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Biomedical subjects

J Choi

Publications and source records attributed to J Choi.

At least 163 records · Page 9Linked to original sources
PubMed1998

Features for a B-ISDN telemedicine system and its application.

Telemedicine technology is emerging as a new way of medical practice. It will provide more cooperative activity between departments and more comfortable access for disabled patients home. We developed two types of telemedicine system: a telediagnosis system and a home care system. Our telemedicine application is aimed to be run on the broadband-integrated services digital network (B-ISDN). The legacy network is also considered. The user interface is designed to help doctors to communicate easily. The key elements of telemedicine systems are user friendly interface, medical multimedia database design highly refined display technique.

Computer Communication Networks↗
PubMed1998

Effects of 8-bromo-cyclic GMP on membrane potential of single swine tracheal smooth muscle cells.

Cyclic GMP relaxes swine tracheal smooth muscle. Relaxation occurs because of decreases in intracellular calcium concentration ([Ca++]i) that are thought to occur through hyperpolarization which inhibits calcium influx. Activation of K+ channels has been suggested as the underlying mechanism for the hyperpolarization. In the present study, the effects of 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP, a membrane-permeable analog of cyclic GMP) on acetylcholine (ACh)-induced increases in [Ca++]i were examined by laser scanning confocal microscopy in fluo 3-loaded single cells. Membrane potential and currents were measured by the perforated-configuration of patch-clamp method, 8-Bromo-cGMP (1 microM-0.1 mM) inhibited 0.1 microM ACh-induced oscillations in [Ca++]i in a concentration-dependent manner. Spontaneous changes in membrane potential were observed by the patch-clamp method. Acetylcholine (0.03 microM) did not affect the time-averaged mean potential. The spontaneous changes in membrane potential were reduced and the cells were depolarized by 0.1 microM ACh and to a greater degree by 1 microM ACh. This result is consistent with previous observations of ACh-induced depolarization in intact tissue. The application of 0.1 mM 8-Br-cGMP had no significant effects on spontaneous changes in membrane potential and did not induce changes in membrane potential in cells treated with 0.1 microM ACh. In voltage-clamped cells, ACh (0.1 microM) induced oscillations in calcium-activated K+ currents. 8-Bromo-cGMP (0.1 mM) inhibited these ACh-induced oscillations in currents, but had no significant effects on spontaneous changes in membrane current in unstimulated cells. These data indicate that 8-Br-cGMP inhibits ACh-induced increases in [Ca++]i by mechanisms other than regulation of membrane potential.

Acetylcholine↗
PubMed1998

The effect of N-alkyloxycarbonyl group on the anticonvulsant activities of N-alkyloxycarbonyl-alpha-amino-N-methylsuccinimides.

In connection with the development of new anticonvulsant agents with a broad spectrum, we found that N-Cbz-alpha-amino-N-alkylsuccinimides showed significant anticonvulsant activities, and the pharmacological activities of these compounds were dependent on their stereochemistry and N-substituted alkyl group. These results prompted us to define the effects of other functional group on the anticonvulsant activities of these compounds. Therefore a series of N-alkoxycarbonyl-alpha-amino-N-methylsuccinimide were prepared from N-Cbz-aspartic acid and were evaluated with their anticonvulsant activities against the MES and PTZ tests, in order to define the effect of N-substituted alkoxy carbonyl group with the anticonvulsant activities. From these studies, it was found that all the tested N-alkoxycarbonyl-alpha-amino-N-methylsuccinimides exhibited significant anticonvulsant activities in the PTZ test and were not active in the MES test. The most active compound in the PTZ test was (S) N-ethoxycarbonyl-alpha-amino-N-methyl-succinimide. We found that the pharmacological activities in the PTZ test were dependent on their N-alkoxycarbonyl groups. They follow as such; The order of anticonvulsant activities for (R) series as evaluated by ED50 was N-phenoxycarbonyl = N-4-nitrobenzyloxycarbonyl > N-ethoxycarbonyl > N-allyloxycarbonyl > N-tert. butoxycarbonyl compound; For the (S) series N-ethoxycarbonyl > N-phenoxycarbonyl > N-allyloxycarbonyl compound. From the above results, it was conceivable that N-substituted alkoxycarbonyl group had certain effects on the anticonvulsant activities of N-alkoxycarbonyl-alpha-amino-N-methylsuccinimides.

