BACKGROUND: In response to numerous pathologic stimuli, the myocardium undergoes a hypertrophic response characterized by increased myocardial cell size and activation of fetal cardiac genes. Recently, the calcineurin inhibitor, cyclosporine has been reported to prevent the development of cardiac hypertrophy, however, others reported data which are disagreed to the cyclosporine effect on the prevention of cardiac hypertrophy. METHOD: To clarify whether the calcineurin signaling pathway is a critical for overloaded hypertrophy in vivo and to characterize the cyclosporine effect on the develpment of cardiac hypertrophy, I examined the effects of cyclosporine on the left ventricular overload in the experimental model of clipping of abdominal aorta between the diaphragm and renal artery for three weeks in rats. RESULTS: Left ventricular mass was larger in the group of clipping of abdominal aorta than in the group of cyclosporine injection after clipping of abdominal aorta, however, which had larger ventricular mass rather than control group. It means that cyclosporine suppress hypertrophic growth. Both treated and untreated animals showed increased nuclear polymorphism and euchromatin pattern, and also, ultrastructurally, showed degenerative changes in the cardiac myocytes such as swelling of subsarcolemmal cytoplasm with indistinct sarcoplasmic reticulum and "T" tubules, loosening of myofibril bundles with decreased electron density, and electron dense mitochondria with decreased number. Characteristically, the group of cyclosporine injection after clipping of abdominal aorta showed polymorphic electron dense unswollen giant mitochondria which was not characteristic in other groups. alpha-MyHC mRNA including non-spliced mRNA of the group of abdominal aortic clipping was downregulated in the both groups of clipping of abdominal aorta. beta-MyHC mRNA was upregulated in the group of clipping of abdominal aorta and downregulated in the group of cyclosporine injection after clipping of abdominal aorta. From the above results, initial response to overload is a degenerative changes of cardiac myocytes and cyclosporine may suppress hypertrophic response and the fetal gene reactivation such as beta-MyHC mRNA in this experiment.
Animals ; Aorta, Abdominal ; Calcineurin ; Cardiomegaly ; Cell Size ; Cyclosporine* ; Cytoplasm ; Diaphragm ; Euchromatin ; Heart Ventricles* ; Hypertrophy ; Mitochondria ; Models, Theoretical ; Myocardium* ; Myocytes, Cardiac ; Myofibrils ; Myosin Heavy Chains* ; Myosins* ; Rats* ; Renal Artery ; RNA, Messenger ; Sarcoplasmic Reticulum

The heart, 500g in weight, with subacute myocarditis associated with granulomatous myocarditis may be a good model for the study on the pathophysiologic mechanism of cardiac failure. Furthermore, the clinical data of this case is enough to clarify his all clinical course from admission to death due to cardiac failure. So, we analyzed the clinical data, histologic findings, and morphometric pattern of histologically intact myocardial cells and inflammatory reaction to investigate the pathophysiologic mechanism of the cardiac failure. The results were summarized as follows. 1. Clinically, the heart showed cardiac failure of diastolic phase and abnormal conduction system related to sudden cardiac death. However, it might be adapted to the relatively stable wital signs due to pericardial positive pressure by slowlyprogressed pericardial effusion. 2. The distribution pattern of area of intact myocardial cell area and inflammtion reaction showed relatively even spread of inflammatory reaction and extremely decreased area of myocardial cells to about 21% of total heart. So, its contractility might be decreased below to the 21% of the normal cardiac contractility. 3. The mechanism of the cardiac failure in myocarditis may be sudden inflammatory involvement of conduction system and/or extremely decreased myocardial cell volume due to inflammatory destruction. 4. Morphometric analysis may be a useful objective method to grading the severity of old and recent form of myocarditis. From the above results, the cardiac failure of myocarditis is influenced by the adaptability at the inflammatory abnormality of the conduction system, contractility of injured myocardial cells, and compensation activity of pericardial effusion.
Cell Size ; Compensation and Redress ; Death, Sudden, Cardiac ; Heart ; Heart Failure* ; Myocarditis* ; Pericardial Effusion

Alleles and genotype frequencies and its distribution pattern for the highly polymorphic D1S80 locus were determined in a Korean population sample, especially in Kwangju and Chonnam, by using PCR followed by agarose gel electrophoresis with ethidium bromide staining, a procedure called the amplified-fragment-length polymorphism(Amp-FLP) technique. And the data were compared with the alleles and genotype frequencies of Finnish population, North American Caucasian, and Korean population(Seoul) which had been reported. In 203 unrelated Korean individuals 27 alleles and 84 genotypes were observed. The highest allele frequency was in allele M24(0.128) and tne next orders were inalleles M18(0.126), M29, M30, M31, and M28 and the other alleles showed relatively low frequencies. The highest frequency of genotype was in M18/M24 and the next order frequencies were M18/M30, M19/M27 M29/M29, and M18/M29. The homozyous genotypes were in 9 alleles such as M29, M24, M31, and M18, and most of heterozygous genotypes were composed of alleles of each homozygous genotypes and /or the other alleles, its composition of genotypes was 0.881(74/84), 183(0.901) of the 203 individuals alleles, its composition of genotypes was 0.881(74/84), 183(0.901) of the 203 individuals alleles, its composition of genotypes was 0.881(74/84), 183(0.901) of the 203 individuals were included. The VNTR D1S80 locus demonstrated a heterozygosity of 0.872. From the above results, VNTR D1S80 locus may be a powerful locus to identify individuals, however, the allele frequencies was not closely related to the genotype pattern, and the alleles of homozygous genotypes influenced on the chance of the recombination of the various genotypes. It is necessary to analyze the genotype distribution and the recombination pattern of alleles as well as alleles and genotype frequencies in each populations for statistical test at most highly polymorphic loci.
Alleles* ; Electrophoresis, Agar Gel ; Ethidium ; Gene Frequency ; Genotype* ; Gwangju ; Jeollanam-do ; Polymerase Chain Reaction ; Recombination, Genetic

