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Biomedical subjects

M J Kim

Publications and source records attributed to M J Kim.

At least 217 records · Page 12Linked to original sources
PubMed1997

The role of thiols in protecting against simultaneous toxicity of menadione to platelet plasma and intracellular membranes.

Our previous study suggested that menadione (MEN) is cytotoxic to platelets of rats due to oxidative stress. To elucidate the mechanism of this toxicity, MEN-induced depletion of total cellular thiols or depletion of gutathione was studied in intact rat platelets. Treatment with MEN resulted in dose and time dependent damage to plasma (assessed by lactate dehydrogenase leakage) and intracellular (assessed by serotonin release) membranes. These events were well correlated with total cellular thiol depletion by MEN treatment, however MEN-induced glutathione depletion occurred rapidly and before plasma and intracellular membrane damage. Unlike hepatocytes, oxidized glutathione was not formed, suggesting that protein arylation, rather than oxidative stress, might be the ultimate mechanism for MEN cytotoxicity in platelets. Platelets were pretreated with dithiothreitol to supplement the total cellular thiol pool or with 1-chloro-2,4-dinitrobenzene to deplete glutathione, a soluble thiol. Dithiothreitol pretreatment to platelets protected against MEN-induced toxicity to both plasma membranes (prevented lactate dehydrogenase leakage and changes in platelet turbidity) and intracellular membranes (prevented serotonin release), although 1-chloro-2,4-dinitrobenzene pretreatment potentiated these toxicities. These results indicate that the total cellular pool of thiols plays a vital role in maintaining plasma and intracellular membrane integrity.

Animals↗
PubMed1996

Inhibition of phospholipase D by a protein factor from bovine brain cytosol. Partial purification and characterization of the inhibition mechanism.

A specific protein inhibitor of partially purified bovine brain phospholipase D (PLD) was identified from bovine brain cytosol. The PLD inhibitor has been enriched through several chromatographic steps and characterized with respect to size and mechanism of inhibition. The inhibitor showed an apparent molecular mass of 30 kDa by Superose 12 gel exclusion chromatography and inhibited PLD activity with an IC50 of 7 nM. The inhibitor had neither proteolytic activity nor phospholipid-hydrolyzing activity. Because phosphatidylinositol 4,5-bisphosphate (PIP2), which is included in substrate vesicles, is an essential cofactor for PLD, we examined whether the inhibition might be mediated by sequestration of PIP2. PIP2 hydrolysis by phospholipase C (PLC)-beta1 was not affected by the inhibitor and the inhibitor did not bind to substrate vesicles containing PIP2. In contrast, a PH domain derived from PLC-delta1, which could bind to PIP2, showed a nearly identical inhibition of both PLC-beta1 and PLD activities. Thus, the PLD inhibition by the inhibitor is due to the specific interaction with not PIP2 but PLD. The suppression of PLD activity by the inhibitor was largely eliminated by the addition of ADP-ribosylation factor (ARF) and GTPgammaS. We propose that the inhibitor plays a negative role in regulation of PLD activity by PIP2 and ARF.

Animals↗
PubMed1996

Identification of the DNA damage-responsive elements of the rhp51+ gene, a recA and RAD51 homolog from the fission yeast Schizosaccharomyces pombe.

The Schizosaccharomyces pombe rhp51+ gene encodes a recombinational repair protein that shares significant sequence identities with the bacterial RecA and the Saccharomyces cerevisiae RAD51 protein. Levels of rhp51+ mRNA increase following several types of DNA damage or inhibition of DNA synthesis. An rhp51::ura4 fusion gene was used to identify the cis-acting promoter elements involved in regulating rhp51+ expression in response to DNA damage. Two elements, designated DRE1 and DRE2 (for damage-responsive element), match a decamer consensus URS (upstream repressing sequence) found in the promoters of many other DNA repair and metabolism genes from S. cerevisiae. However, our results show that DRE1 and DRE2 each function as a UAS (upstream activating sequence) rather than a URS and are also required for DNA-damage inducibility of the gene. A 20-bp fragment located downstream of both DRE1 and DRE2 is responsible for URS function. The DRE1 and DRE2 elements cross-competed for binding to two proteins of 45 and 59 kDa. DNase I footprint analysis suggests that DRE1 and DRE2 bind to the same DNA-binding proteins. These results suggest that the DRE-binding proteins may play an important role in the DNA-damage inducibility of rhp51+ expression.

Base Sequence↗
PubMed1996

Mechanism of menadione-induced cytotoxicity in rat platelets.