Animals↗
PubMed1998

The effect of N-alkyloxycarbonyl group on the anticonvulsant activities of N-alkyloxycarbonyl-alpha-aminoglutarimides.

In connection with the development of new anticonvulsant agents with a broad spectrum, we reported that N-Cbz-alpha-aminoglutarimides, combining common structures of other anticonvulsants such as N-CO-C-N and cyclic imides in a single molecule, showed significant anticonvulsant activities in the MES (maximal electroshock seizure) and PTZ (pentylenetetrazole induced seizure) tests. In these studies, a series of (R) and (S) N-alkyloxycarbonyl-alpha-aminoglutarimides 7a-7e and 8a-8e, which were substituted with various alkyloxycarbonyl group instead of Cbz group, were prepared from the corresponding (R) and (S) N-Cbz-glutamic acid 3 and 4, and were evaluated with their anticonvulsant activities against the MES and PTZ tests, including neurotoxicity, in order to define the effect of N-alkyloxycarbonyl group on the anticonvulsant activities of N-alkyloxycarbonyl-alpha-aminoglutarimides. Among them, (S) N-4-nitrobenzyloxycarbonyl-alpha-amino-N-methylglutarimide 8e was the most active in MES (ED50 = 35.6 mg/kg, PI = 2.7) and PTZ tests (ED50 = 15.6, PI = 6.1). Interestingly, (R) and (S) N-4-nitrobenzyloxycarbonyl-alpha-amino-N-methylglutarimide 7e and 8e and (R) N-phenoxycarbonyl-alpha-amino-N-methylglutrimide 7d showed significant anticonvulsant activities in both the MES and PTZ tests and other compounds showed anticonvulsant activities in only the PTZ test. In addition, it was found that their anticonvulsant activities were dependent on their stereochemistries and N-substituted alkyloxycarbonyl groups.

Animals↗
PubMed1997

An RXR-selective analog attenuates the RAR alpha-selective analog-induced differentiation and non-G1-restricted growth arrest of NB4 cells.

NB4, a human acute promyelocytic leukemia cell line expressing the promyelocyte-retinoic acid receptor alpha (PML-RAR alpha) hybrid protein was treated with RAR- and retinoid X receptor (RXR)-selective analogs to determine their effects on cell proliferation, retinoblastoma (RB) tumor-suppressor protein phosphorylation, and differentiation. An RAR- or just RAR alpha-selective analog alone induced similar cell population growth arrest, cell cycle arrest without restriction to G1, hypophosphorylation of RB, and myelomonocytic cell surface differentiation marker expression (CD11b). In addition, an RAR alpha antagonist could inhibit the effects of the RAR alpha agonist completely. The RAR alpha-selective analog-elicited response was attenuated by simultaneous addition of various RXR-selective analogs. In contrast, each of the RXR-selective analogs was unable to induce any of the cellular responses analyzed. The growth arrest of NB4 cells is not G1-restricted and occurs at all points in the cell cycle. Cells growth arrested by treatment with an RAR alpha-selective analog show primarily hypophosphorylated RB. When these cells are sorted into G1 or S + G2/M subpopulations by flow cytometry, hypophosphorylated RB protein was in G1 as well as S + G2/M cells. This suggests that the hypophosphorylated RB protein may be mediating the growth arrest of NB4 cells at all points in the cell cycle. These results are consistent with an involvement of PML-RAR alpha and/or RAR alpha in the transduction of the retinoid signal in NB4 cells.

Cell Cycle↗
PubMed1997

Adaptation to oxidative stress: quinone-mediated protection of signaling in rat lung epithelial L2 cells.

