Biomedical subjects

J H Oh

Publications and source records attributed to J H Oh.

At least 37 records · Page 2Linked to original sources

PubMed2000

Treatment of prostatic abscess: value of transrectal ultrasonographically guided needle aspiration.

The purpose of this study was to assess the effectiveness of transrectal ultrasonographically guided needle aspiration in the treatment of prostatic abscess. Fourteen patients with prostatic abscess were evaluated with this technique and treated with sonographically guided needle aspiration. Using this technique, all cases (100%) had one or more hypoechoic areas within the prostate that contained inhomogeneous materials; in 10 patients (71.0%), the lesion showed internal septa or solid portion. The margins of the hypoechoic area were well defined and thick in 11 patients (79.0%) and poorly defined in 3 patients (21.0%). The estimated volume of the prostatic abscess ranged between 2 and 28 ml (mean, 12.0 ml). The presence of a pus collection within the prostate was confirmed by transrectal ultrasonographically guided aspiration in all patients. However, successful treatment of prostatic abscess with transrectal needle aspiration was done in 12 (86.0%) of 14 patients; the treatment failed in 2 (14.0%) of 14 patients. One patient was treated with perineal incision and drainage and the other with transurethral resection. The amount of pus drained ranged between 1 and 39 ml (mean, 12.0 ml). On follow-up transrectal ultrasonographic examination, no remaining abscess pocket was found within the prostate in any of the cases. One year later, the prostatic abscess recurred in one case. In conclusion, transrectal ultrasonographic guidance is useful in the diagnosis of prostatic abscess as well as in the guidance for aspiration and the drainage of such abscesses. Transrectal ultrasonographically guided needle aspiration could be an effective method for treating prostatic abscess.

Abscess↗

PubMed1999

Establishment and characterization of 12 human colorectal-carcinoma cell lines.

In this article, we describe the characteristics of 12 human colorectal-carcinoma cell lines established from 6 primary tumors and 6 metastatic sites of 11 Korean colorectal-carcinoma patients, including the morphology in vivo and in vitro and mutations of K-ras2, p15, p16, p53, APC, beta-catenin, hMLH1 and hMSH2 genes in vitro. No lines were contaminated with Mycoplasma or bacteria. All lines were proven to be unique by DNA-fingerprinting analysis. All lines expressed the surface carcino-embryonic antigen and secreted it into the supernatant fluid. The morphological correlation between the original tumors and cultured cells suggested that the original tumors showing mucinous adenocarcinoma correlated with floating aggregates in culture, and degree of desmoplasia in the original tumor correlated with attached growth in culture. Five of the cell lines showed mutations in the K-ras2 gene, and 6 of the cell lines showed mutations in the p53 gene. The p15 gene was deleted in 2 cell lines, and the p16 gene was hypermethylated in 3 cell lines. The mutation of mismatch-repair genes (hMLH1 and hMSH2) was found in 4 lines, the APC gene and beta-catenin gene were mutated in 9 and 2 lines respectively. These well-characterized colorectal-cancer cell lines should serve as useful tools for investigating the biological characteristics of colorectal cancer.

Adaptor Proteins, Signal Transducing↗

PubMed1999

Do symptoms predict cardiac arrhythmias and mortality in patients with syncope?

