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Biomedical subjects

J-H Choi

Publications and source records attributed to J-H Choi.

At least 19 recordsLinked to original sources
PubMed2006

Chloroquine inhibits production of TNF-alpha, IL-1beta and IL-6 from lipopolysaccharide-stimulated human monocytes/macrophages by different modes.

OBJECTIVES: TNF-alpha, IL-1 and IL-6 are known to have primary roles in the pathogenesis of rheumatoid arthritis and other inflammatory diseases. The anti-rheumatic drug chloroquine has been shown to inhibit TNF-alpha, IL-1 and IL-6 production from mononuclear phagocytes. We examined the underlying mechanisms involved in the chloroquine-induced inhibition of cytokine production. METHODS: Human peripheral blood mononuclear cells and monocytes/macrophages and monocytic U-937 and THP-1 cells were stimulated with lipopolysaccharide, and TNF-alpha, IL-1beta and IL-6 production was measured by ELISA. Levels of mRNA were measured by northern blotting and reverse transcription-polymerase chain reaction. Synthesis of 26-kDa TNF-alpha precursor was measured by metabolic labelling and immunoprecipitation analysis. Transcription rate was determined by nuclear run-on assay. RESULTS: TNF-alpha release from the cells was inhibited by chloroquine, whereas the steady-state level of TNF-alpha mRNA and synthesis of 26-kDa TNF-alpha precursor were not changed by chloroquine. In contrast, chloroquine-induced inhibition of IL-1beta and IL-6 release was accompanied by a decrease in their steady-state mRNA levels. The transcription rates of the IL-1beta and IL-6 genes were not changed by chloroquine, whereas the stability of IL-1beta and IL-6 mRNA was decreased by chloroquine. Weak-base amines such as methylamine and ammonium chloride had no effect on the production of TNF-alpha, whereas they partially blocked the production of IL-1beta and IL-6. CONCLUSIONS: Our results indicate that chloroquine-mediated inhibition of TNF-alpha, IL-1beta and IL-6 synthesis occurs through different modes in lipopolysaccharide-stimulated human monocytes/macrophages: it blocks the conversion of cell-associated TNF-alpha precursor to mature soluble protein, whereas it reduces the levels of IL-1beta and IL-6 mRNA, at least in part, by decreasing their stability and by a pH-dependent mechanism.

Antirheumatic Agents↗
PubMed2006

Expression of 5-lipoxygenase and cyclooxygenase pathway enzymes in nasal polyps of patients with aspirin-intolerant asthma.

In aspirin-intolerant subjects, adverse bronchial and nasal reactions to cyclooxygenase (COX) inhibitors are associated with over-production of cysteinyl-leukotrienes (cys-LTs) generated by the 5-lipoxygenase (5-LO) pathway. In the bronchi of patients with aspirin-intolerant asthma, we previously linked cys-LT over-production and aspirin hyper-reactivity with elevated immunoexpression in eosinophils of the terminal enzyme for cys-LT production, LTC4 synthase. We investigated whether this anomaly also occurs in the nasal airways of these patients. Immunohistochemical expression of 5-LO and COX pathway proteins was quantified in nasal polyps from 12 patients with aspirin-intolerant asthma and 13 with aspirin-tolerant asthma. In the mucosa of polyps from aspirin-intolerant asthmatic patients, cells immunopositive for LTC4 synthase were four-fold more numerous than in aspirin-tolerant asthmatic patients (p=0.04). There were also three-fold more cells expressing 5-LO (p=0.037), with no differences in 5-LO activating protein (FLAP), COX-1 or COX-2. LTC4 synthase-positive cell counts correlated exclusively with mucosal eosinophils (r=0.94, p<0.001, n=25). Co-localisation confirmed that five-fold higher eosinophil counts (p=0.007) accounted for the increased LTC4 synthase expression in polyps from aspirin-intolerant asthmatic patients, with no alterations in mast cells or macrophages. Within the epithelium, increased counts of eosinophils (p=0.006), macrophages (p=0.097), and mast cells (p=0.034) in aspirin-intolerant asthmatic polyps were associated only with 2.5-fold increased 5-LO-positive cells (p<0.05), while the other enzymes were not different. Our results indicate that a marked over-representation of LTC4 synthase in mucosal eosinophils is closely linked to aspirin intolerance in the nasal airway, as in the bronchial airways.

