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Biomedical subjects

Y Choi

Publications and source records attributed to Y Choi.

At least 235 records · Page 13Linked to original sources
PubMed1997

Renovascular hypertension in children with moyamoya disease.

OBJECTIVES: To examine the incidence, clinical and radiologic findings, and response to treatment of renovascular hypertension (RVHT) in moyamoya disease (MMD). METHODS: A retrospective analysis of medical records in six RVHT cases (8.3%) among 72 MMD patients observed from November 1987 to December 1995. RESULTS: The age at onset of MMD ranged from 9 months to 7 years 1 month (mean, 3.3 years). The most common initial manifestation of MMD was transient ischemic attack. Hypertension was detected between 4 years 4 months and 12 years 3 months (mean, 7.87 years). Unstimulated plasma renin activity was elevated in all six cases. Renal ultrasonography and captopril technetium 99m-labeled dimercaptosuccinic acid scan showed abnormal findings in four of five and in three of four available studies, respectively. However, both imaging studies showed abnormal findings only in the most severely affected kidneys even with bilateral renal artery stenosis. Renal arteriography revealed bilateral lesions in three of the patients and unilateral lesions in the others. Renal angioplasty was performed in four cases but was successful in only one and partially successful in another. A renal artery specimen obtained during renal autotransplantation showed intimal fibroplasia. At the last follow-up, one patient had normal blood pressure without the use of antihypertensive agents, but the other five patients needed this medication to control blood pressure. CONCLUSION: Because RVHT may be more commonly associated with MMD than has hitherto been appreciated, it is recommended that blood pressure be carefully followed and that diagnostic procedures for RVHT be carried out in hypertensive patients with MMD.

Adolescent↗
PubMed1997

Bovine cytokine expression during different phases of bovine leukemia virus infection.

The potential role of aberrant cytokine production in the pathogenesis of bovine leukemia virus (BLV) was studied by analyzing cytokine mRNA expression in pokeweed-stimulated PBMLs of cows in different phases of disease progression. To analyze the mRNA, a semi-quantitative RT-PCR assay was developed. The RT-PCR assay was developed for detection of IL-2, -4, -6, -10, -12, IFN-gamma and actin using cDNA derived from phorbol-stimulated peripheral blood mononuclear leukocytes. Using a PCR specific for BLV tax, agar gel immunodiffusion and white blood cell counts, BLV-negative, BLV-positive aleukemic (AL), and BLV-positive persistently lymphocytotic (PL) cattle were identified. Peripheral blood lymphocytes cultured in vitro for 24 h in pokeweed mitogen were analyzed for cytokine production using the RT-PCR assay. Consistently elevated levels of IL-2 and IL-12 in AL and PL cattle in pokeweed mitogen-stimulated cells was detected, while IFN-gamma was elevated in the AL but not the PL cattle.

Animals↗
PubMed1997

Pathways leading to cell death in T cells.

Antigen-induced apoptosis of T cells is a highly regulated process which plays a key role in the elimination of self-reactive T cells and, thus, in the prevention of autoimmunity. It has recently become apparent that members of the tumor necrosis factor (TNF) and TNF receptor (TNFR) superfamily regulate antigen-induced T-cell death. Studies characterizing genes which control TNF/TNFR superfamily expression and how TNF/TNFR signal transducers activate cell death machinery, such as caspases, have begun to reveal the molecular control of antigen-induced T-cell death.

Animals↗
PubMed1997

TRAF2 is essential for JNK but not NF-kappaB activation and regulates lymphocyte proliferation and survival.

TRAF2 is believed to mediate the activation of NF-kappaB and JNK induced by the tumor necrosis factor receptor (TNFR) superfamily, which elicits pleiotropic responses in lymphocytes. We have investigated the physiological roles of TRAF2 in these processes by expressing a lymphocyte-specific dominant negative form of TRAF2, thereby blocking this protein's effector function. We find that the TNFR superfamily signals require TRAF2 for activation of JNK but not NF-kappaB. In addition, we show that TRAF2 induces NF-kappaB-independent antiapoptotic pathways during TNF-induced apoptosis. Inhibition of TRAF2 leads to splenomegaly, lymphadenopathy, and an increased number of B cells. These findings indicate that TRAF2 is involved in the regulation of lymphocyte function and growth in vivo.

