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Biomedical subjects

K S Jeong

Publications and source records attributed to K S Jeong.

At least 19 recordsLinked to original sources
PubMed2006

Supplementation of whole persimmon leaf improves lipid profiles and suppresses body weight gain in rats fed high-fat diet.

The objective of this study was to investigate the hypolipidemic effects of powdered whole persimmon leaf supplement in rats fed high-fat diet. Three groups of male Sprague-Dawley rats during 6 weeks were fed different diet: normal control (NC), high-fat (HF), and high-fat supplemented with powdered whole persimmon leaf (PL; 5%, wt/wt) groups. Body weight and relative weight of interscapular brown adipose tissue were significantly lower in the PL group than in the HF group, while plasma leptin concentration was higher. The supplementation of persimmon leaf significantly lowered the plasma total cholesterol and triglyceride concentrations, whereas elevated the ratio of HDL-C/total-C and improved the atherogenic index. Persimmon leaf supplementation led the hepatic cholesterol and triglyceride values to similar levels to the NC group. Accumulation of hepatic lipid droplets and the epididymal white adipocyte size of PL group were diminished comparing to the HF group. Hepatic HMG-CoA and ACAT activities were significantly higher in the PL group than in other groups. Contents of fecal triglyceride, cholesterol and acidic sterol were significantly higher in the PL group than in the HF group. Accordingly, we suggest that supplementation of the powdered whole persimmon leaf improves plasma and hepatic lipid levels profile partly via the increased fecal lipids in high-fat fed rats. These beneficial effects may be due to the properties of its phenolic compounds (1.15 g/100g) and high fiber (63.48 g/100g) content in the powdered persimmon leaf.

Acyl Coenzyme A↗
PubMed2005

Measurement of estrogen effect on bone turnover by 2H2O labeling.

Estrogen loss has been known to increase bone turnover through accelerated bone resorption coupled by increased bone formation. In the present study, we measured estrogen effect on bone turnover by incorporation of 2H from 2H2O into amino acids. At 6 weeks of age, rats were either sham-operated (sham) or ovariectomized (ovx). Two weeks after surgery, 17beta-estradiol (est) was implanted subcutaneously to ovx rats. At 9 weeks of age, 2H2O labeling started by administration of 4% 2H2O to rats for 4 or 7 weeks in drinking water after a single intraperitonial bolus injection with 99.9% 2H2O. Body 2H2O enrichments were stable at approximately 3.0% over labeling period. Fractional replacements (f) of the midshaft femur were higher in the sham group (40.36 +/- 4.89% vs 42.47 +/- 11.22%) than the ovx (28.57 +/- 9.67% vs 37.47 +/- 8.34%) and est (26.57 +/- 4.00% vs 30.35 +/- 5.34%) groups 4 and 7 weeks after labeling, respectively. Ovariectomy-induced bone loss was observed in the trabecular bone along with a significantly increased number of osteoclasts, all of which were normalized after estradiol treatment. Taken together, our results indicate that estrogen deficiency significantly reduces the proportion of newly synthesized bone matrix as well as the total amount of bone matrix. The reduced portion of new matrix in ovx rats, presumably caused by activated osteoclastic degradation, was compensated rapidly with time. In addition, estradiol treatment protected the bone matrix by decreasing bone turnover rate.

Alanine↗
PubMed2005

Hepatocellular carcinoma with metastasis to the spleen in a Holstein cow.

Hepatocellular carcinoma (HCC) with metastasis to the spleen in a Holstein cow was studied by histopathologic and immunohistochemical methods. The tumor was characterized by a pseudoglandular (acinar) pattern with an associated fibrous stroma. Individual cells often had a "hepatoid" appearance but were interspersed with scattered cells exhibiting a clear, periodic acid-Schiff (PAS)-positive cytoplasm and small eccentric nuclei. This pattern was present in nodules found in both liver and spleen. Moreover, hepatoid tumor cells were positive for alpha-fetoprotein. Immunohistochemical studies suggest that myofibroblasts were responsible for the production of fibrous septa surrounding the pseudoglandular structures of bovine HCC. In summary, our histologic and immunohistochemical findings support a diagnosis of primary HCC with splenic metastasis. Furthermore, the associated stromal response appears to be of a myofibroblast origin. The primary etiology of bovine HCC and the significance of the intralesional, PAS-positive clear cells remain undetermined.