BACKGROUND: Patients with syncope frequently present with multitude of other symptoms but their significance in predicting morbidity or mortality has not been previously studied. OBJECTIVE: To determine if certain symptoms can be used to identify syncope patients at risk for cardiac arrhythmias, mortality, or recurrence of syncope. PATIENTS AND METHODS: From August 1987 to February 1991, we prospectively evaluated patients with syncope from outpatient, inpatient, and emergency department services of a university medical center. These patients were interviewed, charts were reviewed, and detailed information on 19 symptoms and comorbidities was obtained. A cause of syncope was assigned using standardized diagnostic criteria. All patients were followed up at 3-month intervals for at least 1 year for recurrence of syncope and mortality. Patients in whom the cause of syncope was determined by medical history and physical examination alone were not included in our analysis. RESULTS: History and physical examination led to the cause of syncope in 222 of 497 patients enrolled. In the remaining 275 patients, the absence of nausea and vomiting before syncope (odds ratio, 7.1) and electrocardiographic abnormalities (odds ratio, 23.5) were predictors of arrhythmic syncope. Underlying cardiac disease was the only predictor of 1-year mortality. No symptom remained as independent predictor for 1-year mortality or syncope recurrence. CONCLUSIONS: Symptoms, although important in assigning many noncardiac causes, are not useful in risk-stratifying patients whose cause of syncope cannot be identified by other history and physical examination. Triage decisions and management plans should be based on pre-existing cardiac disease or electrocardiographic abnormalities, which are important predictors of arrhythmic syncope and mortality.

Adolescent↗

PubMed1999

Ginsenoside RH-2 induces apoptotic cell death in rat C6 glioma via a reactive oxygen- and caspase-dependent but Bcl-X(L)-independent pathway.

We used the rat C6 gliomal cell line to investigate the potential role of ginsenoside Rh2 (G-Rh2) in brain tumor. G-Rh2 induced many apoptotic manifestations in C6 gliomal cells as evidenced by changes in cell morphology, generation of DNA fragmentation, activation of caspase and production of reactive oxygen species (ROS). As a result, cotreatment with antioxidants or a broad-spectrum caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone effectively attenuated G-Rh2-induced cell death. However, specific cleavage of poly(ADP-ribose)polymerase into 85 kDa protein was not detected as demonstrated in many other apoptotic paradigms. Expression levels of Bcl-2 and Bax remained unchanged following G-Rh2 treatment. Furthermore, G-Rh2-induced cell death in C6 gliomal cells overexpressing antiapoptotic protein, Bcl-X(L), was comparable to that in parental cells. Taken together, our data indicate that G-Rh2-induced cell death is mediated by the generated ROS and the activation of caspase pathway in a Bcl-X(L)-independent manner.

Animals↗

PubMed1999

Sequential cleavage of poly(ADP-ribose)polymerase and appearance of a small Bax-immunoreactive protein are blocked by Bcl-X(L) and caspase inhibitors during staurosporine-induced dopaminergic neuronal apoptosis.

To assess the role of Bcl-X(L) and its splice derivative, Bcl-X(S), in staurosporine-induced cell death, we used a dopaminergic cell line, MN9D, transfected with bcl-xL (MN9D/Bcl-X(L)), bcl-xS (MN9D/Bcl-X(S)), or control vector (MN9D/Neo). Only 8.6% of MN9D/Neo cells survived after 24 h of 1 microM staurosporine treatment. Caspase activity was implicated because a caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-fmk), attenuated staurosporine-induced cell death. Bcl-X(L) rescued MN9D cells from death (89.4% viable cells), whereas Bcl-X(S) had little or no effect. Bcl-X(L) prevented morphologically apoptotic changes as well as cleavage of poly(ADP-ribose)polymerase (PARP) induced by staurosporine. It is interesting that a small Bax-immunoreactive protein appeared 4-8 h after PARP cleavage in MN9D/Neo cells. The appearance of the small Bax-immunoreactive protein, however, may be cell type-specific as it was not observed in PC12 cells after staurosporine treatment. The sequential cleavage of PARP and the appearance of the small Bax-immunoreactive protein in MN9D cells were blocked either by Z-VAD-fmk or by Bcl-X(L). Thus, our present study suggests that Bcl-X(L) but not Bcl-X(S) prevents staurosporine-induced apoptosis by inhibiting the caspase activation that may be directly or indirectly responsible for the appearance of the small Bax-immunoreactive protein in some types of neurons.

Animals↗

PubMed1999

Screening of Korean forest plants for rat lens aldose reductase inhibition.