Animals↗
PubMed1997

Nucleoside Oxidase, a Hydrogen Peroxide-Forming Oxidase, from Flavobacterium meningosepticum.

A novel enzyme which catalyzes the oxidation of nucleosides to nucleoside-5(prm1)-carboxylic acids, forming hydrogen peroxide, was purified to homogeneity from Flavobacterium meningosepticum T-2799. The enzyme has a molecular weight of about 500,000, and four nonidentical subunits (molecular weights of 81,000, 69,000, 33,000, and 16,000) were detected on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. On the basis of visible absorption spectra of the purified enzyme, the enzyme is concluded to be a hemoprotein. It also contains covalently bound flavin adenine dinucleotide. The various nucleosides, such as adenosine (K(infm) = 48 (mu)M), inosine (K(infm) = 66 (mu)M), guanosine (K(infm) = 21 (mu)M), thymidine (K(infm) = 50 (mu)M), uridine (K(infm) = 80 (mu)M), and cytidine (K(infm) = 50 (mu)M), were oxidized by the enzyme, but nucleotides, bases, and ribose were not.

Journal Article↗
PubMed1997

Six novel mutations in the vasopressin V2 receptor gene causing nephrogenic diabetes insipidus.

X-linked nephrogenic diabetes insipidus (NDI) is a rare disease caused by mutations in the vasopressin V2 receptor (AVPR2) gene. We analyzed the AVPR2 gene in 6 unrelated Korean families with X-linked NDI, and found 6 novel mutations. Two of them were missense point mutations, 2 were short deletions causing frameshifts, 1 was a duplication of 9 bases, and 1 was a compound gene rearrangement. Four mutations cosegregated with the clinical phenotype in corresponding family members, and one was a de novo mutation. In 1 family, prenatal diagnosis was made by amniocentesis. In conclusion, we found 6 novel mutations in the AVPR2 gene causing X-linked NDI in 6 families, and direct mutational analysis is now applicable for carrier detection and early (prenatal) diagnosis.

Adult↗
PubMed1997

Polymorphism of angiotensin converting enzyme gene is associated with circulating levels of plasminogen activator inhibitor-1.

The deletion (D) allele of the insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene is strongly associated with an increased level of circulating ACE. The ACE gene polymorphism may influence the production of angiotensin II (Ang II). It has been shown that Ang II modulates fibrinolysis, that is, Ang II increases plasminogen activator inhibitor-1 (PAI-1) mRNA and plasma PAI-1 levels in vitro and in vivo. Considered together, we tested the hypothesis that the deletion allele of the ACE gene might be associated with increased levels of PAI-1. We related the ACE genotype to PAI-1 antigen levels in 603 men and 221 women attending a routine health screening. As a whole, the plasma PAI-1 level was not strongly associated with ACE genotype. Since the PAI-1 level was significantly influenced by well-known risk factors for coronary artery disease (CAD), we further analyzed the data after excluding subjects with major cardiovascular risk factors. In low-risk male subjects, the DD genotype had significantly higher levels of plasma PAI-1 (DD: 20.3 +/- 2.2; DI: 13.9 +/- 1.1; II: 13.6 +/- 1.3 ng/mL, P = .010 by ANOVA). In low-risk female subjects, the DD genotype showed a tendency to a high level of plasma PAI-1 without statistical significance. When analysis was restricted to postmenopausal women (age > or = 55 or FSH > or = 35 ng/mL), the DD genotype showed a significantly higher level of PAI-1 than subjects with the DI and II genotypes (27.7 +/- 6.2 versus 15.6 +/- 1.8 ng/mL, P = .028). The DD polymorphism of the ACE gene is associated with high PAI-1 levels in male and possibly in postmenopausal female subjects who have lower conventional cardiovascular risk factors. These results suggest that the increased ACE activity caused by DD polymorphism may play an important role in elevating the level of plasma PAI-1. Our data support the notion that the genetic variation of ACE contributes to the balance of the fibrinolytic pathway.

Alleles↗
PubMed1997

Lipoprotein(a) in Korean children and a history of coronary or cerebral vascular events in their older family members.

