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Biomedical subjects

J C Kim

Publications and source records attributed to J C Kim.

At least 145 records · Page 8Linked to original sources
PubMed1998

Usefulness of CT in patients with intestinal obstruction who have undergone abdominal surgery for malignancy.

OBJECTIVE: The purpose of this study was to evaluate the usefulness of CT in determining the causes of intestinal obstruction in patients who have undergone abdominal surgery for malignancy. MATERIALS AND METHODS: We analyzed the CT scans of 55 patients with benign (n = 26) or malignant (n = 29) intestinal obstruction that developed after abdominal surgery for malignancy. After calculating the diagnostic accuracy of interpretations by three radiologists, we compared CT findings for benign and malignant intestinal obstructions with respect to peritoneal involvement patterns and other ancillary findings. Multivariate logistic regression analysis was used to determine the diagnostic performance of CT in revealing causes of obstruction. RESULTS: Diagnostic accuracies of the three radiologists were 67%, 75%, and 78%. CT findings indicating malignant obstruction were a mass at the site of obstruction or prior surgery, lymphadenopathy, or an abrupt transition zone and irregular bowel wall thickening at obstructed sites (p < .05). Conversely, the chance for benign obstruction increased when CT revealed mesenteric vascular changes, a large amount of ascites, or a smooth transition zone and smooth bowel wall thickening at the obstructed site (p < .05). With multivariate logistic regression analysis using two variables (a mass at the site of obstruction or prior surgery and lymphadenopathy), we calculated the overall accuracy of CT as 84% (46/55 patients). CONCLUSION: CT is useful in differentiating benign from malignant intestinal obstructions in patients who have undergone abdominal surgery for malignancy. However, CT has limitations in patients not having a demonstrable peritoneal mass.

Abdomen↗
PubMed1998

Glutathione transferase (class pi) and tissue transglutaminase (Tgase C) expression in pterygia.

Pterygia are considered to be induced by predisposing factors such as the external toxic environment. Glutathione transferases (GSTs) have a role in the detoxication of toxic chemicals. Transglutaminases (TGases) are involved in apoptosis, cellular adhesion and the wound healing process. As their expressions may be changed in abnormal conditions, we evaluated the clinicopathological status of pterygia by immunohistochemical study with GST-pi and TGase C. Twenty one pterygia, two pseudopterygia and five normal conjunctival specimens were used. The formalin-fixed samples were embedded in paraffin blocks, which were subjected to be stained with anti-GST-pi and anti-TG polyclonal antibodies immunohistochemically. They were graded from negative to strong. Staining patterns of GST-pi ranged from negative to weak in normal conjunctival epithelium, while in pterygia and pseudopterygia, one was weak, seven mild, ten moderate and five strong. As for TGase C expression, normal tissues were weak to mild, but ten were mild, nine moderate and four strong in pterygia and pseudopterygia. The general staining patterns of GST-pi and TGase C were prominent, ranged from moderate to strong in pterygia and pseudopterygia with basophilic degeneration and keratinization. On the corneal side of pterygia, TGase C was strongly positive in the basal epithelium on destroyed Bowman's layer and in conjunctival fibrous tissue. We suggest that GST-pi and TGase C are responsible for the process of pathogenesis of pterygia and pseudopterygia.

Fluorescent Dyes↗
PubMed1997

Differential activation of NAD kinase by plant calmodulin isoforms. The critical role of domain I.