Adolescent↗
PubMed2006

Association of TNF-alpha genetic polymorphism with HLA DPB1*0301.

BACKGROUND: We speculated TNF-alpha can be one of candidate gene for aspirin-intolerant asthma (AIA) because TNF-alpha is pro-inflammatory cytokine and known to be increased level in asthmatic airways. In addition, genetic interaction between TNF-alpha and human antigen leucocyte (HLA) DPB1*0301, which is a strong genetic marker for AIA, was examined for its close location within chromosome 6. METHOD: To investigate genetic association of TNF-alpha with an AIA phenotype, three study groups (163 patients with AIA, 197 patients with aspirin-tolerant asthma (ATA), 257 normal control subjects) were enrolled. Single nucleotide polymorphisms (SNPs) were genotyped using a single-base extension method and HLA DPB1 genotyping was determined by high-throughput sequencing method. RESULTS: All five SNPs of TNF-alpha were tested; there were no significant differences in allele and genotype frequencies among the three groups. However, significant association between TNF-alpha-308G>A polymorphism and atopy status was noted (P<0.05). Gene to gene interaction between TNF-alpha-1031T>C (or -863C>A or -857C>A) and HLA DPB1*0301could synergistically increase the susceptibility to AIA with odds ratio (OR) to 7.738 (or OR=8.184 for -863C>A, OR=7.500 for -857C>T, P<0.001, respectively). CONCLUSION: TNF-alpha promoter polymorphism may significantly increase susceptibility to AIA by gene-to-gene interaction with HLA DPB1*0301.

Adult↗
PubMed2006

The addition of induction chemotherapy with etoposide, ifosfamide, and cisplatin failed to improve therapeutic outcome of concurrent chemoradiotherapy in patients with locally advanced non-small cell lung cancer -- single institution retrospective analysis.

Although chemoradiotherapy (CRT) is a standard treatment for unresectable locally advanced non-small cell lung cancer (NSCLC), the optimal sequencing remains to be determined. We retrospectively compared the treatment results of induction chemotherapy followed by concurrent CRT (induction group, 32 patients) with those of concurrent CRT alone (concurrent group, 41 patients) in unresectable stage IIIA/IIIB NSCLC patients. In induction group, 2 cycles of induction chemotherapy (etoposide/ifosfamide/cisplatin: 24 patients, others: 8 patients) were followed by concurrent CRT (60 Gy/30 fractions, 6 mg/m2 of cisplatin daily), while the same concurrent CRT was administered in concurrent group. Clinicopathologic characteristics including age, weight loss, histologic types, and clinical stage did not show significant differences between two groups except for a higher proportion of patients with ECOG performance status 2 in concurrent group (3% vs. 27%, p=0.015). Overall toxicity was generally acceptable with 1 treatment-related death from tracheoesophageal fistula in induction group. The response rates after concurrent CRT were 41% for induction group and 54% for concurrent group, which showed no significant difference (p=0.560). With median follow-up of 13 (1-92) months, there was a trend toward an advantage for concurrent group in median progression-free survival (6 months vs 8.3 months, p=0.067) and overall survival (12 months vs. 14.5 months, p=0.059). In multivariate analysis, only more than 10% weight loss within 6 months was significantly associated with poor survival (p=0.001). In conclusion, the addition of induction chemotherapy to concurrent CRT did not show any advantage over concurrent CRT alone in locally advanced NSCLC.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

Concurrent chemoradiotherapy in patients with nasopharyngeal cancer: prognostic significance of low expression of bax.