Naturally occurring substances which can prevent and treat diabetic complications were sought by examining ethanol extracts prepared from Korean forest plants for their inhibitory effects on rat lens aldose reductase activity in vitro. Among the plants examined, Acer ginnala, Illicium religiosum and Cornus macrophylla exerted the most strong inhibitory activity on aldose reductase.

Aldehyde Reductase↗

PubMed1999

Effect of eradication of Helicobacter pylori on the benign gastric ulcer recurrence--a 24 month follow-up study.

OBJECTIVES: To evaluate the effect of eradication of Helicobacter pylori (H. pylori) on the recurrence of benign gastric ulcer (BGU) in the patients with BGU. METHODS: This study was performed for 40 H. pylori-positive BGU patients cured of BGU and H. pylori eradicated, and for 25 H. pylori-positive patients (non-eradicated group) who were not treated with H. pylori eradication regimen or H. pylori was not eradicated. Four different methods--CLOtest, microscopy of Gram stained mucosal smear, culture and histology of modified Giemsa staining--were taken for identifying colonization of H. pylori before treatment, and 4 weeks after completion of triple therapy. For the control group in which triple therapy was not tried, follow-up gastroscopy was done to confirm the healing of the ulcer. To detect BGU recurrence, the gastroscopy was performed at 6, 12, 18, and 24 months after therapy. RESULTS: In the non-eradicated group, the BGU recurrence rate was 16% within 6 months, 40% within 1 year, 56% within 18 months and 60% within 2 years. The respective recurrence rates in the 40 patients in whom the bacteria had been eradicated were 0%, 7.5%, 10% and 10% (4 patients), respectively. Among the four BGU-recurred patients in whom H. pylori had been eradicated, one patient was found to have BGU recurring with H. pylori positive again in one year, and another two patients had NSAIDs ingestion history. CONCLUSION: The eradication of H. pylori in patients with BGU reduces the recurrence of BGU. In addition, the major causes of BGU recurrence look like NSAIDs ingestion and reinfection of H. pylori.

Adult↗

PubMed1998

Analysis of the gene encoding cyclomaltodextrinase from alkalophilic Bacillus sp. I-5 and characterization of enzymatic properties.

The gene encoding cyclomaltodextrinase (CDase) was cloned from alkalophilic Bacillus sp. I-5. The nucleotide sequence of the gene was determined and the physicochemical properties of the enzyme were investigated. The gene had an open reading frame of 559 amino acids with a predicted molecular weight of 64,884. The enzyme was purified to near homogeneity from Escherichia coli cells carrying a recombinant plasmid that contained the CDase gene. The enzyme hydrolyzed cyclomaltoheptaose (beta-CD) 13 times better than starch and 33 times better than pullulan, and it had transglycosylation activity. The enzyme also hydrolyzed acarbose, a pseudotetrasaccharide inhibitor of glucosidases. The enzyme was stabilized by Ca2+ and the activity was increased more than twofold in the presence of 5 mM EDTA. The optimum temperature of the enzyme was elevated from 40 to 50 degrees C by Ca2+ ion and the thermal activity was maintained more than 80% at 60 degrees C in the presence of Ca2+. Comparison of known amino acid sequences of several amylolytic enzymes with cyclomaltodextrinase activity, site-directed mutagenesis of the enzyme, and substrate specificity of the enzyme imply that the region between the third and the fourth conserved regions of the enzyme may play an important role in binding and degradation of cyclomaltodextrin.

Acarbose↗

PubMed1998

Overexpression of HA-Bax but not Bcl-2 or Bcl-XL attenuates 6-hydroxydopamine-induced neuronal apoptosis.

