We describe a case of xanthoma on the corneoscleral limbus in a 21-year-old man. It was characterized by a localized, round, elevated, yellowish mass on the right superonasal limbus with 6mm in size. There was no correlation with systemic or metabolic diseases such as hyperlipidemia and the microscopic examination revealed scanty fibrous element.
Humans ; Hyperlipidemias ; Metabolic Diseases ; Xanthomatosis* ; Young Adult

We describe a case of xanthoma on the corneoscleral limbus in a 21-year-old man. It was characterized by a localized, round, elevated, yellowish mass on the right superonasal limbus with 6mm in size. There was no correlation with systemic or metabolic diseases such as hyperlipidemia and the microscopic examination revealed scanty fibrous element.
Humans ; Hyperlipidemias ; Metabolic Diseases ; Xanthomatosis* ; Young Adult

BACKGROUND: Herpes simplex virus thymidine kinase (HSVtk) phosphorylates the prodrug ganciclovir to a nucleoside analog that inhibits DNA synthesis, causing cell death. Neighbouring nontransfected cells may be affected through a 'bystander effect', thereby amplifying the antiproliferative actions. This study was carried out to determine whether retrovirus-mediated HSVtk gene therapy could reduce intimal hyperplasia and prevent stenosis following balloon injury of the rat carotid artery. METHODS: A replication-defective recombinant retroviral vector containing HSVtk cDNA (LtkSN) was constructed. Cultured primary rat smooth muscle cells (SMCs) infected with this vector (SMC/LtkSN) were transplanted to the balloon injured rat right carotid artery. One week after transplantation, HSVtk gene therapy group was administered a 2-week treatment of ganciclovir (30 mg/kg/d). Three weeks after balloon injury and SMC/LtkSN transplantation, carotid arteriography was performed and carotid arteries were perfusion-fixed for histologic examination. RESULTS: Carotid arteriographic evaluation comparing with the uninjured left carotid artery showed that the mean luminal diameter of HSVtk gene therapy group (n=5, 85+/-3%) was significantly larger than that of balloon injury only group (n=5, 65+/-5%). The neointimal mass of HSVtk gene therapy group was less than that of balloon injury only group. SMC/LtkSN transplantation without ganciclovir treatment group (n=3) showed asymmetric intimal proliferation probably because of gravitational pooling of seeding. There were inflammatory cell infiltrations at the gravity dependent portion of HSVtk gene therapy group. CONCLUSION: Retrovirus-mediated HSVtk gene therapy following balloon injury of the rat carotid artery reduced neointimal expansion and arteriographic stenosis.
Angiography ; Animals ; Carotid Arteries* ; Carotid Artery Injuries* ; Cell Death ; Constriction, Pathologic* ; DNA ; DNA, Complementary ; Ganciclovir ; Genetic Therapy* ; Gravitation ; Herpes Simplex* ; Hyperplasia ; Myocytes, Smooth Muscle ; Phenobarbital ; Phosphotransferases* ; Rats* ; Simplexvirus* ; Thymidine Kinase ; Zidovudine

BACKGROUND: Clinical and experimental studies have suggested that brain death may cause hemodynamic, electrocardiographic, functional or histopathologic changes of the heart. METHODS: Brain death was induced by increasing intracranial pressure(ICP) abruptly by intermittent bolus injection of saline(model ) or gradually by continuous infusion of saline(model ) to the epidural catheter in 5 mongrel dogs, respectively. Hemodynamic and biochemical changes during the process of brain death and histopathologic changes of the myocardium were analyzed and compared in two brain death models, and the association of apoptosis was also evaluated. RESULTS: 1) Two predominant subsets of acute contraction band lesion were produced in both brain death models : paradiscal and holocystic contraction band lesions. Both contraction band lesions were more prevalent in brain death model . 2) The frequency of both contraction band lesions was lowest in the epicardial layer and highest in the endocardial layer in both models, but no correlation was observed between the degree of contraction band lesions and ICP, LV maximum +dp/dt or catecholamine levels. There was no statistical difference between any of the LV circumferential blocks and either type of contraction band lesion, and transaxial distribution was not also different in both models. 3) There was no remarkable histopathologic changes in the analysis of major epicardial coronary arteries. Apoptotic cells were suggested in the scattered myocytes in the light microscopy and apoptosis was detected by in situ nick end labeling method. Electron microscopy revealed a condensation of nuclear chromatin and convolution of nuclear membrane in those myocytes. CONCLUSIONS: Myocardial changes due to brain were observed frequently, and few apoptotic cells were found in the brain death heart. Studies on the treatment strategy to minimize damages of myocardial structure and function caused by brain death should be followed in the near future.
Animals ; Apoptosis ; Brain Death* ; Brain* ; Catheters ; Chromatin ; Coronary Vessels ; Dogs ; Electrocardiography ; Heart ; Hemodynamics ; In Situ Nick-End Labeling ; Microscopy ; Microscopy, Electron ; Muscle Cells ; Myocardium* ; Nuclear Envelope

