Biomedical subjects

S T Park

Publications and source records attributed to S T Park.

At least 19 recordsLinked to original sources

PubMed2004

Magnetic resonance imaging of metaplastic carcinoma of the breast: sonographic and pathologic correlation.

Metaplastic carcinoma of the breast is a rare disease. We describe the MRI findings with the correlative sonographic and pathologic features of two cases. On MRI, T2-weighted images demonstrate a relatively well-defined mass with high signal intensity cystic components. Dynamic enhancement subtraction images showed an early enhancing and delayed washout peripheral rim and non-enhancing internal components. A microlobulated, isoechogenic mass with cystic components was seen sonographically, and was histopathology related to necrosis and cystic degeneration. Although these features are not unique, metaplastic carcinoma should be included in the differential diagnosis for breast masses.

Adult↗

PubMed2001

Implication of co-measured platelet factor 4 in the reliability of the results of the plasma transforming growth factor-beta 1 measurement.

We examined the possible alteration of circulating transforming growth factor-beta1 (TGF-beta1) concentrations in a time-dependent fashion in human plasma. Plasma TGF-beta1 was measured three times at 2 week-intervals from each of 12 healthy participants. Platelet factor 4 (PF4) was measured in parallel with TGF-beta1 to estimate the degree of platelet degranulation. TGF-beta1 levels of the second and third plasma samples, in which PF4s were measured as < approximately 1000 IU/ml, were relatively low and fell in a narrow range. However, TGF-beta1 levels of the first samples, in most of which PF4s were > approximately 1000 IU/ml, appeared much higher and more variable than those of the second or third samples. These results indicate that the platelet degranulation accounted for the higher TGF-beta1 levels in the first samples, and thus did not support our initial assumption. We, nevertheless, could propose a useful guidance in the assessment of TGF-beta1 levels in plasma. When the PF4 level is measured as < approximately 1000 IU/ml under our assay conditions, the TGF-beta1 level in a given plasma sample might be accepted as a reliable value considering the effect of platelet degranulation on TGF-beta1 level.

Adult↗

PubMed2001

Inhibitory action of water soluble fraction of Terminalia chebula on systemic and local anaphylaxis.

We investigated the effects of the water soluble fraction of Terminalia chebula (Combretaceae) (WFTC) on systemic and local anaphylaxis. WFTC administered 1h before compound 48/80 injection inhibited compound 48/80-induced anaphylactic shock 100% with doses of 0.01-1.0 g/kg. When WFTC was administered 5 or 10 min after compound 48/80 injection, the mortality also decreased in a dose-dependent manner. Passive cutaneous anaphylaxis was inhibited by 63.5+/-7.8% by oral administration of WFTC (1.0 g/kg). When WFTC was pretreated at concentrations ranging from 0.005 to 1.0 g/kg, the serum histamine levels were reduced in a dose-dependent manner. WFTC (0.01-1.0 mg/ml) also significantly inhibited histamine release from rat peritoneal mast cells (RPMC) by compound 48/80. However, WFTC (1.0 mg/ml) had a significant increasing effect on anti-dinitrophenyl IgE-induced tumor necrosis factor-alpha production from RPMC. These results indicate that WFTC may possess a strong antianaphylactic action.

Anaphylaxis↗

PubMed2001

Disodium cromoglycate inhibits production of immunoglobulin E.

Disodium cromoglycate (DSCG) has been shown to inhibit the release of mediators from mast cells. In the present study, the effect of DSCG on active anaphylactic reaction was studied in mice. DSCG dose-dependently inhibited the active systemic anaphylactic reaction and serum immunoglobulin (Ig)E production induced by immunization with ovalbumin, Bordetella pertussis toxin and aluminum hydroxide gel. DSCG strongly inhibited IL-4-dependent IgE production by lipopolysaccharide-stimulated murine whole spleen cells. In the case of U266 human IgE-bearing B cells, DSCG also showed an inhibitory effect on the IgE production. These results suggest that DSCG has an anti-anaphylactic activity by inhibition of IgE production from B cells.