The elevation of intracellular Ca2+ in various tissue through oxidative stress induced by menadione has been well documented. Increase of Ca2+ level in platelets results in aggregation of platelets. To test the hypothesis that menadione-induced Ca2+ elevations can play a role in platelet aggregation, we have studied the effect of menadione on aggregation of platelets isolated from female rats. Treatment with menadione to platelet-rich plasma (PRP), which proved to be an adequate system, appeared to induce dose-dependent platelet aggregations up to 60%, as determined by aggregometry. However, exposure of PRP to menadione led to slow reduction of platelet cell number coincident with a loss of viability, as measured by lactate dehydrogenase leakage, suggesting that menadione might induce cell lysis rather than aggregation of platelets. Light microscopy confirmed that menadione reduced the number of platelets and failed to show aggregates of platelets. To elucidate the mechanism of this cytotoxicity, menadione-induced oxygen consumption was studied in intact rat platelets. Incubation of platelets with menadione resulted in rapid dose-dependent increases of oxygen consumption, which were not inhibited by indomethacin and nordihydroguaiaretic acid, suggesting that menadione did not affect the cyclooxygenase and lipoxygenase pathways in platelets. Oxygen consumption, as well as cytotoxicity by menadione, was unaffected by addition of dicoumarol, which is a quinone reductase (QR) inhibitor. Consistent with these findings, no activity of QR was detected in any subcellular fractions of platelets. Oxygen consumption by several subcellular platelet fractions treated with menadione was examined in the presence of NADPH or NADH. Additions of NADPH or NADH to microsomal fractions or a 9000 g pellet (which contains plasma membranes) led to 2-fold to 18-fold elevations in platelets may contribute to the oxidative damage associated with menadione-induced oxygen consumption, respectively. These results suggest that NADPH and/or NADH-dependent enzyme systems in menadione-induced cytotoxicity.

Animals↗
PubMed1996

Bronchiolitis obliterans in children with Stevens-Johnson syndrome: follow-up with high resolution CT.

About one third of children with Stevens-Johnson syndrome have pulmonary involvement. As a consequence of airway epithelial injury, bronchiolitis obliterans can occur in these patients. Two cases of Stevens-Johnson syndrome-associated bronchiolitis obliterans in children were diagnosed and followed by high resolution CT without open lung biopsy. Serial changes of high resolution CT features of bronchiolitis obliterans are discussed and the literature is reviewed.

Bronchiolitis Obliterans↗
PubMed1996

Effects of mixed leukocyte reaction, hydrocortisone and cyclosporine on expression of leukocyte adhesion molecules by endothelial and mesangial cells.

We investigated the effects of mixed leukocyte reaction (MLR), hydrocortisone (HC) and cyclosporine A (CsA) on the expression of leukocyte adhesion molecules on the mesangial (MC) and endothelial cells (EnC). Cell surface enzyme immunoassay showed that INFnu, IL-1beta, or TNF alpha stimulated expression of ICAM-1, or VCAM-1 on MC after 24 hours. Flow cytometric analysis demonstrated that MLR supernatant induced a marked increase in mean fluorescence of or % of cells highly expressing intercellular adhesion molecule(ICAM)-1 or vascular cell adhesion molecule (VCAM)-1 on both cells after 24 hours (p<0.001). HC treatment(300 ng/ml) during MLR effectively inhibited MLR-induced upregulation of ICAM-1 and VCAM-1 on both cells (p<0.005). When MLR supernatant with HC was added to adhesion molecule assay, there was no inhibitory effect of HC on VCAM-1. CsA treatment (500 ng/ml) during MLR caused a modest decrease in upregulation of VCAM-1 on EnC (p<0.05), but had no effects on ICAM-1 on both cells. CsA directly decreased expression of VCAM-1 on MC. In conclusion, alloreactive lymphocytes and monocytes upregulate the expression of VCAM-1 and ICAM-1 on target cells probably by the mediation of cytokines. HC effectively prevents MLR-induced upregulation of VCAM-1 and ICAM-1. CsA does not increase the expression of VCAM-1 and ICAM-1.

Cells, Cultured↗
PubMed1996

Post-exercise response of ventricular ejection fraction after total repair of congenital heart disease with left to right shunt.