NAD kinase is a Ca2+/calmodulin (CaM)-dependent enzyme capable of converting cellular NAD to NADP. The enzyme purified from pea seedlings can be activated by highly conserved soybean CaM, SCaM-1, but not by the divergent soybean CaM isoform, SCaM-4 (Lee, S. H., Kim, J. C., Lee, M. S., Heo, W. D., Seo, H. Y., Yoon, H. W., Hong, J. C., Lee, S. Y., Bahk, J. D., Hwang, I., and Cho, M. J. (1995) J. Biol. Chem. 270, 21806-21812). To determine which domains were responsible for this differential activation of NAD kinase, a series of chimeric SCaMs were generated by exchanging functional domains between SCaM-4 and SCaM-1. SCaM-4111, a chimeric SCaM-1 that contains the first domain of SCaM-4, was severely impaired (only 40% of maximal) in its ability to activate NAD kinase. SCaM-1444, a chimeric SCaM-4 that contains the first domain of SCaM-1 exhibited nearly full ( approximately 70%) activation of NAD kinase. Only chimeras containing domain I of SCaM-1 produced greater than half-maximal activation of NAD kinase. To define the amino acid residue(s) in domain I that were responsible for this differential activation, seven single residue substitution mutants of SCaM-1 were generated and tested for NAD kinase activation. Among these mutants, only K30E and G40D showed greatly reduced NAD kinase activation. Also a double residue substitution mutant, K30E/G40D, containing these two mutations in combination was severely impaired in its NAD kinase-activating potential, reaching only 20% of maximal activation. Furthermore, a triple mutation, K30E/M36I/G40D, completely abolished NAD kinase activation. Thus, our data suggest that domain I of CaM plays a key role in the differential activation of NAD kinase exhibited by SCaM-1 and SCaM-4. Further, the residues Lys30 and Glu40 of SCaM-1 are critical for this function.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1997

NF-kappaB activation and modulation in hepatic macrophages during cholestatic injury.

Cholestatic liver injury induces an inflammatory response that follows the activation of hepatic macrophages. Constitutive activation of the transcription factor, NF-kappaB, was found in these macrophages over the course of hepatic injury. Since NF-kappaB activation has been shown to have a key role in the inflammatory process, the modulatory effects of the antioxidant, alpha-tocopherol succinate, and the glucocorticoid, dexamethasone, on NF-kappaB activation were examined in this study. Male Sprague Dawley rats underwent 2-7 days of common bile duct division and ligation (CBDL) or sham laparotomy. Hepatic macrophages were isolated by collagenase Pronase perfusion and purified by centrifugal elutriation. Activation was determined by electrophoretic mobility shift assay and ELISA. We determined that NF-kappaB activation in injured hepatic macrophages could only be inhibited by dexamethasone. Dexamethasone-mediated inhibition of NF-kappaB activation required the synthesis of a regulatory protein since cycloheximide-treated cells were resistant to its effects. Furthermore, dexamethasone-treated hepatic macrophages showed elevated steady-state levels of IkappaB-alpha mRNA, suggesting the role of IkappaB-alpha as a potential regulatory mediator. Consistent with constitutive transcriptional activation we showed constitutive secretion of TNF-alpha from injured hepatic macrophages which could be inhibited by dexamethasone. These data show for the first time, in a biologically significant model of hepatic injury, constitutive activation of the key inflammatory transcription factor NF-kappaB and cytokine TNF-alpha. These results support an approach focused on the NF-kappaB/IkappaB-alpha pathway as a critical target for therapeutic intervention during hepatic injury, and the consideration of possible steroid-based therapies.

Analysis of Variance↗
PubMed1997

Adhesive function of carcinoembryonic antigen in the liver metastasis of KM-12c colon carcinoma cell line.

PURPOSE: Both experimental and clinical results reveal that carcinoembryonic antigen (CEA) seems to mediate some important role in the liver metastasis of colorectal carcinoma cells. The intent of this study was to verify whether adhesive function of CEA might affect liver metastasis in the CEA-expressing colon carcinoma cell line, KM-12c. METHODS: The hepatic binding of [125I]iododeoxyuridine KM-12c cells was measured with or without intravenous CEA pretreatment in four nude mice each. Then, 2 x 10(6) cells of KM-12c were injected into the splenic subcapsule of 57 CEA-pretreated nude mice. KM-12c cells were prepared in phosphate-buffered saline (control, 27 mice) or anti-CEA monoclonal antibody, T84.66 (30 mice). All mice were killed at the end of the eighth week after implant, and tumor nodules were confirmed histologically. RESULTS: Marginal differences of hepatic sequestration were found between the CEA-pretreated mice and the control group. Splenic tumor occurred in 75 percent (18/24) of the control group and in 40 percent (10/25) of the T84.66-pretreated group (P = 0.0107). Forty-two percent (10/24) incurred liver metastasis in the control group, whereas 20 percent (5/25) did so in the T84.66-pretreated group. The number of splenic tumor cells was significantly related to the number and volume of liver metastasis (P = 0.0065). CONCLUSIONS: CEA enhanced liver metastasis predominantly by successful primary tumor implant, whereas primary hepatic entrapment also supported it to some extent in a weakly metastatic colon carcinoma cell line, KM-12c. Tumor cell aggregates seem to be mediated by homophilic binding of CEA molecules, and it is an important mechanism to yield liver metastasis.