Animals↗
PubMed2003

Multiple congenital malformation in a Holstein calf.

A 10-day-old male Holstein dairy calf with orthopaedic abnormalities was unable to stand but was alert with a suckle reflex. At necropsy, the calf showed multiple defects, including partial agenesis of the left rib plate, deformed left scapula, shortened left humerus, agenesis of the left kidney, atresia ani and scoliosis. The cause of these anomalies could not be determined. This report is the first to describe partial agenesis of ribs in a calf.

Abnormalities, Multiple↗
PubMed2001

Regulation of apoptosis by somatostatin and substance P in peritoneal macrophages.

Recent studies have shown that somatostatin (SOM) inhibits interleukin 6 (IL-6) and interferon gamma (IFNgamma) production by lymphocytes and peritoneal macrophages, whereas substance P (SP) enhances these cytokines production. To define the mechanism of the cytokine production enhancements and inhibitions by SOM and SP, we examined the expression of apoptosis modulator, p53, Bcl-2, Bax, inducible nitric oxide synthase (iNOS), Fas, caspase-8 and nitric oxide (NO) in thioglycolate-elicited peritoneal macrophages. SOM caused up-regulation of p53, Bcl-2, Fas and caspase-8 activities, and down-regulation of iNOS expression and NO production. On the other hand, SP slightly induces p53 and highly induces Bcl-2, iNOS expression and NO production. These data suggest that apoptosis by SOM may occur by a Bax- and NO-independent p53 accumulation, and through Fas and caspase-8 activation pathways, and that the inducible expression of Bcl-2 and NO production by SP may contribute to prevent the signals of apoptosis by Bax, and via Fas and caspase-8 activation.

Animals↗
PubMed2001

Self-assembly and dynamics of [2]- and [3]rotaxanes with a dinuclear macrocycle containing reversible Os-N coordinate bonds.

With a dinuclear macrocycle 2 that contains weak reversible OsVI-N coordinate bonds, self-assembly and equilibrium dynamics of [2]- and [3]rotaxanes have been investigated. When the macrocycle 2 was mixed together with threads 4a-e, which all contain an adipamide station but different sizes of end groups, [2]pseudorotaxane- and rotaxane-like complexes were immediately formed with large association constants of >7 x 103M(-1) in CDCl3 at 298 K. Exchange dynamics, explored by 2D-EXSY experiments, suggest that assembly and disassembly of complexes occur through two distinct pathways, slipping or clipping, and this depends on the size of the end groups. The slipping pathway is predominant with smaller end groups that give pseudorotaxane-like complexes, while the clipping pathway is observed with larger end groups that yield rotaxane-like complexes. Under the same conditions, exchange barriers (deltaG++) were 14.3 kcalmol(-1) for 4a and 16.7 kcalmol(-1) for 4d, and indicate that the slipping process is at least one order of magnitude faster than the clipping process. Using threads 13a and 13b that contain two adipamide groups, more complicated systems have been investigated in which [2]rotaxane, [3]rotaxane, and free components are in equilibrium. Concentration- and temperature-dependent 1H NMR spectroscopic studies allowed the identification of all possible elements and the determination of their relative distributions in solution. For example, the relative distribution of the free components, [2]rotaxane, and [3]rotaxane are 30, 45, and 25 %, respectively, in a mixture of 2 (2mM) and 13a (2mM) in CDCl3 at 10 degrees C. However, [3]rotaxane exists nearly quantitatively in a mixture of 2 (4 mM) and 13 a (2 mM) in CDCl3 at a low temperature - 10 degrees C.

Journal Article↗
PubMed2001

Control of mitochondrial redox balance and cellular defense against oxidative damage by mitochondrial NADP+-dependent isocitrate dehydrogenase.

