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Biomedical subjects

C Choi

Publications and source records attributed to C Choi.

At least 73 records · Page 4Linked to original sources

Seroprevalence of porcine respiratory coronavirus in selected Korean pigs.

A total of 446 serum samples from 88 herds in Korea were examined for antibody to porcine respiratory coronavirus (PRCV) using blocking enzyme-linked immunosorbent assay (ELISA). All serum samples were collected from 24- to 26-week-old finishing pigs between December 1998 and June 1999. By ELISA, 237 out of 446 sera tested (53.1%) and 54 out of 88 sampled herds (61.3%) were positive against PRCV. Of 446 sera from 88 herd tested, 185 (41.5%) serum samples from 22 (25%) herds were seronegative against PRCV and transmissible gastroenteritis virus infection. Our data suggested that seropositive herds for PRCV are distributed diffusely throughout South Korea.

Animals↗

Detection and differentiation of porcine epidemic diarrhoea virus and transmissible gastroenteritis virus in clinical samples by multiplex RT-PCR.

A multiplex reverse-transcriptase-PCR (RT-PCR) procedure was developed for the simultaneous detection of porcine epidemic diarrhoea virus (PEDV) and transmissible gastroenteritis virus (TGEV) in preweaning pigs with diarrhoea. The membrane gene of PEDV and the nucleocapsid gene of TGEV were chosen as targets. The PCR products of PEDV and TGEV had molecular sizes of 412 and 612 base pairs, respectively. Primers from PEDV did not react with any TGEV tested and vice versa. In addition, the primers did not react with other pig viruses. The multiplex RT-PCR was able to detect 10 tissue culture-infective doses 50 per cent (TCID50)/ml of PEDV or TGEV with each of the primer sets for PEDV and TGEV, respectively. The RNAS of PEDV and TGEV were detected directly in intestinal and faecal samples from pigs infected experimentally with either virus. The results of the assay correlated well with the results of virus isolation. None of the five control specimens was positive. PEDV was detected in 10 intestinal and nine faecal samples, and among the nine positive faecal samples two were culture-negative. TGEV was also detected in 10 intestinal and nine faecal samples, and among the nine positive faecal samples, three were culture-negative.

Animals↗

Loss of heterozygosity at chromosome segments 8p22 and 8p11.2-21.1 in transitional-cell carcinoma of the urinary bladder.

To identify the putative tumor-suppressor gene (TSG) involved in transitional-cell carcinoma (TCC) of the urinary bladder, we undertook an allelotyping analysis in 48 cases of TCC. Relatively high percentages of allelic loss were found in 2p (5 of 23, 21.7%), 8p (9 of 21, 42.9%), 9p (4 of 20, 20.0%), 12q (6 of 28, 21.4%), 15q (1 of 5, 20%; 4 of 20, 20%), 17p (7 of 26, 26.9%) and 22q (6 of 23, 26.1%). On the basis of these results, fine-deletion mapping was performed on chromosome 8 in 52 cases by PCR of 15 microsatellite markers. Two distinct regions of common deletion were found. A 10 cM telomeric region was located to 8p22, defined by D8S511 and D8S258. A 17 cM centromeric region was located to 8p11.2-21.1, flanked by D8S298 and D8S535. The distance between the telomeric and the centromeric regions of common deletion was 3 cM. Loss of heterozygosity of 8p22 was frequently observed in tumors of high grade or advanced stage.

Carcinoma, Transitional Cell↗

Acetylcholine receptor extracellular domain determines sensitivity to nicotine-induced inactivation.