Animals↗
PubMed1997

Natural occurrence of trichothecenes and zearalenone in Korean and imported beers.

In order to survey the natural occurrence of Fusarium mycotoxins including deoxynivalenol (DON), nivalenol (NIV), and zearalenone (ZEN) in beers consumed in Korea, a total of 54 extracts of Korean and imported beers were derivatized with heptafluorobutyric anhydride and analysed by gas chromatography-mass spectrometry with selected ion monitoring mode. DON was detected in 14 samples (26%) and NIV was detected in 43 samples (80%). ZEN was not detected in any of the samples tested. The incidence of DON was 19% for Korean beers and 50% for imported beers, whereas the incidence of NIV was 85% for Korean beers and 58% for imported beers. This is the first report that the beers consumed in Korea are contaminated with DON and NIV.

Beer↗
PubMed1997

Temperature-sensitivity of liposomal lipid bilayers mixed with poly(N-isopropylacrylamide-co-acrylic acid).

Temperature-sensitive drug release was examined using liposomes mixed with a copolymer of N-isopropylacrylamide (NIPAM) and acrylic acid [P(NIPAM-AA)] i.e., thermally responsive liposomes. P(NIPAM-AA) copolymers with transition temperatures of about 30, 33, 37, and 43 degrees C were synthesized by copolymerizing NIPAM and acrylic acid. Thermally responsive liposomes were prepared by mixing hydrophobically modified PNIPAM, or P(NIPAM-AA) with various liposomes, composed of egg phosphatidylcholine (PC), dimyristoylphosphatidylcholine (DMPC)/dipalmitoylphosphatidylcholine (DPPC) mixture (5: 5, w/w), DPPC, or distearoylphosphatidylcholine (DSPC). The release of a fluorescent marker, calcein, from liposomes was monitored by injecting the liposomal suspension at 17 degrees C into phosphate-buffered saline (PBS, pH 7.4) preadjusted to a temperature ranging from 20 to 46 degrees C. For liposomes of egg PC and DSPC, which do not undergo a phase transition during the temperature jump (17-->20-46 degrees C), the release temperature of the liposomes increased as the content of acrylic acid in the copolymers increased. The interaction between copolymer and lipid may induce the release of calcein at LCST of the copolymer. For DPPC liposomes, the release patterns were similar to those of egg PC and DSPC liposomes at 20-36 degrees C, where the phase transition of the liposomal membrane did not occur, while at 36-46 degrees C, where the phase transition of liposomal membrane occurred, the degree of release was almost the same. For DMPC/DPPC (5:5, w/w) liposomes, where the transition occurred below those of PNIPAMs, equally enhanced releases were observed as compared with PNIPAMs, even below the LCSTs of PNIPAMs. Thus, regardless of the occurrence of the transition of PNIPAMs, phase transition of DMPC/DPPC liposomes controlled the release of calcein.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1997

Hemolytic and antifungal activity of liposome-entrapped amphotericin B prepared by the precipitation method.