Bax, a member of the Bcl-2 gene family, is known to promote apoptosis in many cases but to block cell death under certain conditions. To investigate the potential role of Bax in 6-hydroxydopamine (6-OHDA)-induced cell death, we first established and characterized a dopaminergic neuronal cell line (MN9D) stably overexpressing hemagglutinin epitope-tagged Bax (MN9D/HA-Bax) as well as control clones (MN9D/Neo). Treatment of MN9D/Neo cells with 6-OHDA induced typical apoptotic cell death accompanied by shrinkage of the cell, nuclear condensation, and DNA fragmentation as demonstrated by light microscopy and agarose gel analysis. Overexpression of HA-Bax in MN9D cells was shown to attenuate 6-OHDA-induced cell death as determined by the MTT reduction assay and agarose gel analysis for DNA fragmentation. Western blot analysis revealed that cleavage of poly(ADP-ribose)polymerase induced by 6-OHDA was attenuated in MN9D/HA-Bax cells. In contrast, overexpression of a well-known cell death-inhibiting protein such as Bcl-2 or Bcl-XL did not attenuate 6-OHDA-induced cell death. Interestingly, cell death induced by hydrogen peroxide (0.25-2.0 mM) was significantly accelerated, whereas the rate of cell death induced by menadione (10-50 microM) was not affected in MN9D/HA-Bax cells. Thus, our present data suggest that the functionally diverse roles of Bax may be determined by the type of stress applied to the cell.

Animals↗

PubMed1998

Mechanisms of cardiomyoplasty: comparative effects of adynamic versus dynamic cardiomyoplasty.

BACKGROUND: The apparent paradox seen in patients who have undergone dynamic cardiomyoplasty and shown substantial clinical and functional improvements with only modest hemodynamic changes may be due to inappropriate end points chosen for study, a result of incomplete understanding of mechanisms involved. The purpose of this study was to compare the relative role of the passive "girdling effect" and the dynamic "systolic squeezing effect" of the wrapped muscle in cardiomyoplasty. METHODS: The control group of 6 dogs underwent 4 weeks of rapid pacing (250 beats/min) to induce severe heart failure followed by 8 weeks of observation without rapid pacing. The trajectory of recovery in hemodynamics and cardiac dimensions was followed with echocardiography and Swan-Ganz catheters. In the "adynamic" cardiomyoplasty group (n=4), the left latissimus dorsi muscle was wrapped around the ventricles and allowed to stabilize and mature for 4 weeks. This was followed by rapid pacing and recovery as in the control group. In the "dynamic" cardiomyoplasty group (n=3), the same protocol for the adynamic group was followed except that a synchronizable cardiomyostimulator was attached to the thoracodorsal nerve of the muscle wrap. This allowed the latter to be transformed during the rapid-pacing phase and permitted dynamic squeezing of the muscle wrap to be generated by burst stimulation synchronized with cardiac contraction in a 1:2 ratio. RESULTS: Baseline data were comparable in all groups prior to rapid pacing. After 4 weeks of rapid pacing, the left ventricular ejection fraction was higher in the adynamic (27.0%+/-3.9%; p < 0.05) and dynamic (33.3%+/-2.3%; p < 0.02) cardiomyoplasty groups compared with controls (18.8%+/-8.3%). Similarly, ventricular dilatation in both systole and diastole was less in the adynamic (51.8+/-8.7 mL, [p < 0.002] and 38.2+/-7.2 mL [p < 0.001], respectively) and dynamic (62.0+/-7.2 [p < 0.02] and 41.3+/-3.5 mL [p < 0.005], respectively) cardiomyoplasty groups compared with controls. In the dynamic group, on and off studies were carried out after cessation of rapid pacing while the heart was still in severe failure, and they demonstrated a systolic squeezing effect in stimulated beats. Only this group recovered fully to baseline after 8 weeks. CONCLUSIONS: By reducing myocardial stress, both the passive girdling effect and the dynamic systolic squeezing effect have complementary roles in the mechanisms of dynamic cardiomyoplasty.

Animals↗

PubMed1998

The effects of prosthetic cardiac binding and adynamic cardiomyoplasty in a model of dilated cardiomyopathy.