No abstract available.
Lip*

We report a case of multiple Bowen's disease associated with leprosy. A 68-year-old man was seen because of slightly pruritic multiple erythematous scaly patches and plaques on the trunk and the both extremities for 5 years. He has been treated for leprosy with many kinds of drugs consisting of the herb medications for over 40 years. He also showed decreased cell-mediated immunity in skin tests. It is considered that depressed cellular immunity may be an important predisposing factor in the development of mutiple Bowen's disease in this case, .although arsenics can not be completetly excluded.
Aged ; Bowen's Disease ; Causality ; Extremities ; Humans ; Immunity, Cellular ; Leprosy* ; Skin Tests

A 31-year-old woman had a livedo reticularis of reticulated, bluish discoloration on both arms and legs for 18 months with a burning pain in the right hand and numbness in both lower legs. The findings of the electromyography were consistent with mononeuropathy multiplex and bilateral ulnar-median nerve anastomosis. A biopsy specimen from the right sural nerve showed perivascular lymphocytic infiltration and occasional myelin digestion chambers, which were consistent with vasculitic neuropathy. We present a patient with livedo reticularis idiopathica associated with mononeuropathy multiplex syndrome who also has bilateral ulnar-median nerve anastomosis.
Adult ; Arm ; Biopsy ; Burns ; Digestion ; Electromyography ; Female ; Hand ; Humans ; Hypesthesia ; Leg ; Livedo Reticularis* ; Mononeuropathies* ; Myelin Sheath ; Sural Nerve

Genes encoding sequence-specific DNA binding proteins have been isolated by screening cDNA libraries constructed in rgt11 expression vector with recognition site DNAs. We isolated a rgt11 recombinant human cDNA clone, designated to C2, using a DNA probe consisted of heptamer of the perfect palindrome (PP; GGGGATTCCCC) of enhancer A (Enh A) of HLA dass I promoter. Sequencing analysis showed that this clone contained a partial cDNA homologous to NF-kB2. Lysogenic E. coli containing the C2 was generated and crude cell extract was prepared. Immunoblot using anti-B-galactosidase antibody showed that this lysogenic E. coli expressed B-galactosidase fusion protein. Electrophoretic mobility shift assay (EMSA) and DNase I footprinting assay were done using crude cell extract and their patterns were compared with nuclear protein extracted from an EBV transformed B lymphoblastoid cell line (BLCL). EMSA showed that crude cell extract prepared from E. coli lysogen speci5cally bound to the PP of Enh A region of HLA class I gene. DNase I footprinting assay showed that the binding sequence of this recombinant B-galactosidase fusion protein was identical to that of nuclear protein extracted from a BLCL. Our data indicate that a Agt11 recombinant cDNA clone was isolated from a human cDNA library using the PP of Enh A of the HLA class I promoter and this clone encoded a B-galactosidase fusion protein capable of binding to the PP and belongs to a NF-xB subunit.
Cell Line ; Clone Cells ; Deoxyribonuclease I ; DNA ; DNA, Complementary* ; DNA-Binding Proteins ; Electrophoretic Mobility Shift Assay ; Gene Library ; Genes, MHC Class I ; Herpesvirus 4, Human ; Humans* ; Mass Screening ; Nuclear Proteins

No abstract available.

No abstract available.
Hydronephrosis*

Many investigators were interested in the pathogenesis and the relationship between microscopical features and clinical behavior of hydatidiform mole. Trophoblastic cells in the trophoblastic disease were intensively examined histologically, ultrastructurally, immunohistochemically, and with hormone assay method, etc. But ultrastructural study on the stroma of hydatidiform mole was scarcely reported. In this paper, hydatidiform mole was examined at light and electron microscopic levels, with emphasis on the stroma. The results were as follows: 1) Hydropic degeneration of H-mole is more severe in the center of stroma and is not related with the degree of trophoblastic proliferation. Hofbauer cell and vascular structure are extremely rarely observed in the periphery of stroma which has relatively preserved cellular components. 2) Basement membrane is sometimes separated from trophoblastic layer. Degenerated cells in the stroma contain vacuoles, autophagosomes, and lipid droplets. Collagen is abundant in the loose interstitium. Hofbauer cells have no lysosome or phagosome. Vascular lumen is patient and endothelial cells are degenerated. From the above results, H-mole may be produced due to abnormal changes of trophoblasts and stromal changes may be a secondary process, so called autolysis. Hofbauer cells are not engaged in the stromal degeneration and may be different from usual tissue macrophages.