BACKGROUND: Pacing-induced atrial electrical remodeling (AER) is characterized by shortening of atrial effective refractory period (A-ERP) and its altered rate adaptation. In paroxysmal atrial fibrillation (AF), periods of AF occur with interveneing normal sinus rhythm (NSR) when atria recover from the preceding AER. Previous episodes of AF may precondition the atrial myocardium and cause different time course of AER in subsequent episodes of AF. But the influence of the preceding AER on the subsequent AER has not been described. METHODS: Four mongrel dogs were anesthetized with enflurane. After thoracotomy, silicon band with 3 pairs of electrodes was sutured to the lateral wall of the left atrium. Atrial pacing was performed after 2 wks of recovery and autonomic blockade. Pacing protocol consisted of rapid atrial pacing (RAP) at 500 bpm (for 60 min) and recovery in NSR (for 60 min) which was repeated three times. A-ERP was measured every 10 min. The same pacing protocol was repeated after pretreatment with verapamil (0.1 mg/kg/hr). RESULTS: 1) With 60 min of RAP, A-ERP decreased significantly (126+/-6 ms vs. 105+/-7 ms, p<0.005). 2) After cessation of pacing, A-ERP returned to 98% of baseline value in 15 minutes. Recovery from AER occurred faster than AER (78 vs 21 ms/h). 3) After pretreatment with verapamil, RAP decreased A-ERP from 127+/-5 ms to 116+/-5 ms. AER, the reduction in A-ERP, was significantly attenuated by pretreatment with verapamil (deltaERp=17+/-7 vs. 9+/-0.2 %, p<0.05). 4) When RAPs were repeated, AER showed a tendency of acceleration, but it was not statistically significant (deltaERp=22 ms, 24 ms, 28 ms at the end of 60 min pacing for the 1st, 2nd, 3rd pacing). CONCLUSION: RAP induced AER in conscious dog atria and it was reduced by pretreatment with calcium channel blocking agent, verapamil. Upon repeated atrial stimulations, AER did not accelerate or decelerate when the atria recovered from the preceding AER.
Acceleration ; Animals ; Atrial Fibrillation ; Atrial Remodeling* ; Calcium ; Calcium Channels ; Dogs* ; Electrodes ; Enflurane ; Heart Atria ; Myocardium ; Silicones ; Thoracotomy ; Verapamil