We have shown previously that chronic exposure to submicromolar concentrations of nicotine permanently inactivates alpha4beta2 and alpha7 neuronal nicotinic acetylcholine receptors while alpha3beta2 acetylcholine receptors are resistant to inactivation. Phosphorylation of the large cytoplasmic domain has been proposed to mediate functional inactivation. Chimeric subunits consisting of human alpha4 sequence from their N-terminus to either the beginning of the first transmembrane domain or the large cytoplasmic domain and alpha3 sequences thereafter formed acetylcholine receptors with beta2 subunits which were as susceptible to nicotine-induced inactivation as wild-type alpha4 acetylcholine receptors. The converse chimeras, containing the N-terminal parts of the alpha3 subunit and the C-terminal parts of the alpha4 subunit, formed acetylcholine receptors with beta2 subunits which were as resistant to nicotine-induced inactivation as wild-type alpha3beta2 acetylcholine receptors. Thus, inactivation of acetylcholine receptors produced by chronic exposure to nicotine results primarily from effects of the agonist on the extracellular and transmembrane domains of the alpha subunit.

Animals↗

Differential regulation and function of Fas expression on glial cells.

Fas/Apo-1 is a member of the TNF receptor superfamily that signals apoptotic cell death in susceptible target cells. Fas or Fas ligand (FasL)-deficient mice are relatively resistant to the induction of experimental allergic encephalomyelitis, implying the involvement of Fas/FasL in this disease process. We have examined the regulation and function of Fas expression in glial cells (astrocytes and microglia). Fas is constitutively expressed by primary murine microglia at a low level and significantly up-regulated by TNF-alpha or IFN-gamma stimulation. Primary astrocytes express high constitutive levels of Fas, which are not further affected by cytokine treatment. In microglia, Fas expression is regulated at the level of mRNA expression; TNF-alpha and IFN-gamma induced Fas mRNA by approximately 20-fold. STAT-1alpha and NF-kappaB activation are involved in IFN-gamma- or TNF-alpha-mediated Fas up-regulation in microglia, respectively. The cytokine TGF-beta inhibits basal expression of Fas as well as cytokine-mediated Fas expression by microglia. Upon incubation of microglial cells with FasL-expressing cells, approximately 20% of cells underwent Fas-mediated cell death, which increased to approximately 60% when cells were pretreated with either TNF-alpha or IFN-gamma. TGF-beta treatment inhibited Fas-mediated cell death of TNF-alpha- or IFN-gamma-stimulated microglial cells. In contrast, astrocytes are resistant to Fas-mediated cell death, however, ligation of Fas induces expression of the chemokines macrophage inflammatory protein-1beta (MIP-1beta), MIP-1alpha, and MIP-2. These data demonstrate that Fas transmits different signals in the two glial cell populations: a cytotoxic signal in microglia and an inflammatory signal in the astrocyte.

Animals↗

The effect of long-term levodopa therapy on depression level in de novo patients with Parkinson's disease.

20) became non-depressed, while five patients (22%) among 23 initially non-depressed became depressed. With long-term levodopa therapy, the UPDRS-motor score significantly improved (35+/-15. 7-18+/-7.6), but the BDI score was unchanged (18+/-9.3-19+/-9.2). The initial BDI score was significantly and inversely correlated to the parkinsonian motor symptoms, but their percentage changes were not correlated to each other. These results provide strong support to previous observations that levodopa therapy does not alter parkinsonian depression as well as providing additional evidence to support the role of non-dopaminergic mechanisms in parkinsonian depression.

Depressive Disorder↗

A distinct tumor suppressor gene locus on chromosome 15q21.1 in sporadic form of colorectal cancer.

The SM1311 family is an Ashkenazi family with dominantly inherited predisposition to colorectal adenomas and carcinomas and has a high-penetrance locus in chromosome 15q, with a multipoint logarithm of the odds score of 3.06 at marker D15S118. In the present study, we performed a high-density loss of heterozygosity study with 13 polymorphic microsatellite markers, including D15S118, spanning 15q15.3-q22.1, on 70 cases of the sporadic form of colorectal tumors. Our deletion mapping data showed a locus at D15S968 in chromosomal sub-band 15q21.1 may harbor a tumor suppressor gene in an area <0.521 Mb in physical map distance defined by markers D15S514 and D15S222. THBS1, 0.185 Mb proximal to D15S968, is the nearest known gene to this specific narrow loss of heterozygosity region. Thus, we speculate that THBS1 might be the most probable candidate gene involved in colorectal cancer carcinogenesis.