Anaphylaxis↗

PubMed2001

Phosphatidylinositol 3-kinase regulates proliferation of RAW 264.7 macrophages.

Phosphatidylinositol 3-kinase (P13-kinase) is an enzyme that acts as a direct biochemical link between a novel phosphatidylinositol pathway and a number of proteins containing intrinsic or associated kinase activities. Here we demonstrate that wortmannin, P13-kinase inhibitor, decreases the proliferation of RAW 264.7 macrophages and that another structurally unrelated inhibitor of P13-kinase, LY294002. also inhibits the proliferation. These results indicate a possible involvement of P13-kinase in RAW 264.7 macrophages growth regulation. Wortmannin stimulation of RAW 264.7 macrophages is followed by sustained expression of the mRNA of c-fos and a transient expression of the mRNA of c-jun. We also show that the wortmannin and LY294002 induce a cell cycle arrest in asynchronously growing cells leading to an inhibition of cell proliferation after 12 h of treatment. In addition, wortmannin or LY294002 inhibited the phorbol 12-myristate 13-acetate-induced macrophages proliferation potently. These results suggest that P13-kinase plays an important role in growth regulation of RAW 264.7 macrophages and that protein kinase C is a down stream effector of P13-kinase.

Androstadienes↗

PubMed2001

Polymorphism of the angiotensin-converting enzyme gene in patients with cerebral infarction in Koreans.

The relationship between cerebrovascular disease and an insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is still being debated. The frequency of the DD genotype of the ACE gene was significantly higher in subjects with than those without cerebral infarction in Japan. The aim of the present study was to assess the relationship between ACE gene polymorphism and the development of cerebral infarction in a population from Korea. We examined its possible role as a risk factor in patients with cerebral infarction. The association between ACE gene polymorphism and cerebral infarction was examined in 106 patients with cerebral infarction and 498 controls without cerebral infarction. Frequencies of the genotypes and alleles of the ACE gene were investigated. The ACE genotype was analyzed by the polymerase chain reaction (PCR). The frequency of D allele was 37.7% in patients and 39.1% in controls (chi2 = 0.128, p = 0.720). The frequencies of the genotypes of the ACE gene were II: 39.6%, ID: 45.3%, and DD: 15.1% in patients, and II: 37.1%, ID: 47.6%, and DD: 15.3% in controls (chi2 = 0.127, p = 0.721). There was no significant difference in the frequency of the DD genotype of the ACE gene, and we did not find any association between ACE polymorphism and cerebral infarction. These results indicate that ACE polymorphism is not a risk factor for the development of cerebral infarction in a Korean population.

Adult↗

PubMed2001

Inhibition of heat shock-induced apoptosis by peppermint oil in astrocytes.

Exposure to environmental stresses and toxins is linked to the pathogenesis of neuropsychiatric disorders. Astrocytes, the most abundant glial-cell type in the brain, are considered to have physiological and pathological roles in neuronal activities. We have investigated whether peppermint oil inhibits heat shock-induced apoptosis of astrocytes. We found that peppermint oil inhibits the heat shock-induced apoptosis in both human astrocyte CCF-STTG1 cells and rat astrocytes. Pretreatment of the cells with peppermint oil inhibited the heat shock-induced DNA fragmentation and condensation of nuclear chromatin. Peppermint oil also inhibited the caspase-3 activation and poly-ADP-ribose polymerase fragmentation in CCF-STTG1 cells. These results suggest that peppermint oil may modulate the apoptosis of astrocytes via the activation of the caspase-3.

Animals↗

PubMed2000

Expression of 3 beta-hydroxysteroid/dehydrogenase/delta5-delta4/isomerase in the tracheal cartilage of the rat.