A new method of preparing liposomes containing amphotericin B (AmB) was developed with the purpose of reducing the toxicity of AmB without causing a loss in its antifungal activity. The procedure involved the precipitation of AmB and egg phosphatidylcholine (PC) in phosphate buffered saline (PBS, pH 7.4) or tris buffered saline (TBS, pH 7.4) by evaporating methanol and chloroform, which had been previously mixed in the buffer solution, at 4 degrees C and 600 mm Hg. The in vitro toxicity of the precipitated liposomes containing 3, 6, 9, 12, and 15 wt% AmB was compared with that of the film-swollen liposomes containing the equivalent contents of the drug. The hemolytic ability of the precipitated liposomes at 37 degrees C was 50.3% at maximum of the film-swollen liposomes at a dose of 30 micrograms AmB/ml, as measured after 17-hr incubation. The significant reduction in the hemolysis effect may in fact be attributed to the reduced rate of drug release from the precipitated liposomes. The precipitated liposomes were multilayered and aggregates of AmB were embedded in the bilayers. These aggregates of AmB would be responsible for an intensive positive peak around 330 nm and reduced toxicity. Despite the decrease in toxicity, the activity of the precipitated liposomes against Candida albicans remained almost equipotent to that of the film-swollen liposomes. Therefore, liposomes prepared by the precipitation method are less toxic but equally as active.

Amphotericin B↗
PubMed1997

A randomized trial comparing cisplatin plus 5-fluorouracil with or without levamisole in operable gastric cancer.

OBJECTIVES: To determine the effectiveness and toxicity when levamisole was added to the adjuvant combination chemotherapy in patients with operable gastric cancer. METHODS: After en bloc resection of gastric cancer without gross or microscopic evidence of residual disease from April 1991 to December 1992, 100 patients were randomized to 6 months of 5-fluorouracil 1,000 mg/m2/day administered as continuous infusion for 5 days, cisplatin 60 mg/m2/day as intravenous infusion for 1 day with or without levamisole (50 mg every eight hours P.O for a period of three days every 2 weeks for 6 months). This chemotherapy treatment was begun within 2 to 4 weeks after the surgery. The chemotherapy consisted of discrete 5-day courses administered at 4-weeks intervals. All 100 patients are assessable. RESULTS: The fifty patients were assigned to each treatment group. There was no statistical difference and no bias in the distribution of characteristics of the 100 evaluable patients between the two groups. A total of 274 courses of treatment were given in the levamisole group and 260 courses of treatment in non-levamisole group. Eleven patients in each group did not finish planned 6 courses of treatment mainly due to non-compliance. At median follow up of 39 months, 32 patients relapsed 19 in the levamisole group and 13 in the non-levamisole group (p = 0.284). Twenty five patients died of relapsed diseases, 15 in the levamisole group and 10 in the non-levamisole group. The levamisole group tended to show more risk of overall death rate and recurrence than the non-levamisole group. However, this result was not statistically significant at 3 years. The treatment was well tolerated in both treatment groups. The grade 2-3 toxicities were nausea/ vomiting (levamisole, non-levamisole group; 31.7%, 29.3% of treatment courses respectively), diarrhea (7.6%, 8.4%), mucositis (11.6%, 12.3%), and leukopenia (9.8%, 9.6%). CONCLUSION: Levamisole had negative effects on disease-free survival and overall survival when added to adjuvant combination chemotherapy of cisplatin and 5-fluorouracil in patients with operable gastric cancer. Both treatment arms were generally well tolerated and the toxicity profile was similar with or without levamisole.

Adjuvants, Immunologic↗
PubMed1997

Light-dependent corneal toxicity in streptozocin-treated rats.