OBJECTIVE: Because adynamic cardiomyoplasty, or wrapping skeletal muscle around the heart, had been shown to provide a girdling effect and delay progressive ventricular dilatation in heart failure, a similar girdling effect by the much simpler procedure of cardiac binding, using a prosthetic membrane to wrap the heart, was studied and compared with that of adynamic cardiomyoplasty. METHODS: Twenty-one dogs were divided into control, adynamic cardiomyoplasty, and cardiac binding groups. Cardiac dimension and hemodynamic studies were carried out before and 4 weeks after rapid pacing at 250 beats/min. For adynamic cardiomyoplasty, the left latissimus dorsi muscle was used for the cardiac wrap; for cardiac binding, a Marlex sheet (C. R. Bard, Inc., Murray Hill, N.J.) was used. Serial two-dimensional echocardiography, right heart catheterization, and in the cardiac binding group, left heart catheterization were performed. RESULTS: Four weeks of rapid pacing induced severe heart failure and cardiac dilatation. The magnitude of ventricular dilatation at the end of rapid pacing was less in the cardiac binding group than in the control group and least in the adynamic cardiomyoplasty group. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were 82.1 +/- 21.1 ml, 67.1 +/- 16.0 ml, and 17.5% +/- 5.8%, respectively, in the control group; 61.9. +/- 8.1 ml, 44.1 +/- 7.8 ml, and 30.1% +/- 3.6%, respectively, in the cardiac binding group; and 51.8 +/- 8.7 ml, 30.3 +/- 10.4 ml, and 27.0% +/- 4.0%, respectively, in the adynamic cardiomyoplasty group. CONCLUSIONS: Both adynamic cardiomyoplasty and cardiac binding reduced cardiac enlargement and functional deterioration after rapid pacing, with adynamic cardiomyoplasty appearing to be more effective, perhaps because of the adaptive capabilities of the skeletal muscle wrap. However, cardiac binding is a simpler and less invasive procedure, which may be useful as an adjunct to prevent or delay progressive ventricular dilatation in heart failure.

Animals↗

PubMed1998

Sequential effects of high glucose on mesangial cell transforming growth factor-beta 1 and fibronectin synthesis.

BACKGROUND: Transforming growth factor (TGF)-beta is recognized as the final common mediator of the principal lesions of diabetic nephropathy such as renal hypertrophy and mesangial expansion. To gain better understanding of the temporal relationships between high glucose (HG) and mesangial cell (MC) TGF-beta 1 synthesis and between TGF-beta 1 and extracellular matrix (ECM) synthesis, the present study examined early and sequential effects of HG on TGF-beta 1 and fibronectin (FN) mRNA expression and protein synthesis. METHODS: Confluent primary rat MC was stimulated with 5.6 (control) or 30 (high) mM glucose after synchronizing the growth by incubation with serum-free media for 48 hours. RESULTS: Mesangial cell TGF-beta 1 mRNA expression increased significantly in six hours and continued to increase until 48 hours in response to HG. The level of TGF-beta 1 mRNA was 1.5-fold higher than that of control glucose at six hours and 1.8-fold at 48 hours. TGF-beta activity in heat-activated conditioned media under HG increased 1.5- and 1.6-fold at 24 and 48 hours, respectively, compared to control glucose. FN mRNA increased significantly at 24 and 48 hours and 1.4-fold that of control glucose at both time points. FN protein also increased 1.5-fold that of control glucose at 48 hours. Anti-TGF-beta antibody completely abolished HG-induced FN synthesis. CONCLUSIONS: The present finding demonstrate that HG stimulates TGF-beta 1 very early and prior to FN production and that HG-induced FN production is mediated by TGF-beta. This finding is consistent with the view that TGF-beta mediates increased ECM accumulation by MC under high glucose conditions.

Animals↗

PubMed1998

Treatment of suprachoroidal hemorrhage with tissue plasminogen activator.