The enzyme complex 3beta-hydroxysteroid dehydrogenase isomerase/delta5-delta4 (3beta-HSD) is involved in the biosynthesis of all classes of active steroids. In this study, the presence of 3beta-HSD was defined in rat tracheal cartilage. The expression of the 3beta-HSD gene was examined by Northern blot analysis from 30-day-old rats. Western blot and immunohistochemical localization were also performed with antibodies raised against purified human placental 3beta-HSD to obtain further information on the expression of 3beta-HSD protein during fetal and postnatal periods of development in rat cartilage. Northern blot analysis using an oligonucleotide common to the 4 known 3beta-HSD isoforms showed 3beta-HSD mRNA corresponding to a transcript of 1.7 kb. Furthermore, a 42 KDa protein band was detected in the tracheal cartilage extracts by Western blot analysis. Immunostaining for 3beta-SD was observed in chondrocytes. The first expression was detected on the 17th day of fetal life by Western blot and immunohistochemistry. Immunoreactivity of 3beta-HSD showed a significant increase at 7 and 15 days after birth, and then remained unchanged through adulthood, in agreement with the data of the Western blot. Our results demonstrated the expression for 3beta-HSD in the tracheal cartilage at both the mRNA and protein levels during fetal life and postnatal development of the rat. These results suggest that 3beta-HSD may synthesize certain steroids which play major roles in differentiation and maintenance of function during development of rat cartilage.

3-Hydroxysteroid Dehydrogenases↗

PubMed2000

Human chorionic gonadotropin induces nitric oxide synthesis by murine microglia.

This study investigated the effects of human chorionic gonadotropin (hCG) on the synthesis of nitric oxide (NO) in murine neonatal microglial cells. When hCG was used in combination with interferon-gamma (IFN-gamma), there was a marked cooperative induction of NO synthesis in a dose-dependent manner. This increase in NO synthesis was reflected as an increased amount of iNOS protein. The increase of NO synthesis by IFN-gamma-plus-hCG was associated with the increase of tumor necrosis factor-alpha (TNF-alpha) secretion and hCG-induced NO production was decreased by the treatment with anti-murine TNF-alpha neutralizing antibody. This study provides evidence that hCG activates expression of iNOS protein in murine microglial cells accompanied by NO accumulation via pathway dependent on L-arginine in the culture medium, and further offers that TNF-alpha acts on the NO synthesis from IFN-gamma-primed murine microglial cells.

Animals↗

PubMed2000

Nitric oxide production by high molecular weight water-soluble chitosan via nuclear factor-kappaB activation.

High molecular weight water-soluble chitosan (WSC), having an average molecular weight of 300000 Da and a degree of deacethylation over 90%, can be produced using a simple multi-step membrane separation process. In this study, the effect of WSC on the production of nitric oxide (NO) in RAW 264.7 macrophages was evaluated. Water-insoluble chitosan alone has been previously shown to exhibit in vitro stimulatory effect on macrophages NO production. However, WSC had no effect on NO production by itself. When WSC was used in combination with recombinant interferon-gamma (rIFN-gamma), there was a marked cooperative induction of NO synthesis in a dose-dependent manner. The optimal effect of WSC on NO synthesis was shown 24 h after treatment with rIFN-gamma. The increased production of NO from rIFN-gamma plus WSC-stimulated RAW 264.7 macrophages was decreased by the treatment with N(G)-monomethyl-L-arginine (N(G)MMA). The increase in NO synthesis was reflected, as an increased amounts of inducible NO synthase protein. In addition, synergy between rIFN-gamma and WSC was mainly dependent on WSC-induced tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) activation. The present results indicate that the capacity of WSC to increase NO production from rIFN-gamma-primed RAW 264.7 macrophages is the result of WSC-induced TNF-alpha secretion via the signal transduction pathway of NF-kappaB activation.

Animals↗

PubMed2000

Inhibition of tumor necrosis factor-alpha-induced apoptosis by Asparagus cochinchinensis in Hep G2 cells.

A human hepatoma cell line, Hep G2 cells, is a reliable system for the study of alcohol-induced hepatotoxicity. In this study, we investigated the effect of an aqueous extract of Asparagus cochinchinensis(MERRIL) (Liliaceae) roots (ACAE) on ethanol (EtOH)-induced cytotoxicity in Hep G2 cells. ACAE (1-100 microg/ml) dose-dependently inhibited the EtOH-induced tumor necrosis factor-alpha (TNF-alpha) secretion. ACAE (1-100 microg/ml) also inhibited the EtOH and TNF-alpha-induced cytotoxicity. Furthermore, we found that ACAE inhibited the TNF-alpha-induced apoptosis of Hep G2 cells. These results suggest that ACAE may prevent the EtOH-induced cytotoxicity through inhibition of the apoptosis of Hep G2 cells.