Cells can respond to a sublethal oxidative stress by up-regulating their intracellular glutathione (GSH) pool. Such increased GSH concentration is likely to be protective against further oxidative challenge, and, in fact, pre-exposure to low levels of oxidants confers increased cellular resistance to subsequent greater oxidative stress. Previously, we have shown that pretreatment of rat lung epithelial L2 cells with sublethal concentrations of tert-butylhydroquinone (TBHQ) increases intracellular GSH concentration in a concentration- and time-dependent manner. This increase resulted from up-regulation of both gamma-glutamyltranspeptidase (GGT) and gamma-glutamylcysteine synthetase (GCS). Therefore, we investigated whether such increased GSH concentration protected these cells against a subtle loss in function caused by a subsequent challenge with sublethal concentrations of tert-butyl hydroperoxide (tBOOH) (< or = 200 microM), mimicking a physiological oxidative stress. Activation of L2 cell purinoreceptors with 100 microM ADP caused an elevation of intracellular Ca2+. This response was suppressed by a brief pre-exposure to tBOOH. The inhibition, however, was alleviated dramatically by a 16-hr pretreatment with 50 microM TBHQ. The same TBHQ pretreatment also protected the cells from ATP-depletion induced by tBOOH. L-Buthionine S,R-sulfoximine (BSO), an irreversible inhibitor of GCS, prevented the increase in intracellular GSH and also completely removed the protection by TBHQ in maintaining the ATP level. Thus, pre-exposure to a sublethal level of TBHQ results in protection of cell functions from hydroperoxide toxicity. This protection appears to depend on alteration of the intracellular GSH pool, the modulation of which constitutes an adaptive response to oxidative stress.

Adenosine Diphosphate↗
PubMed1997

Unanticipated temporal and spatial effects of sarcomeric alpha-actinin peptides expressed in PtK2 cells.

To understand the multiple roles of alpha-actinin in the assembly of (1) Z bands in muscle, and (2) a variety of cytoskeletal structures in non-muscle cells, 4 sarcomeric alpha-actinin derived cDNAs tagged with a MYC epitope were constructed. The constructs were: (1) full-length (FL/MYC); (2) minus EF-hands (-EF/MYC); (3) actin-binding site (+A/MYC); and (4) minus actin-binding site (-A/MYC). These four cDNAs were individually transfected into PtK2 cells. The exogenous sarcomeric alpha-actinin (s-alpha-actinin/MYC) was followed with labeled anti-MYC, the endogenous non-sarcomeric alpha-actinin (non-s-alpha-actinin) with labeled anti-non-s-alpha-actinin. The salient findings were: (1) the selective intracellular localizations of each expressed MYC-tagged peptide differed one from the other; (2) their respective localizations in the 10-24-h post-transfection (p.t.) period differed from their localizations in the 48-72-h p.t. period; (3) each MYC-positive peptide was cytotoxic, but each in a distinctive way; and (4) while the selective targeting of FL/MYC to dense bodies, adhesion plaques, adherens junctions, and ruffled membranes was consistent with binding studies in cell-free systems, the incorporation of the mutated peptides, particularly +A/MYC and -A/MYC was not. Changes in localization over time and the distinctive cytopathologies probably reflect domain-specific targeting. They also suggest unexpected cooperative involvement of multiple domains of alpha-actinin with specific receptors in distal cytoskeletal structures. To date, such qualitative in vivo interactions have not been described either in in vitro binding studies, or in short-term experiments involving localization and/or fate of microinjected labeled molecules into living cells.

Actinin↗
PubMed1997

Seroimmunological characteristics of Korean workers exposed to toluene diisocyanate.

Since type I allergy caused by specific IgE antibodies may play principal roles and IgG antibody-mediated reactions have been thought to be involved in some parts of the pathogenesis, this study was performed to investigate the role of IgE- or IgG-mediated hypersensitivity reactions in development of toluene diisocyanate (TDI) asthma in Korean workers. For 81 TDI spray painters, self-administrative questionnaires and direct interviews on respiratory symptoms, chest auscultation, and measurements of forced vital capacity (FVC) and forced expiratory volume in 1 sec (FEV1.0) were performed. The TDI concentration in their working environments was measured. Levels of serum IgE and IgG specific to TDI were estimated by radioallergosorbent test (RAST) and ELISA using p-tolyl isocyanate-human serum albumin (TMI-HSA) as the antigen. When sputum, cough, and dyspnea aggravated by work or wheezing existed, when FVC or FEV1.0 was less than 80% of the normal reference value, or when IgE RAST for TDI was positive, the peak expiratory flow rate (PEFR) was recorded four times per day for over 2 weeks. If decrease of PEFR was over 20% of baseline PEFR and changing pattern of PEFR was closely related to workshift in time, then a diagnosis of TDI asthma was made. Changing patterns of PEFR of 8 (9.9%) workers corresponded to the diagnostic criteria of TDI-related occupational asthma. Levels of the specific IgE were increased in 9 (11.1%) of the 81 subject workers and in 3 (37.5%) of the 8 PEFR-positive workers. Levels of the specific IgG were increased in 9 (11.1%) workers, and in only 1 (12.5%) of the asthmatics sensitive to TDI. Neither elevated TDI-specific IgE levels nor PEFR test positivities were associated with increased IgG levels. The mean titer of the PEFR-test-positive workers was slightly lower than that of the PEFR-negative workers and that of the IgE RAST-positive workers lower than that of the test-negative workers, but there was no statistical significance. These results suggest that IgG is not deeply involved in the pathogenesis of TDI-induced occupational asthma in Korean workers.