The purpose of this study was to determine the relationships between serum apolipoprotein concentration and family history of coronary or cerebral events in schoolchildren. In 269 primary schoolchildren aged 6-11 years (145 boys and 124 girls) we measured the blood concentrations of total cholesterol, apolipoproteins B and A-1, and lipoprotein(a), and questioned their parents about coronary or cerebral vascular events. Serum concentrations of apo B, A-1 and Lp(a) significantly increased with age. In children with serum cholesterol concentration > 5.18 mmol/L the concentrations of apo B, A-1, Lp(a) and apo B/apo A-1 ratio were significantly higher. The concentrations of total cholesterol, apo B, Lp(a), and apo B/apo A-1 ratio in the obese group (body weight 20% above the median body weight for age and height) differed significantly from those in the non-obese group. Serum concentrations of Lp(a) in the children who had positive family histories of coronary or cerebral events (geometric mean = 0.174 x/divided by 0.036g/L) and was significantly higher than that in the children with negative history (geometric mean = 0.086 x/divided by 0.36g/L). Family history was an independent and major contributor to high Lp(a). In evaluating children's lipid profiles, measurement of Lp(a) may help to identify children and their families at increased risk and this may facilitate the targeting of preventive measures.

Cerebrovascular Disorders↗
PubMed1997

Growth hormone response to the hypothalamic somatostatinergic activity in acromegalic patients.

Oral glucose administration suppresses the TRH-induced TSH response by enhancing the hypothalamic somatostatinergic activity (HSA). We assessed the HSA in 13 acromegalic patients by measuring glucose-induced suppression of TRH-stimulated TSH secretion. The HSA showed wide variation with up to 64% suppression. The mean HSA of the patients (25 +/- 6%) did not differ from that in normal young men (19 +/- 4%) in our previous study. Six patients had normal or low HSA, and the other 7 patients had high HSA. The mean TRH-stimulated TSH levels of the patients with normal or low HSA was significantly lower than that of the patients with high HSA (5.13 +/- 0.10 vs. 11.30 +/- 2.80 mU/L). The HSA did not relate to sex, age, tumor size, basal GH levels, the paradoxical responses to TRH and GnRH, octreotide response, or the gsp oncogene. In the combined glucose-TRH test, glucose pretreatment completely suppressed the paradoxical increase in GH level at 30 min in 4 patients. However, it could suppress the paradoxical GH response by only 6-51% in the other 5 patients who also showed the paradoxical response in TRH test. The tumor diameter of patients with good response to the HSA was significantly larger than that of the patients with poor response (31 +/- 5 vs. 14 +/- 2 mm) as was the tumor grade (3.3 +/- 0.3 vs. 1.7 +/- 0.2). This study supports the idea that a reduction of HSA is not a primary cause of acromegaly, and the HSA seems to increase to suppress the autonomous secretion of GH from the pituitary adenomas. HSA as well as the response of tumors to HSA do not determine tumor growth.

Acromegaly↗
PubMed1997

Molecular analysis of hypoxanthine guanine phosphoribosyltransferase (HPRT) gene in five Korean families with Lesch-Nyhan syndrome.

Lesch-Nyhan syndrome is caused by the complete deficiency of hypoxanthine guanine phosphoribosyl-transferase (HPRT). By the analysis of genomic DNA and mRNA using the polymerase chain reaction (PCR) technique coupled with direct sequencing, five independent mutations in HPRT genes have been identified in Korean Lesch-Nyhan families. Two novel mutations and three previously reported mutations have been found in five independent families. Heterozygous carriers were detected in all the families, and prenatal diagnosis was carried out in two families.

Exons↗
PubMed1997

Compartment model for measuring myocardial oxygen consumption using [1-11C]acetate.

UNLABELLED: Although [1-11C]acetate has been validated as a PET tracer for myocardial oxygen consumption (MVO2) in animals and humans, mono- and biexponential fitting of the tissue time-activity curve yields only estimates of MVO2. This study attempts to develop and validate a simple tracer kinetic model in vivo for estimation of regional MVO2. METHODS: Twenty-seven experiments were performed in 12 anesthetized dogs with [1-11C]acetate and serial PET images under different MBF and MVO2 (baseline, ischemia, xylazine, dobutamine and dipyridamole). Estimates of MVO2 were obtained from dynamic [1-11C]acetate PET and model fitting. MBF was measured by radiolabeled microspheres, and MVO2 was calculated by the Fick method using arterial and coronary blood samples. RESULTS: The proposed model fitted equally well for all study conditions with a multiple correlation coefficient of 0.985 +/- 0.026. Estimated MVO2 correlated linearly with measured MVO2 (y = 0.033 + 0.690x, r = 0.92, s.e. of estimates = 0.020). CONCLUSION: This study indicates that MVO2 can be assessed with PET and [1-11C]acetate over a wide range with a simple tracer kinetic model.