A radioisotope first pass study was done on patients over a period of 1 to 15 years (average 4.6 years) after repair for ventricular septal defect or arterial septal defect with a left to right shunt. The age of the patients ranged from 6 to 32 years (average 14.2 year) at the time of the study. The total work of exercise and the right and left ventricular ejection fraction(EF) were evaluated at rest and after exercise. The results were compared with the preoperative hemodynamic findings and with the age of patient at the time of the operation. 1) When the total work of exercise was divided with the maximal exercise capacity of the normal individual corresponding to the patients' height and body surface area (the percentage of total work), it were very low with the average of 40% of normal. There was no sexual difference, but the percentage of total work of exercise had significant correlation with the patients' age at the time of operation (r = -0.52, p < 0.01) and post-exercise left ventricular ejection fraction (LVEF)(r = -0.39, p < 0.05). 2) LVEF at rest had some correlation with the preoperative mean pulmonary arterial pressure (r = -0.29, p = 0.05), but showed no relationship with Qp/Qs or Rp/Rs ratios. The right ventricular ejection fraction (RVEF) at rest had no relations with the preoperative hemodynamic findings with maximal workload. 3) The post-exercise RVEF showed linear correlation with the preoperative Rp/Rs ratio (r = -0.49, p < 0.005), and mean pulmonary arterial pressure (r = -0.37, p < 0.05). The post-exercise LVEF had no significant correlation with any preoperative hemodynamic factors. 4) When greater than 5% increase in ventricular EF after exercise is considered normal, the group with the normal right and left ventricular responses (n = 11) showed normal preoperative Rp/Rs ratio (7.6 +/- 4.1). In the group with normal left, but abnormal right ventricular response (n = 9) and the group with abnormal biventricular response (n = 11), both demonstrated incremental increase in Rp/Rs ratio (20.1 +/- 11.3, 26.3 +/- 19.8 respectively). Normal right, but abnormal left ventricular reaction (n = 2) was noted in patients with residual aortic valvular insufficiency and residual ventricular septal defect. In conclusion, post-operative ventricular response was much more sensitive and informative than that of ventricular function at rest and to detect subclinical cardiac dysfunction. Post-exercise RVEF was closely correlated with preoperative pulmonary vascular hemodynamics, while post-exercise LVEF seemed to be a major determinant of working capacity after repair.

Adolescent↗
PubMed1995

Homogeneous assays for riboflavin mediated by the interaction between enzyme-biotin and avidin-riboflavin conjugates.

Homogeneous-type enzyme-linked competitive binding assays utilizing the synthetic enzyme-biotin and avidin-riboflavin conjugates are developed for the detection of riboflavin as well as its binder protein. The activity of the enzyme-biotin conjugate is inhibited in the presence of the avidin-riboflavin conjugate, and the observed inhibition is reversed in an amount dependent on the concentration of riboflavin binding protein (RBP) added. Upon additions of free riboflavin to the mixture, activity is reinhibited in an amount proportional to the riboflavin concentration. Three different enzymes are examined as the labels: glucose-6-phosphate dehydrogenase, adenosine deaminase, and alkaline phosphatase. The catalytic activity of these enzymes, when conjugated with biotin, is shown to be inhibited to a significant degree (> 90%) by the binding of the avidin-riboflavin conjugate, and reversed upon additions of RBP.

Adenosine Deaminase↗
PubMed1995

Characterization of SFP2, a putative sulfate permease gene of Saccharomyces cerevisiae.

The SFP2 gene of Saccharomyces cerevisiae has been characterized. The deduced amino acid sequence contained twelve highly hydrophobic domains and showed 50, 47, 44 and 48% homologies to Neurospora crassa sulfate permease II (CYS14), soybean GMAK170 nodulin, human colon mucosa protein (DRA) and a putative open reading frame (ORF) downstream of Escherichia coli prs (phosphoribosyl pyrophosphatate synthetase) gene, respectively, in the aligned regions. Cells lacking SFP2 were viable and displayed no obvious decrease in their growth rate. Southern blot analysis revealed that SFP2 exists as a single copy in haploid genome. Northern blot analysis showed that SFP2 produced a 2.8-kb transcript which was highly expressed under sulfur derepressing condition. SFP2 mRNA was found to turn over with a half-life of approximately 15 min, which may contribute to the regulation of sulfate permease function, and reached its maximal level in about 22 h after depression.

Amino Acid Sequence↗
PubMed1995

Staurosporine induces de novo synthesis of prostaglandin H synthase-2 in rat alveolar macrophages.

This study was initiated to investigate the possible involvement of prostaglandin H synthase in the staurosporine-induced prostaglandin production. The time course of prostaglandin H synthase activity in macrophages treated with staurosporine (20 nM) showed that the maximum activity was reached in 20 h. The stimulatory effect of staurosporine on thromboxane B2 production was maximum at 50 nM staurosporine and this effect was reversed at higher concentrations. Immunoprecipitation of 35S-labeled enzyme using an antibody specific for prostaglandin H synthase-2 paralleled the changes in enzyme activity. These results indicate that increased de novo synthesis of prostaglandin H synthase-2 is largely, if not solely, responsible for staurosporine-stimulated prostaglandin production in macrophages.

Alkaloids↗
PubMed1995

Mandibular reconstruction with free vascularized fibular flap.

