BACKGROUND AND OBJECTIVES: Compared to other target cells examined for gene therapy, vascular smooth muscle cells (VSMCs) have the unique advantages including proximity to blood stream and relative abundance in vasculature. With an ultimate goal of developing VSMC-based therapies for cardiovascular disorders, we explored the utility of VSMC as a target cell for ex vivo gene therapy using a set of retroviral vectors. MATERIALS AND METHODS: Cultured VSMCs were transduced with replication-defective recombinant retroviruses harboring LacZ, nlsLacZ, mVEGF, mGM-CSF or bacterial CAT reporter. The VSMCs were examined for G418-selection, transduction efficiency, the level of transgene expression, and longevity of gene expression. ResultsVSMCs were readily transduced with different kinds of retroviral vectors. The bacterial neo r gene-transduced VSMCs were successfully selected with G418. The G418-selected VSMCs could express the transduced genes at a level comparable to NIH3T3. The level of transgene expression did not appear to be affected by the increasing number of passages. CONCLUSION: The results demonstrate an efficient transduction of VSMCs by retroviral vectors in vitro and an sustained expression of retrovirally transduced genes in VSMCs. VSMCs could be one of the ideal target cells for ex vivo cardiovascular gene therapy employing retroviral vector.
Animals ; Cats ; Gene Expression ; Genetic Therapy* ; Longevity ; Muscle, Smooth, Vascular* ; Retroviridae ; Rivers ; Transgenes ; Zidovudine

Actinomycosis is an oppoturnistic infection of actinomyces, which are relatively avirulent endogenous oral commensals. After trauma or infection, they breach the normally protective mucosal barriers to invade adjacent soft tissue structures. Lesions routinely contain other bacteria, the normal resident flora at the site of primary infection, which act synergistically with actinomyces species to provoke this unique infection, which range from an acute suppurative process to a chronic fibrotic process. According to epidemic studies about pelvic actinomycosis, it should be significantly related to IUD(intrauterine device). It is accounted that IUD cause chronic intrauterine infection, tissue injury and act as nucleus for parasitic infestation. Here we present a case of pelvic actinomycosis related to IUD with brief review of the concerned literature.
Actinomyces ; Actinomycosis* ; Bacteria

No abstract available.
Atrial Natriuretic Factor* ; Humans* ; Lymph Nodes* ; Polymerase Chain Reaction*

No abstract available.
Liver Cirrhosis* ; Liver* ; Polycythemia Vera* ; Polycythemia*

BACKGROUND AND OBJECTIVES: ovastatin, a HMG-CoA reductase inhibitor, is known to show antiproliferative effects on VSMC after vessel injury, but a large amount of the drug is needed orally for this purpose. This study investigated the effects of lovastatin given locally to injured carotid arteries of rats on reducing neointimal hyperplasia. MATERIALS AND METHOD: Lovastatin was given perivascularly to balloon-injured carotid arteries of 21 rats in 1 microM to the low-dose group, and 30 microM to the high-dose group. The control group was treated with pluronic gel only. Two weeks later, the lumen area, neointimal areas and the number of actively proliferating cells were obtained and compared. RESULTS: eointimal area was 0.113+/-0.032 mm2, 0.065+/-0.017 mm2, 0.072+/-0.017 mm2 in the control, low-dose and high-dose groups respectively. The area was significantly smaller in the treatment groups (p<0.05), but no significant difference was observed between the treatment groups. The number of actively proliferating cells per mm2 of neointimal area were 714.5+/-227.4, 688.4+/-333.7, and 1526.3+/-744.0 in the groups respectively, and the number was significantly high in the high-dose group (p<0.05). CONCLUSION: Local administration of lovastatin is effective in reducing neointimal hyperplasia after vascular injury, but extremely high doses are not needed locally for this purpose.
Animals ; Carotid Arteries* ; Carotid Artery Injuries* ; Hyperplasia* ; Lovastatin* ; Oxidoreductases ; Rats* ; Vascular System Injuries