Mitochondria are the major organelles that produce reactive oxygen species (ROS) and the main target of ROS-induced damage as observed in various pathological states including aging. Production of NADPH required for the regeneration of glutathione in the mitochondria is critical for scavenging mitochondrial ROS through glutathione reductase and peroxidase systems. We investigated the role of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) in controlling the mitochondrial redox balance and subsequent cellular defense against oxidative damage. We demonstrate in this report that IDPm is induced by ROS and that decreased expression of IDPm markedly elevates the ROS generation, DNA fragmentation, lipid peroxidation, and concurrent mitochondrial damage with a significant reduction in ATP level. Conversely, overproduction of IDPm protein efficiently protected the cells from ROS-induced damage. The protective role of IDPm against oxidative damage may be attributed to increased levels of a reducing equivalent, NADPH, needed for regeneration of glutathione in the mitochondria. Our results strongly indicate that IDPm is a major NADPH producer in the mitochondria and thus plays a key role in cellular defense against oxidative stress-induced damage.

3T3 Cells↗
PubMed2001

Design of a wavelet interpolation filter for enhancement of the ST-segment.

A wavelet interpolation filter (WIF) is designed for the removal of motion artifacts in the ST-segment of stress ECGs. The WIF consists of two parts. One part is a wavelet transform that decomposes the stress ECG signal into several frequency bands using a Haar wavelet. The other part is an interpolation method, such as the spline technique, that is used to enhance the reconstruction performance of the signal decomposed by the wavelet transform. To evaluate the performance of the WIF, three indices are used: signal-to-noise ratio (SNR), reconstruction square error (RSE) and standard deviation (SD). The MIT/BIH arrhythmia database, the European ST-T database and the triangular wave are used for evaluation. A noisy ECG signal, corrupted by motion artifacts, is simulated by the addition of two types of random noise to the original ECG signal. For comparison, three indices for the other methods are also computed: mean, median and hard thresholding. The performance of the WIF shows that RSE, SNR and SD are 392.7, 18.3dB and 2.6, respectively, in the case of a noisy signal with an SNR of 7.1 dB. This result is much better than those for the other methods.

Artifacts↗
PubMed2001

Subcellular redistribution of protein kinase C isozymes is associated with rat liver cirrhotic changes induced by carbon tetrachloride or thioacetamide.

BACKGROUND AND AIMS: Protein kinase C (PKC) plays a key role in the alteration of signal transduction in the liver, which may contribute to the development of liver cirrhosis. The aim of the present study was to examine the subcellular redistribution of PKC isozymes in rat liver cirrhosis, which is induced by two different cirrhotic chemical agents, carbon tetrachloride (CCl4) and thioacetamide (TAA). METHODS AND RESULTS: Thioacetamide and CCl4 were administered to rats for 8 and 30 weeks, respectively before rats were killed and autopsies performed at 9, 20 and 30 weeks later. The TAA induced a fibrotic pattern in the liver that differed from that produced by CCl4, notably in the formation of fibrous connective tissue and the proliferation of bile ductule cells. Cholangiofibrosis and clear-cell foci were also observed in TAA-treated rats at 30 weeks. Histological examination revealed that severe cirrhotic changes were present 9 weeks after the commencement of CCl4 treatment and 30 weeks after TAA treatment. DISCUSSION: When the subcellular redistribution of PKC isozymes (PKCalpha, -beta1, -delta, and -epsilon) was examined, all the PKC isozymes in CCl4-treated rats were found to be translocated to the membrane fraction, which may mean PKC activation, and then downregulated by proteolytic degradation after 9 weeks of treatment, which coincided with peak cirrhotic changes. All rats treated with CCl4 recovered to the control level after 20 weeks of treatment. In the case of TAA-treated rats, PKC isozymes were translocated to the particulate fraction of the liver after 9 weeks of treatment and this persisted in most of the rats for the duration of the experiment. CONCLUSIONS: From these results, it would appear that PKC translocation preceded morphologic changes, and that an altered subcellular distribution of the PKC isozyme may be associated with the response to liver damage and carcinogenesis.

