PURPOSE: Congenital anomalies are known as a major cause of neonatal death with prematurity and birth injuries. We surveyed the incidence of congenital anomalies among livebirths and stillbirths delivered at our hospital, and detected in neonatal and postneonatal period. METHODS: The statistical study was done about congenital anomalies among 9,569 deliveries (9,438 livebirths and 131 stillbirths) at Ulsan University Hospital during the periods of 5 years from Jan 1992 to Dec 1996. We reviewed delivery and newborn record, OPD chart, admission chart retrospectively. We investigated the incidence of congenital anomaly according to each year, period, outcome of delivery, sex, birth weight, gestational age, maternal age, Apgar score, multiple pregnancy, and each system. RESULTS: 1) The overall incidence of congenital anomalies was 5.0% (481 cases) among 9,569 deliveries. The annual incidence was 4.5% in 1992, 5.1% in 1993, 5.2% in 1994, 5.8% in 1995, 4.7% in 1996. 2) The incidence of congenital anomalies detected in neonatal period was 3.5% (333 cases) and 1.5% (148 cases) in postneonatal periods. 3) The incidence of congenital anomalies was 4.9% among live births and 9.2% among stillbirths. 4) The incidence of congenital anomalies was 5.3% in male and 4.7% in female. 5) The incidence of congenital anomalies among the babies, below 2,500g of birth weight was 7.7%, between 2,500g and 3,999g was 4.7%, and over 4,000g was 6.8N. 6) The incidence of congenital anomalies among the babies, below 32 weeks of gestational age was 12.9%, between 32 weeks and 36 weeks was 7.4%, between 37 weeks and 41 weeks was 4.7%, and over 42 weeks was 5.1%. 7) The babies born to mothers younger than 20 years of age have anomalies in 7.1%, mother between 20 years of age and 35 years of age in 5.0%, and older than 35 years of age in 6.5%. 8) The incidence of congenital anomalies according to Apgar score among live births between 0 and 3 was 9.8%, between 4 and 6 was 6.0%, and between 7 and 10 was 5.0%. 9) The incidence of congenital anomalies according to multiple pregnancy was 8.6%. 10)The systems of congenital anomalies in order of incidence were as follows; The digestive system (25.6%), the cardiovascular system (22.1%), the genitourinary system (18.9%), the musculoskeletal system (15.5%), the skin and soft tissue (11.7%), the central nervous system (1.6%), the respiratory system (l%), the others (3.6%). CONCLUSIONS: Regular examination and screening on congenital anomaly is required from newborn period to infant and childhood. In view of these considerations, the incidence of congenital anomaly may be increased more than the past reports because of development of recent diagnostic techniques.
Apgar Score ; Birth Injuries ; Birth Weight ; Cardiovascular System ; Central Nervous System ; Digestive System ; Female ; Gestational Age ; Humans ; Incidence ; Infant ; Infant, Newborn ; Live Birth ; Male ; Mass Screening ; Maternal Age ; Mothers ; Musculoskeletal System ; Pregnancy ; Pregnancy, Multiple ; Respiratory System ; Retrospective Studies ; Skin ; Statistics as Topic* ; Stillbirth ; Ulsan ; Urogenital System

No abstract available.
Mesenteric Artery, Superior* ; Superior Mesenteric Artery Syndrome*

The bond failure of resin teeth to denture base resin is one of the failure in prosthodontic treatment. The purpose of this study was to evaluate the bond strength of artificial resin teeth to the denture base resins. Specimens were made with heat curing acrylic resins (Vertex Rs, Lucitone 199) and artificial resin teeth (Tiger, Trubyte biotone, Endura, Orthosit, Trubyte bioform IPN) and the bond strength were measured with testing machine (Zwick, Germany) and the mode of bond failure were observed. The results were as follows; 1. The bond strength of Vertex Rs to artificial resin teeth was the highest in Trubyte biotone, and It was the lowest in Tiger and Trubyte bioform IPN 2. The bond strength of Lucitone 199 to artificial resin teeth were higher in Orthosit and Trubyte bioform IPN than in Tiger and Trubyte biotone. 3. The bond strength of Trubyte biotone to Vertex Rs was higher than to Lucitone 199 and that of the Trubyte bioform IPN to Lucitone 199 was higher than to Vertex Rs. 4. Nearly all bond failures of specimens occured cohesively within the resin teeth.
Acrylic Resins ; Denture Bases* ; Dentures* ; Hot Temperature ; Prosthodontics ; Tigers ; Tooth*

No abstract available.

A putative polypeptide hormone identified as amylin[islet amyloid polypeptide] is synthesized and co-localized with insulin in B cells of pancreatic islets in several animal species including man. However, there is growing evidence that somatostatin cells are also expressed and contained amylin in the pancreatic islets of the rat The aim of the present study was to investigate the immunocytochemical expression of the amylin within the endocrine pancreas of the man, rabbit and guinea pig, with special reference to the possible ability of islet cells other than insulin cells to synthesize amylin. For this purpose serial sections of the pancreatic islets were stainedimmunocytochemically using anti-amylin, anti-insulin, anti-glucagon, anti-somatostatin antisera. In serial sections of pancreatic islets of the man and rabbit, it was shown that amylin immunoreactivity occurred in insulin-reactive B cells predominantly located in interior of the islets. In contrast, amylin immunoreacivity appeared in glucagon-reactive A cells peripherally located in the islets of the guinea pig. These results suggest that in both the man and rabbit, amylin is synthesized by B cells for subsequent co-secretion with insulin, and that in guinea pig, amylin is synthesized by A cells for co-secretion with glucagon. It thus appears that amylin release may be mediated by different secretory mechanisms according to animal species.
Amyloid ; Animals ; B-Lymphocytes ; Glucagon ; Guinea Pigs* ; Guinea* ; Immune Sera ; Immunohistochemistry ; Insulin ; Islet Amyloid Polypeptide* ; Islets of Langerhans* ; Rats ; Somatostatin-Secreting Cells