Adenocarcinoma↗

Androgen receptor gene mutation identified by PCR-SSCP and sequencing in 4 patients with complete androgen insensitivity syndrome.

To study the genetic defect of the human androgen receptor (hAR) gene in the complete androgen insensitivity syndrome (CAIS), we amplified each of the eight exons by PCR in genomic DNA extracted from the paraffin blocks of the resected gonads. We analyzed using SSCP, and directly sequenced the abnormally shifted bands. Mutations were found in 4 cases of CAIS. Patient 1 carried a point mutation; a G to A transition in exon 7 resulted in a change from arginine to glutamine at codon 831. Patient 2 carried a point mutation; a C to T transition in exon 7 resulted in a change from arginine to stop at codon 831. Patient 3 carried a point mutation and deletion in exon 7. A point mutation was an A to G transition that caused a glutamine to be substituted for the asparagine present at codon 819. A deletion of a G at codon 820 resulted in a frameshift and consequently in the introduction of a premature stop at codon 821. Patient 4 carried a mutation in 5' splice donor site of intron 7; a G to T transition might have caused an abnormal splicing of the exon 7. All of the mutations were found in exon 7. These mutations of hAR gene might be related to the pathogenesis of CAIS.

Adolescent↗

Intravascular papillary endothelial hyperplasia in the kidney of a child.

Intravascular papillary endothelial hyperplasia (IPEH) is a benign vascular lesion which is thought to represent an unusual form of organizing thrombus. A case of IPEH in the kidney of a 7-year-old girl is described. She suffered from intermittent flank pain and gross hematuria for 6 months. On radiological examinations, well-defined hypoechoic lesions were identified in the medullary portion of the left kidney. A well-demarcated, sponge-like mass was noted on gross examination. It was an intravascular mass lined by a fibrous capsule of various thicknesses. It was characterized by papillary fronds lined with benign endothelial cells. This is the first description of a renal IPEH in a child.

Child↗

Human alpha6 AChR subtypes: subunit composition, assembly, and pharmacological responses.

Many nicotinic acetylcholine receptor (AChR) subunits are known to be co-expressed with the alpha6 subunit in neurons. Because alpha6beta4 AChRs assemble inefficiently and alpha6beta2 AChRs not at all, more complex mixtures of human subunit cDNAs were tested for their abilities to form functional AChRs when expressed in Xenopus oocytes. alpha6beta4beta3 AChRs produced the largest and most consistent responses. alpha6alpha3beta2 AChRs exhibited reduced potency for ACh and increased potency and efficacy for nicotine compared to alpha3beta2 AChRs, but similar resistance to functional inactivation after prolonged exposure to nicotine. alpha6alpha4beta2 AChRs differed little in potency or efficacy for ACh or nicotine compared to alpha4beta2 AChRs, and had similarly high sensitivity to inactivation by prolonged exposure to nicotine. Co-expression of alpha6 and beta2 cRNAs resulted in large numbers of (3)H-epibatidine binding sites in the form of large aggregates but not in functional pentameric AChRs. Co-expression of alpha6, beta2, and alpha5 resulted in assembly of some functional pentameric AChRs. Chimeras with the large extracellular domain of alpha6 and the rest from either alpha3 or alpha4 efficiently formed functional AChRs. Thus, the extracellular domain of alpha6 efficiently assembles with beta2 to form ACh binding sites, but more C-terminal domains cause difficulties in forming pentameric AChRs. Chimeric alpha6/alpha3 and alpha6/alpha4 AChRs containing either beta2 or beta4 subunits were blocked by alpha-conotoxin MII which had previously been reported to be specific for alpha3beta2 AChRs.

Animals↗

Effect of a global regulatory gene, afsR2, from Streptomyces lividans on avermectin production in Streptomyces avermitilis.

The global regulatory gene, afsR2, from Streptomyces lividans was previously reported to highly stimulate two structurally unrelated antibiotics, actinorhodin and undecylprodigiosin, in both S. lividans and its close relative S. coelicolor. Production of eight avermectin components was also improved in S. avermitilis: the use of wild-type S. avermitilis and its high-producing mutant, transformed by introduction of multiple copies of afsR2, increased the total avermectin productions by 2.3-fold and 1.5-fold, respectively.