BACKGROUND AND OBJECTIVES: It has been well known that the Braunwald classification is an appropriate clinical parameter in the prediction of the outcome in patients with unstable angina. However, the ability of the classification to predict prognosis of unstable angina according to treatment strategy is not established. We evaluated the relation between severity of angina on admission and outcome of primary unstable angina with early invasive strategy. MATERIALS AND METHOD: 148 patients (M 85, F 63, age 61+/-10) with suspected unstable angina were divided into three subgroups on the basis of the Braunwald classification on admission. The patients were followed up to 6 months prospectively if the final diagnosis was primary unstable angina. Early invasive strategy was used for the treatment of unstable angina. Major cardiac events were assessed during hospitalization and 6 months follow-up period according to the Braunwald classification. RESULTS: Unstable angina was diagnosed in 95 patients (64%). Among these patients, 89 patients with primary unstable angina were followed up to 6 months. Clinical characteristics including number of patients, mean age, sex ratio, risk factors, coronary angiographic findings and revascularization rate during hospitalization were not different in three subgroups of these patients. Among these patients, early coronary revascularizations was performed in 67 patients (75%) and 2 (2%) deaths/myocardial infarctions occurred during hospitalization. During the follow-up period, 1 (1%) myocardial infarction/death and 12 (13%) revascularizations occurred. Cardiac event rate (death, myocardial infarction or revascularization) was not different during hospitalization and 6 months follow-up period among subgroups of severity class. CONCLUSION: Clinical outcome should be reevaluated after early coronary intervention to predict cardiac event in patients with unstable angina.
Angina, Unstable* ; Classification ; Diagnosis ; Follow-Up Studies ; Hospitalization ; Humans ; Infarction ; Myocardial Infarction ; Prognosis ; Prospective Studies ; Risk Factors ; Sex Ratio

BACKGROUND: It has been suggested that all components of the renin-angiotensin-aldosterone system (RAAS) are present in the vascular wall and that the vascular RAAS modulates vascular tone and vascular hypertrophy. One of the catalytic step in the RAAS cascade is the local conversion of angiotensin I to angiotensin II (Ang II) by angiotensin converting enzyme (ACE). One of the major sources of ACE in the vasculature is vascular smooth muscle cells (VSMC). Here, we provide insight into the intrinsic mechanisms by which the components of RAAS regulate gene expression of ACE in cultured smooth muscle cells of the rat and we also investigated the effects of cytokines on ACE mRNA. METHODS: RNA was extracted from the primary cultured VSMCs. We analyzed the expression levels of ACE by competitive reverse transcription-PCR using recombinant RNA as an internal standard. RESULTS: 1) ACE mRNA level was increased markedly by aldosterone in a dose- and time-dependent manner, indicating that there exists positive feedback mechanism within RAAS. 2) The induction of ACE mRNA by aldosterone was inhibited by spironolactone. 3) Aldosterone-stimulated expression of ACE was also inhibited by Ang II, which shows that Ang II acts as a negative regulator of the expression of ACE in RAAS cascade. 4) Interleukin-1beta or TNF-alpha did not induce ACE mRNA expression. 5) However, mixture of interleukin-1betaand TNF-alpha(CytoMix) significantly increased the expression of ACE. It was also shown that CytoMix increased aldosterone-stimulated ACE mRNA expression in an additative manner. CONCLUSION: These results indicate that the expression of ACE in smooth muscle cells is modulated by the components of RAAS and cytokines. The intrinsic positive and negative feedback controls of RAAS would play an important role in the pathogenesis of vascular diseases.
Aldosterone* ; Angiotensin I ; Angiotensin II ; Angiotensins* ; Animals ; Cytokines* ; Gene Expression ; Hypertrophy ; Interleukin-1beta ; Muscle, Smooth, Vascular* ; Myocytes, Smooth Muscle ; Peptidyl-Dipeptidase A* ; Rats ; Renin-Angiotensin System ; RNA ; RNA, Messenger ; Spironolactone ; Tumor Necrosis Factor-alpha* ; Vascular Diseases