Apoptosis↗

PubMed2000

Expression of protein kinase C genes in normal (+/+) and W mutant alleles (Wsh/Wsh, W/Wv) mice testes.

In the present study, we investigated the expression of mRNA of protein kinase C (PKC) isoenzymes (alpha, beta, gamma, delta, epsilon, zeta, eta, and theta) in normal (+/+) and W mutant alleles mice testes. In +/+ mice testes, abundant expression of PKCdelta and PKCtheta was observed, while other PKCs (alpha, beta, gamma, epsilon, zeta, and eta) generally were not detected by Northern blotting. The PKCdelta and PKCtheta isoenzymes demonstrated a distinctive cellular distribution when evaluated by in situ hybridization. We have previously shown that PKCdelta gene was selectively expressed in spermatid of +/+ testes. Here we show that PKCdelta gene is also present in spermatid of Wsh/Wsh mice testes and PKCtheta gene was present in interstitial cells of +/+, Wsh/Wsh, and W/Wv mice testes. These studies provide the evidence of selective cell distributions of the PKC isoenzymes and suggest that PKC has the functional significance in testes.

Alleles↗

PubMed2000

Inhibitory effect of mast cell-mediated immediate-type allergic reactions by sulfapyridine.

We examined the effect of sulfapyridine on mast cell-mediated immediate-type allergic reactions. Sulfapyridine (1 and 10 microg/kg) significantly inhibited systemic allergic reaction induced by compound 48/80 in rats. Sulfapyridine (1 and 10 microg/kg) also inhibited significantly local mast cell-mediated immediate-type allergic reactions activated by anti-dinitrophenyl (DNP) IgE. Moreover, sulfapyridine inhibited histamine release dose-dependently in the rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. When sulfapyridine was added, the level of cAMP in RPMC, transiently and significantly increased about 4-fold compared with that of basal cells. These results indicate that sulfapyridine inhibits mast cell-mediated immediate-type allergic reactions in vivo and in vitro.

Animals↗

PubMed1999

Growth inhibition and apoptosis due to restoration of E2A activity in T cell acute lymphoblastic leukemia cells.

Two models have been proposed for the molecular mechanism by which the Tal1 oncogene causes T cell acute lymphoblastic leukemia (T-ALL). The activation model suggests that Tal1 as heterodimers with the E2A transcription factor activates the expression of oncogenes. The inhibition model postulates that Tal1 interferes with the tumor-suppressing function of E2A. In the Jurkat T cell line, originally derived from a patient with T-ALL, Tal1 is complexed with E2A proteins and the transcriptional activity of E2A is very low. When E2A activity was restored by expressing an E2A-Tal1 fusion protein, E-T/2, the Jurkat cells underwent growth arrest and subsequently apoptosis, thus supporting the inhibition model and suggesting that E2A loss may contribute to leukemic progression.

Apoptosis↗

PubMed1999

Effect of Korean folk medicine 'Chung-Dae-San' on mast cell-dependent anaphylactic reaction.

We investigated the effect of the herbal formulation 'Chung-Dae-San' (CDS) on anaphylactic reactions. CDS inhibited compound 48/80-induced anaphylactic shock 100% with the dose of 10(0) g/kg body weight (BW). When CDS was given as pretreatment at concentrations ranging from 10(-4) to 10(0) g/kg BW, the serum histamine levels induced by compound 48/80 were reduced in a dose-dependent manner. We also investigated the effect of CDS on mast cell-dependent passive cutaneous anaphylaxis (PCA) activated by anti-dinitrophenyl (DNP) IgE antibody. CDS potently inhibited PCA when administered orally, topically, intraperitoneally or intradermally. However, it did not show inhibitory activity when administered intravenously. CDS dose-dependently inhibited the histamine release from the rat peritoneal mast cells (RPMC) by compound 48/80 and anti-DNP IgE. Moreover, the level of cAMP in RPMC, when CDS was added, significantly increased about 4-fold at 4 min compared with that of basal cells. These results indicate that CDS may possess strong antianaphylactic activity and also suggest the differential activity following administration routes may be caused by difference in bioavailability.