Journal Article↗

Oncostatin M regulation of interleukin-6 expression in astrocytes: biphasic regulation involving the mitogen-activated protein kinases ERK1/2 and p38.

Oncostatin M (OSM) is a member of the interleukin (IL)-6 family of cytokines and has both pro- and anti-inflammatory properties. Of interest, OSM has functional effects within the CNS. We have shown recently that OSM can modulate expression of the cytokine IL-6 in astrocytes. Herein we characterize the molecular mechanisms and signaling cascades involved in this response. OSM induces IL-6 protein expression in a dose- and time-dependent manner in astrocytes. In addition, OSM can synergize with the cytokines tumor necrosis factor-alpha, IL-1beta, and transforming growth factor-beta for enhanced IL-6 expression. Using neutralizing antibodies to gp 130, the OSM receptor (OSMR), and the leukemia inhibitory factor receptor (LIFR), we document that OSM exclusively uses the OSMR/gp 130 heterodimer in signaling events, rather than the LIFR/gp 130 heterodimer. Kinetic analysis of OSM-induced IL-6 mRNA reveals two up-regulatory events. The first, peaking at 1 h, is transient, does not require protein synthesis, and is regulated at the transcriptional level. The second, peaking between 6 and 8 h, is prolonged and sensitive to puromycin, suggesting a requirement for de novo protein synthesis, and also is transcriptionally regulated. OSM-induced IL-6 mRNA and protein expression is inhibited by the mitogen-activated protein kinase (MAPK) inhibitors U0126 and SB202190, suggesting a requirement for the MAPKs ERK1/2 and p38 in this response. Finally, we show that the MAPKs ERK1/2 and p38 are activated by OSM in astrocytes and that this activation is reduced by the MAPK inhibitors. These data demonstrate that OSM induces IL-6 expression in astrocytes and that the MAPKs ERK1/2 and p38 participate in this response.

Adult↗

Distribution of porcine parvovirus in porcine circovirus 2-infected pigs with postweaning multisystemic wasting syndrome as shown by in-situ hybridization.

In-situ hybridization with a nonradioactive digoxigenin-labelled probe was used to study the distribution of porcine parvovirus (PPV) in formalin-fixed paraffin wax-embedded tissues from 10 porcine circovirus 2 (PCV2)-infected weaned pigs with naturally occurring postweaning multisystemic wasting syndrome (PMWS). A 226 base pair DNA fragment from a VP2 structural gene was generated by polymerase chain reaction (PCR) and used as a probe. Lymph node, spleen, thymus and tonsil were positive by PCR, demonstrating the presence of PPV DNA in the tissue samples from four of 10 pigs tested. PPV nucleic acid was also detected consistently in lymph node, spleen, thymus and tonsil by in-situ hybridization. Detection of PPV DNA from PCV2-infected pigs with PMWS suggests that PPV also plays a role in the pathogenesis of PMWS.

Animals↗

Porcine postweaning multisystemic wasting syndrome in Korean pig: detection of porcine circovirus 2 infection by immunohistochemistry and polymerase chain reaction.

This report describes the first diagnosis of porcine circovirus (PCV) infection in weaned pigs with postweaning multisystemic wasting syndrome in Korea by immunohistochemistry and polymerase chain reaction. The most unique lesions were multifocal granulomatous inflammation affecting lymph nodes, liver, and spleen, characterized by infiltrates of epithelioid macrophages and multinucleated giant cells. Circoviral antigen was detected in formalin-fixed sections and was usually present in large, round, dendritic cells in the white pulp of spleen and remnants of follicles in lymph nodes. Lymphoid follicles in the tonsils also contained PCV antigen. A 530-bp DNA fragment of circovirus was successfully amplified from all tested lymph nodes, liver, and spleen.

Animals↗

Immunohistochemistry and polymerase chain reaction for the detection of Lawsonia intracellularis in porcine intestinal tissues with proliferative enteropathy.