PURPOSE: To find the role of nitric oxide (NO) in streptozocin-induced corneal toxicity in rats. METHODS: Sprague-Dawley rats were injected intraperitoneally with streptozotocin (65 mg/kg). For exposure to light, each rat cage was placed in a box surrounded with aluminum foil and illuminated for 6 hours per day with two 20-W fluorescent lamps at a distance of 50 cm. When not exposed to light, each cage was placed in a dark room. Some animals with and without light exposure also were treated with and without streptozotocin treatment. Control animals did not receive streptozotocin and were housed in a dark room 24 hours a day. Each group contained 15 rats. After 1, 3, 7, and 10 days of light exposure, concentrations of nitrite and nitrate, stable oxidation products of NO, were measured in the aqueous humor. Corneal changes also were examined by electron microscopy after 10 days. To examine specific NO-induced histopathologic changes, several rats were injected subconjunctivally with a balanced saline solution containing the NO-generating agent (S-nitroso-N-acetyl-D,L-penicillamine or (Z)-I-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1- ium-1, 2-diolate]). RESULTS: Concentrations of nitrite and nitrate were highest in the streptozocin-injected rats irradiated while under the fluorescent lamp. On the 10th day of the streptozotocin injection, the concentrations of nitrite and nitrate in streptozocin-treated rats irradiated while under the fluorescent lamp was almost two-and-a-half times greater than that of nontreated rats reared in the dark (111.37 +/- 7.47 microM, 45.43 +/- 3.91 microM, respectively). Slit-lamp biomicroscopy showed that the corneas swelled gradually and opacified by the third day in the irradiated streptozocin-injected group. The corneas became hazy to the point of indistinguishable detail structures by the 10th day, although those of the other rats were relatively clear at the same time. Histopathologically, ultrastructural changes included the remarkable swelling of intracytoplasmic organelles, including mitochondria, and denaturation of collagen fibril was shown in the streptozocin-injected-irradiated rats by the 10th day. The corneas injected with two NO-generating agents, S-nitroso-N-acetyl-D,L-penicillamine and (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1- ium-1, 2-diolate, showed similar but more severe changes. CONCLUSIONS: Nitric oxide can cause damage to the mitochondria, the most important energy source of the cell, and induce ultrastructural damage to the corneal endothelium and fibroblast. The authors suggest that NO is associated with the development of corneal cytotoxicity and that NO production and subsequent cytotoxicity can be prevented by blocking to photoactivation.

Animals↗
PubMed1997

Familial juvenile polyposis coli with APC gene mutation.

Familial juvenile polyposis has been known to have malignant potential, but their genetic relation to familial adenomatous polyposis has not been proven yet. Two young brothers with intermittent rectal bleeding revealed multiple juvenile polyposis. Their father had a history of rectal cancer with multiple colonic polyps. Four frequent exons of APC gene mutation were tested from these patients' white blood cells by polyacrylamide gel electrophoresis and sequencing. The 21-yr-old brother had a missense mutation (GAA-->GGA) at codon 1309, whereas the 18-yr-old brother showed a missense mutation (ATA-->GTA) at codon 1304 in exon 15 of APC gene. Three of four first-degree relatives were affected with familial juvenile polyposis, familial juvenile polyposis with adenomatous change, and rectal cancer with multiple polyps. The APC gene mutation of familial juvenile polyposis in this case suggests a genetic relationship with familial adenomatous polyposis.

Adenomatous Polyposis Coli↗
PubMed1996

Isolation and characterization of two new type C fumonisins produced by Fusarium oxysporum.

Two new fumonisins, hydroxylated fumonisin C1 (1) and fumonisin C3 (3), were isolated from wheat cultures of Fusarium oxysporum together with known fumonisin C1 (2) and C4 (4). Compound 1 is structurally similar to 2 except for the presence of an additional hydroxy group at C-3. Compound 3 is similar in structure to fumonisin B3 except that the C-1 terminal methyl group is missing.

Carboxylic Acids↗
PubMed1996

Clinical evaluation of corneal diseases associated with floppy eyelid syndrome.

We examined 18 cases of floppy eyelid syndrome, first reported in the Orient, in patients ranging in age from 11 to 55 years (mean 24 years); 16 were men and two were women. In contrast to previous reports in which almost all patients were obese men, only three of our patients were mildly obese. The most common abnormal corneal finding was punctate epithelial keratopathy (five patients-28%). Keratoconus was detectable in three patients (17%) overall; it was bilateral in one case and unilateral in two. Other miscellaneous corneal findings were corneal astigmatism and corneal opacity. In two cases, we found a familial tendency to skin hyperextensibility and joint hypermobility, and in one case, floppy eyelid syndrome developed after pars plana vitrectomy. The pathogenesis of the syndrome is still unknown, but our findings suggest that the more important pathogenetic risk factors are not obesity and sleeping pattern, but genetic collagen and/or elastin abnormality.

Adolescent↗
PubMed1996

Effect of amniotic fluid in corneal sensitivity and nerve regeneration after excimer laser ablation.

