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

No abstract available.
Mandibular Osteotomy*

No abstract available.
Lip*

Coronary artery calcification(CAC) is found frequently in the atheromatous plaques CAC is known to have increased frequency above 40 years. CAC without evidence of atherosclerosis in young adults is quite rare, however, CAC combined with aneurysms in young adults have been infrequently reported in patients with a past history of a Kawasaki disease in child. We report an autopsy case showing CAC and aneurysm in the absence of macroscopically identified atherosclerotic lesions in a healthy 23-year-old man. The autopsy examination revealed aneurysmal dilatation of the right coronary artery which was connected with calcified lesion. A calcified lesion of the left anterior descending coronary artery was aslo noted. Microscopically, aneurysmal wall was non-specific except for hyalinized wall and foci of calcification. A striking histologic finding of calcified mass was ring calcification along the wall of the coronary artery. Antecedent Kawasaki disease in the past was suggestive as other reports.
Aneurysm* ; Atherosclerosis* ; Autopsy ; Child ; Coronary Vessels* ; Dilatation ; Humans ; Hyalin ; Mucocutaneous Lymph Node Syndrome ; Plaque, Atherosclerotic ; Strikes, Employee ; Young Adult*

Aortic dissection may be considered the result of a discrepancy between the strength of the aortic wall and the intramural pressure. And factors that predispose to aortic dissection may include systemic hypertension, cystic medial necrosis, Marfan's syndrome, atherosclerosis, disease of aortic valve, pregnancy, giant cell arteritis, hyperthyrosis, disease of aortic valve, pregnancy, giant cell arteritis, hyperthyroidism, and blunt chest trauma. A few of aortic dissection may extend retrograde toward the aortic valve and involve the coronary arteries. Coronary artery occlusions due to mural dissection are an uncommon but well documented cause of myocardial infarction. Although rare, extramural hematoma compressing the coronary artery is another cause of myocardial infarction. At autopsy of 43 years old male who had no critical external wound, pericardial sac was distended and contained 400ml of dark red and clotted blood. Examination of the aorta revealed only minute atherosclerosis, intact aortic valve, and patent coronary ostia. 0.5cm sized aortic rupture was noted at the 3.5cm distal to the aortic valve. DeBakey type II aortic dissection was found to involve the ascending aorta and brachiocephalic trunk. Three intimal tears were 1.5cm, 8cm. 11.5cm distal to the aortic valve and two false lumens which had intact area between them extended 3.5cm distal to the third intimal tear and proximally in a retrograde fashion to the aortic root. Microscopically, sections of aorta showed relatively intact arrangement of smooth muscle and elastic fibers, except mild vascular ectasia and scattered several foci of the small sized aggregation of foamy histiocytes, and there was no evidence of cystic medial degeneration in aorta. Sections of both coronary arteries did not show mural dissection or atherosclerosis. Sections of right atrium and sinus node showed inflammatory reaction, extensive replacement of myocardium by active fibrous tissue consistent with infarction. There was no histologic evidence of myocardial infarction in the walls of other chambers or septum of the heart. We believe that extramural compression of the artery to sinus m\node by the dissecting hematoma was the cause of myocardial infarction involving the right atrium and the sinus node.
Adult ; Aorta ; Aortic Rupture ; Aortic Valve ; Arteries ; Atherosclerosis ; Autopsy ; Brachiocephalic Trunk ; Coronary Vessels ; Dilatation, Pathologic ; Elastic Tissue ; Giant Cell Arteritis ; Heart ; Heart Atria ; Hematoma ; Hemodynamics* ; Histiocytes ; Humans ; Hypertension ; Hyperthyroidism ; Infarction ; Male ; Marfan Syndrome ; Muscle, Smooth ; Myocardial Infarction* ; Myocardium ; Necrosis ; Pregnancy ; Sinoatrial Node ; Thorax ; Wounds and Injuries

No abstract available.
Heart Septal Defects, Ventricular*

Percutaneous catheter drainage has been reported to bean effective method in the management of selectedpatients with abscess and fluid collection. Its high sucess rate and relatively low complications make theprocedure an alternative to surgery in the individual cases. During past two years percutaneous catheter dainagein 25 patients with intraabdominal abscesses and fluid collection was performed at the Department of Radiology,Yonsei Universtiy College of medicine. Here the technique and auathor's results were summarized; 1. The total 25patients who had percutaneous catheter drainage are 10 liver abscesses, 3 subphrenic, one subhepatic, 4 renal andperirenal, 2 pelvic, one psoas, one anterior pararenal fluid from acute pancreatitis, one pancreas pseudocyst and2 malignant tumor necrosis. 2. The modified Seldinger technique used for all cases of abscess and fluid draingeunder guidence of ultrasound scan. The used catheters were 10F. Pigtail and 14F. Malecot (Cook c/o) catheters. 3.The abscesses and fluid of 17 patients among 25 were cured by the percutaneous catheter drainage and 4 patientswere clinically improved. The catheter drainage was failed in 2 patients and 3 complications were developed. 4.The success rate of this procefure was 91.3%, failure rate was 8.7% and complication rate was 12%.
Abscess ; Catheters ; Drainage ; Humans ; Liver Abscess ; Methods ; Necrosis ; Pancreas ; Pancreatitis ; Ultrasonography

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

Myeloid body formation is an ultrastructural feature of gentamicin induced nephrotoxicity in human being and experimental animals. The origin of the myeloid body is not satisfactorily understood and morphological verification of the developing process of this structure is not fully accomplished. We injected 100 mg/kg/12 hour of gentamicin in 20 Spraque-Dawley rats and examined the ultrastructural feature of the proximal convoluted tubular cells of the kidney every 30 minutes in the first 4 hours, and in 5 hours, 6 hours, 12 hours, 24 hours and 48 hours after injection of gentamicin, with a TEM and a SEM. Myeloid bodies were noted as concentric layers of membranous structures of degenerated endoplasmic reticulum and mitochondria in the lysosome. The number and size of the myeloid body containing lysosomes were increased with time. We can deduce from this observation that injured cell organelles by diffusible gentamicin within the cells are autophagocytosed by lysosomes which were also injured by the drug from pinocytotic vesicles, and incompletely digested organellar remnants are retained in the lysosomes as myeloid bodies. So we think that the myeloid body formation is a result of an exaggerated and a pathologic autophagocytic process due to cell injury induced by gentamicin.
Animals ; Endoplasmic Reticulum ; Gentamicins* ; Humans ; Kidney ; Lysosomes ; Mitochondria ; Organelles ; Rats*

No abstract available.
Carcinoma, Transitional Cell* ; Urinary Bladder*