We evaluated the efficacy of tissue plasminogen activator in treating experimental suprachoroidal hemorrhage. Suprachoroidal hemorrhage was created in 30 white rabbit eyes by implanting four pieces of small, exogenously formed blood coagula into the suprachoroidal space. Animals were randomized for treatment with a surgical sponge soaked in 25, 50, or 75 microg of tissue plasminogen activator (tPA) or balanced salt solution (BSS) as a control. The time when initiation and completion of clot dissolution occurred was established, and histological examination was performed to assess damage. Clot dissolution started within 30 min in the 50- and 75-microg tPA group, whereas it took 2.75 days in the control group; complete dissolution of blood clots took 4.5 h in the 75-microg tPA group and 14 days in the control group. Histological examination revealed a minimal change in photoreceptors within 6 h after treatment with 75 microg tPA. Treatment of suprachoroidal hemorrhage with tPA seems to be effective, but further investigations for determining the effective and nontoxic dose are required.

Administration, Topical↗

PubMed1998

Massive bleeding from left colonic arteriovenous malformation in a young patient with ventricular septal defect.

Arteriovenous malformation of the gut is well known to have been an important bleeding focus in past ages. We report a young Korean male patient, who had been known to have ventricular septal defect, presenting massive lower gastrointestinal bleeding from an arteriovenous malformation involving a long segment of the left colon. Angiographic, gross and histologic findings are presented and the literature is reviewed.

Adult↗

PubMed1998

Antihypertensive effects of the novel potassium channel activator SKP-450 and its major metabolites in rats.

Antihypertensive effects of SKP-450 (KR-30450, CAS 172489-10-0, (-)-(2R)-2"-(1",3"-dioxolan-2-yl)-2-2methyl-4-(2'-oxopyrr olidin-1-yl)-6- nitro-2H-1-benzopyran), a newly synthesized potassium channel activator, and its major metabolites SKP-818 ((-)-(2R)-2"-hydroxymethyl-2-methyl-4-(2'-oxopyrrolidin-1-yl)-6-ni tro- 2H-1-benzopyran) and SKP-310 ((-)-(2R)-2"-carboxy-2-methyl-4-(2'-oxopyrrolidin-1-yl)-6-nitro-2H -1- benzopyran) were evaluated in freely moving spontaneously hypertensive (SHR), renally hypertenisve (RHR), DOCA/salt-induced hypertensive (DHR) and normotensive rats (NR). The effects of long-term treatment with SKP-450 on blood pressure and arterial reactivity were also studied in SHR. SKP-450 (3-300 micrograms/kg, p.o.) and SKP-818 (3-100 micrograms/kg, i.v.) dose-dependently decreased mean arterial pressure (MAP) (potency order: SKP-450, RHR > SHR = DHR > NR; SKP-818, DHR = SHR = RHR > NR); however, SKP-310 did not influence MAP. Compared with lemakalim, SKP-450 was 2 to 5 fold more potent in SHR and NR, and equipotent in RHR and DHR. Repeatedly administration of SKP-450 to SHR over 21 days (10 and 30 micrograms/kg, p.o., once a day), had no significant effect on the degree and pattern of its antihypertensive effects and on the reactivity of isolated aorta to various vasoconstrictors and vasodilators. These results suggest that SKP-450 is a potent peripheral vasodilator acting without the development of tolerance and the alteration in vascular reactivity. SKP-818 and SKP-310 may play a role as an active metabolite and inactive intermediary, respectively.

Animals↗

PubMed1997

Bax accelerates staurosporine-induced but suppresses nigericin-induced neuronal cell death.