Adult↗
PubMed1997

Butyrate inhibits deoxycholate-induced increase in colonic mucosal DNA and protein synthesis in vivo.

PURPOSE: Crypt surface hyperproliferation is an intermediate biomarker of colon cancer risk. In vitro studies indicate that the short-chain fatty acid and antineoplastic agent butyrate may reverse the crypt surface hyperproliferation induced by the secondary bile acid and tumor promoter, deoxycholate. We hypothesized that butyrate may reverse deoxycholate-induced crypt surface proliferation in vivo. METHODS: Thirty-one Sprague-Dawley rats (250-300 g) underwent surgical isolation of the colon and 24-hour luminal instillation of either sodium chloride, butyrate, deoxycholate, or butyrate plus deoxycholate (all solutions, 2 ml; pH 7; total sodium = 20 mM). Study variables included colon weight, mucosal DNA, mucosal protein, and proliferating cell nuclear antigen immunohistochemistry, labeling of which was determined in five crypt compartments from base to surface (12 crypts per rat). Labeling indexes were calculated as proliferating cell nuclear antigen immunohistochemistry-labeled cells divided by total counted cells in the whole colonic crypt and each of five crypt compartments. The phi(h) value (an index of premalignant risk) was calculated as the ratio of labeled cells in the two surface compartments divided by the total labeled cells. RESULTS: Deoxycholate significantly increased colon wet weight, mucosal protein, total crypt labeling indexes, crypt surface labeling indexes, and the phi(h) value and raised the mucosal DNA content. Butyrate alone slightly reduced total mucosal DNA and protein content. The combination of butyrate plus deoxycholate significantly decreased mucosal DNA and tended to reduce mucosal protein compared with deoxycholate alone. In contrast to prior in vitro findings, butyrate plus deoxycholate did not reverse the deoxycholate-induced surface hyperproliferative changes as measured by proliferating cell nuclear antigen labeling. CONCLUSIONS: Because co-treatment with butyrate plus deoxycholate inhibits deoxycholate-induced increases in total mucosal DNA and protein content, we conclude that butyrate may play a role in maintaining the proliferative balance of the colonic mucosa, in vivo. However, co-treatment with butyrate plus deoxycholate does not reverse the deoxycholate-induced increases in colon weight and proliferating cell nuclear antigen labeling indexes under the studied experimental conditions.

Animals↗
PubMed1997

Transduction of murine and human tumors using recombinant adenovirus vectors.

BACKGROUND: Most cytokine-based cancer gene therapy clinical trials have used labor-intensive, retrovirus-mediated strategies resulting in unpredictable gene expression. Recombinant AdV vectors were evaluated for easier, more reproducible gene transfer into 12 human melanoma, 2 murine fibrosarcomas, and 8 other tumor cell lines. METHODS: AdV vectors contained a reporter (Escherichia coli beta-galactosidase or firefly luciferase) or cytokine gene (human interleukin-2 [IL-2] or IL-7). Transduction efficiencies and expression levels were assessed by histochemical staining, flow cytometry, polymerase chain reaction, fluorometry, and enzyme-linked immunosorbent assay. Tumorigenicity was determined by subcutaneous injection of cells into syngeneic mice. RESULTS: All cell lines studied were transduced with AdV. Most cell lines exhibited 100% transduction efficiencies (by flow cytometry) at multiplicities of infection (MOI) epsilon 10. Gene expression correlated linearly with MOI, but a cytopathic effect was observed at MOI > 100 with all vectors. Nanogram gene expression levels were routinely achieved. Irradiation (30 Gy) minimally affected expression levels. Tumorigenicity of AdV-IL-2-transduced fibrosarcoma cells in mice was inversely related to IL-2 production. A majority of mice that rejected their tumor challenge were immune to tumor rechallenge. CONCLUSIONS: E1-deleted AdV vectors may prove useful in generating tumor vaccines ex vivo with high, transient cytokine expression levels.