No abstract available.
Cough* ; Humans ; Sarcoidosis* ; Skin*

BACKGROUND: Several kinds of stents have shown their safety and efficacy to treat acute or subacute closure after balloon angioplasty as well as to reduce restenosis rate. However, one of the limitations of stents is difficult to deploy especially in tortuos vessels, lesions at a bend, and distal to previously deployed stents. The Micro stent II, which was one of the most recently developed stents, ia a rapid-exchage balloon expandable stainless steel stent with a zigzag design connected with a continuous single weld in each 3mm segments. It scores over excellent trackability and optimum radio-opacity. Therefore, it is easy to operate and feasible in tortuous, distal lesions and variety of lesion lengths. We report our experiences with Micro-II stent implanatation in the first 76 patients at Tonsei cardiovascular center to assess its safety and efficacy in patients with complex coronary anatomy and clinical results in the first months. METHODS: Between January 1996 and July 1996, eighty-six Micro-II stent were implanted in the coronary arteries of 76 patients(male 65.8%, age 59+/-10 year). Forty-five patients had unstable angina, the others had stable angina(17pts), acute myocardial infarction(14pts). RESULTS: 1) Indication of stenting was de novo 51(59.3%), suboptimal result 25(29.1%), restenosis 1(1.2%) and 9(10.4%) of lesions were stented in bail out situation. 2) Single stent were implanted in 76(88.4%)lesions, overlapping stent in 10(11.6%)lesions. Among overlapping stents, the second stent with Micro-II stent and with another kind of stent were 4.6%, 7.0%, respectively. 3) Procedure related complication including a subacute closure was occurred in 1(1.2%) patient who had distal dissection and 45% residual stenosis. In 12(14%) lesions, preistent dissection has been noticed after stent impantation. 4) Angiographic success(defined as a residual stenosis of <30% without major dissection) was achieved in 82 of 86 attempts(95.3%). The procedual success rate(defined as a residual stenosis of <30% without occurrence of major clinical events within 4 weeks after procesure) was 96.1%(73/76 patients). Angiographic success and procedural success rate in calcified lesion were 100% and 100%, respectively. Angiographic success and procedural success rate in more than 45` angulated lesion were 97% and 100%, respectively. 5) The mean minimal luminal diameter of the target lesions was increased from 0.42+/-0.40mm before stent implantation to 2.93+/-0.50mm(p<0.001). The percentage of diameter stenosis was reduced from 86.49+/-13.04% to 1.40+/-7.11%(p<0.001) after stent implantation. CONCLUSION: Coronary stenting with AVE Micro-II stent can be safety performed and is particularly beneficial in tortuous and calcified arteries. There was a high tendency for peristent dissection which need to special consideration to avoid. Follow-up data is needed to assess mid and term patency. Coronary artery disease . AVE Micro-II stent . Immediate results.
Angina, Unstable ; Angioplasty, Balloon ; Arteries ; Constriction, Pathologic ; Coronary Artery Disease ; Coronary Vessels ; Follow-Up Studies ; Humans ; Phenobarbital ; Stainless Steel ; Stents*

Viral myocarditis is considered an important cause of dilated cardiomyopathy. At preseent, two mechanisms are known to be involved in the pathogenesis of viral myocarditis and subse-quent cardiomyopathy: viral direct toxicity and immune mediated toxicity. Some authors have reported that IL-6 influences the immunologic mechanism and the virus-induced tissue damage in myocarditis. We injected encephalomyocarditis(EMC) virus to induce viral myocarditis in ICR mice. In order to study the lymphocyte subset and IL-6 expression to clarify the immune mechanism and to demonstrate the role of IL-6 in viral induced myocardial damage. The following results were obtained: 1) In virus inoculated mice, inflammation was severest at 10 days, and some serious complications developed, indicating a possible transition to dilated cardiomyopathy. 2) On analysis of the lymphocyte subset, CD4 cells were most prevalent at 5 days and CD8 cells were most prevalent at 10 and 20 days. 3) IL-6 was significantly increased and expression of IL-6 was constant, but its intensity was strongest at 5 days. In conclusion, IL-6, produced by inflammatory cells, fibroblasts, and endothelial cells, might play an important role in myocardial damage in experimentally induced EMC viral myocarditis by its direct cytotoxicity or cytokine mediated activation of cytotoxic cells.
Mice ; Animals

BACKGROUND: Many autopsy studies have shown that the extent of extracranial carotid and coronary artherosclerosis is correlated and B-mode ultrasonographic intima-media thickness(IMT) and histologic IMT have been good correlation. In recent years. as it has been reported that IMT of carotid artery had something to do with risk factors of atherosclerosis and occurrence of coronary artery disease, in this study, we tried to investigate if the grade of atherosclerosis in B-mode ultrasonography of carotid artery could predict coronary artery disease and have something to do with the severity of coronary artery disease. METHODS: We classified the patients who were examined coronary angiography into control group without significant(>50%) stenosis(11 patients) and coronary artery disease(CAD) group(45 patients) according to the existence of significant stenosis, and we subdivided CAD group into single vessel disease(SVD) group(25 patients) and multivessel disease(MVD) group(20 patients). Practicing B-mode ultrasonography of common carotid artery(CCA), carotid artery bifurcation(BIF) and internal carotid artery(ICA), we measured IMT and IMT/L(lumen diameter) of each segment. Adding all values of each segment, we got mean aggregated IMT and mean aggregated IMT/L. RESULTS: 1) As IMT of left BIF in both six segments, control group was 0.55+/-0.16mm, SVD group was 0.71+/-0.36mm and MVD group was 1.02+/-0.61mm. So compared with control group and SVD, MVD group were significantly thick. As IMT/L, control group was 0.07+/-0.02, SVD group 0.08+/-0.05 and MVD group was 0.13+/-0.08. So compared with control group and SVD, MVD group was ignificantly high. 2)IMT of BIF in three segments, control group was 0.59+/-0.16mm, CAD group was 0.82+/-0.47mm and MVD group was 0.90+/-0.54mm. So compared with control group and CAD, MVD group were significantly thick. Also as IMT/L of BIF, compared with control group(0.07+/-0.02) and CAD(0.10+/-0.06), MVD(0.11+/-0.07) group was high.= 3) As mean aggregated IMT, control group was 0.57+/-0.34mm, CAD group was 0.69+/-0.45mm, SVD group was 0.63+/-0.12mm and MVD group was 0.74+/-0.21mm. So CAD group was thicker than control group and MVD group was thicker than SVD group. As mean aggregated IMT/L, control group was 0.07+/-0.03, CAD group was 0.10+/-0.05, SVD group was 0.09+/-0.01 and MVD group was 0.11+/-0.03. So CAD group was higher than control group and MVD group was higher than SVD group. CONCLUSION: These data support use of the mean aggregated B-mode ultrasonographic IMT and IMT/L in carotid bifurcation for correlation with the status of coronary atherosclerosis.
Atherosclerosis ; Autopsy ; Carotid Arteries* ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease* ; Coronary Vessels* ; Humans ; Risk Factors ; Ultrasonography