Anaphylaxis↗

PubMed1999

Inhibition of immunoglobulin E production by Poncirus trifoliata fruit extract.

Immunoglobulin E (IgE) is the principal immunoglobulin involved in immediate hypersensitivities and chronic allergic diseases. The effect of an aqueous extract of Poncirus trifoliata (L) Raf. (Rutaceae) fruits (PTFE) on in vivo and in vitro IgE production was investigated. PTFE dose-dependently inhibited the active systemic anaphylaxis and serum IgE production induced by immunization with ovalbumin, Bordetella pertussis toxin and aluminum hydroxide gel. PTFE strongly inhibited interleukin 4 (IL-4)-dependent IgE production by lipopolysaccharide-stimulated murine whole spleen cells. In the case of U266 human IgE-bearing B cells, PTFE also showed an inhibitory effect on the IgE production. These results suggest that PTFE has an anti-allergic activity by inhibition of IgE production from B cells.

Aluminum Hydroxide↗

PubMed1998

The Tal1 oncoprotein inhibits E47-mediated transcription. Mechanism of inhibition.

The Tal1 oncogene is a class II basic helix-loop-helix (bHLH) transcription factor, overexpressed in as much as 60% of T cell acute lymphoblastic leukemia cases. Like other class II bHLH proteins, Tal1 can heterodimerize with the class I bHLH proteins, such as E47, and bind to a DNA recognition sequence termed E box. Therefore, it is believed that the oncogenic capacity of Tal1 lies in its ability, as a heterodimer with E47, to activate aberrantly a set of "leukemogenic" genes in T cells. However, compared with E47 homodimers, Tal1/E47 heterodimers are very poor transactivators. Thus the effect of Tal1 is actually to inhibit E47 homodimer activity. Here we propose that the transforming properties of Tal1 are the result of its ability to inhibit E47 activity. We address the mechanism of Tal1 inhibition and demonstrate that Tal1/E47 heterodimers cannot activate transcription because their respective activation domains are incompatible. Furthermore, we present data showing that Tal1 can inhibit E47-mediated activation of the CIP1 gene. Finally, we demonstrate that Tal1 inhibits E47 activity in leukemic T cells.

Basic Helix-Loop-Helix Proteins↗

PubMed1998

Immunohistochemical study of 3beta-hydroxysteroid dehydrogenase/delta5-delta4 isomerase in the rat cardiovascular system.

The enzyme complex 3beta-hydroxysteroid dehydrogenase (3beta-HSD) is involved in the biosynthesis of all classes of active steroids. It is known that the enzymatic activity of 3beta-HSD is present not only in classical steroidogenic tissues, but also in many peripheral tissues including cardiac tissue. To determine whether 3beta-HSD is present in rat non-steroidogenic tissues, we examined cardiovascular tissues including the ventricle, atrium, aortic arch, abdominal aorta, and inferior vena cava by immunohistochemistry and Western blotting using polyclonal antibody raised against a synthetic peptide of human placental 3beta-HSD. By Western blotting, protein bands immunoreactive for anti-3beta-HSD were detected at molecular weights of 42 and 37 kDa in both the ventricle and atrium, whereas only a 37 kDa band was recognized in both the aortic arch and abdominal aorta. By immunohistochemistry, immunoreactivity for 3beta,-HSD was detected in both the ventricular and atrial cardiocytes, while immunostaining was also found, though faintly, in the smooth muscles of the aortic arch, abdominal aorta, and inferior vena cava. These results suggest that cardiocytes may synthesize the steroidogenic 3beta,-HSD enzyme.

Animals↗