Animals↗
PubMed2001

Exchange of the basic domain of human immunodeficiency virus type 1 Rev for a polyarginine stretch expands the RNA binding specificity, and a minimal arginine cluster is required for optimal RRE RNA binding affinity, nuclear accumulation, and trans-activation.

The Rev regulatory protein of human immunodeficiency virus (HIV) facilitates the nuclear export of unspliced and partially spliced HIV RNAs. Using a Rev:MS2 phage coat protein fusion that could be targeted to bind and activate the Rev-responsive element (RRE) RNA or heterologous MS2 phage operator RNA, we analyzed the role(s) of the arginine-rich RNA binding domain in RNA binding and transactivation. The arginine-rich domain could be functionally replaced by a stretch of nine arginines. However, polyarginine substitutions expanded the RNA binding specificity of the resultant mutant Rev protein. Polyarginine insertions in place of residues 24 to 60 that excised the RNA binding and oligomerization domains of Rev preserved the activation for MS2 RNA, but not for the RRE. A nine-arginine insertion outside of the natural context of the Rev nuclear localization signal domain was incompatible with activation of either RNA target. Insertions of fewer than eight arginines impaired RRE activation. Interrupted lysine clusters and disruption of the arginine stretch with lysine or neutral residues resulted in a similar phenotype. Some of these mutants with a null phenotype for RRE activated the heterologous MS2 RNA target. Under steady-state conditions, mutants that preserved the Rev response for RRE RNA localized to the nuclei; those with poor or no Rev response accumulated mostly in the cytoplasm. Many of the cytoplasmically resident derivatives became nuclear when leptomycin B (LMB) treatment inhibited nuclear export of nuclear export signal-containing proteins. Mutants that had a null activation potential for either RNA target were particularly resistant to LMB treatment. Abbreviated nuclear residence times and differences in RRE binding affinity may have compromised their activation potential for RRE. High-affinity binding to MS2 RNA through the intact coat protein was sufficient to overcome the short nuclear residence times and to facilitate MS2 activation by some derivatives.

Animals↗
PubMed2000

Cytochrome P450 2E1 (CYP2E1)-dependent production of a 37-kDa acetaldehyde-protein adduct in the rat liver.

Ethanol-inducible cytochrome P450 2E1 (CYP2E1) has been shown to be involved in the metabolism of both ethanol and acetaldehyde. Acetaldehyde, produced from ethanol metabolism, is highly reactive and can form various protein adducts. In this study, we investigated the role of CYP2E1 in the production of a 37-kDa acetaldehyde-protein adduct. Rats were pairfed an isocaloric control or an alcohol liquid diet with and without cotreatment of YH439, an inhibitor of CYP2E1 gene transcription, for 4 weeks. The soluble proteins from rat livers of each group were separated on SDS-polyacrylamide gels followed by immunoblot analysis using specific antibodies against the 37-kDa protein acetaldehyde adduct. In addition, catalytic activities of the enzymes involved in alcohol and acetaldehyde metabolism were measured and compared with the adduct level. Immunoblot analysis revealed that the 37-kDa adduct, absent in the pair-fed control, was evident in alcohol-fed rats but markedly reduced by YH439 treatment. Immunohistochemical analysis also showed that the 37-kDa adduct is predominantly localized in the pericentral region of the liver where CYP2E1 protein is mainly expressed. This staining disappeared in the pericentral region after YH439 treatment. The levels of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase isozymes were unchanged after YH439 treatment. However, the level of the 37-kDa protein adduct positively correlated with the hepatic content of P4502E1. These data indicate that the 37-kDa adduct could be produced by CYP2E1-mediated ethanol metabolism in addition to the ADH-dependent formation.

Acetaldehyde↗
PubMed2000

Deletions near the N-terminus of HIV-1 Rev reduce RNA binding affinity and dominantly interfere with Rev function irrespective of the RNA target.

