (HCV) was investigated in 212 viraemic blood donors from Hong Kong. A subset of the samples was investigated using three different genotyping assays to establish the accuracy of each in this population. These assays were restriction fragment length polymorphism (RFLP) of amplified 5' noncoding region (5'NCR) sequences, RFLP of the core region, and a serotyping assay using peptides from two antigenic regions of NS4. Genotypes detected in Hong Kong blood donors were 1a (6.2%), 1b (58.8%), 2a (1.4%), 2b (1.4%), 3a (1.9%), and 6a (27.0%). All genotyping assays produced concordant results. No evidence was obtained for the presence of type 6 group variants recently identified in Southeast Asia, other than type 6a. A serotyping assay based upon the detection of type-specific antibody to epitopes in NS4 produced similar results to the genotyping assays (98% concordance), but a reduced sensitivity (75%) compared with genotyping methods. Sequence variation in NS4 was not the cause of the reduced rate of detection of type 6 antibody in this population. Eighty-four percent donors infected with type 6a were male, compared to 75% donors infected with type 1b. The median alanine transaminase (ALT) level in type 6 infected donors was lower than in type 1b, (43.8 and 51.1 U/l, respectively) although these values were not statistically significant (P = 0.094). There was no significant difference between the ages of donors infected with types 1b and 6a. Risk factors for HCV infection in the blood donors included blood transfusion, intravenous drug abuse, and tattooing. A significantly greater number of donors infected with HCV-6a reported a history of drug abuse (66%) than donors infected with HCV-1b (7%).

Adolescent↗

When to discharge patients with bleeding peptic ulcers: a prospective study of residual risk of rebleeding.

BACKGROUND: From January 1993 to December 1994, we conducted a prospective study to investigate the evolutionary change of rebleeding risk in bleeding peptic ulcers. To obviate possible confounding factors that would influence decision making for discharge of patients, subjects with coexistent acute illnesses, systemic bleeding disorders, alcoholism, and use of nonsteroidal anti-inflammatory drugs were excluded. METHODS: Emergency endoscopies were performed in patients with hematemesis or a melena within 24 hours of admission. Ulcer lesions were divided into six categories according to endoscopic findings. The residual risks of rebleeding of each type of ulcers were calculated for 10 days, and the critical point of acceptable rebleeding risk after discharge was set at 3%. RESULTS: Three hundred ninety-two patients with bleeding peptic ulcers completed the study. The ulcers, characterized by clean bases, red or black spots, adherent clots, nonbleeding visible vessels without local therapy, nonbleeding visible vessels with local therapy, and bleeding visible vessels with local therapy took 0, 3, 3, 4, 4, and 3 days, respectively, to decrease rebleeding risk to below the critical point. All episodes of fatal rebleeding (n = 4) occurred within 24 hours after admission. CONCLUSIONS: Patients with clean-based ulcers can be discharged in the first day of admission. The optimal duration required for hospitalization of patients with ulcers characterized by nonbleeding visible vessels at initial endoscopy is 4 days. The remaining patients with ulcers marked by other bleeding stigmata may be discharged after a 3-day observation.

Adolescent↗

The impact of endoscopic variceal ligation on the pressure of the portal venous system.

BACKGROUND/AIMS: Endoscopic variceal ligation is a viable substitute for injection sclerotherapy. It is still not known how endoscopic variceal ligation may influence the portal venous system. To clarify this issue we investigated the impact of endoscopic variceal ligation on the pressure of the portal venous system. METHODS: Twenty-nine patients with a history of esophageal variceal bleeding but without ascites were enrolled. All had cirrhosis; 63% of them were post-hepatitic. Ligation was performed at intervals of 2-3 weeks until all the varices were obliterated. Portal venograms were performed before institution of ligation and after variceal obliteration to assess venographic findings and pressure changes. The pressures of the main portal vein, splenic vein and superior mesenteric vein were recorded. RESULTS: Twenty-five patients completed the study. A mean of 4.4 sessions (range: 2-7) of ligation over a period of 2 months was needed. Seventeen (68%) patients experienced elevated pressure and eight (32%) patients reduced pressure after ligation. Mean (median) pressure changes were as follows: portal venous pressure, 26.5 +/- 4.7 (25.0) mmHg vs. 28.2 +/- 7.2 (28.0) mmHg (p > 0.05); splenic venous pressure, 28.2 +/- 4.9 (26.0) mmHg vs. 29.0 +/- 6.8 (29.0) mmHg (p > 0.05); superior mesenteric venous pressure, 28.4 +/- 6.0 (27.0) mmHg vs. 29.5 +/- 7.0 (29.0) mmHg (p > 0.05). Five patients (20%) experienced rebleeding before variceal obliteration; all of them presented elevated portal pressures after variceal obliteration. Among the eight patients with decreased portal pressure, seven (87%) had other major collaterals apart from esophageal varices, compared to three out of the 17 (18%) patients with elevated portal pressure who had other major collaterals (p < 0.01). CONCLUSIONS: Among patients receiving endoscopic variceal ligation, 68% experienced elevated portal pressure, while 32% had decreased portal pressure. Elevation of portal pressure after variceal ligation may be an important factor in variceal rebleeding. The presence of other major collaterals apart from esophageal varices may be responsible for the decrease in portal pressure after obliteration of esophagel varices.

Adult↗

First case of haemolytic disease of the newborn due to anti-Mur in Hong Kong.

The fifth child of a Hong Kong Chinese mother developed moderate jaundice, attributable to antibodies (anti-Mi) against antigenic determinants in GP.Mur (Miltenberger, class III) red cells. Both the father and the eldest sister were of the phenotype GP.Mur. Testing of maternal serum against a red cell panel including cells known to carry the antigenic determinants of some Miltenberger phenotypes revealed the presence of anti-Mur. This report documents the first case of haemolytic disease of the newborn (HDN) due to anti-Mur in Hong Kong.

Antibodies↗

Use of two 16S DNA targeted oligonucleotides as PCR primers for the specific detection of Salmonella in foods.

A 16S DNA targeted polymerase chain reaction (PCR) method specific for the detection of Salmonella isolates with various serotypes was developed. The primers used for such a PCR method were 16SF1 and 16SIII. 16SF1 is the reverse and complementary strand of 16SI which has been shown to be able to hybridize with Salmonella and Citrobacter spp. 16III on the other hand, is able to hybridize with Klebsiella and Serratia spp. in addition to Salmonella. Although 16SF1 and 16SIII were not specific to Salmonella only, when they were used as PCR primers, only the Salmonella isolates could be specifically detected. The interference from Citrobacter, Klebsiella and Serratia spp. could be prevented. None of the other non-Salmonella isolates including strains of the family of Enterobacteriaceae closely related to Salmonella would generate the false-positive reaction. When this PCR system was used for the detection of Salmonella cells artificially contaminated in food samples, results obtained were satisfactory. A detection limit of N x 10(0) cells per assay could be obtained.

Base Sequence↗