To examine the effect of topical application amniotic fluids on the recovery of corneal sensitivity and nerve regeneration after excimer laser photokeratectomy, excimer laser was applied to 18 rabbits (VISX 20/20, 5 Hz, 7 microns depth: nine rabbits; 100 microns depth: nine rabbits). Human amniotic fluid (AF) was topically applied to the right eyes (AF group), and a balanced salt solution (BSS) was applied to the left eyes (BSS group). Corneal sensitivity was measured by using a Cochet-Bonnet aesthesiometer after weeks 1, 2, 4, 5, 8, and 12. Nerve-regeneration status was evaluated after weeks 2, 4, 5, 8, and 12 by gold chloride staining. Corneal sensitivity was initially subnormal and recovered close to the normal level at week 8. The sensitivity was higher in the AF group than in the BSS control group, except at week 2. Subepithelial nerve regeneration at the laser site was detected both at week 4 in the AF group and at week 5 in the BSS group. There was no significant correlation between the nerve-regeneration state and sensitivity changes. Long striated nerve regeneration from the deep stromal nerve was remarkable at the third month, especially in the BSS group. The BSS group showed more marked scarring of the superficial stroma, compared with the AF group. The nerve regeneration at the scar site was discontinued and delayed. Subepithelial leash nerves in the AF group were more abundant than those in the BSS group. The recovery of sensitivity and nerve regeneration were faster in the AF cornea than in the BSS cornea. These results suggest that the factors in AF helped the recovery of corneal sensitivity, nerve regeneration, and reduced scar formation.

Administration, Topical↗
PubMed1995

Ulex europaeus I lectin induces activation of matrix-metalloproteinase-2 in endothelial cells.

In this report, we show that the lectin Ulex europaeus agglutinin I (UEA I), which binds to alpha-linked fucose residues on the surface of endothelial cells, mediates activation of the 72-kDa matrix metalloproteinase-2 (MMP-2). A dose-dependent increase in the active 62-kDa form of MMP-2 was observed in conditioned medium from monkey aortic endothelial cells (MAEC) following incubation with concentrations of UEA I ranging from 2 to 100 micrograms/ml. The increase in the 62-kDa MMP-2 gelatinolytic activity was not reflected by a rise in MMP-2 gene expression. The UEA I-mediated activation of MMP-2 was blocked by L-fucose, which competes with UEA I for binding to alpha-fucose. These findings may suggest that a similar in vivo mechanism exists, whereby adhesive interactions between tumor cell lectins and endothelial cells can mediate MMP-2 activation.

Animals↗
PubMed1995

Identification of a novel divergent calmodulin isoform from soybean which has differential ability to activate calmodulin-dependent enzymes.

Calmodulin plays pivotal roles in the transduction of various Ca(2+)-mediated signals and is one of the most highly conserved proteins in eukaryotic cells. In plants, multiple calmodulin isoforms with minor amino acid sequence differences were identified but their functional significances are unknown. To investigate the biological function of calmodulins in the regulation of calmodulin-dependent enzymes, we cloned cDNAs encoding calmodulins in soybean. Among the five cDNAs isolated from soybean, designated as SCaM-1 to -5, SCaM-4 and -5 encoded very divergent calmodulin isoforms which have 32 amino acid substitutions from the highly conserved calmodulin, SCaM-1 encoded by SCaM-1 and SCaM-3. SCaM-4 protein produced in Escherichia coli showed typical characteristics of calmodulin such as Ca(2+)-dependent electrophoretic mobility shift and the ability to activate phosphodiesterase. However, the extent of mobility shift and antigenicity of SCaM-4 were different from those of SCaM-1. Moreover, SCaM-4 did not activate NAD kinase at all in contrast to SCaM-1. Also there were differences in the expression pattern of SCaM-1 and SCaM-4. Expression levels of SCaM-4 were approximately 5-fold lower than those of SCaM-1 in apical and elongating regions of hypocotyls. In addition, SCaM-4 transcripts were barely detectable in root whereas SCaM-1 transcripts were as abundant as in apical and elongating regions of hypocotyls. In conclusion, the different biochemical properties together with differential expression of SCaM-4 suggest that this novel calmodulin may have different functions in plant cells.

Animals↗