BACKGROUND AND OBJECTIVES: Heart rate variability(HRV) reflects the autonomic integration of heart. There were many reports that HRV in patients with myocardial infarction or heart failure is an independent prognostic factor to predict fatal arrhythmia and sudden cardiac death. But, the role of HRV is still controversial in stable angina patients without history of myocardial infarction. In this study, we tried to compare HRV indices between stable angina patients and normal subjects. MATERIALS AND METHODS: Twenty-one stable anginal patients without history of myocardial infarction (mean age : 57 +/- 2 years) and twenty-one relatively healthy persons without history of coronary heart disease (mean age : 53 +/- 2 years) were included in the study and underwent 24-hour ambulatory ECG monitoring. In patients group, all underwent coronary angiography after 24-hour ambulatory ECG monitoring. HRV was analyzed over the whole 24 hours, using time and frequency domain parameters, according to time phases and coronary angiographic severity. RESULTS: There were no significant differences in age, sex and cardiovascular risk factors, except hypertension (p=.001) between two groups. HRV indices such as rMSSD, pNN50, LF, HF, LFnorm and HFnorm were significantly decreased (p<0.05) in patients group. But the angiographic severity of coronary arteries did not show any significant effect on the HRV indices in patients group. CONCLUSIONS: We observed significantly reduced HRV indices in patients with stable angina without history of myocardial infarction.
Angina, Stable* ; Arrhythmias, Cardiac ; Coronary Angiography ; Coronary Disease ; Coronary Vessels ; Death, Sudden, Cardiac ; Electrocardiography ; Heart Failure ; Heart Rate* ; Heart* ; Humans ; Hypertension ; Myocardial Infarction* ; Risk Factors

BACKGROUND AND OBJECTIVES: This study was performed to investigate the antiproliferative effect of lovastatin on vascular smooth muscle cell, especially to determine whether lovastatin induces apoptosis in vascular smooth muscle cell and the products of mevalonate pathway can reverse the antiproliferative effect of lovastatin. METHODS AND MATERIALS: Lovastatin only and lovastatin with one of the products of mevalonate pathway such as isopentenyl adenine, farnesol, mevalonate, cholesterol were added respectively in cultured rat vascular smooth muscle cells stimulated with 10% fetal calf serum. DNA synthesis was measured by tritiated-thymidine incorporation. Cell number was determined by hemocytometric counting. Cells were Giemsa-stained to evaluate morphological changes of apoptosis. Extracted DNA from the cells treated with lovastatin was assessed by gel electrophoresis. RESULTS: 1)Lovastatin inhibited DNA synthesis and cell proliferation in a dose-dependent manner. 2)The inhibitory effects of lovastatin could be reversed almost completely by mevalonate, partially by farnesol. 3)Lovastatin-treated vascular smooth muscle cells showed typical morphological changes of apoptosis. 4)A distinct ladder of DNA bands was visualized by gel electrophoresis of the DNA from the cells treated with lovastatin. CONCLUSION: Mevalonate metabolism is essential for vascular smooth muscle cell proliferation. The antiproliferative effect of lovastatin may result from the induction of apoptosis in vascular smooth muscle cells.
Adenine ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cholesterol ; DNA ; Electrophoresis ; Farnesol ; Lovastatin* ; Metabolism ; Mevalonic Acid ; Muscle, Smooth, Vascular* ; Rats

BACKGROUND AND OBJECTIVES: Neurocardiogenic syncope is believed to be caused by a transient imbalance of autonomic nervous system. Actually, there were significant differences in heart rate variability (HRV) indices during head-up tilt test between patients with neurocardiogenic syncope and normal controls. But there was no definite evidence for it during daily activity. So, we tried to evaluate HRV during daily activity with 24-hour ambulatory electrocardiography monitoring. MATERIALS AND METHODS: 27 patients with neurocardiogenic syncope or presyncope (mean age 45+/-3) and 25 normal volunteers (mean age 47+/-2) comparable for age and sex underwent 24-hour ambulatory electrocardiography. Head-up tilt test was used to diagnose neurocardiogenic syncope or presyncope in patients group. HRV was analysed over the whole 24 hours, using time and frequency domain parameters. Student's t-test was applied. ResultsThere were no significant differences in HRV measures between two groups, over 24-hour period and day-time and night-time period. But the hourly HRV measures showed a transient decrease of LF, LFnorm and LF/HF ratio in patients group compared to normal control group. CONCLUSIONS: These results indicate that patients with neurocardiogenic syncope or presyncope suffer from temporarily decreased sympathetic tone with normal parasympathetic tone. So, transient additive change of autonomic nervous tone may cause syncope or presyncope in these patients. (Korean Circulation J 2000;30 (6):716-723)
Autonomic Nervous System ; Electrocardiography, Ambulatory ; Healthy Volunteers ; Heart Rate* ; Heart* ; Humans ; Syncope* ; Syncope, Vasovagal*