Adenoviridae↗
PubMed1997

Heparan sulfate potentiates the autocrine action of basic fibroblast growth factor in astrocytes: an in vivo and in vitro study.

Increasing evidence indicates that heparan sulfate proteoglycans have a critical role in the regulation of the activity of basic fibroblast growth factor by interacting with it or its receptor. In this study we examined the possibility that heparan sulfate can modulate the basic fibroblast growth factor system at a more fundamental level than activity regulation, by influencing the synthesis of basic fibroblast growth factor and its receptor messenger RNAs. Previous studies in vitro indicate that basic fibroblast growth factor promotes proliferation and differentiation of astrocytes. Accordingly, we examined the possibility that the action of heparan sulfate on the basic fibroblast growth factor system could have a critical role in the modulation of reactivity and/or proliferation of astrocytes in vitro and in vivo. We report that basic fibroblast growth factor applied to pure astrocyte cultures or rat neocortex promoted an increase in the messenger RNA for basic fibroblast growth factor itself and for its receptor. Furthermore, basic fibroblast growth factor applied directly into the brain elicited an increase in messenger RNA for the astrocytic marker glial fibrillary acidic protein. All of these actions, both in vitro and in vivo, were highly potentiated when heparan sulfate was applied in combination with basic fibroblast growth factor. These results suggest that basic fibroblast growth factor regulates astrocytic proliferation or reactivity via an autocrine cascade that involves induction of its own receptor and that this action is modulated by heparan sulfate.

Animals↗
PubMed1997

Assessment of proliferating cell nuclear antigen in nasopharyngeal carcinoma tissue and its relation to clinical findings.

47 newly diagnosed patients with nasopharyngeal carcinoma (NPC) were studied using the proliferating cell nuclear antigen (PCNA) immunostaining technique. The results were reproducible as shown by assessment of three separate sections performed for each patient. No statistical correlation was found between PCNA labelling index (LI) and Ho's clinical staging or time required to achieve complete remission of the local disease. A higher PCNA LI was associated with a poorer disease-free survival. The literature on the use of PCNA in human tumours is reviewed.

Adolescent↗
PubMed1997

NADPH-cytochrome P-450 reductase, cytochrome P-450 2C11 and P-450 1A1, and the aryl hydrocarbon receptor in livers of rats fed methyl-folate-deficient diets.

We investigated three hepatic cytochrome P-450 isozymes and the aryl hydrocarbon (Ah) receptor in rats fed one of the following three diets for 15 months: a diet containing the AIN vitamin mixture (control), the control diet devoid of choline and folate (CFD), or the CFD diet devoid of niacin (CFND). Hepatic tumors developed in all CFD- and CFND-fed rats. Western blot analyses of nontumor hepatic tissue showed that NADPH-cytochrome P-450 reductase (P-450 reductase) increased significantly in the CFD and CFND groups compared with the control group. Hepatic cytochrome P-450 2C11 (CYP2C11) was not detectable in the CFD and CFND groups compared with the control group. Ah receptor and cytochrome P-450 1A1 (CYP1A1) were detected in higher amounts in livers of both deficient groups. CYP1A1 is an enzyme associated with bioactivation of exogenous genotoxins. To our knowledge, this is the first time it has been shown that CYP1A1 and the Ah receptor are induced by dietary deficiencies.

Animals↗
PubMed1997

Fluorescence polarization immunoassay of progesterone.