Acetates↗
PubMed1996

CD30/TNF receptor-associated factor interaction: NF-kappa B activation and binding specificity.

CD30 is a member of the tumor necrosis factor (TNF) receptor superfamily. CD30 is expressed on normal activated lymphocytes, on several virally transformed T- or B-cell lines and on neoplastic cells of Hodgkin's lymphoma. The interaction of CD30 with its ligand induces pleiotropic effects on cells resulting in proliferation, differentiation, or death. The CD30 cytoplasmic tail interacts with TNF receptor-associated factors (TRAFs), which have been shown to transduce signals mediated by TNF-R2 and CD40. We demonstrate here that TRAF2 also plays an important role in CD30-induced NF-kappa B activation. We also show that TRAF2-mediated activation of NF-kappa B plays a role in the activation of HIV transcription induced by CD30 cross-linking. Detailed site-directed mutagenesis of the CD30 cytoplasmic tail reveals that there are two independent binding sites for TRAF, each interacting with a different domain of TRAF. Furthermore, we localized the TRAF-C binding site in CD30 to a 5-7 amino acid stretch.

Amino Acid Sequence↗
PubMed1996

Iron metabolism-related genes and mitochondrial genes are induced during involution of mouse mammary gland.

To understand molecular mechanisms of mammary gland involution, several clones were isolated after the primary differential screening of a total 40,000 pfu of involution-specific cDNA library, and further characterized. The partial sequences and Northern analysis revealed that iron metabolism-related genes and mitochondrial genes were induced during mammary gland involution. The expression of the lactoferrin gene was induced at involution days 1, 2, and 3. The expression of ferritin heavy chain gene was induced at involution days 1, 2, 3 and 4. Cytochrome oxidase subunit 1 and cytochrome oxidase subunit 2 genes were induced at involution days 4 and 7. The expression of cytochrome b gene was induced at involution day 7. These results imply that iron metabolism and mitochondrial function may be altered during mammary gland involution.

Animals↗
PubMed1996

The proinflammatory cytokine response to coagulation and endotoxin in whole blood.

Acute inflammatory illnesses, including the sepsis syndrome, often include a component of coagulation. A human whole blood culture system was developed so that the relationship between coagulation activation and cytokine responses in the presence or absence of lipopolysaccharide (LPS) could be evaluated. In the absence of LPS stimulation, coagulation activation resulted in a novel pattern of cytokine production. During a 4-hour culture of coagulating blood, significant production of interleukin-8 (IL-8; >2,000 pg/mL) was observed, whereas other proinflammatory cytokines including IL-1 beta, IL-6, or tumor necrosis factor a were undetectable or less than 35 pg/mL. The cytokine profile was distinct from that of fully anticoagulated, LPS-stimulated blood, which showed levels of all the indicated proinflammatory cytokines > or = 2,000 pg/mL over the same time period. Over 24 to 48 hours, the coagulation-induced cytokine response was characterized by marked and sustained IL-8 production, limited IL-6 generation (with kinetics delayed relative to IL-8), and minimal or undetectable tumor necrosis factor alpha levels. The magnitude of the whole blood IL-8 response correlated with the level of coagulation activation as determined by measurement of thrombin-antithrombin III complex formation. The combined stimuli of coagulation activation and LPS challenge induced a synergistic enhancement of IL-8 production but not of IL-6. Coagulation-induced cytokine production and the synergistic production of IL-8 by coagulation and LPS could be attenuated by hirudin or tissue factor pathway inhibitor (TFPI). Studies to elucidate mechanisms implicated (1) the TFPI third Kunitz and carboxy-terminus as important structural components for TFPI regulation of coagulation activation and (2) thrombin as a candidate mediator of the mononuclear cell cytokine response to coagulation activation. In summary, a unique aspect of the crosstalk between the coagulation and cytokine cascades in whole blood is shown with the identification of IL-8 as a key proinflammatory participant.