A randomized trial has demonstrated that concurrent chemoradiotherapy (CRT) is superior to radiotherapy (RT) alone in locally advanced nasopharyngeal cancer (NPC). Our study comprise 35 patients with locally advanced NPC (stage I: 1, II: 12, III: 7, IV: 15) with 1 cycle of induction chemotherapy (5-fluorouracil 1,000 mg/m(2)/day and cisplatin 20 mg/m(2)/day, days 1- 4) followed by concurrent CRT starting on day 22. Concurrent CRT consisted of RT (70 Gy/35 fractions for 7 weeks) with cisplatin 20 mg/m(2)/day for 4 days on weeks 1, 4, 7 of RT. Complete response (CR) was achieved in 33 patients (94%). Four-year progression-free survival (PFS) and overall survival (OS) of all patients were 57% and 65%, respectively. In analysis of prognostic factors, low expression of bax was the most significant independent predictor of poor prognosis in both PFS (p=0.002) and OS (p=0.008). In conclusion, the outcome of patients treated with this combined therapeutical modality appears to be comparable with that of Intergroup 0099 trial with high CR rate. Low expression of bax was significantly associated with poor PFS and OS.

Adult↗
PubMed2005

Landau quantization and time dependence in the ionization of cold, strongly magnetized Rydberg atoms.

The electric-field-ionization and autoionization behavior of cold Rydberg atoms of 85Rb in magnetic fields up to 6 T is investigated. Multiple ionization potentials and field-ionization bands reflecting the Landau energy quantization of the quasifree Rydberg electron are observed. The time-resolved and state-selective field-ionization study provides evidence of mixing and spin flips of the Rydberg electron. Spin-orbit coupling combined with mixing gives rise to a Feshbach-type autoionization of metastable positive-energy atoms.

Journal Article↗
PubMed2005

Magnetic trapping of long-lived cold Rydberg atoms.

We report on the trapping of long-lived strongly magnetized Rydberg atoms. 85Rb atoms are laser cooled and collected in a superconducting magnetic trap with a strong bias field (2.9 T) and laser excited to Rydberg states. Collisions scatter a small fraction of the Rydberg atoms into long-lived high-angular momentum "guiding-center" Rydberg states, which are magnetically trapped. The Rydberg atomic cloud is examined using a time-delayed, position-sensitive probe. We observe magnetic trapping of these Rydberg atoms for times up to 200 ms. Oscillations of the Rydberg-atom cloud in the trap reveal an average magnetic moment of the trapped Rydberg atoms of approximately -8microB. These results provide guidance for other Rydberg-atom trapping schemes and illuminate a possible route for trapping antihydrogen.

Journal Article↗
PubMed2005

Laser cooling and magnetic trapping at several tesla.

Laser cooling and magnetic trapping of (85)Rb atoms have been performed in extremely strong and tunable magnetic fields, extending these techniques to a new regime and setting the stage for a variety of cold atom and plasma experiments. Using a superconducting Ioffe-Pritchard trap and an optical molasses, 2.4 x 10(7) atoms were laser cooled to the Doppler limit and magnetically trapped at bias fields up to 2.9 T. At magnetic fields up to 6 T, 3 x 10(6) cold atoms were laser cooled in a pulsed loading scheme. These bias fields are well beyond an order of magnitude larger than those in previous experiments. Loading rates, molasses lifetimes, magnetic-trapping times, and temperatures were measured using photoionization and electron detection.

Journal Article↗
PubMed2005

Comparative genomic hybridization in extramammary Paget's disease.

BACKGROUND: Extramammary Paget's disease (EMPD) is a distinct skin cancer of unknown histogenesis. Data from genome-wide surveys for chromosomal aberrations in EMPD are limited. OBJECTIVES: To identify chromosomal aberrations that are present in EMPD. METHODS: Fifteen cases of EMPD were analysed by comparative genomic hybridization (CGH). We used pooled DNA CGH, instead of studying a single sample. In addition, immunohistochemistry was performed for detection of androgen receptor (AR). RESULTS: The most recurrent change was amplification at chromosomes Xcent-q21 and 19, and loss at 10q24-qter. In addition, expression of AR, located in chromosome X, was found in six cases. CONCLUSIONS: Results suggest that AR may play a role in EMPD tumorigenesis.

Chromosome Aberrations↗