Although various sources of vascularized bone/composite tissue have been used for mandibular reconstruction, the vascularized fibular flap has been reported to have many advantages over the others and to be the most suitable for bridging a long-span mandibular defect. In this paper, positive experience of 14 consecutive cases in which a free vascularized fibular graft with or without a skin paddle has been used to reconstruct a long mandibular defect is reported. Half of the cases were primarily reconstructed, the rest secondarily. The average length of the fibula graft harvested was 16.7 cm, with a range of 12 to 22 cm. The number of wedge osteotomies ranged from 0 to 4, with an average of 1.67. In ten flaps, a peroneal skin paddle was included. The donor wound was typically closed directly, except in three cases, where a skin graft was used. Vein grafts were performed in five cases to lengthen the pedicle. In two cases, the skin partially necrosed. All scintigrams except one showed good bone viability. But there was no total flap failure. Postoperative facial appearances were fair to excellent, with mouth opening ranging from 21 to 50 mm. Although unusual serious donor wound rupture was experienced in one case, in general the donor site complications were minimal.

Adult↗
PubMed1995

A case of rectal cancer with sternal metastasis as initial presentation.

Colorectal cancer with bone metastasis as initial manifestation is a very rare event. We have reported a case of rectal cancer presenting with sternal metastasis. A 30 year-old man was evaluated due to pain in the sternal area with a bulging mass. History and physical examination did not suggest any specific disease. A radionuclide bone scan revealed increased uptake in the sternal area, right 6th rib, and sacrum. Microscopic examination of a biopsy specimen from the sternum showed metastatic adenocarcinoma. A barium enema and CT scan of the pelvis suggested carcinoma of the upper rectum. Adenocarcinoma of the rectosigmoid junction area was demonstrated by colonoscopic examination with biopsy. He received palliative transverse colostomy for obstruction without further treatment.

Adult↗
PubMed1995

Augmentation of vascular endothelial barrier function by heparin and low molecular weight heparin.

Glycosaminoglycans (GAGs) are an important component of endothelial barrier function. Early passage human umbilical vein endothelial cells were grown to confluence on transparent micropore filters and barrier function assessed as transendothelial electrical resistance (TEER) and permeability to albumin and sucrose. Unfractionated heparin and the LMW heparin Clexane decreased endothelial permeability to both sucrose and albumin and increased TEER. Chondroitin 6-sulphate also augmented barrier function, but other GAGs had no effect. Interleukin-1 increased permeability to albumin and sucrose and decreased TEER. Although heparin attenuated the effect of IL-1 on TEER and sucrose permeability, it could not restore the barrier to albumin transfer. Denuded endothelial matrix presented a negligible barrier, which was not enhanced by heparin. When sulphation of endogenous GAGs was inhibited by chlorate, barrier function was compromised and was not restored by exogenous heparin. Thus heparin enhances the barrier function of resting endothelium, but cannot completely overcome the increased permeability resulting from exposure to IL-1 or substitute for endogenous GAGs.

Albumins↗
PubMed1995

The efficacy of cyclosporine A in adult nephrotic syndrome with minimal change disease and focal-segmental glomerulosclerosis: a multicenter study in Korea.

A multicenter prospective study conducted in four university hospitals in Korea investigated the efficacy and tolerance of cyclosporine A (CyA, Sandimmun) in 30 patients with adult nephrotic syndrome [25 patients with minimal change disease (MCD) and 5 with focal-segmental glomerulosclerosis (FSGS)]. After a 6-week washout period, CyA 5 mg/kg/day and prednisolone 10 mg/day were administered for up to 8 months, depending on responses to CyA. The rate of relapse after withdrawal of CyA was assessed up to 10 months. Of the 30 patients enrolled, 3 withdrew prematurely due to adverse events. Of the 27 patients who completed the study, 22 had MCD and 5 had FSGS. The prior steroid responses of these patients were 19 steroid-dependent (SD), 4 frequent-relapser (FR) and 4 steroid-resistant (SR) type. High rates of complete remission were obtained after CyA treatment in both MCD and FSGS patients, 86.4% (19/22) and 80% (4/5) respectively. Previous steroid responses did not affect the response to CyA; complete remission was obtained in 84.2% (16/19) of SD patients and in 75% (3/4) of SR patients. The mean (+/- SEM) duration of CyA treatment to attain complete remission in SD and SR patients was 3.8 (+/- 0.6) weeks and 10.7 (+/- 2.7) weeks, respectively (not significantly different). Tapering or withdrawal of CyA was followed by release of nephrotic syndrome in many patients, and the cumulative relapse rates at month 10 were 68.4% (13/19) in MCD patients and 50% (2/4) in FSGS patients. When considered according to prior steroid responses, the relapse rate was 73.3% (11/15) in SD patients and 50% (2/4) in SR patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Overemphasized use of GPA for admission decisions.

When nursing schools have too many applicants for the number of students they can take, many use the cumulative Grade Point Average (GPA) as an important factor in the selection process. However, this practice continues to exclude students, many from minorities, which need to be included in preparing nurses to care for all populations. These authors describe how to use GPA only as an initial preliminary screening tool to determine qualified applicants, but not as a factor in the final decision in selecting students.

Bias↗