BACKGROUND AND OBJECTIVES: The FK-506 binding protein 12 (FKBP12) regulates intracellular Ca2+ release by stabilizing the Ca2+-induced Ca2+-release channel (ryanodine receptor) in skeletal muscle. It has been recently shown that a different FKBP, FKBP12.6, is specifically associated with cardiac ryanodine receptor. Since the role of FKBP12.6 in excitation-contraction coupling in the cardiac muscle has not been precisely determined, its biological function was assessed and expression patterns of FKBP12.6 were evaluated in the various models of heart disease. MATERIAL AND METHODS: The mouse (m) FKBP12.6 gene was cloned and characterized after screening a mouse genomic DNA library using a mFKBP12.6 cDNA obtained through reverse transcriptase-polymerase chain reaction. Expression levels of mFKBP12.6 was evaluated during cardiac development and in the models of cardiac hypertrophy and failure. RESULTS: Both mFKBP12.6 and mFKBP12 contain an open reading frame of 327 nucleotides encoding 108 amino acids. Comparison of mFKBP12.6 cDNA to rat FKBP12.6, human FKBP12.6 and mFKBP12 cDNA revealed 95%, 94% and 74% identity in nucleotide sequence and 98%, 97% and 80% identity in amino acid sequence, respectively. Purified recombinant mFKBP12.6 migrated slower than either mFKBP12 or human FKBP12 on an SDS-polyacrylamide gel, despite having the same number of amino acids and a slightly lower calculated molecular mass. Northern blot analysis showed that the expression of FKBP12 and FKBP12.6 to be highest in brain. While the expression of FKBP12 was much stronger in adult than in embryonic hearts, it was further increased following pressure overload hypertrophy. FKBP12.6 mRNA expression analyzed by RNase protection assay was upregulated after induction of cardiac hypertrophy like FKBP12, whereas it was decreased in the failing heart. The mFKBP12.6 gene contains 5 exons and the proteincoding region of the gene was divided into 4 exon modules. CONCLUSION: We report the molecular cloning and characterization of the mouse FKBP12.6 gene. According to these results, FKBP12 and FKBP12.6 may play a role in the development of cardiac hypertrophy and transition to heart failure. To precisely determine the role of FKBP12 and FKBP12.6 in the heart, a strategy using homologous recombination in embryonic stem cells to conditionally ablate exon 2 of mFKBP12.6 gene has been developed and initial characterization is now underway.
Adult ; Amino Acid Sequence ; Amino Acids ; Animals ; Base Sequence ; Blotting, Northern ; Brain ; Cardiomegaly ; Carrier Proteins* ; Clone Cells ; Cloning, Molecular* ; Cloning, Organism ; DNA, Complementary ; Embryonic Stem Cells ; Exons ; Gene Library ; Heart Diseases* ; Heart Failure ; Heart* ; Homologous Recombination ; Humans ; Hypertrophy ; Mass Screening ; Mice* ; Muscle, Skeletal ; Myocardium ; Nucleotides ; Open Reading Frames ; Rats ; Ribonucleases ; RNA, Messenger ; Ryanodine Receptor Calcium Release Channel ; Tacrolimus Binding Protein 1A ; Tacrolimus Binding Proteins ; Tacrolimus*