Detection method of Lawsonia intracellularis was studied in formalin-fixed paraffin-embedded intestinal tissues from 5 naturally infected pigs by immunohistochemistry with a monoclonal antibody against outer membrane protein of L. intracellularis. Warthin-Starry silver stain revealed clusters of argyrophilic, slightly curved rod-shaped organisms in the apical cytoplasm of enterocytes. Immunohistochemical staining with a L. intracellularis-specific monoclonal antibody confirmed the presence of the organism in the apical cytoplasm of hyperplastic enterocytes. The presence of L. intracellularis in the ileum of pig with proliferative enteropathy was confirmed by polymerase chain reaction (PCR) further on the basis of amplification of 319 base pair products specific for porcine L. intracellularis chromosomal DNA. Immunohistochemistry and PCR may be a complementary method to confirm the diagnosis of L. intracellularis infection in pigs.

Animals↗

Congenital cytomegalovirus infection: three autopsy case reports.

We report three autopsy cases of congenital cytomegalovirus (CMV) infection in fetuses with a review of literature. The clinical manifestations in these cases of congenital CMV infection include intrauterine fetal death, hydrops fetalis, and CMV pneumonia associated with cardiovascular defect. The pathological characteristics were as follows: 1) the kidney was the most frequently involved organ, followed by lung and liver, 2) CMV inclusions were found predominantly in epithelial cells and to a lesser degree in endothelial cells, 3) intrahepatic bile duct epithelial cells were frequently involved, and 4) inflammatory reaction around CMV inclusions was not prominent in the early stage of pregnancy. Diagnostic confirmation was obtained by in situ hybridization (ISH) using a biotinylated CMV-DNA probe, which demonstrated intranuclear inclusions and sometimes recognized cells that did not show intranuclear inclusion.

Autopsy↗

Transient improvement of pyruvate metabolism after coenzyme Q therapy in Kearns-Sayre syndrome: MRS study.

Coenzyme Q therapy has been used to support metabolic derangements in patients with mitochondrial encephalomyopathies. Biochemical analysis of the living human brain can be performed by magnetic resonance spectroscopy (MRS). We report upon a KSS patient who was serially imaged with localized proton MRS to monitor the efficacy of CoQ treatment. A 17-year-old girl with KSS was serially imaged with localized proton MRS performed on a GE 1.5 T SIGNA MRI/MRS system. The elevated lactate contents of lesions decreased after one month of CoQ therapy but were re-elevated 10 months after treatment. We conclude that MRS presents us with a powerful tool for monitoring the effects of therapeutic trials in mitochondrial encephalomyopathies.

Adolescent↗

Potentiation of carbon monoxide-induced relaxation of rat aorta by YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole].

The hypothesis that endogenous carbon monoxide (CO), produced during the oxidation of heme catalyzed by heme oxygenase (HO), plays a role similar to that of nitric oxide (NO) in the regulation of cardiovascular tone has been criticized because of the low potency of CO compared with NO in relaxing blood vessels and stimulating soluble guanylyl cyclase (sGC). This criticism has been muted by the demonstration that, in the presence of YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole], CO has similar potency to NO in stimulating sGC activity. In this study, we determined that YC-1 potentiated CO-induced relaxation of rat aortic strips (RtAS) by approximately ten-fold. Furthermore, CO-induced relaxation of RtAS was shown to be mediated through stimulation of sGC because vasorelaxation was inhibited by ODQ (1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one), a selective sGC inhibitor, in the absence and presence of YC-1. A gas chromatographic-headspace method was used to measure CO concentration in Krebs' solution following the addition of CO-saturated saline solution to the tissue bath, in order to provide an accurate determination of RtAS exposure to CO. The tissue bath concentration of CO was shown to be approximately one-half of that calculated to be present. We conclude that should an endogenous compound exist with properties similar to that of YC-1, then the potency of CO as a vasorelaxant in the presence of this factor would be increased. As a consequence, CO could play a role in the regulation of cardiovascular tone, comparable to that of NO.

Animals↗