The contributions of the near N-terminal residues of Rev protein of HIV were investigated by analyzing N-terminal deletions of Rev in the context of a Rev/MS-C fusion protein that can bind and activate both the Rev responsive element (RRE) and the MS2 phage translational operator RNAs. Rev/MS-C fusion proteins deleted for residues 3-19 of Rev retained trans-activation potential for both RRE and MS2 targets. Coincidentally, peptides spanning residues 17-87 or 22-85 were functionally competent for trans-activation of RRE containing HIV-1 gag mRNA. Deletion of residues 18-24 of Rev in the Rev/MS-C fusion protein abolished the activation potential for both RRE and MS2 targets, although this mutant was competent for specific RNA binding, protein multimerization, and nuclear and nucleolar localization. Four mutants dominantly interfering with Rev activation of RRE were mapped near the N-terminus of Rev; (i) between residues 18 and 24, (ii) 25-34, (iii) 43-50, and (iv) 51-60. Of these, the mutant lacking residues 18-24 was a novel trans-dominant inhibitor of Rev and Rev/MS-C for activation of RRE or MS2 RNA, while the oligomerization domain mutants mapping between residues 25-34 or 51-60 inhibited the activation of RRE rather than MS2 RNA.

Amino Acid Sequence↗
PubMed2000

Adaptive response is differently induced depending on the sensitivity to radiation-induced cell death in mouse epidermal cells.

We investigated the relationship between induction of radio-adaptive response and cell death in mouse normal and neoplastic epidermal cells. Mouse normal primary keratinocytes (PK), cancer-prone cells [v-rasHa-transfected mouse keratinocytes (ras-PK), and line 308 cells (mouse skin papilloma cells which have activated rasHa gene with A-to-T transversion at codon 61) were primed with a low dose of gamma-rays (0.01 Gy), and were challenged with a high dose (4 Gy) after a 4 or 7 h interval. The induction of cell death in PK was 2-10 times higher and was also more rapid in PK than in ras-PK or 308 cells. Low-dose pretreatment with a 4 h interval decreased cell death, and this adaptive response was prominent in PK, whereas it was less obvious in the cases of ras-PK and 308 cells. The response of each protein kinase C (PKC) isozymes to high-dose radiation, especially PKCalpha, PKCdelta, PKCepsilon, and PKCeta, were different between the normal and ras oncogene-activated neoplastic keratinocytes; translocation of these isozymes to membrane occurred more rapidly in normal than in neoplastic cells. Furthermore, low-dose pretreatment did not induce the translocation of PKCdelta in PK significantly more than in ras-PK and 308. Thus, the difference in the induction of radio-adaptive responses between mouse normal and neoplastic epidermal cells reflects difference in the rapidity of cell death, and responsiveness of PKC may affect this adaptive response.

Adaptation, Physiological↗
PubMed2000

Selective activation of the c-Jun N-terminal protein kinase pathway during 4-hydroxynonenal-induced apoptosis of PC12 cells.

The by-product of lipid peroxidation, 4-hydroxynonenal (HNE), was shown to cause apoptosis in PC12 cells. In this study, we investigated the molecular mechanism of HNE-induced apoptosis in these cells. Specifically, we determined the effect of HNE on the activities of mitogen-activated protein (MAP) kinases involved in early signal transduction. Within 15 to 30 min after HNE treatment, c-Jun N-terminal protein kinase (JNK) was maximally activated, before it returned to control level at 1 h post-treatment. In contrast, activities of extracellular signal-regulated kinase and p38 MAP kinase remained unchanged from their baseline levels. Stress-activated protein kinase kinase (SEK1), an upstream kinase of JNK, was also activated within 5 min after HNE treatment and remained activated for up to 60 min. Marked activation of the JNK pathway through SEK1 and apoptosis signal-regulating kinase 1 (ASK1), an upstream kinase of SEK1, was demonstrated by the transient transfection of cDNA for wild-type SEK1 or ASK1 together with JNK into COS-7 cells. Furthermore, significant reductions in JNK activation and HNE-induced cell death were observed when either of the dominant negative mutant of SEK1 or ASK1 was cotransfected with JNK. Pretreatment of PC12 cells with a survival-promoting agent, 8-(4-chlorophenylthio)-cAMP, prevented both the HNE-induced JNK activation and apoptosis. Nonaldehyde, a nontoxic aldehyde, neither caused apoptosis nor JNK activation. Pretreatment of PC12 cells with SB203580, a specific inhibitor of p38 MAP kinase, had no effect on HNE-induced apoptosis. All these data suggest that the selective JNK activation by HNE is critical for the apoptosis of PC12 cells and that the HNE-mediated apoptosis is likely to be mediated through the activation of the ASK1-SEK1-JNK pathway without activation of extracellular signal-regulated kinase or p38 MAP kinase.