Blood Coagulation↗
PubMed1996

Noninvasive quantification of myocardial blood flow in humans. A direct comparison of the [13N]ammonia and the [15O]water techniques.

BACKGROUND: [13N]Ammonia has been validated in dog studies as a myocardial blood flow tracer. Estimates of myocardial blood flow by [13N]ammonia were highly linearly correlated to those by the microsphere and blood sample techniques. However, estimates of myocardial blood flow with [13N]ammonia in humans have not yet been compared with those by an independent technique. This study therefore tested the hypothesis that the [13N]ammonia positron emission tomographic technique in humans gives estimates of myocardial blood flow comparable to those obtained with the [15O]water technique. METHODS AND RESULTS: A total of 30 pairs of positron emission tomographic flow measurements were performed in 30 healthy volunteers; 15 volunteers were studied at rest and 15 during adenosine-induced hypermia. Estimates of average and of regional myocardial blood flow by the [13N]ammonia and the [15O]water approaches correlated well (y = 0.02 + 1.02x, r = .99, P < .001 SEE = 0.023 for average and y = 0.06 + 1.00x, r = .97, P < .001, SEE = 0.025 for regional values) over a flow range of 0.45 to 4.74 mL.min-1.g-1. At rest, mean myocardial blood flow was 0.64 +/- 0.09 mL.min-1.g-1 for [13N]ammonia and 0.66 +/- 0.12 mL.min-1.g-1 for [15O]water (P = NS). For adenosine-induced hyperemia, mean myocardial blood flow was 2.63 +/- 0.75 mL.min-1.g-1 for [13N]ammonia and 2.73 +/- 0.77 mL.min-1.g-1 for [15O]water (P = NS). The coefficient of variation as an index of the observed heterogeneity of myocardial blood flow averaged, for [13N]ammonia, 9 +/- 4% at rest and 12 +/- 7% during stress and, for [15O]water, 14 +/- 11% at rest and 16 +/- 9% during stress. The coefficients of variation for [15O]water were significantly higher than those for [13N]ammonia (P = .004 at rest and P = .03 during stress). CONCLUSIONS: The two approaches yield comparable estimates of myocardial blood flow in humans, which supports the validity of the [13N]ammonia method in human myocardium previously shown only in animals. However, the [15O]water approach reveals a greater heterogeneity (presumably method-related), which might limit the accuracy of sectorial myocardial blood flow estimates in humans.

Adenosine↗
PubMed1996

Clonal evolution in B-lineage acute lymphoblastic leukemia by contemporaneous VH-VH gene replacements and VH-DJH gene rearrangements.

B-cell acute lymphoblastic leukemia (B-ALL), more frequently than any other B-lineage neoplasm, exhibits oligoclonal Ig heavy chain (IgH) gene rearrangement in 15% to 43% of all cases studied. To study the molecular processes that promote multiple IgH rearrangements, a comprehensive sequence analysis of a B-ALL case was performed in which seven clonal IgH gene rearrangements were identified. The genetic profiles suggested that a single leukemic progenitor clone evolved into several subclones through dual processes of variable (VH) to preexisting diversity-joining (DJH) gene segment rearrangement and VH to VH gene replacement. Predominant IgH-V usage and the uniquely rearranged clonotype-specific VHDJH region gene sequences were identified using a novel DNA-based gene amplification strategy. Polymerase chain reaction (PCR) was directed by an IgH-J generic primer and a complement of family-specific IgH-V primers that defined the major B-cell IgH-V gene usage. Clonality of rearranged VHDJH bands was substantiated by high resolution denaturant gel electrophoretic analysis. Sequence patterns of the amplified VHDJH fragments segregated into two groups defined by common DJH sequences. Partial N region homology at the VHD junction as well as shared DJH sequences firmly established VH to VHDJH gene replacement as a mechanism generating clonal evolution in one group. In the second subset, oligoclonality was propagated by independent VH gene rearrangements to a common DJH precursor. The contributions of all clonal Ig-VHDJH repertoires for each group was approximately 50% and reflected a symmetric distribution of leukemic subclones generated by either process. Thus, oligoclonal rearrangements evolved by two independent, yet seemingly contemporaneous molecular genetic mechanisms. All seven clones displayed nonfunctional Ig-VHDJH recombinations. These observations may have relevance to the recombinatorial opportunities available during normal B-cell maturation.

Base Sequence↗