A homogeneous fluorescence polarization immunoassay (FPIA) was developed to measure levels of progesterone in urine using a TDx analyzer in photocheck mode (Abbott Labs). Two tracers of ethylenediamine fluorescein thiocarbamyl (EDF) were employed; one was synthesized from 11 alpha-hydroxyhemisuccinate progesterone (Prog-11OH-HS) and the other was synthesized from 3-(o-carboxymethyl)oxime progesterone (Prog-3CMO). Each derivative of progesterone was conjugated with bovine serum albumin and used as an immunogen which produced monoclonal antibody clone 15A (MAb 15A, anti-Prog-11OH-HS) and clone 2B7 (MAb 2B7, anti-Prog-3CMO), respectively. Different combinations of tracers and antibodies were investigated in the FPIA system. Similar sensitivity was observed when using the pair, MAb 2B7 and its homologous tracer, Prog-3CMO-EDF, or MAb 15A and its homologous tracer, Prog-11OH-HS-EDF. In this immunoassay, no separation step was required and the total time for an assay of 10 samples was approximately 7 min. The progesterone detection limit in a 10 microliters sample was 3 ng/ml. The cross-reactivity results indicate that the A-, B- and D-ring of a steroid are buried in the binding pocket of MAb 15A, while the C-ring faced outward, resulting in cross-reactivity with 11-alpha hydroxy progesterone. The A-, B- and C-ring of a steroid of MAb 2B7, in contrast, are buried deep in the pocket leaving the D-ring facing outward, resulting in some different degrees of cross-reactivity with C17 position substituted steroids.

Fluorescence Polarization Immunoassay↗
PubMed1997

Alterations in the carnitine metabolism in epileptic children treated with valproic acid.

Serum concentrations of total carnitine, free carnitine and acylcarnitine were measured in forty-one epileptic patients treated with valproic acid (VPA). Among them, 14 patients were on VPA monotherapy and 27 were on VPA polytherapy. Forty-one age and sex matched healthy normal controls were also evaluated for carnitine metabolism. The mean total and free carnitine were significantly lower in both the VPA monotherapy and polytherapy groups compared with the controls. However, there were no significant differences in concentrations of carnitine between the VPA polytherapy and VPA monotherapy groups. Patients treated with VPA polytherapy had lower carnitine than those treated with VPA monotherapy. An inverse correlation was found between serum concentrations of carnitine and duration of treatment in patients treated with VPA. However, there was no significant correlations between serum concentrations of carnitine and those of VPA. Also, correlation between serum concentrations of carnitine and the activities of serum GOT and GPT was not significant. After L-carnitine supplementation in eleven patients with hypocarnitinemia, the concentrations of carnitine were significantly increased.

Administration, Oral↗
PubMed1996

FISH-Mapped CEPH YACs spanning 0 to 46 cM on human chromosome 6.

Seventy-six CEPH YACs were mapped by fluorescence in situ hybridization (FISH) to human metaphase chromosomes. These clones have been ordered from pter to 46 cM by combining the results of FISH with sequence-tagged site content mapping using data from the public databases. This created a minimal tiling path containing at least 37 Mb of human genomic DNA from 0 to 46 cM on chromosome 6 that contains up to four gaps not greater than 200 kb. These data provide an integration of the FLpter physical map values with cytogenetic band localization and markers on the genetic and radiation hybrid maps. We also assessed YAC chimerism and placed three additional Whitehead contigs (WC952, WC799, WC436) within the integrated map.

Chromosome Mapping↗
PubMed1996

Structure of the FKBP12-rapamycin complex interacting with the binding domain of human FRAP.

Rapamycin, a potent immunosuppressive agent, binds two proteins: the FK506-binding protein (FKBP12) and the FKBP-rapamycin-associated protein (FRAP). A crystal structure of the ternary complex of human FKBP12, rapamycin, and the FKBP12-rapamycin-binding (FRB) domain of human FRAP at a resolution of 2.7 angstroms revealed the two proteins bound together as a result of the ability of rapamycin to occupy two different hydrophobic binding pockets simultaneously. The structure shows extensive interactions between rapamycin and both proteins, but fewer interactions between the proteins. The structure of the FRB domain of FRAP clarifies both rapamycin-independent and -dependent effects observed for mutants of FRAP and its homologs in the family of proteins related to the ataxia-telangiectasia mutant gene product, and it illustrates how a small cell-permeable molecule can mediate protein dimerization.

Binding Sites↗