Aldehydes↗
PubMed2000

Somatostatin and substance P induced in vivo by lipopolysaccharide and in peritoneal macrophages stimulated with lipopolysaccharide or interferon-gamma have differential effects on murine cytokine production.

We have investigated whether lipopolysaccharide (LPS) induces substance P (SP) and somatostatin (SOM) in popliteal lymph nodes in vivo and whether macrophages are a source of SP and SOM in vitro. We have also investigated the effect of SP and SOM treatment on the production of cytokines. SP reached a maximum 3 days after injection of LPS (100 microg/footpad) and then declined. SOM expression after LPS injection reached a maximum at 5-7 days. Stimulation of thioglycolate-elicited peritoneal macrophages with LPS (20 microg/ml), recombinant interferon-gamma (rIFN-gamma, 100 U/ml), and LPS plus rIFN-gamma induced SOM and SP. Thioglycolate-elicited, unstimulated peritoneal macrophages also synthesized these peptides. SOM (10(-12)-10(-8) M) significantly inhibited IL-6 and IFN-gamma production, whereas SP at those concentrations enhanced cytokine production by activated lymphocytes and macrophages. These findings suggest that neuropeptides which originate from macrophages and nerve fibers act as immunomodulators to mediate changes in the pattern of cytokine production.

Animals↗
PubMed1999

Identification and functional characterization of a novel, tissue-specific NAD(+)-dependent isocitrate dehydrogenase beta subunit isoform.

To understand the interactions and functional role of each of the three mitochondrial NAD(+)-dependent isocitrate dehydrogenase (IDH) subunits (alpha, beta, and gamma), we have characterized human cDNAs encoding two beta isoforms (beta(1) and beta(2)) and the gamma subunit. Analysis of deduced amino acid sequences revealed that beta(1) and beta(2) encode 349 and 354 amino acids, respectively, and the two isoforms only differ in the most carboxyl 28 amino acids. The gamma cDNA encodes 354 amino acids and is almost identical to monkey IDHgamma. Northern analyses revealed that the smaller beta(2) transcript (1.3 kilobases) is primarily expressed in heart and skeletal muscle, whereas the larger beta(1) mRNA (1.6 kilobases) is prevalent in nonmuscle tissues. Sequence analysis of the IDHbeta gene indicates that the difference in the C-terminal 28 amino acids between beta(1) and beta(2) proteins results from alternative splicing of a single transcript. Among the various combinations of human IDH subunits co-expressed in bacteria, alphabetagamma, alphabeta, and alphagamma combinations exhibited significant amounts of IDH activity, whereas subunits produced alone and betagamma showed no detectable activity. These data suggest that the alpha is the catalytic subunit and that at least one of the other two subunits plays an essential supporting role for activity. Substitution of beta(1) with beta(2) in the co-expression system lowered the pH optimum for IDH activity from 8.0 to 7.6. This difference in optimal pH was analogous to what was observed in mouse kidney and brain (beta(1) prevalent; optimal pH 8.0) versus heart (beta(2) prevalent; pH 7.6) mitochondria. Experiments with a specially designed splicing reporter construct stably transfected into HT1080 cells indicate that acidic conditions favor a splicing pattern responsible for the muscle- and heart-specific beta(2) isoform. Taken together, these data indicate a regulatory role of IDHbeta isoforms in determining the pH optimum for IDH activity through the tissue-specific alternative splicing.

Alternative Splicing↗