It has been clarified that myoepithelial cells contain S-100 protein which is known to be a marker protein of neural tissue. To evaluate the participation of myoepithelial cells in the histogenesis of the salivary gland tumors, normal salivary glands and various salivary gland tumors were stained by immuno-peroxidase method. PAP kits (DAKO Co, USA) for the S-100 protein and the Cytokeratin were used and the following resulting were obtained. Acinic cells of the normal salivery gland were negative for both cytokeratin and S-100 protein. The intercalated duct cells were weakly positive for cytokeratin and S-100 protein. The normal myoepithelial cells scattered around the acini and the intercalated ducts were positive only S-100 protein. In contrast, the striated duct were positive only for cytokeratin. In plemorphic adenoma, the S-100 protein positive cells were found in solid sheets of tumor cells, in chondromyxoid areas and in areas of spindle-cell stroma as well as in the outer layer of the tubular structures. Only the inner lining of the tubules were positive for cytokeratin. In basal cell adenoma, the stromal spindle cells were strongly positive for S-100 protein and the epithelial cells weakly positive. When tubules were present within the epithelial sheets, the inner most lining cells were positive for cytokeratin. The peripheral palisaded tumor cells were negative for both substances. By immunostaining of the adenoid cystic carcinoma, S-100 protein containing cells were found focally scattered independently on the variety of histologies. The lining cells of true cystic structure were positive for cytokeratin. Immunostaining of the mucoepidermoid carcinoma demostrated that the squamous cells and the tubular epithelial cells contained cytokeraitn, whereas only a few intermediate cells were positive for S-100 protein. In Warthin's tumor there were no S-100 protein positive cells, although basally located epithelial cells of the papillae were positive for cytokeratin. These findings suggest that salivary gland tumors other than the Warthin's tumor arise from myoepithelial cells or reserve cells having dual potentiality differentating into myoepithelial and intercalcated duct cells.

Serum zinc is an essential element in men and animals. Recently on the dermatologic fields, the serum and the skin levels and the roles of zinc have been studied especially in acne vulgaris, but the results were controversial. So to confirm the previous reports and for evaluation of the relationship between the various aspects of acne vulgaris and the serum levels of zinc, the serum levels of zinc were measured by atomic absorption spectrophotometer in 13 healthy controls and 46 patients with acne vulgaris. In the healthy controls, their mean values of zinc were 0.843+0.251 ppm in total, 0.920+0.219 ppm, in females and 0.777+0.260 ppm in males. There was no statistical difference attributable to sex. In the 46 patients with acne vulgaris, their mean value of zinc was 0.741+0.195 ppm. There was no significant difference in the mean serum zinc level compared with the controls. In the males with acne, the mean va1ue of zinc was 0.727+0.166 ppm, and 0.748+0.208 ppm in females with acne. There was no significant statistical difference between males and females with acne. And females, but not males, with acne had significantly lower serum zinc levelss than controls of the corresponding sex. (p<0.1) By clinical severity, classifying the 46 patients with acne vulgaris into three groups: mild type (only comedones), moderate type (comedones with pa.pules) and severe type (includes pustules, comedones, and papules, etc.), the serum zinc levels of each group were 0.774+0.185 ppm, 0.7880. 200 ppm and 0.666+0.176 ppm. The significant statistical difference was found only in the severe type of acne compared with the healthy controls (p<0.05). Also classifying the patients into three groups (acute, moderate and chronic types of acne) by duration of acne, the serum values of zinc were 0.738+0.158 ppm, 0.692+0.283 ppm and 0.769+0.241 ppm, respectively. Only in the moderate type of acne, the mean serum level of zinc was significantly reduced compared with the control group (p<0.1)
Absorption ; Acne Vulgaris* ; Animals ; Female ; Humans ; Male ; Skin ; Zinc*

No abstract available.
Hepatocytes*

Industrial exposure to toxic agent may produce a wide variety of respiratory damage. Acetic acid is a colorless liquid with a pungent vingar-like odor. It is a rare case that acute lung injury is caused by inhalation of acetic acid. Acetic acid is miscible with water, and may directly produce damage to mucosa of respiratory tract due to its irritant quality. The outcome of the reaction is dependent on the intensity and duration of exposure and varies from death or pulmonary edema in acute phase to resolution or bronchiolitis obliterans or bronchiectasis. We experienced a rose of acute lung injury due to accidental inhalation of acetic acid. The patient was a 31-year-old male who had developed progressive chest discomfort, chilling sense, and mild dyspnea after accidental inhalation of acetic acid. He had severe hypoxemia and chest radiograph showed diane bilateral alveolar edema. He responded to conservative treatment with oxygen inhalation and was discharged with improved condition on the 7th hospital day.
Acetic Acid* ; Acute Lung Injury* ; Adult ; Anoxia ; Bronchiectasis ; Bronchiolitis Obliterans ; Dyspnea ; Edema ; Humans ; Inhalation* ; Male ; Mucous Membrane ; Odors ; Oxygen ; Pulmonary Edema ; Radiography, Thoracic ; Respiratory System ; Thorax ; Water

Congenital diverticulosis of the left ventricle is an extremely are rare maldevelopment. We report a 9 year old girl with probable isolated left ventricular diverticulum in whom the diagnosis was made by cross sectional echocardiography and by angiography.
Angiography ; Diagnosis ; Diverticulum* ; Echocardiography ; Female ; Heart Ventricles ; Humans