No abstract available.
Stomach Neoplasms*

No abstract available.
Alleles* ; Base Sequence* ; DNA* ; HLA-DR4 Antigen* ; HLA-DRB1 Chains*

No abstract available.
Genetic Loci* ; Loss of Heterozygosity* ; Stomach Neoplasms*

No abstract available.
DNA Fingerprinting* ; DNA* ; Oligonucleotide Probes* ; Polymerase Chain Reaction*

No abstract available.
Digestion* ; Exons* ; Humans* ; Polymerase Chain Reaction* ; Stomach Neoplasms*

BACKGROUND: It is not yet clear whether the abnormal cytokine production in relation to serum IgE levels in atopic dermatitis (AD) is associated with the amount of mRNA of cytokine gene. OBJECTIVE: Our purpose was to delineate the effect of reciprocal correlation in the level of mRNA between interleukin-4 (I") and interferon-gamma (IFN-γ) in severe AD. METHODS: We examined 15 cases including 5 AD patients with high serum IgE (>2,000 kU/liter), 5 AD patients with low serum IgE (<100 kU/liter), and 5 healthy controls. Using semi quantitative reverse transcription-polymerase chain reaction, IL-4 and IFN-γ gene expressions in peripheral mononuclear cells (PBMC) were examined. RESULTS: 1) IL-4 gene expression in spontaneous PBMC was higher in AD patient groups than in control group, significantly higher only in AD patient group with high serum IgE level (p < 0.05). 2) IFN-γ gene expression in spontaneous PBMC showed increased tendency in AD patient groups than in control group without statistical significance. 3) IL-4 and IFN-γ gene expressions in stimulated PBMC were not different among all three groups. CONCLUSION: In light of our results, high and low IgE subgroups in AD can exist and AD may not be R characterized by the shift in the reciprocal relationship between IL-4 and IFN-γ when T cells are stimulated under antigen presenting cell-independent conditions.
Dermatitis, Atopic ; Gene Expression ; Humans ; Immunoglobulin E* ; Interferon-gamma* ; Interleukin-4* ; RNA, Messenger ; T-Lymphocytes

No abstract available.
HLA-A2 Antigen* ; Isoelectric Focusing*

We exploited the serial analysis of gene expression (SAGE) libraries and human genome database in silico to correlate the breadth of expression (BOE; housekeep-ing versus tissue-specific genes) and peak rate of expression (PRE; high versus low expressed genes) with the density distribution of the retroelements. The BOE status is linearly associated with the density of the sense Alus along the 100 kb nucleotides region upstream of a gene, whereas the PRE status is inversely correlated with the density of antisense L1s within a gene and in the up- and downstream regions of the 0-10 kb nucleotides. The radial distance of intranuclear position, which is known to serve as the global domain for transcription regulation, is reciprocally correlated with the fractions of Alu (toward the nuclear center) and L1 (toward the nuclear edge) elements in each chromosome. We propose that the BOE and PRE statuses are related to the reciprocal distribution of Alu and L1 elements that formulate local and global expression domains.
Alu Elements/*genetics ; Chromosome Mapping/*methods ; Comparative Study ; Databases, Genetic ; Gene Expression Profiling/*methods ; Gene Expression Regulation/*genetics ; Genome, Human ; Humans ; Long Interspersed Nucleotide Elements/*genetics ; Retroelements/genetics ; Sequence Analysis, DNA/*methods ; Statistics ; Tissue Distribution

Recently the adenomaatous polyposis coli(APC) gene, a tumor suppressor gene, was identified and the cDNA was cloned from chromosome 5q21. Allelic deletion or point mutation of tumor suppressor genes(TSGs) has been considered as an important mechanism in development of human tumor. Point mutations affecting APC gene are seen in the hereditary syndrome, adenomatous polyposis and spordic colon cancer. However, the mutation of APC gene and other TSGs have not been described in gastric cancer. In order to identify the mutation of exon 11 of APC gene for gastric cancer, we amplified DNA extracted from paraffin-embedded tissues by polymerase chain reaction(PCR) and digested the PCR products with restriction enzyme Rsa I. We examined the DNA extracted from paraffin-embedded 44 gastric cancer tissues with lymph nodes. Eighteen(41%) among 44 were informative for the study exon 11 of the APC gene, and we found loss of heterozygosity(LOH) for APC in 6/18(33.3%). These data suggest that the point mutation or the base change of APC gene commonly occurs in gastric cancer. We conclude that the mutation of APC gene is strongly connected with development of human gastric cancer.
Humans ; Genes, Tumor Suppressor ; Stomach Neoplasms

Five retroelement families, L1 and L2 (long interspersed nuclear element, LINE), Alu and MIR (short interspersed nuclear element, SINE), and LTR (long terminal repeat), comprise almost half of the human genome. This genome-wide analysis on the time-scaled expansion of retroelements sheds light on the chronologically synchronous amplification peaks of each retroelement family in variable heights across human chromosomes. Especially, L1s and LTRs in the highest density on sex chromosomes Xq and Y, respectively, disclose peak activities that are obscured in autosomes. The periods of young L1, Alu, LTR, and old L1 peak activities calibrated based on sequence divergence coincide with the divergence of the three major hominoid divergence as well as early eutherian radiation while the amplification peaks of old MIR and L2 account for the marsupial-placental split. Overall, the peaks of autonomous LINE (young and old L1s and L2s) peaks and non-autonomous SINE (Alus and MIRs) have alternated repeatedly for 150 million years. In addition, a single burst of LTR parallels the Cretaceous-Tertiary (K-T) boundary, an exceptional global event. These findings suggest that the periodic explosive expansions of LINEs and SINEs and an exceptional burst of LTR comprise the genome dynamics underlying the macroevolution of the hominoid primate lineage.
Animals ; Chromosomes, Human ; *Evolution, Molecular ; Genome, Human ; Hominidae/*genetics ; Human ; Primates ; Sex Chromosomes ; Support, Non-U.S. Gov't ; Terminal Repeat Sequences/*genetics