Bax, a member of the Bcl-2 multigene family, is known to promote apoptosis. To investigate the role of Bax in an experimentally induced cell death of the murine dopaminergic neuronal cell line (MN9D), we established MN9D cells stably over-expressing murine Bax (MN9D/ Bax) or vector alone (MN9D/Neo). In MN9D/Neo cells treated with either 1 microM staurosporine or 0.1 microM nigericin, a ladder pattern of DNA fragmentation was induced. As expected, over-expression of Bax in MN9D cells accelerated staurosporine-induced cell death as measured by the MTT reduction assay (62.3% survival in MN9D/Neo vs 27.0% survival in MN9D/Bax). Surprizingly, both nigericin-induced cell death and its accompanying DNA fragmentation were largely attenuated in MN9D/Bax cells (22.0% survival in MN9D/Neo vs 86.7% survival in MN9D/Bax). Similar patterns were observed in two other MN9D/Bax cell lines. Cleavage of poly(ADP-ribose)polymerase caused by nigericin was greatly attenuated in MN9D/Bax cells suggesting that, like Bcl-2, Bax suppresses nigericin-induced cell death by inhibiting the activation of cysteine proteases. Thus, our data imply that Bax acts as a negative or positive regulator of cell death depending on the type of death stimulus applied to the cell.

Animals↗

PubMed1997

Establishment and characterization of human gastric carcinoma cell lines.

We report 8 newly established gastric-carcinoma cell lines (SNU-216, 484, 520, 601, 620, 638, 668, 719) from Korean patients. Morphologic study was carried out using light and electron microscopes. CEA, alpha FP, and CA 19-9 and TPA in supernatant and in cell lysate were measured by radioimmunoassay. p53 and c-Ki-ras gene mutations were screened and confirmed by sequencing. The cell lines, derived from tumors with moderate differentiation, grew as a diffuse monolayer, and those from tumors with poor differentiation and minimal desmoplasia grew exclusively as non-adherent. Out of the 8 gastric-cancer cell lines, 5 had detectable levels of CEA both in supernatant and in cell lysate; there was no expression or secretion of alpha FP in these cells; 4 cell lines showed high levels of CA 19-9 in cell pellets. All cell lines except SNU-484 had high concentrations of TPA both in cell lysate and in supernatants. p53 mutation was found in 6 cell lines (75%): 2 (SNU-216 and SNU-668) had mutations in exon 6, and other 3 in exon 8. The c-Ki-ras mutation was found in 2 cell lines (25%), SNU-601 and SNU-668. The former showed GGT-to-GAT transition mutation at codon 12, while the latter showed CAA-to-AAA transversion mutation at codon 61. DNA profiles using restriction endonuclease HinfI and polymorphic DNA probes ChdTC-15 and ChdTC-114 showed different unique patterns; which suggests that these cell lines are unique and not cross-contaminated. We believe that the newly characterized gastric-cancer cell lines presented in this paper will provide a useful in vitro model for studies related to human gastric cancer.

Adult↗

PubMed1997

Genetic variations of the apo E-CI-CII cluster gene in Koreans.

OBJECTIVES: To investigate the allele frequencies of the apolipoprotein (apo) E-CI-CII cluster gene in Koreans, and its relation to plasma lipid and lipoprotein levels. METHODS: The study subjects consisted of healthy Korean individuals (apo E, 145; apo CI and CII, 81) who were randomly selected via health screening. For polymorphism analysis, DNA was amplified by polymerase chain reaction (PCR). The one-way analysis of variance (ANOVA) test was performed to compare the mean of lipid levels among different genotypes. RESULTS: The apo E polymorphism in the Korean population appeared as the E4/2, E3/2, E3/3, E4/3, and E4/4 genotypes. The epsilon 3 allele was the most frequent, as in other populations. The apo E polymorphism showed the lack of association with plasma lipid levels in this population. On the other hand, we demonstrated AvaII polymorphism of the apo CII gene by PCR technique. Cholesterol and triglyceride levels were varied significantly among the AvaII genotypes (p < 0.05). CONCLUSION: No effect of the apo E allele on lipid levels was seen in the Korean population. This result suggests that it might be one of the factors in explaining the low prevalence rate of atherosclerosis in the Korean population. Also, the AvaII polymorphism analysis by PCR is a simple and less time-consuming method.

Apolipoprotein C-I↗